Internal Medicine 2 Module

UNITED REPUBLIC OF TANZANIA

Ministry of Health and Social Welfare
CMT 05211 Internal

Medicine II
NTA Level 5 Semester 2

Facilitator Guide

August 2010

Copyright © Ministry of Health and Social Welfare – Tanzania 2010
CMT 05211 Internal Medicine II NTA Level 5 Semester 2 Facilitator Guide

ii
Table of Contents

Background and Acknowledgement ........................................................................ iv
Introduction .............................................................................................................. ix
Abbreviations ........................................................................................................... xi
Module Sessions
Session 1: Status Asthmaticus, Respiratory Obstruction (Asphyxia) and
Pulmonary Oedema ....................................................................................................1
Session 2: Shock, Anaphylaxis and Poisoning ........................................................19
Session 3: Meningitis, Convulsions and Coma .......................................................33
Session 4: Urinary Tract Infections and Acute Glomerulonephritis .......................45
Session 5: Nephrotic Syndrome and Chronic Kidney Disease................................61
Session 6: Pyogenic and Viral Skin Infections, Urticaria & Drug Allergies ..........73
Session 7: Diabetes Mellitus ....................................................................................93
Session 8: HIV Care at First Level Health Facilities .............................................105
Session 9: Tuberculosis and HIV Co-Infection .....................................................119
Session 10: Diagnosis and Management of Opportunistic Infections ...................133
Session 11: Introduction to Psychiatry and Mental Health ..................................143
Session 12: Epilepsy ..............................................................................................153
Session 13: Non-Organic (Functional) Psychiatric Disorders ..............................165
Session 14: HIV and AIDS and Mental Health .....................................................181
Session 15: Drug and Alcohol Abuse ...................................................................193
Session 16: Cerebrovascular Accident/Stroke .......................................................207

iii
Background and Acknowledgement
In April 2009, a planning meeting was held at Kibaha which was followed up by a Task
Force Committee meeting in June 2009 at Dodoma and developed a proposal which guided
the process of the development of standardised Clinical Assistant (CA) and Clinical Officer
(CO) training materials which were based on CA/CO curricula. The purpose of this process
was to standardize the entire curriculum with up-to-date content which would then be
provided to all Clinical Assistant and Clinical Officer Training Centres (CATCs/COTCs).
The perceived benefit was that, by standardizing the quality of content and integrating
interactive teaching methodologies, students would be able to learn more effectively and that
the assessment of students’ learning would have more uniformity and validity across all
schools.
In September 2009, MOHSW embarked on an innovative approach of developing the

standardised training materials through the Writer’s Workshop (WW) model. The model
included a series of three-week workshops in which pre-service tutors and content experts
developed training materials, guided by facilitators with expertise in instructional design and
curriculum development. The goals of WW were to develop high-quality, standardized
teaching materials and to build the capacity of tutors to develop these materials.
The new training package for CA/CO cadres includes a Facilitator Guide, Student Manual
and Practicum. There are 40 modules with approximately 600 content sessions. This product
is a result of a lengthy collaborative process, with significant input from key stakeholders and
experts of different organizations and institutions, from within and outside the country.
The MOHSW would like to thank all those involved during the process for their valuable
contribution to the development of these materials for CA /CO cadres. We would first like to
thank the U.S. Centers for Disease Control and Prevention’s Global AIDS Program
(CDC/GAP) Tanzania, and the International Training and Education Center for Health (I-
TECH) for their financial and technical support throughout the process. At CDC/GAP, we
would like to thank Ms. Suzzane McQueen and Ms. Angela Makota for their support and
guidance. At I-TECH, we would especially like to acknowledge Ms. Alyson Shumays,
Country Program Manager, Dr. Flavian Magari, Country Director, Mr. Tumaini Charles,
Deputy Country Director, and Ms. Susan Clark, Health Systems Director. The MOHSW
would also like to thank the World Health Organization (WHO) for technical and financial
support in the development process.
Particular thanks are due to those who led this important process: Dr. Bumi L.A.
Mwamasage, the Assistant Director for Allied Health Sciences Training, Dr. Mabula Ndimila
and Mr. Dennis Busuguli, Coordinators of Allied Health Sciences Training, Ministry of
Health and Social Welfare, Dr. Stella Kasindi Mwita, Programme Officer Integrated
Management of Adults and Adolescent Illnesses (IMAI), WHO Tanzania and Stella M.
Mpanda, Pre-service Programme Manager, I-TECH.
Sincere gratitude is expressed to small group facilitators: Dr. Otilia Gowele, Principal, Kilosa
COTC, Dr. Violet Kiango, Tutor, Kibaha COTC, Ms. Stephanie Smith, Ms. Stephanie
Askins, Julie Stein, Ms. Maureen Sarewitz, Mr. Golden Masika, Ms. Kanisia Ignas, Ms.
Yovitha Mrina and Mr. Nicholous Dampu, all of I-TECH, for their tireless efforts in guiding
participants and content experts through the process. A special note of thanks also goes to

iv
Dr. Julius Charles and Dr. Moses Bateganya, I-TECH’s Clinical Advisors, and other Clinical
Advisors who provided input. We also thank individual content experts from different
departments of the MOHSW and other governmental and non-governmental organizations,
including EngenderHealth, Jhpiego and AIHA, for their technical guidance.
Special thanks goes to a team of I-TECH staff namely Ms. Lauren Dunnington, Ms.
Stephanie Askins, Ms. Stephanie Smith, Ms Aisling Underwood, Golden Masika, Yovitha
Mrina, Kanisia Ignas, Nicholous Dampu, Michael Stockman and Stella M. Mpanda for
finalising the editing, formatting and compilation of the modules.
Finally, we very much appreciate the contributions of the tutors and content experts
representing the CATCs/COTCs, various hospitals, universities, and other health training
institutions. Their participation in meetings and workshops, and their input in the
development of content for each of the modules have been invaluable. It is the commitment
of these busy clinicians and teachers that has made this product possible.
These participants are listed with our gratitude below:
Tutors
Ms. Magdalena M. Bulegeya – Tutor, Kilosa COTC
Mr. Pius J.Mashimba – Tutor, Kibaha Clinical Officers Training Centre (COTC)
Dr. Naushad Rattansi – Tutor, Kibaha COTC
Dr. Salla Salustian – Principal, Songea CATC
Dr. Kelly Msafiri – Principal, Sumbawanga CATC
Dr. Joseph Mapunda - Tutor, Songea CATC
Dr. Beda B. Hamis – Tutor, Mafinga COTC
Col Dr. Josiah Mekere – Principal, Lugalo Military Medical School
Mr. Charles Kahurananga – Tutor, Kigoma CATC
Dr. Ernest S. Kalimenze – Tutor, Sengerema COTC
Dr. Lucheri Efraim – Tutor, Kilosa COTC
Dr. Kevin Nyakimori – Tutor, Sumbawanga CATC
Mr. John Mpiluka – Tutor, Mvumi COTC
Mr. Gerald N. Mngóngó –Tutor, Kilosa COTC
Dr. Tito M. Shengena –Tutor, Mtwara COTC
Dr. Fadhili Lyimo – Tutor, Kilosa COTC
Dr. James William Nasson– Tutor, Kilosa COTC
Dr. Titus Mlingwa – Tutor, Kigoma CATC
Dr. Rex F. Mwakipiti – Principal, Musoma CATC
Dr. Wilson Kitinya - Principal, Masasi ( Clinical Assistants Training Centre (CATC)
Ms. Johari A. Said – Tutor, Masasi CATC
Dr. Godwin H. Katisa – Tutor, Tanga Assistant Medical Officers Training Centre (AMOTC)
Dr. Lautfred Bond Mtani – Principal, Sengerema COTC
Ms Pamela Henry Meena – Tutor, Kibaha COTC
Dr. Fidelis Amon Ruanda – Tutor, Mbeya AMOTC
Dr. Cosmas C. Chacha – Tutor, Mbeya AMOTC
Dr. Ignatus Mosten – Ag. Principal, Tanga AMOTC
Dr. Muhidini Mbata – Tutor, Mafinga COTC
Dr. Simon Haule – Ag. Principal, Kibaha COTC
Ms. Juliana Lufulenge - Tutor, Kilosa COTC
Dr. Peter Kiula – Tutor, Songea CATC

v
Mr. Hassan Msemo – Tutor, Kibaha COTC
Dr. Sangare Antony –Tutor, Mbeya AMOTC
Content Experts
Ms. Emily Nyakiha – Principal, Bugando Nursing School, Mwanza
Mr. Gustav Moyo - Registrar, Tanganyika Nursesand Midwives Council, Ministry of Health
and Social Welfare (MOHSW).
Dr. Kohelet H. Winani - Reproductive and Child Health Services, MOHSW
Mr. Hussein M. Lugendo – Principal, Vector Control Training Centre (VCTC), Muheza
Dr. Elias Massau Kwesi - Public Health Specialist, Head of Unit Health Systems Research
and Survey, MOHSW
Dr. William John Muller - Pathologist, Muhimbili National Hospital (MNH)
Mr. Desire Gaspered - Computer Analyst, Institute of Finance Management (IFM), Dar es
Salaam
Mrs. Husna Rajabu - Health Education Officer, MOHSW
Mr. Zakayo Simon - Registered Nurse and Tutor, Public Health Nursing School (PHNS)
Morogoro
Dr. Ewaldo Vitus Komba - Lecturer, Department of Internal Medicine, Muhimbili University
of Health and Allied Sciences School (MUHAS)
Mrs. Asteria L.M. Ndomba - Assistant Lecturer, School of Nursing, MUHAS
Mrs. Zebina Msumi - Training Officer, Extended programme on Immunization (EPI),
MOHSW
Mr. Lister E. Matonya - Health Officer, School of Environmental Health Sciences (SEHS),
Ngudu, Mwanza.
Dr. Joyceline Kaganda - Nutritionist, Tanzania Food and Nutrition Centre (TFNC),
MOHSW.
Dr. Suleiman C. Mtani - Obstetrician and Gynecologist, Director, Mwananyamala Hospital,
Dar es salaam
Mr. Brown D. Karanja - Pharmacist, Lugalo Military Hospital
Mr. Muhsin Idd Nyanyam - Tutor, Primary Health Care Institute (PHCI), Iringa
Dr. Judith Mwende - Ophthalmologist, MNH
Dr. Paul Marealle - Orthopaedic and Traumatic Surgeon, Muhimbili Orthopedic Institute
(MOI),
Dr. Erasmus Mndeme - Psychiatrist, Mirembe Refferal Hospital
Mrs. Bridget Shirima - Nurse Tutor (Midwifery), Kilimanjoro Chrician Medical Centre
(KCMC)
Dr. Angelo Nyamtema - Tutor Tanzania Training Centre for International Health (TTCIH),
Ifakara.
Ms. Vumilia B. E. Mmari - Nurse Tutor (Reproductive Health) MNH-School of Nursing
Dr. David Kihwele - Obs/Gynae Specialist, and Consultant
Dr. Amos Mwakigonja – Pathologist and Lecturer, Department of Morbid Anatomy and
Histopathology, MUHAS
Mr. Claud J. Kumalija - Statistician and Head, Health Management Information System
(HMIS), MOHSW
Ms. Eva Muro, Lecturer and Pharmacist, Head Pharmacy Department, KCMC
Dr. Ibrahim Maduhu - Paediatrician, EPI/MOHSW
Dr. Merida Makia - Lecturer Head, Department of Surgery, MNH
Dr. Gabriel S. Mhidze - ENT Surgeon, Lugalo Military Hospital
Dr. Sira Owibingire - Lecturer, Dental School, MUHAS
Mr. Issai Seng’enge - Lecturer (Health Promotion), University of Dar es Salaam (UDSM)

vi
Prof. Charles Kihamia - Professor, Parasitology and Entomology, MUHAS
Mr. Benard Konga - Economist, MOSHW
Dr. Martha Kisanga - Field Officer Manager, Engender Health, Dar es Salaam
Dr. Omary Salehe - Consultant Physician, Mbeya Referral Hospital
Ms Yasinta Kisisiwe - Principal Nursing Officer, Health Education Unit (HEU), MOHSW
Dr. Levina Msuya - Paediatrician and Principal, Assistant Medical Officers Training Centre
(AMOTC), Kilimanjaro Christian Medical Centre (KCMC)
Dr. Mohamed Ali - Epidemiologist, MOHSW
Mr. Fikiri Mazige - Tutor, PHCI-Iringa
Mr. Salum Ramadhani - Lecturer, Institute of Finance Management
Ms. Grace Chuwa - Regional RCH Coordinator, Coastal Region
Mr. Shija Ganai - Health Education Officer, Regional Hospital, Kigoma
Dr. Emmanuel Suluba - Assistant Lecturer, Anatomy and Histology Department, MUHAS
Mr. Mdoe Ibrahim - Tutor, KCMC Health Records Technician Training Centre
Mr. Sunny Kiluvia - Health Communication Consultant, Dar es Salaam
Dr. Nkundwe Gallen Mwakyusa - Ophthalmologist, MOHSW
Dr. Nicodemus Ezekiel Mgalula -Dentist, Principal Dental Training School, Tanga
Mrs. Violet Peter Msolwa - Registered Nurse Midwife, Programme Officer, National AIDS
Control Programme (NACP), MOHSW
Dr. Wilbert Bunini Manyilizu - Lecturer, Mzumbe University, Morogoro
Editorial Review Team

Dr. Kasanga G. Mkambu - Obstertric and Gynaecology specialist, Tanga Assistant Medical
Officers Training Centre (AMOTC)
Dr. Ronald Erasto Msangi - Principal, Bumbuli COTC
Mr. Sita M. Lusana - Tutor, Tanga Environmental Health Science Training Centre
Mr. Ignas Mwamsigala - Tutor (Entrepreneurship) RVTC Tanga
Mr. January Karungula - RN, Quality Improvement Advisor, Muhimbili National Hospital
Prof. Pauline Mella - Registered Nurse and Profesor, Hubert Kairuki Memorial University
Dr. Emmanuel A. Mnkeni – Medical Officer and Tutor, Kilosa COTC
Dr. Ronald E. Msangi - Principal, Bumbuli COTC
Mr. Dickson Mtalitinya - Pharmacist, Deputy Principal, St Luke Foundation, Kilimanjaro
School of Pharmacy
Dr. Janeth C. Njau - Paediatrician/Tutor, Kibaha COTC
Mr. Fidelis Mgohamwende - Labaratory Technologist, Programme Officer National Malaria
Control Programme (NMCP), MOHSW
Mr. Gasper P. Ngeleja - Computer Instructor, RVTC Tanga
Dr. Shubis M Kafuruki - Research Scientist, Ifakara Health Institute, Bagamoyo
Dr. Andrew Isack Lwali - Director, Tumbi Hospital
Librarians and Secretaries

Mr. Christom Aron Mwambungu - Librarian MUHAS
Ms. Juliana Rutta - Librarian MOHSW
Mr. Hussein Haruna - Librarian, MOHSW
Ms. Perpetua Yusufu - Secretary, MOHSW
Mrs. Martina G. Mturano -Secretary, MUHAS
Mrs. Mary F. Kawau - Secretary, MOHSW

vii
IT support
Mr. Isaac Urio - IT Consultant, I-TECH
Mr. Michael Fumbuka - Computer Systems Administrator – Institute of Finance and
Management (IFM), Dar es Salaam
Dr. Gilbert Mliga

Director of Human Resources Development, Ministry of Health and Social Welfare

viii
Introduction
Module Overview
This module content has been prepared as a guide for tutors of Clinical Assistant (CA) and
Clinical Officer (CO) schools for training of students. The session contents are based on the
sub-enabling outcomes of the curriculum of CA and CO. The module sub-enabling outcomes
are as follows:
3.1.2 Manage People Living with HIV (PLHIV) effectively using national protocols
3.1.3 Manage medical emergencies and give first line treatment before referral.
3.1.4. Manage complicated medical conditions of Genito – Urinary, Bones, Joints, Muscles
and Skin, Nervous and Endocrine system
3.1.5. Diagnose and manage common mental disorders and refer complicated cases
3.1.6. Manage patients with drug/substance abuse
Who is the Module For?

This module is intended for use primarily by tutors of CA and CO schools. The module’s
sessions give guidance on the time and activities of the session and provide information on
how to teach the session to students. The sessions include different activities which focus on
increasing students’ knowledge, skills and attitudes.
How is the Module Organized?

The module is divided into16 sessions; each session is divided into several sections. The
following are the sections of each session:
• Session Title: The name of the session.
• Total Session Time: The estimated time for teaching the session, indicated in minutes.
• Pre-requisites: A module or session which needs to be covered before teaching the
session.
• Learning Objectives – Statements which indicate what the student is expected to learn at
the end of the session.
• Resources Needed – All of resources needed for the session are listed including handouts
and worksheets.
• Session Overview – The session overview box lists the steps, time for each step, the
activity or method used in each step and the step heading.
• Session Content – All the session contents are divided into steps. Each step has a heading
and an estimated time to teach that step. Also, this section includes instructions for the
tutor and activities with their instructions to be done during teaching of the contents.
• Key Points – Each session has a step which concludes the session contents near the end
of a session. This step summarizes the main points and ideas from the session.
• Evaluation – The last section of the session consists of short questions based on the
learning objectives to check the understanding of students.
• Handouts – Additional information which can be used in the classroom while teaching or
later for students’ further learning. Handouts are used to provide extra information related
to the session topic that cannot fit into the session time. Handouts can be used by the
participants to study material on their own and to reference after the session. Sometimes,
a handout will have questions or an exercise for the participants. The answers to the
questions are in the Facilitator Guide Handout, and not in the Student Manual Handout.

ix
How Should the Module be Used?
Tutors are expected to use the module as a guide to train students in the classroom and
clinical settings. The contents of the modules are the basis for teaching and learning Internal
Medicine II. The tutors are therefore advised to read each session and the relevant handouts
and worksheets as preparation before facilitating the session. Also, tutors need to prepare all
the resources, as indicated in the resource section or any other item, for an effective teaching
and learning process.
What Should the Facilitators Do?

• Plan a schedule (timetable) of the training activities.
• Use the session contents as a guide. Facilitators are expected to be innovative to make the
teaching and learning process effective.
• Read the sessions before facilitation; make sure you understand the contents in order to
clarify points during facilitation.
• Time allocated is estimated, but you are advised to follow the time as much as possible,
and adjust as needed.
• Use session activities and exercises suggested in the sessions as a guide.
• Always involve participants in their own learning. When participants are involved, they
learn more effectively.
• Facilitators are encouraged to use real life examples to make learning more realistic.
• Make use of appropriate reference materials and teaching resources available locally.
What You Need to Do Before Teaching with Handouts and Worksheets

• Go through the session and identify handouts and worksheets needed for the session.
• Reproduce pages of these handouts and worksheets for student use while teaching the
session. This will enable students to refer to handouts and worksheets during the session
in the class. You can reproduce enough copies for students or for sharing.
• Give clear instructions to students on the student activity in order for the students to
follow the instructions of the activity.
• Refer students to the specific page in the student manual as instructed in the facilitator
guide.
How to Use the Students Manual

The student manual is a document which has the same content as the facilitator guide, which
excludes facilitator instructions and answers for exercises. The student manual is for assisting
students to learn effectively and acts as a reference document during and after teaching the
session. Some of the activities included in facilitator guide are in the student manual without
facilitator instructions.

x
Abbrreviation
ns
ABC Air way, Breeathing and Circulation
A n
ABG A
Arterial Bloood Gases
ACE A
Angiotensin Convertingg Enzyme
ADC A
AIDS Demenntia Compleex
ADHD A
Attention Deeficit Hyperactivity Dissorders
AFB A Fast Baacilli
Acid
AGN A
Acute Glomeerulonephrittis
AIDS A
Aquired Immmune Defficciency Synd drome
ALT A
Alamine Ammoinotransfeerase
ARDS A
Acute Respirratory Distress Syndrom me
ART A Retrovirral Therapyy
Anti
ARV A Retro Viral
Anti V
ASOT A
Antistreptolyysin O Titree
Bd (bidd) Two times a day
BMI B
Body Mass Index
BUN B
Blood Urea and
a Nitrogeen
CA C
Cronological l Age
Ca+ C
Calcium
CBC C
Complete Blood Count
CCF C
Congestive C
Cardiac Faillure
CD4 C
Cluster Diffeerentiated Cells
C
CMV C
Cytomegalo Virus
CNS C
Central Nervvous System m
COX C
Cyclooxygen nase
CPE C
Cardiogenic Pulmonary Edema
CSF C
Cerebral Spinnal Fluid
CT C
Computerize ed Tomograaphy
CTC C and Treeatment Cenntre
Care
CVA C
Carebral Vasscular Acciddent
CX-R C
Chest X- rayy
DIC D
Disseminated d Intravascuular Coagulopathy
DKA D
Diabetic Keto Acidosis
DL D
Deciliter
DM D
Diabetes Mellitus
DNA D
Deoxyribose Neucleic Acid
A
DOT D
Direct Obserrved Treatm ment
ECG Electrocardioograph
EEG Electroencepphalocardioggraph
EFV Efaverenz
EGF – R Eppidermal Growth
G Factoor Receptorr
eGFR esstimated Glomerular Fiiltration Ratte
EPTB Extra Pulmonnary Tubercculosis
ESR Erythrocyte Sedimentati
S ion Rate
ESRD End Stage Reenal Disease
ETT Endotracheall Tube
CMT 052211 Internal Medicine

M II NTA Level 5 Semester 2 Facilitattor Guide
xi
FBG Full Blood Count
FEV1 Forced Expiration Volume in one second
FPG Fasting Plasma Glucose
FSGS Focal Segmental Glomerulo Sclerosis
G/dl Gram per deciliter
GCS Glasgow Coma Scale
GDM Gestational Diabetes Mellitus
GFR Glomerular Filtration Rate
GGT Gamma Glutamyl Transferase
GHb Glycosylated Haemoglobin
GIT Gastro Intestinal Tract
GN Glomerulonephritis
GUD Genital Urinary Disease
Hb Haemoglobin
HCWs Health Care Workers
HIV Human Immunodeficiency Virus
HPV Human Papiloma Virus
HSV Herpes Simplex Virus
ID Identity
IDDM Insulin Dependent Diabetes Mellitus
IFG Impaired Fasting Glucose
IgA Immunoglobulin A
IgE Immunoglobulin E
IGT Impaired Glucose Tolerance Test
IM Intramuscular
IMAI Integrated Management of Adult and Adolescent Illnesses
INH Isoniazid (Isonicotinic acid hydrazide)
IOP Intraoccular Pressure
IPT Isoniazid Preventive Teatment
IQ Intelligent Quotient
ISTC International Standards for Tuberculosis Care
IU International Units
IV Intravenous
K+ Potasium
KOH Potassium Hydroxide
LF Left Ventricle
LP Lumbar Puncture
LVF Left Ventricular Hypertrophy
MA Mental Age
Mcg Micrograms
MCV Mean Corpuscular Volume
MDI Metered Dose Inhalers
MDR Multiple Drug Resistance
Mg/h Milligram per hour
Mg/kg/h Milligram per Kilogram per hour
Mm Hg Millimeter of Mercury
Mmol/l Millimol per liter
MOHSW Ministry of Health and Social Welfare
MRI Magnetic Resonance Image
MRSA Methicillin Ressistant Staphylococcus aureus

xii
Na+ Sodium
Nacl Sodium Chloride
NCPE Noon Cardiogenic Pulmonary Oedema
NIDDM Non Insulin Dependent Diabetes mellitus
NKHS Non Ketotic Hyperosmolar State
NS Normal Saline
NSAID Non Steroidal Ant inflammatory Drugs
NTA National Technical Award
NTLP National Tuberculosis and Leprosy Programme
NVP Niverapine
O2 Oxygen
Od Once per day
OI Opportunistic Infection
OPD Out Patient Department
PaO2 Partial Pressure of Oxygen
PITC Provider Initiated Testing and Counseling
PJP Pneumocytis jirovecii Pneumonia
PLHIV People Living with HIV
PMTCT Prevention of Mother To Child Transmission
PO Per Orally
PSGN Post Streptococcal Glomerulo Nephritis
PTB Pulmonary Tuberculosis
Qid Four times a day
RBC Red Blood Cells
RV Right Ventricle
SaO2 Oxygen Saturation
SARS Severe Acute Respiratory Syndrome
SSRIs Serotonin selective reuptake inhibitors
STI Sexually Transmitted Disease
TB Tuberculosis
TIA Transient Ischaemic Attack
Tid Three times a day
TMP/SMZ Trimethoprim/Sulfamethoxazole
TV Television
URTI Upper Respiratory Tract Infection
UTI Urinary Tract Infection
VDRL Venereal Disease Research Laboratory
VZV Varricela Zoster Virus
WBC White Blood Cells
WHO World Health Organization
ZN Ziehl Neelsen

xiii
xiv
Session 1: Status Asthmaticus, Respiratory Obstruction
(Asphyxia) and Pulmonary Oedema
Total Session Time: 120 minutes
Prerequisites
• None
Learning Objectives
By the end of this session, students will be able to:
• Describe status asthmaticus, respiratory obstruction and pulmonary oedema
• Explain causes of status asthmaticus, respiratory obstruction and pulmonary oedema
• Describe clinical features of status asthmaticus, respiratory obstruction and pulmonary
oedema
• Discuss management of status asthmaticus, respiratory obstruction and pulmonary
oedema
• Outline complications of status asthmaticus, respiratory obstruction and pulmonary
oedema
Resources Needed
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Handout 1.1: Drugs for Treatment of Status Asthmaticus
• Handout 1.2: Heimlich Maneuver for Infants, Adults and Children
• Handout 1.3: Complications of Respiratory Obstruction
SESSION OVERVIEW
Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction , Learning Objectives
Causes and Clinical Features of Status
2 20 minutes Presentation
Asthmaticus
Differential Diagnoses, Investigations,
Presentation,
3 20 minutes Treatment and Complications of Status
Brainstorm
Asthmaticus
Epidemiology, Causes, Pathophysiology and
Clinical Features of Respiratory Obstruction
Differential Diagnosis, Investigations and
Treatment of Respiratory Obstruction
Classification and Clinical Features of
Pulmonary Oedema
Treatment of Pulmonary Oedema
8 05 minutes Presentation Key Points
9 05 minutes Presentation Evaluation

Session 1: Status Asthmaticus, Respiratory Obstruction (Asphyxia) and Pulmonary Oedema 1
SESSION CONTENT
Step 1: Presentation of Session Title and Learning Objectives (5 minutes)

READ or ASK the students to read the learning objectives, and clarify.
ASK students if they have any questions before continuing.
Step 2: Causes and Clinical Features of Status Asthmaticus (20 minutes)
Introduction
• Status asthmaticus is a medical emergency in which asthma symptoms are refractory to
initial bronchodilator therapy.
• Patients report
o Chest tightness
o Rapidly progressive shortness of breath
o Dry cough
o Wheezing
• Typically patients present a few days after
o The onset of a viral respiratory illness
o Following exposure to a potent allergen or irritant or
o Exercise in a cold environment
• Frequently patients have underused or have been under prescribed anti-inflammatory
therapy.
Causes of Status Asthmaticus

• In persons with acute asthma, bronchospasms occur as a result of one or more inciting
factors that may include
o A viral upper or lower respiratory tract infection
o Significant allergic response to an allergen such as
Pollen
Mold
Animal dang
House dust mites
o Exposure to an irritant or
o Vigorous exercise in a cold environment
o Infection
o Poor adherence to the medical regimen
o Rapid decrease in long-term oral steroid therapy
• Inflammation can be the result of
o Infection
o Lymphocyte, mast cell, eosinophilic, and neutrophilic responses
o Airway epithelial damage
Clinical Features of Status Asthmaticus

• History
o Patients with status asthmaticus have severe dyspnea that has developed over hours to
days
o Patients usually present with audible wheezing

Physical Findings
• Patients are usually upon examination and, in early stages of status asthmaticus, may have
significant wheezing.
• Initially wheezing is heard only during expiration but later wheezing occurs during both
expiration and inspiration.
• The chest is hyper expanded and accessory muscles particularly the sternocleidomastoid,
scalene, and intercostal muscles are used.
• Later as bronchoconstriction worsens patients' wheezing may disappear which may
indicate severe airflow obstruction.
• Normally the pulsus paradoxus (i.e. the difference in systolic blood pressure between
inspiration and expiration) does not exceed 15 mm Hg.
• In patients with severe asthma a pulsus paradoxus of greater than 25 mm Hg usually
indicates severe airway obstruction.
• Status asthmaticus is a medical emergency, if not managed initially can lead to the need
for intubation and ventilation.
Step 3: Differential Diagnoses, Investigations, Treatment and

Complications of Status Asthmaticus (20 minutes)
Activity: Brainstorm (5 minutes)
ASK students to mention differential diagnoses of status asthmaticus.
INVITE few students to give their responses.
RECORD the responses on the board/ flip chart.
SUMMARIZE the discussion by using the content below.
Differential Diagnoses
• Pulmonary hypertension
• Congestive heart failure
• Upper airway obstruction
• Pneumonia (bacterial or viral)
• Chronic Obstructive Pulmonary Disease (COPD) exacerbation
• Pneumothorax
Investigations
• Note: Investigations are available in equipped hospitals and therefore patients may be
referred after receiving pre-referral management. In hospitals, the investigations that can
be done are outlined below
• Pulse oximetry values should be used to monitor the progression of asthma
• Obtain a complete blood count (CBC) and differential count
• Obtain an arterial blood gas
• Obtain a chest radiograph to evaluate for
o Pneumonia
o Pneumothorax
o Congestive heart failure

o Signs of chronic obstructive pulmonary disease
• These conditions may complicate patient's response to treatment
Treatment of Status Asthmaticus

• Patients with status asthmaticus need close monitoring as well as oxygen therapy and
therefore referring them to hospitals with equipments is important.
• After confirming the diagnosis and assessing the severity of the asthma attack, direct
treatment is toward controlling bronchoconstriction and further inflammation.
• Bronchodilator Treatment with Beta-2 Agonists
o The first line of therapy is bronchodilator treatment with a beta-2 agonist is albuterol
(Salbutamol).
o Handheld nebulizer treatments may be administered either continuously (10-15 mg/h)
or by frequent timing (e.g. q5-20min), depending on the severity of the
bronchospasm.
• Oxygen therapy
• Glucocorticosteroids
o Steroids are the most important treatment for status asthmaticus
• Fluid replacement
o Intravenous fluids are administered to restore blood volume, however should make
sure the patients are not in congestive heart failure
• Antibiotics
o The routine administration of antibiotics is discouraged
o Patients are administered antibiotics only when they show evidence of infection such
as pneumonia, sinusitis
• Aminophylline (theophylline)
o Starting intravenous aminophylline may be reasonable in patients who do not respond
to medical treatment with bronchodilators, oxygen, corticosteroids, and intravenous
fluids within 24 hours
o The loading dose is usually 5-6 mg/kg followed by a continuous infusion of 0.5-0.9
mg/kg/h
o Aminophylline has some significant side effects and need to monitor for therapeutic
range
Complications
• Pneumothorax may complicate acute asthma either because of increased airway pressure
or as a result of mechanical ventilation.
• Superimposed infection can also occur in intubated patients.
• Patients may require a chest tube for pneumothorax or aggressive antibiotic therapy for a
superimposed infection.
Refer students to Handout 1.1: Drugs for Treatment of Status Asthmaticus
Step 4: Epidemiology, Causes, Pathophysiology and Clinical Features of

Respiratory Obstruction (20 minutes)
Background
• Foreign body aspiration can be a life-threatening emergency
• An aspirated solid or semisolid object may lodge in the larynx or trachea

• If the object is large enough to cause nearly complete obstruction of the airway asphyxia
may rapidly cause death.
• Lesser degrees of obstruction or passage of the obstructive object beyond the carina can
result in less severe signs and symptoms.
• Chronic debilitating symptoms with recurrent infections might occur with delayed
extraction or the patient may remain asymptomatic.
• The actual aspiration event can usually be identified although it is often not immediately
appreciated.
• The aspirated object might even escape detection.
• Most often the aspirated object is food but a broad spectrum of aspirated items has been
documented over the years.
• Commonly retrieved objects include
o Seeds
o Nuts
o Bone fragments
o Nails
o Small toys
o Coins, pins
o Medical instrument fragments and
o Dental appliances
• Geographic differences in the spectrum of objects commonly found in a particular
environment and variations in dietary and eating habits affect the relative frequency with
which various objects are aspirated
Pathophysiology
• Near-total obstruction of the larynx or trachea can cause immediate asphyxia and death.
• Should the object pass beyond the carina, its location would depend on the patient's age
and physical position at the time of the aspiration.
• Because the angles made by the main stem bronchi with the trachea are identical until age
of 15 years, foreign bodies are found on either side with equal frequency in persons in
this age group.
• With normal growth and development, the adult right and left main stem bronchi diverge
from the trachea with very different angles, with the right main stem bronchus being more
acute and therefore making a relatively straight path from larynx to bronchus.
• Objects that descend beyond the trachea are more often found in the right endobronchial
tree than in the left.
• Cough, wheeze, stridor, dyspnea, cyanosis, and even asphyxia might ensue.
• Organic foreign bodies such as oily nuts (commonly peanuts) induce inflammation and
Oedema.
• Local inflammation, Oedema, cellular infiltration, ulceration, and granulation tissue
formation may contribute to airway obstruction while making bronchoscopic
identification and removal of the object more difficult.
• The airway becomes more likely to bleed with manipulation and the object becomes
more likely obscured and more difficult to dislodge.
• Mediastinitis or tracheoesophageal fistulas may result.
• Distal to the obstruction air trapping may occurs leading to local
o Emphysema
o Atelectasis
o Hypoxic vasoconstriction

o Post obstructive pneumonia and the
o Possibility of volume loss
o Necrotizing pneumonia or abscess
o Suppurative pneumonia, or bronchiectasis
• Bronchoscopically, the object may appear as a tumor.
• Even if the object is removed, the inflammatory changes may not be completely
reversible.
• Some investigators believe scar carcinoma may develop over time.
• The likelihood of complications increases after 24-48 hours making expeditious removal
of the foreign body imperative.
• Speaking while eating increases the likelihood of food aspiration.
• Impaired consciousness also increases the likelihood of aspiration while eating.
Causes
• Children are at risk for putting small toys, candies, or nuts into their mouths.
• Children aged 1-3 years chew incompletely with incisors before their molars erupt, and
objects or fragments may be propelled posteriorly, triggering a reflex inhalation
• Among adults, the following conditions, actions, and procedures facilitate foreign body
aspiration
o Impaired swallowing reflex
o Impaired cough reflex
o Mental retardation
o Alcohol or sedative use
o General anesthesia
o Poor dentition
o Dental, pharyngeal, or airway procedures
o Altered sensorium
o Loss of consciousness
o Convulsions
o Maxillofacial trauma
• Frequently aspirated objects include food such as nuts and seeds, teeth, dental appliances
and medical instruments.
• The original event might have been forgotten.
• Choking with severe dyspnea leading to respiratory or cardiac arrest while eating might
be initially misdiagnosed as myocardial ischemia.
Epidemiology
• The often-fatal syndrome of acute asphyxia from upper airway obstruction associated
with eating (acute asphyxia), and aspiration of gastric contents are usually not considered
with other foreign body aspiration syndromes.
• For these reasons, the true incidence and prevalence of foreign body aspiration is
unknown.
• The overall risk of death from acute asphyxia is estimated to be 0.66 deaths per 100,000
people.
• Morbidity increases if extraction of the object is delayed beyond 24 hours.
• The male-to-female ratio is 2:1.
• Children especially those aged 1-3 years are at risk for foreign body aspiration because of
their tendency to put everything in their mouths and because of the way they chew.
• Young children chew their food incompletely with incisors before their molars erupt.

• Objects or fragments may be propelled posteriorly triggering a reflex inhalation.
• Adults are at increased risk of aspirating foreign bodies enduring oropharyngeal
procedures as they are sedated.
Clinical Features
• History
o In the acute asphyxia a large object (often poorly chewed meat) lodges in the larynx
or trachea causing nearly complete airway obstruction.
o Respiratory distress, aphonia, cyanosis, loss of consciousness, and death occur in
quick succession unless the object is dislodged.
o When the degree of obstruction is less severe or when the aspirated object descends
beyond the carina, the presentation is less dramatic.
o Sudden onset of the classic triad of coughing, wheezing and decreased breathing
sounds is frequently not observed.
o Presenting symptoms other than cough include
Fever (although this might be uncommon in early stage)
Hemoptysis
Dyspnea and
Chest pain
• A history of a choking episode is not always obtained or may have initially been ignored
or misdiagnosed
• Most patients or parents can identify a specific episode of choking, however presentation
is often delayed by more than a week.
• The latency period prior to the onset of symptoms may last months or years if the foreign
body is inert bone or inorganic material.
• Patients may have been empirically treated for other conditions even when a choking
episode was witnessed.
• Patients with chronic symptoms may have been erroneously diagnosed as having asthma
or chronic bronchitis.
• Young children and patients with neurologic or psychiatric disorders are at increased risk
for aspiration but might not be able to describe symptoms or to report choking episodes
• Other risk factors include
o Institutionalization
o Old age
o Abnormal dentition
o Alcohol or sedative use
• A presentation of cyanosis, cough, wheeze, incompletely resolved pneumonia, or
localized bronchiectasis should raise suspicion of foreign body aspiration, particularly in
individuals at risk for foreign body aspiration.
• Seek information about a history of
o Impaired swallowing
o Impaired coughing
o Traumatic loss of consciousness
o Intoxication or
o Oropharyngeal surgery
Physical Findings
• A small number of foreign body aspirations are incidentally found after chest radiography
or bronchoscopic inspection.

• Patients may be asymptomatic or may be undergoing testing for other diagnoses
• Physical findings may include
o Stridor
o Wheeze,
o Diminished breath sounds
• If obstruction is severe cyanosis may occur
• Signs of consolidation can accompany post obstructive pneumonia
Step 5: Differential Diagnosis, Investigations and Treatment of Respiratory

Obstruction (15 minutes)
Differential Diagnoses of Respiratory Obstruction
• Pneumonia
• Pneumothorax
• Lung Abscess
• Pulmonary Embolism
• Respiratory Failure
• Chronic Obstructive Pulmonary Disease (COPD)
• Emphysema
• Atelectasis
• Myocardial infarction
Investigations
• Investigations for respiratory obstruction cannot be done at primary health care facilities
and therefore patients suspected of having the condition must be referred to hospitals.
The investigations are listed here below.
o Chest radiography
o CT scanning of the chest
o Bronchoscope (both rigid and flexible) can be both diagnostic and therapeutic
o Fluoroscopy
o Radioisotope lung perfusion scanning
Treatment
Medical Care
• Acute choking, with respiratory failure associated with tracheal or laryngeal foreign body
obstruction, may be successfully treated at the scene with the heimlich maneuver back
blows and abdominal thrusts.

Heimlich Maneuver
• It is an emergency treatment for obstruction of the airway in adults.
• It may be needed when someone chokes on a piece of food that has ‘gone down the
wrong way’.
• To perform the Heimlich maneuver.
o Stand behind the victim.
o Wrap your arms around their waist.
o Make a fist with one hand and hold the fist with the thumb side just below the breast
bone.
o Place your other hand over this first and use it to pull sharply into the top of the
choking person's abdomen and forcefully press up into the victim's diaphragm to
expel the obstruction (most commonly food).
o Repeat as necessary.
o Children and infants need a different approach for the Heimlich maneuver
• Even in non emergency situations expeditious removal of tracheobronchial foreign bodies
is recommended.
Refer students to Handout 1.2: Heimlich Maneuver for Infants, Adult and
Children
• Refer the patient after performing this emergency procedure for farther evaluation e.g.
o Bronchoscopy
o Surgical care
Prevention
• In order to prevent food aspiration the diet should be appropriate for the patient's ability
to chew and swallow.
• The size and shape of food bits should be appropriate for the patient's age and the size of
the larynx and tracheobronchial tree.
• Pay attention to the size and texture of foods and objects available to children and adults
with impaired mentation or ability to protect the airway such as impaired chewing,
swallowing or coughing.
• Removal of appliances prior to manipulation of the teeth or airway is essential.
• Note the condition of medical equipment at the beginning and end of procedures
involving the pharynx, larynx, respiratory tract, or digestive tract.
• Sedatives and topical anesthetics increase the risk for aspiration therefore use them
cautiously.
• Children should not be given toys or food substances that they can choke on.
Complications
• The severity of the complications of foreign body aspiration depends on the
o Size
o Shape
o Composition
o Location and
o Orientation of the aspirated object
• The following complications may ensue
o Cough

o Dyspnea
o Wheeze
o Stridor
o Hemoptysis
o Asphyxia
o Laryngeal oedema
o Pneumothorax
o Pneumomediastinum
o Tracheobronchial rupture
o Cardiac arrest
Refer students to Handout 1.3: Complications of Respiratory Obstruction
Step 6: Classification and Clinical Features of Pulmonary Oedema

(20 minutes)
Introduction
• Pulmonary oedema refers to extravasation of fluid from the pulmonary vasculature into
the interstitium and alveoli of the lung.
• The formation of pulmonary oedema may be caused by 4 major pathophysiologic
mechanisms.
o Imbalance of starling forces which are
Increased pulmonary capillary pressure
Decreased plasma oncotic pressure
Increased negative interstitial pressure
o Damage to the alveolar-capillary barrier
o Lymphatic obstruction
o Idiopathic or unknown mechanism
Classification of Pulmonary Oedema

• Cardiogenic pulmonary oedema (CPE): This is defined as pulmonary oedema due to
increased capillary hydrostatic pressure secondary to elevated pulmonary venous
pressure.
• Non-Cardiogenic pulmonary oedema: This include several clinical conditions that are
associated with pulmonary oedema based on an imbalance of starling forces other than
through primary elevations of pulmonary capillary pressure.
Clinical Features of Pulmonary Oedema
Symptoms
• Breathlessness
• Anxiety
• Profuse diaphoresis
• Patients with symptoms of gradual onset CPE (e.g. over 24 h) often report dyspnea on
exertion, orthopnea (respiratory discomfort when supine), and paroxysmal nocturnal
dyspnea (patient awakens gasping for air and must sit up).
• Cough is a frequent complaint that may provide an early clue to worsening pulmonary
oedema in patients with chronic left ventricle (LV) dysfunction.

• Pink frothy sputum may be present in patients with severe disease.
• Chest pain should alert the physician to the possibility of acute myocardial ischemia,
infarction, or aortic dissection with acute aortic regurgitation as the precipitant of
pulmonary oedema.
Physical Findings
• Tachypnea and tachycardia
• Patients may be sitting upright, they may demonstrate air hunger, and they may become
agitated.
• Patients usually appear anxious and diaphoretic
• Hypertension is often present because of the hyper adrenergic state.
• Hypotension indicates severe LV systolic dysfunction and the possibility of cardiogenic
shock.
• Auscultation of the lungs usually reveals fine crepitations, but rhonchi or wheezes may
also be present.
• Rales (crepitations) are usually heard at the bases first; as the condition worsens, they
progress to the apices.
• Auscultation of murmurs can help in the diagnosis of acute valvular disorders manifesting
with pulmonary oedema.
• Another notable physical finding is skin pallor or mottling resulting from peripheral
vasoconstriction and shunting of blood to the central circulation in patients with poor LV
function and substantially increased sympathetic tone.
• Patients with concurrent right ventricular (RV) failure may present with hepatomegaly,
positive hepatojugular reflux (seen in the neck region) and peripheral oedema.
• Severe cardio pulmonary oedema may be associated with a change in mental status which
may be the result of hypoxia or hypercapnia (a condition where there is too much carbon
dioxide in the blood).
Step 7: Differential Diagnosis, Investigations and Treatment of Pulmonary

Oedema (10 minutes)
Differential Diagnosis
• Pneumonia
• Pneumothorax
• Pulmonary Embolism
• Diffuse pulmonary infections
• Aspiration
• Shock
• Acute Respiratory Distress Syndrome (ARDS)
• Asthma
• Cardiogenic Shock
• Emphysema
• Myocardial Infarction
• Diffuse pulmonary infections
• Aspiration

• Shock
• Acute Respiratory Distress Syndrome (ARDS)
• Asthma
• Cardiogenic Shock
• Emphysema
• Myocardial Infarction
Investigations
• Laboratory Studies
o Blood count
o Serum electrolyte measurements
o BUN and creatinine determination
o Cardiac enzymes if available
o Electrocardiogram would be very helpful
• Imaging Studies
o Chest radiography
o Echocardiography
Note: Most of these investigations are done at hospital levels and therefore patients
suspected of having pulmonary oedema must be referred for proper investigations.
Treatment of Pulmonary Oedema

• Pulmonary oedema is life-threatening and must be considered a medical emergency
• In the treatment of pulmonary oedema attention must be directed to identifying and
removing any precipitating causes
• Because of the acute nature of the problem, a number of additional nonspecific measures
are necessary before referring the patient to the hospital, these includes
o Oxygen therapy (whenever possible)
o Diuretics e.g. furosemide (lasix)
o Keep patient in semi sitting position
Step 8: Key Points (5 minutes)
• Beta-agonists and steroids and theophylline are mainstays in the treatment of status
asthmaticus.
• Foreign body aspiration can be a life-threatening emergency.
• Pulmonary oedema refers to extravasation of fluid from the pulmonary vasculature into
the interstitium and alveoli of the lung.
• Cough is a frequent complaint that may provide an early clue to worsening pulmonary
oedema in patients with chronic LV dysfunction.
• Pulmonary oedema is life-threatening and must be considered a medical emergency.
Step 9: Evaluation (5 minutes)

• Describe the causes of respiratory obstruction
• List eight complications of respiratory obstruction
• List the clinical features of pulmonary oedema
ASK students if they have any comments or need clarification on any points.

References
• Braunwald, E. & Fauci, A.S. (2001). Harrison’s Principles of Internal Medicine.
McGraw Hill.
• Cumming, A.D. (2003). Davidson’s Principles and Practice of Medicine. Edingurgh,
Oxford: Elsevier Saunders.
• Kumar, P. & Clark, M. (2007). Clinical Medicine (6th ed.). Edingurgh, Oxford: Elsevier
Saunders.
• Johor Bahru's Doctors Don't Know Heimlich. (2009). Retrieved July 15th 2010 from
http://www.preparednessresource.com/first_aid.html
• Heimlich Maneuver for an Infant (younger than 1 years. (2008). Retrieved July 15th, 2010 from
http://www.nlm.nih.gov/medlineplus/ency/article/000047.htm

Handout 1.1: Drugs for Treatment of Status Asthmaticus
Beta Adrenergic Agonists Bronchodilators

• Act to decrease muscle tone in both small and large airways in lungs, thereby increasing
ventilation.
• Relieve reversible bronchospasm by relaxing smooth muscles of the bronchi.
• Albuterol (Salbutamol)
o Inhalers: 1-2 puffs q4-6h; not to exceed 12 puffs/day. For severe asthma and
bronchospasm can give 4 puffs every 20 minutes x 3 doses then every 1-4 hours as
needed- need to monitor for tachycardia, hypertension and agitation.
o Nebulizer: Dilute 0.5 ml (2.5 mg) of 0.5% inhalation solution in 1-2.5 ml of NS;
administer 2.5-5 mg diluted in 2-5 ml sterile saline or water ( in acute situation can
give every 20 minutes for 3 doses) then every 1-6h as needed. There is a need to
monitor for side effects of medication as noted (for severe bronchospasm nebulizer
administration is the preferred method)
o Pediatric/childrens dosing will be covered in the pediatric modules
Mast Cell Stabilizers

• These agents prevent histamine release from mast cells following stimuli by specific
antigens.
• Inhibits degranulation of sensitized mast cells following their exposure to specific
antigens.
Corticosteroids
• Maintenance medications that decrease inflammatory mediators to limit airway
remodeling.
• Must be taken regularly to be beneficial (for control of asthma). Inhaled steroids are the
drug of choice for controlling asthma. IV dosing is usually given in context of severe
bronchospasm.
• Glucocorticoids do not relieve acute bronchospasm, and short-acting bronchodilators
must be available.
• Multiple formulations are available that are not equivalent on a per-dose or per-mcg basis.
• Inhaled corticosteroids are one of the most important developments in asthma
management because they decrease inflammation.
• These agents are proven to improve lung function (FEV1 and airway hyperactivity) and
decrease symptoms, exacerbation frequency, and the need for rescue inhalers.
Methylprednisolone (Solu-medrol)
• Loading dose: 125-250 mg IV
Maintenance dose: 4 mg/kg/d IV divided q4-6h (usually 125 mg IV every 6 hours, reduce
dose quickly as patient improves to avoid side effects of corticosteroids)
Theophylline (Aminophylline)
• 5mg/kg loading dose (based on aminophylline) IV over 20 min, followed by maintenance
infusion of 0.1-1.1 mg/kg/h (watch for signs of toxicity).

Handout 1.2: Heimlich Maneuver for Infants, Adults and
Children
1) Heimlich maneuver for an infant (younger than 1 year)

A baby who is choking cannot cough or breathe and may turn blue or dusky. The Heimlich
maneuver can help dislodge the food or object.
WARNING: Do not begin the choking rescue procedure unless you are certain that the
baby is choking.
If the baby can cough or make sounds, let him or her cough to try to get the object out. If a
baby can't breathe, cough, or make sounds, then:
• Put the baby face down on your forearm so the baby's head is lower than his or her chest.
• Support the baby's head in your palm, against your thigh. Don't cover the baby's mouth or
twist his or her neck.
• Use the heel of one hand to give up to 5 back slaps between the baby's shoulder blades.
See picture A below.
• If the object does not pop out, support the baby's head and turn him or her face-up on
your thigh. Keep the baby's head lower than his or her body.
• Place 2 or 3 fingers just below the nipple line on the baby's breastbone and give 5 quick
chest thrusts (same position as chest compressions in CPR for a baby). See picture B
below.
• Keep giving 5 back slaps and 5 chest thrusts until the object comes out or the baby faints.
• If the baby faints, call for a help, and
o Do not do any more back slaps or chest thrusts.
o Start CPR. Each time you open the airway, look for an object in the baby's mouth. If
you see the object, take it out. But if you can't see the object, don't stick your finger
down the baby's throat to feel for it. See Picture C below
o Keep doing CPR until the baby is breathing on his or her own or until help arrives.
Picture A Picture B Picture C
Source: http://www.health.com/health/library/mdp/0,,tp12034,00.html

3) Heimlich maneuver for Adults and Children over 1 Year Old
Source: http://www.preparednessresource.com/first_aid.html,2009

Handout 1.3: Complications of Respiratory Obstruction
• Delay in treatment of respiratory obstruction can result in the following conditions:

o Obstructive emphysema
o Atelectasis
o Tracheoesophageal fistula
o Bronchial stricture
o Pneumonia
o Persistent cough
o Hemoptysis
o Polyp formation
o Localized bronchiectasis
o Chronic post obstructive pneumonia
o Lung abscess
o Bronchopleural fistula
o Decreased lung perfusion
o Chronic complications may be due to the foreign body itself or to trauma induced
during attempts to remove the object
o The complication rate increases if extraction of foreign body is delayed

Session 2: Shock, Anaphylaxis and Poisoning
Prerequisites
• None
Learning Objectives
• Define shock, anaphylaxis and poisoning
• Describe cause, classification, clinical features, and management of shock
• Describe types of common poisons, clinical features and their management
Resources Needed
• Handout 2.1: Management of Shock
• Handout 2.2: General Management of Poisoning
SESSION OVERVIEW
Activity/
Step Time Content
Method
2 05 minutes Presentation Definitions of Shock

Presentation,
3 30 minutes Aetiology and Classification of Shock
Buzz
4 05 minutes Presentation Clinical Features of Shock
5 05 minutes Presentation Management of Shock

Presentation, Definition and Clinical Features of
6 15 minutes
Brainstorm Poisoning
7 15 minutes Presentation Diagnosis of Poisoning
8 05 minutes Presentation Management Protocols for Poisoning
9 20 minutes Presentation Specific Poisons

Session 2: Shock, Anaphylaxis and Poisoning 19
SESSION CONTENT

Step 2: Definition of Shock (5 minutes)
• Shock: Is a clinical state of cardiovascular collapse characterized by failure of cells

perfusion resulting in
o Hypotension
o Tissue/cellular hypoxia
o Impaired cellular metabolism & death due to acute reduction of effective circulating
blood volume
• Shock is a life-threatening condition that occurs when the body is not getting enough
blood flow. This can damage multiple organs.
• Shock requires immediate medical treatment and can get worse very rapidly.
Step 3: Aetiology and Classification of Shock (30 minutes)
Aetiology
• Shock can be caused by any condition that reduces blood flow including
o Heart problems such as heart attack or heart failure
o Low blood volume as with heavy bleeding or dehydration
o Changes in blood vessels as with infection or severe allergic reactions
o Heavy external or internal bleeding from a serious injury
o Spinal injuries can also cause shock
• Septic shock syndrome is an example of a type of shock from an infection
Activity: Buzz (10 minutes)
TELL students to pair up.
TELL students to list classification of shock.
ALLOW 2 minutes for students to discuss in pairs.
ASK each pair to give their responses.
RECORD the responses on the board/flip chart.

Major Classifications of Shock
• Cardiogenic shock (associated with heart problems)
• Hypovolemic shock (caused by inadequate blood volume)
• Anaphylactic shock (caused by allergic reaction)
• Septic shock (associated with infections)
• Neurogenic shock (caused by damage to the nervous system)
Cardiogenic Shock
• Is an acute circulatory failure with sudden fall in cardiac output without actual reduction
of blood volume (normovolemic).
• Cardiogenic shock is a disease state where the heart is damaged enough that it is unable to
supply sufficient blood to the body.
• Occurs whenever the heart is unable to pump enough blood for the required needs.
• Cardiogenic shock can be caused by disorders of the heart muscle, the valves, or the
heart's conduction system.
• Some related disorders include heart attack, heart failure, cardiomyopathy, rupture of the
heart, abnormal heart rhythms, and heart valve disorders (especially leaky valves).
Hypovolemic Shock
• Hypovolemic shock is an emergency condition in which severe blood and fluid loss
makes the heart unable to pump enough blood to the body.
• Is the type of shock that can cause many organs to stop working.
• Acute reduction in blood volume can result from
o Severe haemorrhage (external or internal): Losing about 1/5 or more of the normal
amount of blood in the body causes hypovolemic shock such as trauma and surgery.
o Severe fluid loss: e.g. Severe burns, crush injury of a limb, persistent diarrhoea &/or
vomiting.
o Blood loss can be due to bleeding from cuts or other injury or internal bleeding such
as gastrointestinal tract bleeding.
o The amount of blood in the body may drop when one loses too many other body
fluids which can happen with diarrhoea, vomiting, burns, and other conditions.
• The greater and more rapid the blood loss the more severe the shock symptoms
Anaphylactic Shock
• Anaphylaxis is a severe whole-body allergic reaction
• After an initial exposure to a substance like bee sting toxin, the person's immune system
becomes sensitized to that allergen
• On a subsequent exposure an allergic reaction occurs
• This reaction is sudden, severe and involves the whole body
• Tissues in different parts of the body release histamine and other substances
• Clinical features develop rapidly often within seconds or minutes
• They may include the following
o Difficulty breathing, wheezing, abnormal (high-pitched) breathing sounds
o Confusion, slurred speech, fainting, light-headedness, dizziness
o Rapid or weak pulse, hypotension
o Cyanosis
o Hives and generalized itching
o Anxiety
o Sensation of feeling the heart beat (palpitations)

o Nausea, vomiting and diarrhoea
o Abdominal pain or cramping
o Nasal congestion and cough
Septic Shock
• Septic shock is a serious condition that occurs when an overwhelming
infection/septicaemia leads to low blood pressure and low blood flow
• The brain, heart, kidneys, and liver may not work properly or may fail
• Commonest bacteria are Gram negative for endotoxic shock or endotoxaemia and Gram
positive for exotoxic shock.
• Complications of Septic Shock include
o Waterhouse-Friderichsen Syndrome in Neisseria meningitidis, Streptococcus
pneumoniae
o DIC (disseminated intravascular coagulation)
o Multiple organ dysfunction syndrome
o Acute Respiratory Distress Syndrome (ARDS)
Step 4: Clinical Features of Shock (5 minutes)
• A person in shock has extremely low blood pressure

• Depending on the specific cause and type of shock, symptoms will include one or more of
the following
o Anxiety or agitation
o Confusion
o Pale, cool, clammy skin
o Low or no urine output
o Bluish lips and fingernails
o Dizziness, light-headedness, or faintness
o Profuse sweating, moist skin
o Rapid but weak pulse
o Shallow breathing
o Chest pain
o Unconsciousness
Step 5: Management of Shock (5 minutes)
Perform Pre-referral Management

• Urgently perform initial resuscitation for priorities to Airway, Breathing and Circulation( ABC)
o Maintain a clear airway. Extend neck, support jaw and suction
o Ensure normal breathing. Use mechanical ventilator as indicated
o Stop external bleeding
o Monitor vital signs
o Initiate I/V line
o Immediately refer the patient to higher center
Refer students to Handout 2. 1: Management of Shock

Step 6: Definition and Clinical Features of Poisoning (15 minutes)
Definition
• Poisoning refers to the development of dose-related adverse effects following exposure to
chemicals, drugs, or other xenobiotics.
• In excessive amounts, substances that are usually innocuous such as oxygen and water
can cause poisoning.
• Poisoning may be local (e.g. skin, eyes, or lungs) or systemic depending on the chemical
and physical properties of the xenobiotic, its mechanism of action and the route of
exposure.
• The severity and reversibility of poisoning also depend on the functional reserve of the
individual or target organ which is influenced by age and preexisting disease.
• All of these factors must be considered when attempting to predict the effects of a
particular exposure.
ASK students to mention clinical features of poisoning
INVITE few students to respond.
Clinical Features of Poisoning

• Clinical features should focus initially on
o Vital signs
o Cardiopulmonary system
o Neurologic status
• On the basis of the pulse, blood pressure, respiratory rate, temperature, and mental status,
the physiologic state can be characterized as
o Excited
o Depressed
o Discordant
o Normal
• More features are obtained from examination of
o Eyes for nystagmus, pupil size and reactivity
o Abdomen for bowel activity and bladder size
o Skin for burns, bullae, color, warmth, moisture, pressure sores, and puncture marks
may narrow the diagnosis to a particular disorder.
• Grading the severity of poisoning is useful for assessing the clinical course and response
to treatment.
• The patient should also be examined for evidence of trauma and underlying illnesses.
• Focal findings should prompt evaluation for a structural central nervous system (CNS)
lesion.
• When the history is unclear all orifices should be examined for the presence of chemical
burns and drug packets.

• The odour of breath or vomitus and the colour of nails, skin or urine may provide
diagnostic clues.
Step 7: Diagnosis of Poisoning (15 minutes)
• Although poisoning can mimic other illnesses, the correct diagnosis can usually be
established by
o History
o Physical examination
o Routine and toxicologic laboratory evaluations
• The history should include
o Time, route, and duration of poisoning
o Circumstances (location, surrounding events, and intent) of exposure
o The name and amount of each drug used
o Chemical or ingredient involved
o The time of onset, nature and severity of symptoms
o The time and type of first aid measures provided
o The medical and psychiatric history
• In many cases the victim is
o Confused
o Comatose
o Unaware of an exposure or unable or unwilling to admit to one
o Suspicious circumstances include unexplained illness in a previously healthy person
• Take history of psychiatric problems particularly depression
• Recent changes in health economic status or social relationships
• Onset of illness while working with chemicals or after ingesting food, drink especially
ethanol or medications
• Patients who become ill soon after arriving from a foreign country or being arrested for
criminal activity should be suspected of ‘body packing’ or ‘body stuffing’ (ingesting or
concealing illicit drugs in a body cavity)
• Relevant history may be available from family, friends, paramedics, police, pharmacists,
physicians and employers who should be questioned regarding the patient's habits,
hobbies, behaviour changes, available medications and antecedent events
• A search of clothes, belongings and place of discovery may reveal a suicide note or a
container of drugs or chemicals
• The imprint code on pills and the label on chemical products may be used to identify the
ingredients and potential toxicity of a suspected poison by consulting a reference text, a
computerized database, the manufacturer or a regional poison information centre
• In the absence of a history of exposure, the clinical course may suggest a diagnosis of
poisoning typically evolves and resolves more rapidly than other disorders
• Signs and symptoms characteristically develop within an hour of acute exposure, peak
within several hours and resolve over hours to days
• The absence of signs and symptoms soon after an overdose does not rule out poisoning

Step: 8 Management Protocols for Poisoning (5 minutes)
General Principles
• Monitoring and support of vital signs
• Prevention of further poison absorption
• Enhancement of poison elimination
• Administration of specific antidotes
• Prevention of re-exposure
• Specific treatment depends on the identity of the poison, the route and amount of
exposure, the time of presentation relative to the time of exposure, and the severity of
poisoning
• Knowledge of the offending agents' pharmacokinetics and pharmacodynamics is essential
Step 9: Specific Poisons (20 minutes)
Non-steroidal Anti-Inflammatory Drugs

• Inhibit prostaglandin and thromboxane synthesis by blocking cyclo-oxygenase (COX)
isoenzymes
• They are absorbed rapidly and blood concentrations peak 1 to 2 hours after ingestion
• They are highly protein bound (>90%) and have volumes of distribution of less than 1.0
L/kg body weight
• They are primarily eliminated by hepatic metabolism
• Half-lives range from 1 to 16 h except for phenylbutazone which has a half-life of 2 to 4
days
Clinical Toxicity
• Effects are usually mild and include
o Nausea
o Vomiting
o abdominal pain
o Drowsiness
o Headache
o Glycosuria
o Hematuria and proteinuria
o Acute renal failure and hepatitis occur rarely but NSAIDS can cause renal failure
even without poisoning.
o Diflunisal can cause hyperventilation, tachycardia and sweating
o Coma, respiratory depression, seizures and cardiovascular collapse may occur with
mefenamic acid and phenylbutazone
o Ibuprofen can cause metabolic acidosis, coma and seizures
o Metabolic acidosis is relatively common in phenylbutazone poisoning and occurs
rarely with naproxen
Treatment
Perform Pre-referral Management

• Urgently perform initial resuscitation with priorities to airway, breathing and circulation.
This includes opening an intravenous (I/V) line and initiation of IV fluids
• Maintain a clear airway, extend neck, support jaw and suction

• Ensure normal breathing and use mechanical ventilator as indicated
• Stop external bleeding (if any)
• Monitor vital signs
• Immediately refer the patient to higher center
Further Treatment at Higher Centre

• Activated charcoal is the preferred method of gastrointestinal decontamination
• Repeated doses may enhance the elimination of indomethacin, phenylbutazone and
piroxicam
• Renal excretion is not increased by diuresis and protein binding limits the efficacy of
hemodialysis
• Hemoperfusion might be useful in patients with hepatic or renal failure and severe
clinical toxicity
• Treatment is otherwise supportive
Organophosphate and Carbamate Insecticides

• Organophosphorus compounds such as the insecticides (Chlorpyrifos, Phosphorothioic
acid (Diazinon), Dichlorvos, Fenthion, Malathion, and Parathion), chemical warfare
‘nerve gases’ such as sarin irreversibly inhibit acetylcholinesterase and cause
accumulation of acetylcholine at muscarinic and nicotinic synapses in the CNS.
• Carbamates such as the insecticides (Aldicarb, Propoxur (Baygon), Carbaryl (Sevin),
bendiocarb (Ficam)), therapeutic agents (Ambenonium, Neostigmine, Physostigmine, and
Pyridostigmine) reversibly inhibit this enzyme.
• Agents that directly stimulate cholinergic receptors such as arecholine (from betel nuts),
bethanechol, pilocarpine and urecholine have the same effect.
• Organophosphates are absorbed through the skin, lungs, gastrointestinal tract and are
distributed widely in tissues.
• Also are slowly eliminated by hepatic metabolism
• Oxidative metabolites of parathion and malathion (paraoxon, malaoxon) are the active
forms of these agents.
• Carbamates are eliminated rapidly by serum and liver enzymes.
Clinical Toxicity
• The time from exposure to the onset of toxicity varies from minutes to hours but is
usually between 30 minutes and 2 hours.
• Muscarinic effects include
o Nausea, vomiting and abdominal cramps
o Urinary and fecal incontinence
o Increased bronchial secretions
o Cough, wheezing and dyspnea
o Sweating
o Salivation
o Miosis, blurred vision, lacrimation, and urinary frequency and incontinence
• In severe poisoning
o Bradycardia, conduction block, hypotension and pulmonary edema may occur.
o Nicotinic signs include
Twitching
Fasciculations
Weakness

Hypertension
Tachycardia
Paralysis and respiratory failure
o CNS effects include
Anxiety
Restlessness
Tremor
Confusion
Weakness
Seizures
Coma
• Toxicity due to Carbamates is shorter in duration and usually less severe than that due to
organophosphates.
• Most patients recover within 24 to 48 hours but fat soluble organophosphates may cause
effects for weeks to months.
• Death is most often due to pulmonary toxicity that consequently leading to respiratory
failure.
Treatment
• Perform Pre-referral Management
o Urgently perform initial resuscitation with priorities to airway, breathing and
circulation. This includes opening an intravenous (I/V) line and initiation of IV fluids.
o Maintain a clear airway, extend neck, support jaw and suction.
o Ensure normal breathing and use mechanical ventilator as indicated.
o Stop external bleeding (if any).
o Monitor vital signs.
o Immediately refer the patient to higher center.
Further Treatment at Higher Centre

• Gastrointestinal decontamination should include use of activated charcoal
• Supportive measures include
o Oxygen administration
o Ventilatory assistance
Treatment of Seizures
• Atropine, a muscarinic receptor antagonist should be administered for muscarinic effects
A dose of 0.5 to 2 mg is given intravenously every 5 to 15 minutes until bronchial and
other secretions have dried and the pupils are dilated to the normal levels (watch for signs
of atropine toxicity).
• Do not use morphine or theophylline.
Refer students to Handout 2.2: Management of Poisoning

• Shock is a life threatening condition which needs immediate life saving resuscitative
measures
• Priority management of shock should be directed to ensure patent air way, breathing and
adequate fluids preferably crystalloids to combat collapsing circulation.
• The severity of poisoning depends on amount exposed and functional reserve of an
individual or target organ under influence of age and preexisting disease
• Diagnosis of poisoning is based by careful history taking and physical examination
• What are the symptoms and signs of shock?

• How is shock managed?
• What are the clinical features of poisoning?
• What are the management protocols of poisoning?
References
McGraw Hill.
• Cumming A.D. (2003). Davidson’s Principles and Practice of Medicine. Edinburgh:
Oxford.
Saunders.
• MOH (2005). Tanzania National Formulary. Dar es Salaam, Tanzania: Ministry of
Health and Social Welfare.

Handout 2.1: Management of Shock
Investigations
• FBP
• ESR
• Serum electrolytes and glucose
• Serum creatinine, BUN, bilirubin, alkaline phosphate and ALT
• Arterial blood gas (ABG)
• Coagulation should be assessed performed to detect the presence of DIC.
• Lumber puncture-meningococcal meningitis
• CXR-severe streptococcal pneumonia
Treatment
• As this is a medical emergency, patients should be referred urgently after initial
resuscitation.
o Priorities: Airway- breathing- circulation.
o Airway - maintain a clear airway. Extend neck, support jaw and suction.
o Administer O2 by nasal catheter or ETT depending on severity.
o Breathing- ensure normal breathing. Use mechanical ventilator as indicated.
o Circulation- stop external bleeding, specific surgery to stop internal bleeding.
o Administer fluids to maintain preload.
Oxygen Therapy
• Administer O2 via face mask, nasal catheter
• O2 saturation maintained at SaO2 > 90% (PaO2 = 60mm Hg)
o Maintain Hb at > 10g/dl by early transfusion
Restore Blood Volume

• Insert large bore IV lines(14-16 gauge) or cut down and administer
• Crystalloids e.g. 0.9% NaCl, Ringer’s lactate
• Adult bolus of 7.5 ml/kg (0.5-2l initially in ½ - 2 hours.)
• Children 20ml/kg as a bolus
• Colloids e.g. Dextran
Further Treatment
• Modify myocardial contractility, heart rate and rhythm
o Bradycardia: (<60/min): Atropine (0.5-1.0 mg IV) or Adrenaline 0.1 mcg/kg/min
(be careful to not induce tachycardia as that will cause further damage to the heart
muscle)
o For Life threatening arrhythmias perform cardio version
o Rhythm disturbances (ECG monitor)
• Treat arrhythmias with specific drugs (depending on the type of rhythm) and or
defibrillation
• The agents listed below should NOT be used unless you have the patient on a cardiac
monitor

Inotropic agents: adult dosing
o Dopamine(renal dose) 2-4 mcg/kg/min IV
o Dobutamine 2.5- 10 mcg/kg/min IV
o Adrenaline (epinephrine) 0.1 mcg/kg/min
o Vasodilators for cardiogenic shock e.g. nitroprusside, nitroglycerine, hydralazine.
Traumatic Shock
• Stabilize chest defects, dress sucking wounds
• Prevent further external loss by direct pressure or large dressing
• Place patient in Trendelenburg position
Cardiogenic Shock
• Exclude tamponade, tension pneumothorax and pulmonary embolism
• Patient in a comfortable position and monitor ECG
• Diuretics if in congestive heart failure with expanded volume
• Improve rate and correct arrhythmias with aid of ECG
Septic Shock
• Antibiotics
o Initial selection of particular agents is empiric based on an assessment of the patient's
underlying host defenses, the potential sources of infection and the most likely
responsible organisms.
o Antibiotics must be broad spectrum and cover gram-positive, gram-negative and
anaerobic bacteria because all classes of these organisms produce an identical clinical
picture.
o Antibiotics must be given parenterally in adequate doses.
o Ant staphylococcal coverage is recommended in patients with an indwelling
intravascular line or devices.
o Coverage directed against anaerobes should be included in patients with intra-
abdominal or perineal infections.
o Antipseudomonal coverage is indicated in patients with neutropenia or burns.
o Immunocompetent patients usually can be treated with a single drug with broad-
spectrum.
o Coverage such as a third generation cephalosporin.
o Immunocompromised patients usually require dual antibiotic coverage with broad-
spectrum antibiotics with overlapping coverage.
o Within these general guidelines no single combination of antibiotics is clearly
superior to others.
o Patients with infected foci should be taken for surgery after initial resuscitation and
administration of antibiotics.
o Little is gained by spending hours to make the patient more stable when an infected
focus persists.
Anaphylactic Shock
• Airway- Intubation may be required and administer O2
• Drugs- Adrenaline (1: 1000) 0.5-1.0mg IM or 0.1-0.2mg (1ml in 9ml N/S) IV over 3-5
min
• Hydrocortisone 100-250 mg IV or Methlprednisolone 50-100mg IM.

Handout 2.2: General Management of Poisoning
Activated Charcoal
• Have comparable or greater efficacy.
• Fewer contraindications and complications.
• Is less aversive and invasive than ipecac or gastric lavage and is the preferred method of
gastrointestinal decontamination in most situations.
• Activated charcoal is prepared as a suspension in water, either alone or with a cathartic
• It is given orally via a nippled bottle (for infants), or via a cup, straw or small-bore
nasogastric tube.
• Do not give to a comatose patient unless the patient is intubated and you have a
nasogastric tube in place.
• The recommended dose is 1g/kg body weight using 8 ml of diluents per gram of charcoal
if a premixed formulation is not available.
• Charcoal adsorbs ingested poisons within the gut lumen allowing the charcoal-toxin
complex to be evacuated with stool.
• The complex can also be removed from the stomach by induced emesis or lavage.
• In vitro, charcoal adsorbs >90% of most substances when given in an amount equal to 10
times the weight of the substance.
• Compounds that are not well adsorbed by charcoal.
o Charged (ionized) chemicals such as
Mineral acids
Alkalis
Highly dissociated salts of cyanide, fluoride, iron, lithium
Other inorganic compounds
• In animal and human volunteer studies, charcoal decreases the absorption of ingestants by
an average of 73% when given within 5 minutes of ingestant administration, 51% when
given at 30 minutes and 36% at 60 minutes.
Complications
• Mechanical obstruction of the airway
• Aspiration
• Vomiting
• Bowel obstruction and infection caused by inspissated charcoal
• Charcoal is not recommended for patients who have ingested corrosives because it
obscures endoscopy
Gastric Lavage
• Is performed by sequentially administering and aspirating about 5 ml fluid per kilogram
of body weight through a no. 28 French orogastric tube in children and no. 40 French tube
in adults.
• Except for infants tap water is acceptable.
• The patient should be placed in trendelenburg and left lateral decubitus positions to
prevent aspiration even if an endotracheal tube is in place.

• Lavage decreases ingestant absorption by an average of 52% if performed within 5
minutes of ingestion administration, 26% if performed at 30 minutes, and 16% if
performed at 60 minutes.
• Its efficacy is similar to that of ipecac.
• Significant amounts of ingested drug are recovered in one-tenth of patients.
• Aspiration is a common complication occurring in up to 10% of patients especially when
lavage is performed improperly.
• Serious complications of tracheal, esophageal and gastric perforation occur in
approximately 1% of patients.
• For this reason the physician should personally insert the lavage tube and confirm its
placement and the patient must be cooperative or adequately restrained with
pharmacologic sedation if necessary during the procedure.
• Gastric lavage is contraindicated in corrosive (such as lye) or petroleum distillate
ingestions because of the respective risks of gastroesophageal perforation and aspiration-
induced hydrocarbon pneumonitis.

Session 3: Meningitis, Convulsions and Coma
Prerequisites
• None
Learning Objectives
• Define meningitis, coma and convulsions
• Outline causes of meningitis, coma and convulsions
• Describe clinical features meningitis, coma and convulsions
• Identify the differential diagnosis of coma and convulsions
• Describe the management of each of meningitis, coma and convulsions
Resources Needed
• Handout 3.1: Cerebrospinal Fluid Indices in Meningitis
• Handout 3.2: Glasgow Coma Scale (GCS)
SESSION OVERVIEW
Activity/
Step Time Content
Method
Definition, Causes and Predisposing
Factors of Meningitis
3 10 minutes Presentation Clinical Features of Meningitis
4 10 minutes Presentation Management of Meningitis

Presentation,
5 15 minutes Definition and Causes of Coma
Brainstorm
Clinical Feature, Differential Diagnosis and
Investigations of Coma
7 10 minutes Presentation Treatment and Prognosis of Coma
Presentation, Definition and Differential Diagnosis of
8 15 minutes
Brainstorm Convulsions
Investigations and Treatment of
9 10 minutes Presentations
Convulsions

Session 3: Meningitis, Convulsions and Coma 33
SESSION CONTENT

READ or ASK the Students to read the learning objectives, and clarify.
Step 2: Definition, Causes and Predisposing Factors of Meningitis

(15 minutes)
Definition
• The name meningitis is derived from the term meninges (dura, pia and arachnoids’
membranes)
• Meninges are the protective membranes covering the central nervous system
• When these membranes are inflamed we use the term meningitis
• Meningitis is a potentially serious condition owing to the proximity of the inflammation
to the brain and spinal cord
Causes of Meningitis
• Most cases of meningitis are caused by microorganisms (infectious meningitis) such as
o Viruses
o Bacteria
o Fungi or
o Parasites
• These microorganisms spread into the blood and into the cerebrospinal fluid (CSF)
• Non-infectious causes of meningitis though not common include
o Cancers, (neoplastic conditions e.g carcinomatous meningitis)
o Systemic lupus erythematosus
o Physical injury (subarachnoid haemorrhages)
o Chemicals (chemical meningitis)
• Neisseria meningitidis (‘meningococcal’) and Streptococcus pneumoniae
(‘pneumococcal’) are the most common pathogens in patients without immune
deficiency
• Meningococcal infection is more common in children
• Staphylococcus aureus may complicate neurosurgical operations, and Listeria
monocytogenes is associated with poor nutritional state and alcoholism
• Acute bacterial meningitis may be caused by the following in order of frequency
o Pneumococci - Streptococcus pneumoniae
o Haemophilus influenzae
o Meningococci - Neisseria meningitidis
o Coliforms - Escherichia coli
o Salmonella - Salmonella typhi
o Staphylococci - Staphylococcus aureus
o Streptococci - Streptococcus pyogene

Figure 1: Causes of Meningitis by Age Group
Age Group of
Common Organisms Less common Organisms
onset
Gram-negative bacilli (Escherichia coli),
Neonate Listeria monocytogenes
Proteus spp and Gram+ve B streptococci
Mycobacterium Tuberculosis
Pre-school
Haemophilus influenzae Neisseria meningitidis
child
Streptococcus pneumoniae
Streptococcus pneumoniae Listeria monocytogenes
Older
Neisseria meningitidis Mycobacterium Tuberculosis
children and
Haemophilus influenzae
adult
Staphylococcus aureus
Predisposing Factors for Meningitis

• Ear infections (otitis media, mastoditis)
• Sinusitis
• Respiratory infections
• Malnutrition
• Head injuries
• Septicaemia and diarrhoea especially in the newborns
• Immune suppression e.g. HIV
Step 3: Clinical Features of Meningitis (10 minutes)

Most Common Clinical Features
• Headache
• Neck stiffness or in ability to flex the neck forward
Others
• Fever
• Altered mental status
• Photophobia (inability to tolerate bright light)
• Delirium (in small children)
• Seizures (in about 20-40% of cases)
• Swelling of the fontanel (in infants 0-6 months)
• Rash (petachial rash) common in meningococcal meningitis, may precede other
symptoms
• The rash consists of numerous small, irregular purple or red spots on the trunk, lower
extremities, mucous membranes, conjunctiva and occasionally on the palms of hands and
soles of feet.
Clinical Signs
• There are two clinical tests that can be done to suggest the diagnosis meningitis namely
Kerning’s and Brudzinski’s sign; however, these signs may be absent as well in many
cases of meningitis.

• Severe malaria
• Viral meningoencephalitis
• Subarachnoid hemorrhage
Step 4: Management of Meningitis (10 minutes)
• Patients suspected of having meningitis should be referred for investigation and treatment
at higher level (hospitals).
Investigations
• Cerebral spinal fluid (CSF) analysis should be done following lumbar puncture
• The CSF sample is examined for
o Check opening pressure
o White blood cells count
o Red blood cells
o Proteins content estimation
o Glucose level estimation
o Gram staining (determines if bacteria are responsible for the disease causation)
o Microbiological culture (in some equipped hospitals)
Refer students to Handout 3.1: Cerebrospinal Fluid Indices in Meningitis
Other Investigations
• Electrolytes
• Liver and kidney function
• Complete blood count
• Chest X-ray
• If the patient is immunocompromised other CSF tests can be done to isolate infections
like:
o Toxoplasmosis
o Epstain-barr virus
o Cytomegalo virus
o Fungal infection (crypyococcal meningitis)
Treatment
• Meningitis cases are best treated at hospital and some few equipped health centres. At
dispensary level, give only pre-referral treatment as shown below;
o First dose antibiotic: if bacterial meningitis is suspected, antibiotics can be given
immediately (preferably within 1 hour of arrival to facility)
o IV fluids
o Antipyretics
o Then refer the patient as soon as possible for prompt management
General Management
• Secure the airway in an unconscious patient.
• Administer of intravenous fluids in hypotension or shock.
• Position the patient on left lateral (if is conscious).

• Administer antibiotics if not already administered.
• Antibiotics of choice are
o Crystalline benzyl penicillin 6 MU at once 3 MU 6-hourly or Ampicillin and
Chloramphenicol 1g every 6-hours.
o These drugs are active against Pneumococci, H. influenzae, Meningococci, E. coli and
Salmonellae spp.
Note: Penicillin is not active against E. coli or Salmonella spp)
• Viral meningitis has no specific treatment except for severe cases where acyclovir can be
given.
• Cryptococcal meningitis is treated with Fluconazole, 400mg OD intravenous or
Amphotericin B 0.7 mg/kg/day IV x 14 days and later on suppressive dosage of
Fluconazole to prevent recurrence.
Step 5: Definition and Causes of Coma (15 minutes)
• Coma: The unnatural situation of reduced alertness and responsiveness represents a

continuum that in its severest form is called coma, a deep sleep-like state from which the
patient cannot be aroused.
ASK students to outline causes of coma.
INVITE students to respond.
Causes of Coma
• Metabolic Disturbances
o Drug overdose
o Diabetes mellitus
Hypoglycaemia
Ketoacidosis
Hyperosmolar coma
o Hyponatraemia
o Uraemia
o Hepatic failure
o Respiratory failure
o Hypothermia
o Hypothyroidism
• Trauma
o Cerebral contusion
o Extradural haematoma
o Subdural haematoma
• Cerebrovascular Disease
o Subarachnoid haemorrhage
o Intracerebral haemorrhage
o Brain-stem infarction/haemorrhage

o Cerebral venous sinus thrombosis
• Infections
o Meningitis
o Encephalitis
o Cerebral abscess
o General sepsis (septicaemia)
• Others
o Epilepsy
o Brain tumour
o Thiamine deficiency
o Alcohol intoxication
Step 6: Clinical Feature, Differential Diagnosis and Investigations of Coma

(10 minutes)
Clinical Feature
• Unconscious for more than half an hour
• Meningitis
• Encephalitis
• Cerebral abscess
• Subarachnoid haemorrhage
• Brain-stem infarction/haemorrhage
• Drug overdose
• Diabetes mellitus
o Hypoglycaemia
o Ketoacidosis
o Hyperosmolar coma
Diagnosis
• Perform Glasgow Coma Score
Refer students to Handout 3.2: Glasgow Coma Scale
Investigations
• Depends on the most likely cause of coma
• Collateral history and physical examination
• Findings may suggest type of investigations to be done
o Blood sugar
o Perform lumbar puncture to obtain cerebral spinal fluid for analysis
o Serum electrolytes analysis
o Liver function tests
o Blood slide for malaria parasites
• Others
o CT scan of brain (when appropriate)

Step 7: Treatment and Prognosis of Coma (10 minutes)
• Refer the patient immediately after initial resuscitation using ABCs protocol.
• The immediate goal in acute coma is the prevention of further nervous system damage.
• Hypotension, hypoglycemia, hypercalcemia, hypoxia, hypercapnia, and hyperthermia
should be corrected rapidly and attentively.
• An oropharyngeal airway is adequate to keep the pharynx open in drowsy patients who
are breathing normally.
• Tracheal intubation is indicated if there is apnea or upper airway obstruction,
hypoventilation, emesis or if the patient is liable to aspirate because of coma.
• Intravenous access is established and naloxone and dextrose are administered if narcotic
overdose or hypoglycemia is even remote possibilities and thiamine is given with glucose
in order to avoid eliciting Wernicke disease in malnourished patients.
• In cases of suspected basilar thrombosis with brainstem ischemia, intravenous heparin or
a thrombolytic agent is often utilized keeping in mind that cerebella and pontine
hemorrhages resemble basilar artery occlusion (this should be done in a hospital).
• In situation of coma hypotonic or hypertonic solutions should NOT be given (it is best to
give isotonic solutions such as normal saline or ringers).
• Cervical spine injuries must not be overlooked particularly prior to attempting intubation
or the evaluation of oculocephalic responses.
• Headache accompanied by fever and meningismus indicates an urgent need for
examination of the CSF to diagnose meningitis.
• If the lumbar puncture in a case of suspected meningitis is delayed for any reason
antibiotics such as a third generation cephalosporin should be administered as soon as
possible (then efforts to do LP should be done without delay).
• Hyperosmolar therapy with mannitol or an equivalent agent is the mainstay of
intracranial pressure reduction.
Prognosis
• The prediction of the outcome of coma must be considered in reference to long-term care
and medical resources.
• Metabolic comas have a far better prognosis than traumatic comas.
• All schemes for prognosis in adults should be taken as approximate indicators and
medical judgments must be tempered by factors such as age, underlying systemic disease
and general medical condition.
Step 8: Definition and Differential Diagnosis of Convulsions (15 minutes)

• Convulsion: Uncontrollable shaking or a violent shaking of the body or limbs caused by
uncontrollable muscle contractions which can be a symptom of brain disorders and other
conditions.
ASK students to mention the differential diagnosis of convulsions.
INVITE students to respond.

• Epilepsy/status epilepticus
• Viral encephalitis
• Febrile seizures (more common in children)
• Migraine
• Malaria
• Hypoglycaemia
• Electrolyte imbalance
• Cerebral hemorrhage
• Space occupying lesions (e.g. toxoplasmosis, neurocysticercosis)
Step 9: Investigations and Treatment of Convulsions (10 minutes)

At Primary Health Care Facilities (Dispensary and Health Centre)
• Blood sugar (preferably using a glucometer)
• Blood slide for malaria parasites
At Higher Centres
• Lumbar puncture & cerebral spinal fluid analysis
• Serum electrolytes analysis
• Liver and renal function tests
Others Investigations
• CT scan of the brain
Treatments
Convulsing patient should be referred to hospital, at primary health care facility level do pre-
referral treatment as follows
• Remove the patient from danger or remove the danger to the patient
• Maintain air way, breathing and circulation
• Remove tight clothes
• Don’t put anything in the mouth
• Don’t try to stop the seizures physically
• Give diazepam 10mg IV initially then repeat after 15 minutes if seizures recur
(max of 30 mg)
• Initiate I/V line and refer the patient to higher centre for management of the cause
• Meningitis is a condition characterized by symptoms of stiff neck, high fever, sensitivity

to light, confusion, headaches and vomiting.
• Severe malaria, viral meningoencephalitis and subarachnoid hemorrhage are important
differential diagnosis of Meningitis.
• Proper management of meningitis needs to be instituted immediately to save patients life.
• Give appropriate antibiotics IV as soon as possible.
• Coma is unnatural situation where an individual has a deep sleep-like state from which
s/he cannot be aroused.

• Blood slide for malaria parasites, blood sugar, cerebral spinal fluid analysis/lumbar
puncture are important investigations to the patient with coma.
• Convulsion is uncontrollable shaking or a violent shaking of the body or limbs caused by
uncontrollable muscle contractions which can be a symptom of brain disorders and other
conditions.
• Differentials of convulsions include severe malaria, hypoglycaemia and electrolyte
imbalance.
• Patients with convulsions should be investigated for blood sugar level and malaria
parasites at the primary level facility before being referred to the higher centre.
• Controlling convulsions is by giving diazepam and then refer the patient for further
management.
• Describe the common aetiologies of meningitis

• List the clinical features of meningitis
• How do you define coma
• Describe management of coma
• Describe the treatment of a patient with convulsions
• List five differential diagnosis of convulsions
References
McGraw Hill.
• Cumming A.D. (2003). Davidson’s Principles and Practice of Medicine. Edinburgh,
Saunders.

Handout 3.1: Cerebral Spinal Fluid Indices in Meningitis
Cell Type Cell Glucose Protein Gram

Count Stain
Normal Lymphocytes 0-4 > 60% Up to 0.45 g/l -
6
of blood
×10 /l
glucose
Viral Lymphocytes 10- Normal Normal -ve
2000
Bacterial Polymorphs 1000- Low Normal/elevated +ve
5000
Tuberculous Polymorphs/lymphocytes/mixed 50- Low Elevated Often
5000 -ve
Fungal Lymphocytes 50- Low Elevated ±ve
500
Malignant Lymphocytes 0-100 Low Normal/elevated -ve

Handout 3.2: Glasgow Coma Scale
Assessment of Level of Consciousness

• Asses the level of consciousness by using Glasgow coma scale
Glasgow Coma Scale (GCS)
Eye Opening
• Spontaneous 4
• To voice 3
• To pain 2
• None 1
Verbal Response
• Oriented 5
• Confused 4
• Inappropriate words 3
• Incomprehensible sounds 2
• None 1
Motor Response
• Obey command 6
• Localises pain 5
• Withdraws (pain) 4
• Flexion (pain) 3
• Extension (pain) 2
• None 1
Total
• Total Score 3-15
• Mildly severe 15-13
• Moderately severe 12-8
• Severe 7-3
• This predicts the severity and expectation of the patients and must be done frequently
• It guides the clinician whether the patient’s condition improves or deteriorates over time

Session 4: Urinary Tract Infections and Acute
Glomerulonephritis
Prerequisites
• None
Learning Objectives
• Define urinary tract infections (UTI) and acute glomerulonephritis
• Describe a brief account of epidemiology of urinary tract infections
• Describe clinical features of urinary tract infections and acute glomerulonephritis
• Identify relevant investigations for the diagnosis urinary tract infections and acute
glomerulonephritis
• Describe treatment of urinary tract infections and acute glomerulonephritis
• Describe prevention of urinary tract infections
Resources Needed
• Handout 4.1: Catheter associated UTI
• Handout 4.2: Treatment of UTI
• Handout 4.3: Treatment of Acute Glomerulonephritis (AGN)
SESSION OVERVIEW
Activity/
Step Time Content
Method
Definition, Aetiology, Epidemiology and
pathogenesis of Urinary Tract Infection
Presentation,
3 15 minutes Clinical Features of UTI
Brainstorm
4 15 minutes Presentation Management of UTI
5 10 minutes Presentation Prevention and Prognosis of UTI

Presentation, Definition and Causes of Acute
6 15 minutes
Brainstorm Glomerulonephritis
Clinical Features and Diagnosis of Acute
Glomerulonephritis
8 05 minutes Presentation Treatment of Acute Glomerulonephritis

Session 4: Urinary Tract Infections and Acute Glomerulonephritis 45
SESSION CONTENT
Step 2: Definition, Aetiology, Epidemiology and pathogenesis of Urinary

Tract Infection [UTI] (25 minutes)
• Urinary tract infection (UTI): Significant bacteriuria in the presence of symptoms of
acute UTI.
o Urethritis
o Cystitis
o Pyelonephritis
Aetiology
• Many different microorganisms can infect the urinary tract but by far the most
common agents are the gram-negative bacilli.
• Escherichia coli cause approximately 80% of acute infections in patients without
catheters, urologic abnormalities or calculi.
• Other gram-negative rods especially Proteus spp and Klebsiella spp and occasionally
Enterobacter spp account for a smaller proportion of uncomplicated infections.
• These organisms plus Serratia spp and Pseudomonas spp assume increasing
importance in recurrent infections and in infections associated with urologic
manipulation, calculi or obstruction.
• They play a major role in nosocomial catheter-associated infections.
• In other women with acute urinary symptoms, pyuria and urine that is sterile (even
when obtained by suprapubic aspiration), sexually transmitted urethritis-producing
agents such as Chlamydia trachomatis, Neisseria gonorrhoeae, and herpes simplex
virus are etiologically important.
• These agents are found most frequently in young sexually active women.
Refer students to Handout 4.1: Catheter Associated UTI
Epidemiology
• Epidemiologically UTIs are subdivided into
o Catheter-associated (or nosocomial) infections.
o Non-catheter-associated (or community-acquired) infections.
• Infections in either category may be symptomatic or asymptomatic.
• Acute community-acquired infections are very common.
• These infections occur in 1 to 3% of schoolgirls and then increase markedly in incidence
with the onset of sexual activity in adolescence.
• Vast majority of acute symptomatic infections involve young women.
• Acute symptomatic UTIs are unusual in men under the age of 50.
• Development of asymptomatic bacteriuria parallels that of symptomatic infection and is
rare among men under 50 but common among women between 20 and 50.

• Asymptomatic bacteriuria is more common among elderly men and women with rates as
high as 40 to 50% in some studies.
Pathogenesis, Sources of Infection and Factors Affecting Pathogenesis

• The urinary tract should be viewed as a single anatomic unit that is united by a
continuous column of urine extending from the urethra to the kidney.
• In the vast majority of UTIs, bacteria gain access to the bladder via the urethra.
• Ascending of bacteria from the bladder may follow and is probably the pathway for most
renal parenchymal infections.
• In females prone to the development of cystitis, enteric gram-negative organisms residing
in the bowel colonize the introitus, the periurethral skin and the distal urethra before and
during episodes of bacteriuria.
• Hematogenous pyelonephritis occurs most often in debilitated patients who are either
chronically ill or receiving immunosuppressive therapy.
• Metastatic staphylococcal or candidal infections of the kidney may follow bacteremia or
fungemia spreading from distant foci of infection in the bone, skin, vasculature or
elsewhere.
Conditions Affecting Pathogenesis

• Gender and Sexual Activity
o The female urethra appears to be particularly prone to colonization with colonic
gram-negative bacilli because of its proximity to the anus, its short length (about 4
cm) and its termination beneath the labia.
o Vigorous sexual intercourse may predispose to introduction of bacteria into the
bladder and is temporally associated with the onset of cystitis.
o More commonly UTI symptoms in men can be associated with a sexually transmitted
disease such as GC or Chlamydia.
o Older men can have UTI symptoms due to prostatitis, kidney stones.
• Pregnancy
o UTIs are detected in 2 -8% of pregnant women
Obstruction
• Any impediment to the free flow of urine (tumor, stricture, stone, or prostatic
hypertrophy) results in hydronephrosis and dilation of the ureters and a greatly increased
frequency of UTI.
Neurogenic Bladder Dysfunction

• Interference with the nerve supply to the bladder as in
o Spinal cord injury
o Tabes dorsalis
o Multiple sclerosis
o Diabetes and other diseases may be associated with UTI
• The infection may be initiated by the use of catheters for bladder drainage and is favored
by the prolonged stasis of urine in the bladder.
Vesicoureteral Reflux
• Defined as reflux of urine from the bladder cavity up into the ureters and sometimes into
the renal pelvis.

• Vesicoureteral reflux is common among children with anatomic abnormalities of the
urinary tract as well as among children with anatomically normal but infected urinary
tracts.
Bacterial Virulence Factors

• Most E. coli strains that cause symptomatic UTIs in non catheterized patients belong to a
small number of specific O, K, and H sero groups.
• These uropathogenic clones have accumulated a number of virulence genes that are often
closely linked on the bacterial chromosome in ‘virulence islands’
Genetic Factors
• Increasing evidence suggests that host genetic factors influence susceptibility to UTI.
• A maternal history of UTI is more often found among women who have experienced
recurrent UTIs than among controls.
Step 3: Clinical Features of UTI (15 minutes)
TELL students to list the clinical features of urinary tract infections.
Cystitis
• Patients with cystitis usually report dysuria, frequency, urgency, and suprapubic pain.
• The urine often becomes grossly cloudy and malodorous and it is bloody in about 30% of
cases.
• Physical examination generally reveals only tenderness of the urethra or the suprapubic
area.
• Prominent systemic manifestations such as a temperature of >38.3°C, nausea and
vomiting usually indicate concomitant renal infection as does costovertebral (renal) angle
tenderness.
• However, the absence of these findings does not ensure that infection is limited to the
bladder and urethra.
Acute Pyelonephritis
• Symptoms of acute pyelonephritis generally develop rapidly over a few hours or a day
and include a fever, shaking chills, nausea, vomiting and diarrhea.
• Symptoms of cystitis may or may not be present.
• Hematuria may be demonstrated during the acute phase of the disease if it persists after
acute manifestations of infection have subsided, a stone, a tumor or tuberculosis should
be considered.
• Besides fever, tachycardia and generalized muscle tenderness, physical examination
reveals marked tenderness on deep pressure in one or both costovertebral angles or on
deep abdominal palpation.

• In some patients signs and symptoms of gram-negative sepsis predominate.
• Except in individuals with papillary necrosis, abscess formation or urinary obstruction
the manifestations of acute pyelonephritis usually respond to therapy within 48 to 72
hours.
Urethritis
• Approximately 30% of women with acute dysuria, frequency, and pyuria have midstream
urine cultures that show either no growth or insignificant bacterial growth
• Clinically these women cannot always be readily distinguished from those with cystitis.
• In this situation a distinction should be made between women infected with sexually
transmitted pathogens such as Chlamydia trachomatis, Neisseria gonorrhoeae, or herpes
simplex virus and those with low-count Eschelichia coli or staphylococcal infection of
the urethra and bladder.
Step 4: Management of UTI (15 minutes)

Investigation at Primary Health Care Facility
• Conduct dipstick urine examination (when available).
• The leukocyte esterase ‘dipstick’ method is less sensitive than microscopy in identifying
pyuria but is a useful alternative where microscopy is not feasible.
• Pyuria in the absence of bacteriuria (sterile pyuria) may indicate infection with unusual
bacterial agents such as C. trachomatis, U. urealyticum, and Mycobacterium tuberculosis
or with fungi.
• Alternatively sterile pyuria may be demonstrated in non-infectious urologic conditions
such as calculi, anatomic abnormality, nephrocalcinosis, vesicoureteral reflux, interstitial
nephritis or polycystic disease.
Investigation at Hospital
• Urine Microscopy (Urinalysis)
o Microscopy of urine from symptomatic patients can be of great diagnostic value
o Microscopic bacteriuria, which is best assessed with Gram-stained uncentrifuged
urine is found in more than 90% of specimens from patients whose infections are
associated with colony counts of at least 105/ml and this finding is very specific.
o Bacteria cannot usually be detected microscopically in infections with lower colony
counts (102 to 104/ml).
o The detection of bacteria by urinary microscopy thus constitutes firm evidence of
infection but the absence of microscopically detectable bacteria does not exclude the
diagnosis.
o When carefully sought by means of chamber-count microscopy, pyuria is a highly
sensitive indicator of UTI in symptomatic patients.
o Pyuria is demonstrated in nearly all acute bacterial UTIs and its absence calls the
diagnosis into question.
• Urine Culture
o Determination of the number and type of bacteria in the urine is an extremely
important diagnostic procedure
• Specimens
o Midstream urine (MSU) specimen
o Suprapubic urine specimen (rarely indicated in adults unless unable to void or
introduce a urethral catheter)

o Urine obtained by catheterization
o Presence of bacteriuria of any degree in suprapubic aspirates or of 102 bacteria per
milliliter of urine obtained by catheterization usually indicates infection
Treatment
• The anatomic location of UTI greatly influences the success or failure of a therapeutic
regimen.
• Treatments listed are those to be prescribed before the etiologic agent is known.
o Cotrimoxazole (TMP/SMZ)
o Furadantin (Nitrofurantoin)
• Gram's staining can be helpful in the selection of empirical therapy.
• Such therapy can be modified once the infecting agent has been identified.
Note: Fluoroquinolones should not be used in pregnancy.
• Gentamicin should be used with caution in pregnancy because of its possible toxicity to
eighth-nerve development in the fetus.
• Multiday oral regimens for cystitis in adults are as follows
o Cotrimoxazole, 960mg (160mg TMP/800mg SMX) q12h x 3 days
o Norfloxacin, 400 mg q12h x 7-10 days
o Ciprofloxacin, 250-500 mg q12h for 7-10 days depending on severity and
susceptibility.
o Ofloxacin, 200-400mg 12 – 24hourly for 7-10 days
o Enoxacin, 200 mg q12h for 7 days for uncomplicated UTI
o Macrocrystalline, amoxicillin 500mg q8h for 5-7 days
Note: Some of the drugs mentioned here might not be readily available in primary health
care facilities.
• Oral regimens for pyelonephritis and complicated UTI are either
• Cotrimoxazole 960mg q12h for 10-14 days or
o Ciprofloxacin, 500 mg q12h for 10-14 days or
o Ofloxacin, 200-300 mg q12h for 14-28 days (in prostatitis) or
o Lomefloxacin,400 mg/d for 10-14 days or
• Parenteral regimens are as follows
o Ciprofloxacin, 200-400 mg q12h or
o Ofloxacin, 200-400 mg q12h or
o Gentamycin, 3-5mg/kg per day divided dosing q 8 hours or
o Ceftriaxone, 1-2 g/daily or
o Ampicillin, 1 g q6h or
o Imipenem, 250-500 mg q6-8h or
Note: UTI in men is always considered complicated and treatment should be targeted at
the likely bacteria.
• It is recommended to add Doxycycline 100 mg twice daily for 7 days to the possible
treatment regimens in this population (men).
• If prostatitis is the cause, a prolonged course (14-21 days) of antibiotic therapy is
recommended
Refer students to Handout 4.2: Treatment of Urinary Tract Infections

Step 5: Prevention and Prognosis of UTI (10 minutes)
Prevention
• Women who experience frequent symptomatic UTIs (3 per year on average) are
candidates for long-term administration of low dose antibiotics directed at preventing
recurrences.
• Such women should be advised to avoid spermicide use soon after intercourse.
• Prophylaxis should be initiated only after bacteriuria has been eradicated with a full-dose
treatment regimen.
• The same prophylactic regimens can be used after sexual intercourse to prevent episodes
of symptomatic infection in women in whom UTIs are temporally related to intercourse.
• Other patients for whom prophylaxis appears to have some merit include
o Men with chronic prostatitis.
o Patients undergoing prostatectomy both during the operation and in the postoperative
period.
o Pregnant women with asymptomatic bacteriuria
• All pregnant women should be screened for bacteriuria in the first trimester at 12-16
weeks of pregnancy and should be treated if bacteriuria is demonstrated/discovered
(quinolones should not be used in pregnancy).
Prognosis
• In patients with uncomplicated cystitis or pyelonephritis, treatment ordinarily results in
complete resolution of symptoms.
• Cystitis may also result in upper tract infection or in bacteremia especially during
instrumentation but little evidence suggests that renal impairment follows.
• Acute uncomplicated pyelonephritis in adults rarely progresses to renal functional
impairment and chronic renal disease.
• Repeated upper urinary tract infections often represent relapse rather than reinfection and
a vigorous search for renal calculi or an underlying urologic abnormality should be
undertaken.
• Repeated symptomatic UTIs in children and in adults with obstructive uropathy,
neurogenic bladder, structural renal disease or diabetes progress to chronic renal disease
with unusual frequency.
• Asymptomatic bacteriuria in these groups as well as in adults without urologic disease or
obstruction predisposes to increased numbers of episodes of symptomatic infection but
does not result in renal impairment in most instances.
Step 6: Definition and Causes of Acute Glomerulonephritis [AGN]

(15 minutes)
Acute Glomerulonephritis (AGN): The abrupt onset of hematuria and proteinuria often
accompanied by azotemia (i.e. decreased Glomerular filtration rate) and renal salt and water
retention.
ASK students to describe the causes of acute glomerulonephritis.
ALLOW few students to respond. Activity continues on the next page

Causes of Acute Glomerulonephritis

• The causal factors that underlie this syndrome can be broadly divided into infectious and
non infectious groups.
• Infectious causes/factors include
o Streptococcal: Post-streptococcal glomerulonephritis (PSGN) usually develops 1-3
weeks following acute infection with specific nephritogenic strains of group A beta-
hemolytic Streptococcus.
o The incidence of GN is approximately 5-10% in persons with pharyngitis and 25% in
those with skin infections.
o Non streptococcal post infectious glomerulonephritis are as outlined below.
Bacterial: Infective endocarditis, shunt nephritis, sepsis, pneumococcal
pneumonia, typhoid, secondary syphilis, meningococcemia, and infection with
methicillin-resistant Staphylococcus aureus (MRSA).
Viral: Hepatitis B, infectious mononucleosis, mumps, measles, varicella, vaccinia,
echovirus, parvovirus, and coxsackievirus.
Parasitic: Malaria, toxoplasmosis
• Non infectious causes/factors include
o Multisystem systemic diseases: Systemic lupus erythematosus, vasculitis, Henoch-
Schönlein purpura, Good pasture syndrome, Wegener granulomatosis.
o Primary glomerular diseases: Membranoproliferative glomerulonephritis, Berger
disease (i.e. immunoglobulin A [IgA] nephropathy), ‘pure’ mesangial proliferative
GN.
o Medications – e.g. cotrimoxazole, NSAIDS, thiazide diuretics, aspirin and penicillins
o Miscellaneous - Guillain-Barré syndrome, radiation of Wilm’s tumor, diphtheria-
pertussis-tetanus vaccine and serum sickness.
Step 7: Clinical Features and Diagnosis of Acute Glomerulonephritis

(15 minutes)
Clinical Features
• Taking a proper history is important and helpful
o Ask the patient about onset and duration of illness
o Identify a possible etiologic agent (e.g. streptococcal throat infection- pharyngitis,
skin infection- pyoderma)
o Recent fever, sore throat, joint pains, hepatitis, travel, valve replacement, and/or
intravenous drug use may be causative factors. Rheumatic fever rarely coexists with
PSGN.
o Identify systemic disease (e.g. arthralgia, diabetes).
o Assess the consequences of the disease process (e.g. uremic symptoms).
o Inquire about loss of appetite, generalized itching, tiredness, listlessness, nausea, easy
bruising, nose bleeds, facial swelling, leg edema, and shortness of breath
o Identify clinical features

o Inquire about edema, decreased volume and frequency of urination, systemic
hypertension, uremic symptoms, costovertebral tenderness (i.e. enlarged kidneys
(rare), and gross hematuria.
o Gross hematuria is the most common abnormality observed in patients with acute post
streptococcal glomerulonephritis and often manifests as smoky, coffee, or cola-
colored urine.
Physical Examination
• Signs of fluid overload
o Periorbital and/or pedal edema
o Edema and hypertension due to fluid overload (in 75% of patients)
o Crackles (i.e. if pulmonary edema)
o Jugular venous distention
• Ascites and pleural effusion
• Rash (i.e. vasculitis, Henoch-Schönlein purpura)
• Pallor
• Renal (costo-vertebral) angle fullness or tenderness
• Joint swelling, or tenderness
• Good pasture syndrome
• Hemolytic uremic syndrome
• Nephritis, interstitial
• Nephritis, lupus
• Drug toxicity
Laboratory Studies
• Investigations are mostly not available in primary health care facilities and therefore
patients suspected of having AGN should be referred for to hospitals for further
evaluation and treatment.
• Investigations can be done by examination of urine and blood, imaging studies and biopsy
as described below.
Urine
• Urinalysis and sediment examination –usually this may be available at the clinic facility-
evidence of blood and protein should prompt referral for further evaluation. Stop
medications that could cause this problem.
o Look for protein, cellular (i.e., RBC, WBC) casts, granular casts, and oval fat bodies.
In some instances, marked sterile pyuria is present.
o Finding RBC casts is an almost pathognomonic sign of AGN.
o Twenty-four–hour urine test for total protein and creatinine clearance.
Blood
• Blood urea and nitrogen (BUN)
• Serum creatinine
• Serum electrolytes especially serum potassium level
• Complete blood cell count
• Erythrocyte sedimentation rate (just supportive)
• Antistreptolysin-O titer (ASOT)

Imaging Studies
• Abdominal ultrasound
o Assesses renal size
o Excludes obstruction
Procedures
• Generally, a renal biopsy is not necessary for a diagnosis of acute glomerulonephritis.
• However in most cases it is important because histology guides both prognosis and
therapy.
Step 8: Treatment of Acute Glomerulonephritis (5 minutes)
• Normally treatment of acute glomerulonephritis requires to be done at higher centers.

• Do the pre-referral treatment and refer the patient to the higher centre.
Refer Students to Handout 4.3: Treatment of Acute Glomerulonephritis
• Escherichia coli cause approximately 80% of acute urinary tract infections in patients
without catheters, urologic abnormalities or calculi.
• The female urethra appears to be particularly prone to colonization with colonic gram-
negative bacilli because of its proximity to the anus, its short length (about 4 cm) and its
termination beneath the labia.
• Patients with cystitis usually report dysuria, frequency, urgency and suprapubic pain
• Microscopy of urine from symptomatic patients can be of great diagnostic value.
• Acute GN is characterized by the abrupt onset of hematuria and proteinuria often
accompanied by azotemia (i.e. decreased GFR) and renal salt and water retention.
• Streptococcal. Poststreptococcal Glomeruolnephritis usually develops 1-3 weeks
following acute infection with specific nephritogenic strains of group A beta-hemolytic
streptococcus.
• Describe clinical features of urinary tract infection.

• Mention the common causative organisms of hospital acquired urinary tract infections.
• What are clinical features of acute glomerulonephritis?
• Describe the treatment of acute glomerulonephritis.
References
McGraw Hill.
• Cumming A.D. (2003). Davidson’s Principles and Practice of Medicine. Edingurgh,

• MOHSW (2005). Tanzania National Formulary. Dar es Salaam, Tanzania: Ministry of
Saunders.

Handout 4.1 Catheter Associated UTI
• Bacteriuria develops in at least 10 to 15% of hospitalized patients with indwelling

urethral catheters. This rate goes up to 100% if a catheter needs to stay in longer than 2
weeks.
• The risk of infection is about 3 to 5% per day of catheterization
• E. coli, Proteus, Pseudomonas, Klebsiella, Serratia, staphylococci, enterococci, and
Candida usually cause these infections.
• Many infecting strains display markedly greater antimicrobial resistance than organisms
that cause community-acquired UTIs.
• Factors associated with an increased risk of catheter-associated UTI include female sex,
prolonged catheterization, severe underlying illness, disconnection of the catheter and
drainage tube and lack of systemic antimicrobial therapy.
• Clinically, most catheter-associated infections cause minimal symptoms and no fever and
often resolve after withdrawal of the catheter.
• Gram-negative bacteremia which follows catheter-associated bacteriuria in 1 to 2% of
cases is the most significant recognized complication of catheter-induced UTIs.
• Catheter-associated UTIs can sometimes be prevented in patients catheterized for <2
weeks by use of a sterile closed collecting system by attention to aseptic technique during
insertion and care of the catheter and by measures to minimize cross-infection.
• Newer studies are recommended to remove catheters after 2 days (i.e. post operatively)
unless they are needed for to maintain strict input and output documentation, for those
seriously ill (e.g. on a ventilator), for those with obstruction or for those with grade 3 or 4
decubitus ulcers and incontinence.
Background Information of UTI

• Acute infections of the urinary tract can be subdivided into two general anatomic
categories.
o Lower tract infection (urethritis and cystitis).
o Upper tract infection (acute pyelonephritis, prostatitis, and intrarenal and perinephric
abscesses).
• Infections at these various sites may occur together or independently and may either be
asymptomatic or present as one of the clinical syndromes described below.
• Infections of the urethra and bladder are often considered superficial (or mucosal)
infections while prostatitis, pyelonephritis, and renal suppuration signify tissue invasion.

Handout 4.2 Treatment of UTI
Treatment Regimens for Bacterial Urinary Tract Infections
Condition Characteristic Mitigating Recommended Empirical

Pathogens Circumstances Treatment
Acute Escherichia None 3-Day regimens: oral
uncomplicated coli, TMP/SMZ, TMP,
cystitis in women Staphylococcus quinolone;
saprophyticus, 7-day regimen:
Proteus macrocrystalline
mirabilis, nitrofurantoin
Klebsiella Diabetes, symptoms for >7 Consider 7 days regimen:
pneumoniae d, recent UTI, use of oral TMP/SMZ, TMP,
diaphragm, age >65 years quinolone
Pregnancy Consider 7-days regimen:
oral amoxicillin,
macrocrystalline
nitrofurantoin, cefpodoxime
proxetil, or TMP/SMZ
Acute E. coli, P. Mild to moderate illness, Oral quinolone **for 7-14
uncomplicated mirabilis, S. no nausea or vomiting; days (initial dose given IV if
pyelonephritis in saprophyticus outpatient therapy desired); or single-dose
women ceftriaxone or gentamycin
IV followed by oral
TMP/SMZ for 14 days
**quinolones are usually not
recommended in pregnancy
but need to weigh potential
side effect of medication vs
damage due to the infection
itself
Severe illness or possible Parenteral ceftriaxone,
urosepsis: hospitalization gentamicin (± ampicillin), ,
required or TMP/SMZ for 14 days
Complicated UTI E. coli, Mild to moderate illness, Oralc quinolone for 10-14
in men and women Proteus, no nausea or vomiting: days
(note that; all UTI Klebsiella, outpatient therapy If Chlamydia is suspected
are considered Pseudomonas, give doxycycline bid x 7
complicated in Serratia, days
men) enterococci, Severe illness or possible IV/IM ampicillin+
staphylococci urosepsis: hospitalization gentamycin, ceftriaxone, or
GC/chlamydia required TMP/SMZ for 10-21 days

Handout 4.3 Treatment of Acute Glomerulonephritis
Medical Care
• Treatment of acute PSGN is mainly supportive because there is no specific therapy for
renal disease.
• Treat the underlying infections when acute GN is associated with chronic infections.
• Antimicrobial therapy
o Antibiotics (e.g. penicillin) are used to control local symptoms and to prevent spread
of infection to close contacts.
o Antimicrobial therapy does not appear to prevent the development of GN except if
given within the first 36 hours.
• Loop diuretic therapy
o Loop diuretics (not thiazides as they can cause AGN) may be required in patients who
are edematous and hypertensive in order to remove excess fluid and to correct
hypertension.
o Relieves edema and controls volume thereby helping to control volume-related
elevation in BP.
o Vasodilator drugs (e.g. nitroprusside, nifedipine, hydralazine, diazoxide) may be used
if severe hypertension or encephalopathy is present.
o Glucocorticoids and cytotoxic agents are of no value except in severe cases of PSGN.
Diet
• Sodium and fluid restriction - For treatment of signs and symptoms of fluid retention
(e.g., edema, pulmonary edema). However if patient is in shock may need to resuscitation
with fluid until stable
Activity
• Recommend bed rest until signs of Glomerular inflammation and circulatory congestion
subside. If patient can ambulate, it might be important to do some ambulation daily to
prevent deep vein thrombosis (DVT).
• Prolonged inactivity does not benefit in the patient recovery process and can increase the
risk of development of DVT
Medication
Penicillin V
• Adult dose of 500,000 IU PO q6-8h
• Pediatric dose of 25,000-90,000 U/kg/d PO in 3-6 divided doses
Furosemide (Lasix)
Adult
• In oedema dose given initially 40-80 mg PO, titrate to satisfactory diuresis in 20 - 40mg
increments q6h not to exceed 200 mg per dose once effective single dose determined,
may repeat qid or tid. Need to watch the renal function carefully with using high dose
furosemide as this can put someone into renal failure. Decrease dosing after initial
therapy and monitor electrolytes (especially potassium), BUN and creatinine

• In hypertension dose given is 20-40 mg PO bid titrated to desired response. If 40 mg PO
bid does not lead to clinically significant response, add another antihypertensive agent
rather than increasing the dose. Note that loop diuretic is a very weak antihypertensive
and may need to use a different agent. Do not lower their blood pressure too fast or too
low as hypotension can cause further damage to the kidneys.
Paediatric
• Dose is 0.5-1 mg/kg PO IV qid.
• In the newborn and premature babies, daily dose should not exceed 1 mg/kg.
Nifedipine (Adalat)
Adult
• 10mg IR cap PO tid, not to exceed 120mg/d (not usually recommended for HTN as it can
cause hypotension)
• 30-60 mg SR(extended release) tab PO daily ; not to exceed 90-120 mg/d
Hydralazine (Apresoline)
Adult
• 10 mg PO bid to qid gradually titrate to 25-50 mg qid (max 300 mg daily)
• Alternatively 5-10 mg slow IV initially then repeat dose after 20-30 minutes if necessary
• Maintenance dose is 25-50 mg 4 times daily.
• Monitor and avoid hypotension.

Session 5: Nephrotic Syndrome and Chronic Kidney
Disease
Prerequisites
• None
Learning Objectives
• Define nephrotic syndrome and chronic kidney disease
• Describe classification of nephrotic syndrome and chronic kidney disease
• Describe the clinical features of nephrotic syndrome and chronic kidney disease
• Identify relevant investigations for the diagnosis nephrotic syndrome and chronic kidney
disease
• Explain treatment of nephrotic syndrome and chronic kidney disease
• Describe prevention of nephrotic syndrome and chronic kidney disease
Resources Needed
• Handout 5.1: Investigations and Treatment of Nephrotic Syndrome
• Handout 5.2: Investigation and Treatment of Chronic Kidney Disease
SESSION OVERVIEW
Activity/
Step Time Content
Method
Definition, Causes and Pathogenesis of
Nephrotic Syndrome
Presentation,
3 25 minutes Clinical Features of Nephrotic Syndrome
Group Discussion
Differential Diagnosis, Management,
4 15 minutes Presentation Complications and Prognosis of Nephrotic
Syndrome
Definition, Causes, Pathophysiology and
Epidemiology of Chronic Kidney Disease
Presentation, Clinical Features of Chronic Kidney
6 15 minutes
Brainstorm Disease
7 10 minutes Presentations
Treatment of Chronic Kidney Disease

Session 5: Nephrotic Syndrome and Chronic Kidney Disease 61
SESSION CONTENT

Step 2: Definition, Causes and Pathogenesis of Nephrotic Syndrome

(15 minutes)
Nephrotic syndrome: A clinical complex characterized by a number of renal and extra-renal
features.
• The most prominent features are
o Proteinuria of >3.5g per 24 hours (in practice, >3.0 to 3.5 g per 24 h)
o hypoalbuminemia
o Edema
o Hyperlipidemia
o Lipiduria
o Hypercoagulability
• It should be stressed that the key component is proteinuria which results from altered
permeability of the glomerular filtration barrier for protein.
• The other components of the Nephrotic syndrome and the ensuing metabolic
complications are all secondary to urine protein loss and can occur with lesser degrees of
proteinuria or may be absent even in patients with massive proteinuria.
Causes of Nephrotic Syndrome

• There are many specific causes of nephrotic syndrome.
• In all cases injury to glomeruli is an essential feature.
• Nephrotic syndrome may affect adults and children of both sexes and of any race.
• It may occur in typical form or in association with nephritic syndrome.
• The latter connotes glomerular inflammation with hematuria and impaired kidney
function.
• Mainly is due to either primary and or secondary causes.
Primary Causes
• Disease specific to the kidneys
• Primary causes of Nephrotic syndrome include in approximate order of frequency
o Minimal-change nephropathy
o Focal glomerulosclerosis
o Membranous nephropathy
o Hereditary nephropathies
Secondary Causes
• Being a renal manifestation of a systemic general illness
• Secondary causes include again in order of approximate frequency
o Diabetes mellitus (DM)

o Systemic lupus erythematosus (SLE)
o Amyloidosis and paraproteinemias
o Viral infections (e.g. hepatitis B, hepatitis C, HIV)
o Pre-eclampsia
Other Causes
• Medication can cause nephrotic syndrome.

• This includes the very infrequent occurrence of minimal-change nephropathy with
NSAID use and the occurrence of membranous nephropathy with the administration of
gold and penicillamine which are older drugs used for rheumatic diseases.
Pathophysiology
• Proteinuria that is more than 85% albumin is selective proteinuria.
• Albumin has a net negative charge and it is proposed that loss of glomerular membrane
negative charges could be important in causing albuminuria.
• Nonselective proteinuria being a glomerular leakage of all plasma proteins would not
involve changes in glomerular net charge but rather a generalized defect in permeability.
• This construct does not permit clear-cut separation of causes of proteinuria except in
minimal-change nephropathy in which proteinuria is selective.
Pathogenesis of Oedema
• An increase in glomerular permeability leads to albuminuria and eventually to
hypoalbuminemia.
• In turn hypoalbuminemia lowers the plasma colloid osmotic pressure causing greater
transcapillary filtration of water throughout the body and thus the development of edema.
Metabolic Consequences of Proteinuria

• In nephrotic syndrome levels of serum lipids are usually elevated.
• The loss of antithrombin III and plasminogen via urine along with the simultaneous
increase in clotting factors especially factors I, VII, VIII and X increases the risk for
venous thrombosis and pulmonary embolism.
• Vitamin D binding protein may be lost in the urine leading to hypovitaminosis D with
malabsorption of calcium and development of bone disease.
• Urinary immunoglobulin losses may lower the patient's resistance to infections and
increase the risk of infections.
Step 3: Clinical Features of Nephrotic Syndrome (25 minutes)
Activity: Small Group Discussion (15 minutes)
DIVIDE students into small manageable groups.
ASK students to describe the clinical features of nephrotic syndrome.
GIVE students 10 minutes to discuss in small groups.
INVITE one group to present their responses and record responses on the board/flip chart.
Activity continued on next page.

History
• The first sign of nephrotic syndrome in children is usually swelling of the face followed
by swelling of the entire body.
• Adults can present with dependent edema.
• Foamy urine may be a presenting feature.
• A thrombotic complication such as deep vein thrombosis of the calf veins or even a
pulmonary embolus may be the first clue indicating Nephrotic syndrome.
• Additional historical features that appear can be related to the cause of Nephrotic
syndrome.
• Recent start of a non steroidal anti-inflammatory drug (NSAID) or a 10-year history of
diabetes may be very relevant.
Physical
• Edema is the predominant feature of nephrotic syndrome and initially develops around
the eyes and legs.
• With time edema becomes generalized and may be associated with an increase in weight
and development of ascites or pleural effusions.
• Haematuria and hypertension manifest in a minority of patients.
• Additional features on exam will vary according to the cause and as a result of whether or
not renal function impairment exists.
• In cases of longstanding diabetes there may be diabetic retinopathy which correlates
closely with diabetic nephropathy.
• If the kidney function is reduced there may be hypertension and/or anemia
Step 4: Differential Diagnosis, Management, Complications and Prognosis

of Nephrotic Syndrome (15 minutes)
• Diabetic nephropathy
• Focal segmental glomerulosclerosis
• Glomerulonephritis
• HIV nephropathy
• IgA nephropathy
• Minimal change kidney disease
• Light chain-associated renal disorders
• Nephritis
• Radiation
• Sickle cell nephropathy
• Heart failure
• Liver cirrhosis with portal hypertension

Investigations
• Perform dipstick screening method for detection of protein concentrations in urine.
• The dipstick is a quick method of screening and detecting proteinuria, hematuria, and
pyuria and provides an estimate of the specific gravity (urine-concentrating capacity).
• More laboratory investigations can be done at higher centers.
Refer Students to Handout 5.1: Investigations and Treatment of Nephrotic
Syndrome
Treatment
• Provide pre-referral treatment
• Refer the patient to the higher centre for further investigation and management
Complications
• Infection is a major concern in nephrotic syndrome.
• Atherosclerotic vascular disease appears to occur in greater frequency in subjects with
nephrotic syndrome than in healthy subjects of the same age.
• Hypocalcemia is common in nephrotic syndrome but rather than being a true
hypocalcemia it is usually caused by a low serum albumin level.
• Venous thrombosis and pulmonary embolism are well known complications of nephrotic
syndrome.
• Hypovolemia is generally observed only when the patient's serum albumin level is less
than 1.5 g/dl.
• Acute renal failure may indicate an underlying glomerulonephritis but is more often
precipitated by hypovolemia or sepsis.
• Hypertension related to fluid retention and reduced kidney function may occur.
• Failure to thrive (in children) may develop in patients with chronic edema including
ascites and pleural effusion.
Prognosis
• The prognosis for patients with primary nephrotic syndrome depends on its cause.
• The prognosis with congenital nephrotic syndrome is poor and survival beyond several
months is possible only with dialysis and kidney transplantation.
• Only about 20% of patients with focal segmental glomerulosclerosis undergo remission
of proteinuria. An additional 10% improve but remain proteinuric.
• Many patients experiencing frequent relapses become steroid-dependent or become
steroid-resistant.
• End-stage renal disease develops in 25-30% of patients with focal segmental
glomerulosclerosis (FSGS) by 5 years and in 30-40% of these patients by 10 years.
• The prognosis for children with minimal-change nephropathy is very good.
Step 5: Definition, Causes, Pathophysiology and Epidemiology of Chronic

Kidney Disease (15 minutes)
Definition
• Chronic kidney disease is characterized by an irreversible deterioration of renal function
that gradually progresses to end-stage renal disease (ESRD)
Or

• As evidence of structural or functional kidney abnormalities (abnormal urinalysis,
imaging studies, or histology) that persist for at least 3 months with or without a
decreased glomerular filtration rate (GFR) as defined by a GFR of less than 60 ml/min
per 1.73 m2
Causes of Chronic Kidney Disease

• Diabetes Mellitus
• Uncontrolled hypertension
• Glomerulonephritis
• Polycystic Kidney Disease
• Chronic urinary tract infections (recurrent Pyelonephritis)
• Nephrolithiasis (obstruction)
• Vasculitis (e.g. Systemic lupus erythematosus)
• Drug toxicity
• Hypoplastic or dysplastic kidneys
• Reflux nephropathy
• Focal segmental glomerulosclerosis
• Polycystic kidney disease (both autosomal-recessive and autosomal-dominant varieties)
Pathophysiology
Despite the diverse etiologies, once chronic kidney disease develops, the subsequent response
of the failing kidney is similar.
Epidemiology
Race
In the United States, ESRD rates in blacks are 2.7 times higher than in whites.
Sex
The incidence and rate of progression to ESRD are equal in both sexes, although obstructive
uropathies are more common in males.
Age
The frequency of chronic kidney disease increases with age and is much more common in
adults than children.
Step 6: Clinical Features of Chronic Kidney Diseases (15 minutes)
ASK students to outline the clinical features of chronic kidney disease.
ALLOW few students to respond.

History
• Chronic kidney disease is asymptomatic in its earliest although urinalysis findings or
blood pressure may be abnormal.
• As chronic kidney disease progresses to more advanced stages signs and symptoms
greatly increase.
o Polydipsia and nocturia (secondary to a reduced capacity to concentrate the urine)
may be one of the earliest symptoms that indicate a diagnosis of chronic kidney
disease.
o The signs and symptoms in advanced chronic kidney disease may including the
following
Volume overload (edema)
Hyperkalemia
Metabolic acidosis
Hypertension
Anemia
Bone disease (termed osteodystrophy)
Anorexia, nausea, vomiting
• The absolute serum levels of BUN or creatinine do not directly correlate with the
development of these symptoms.
• However, estimated glomerular filtration rate (eGFR) seems to be associated with a
stronger correlation.
Physical
The findings vary depending on the severity of kidney failure and can range from an absence
of any physical findings to the presence of one or more of the following
• Anemia
• Short stature
• Hypertension
• Osteodystrophy
• Cardiac abnormalities such as left ventricular hypertrophy (LVH) and pericarditis
• Peripheral neuropathy
• CNS abnormalities such ranging from loss of concentration and lethargy to seizures and
coma
Step 7: Differential Diagnosis, Investigations and Treatment of Chronic

Kidney Disease (10 minutes)
• Acute renal failure
• Rapidly progressive glomerulonephritis
Investigations
• Perform dipstick screening method for detection of proteins, blood and pus in urine
pyuria and provides an estimate of the specific gravity (urine-concentrating capacity).
• More laboratory investigations can be done at higher centers, and therefore refer the
patient to hospital.

Refer Students to Handout 5.2: Investigations and Treatment of Chronic
Kidney Disease
Treatment
• Provide pre-referral treatment.
• One of the most important treatments to prevent worsening kidney disease is to identify
and control blood pressure: goal blood pressure would be <130/80.
• Refer the patient to the higher centre for further investigation and management.
• Nephrotic syndrome is a clinical complex characterized by a number of renal and

extrarenal features.
• An increase in glomerular permeability leads to albuminuria and eventually to
hypoalbuminemia
• Edema is the predominant feature of nephrotic syndrome and initially develops around
the eyes and legs and later on becomes generalized.
• Chronic kidney disease is characterized by an irreversible deterioration of renal function
that gradually progresses to end-stage renal disease (ESRD).
• Polydipsia and nocturia may be one of the earliest symptoms that indicate a diagnosis of
chronic kidney disease.
• Urine examination is perhaps the most important test and should be considered a part of
the physical examination.
• What are the clinical features of nephrotic syndrome?

• Mention differential diagnoses of nephrotic syndrome.
• Mention clinical features of chronic kidney disease.
• Describe the management of nephrotic syndrome and chronic kidney disease.
References
McGraw Hill.
• Cumming A.D. (2003). Davidson’s Principles and Practice of Medicine. Edinburgh,
Saunders.

Handout 5.1: Investigations and Treatment of Nephrotic
Syndrome
Laboratory Studies
• Urinalysis is the first test used in the diagnosis of Nephrotic syndrome
• Nephrotic range proteinuria will be apparent by 3+ or 4+ readings on the dipstick or by
semi quantitative testing by sulfosalicylic acid
• A 3+ reading is 300 mg/dl of urinary protein or more which is 3 g/l or more and thus in
the Nephrotic range
• The chemistry of the dipsticks is such that albumin is the major protein that is tested
• The urine sediment exam may show cells and/or casts
• The presence of more than 2 red blood cells (RBCs) per high power field is indicative of
microhematuria
• Urinary protein is measured by a timed collection or a single spot collection
• In healthy individuals there are no more than 150 mg of total protein in a 24-hour urine
collection
• A single spot urine collection is much easier to obtain
• Serum tests for kidney function are essential
• Serum creatinine will be in the normal range in uncomplicated nephrotic syndrome such
as that occurring in minimal-change nephropathy
• The serum albumin is classically low in nephrotic syndrome being below its normal range
of 3.5-4.5 g/dl
Imaging Studies
• Ultrasonographic
Scanning can be used to determine whether a patient possesses 2 kidneys and to
demonstrate their echogenicity.
Note: Individuals with a single kidney may be prone to developing focal glomerulosclerosis.
Having only one kidney is also a relative contraindication to kidney biopsy.
Treatment
• Acute Management of Adult Nephrotic Syndrome
o The principles for acute management of adults with nephrotic syndrome are similar to
those for children.
o Diuretics will be needed such as Furosemide, Spironolactone and even Metolazone
may be used.
o Volume depletion may occur with diuretic use which should be monitored by
assessment of symptoms, weight, pulse and blood pressure.
o Anticoagulation has been advocated by some for use in preventing thromboembolic
complications but its use in primary prevention is of unproven value.
o Hypolipidemic agents may be used but if the nephrotic syndrome cannot be controlled
there will be persistent hyperlipidemia.
o In secondary Nephrotic syndrome such as that associated with diabetic nephropathy,
angiotensin-converting enzyme (ACE) inhibitors and/or angiotensin II receptor
blockers are widely used.

Specific Treatment of Nephrotic Syndrome
• Depends on the disease's cause.
• Glucocorticosteroids such as prednisone are used for minimal-change nephropathy.
• Prednisone and cyclophosphamide are useful in some forms of lupus nephritis.
• Secondary amyloidosis with Nephrotic syndrome may respond to anti-inflammatory
treatment of the primary disease.
Diet
• For patients with Nephrotic syndrome their diet should provide adequate energy (caloric)
intake and adequate protein (1-2 g/kg/d).
• Supplemental dietary protein is of no proven value.
• A diet with no added salt will help to limit fluid overload.
• Management of hyperlipidemia could be of some importance if the Nephrotic state is
prolonged.
• Fluid restriction per se is not required.
Activity
• There are no activity restrictions for patients with Nephrotic syndrome
• Ongoing activity rather than bed rest will reduce the risk of blood clots

Handout 5.2: Investigation and Treatment of Chronic Kidney
Disease
Laboratory Studies
• Urine examination is perhaps the most important test and should be considered a part of
the physical examination.
• It can be performed at the bedside or in the clinic using a fresh urine sample
• An initial evaluation consists of a multitest detection strip (dipstick) test followed by
urine microscopy
pyuria and provides an estimate of the specific gravity (urine-concentrating capacity)
• Urine microscopy is performed on a centrifuge-spun urine specimen to look for RBCs,
WBCs, and casts.
• BUN and serum creatinine assessments are the most important tests
• Anemia is an important clinical finding in chronic kidney disease and a CBC count is an
important investigation both in the initial evaluation and the subsequent follow-up in
these children.
Imaging Studies
• Imaging studies help in confirming the diagnosis of chronic kidney disease and may also
provide clues to its etiology.
• The following studies are helpful
o Ultrasonography
o Voiding cystourethrography
o CT scanning
o Skeletal survey
Procedures
• Kidney biopsy-rarely needed
Treatment
• Patients with chronic kidney disease should be evaluated to determine the following
o Diagnosis (type of kidney disease)
o Comorbid conditions (such as hyperlipidemia)
o Severity which is based on level of kidney function
o Complications related to level of kidney function
o Risk for loss of kidney function
o Risk for cardiovascular disease
Treatment of Chronic Kidney Disease

• Specific therapy based on diagnosis ( e.g. diabetes, hypertension)
• As above it is essential to treat hypertension. Goal BP is <130/80
• Evaluation and management of reversible causes of renal dysfunction
• Prevention and treatment of complications of decreased kidney function (e.g. anemia,
bone disease, cardiovascular manifestations, hypertension, growth failure)
• Evaluation and management of comorbid conditions
• Slowing the loss of kidney function

• Preparation for kidney failure therapy
• Replacement of kidney function with dialysis and transplantation if signs and symptoms
of uremia are present
Surgical Care
Surgical intervention is often recommended in patients with obstructive uropathy to relieve
acute kidney failure due to initial or recurrent obstruction.
Diet and Electrolytes Required

• Energy
• Protein
• Phosphorus and calcium
• Potassium
• Sodium and fluid
Follow-up
Further Outpatient Care

• All patients require regular follow-up on an outpatient basis in a dedicated chronic kidney
disease clinic until initiation of long-term renal replacement therapy.
• This involves a multidisciplinary team approach that involves the nephrologist, primary
care physician, renal dietitian, nurse and social worker.
• So refer once you make a diagnosis of chronic kidney disease for expert care.
Prognosis
• Once chronic kidney disease occurs, progression to end-stage renal disease (ESRD)
appears certain.
• However, the rate of progression depends on the underlying diagnosis on the successful
implementation of secondary preventive measures and on the individual patient.
Patient Education
• Children with chronic kidney disease and their families should receive education about
the importance of compliance with secondary preventative measures, natural disease
progression, prescribed medications (highlighting their potential benefits and adverse
effects), diet and types of long-term renal replacement modalities.

Session 6: Pyogenic and Viral Skin Infections, Urticaria &
Drug Allergies
Prerequisites
• None
Learning Objectives
At the end of this session, students will be able to:
• Define specific kinds of pyogenic skin infections
• Outline the clinical presentation of pyogenic and viral skin infections
• Identify the treatment methods for the stated skin infections
• Describe causes and clinical features of drug allergies
• Explain causes, clinical features and management of boils
Resources Needed
• Handout 6.1: Various Viral Skin Infections
• Handout 6.2: Other Skin Conditions
• Handout 6.3: Pictures on Angioedema, Urticaria, Morbilliform Drug Rash, Stevens
Johnson Syndrome and Toxic Epidermal Necrolysis (TEN)
SESSION OVERVIEW
Activity/
Step Time Content
Method
Presentation, Definition, Aetiology and Clinical Features
2 20 minutes
Buzz of Impetigo
Investigations, Treatment and Complications
of Impetigo
Presentation, Definition, Clinical Features and Treatment
4 20 minutes
Brainstorm of Different Viral Skin Infections
Definition and Aetiology of Drug Allergy
and Urticaria
Clinical Features, Diagnosis and Treatment
of Drug Allergies
Definition, Aetiology, Clinical Features,
Investigations and Treatment of Boil
8 05 minutes Presentation Key points

Session 6: Pyogenic and Viral Skin Infections, Urticaria & Drug Allergies 73
SESSION CONTENT

READ or ASK the students to read the learning objectives and clarify.
Step 2: Definition, Aetiology and Clinical Features of Impetigo

(20 minutes)
Impetigo: An acute contagious superficial pyogenic skin infection that occurs most
commonly in children especially those who live in hot humid climate
Aetiology
Aetiologically impetigo is grouped into two types
• Non-bullous impetigo caused by Staphylococcus aureus, group A streptococcus
(Streptococcus pyogenes) or both
• Bullous impetigo caused by Staphylococcus aureus, group II type 71 which produce
exfoliatin toxin
TELL students to list down clinical features of impetigo.
SELECT few pairs to respond.
RECORD the answers on the board/flipchart.
Clinical Features
• Impetigo often develops at the site of minor trauma or scratched skin where it is a portal
of entry.
• Non bullous impetigo affects mostly ages 2 - 5 years.
• Bullous impetigo affects mostly newborns and old infants.
• Lesions usually present after days or weeks rather than months.
• The lesions are usually painless although other patients may report burning and pruritis.
• Constitutional symptoms are usually absent.
Non Bullous Impetigo

• Lesion begins as thin walled vesicles or pustules on an erythematous base.
• The lesions promptly rupture releasing their serum which dries and form a light brown
honey-coloured crust.

• Multiple lesions generally occur at the same site often coalescing.
• The affected areas of the skin may enlarge as the infection spread peripherally.
• Skin on any part of the body can be involved but the face and extremities are affected
most common.
• Pruritis of infected area may result into excoriation from scratching.
• As the lesions resolve either spontaneously or after antibiotic treatment, the crusts slough
from affected areas and heal without scarring.
• If the course of disease is prolonged and patients do not seek treatment as many as 90%
will develop regional lymphadenopathy.
Bullous Impetigo
• Lesions may form on grossly normal or previously traumatized skin
• The vesicles do not rupture as easily or quickly as in non bullous lesions but they do
enlarge into bullae that are usually 1-2 cm
• Initially the bullae contain clear yellow fluid that subsequently turns cloudy and dark
yellow
• After 1 to 3 days the lesions rupture to leave a thin light brown vanish like crust
• Central healing results in circinate lesions
Step 3: Investigations, Treatment and Complications of Impetigo

(15 minutes)
Investigations
• Impetigo can usually be diagnosed from the clinical picture, but laboratory is supportive
and mainly for treatment purposes.
• Culture of the fluid and involved skin confirms the diagnosis and definite causation
organisms for choosing appropriate antibiotic therapy.
Treatment
• Medical care
o Topical therapy
First remove the infected crusts with soap and water
Topical mupirocin may be the only necessary therapy
Studies show that topical antibiotics are as effective as oral antibiotics e.g.
erythromycin
Disadvantage of topical treatment is the inability to eradicate organisms from the
blood
• Systemic Therapy
o When infection is moderate to severe accompanied by lymphadenopathy systemic
therapy is indicated
o Streptococci pyogenes are sensitive to penicillin
o Substitute penicillin with clindamycin in patients allergic to penicillin
o In erythromycin resistant Staphylococcus aureus, substitute with cephalosporin
(cephalexin and clidamycin)
o Phenoxymethylpenicillin (penicillin V)500mg/qid PO for 10days (adult dosing)
o Cephalexin 500mg PO every 6 hours for 10 days (adult dosing)
o Clindamycin 300mg PO every 6 hours for 10 days (adult dosing)

Complications
• Acute post streptococcal glomerulonephitis
• Rheumatic carditis
• Erysipelas
• Erthema muliforme
• Urticaria
Step 4: Definition, Clinical Features and Treatment of Different Viral Skin

Infections (20 minutes)
ASK what are types of virus responsible for skin conditions?
RECORD the responses on the board/ flip chart.
• Viral skin infection is inflammation of the skin caused by various types of virus such as
o Herpes virus
o Varicella zoster
o Human papilloma virus
Herpes Zoster (Shingles)

• Herpes zoster (shingles) is an infection with herpes zoster virus result from reactivation of
the varricella zoster virus.
Clinical Features
• Shingles never occurs as primary infection but results from reactivation of latent
varicella zoster virus from dorsal root and/or cranial nerve ganglia
• Reactivation may be preceded by a prodromal phase of tingling or pain that is followed
by eruption of painful and tender blistering in a dermatomal distribution
• Blisters tend to occur in crops and may become pustules which later crust over
• The rash lasts for 2-4 weeks and is usually more severe in the elderly
• It is very rare for more than one dermatome to be involved
• There can be ongoing pain in the area of the shingles lesions long after the blisters have
resolved, this is called post-herpetic neuralgia.
Treatment
• Herpes zoster requires analgesic
• Antibiotics are only given if there is secondary bacterial infection
• Antiviral drugs used for 7 days help to shortage the attack if given early stage of illness.
These drugs include
o Acyclovir 800mg 5 times daily or
o Valacyclovir 1g three times daily or

o Famciclovir 500mg 3 times daily
• If ocular involvement (VI dermatome), this should prompt referral to eye specialist for
appropriate management
Complications
• Complications of herpes zoster include
o Severe persistent pain (post-herpetic neuralgia)
o Ocular disease that can necessitate removal of the eyeball (evisceration)
o Rarely motor neuropathy
Herpes Simplex Virus (HSV)

• This is infection of human being caused by a virus called herpes simplex virus (HSV)
occurring in two genomic subtypes (type I and II).
• HSV type I is transmitted through direct contact and droplet infection.
• HSV type II infection occurs after puberty and usually transmitted through sexual
intercourse.
Epidemiology of Herpes Simplex Virus (HSV)

• HSV I is the major cause herpetic stomatitis, herpes labialis (cold acne),
Keratoconjuctivitis and encephalitis.
• HSV-2 causes genital herpes and may be responsible for systemic infection in immune
compromised host.
• Transmission for HSV I is usually via mouth or occasionally the skin.
• Primary lesion can go unnoticed or can undergo severe inflammatory reaction with
vesicle formation leading to painful ulcers (gingivostomatitis).
• The virus then remain latent most commonly in trigeminal ganglia but may be activated
by stress, trauma, febrile illness and irradiation produce the recurrent form of the disease
as herpes labialis (cold sore).
• Approximately 70% of population is affected with HSV I and recurrent infection occur in
1/3 of individuals.
• Reactivation produces localized paraesthesias in the lip before the appearance of cold sore
• Transmission for HSV 2-infection through genitalia is usually more severe and
recurrences are common.
• The viruses remains latent in sacral ganglia and during recurrence can produce a
radiculomyelopathy with pain in the groin, buttocks and upper thighs.
• Primary anorectal herpes infection is common in male homosexuals.
• In patients with AIDS or receiving intensive cancer treatment may develop disseminated
HSV infected involving viscera.
• In severe cases death may result from hepatitis and encephalitis.
• Neonates may develop primary HSV infection following vagina delivery in the active
genital HSV infected mother.
• The disease in babies varies from localized skin lesions to widespread visceral diseases
with encephalitis.
Clinical Features
• Most people are affected in early childhood and are usually subclinical
• Occasionally it can cause pyrexia as primary illness, with either cluster of painful blister
on the face or gingivostomalitis.

• It can inoculate into site of trauma and present as painful blister/pustules at the fingers
(herpetic Withlow)
• Other complications of HSV infection include
o Corneal ulceration
o Eczema herpeticum
o Chronic perineal ulceration in AIDS patients
Treatment
• Oral valacyclovir (500 mg twice daily for 3-5 days) or Acyclovir (400 mg 3 times a day
for 5 days) for primary HSV and painful genital HSV
• Recurrent cold sore treated with acyclovir cream
• Intravenous Acyclovir may be used in severe lesions such as in immune suppressed
patients
Refer students to:

Handout 6.1: Various Viral Skin Infections
Handout 6.2: Other Skin Conditions
Step 5: Definition and Aetiology of Drug Allergy and Urticaria

(15 minutes)
• Urticaria: A skin reaction characterized by pruritic, red wheals

• Lesions may vary from a small point to a large area
• Individual lesions rarely last more than 24 hours
• When deep dermal and subcutaneous tissues are also swollen, this reaction is known as
angioedema
• Angioedema may involve mucous membranes and may be part of a life-threatening
anaphylactic reaction
• Urticarial lesions along with pruritus and morbilliform (or maculopapular) eruption are
among the most frequent types of cutaneous reactions to drugs
Aetiology
• Drug Induced Urticaria
May be caused by three mechanisms
o IgE-dependent mechanism
o Circulating immune complexes (serum sickness)
o Non-immunologic activation of effector pathways
It may also be idiopathic (unknown cause)
Step 6: Clinical Features, Diagnosis and Treatment of Drug Allergies

(15 minutes)
Clinical Features
• IgE-dependent urticarial reactions usually occur within 36 hours although it can also
occur within minutes.

• Reactions occurring within minutes to hours of drug exposure are termed immediate
reactions whereas those occurring 12 to 36 hours after drug exposure are termed
accelerated reactions.
• Immune complex induced urticaria associated with serum sickness usually occurs from 6
to 12 days after first exposure.
• In this syndrome urticarial eruption may be accompanied by
o Fever
o Haematuria
o Arthralgias
o Hepatic dysfunction, and neurologic symptoms
• Certain drugs such as NSAIDs, angiotensin-converting enzyme (ACE) inhibitors and
radiographic dyes may induce urticarial reactions, angioedema and anaphylaxis in the
absence of drug-specific antibody.
• Although ACE inhibitors, aspirin, penicillin and blood products are the most frequent
causes of urticarial eruptions, urticaria has been observed in association with nearly all
drugs.
• Drugs also may cause chronic urticaria which lasts more than 6 week. Aspirin frequently
exacerbates this problem.
Treatment
• Urticaria or angioedema depends on the severity of the reaction and the rate at which it is
evolving.
• In severe cases especially with respiratory or cardiovascular compromise epinephrine is
the mainstay of therapy but its effect is reduced in patients using beta blockers.
• For more seriously affected patients treatment with systemic glucocorticoids sometimes
intravenously administered are helpful.
• In addition to drug withdrawal for patients with only cutaneous symptoms and without
symptoms of angioedema or anaphylaxis oral antihistamines are usually sufficient.
Diagnosis and Management of Drug Reactions

• Possible causes of an adverse reaction can be assessed as
o Definite
o Probable
o Possible or unlikely
• Based on six variables
o Previous experience with the drug in the general population
o Alternative etiologic candidates
o Timing of events
o Drug levels or evidence of overdose
o Patient reaction to drug discontinuation
o Patient reaction to rechallenge
Refer student to Handout 6.3: Pictures on Angioedema, Urticaria, Morbilliform

Drug Rash, Stevens Johnson Syndrome and Toxic Epidermal Necrolysis (TEN)
Management of Drug Allergies

• Drug discontinuation
• Mild rash could be treated with H1 anti-histamines such as diphenhydramine or
chlorpheniramine

• Treatment with systemic steroids sometimes intravenously administered are helpful for
severe drug reactions
Step 7: Definition, Aetiology, Clinical Features, Investigations and

Treatment of Boil (15 minutes)
A boil: Is a red swollen painful lump under the skin that is caused by an infection. Boil
often starts as an infected hair follicle where bacteria forms pocket of pus which eventually
drain out through the skin.
Aetiology
• The causation agents include
Bacteria Staphylococcus aureus or other bacteria which become secondary to ingrowing
hair, splinter or foreign object lodged in the skin and plugged on the sweat glands or oil
ducts.
Risk Factors to Infection

• Diabetes
• Poor nutrition
• Poor hygiene
• Obesity
• Intravenous drug use
• Immunosuppressant system
• Exposure to hard chemicals
Clinical Features
• Skin lump or bump that is red, swollen and tender
• The lump becomes larger more painful and softer overtime
• Pockets of pus may form on top of the boil
Investigations
• History and performing physical examination
• Bacterial culture to know type of organisms and their sensitivity
Treatment
• Do incision and drainage
• Give systemic antibiotics to which Staphylococcus aureus is sensitive e.g. penicillin
• Application of compressed hot application for 20 minutes in 3-4 times a day will ease the
pain and help to bring the pus to the surface for drainage
• Do not lance (pop) the boil because this can spread the infection and make it worse
• Impetigo mainly affects newborns and children under five years

• Use of antibacterial soaps (medicated soaps) prevents and treats folliculitis
• Boil is superficial collection of pus to the skin which needs incision and drainage
• Most pyogenic skin infections are caused by Staphylococcus aureus

• Skin reactions may be subcutaneous or involve deep dermal depending on severity of the
reaction
• Oral antihistamine may be adequate to control the symptoms
• Systemic steroids given intravenously are helpful in severe cases of allergic reaction
• What are the classifications of impetigo?

• How is impetigo treated?
• What are the predisposing factors for boils?
• What is the difference between urticaria and angioedema?
• What are the treatment approaches of Urticaria/druc reaction?
References
• Braunwald, E. & Fauci, A.N. (2008). Harrison’s Principles of Internal Medicine
(17th ed.). Oxford: McGraw Hill.
• Cumming A.D. (2006). Davidson’s Principles and Practice of Medicine: Edingurgh,
• DermAtlas.Image. Retrieved on July, 16 2010 from http://www.dermatlas.com/derm/
result.cfm?Diagnosis=1669841202
• Integrative Health and Wellness Resource for Angioedema. Angioddema
Pictures.Retrieved July 16, from http://www.goldbamboo.com/pictures-t7568.html
• Kumar, P.J. & Clark, M. (2006). Textbook of Clinical Medicine (6th ed.). Churchill:
Livingstone
• Skinsight (2010). Retrieved on jully,16 2010 from http://www.skinsight.com/
child/urticariaHives.htm

Handout 6.1: Various Viral Skin Infections
Types of Various Viral Skin Infections
‘Slapped Cheek ‘Syndrome (Erythema Infectiosum Fifths Disease)

• This affects children and is caused by parvovirus
• It is mild viral disease which is followed by an intense erythema on the check (slapped
check) and to proximal limb
• Adults can be infected with parvovirus as well and it typically presents as fatigue and
reactive arthritis. Anemia may also be present
Treatment
• Treatment for parvovirus is symptomatic. No antivirals are needed
Varicella Zoster Virus

• Varicella zoster virus (VZV) is the cause of chicken pox as well as the reactivation of
chicken pox known as shingles
•
• The primary infection is chickenpox. It usually occurs in childhood
• Mode of transmission is by airborne virus entering through mucosa of respiratory tract
also by direct contract from fresh skin lesion.
Clinical Features
• Incubation period is 14-21 days
• Followed by a period of fever, headache, malaise and eruption of macules then vesicles
to pustules within several hours
• The lesions occur on the face, scalp and trunk and to lesser extent in the extremities
• It is characteristic to see skin lesion at all stages of development on the same area of skin
Fever subsides as soon as new lesions cease to appear
• Eventually the pustules crust and heal without scarring
Complications
• Pneumonia
• Skin eruption
• Bacteria super infection of skin lesions
• Immunocomprised people are susceptible to disseminated infection with multiorgan
involvement
Treatment
• Usually require no treatment with antiviral therapy
• After recovery a patient develops a lifelong immunity
• Human Papilloma Virus (HPV)
• Is infection responsible of the common cutaneous warts
• There are more than 70 subtypes as detected by DNA hybridization
• All can cause overgrowth of differentiated squamous epithelium

Types of Warts
• There are popular lesions with a coarse roughened surface often seen on hands and feet
but also on can be seen on other sites, namely
o Plantar Warts (verrucal)
o Filiform Warts
o Plan Warts
o Anogenital Warts
• Children and adolescents are usually affected.
• The transmission is by direct contact and is also associated within trauma.
Plantar Warts (verrucal)

• These are lesions on soles of feet
o They often appear flat (inward growing) although they have the same papillomatous
surface change and black dots are often revealed if the skin is pared down
o Warts may be painful or tender if they are over pressure points or around nail folds.
Filiform Warts
• These occur on the face, at the nasal vestibule or around the mouth
• They are elongated with a honey cap
Plane Warts
• These are much less common and caused by certain HPV subtypes.
• They are clinically different and appear as very small, flesh coloured or pigmented, flat
topped lesions (best seen with side-on lighting) with little in the way of surface change
and no black dots within them.
• They are usually multiple and are frequently found on the face or back of hands.
Anogenital Warts
• There are usually seen in adults and are normally transmitted by sexual contact
• They are rare in childhood and when seen sexual abuse should be considered
• HPV subtypes 16 and 18 are potentially oncogenic and are associated with cervical and
anal carcinomos
Treatments
• Warts are difficult to treat effectively but they almost always resolve spontaneously after
months to years
• Regular use of topical kerotolytic agents (e.g. 2-10% salicylic acid) over many months
• A course of cryotherapy (freezing) can help
• Cautery surgery
• Carbon dioxide laser
• Alpha-interfection injection
• Bleomycin injection (rarely used)
• Genital warts are usually treated with either
o Cryotherapy
o Trichloroacetic acid
o Imiquimod cream or
o Topical podophyllin
• Screening of other sexual transmitted diseases should be done especially syphilis

Handout 6.2: Other Skin Conditions
Folliculitis
• Is defined histologically as the presence of inflammatory cells within the wall and ostia of
the hair follicle, creating a follicular base pustule.
o The actual type of inflammatory cells can vary and may be dependent on the aetiology
of the folliculitis, the stage at which the biopsy specimen was obtained or both.
o Folliculitis is a primary inflammation of the hair follicle that occurs as a result of
various infections, or it can be secondary to follicular trauma or occlusion.
o Eosinophilic folliculitis differs with ordinary folliculitis in that it is thought to occur
as a result of an autoimmune process directed against the sebocytes or some
component of the sebum. It is also common in severely immunecompromised persons
(e.g. HIV).
Aetiology
• Papulopustular eruption is secondary to epidermal growth factor receptor (EGF – R)
inhibitor is unknown
• It is hypothesized to occur secondariy to abnormal epidermal differentiation that leads to
follicular obstruction and subsequent inflammation
Clinical Picture
• Acne represents a noninfectious form of folliculitis.
• There is superficial and deep folliculitis.
• Folliculitis occurs in persons of any race but pseudofolliculitis occurs commonly in
African American.
• The patient typically reports an acute onset of papules and pustules associated with
pruritus or mild discomfort.
• Patient with deep folliculitis usually experience more pain and may suppurate and if
develops persistent drainage or recurrent lesion, may result in scarring and permanent hair
loss.
• Patient with papulopustular eruption secondary to EGC-R inhibitors typically occurs
within the first 2 weeks of the initiation of therapy and can be associated with pruritis and
desquamation.
• Superficial folliculitis presents with multiple small papules and pustules on erythematous
base that are pierced by a central hair
• In deep lesions it is manifested as erythematous often fluctuant, sometimes patterned
folliculitis
• One superficial form of infectious folliculitis is known as impetigo and is caused by
Staphylococcus aureus or Streptococcus pyogenes
• When involvement of the follicle is more extensive or follicular centered, a dermal
abscess results
Investigation
• In order to reach to diagnosis the following investigations is formed to confirm as
diagnosis is usually made based on history and physical examination findings alone.
o Gram stain and bacterial culture are performed.
o Gram stain and bacterial culture are performed

o Nasal culture of family members to look for Staphylococcus aureus (usually reserved
for recurrent severe cases)
o Potassium hydroxide (KOH) inspection, fungal culture or both can be used for
diagnosing dermatophytes infection
o Viral culture or biopsy assets in identification of folliculitis caused by herpes simples
virus
o Small punch biopsy (3-4mm) of an active lesion should be performed in atypical
cases or in patients resistant to standard treatments
Treatments
Recurrent Uncomplicated Superficial Folliculitis

• Use antibacterial soaps for hand washing
• If systemic antibiotics are indicated coverage should include S. aureus as is the most
common pathogen
• Pseudomonus folliculitis is usually self limited and does not require treatment. If the
patient is immunocompromised or the lesions are persistent then ciprofloxacin is the drug
of choice
• Eosinophilic pustular folliculitis does not respond to systemic antibiotic, but may respond
to isotretinoin
Eczema
• Eczema or dermatitis is a superficial skin inflammation characterised by epidermal edema
and clinically with red, patches or vesicles that typically are pruritic
• Primary lesions may include
o Papules
o Erythematous macules and vesicles, which can coalesce to form patches and plaques.
o In severe eczema, secondary lesions form infection or excoriation, marked by
weeping and crusting
o Long-standing dermatitis is often dry and is characterized by thickened, scaling skin
(lichenification)
Common Types of Eczema

• Atopic dermatitis
• Contact dermatitis
• Nummular dermatitis
• Lichen Simplex Chronicus
• Asteatotic eczema
• Seborrheic dermatitis
Atopic Dermatitis
• This is the cutaneous expression of the atopic state characterized by a family history of
asthma. Hay fever or dermatitis in up to 70% of patients.
Aetiology
• There is a clear genetic predisposition.
• When both parents are affected by atopic dermatitis over 80% of their children manifest
the disease.
• When only one parent is affected, the prevalence drops to slightly over 50%.

• A number of genes have been tentatively linked to atopic dermatitis including
o Genes coding for IgE
o High affinity IgE receptor
o Mast cell tryptase and
o Interleukin 4
• Patients with atopic dermatits may display a variety of immunoregulatory abnormalities
including increased IgE synthesis.
Clinical Presentation
• Often varies with age
• Half of patients with atopic dermatitis present within the first year of life and 80% present
by 5 years of age.
• Some 80% ultimately coexpress allergic rhinitis or asthma later in life.
• The infantile pattern is characterized by weeping inflammatory patches and crusted
plaques that occur on the face, neck, extensor surfaces, and groin.
• The childhood and adolescent pattern is marked by dermatitis of flexural skin particularly
in the antecubital and popliteal fossae.
• Atopic dermatitis may resolve spontaneously in adults, but the dermatitis will persist into
adult life in over half of individuals affected as children.
• The distribution of lesions may be similar to those seen in childhood
• Adults affected with atopic dermatitis frequently have localized disease manifesting as
hand eczema or lichen simplex chronicus
• Pruritus is a prominent characteristic of atopic dermatitis and many of the cutaneous
findings in affected patients are secondary to rubbing and scratching
• Other cutaneous stigmata of atopic dermatitis are
o Perioral pallor
o An extra fold of skin beneath the lower eyelid (dennie's line)
o Increased palmar markings and
o Increased incidence of cutaneous infections particularly with staphylococcus aureus
• Atopic individuals often have dry itchy skin, abnormalities in cutaneous vascular
responses
Treatment of Atopic Dermatitis

• Therapy of atopic dermatitis should be based on
o Avoidance of cutaneous irritants
o Adequate cutaneous hydration
o Judicious use of low or mid-potency topical steroids to affected areas
o Prompt treatment of secondarily infected skin lesions
o Patients should be instructed to bathe using warm, but not hot, water and to limit their
use of soap.
o Immediately after bathing while the skin is still moist, the skin should be lubricated
using a more oil based lotion
o Potent fluorinated topical steroids should not be used on the face or intertriginous
areas
o (It takes a minimum of 30 g of glucocorticoid ointment to cover the entire body
surface of an average adult)
o Crusted and weeping skin lesions should be treated with systemic antibiotics with
activity against S. aureus and S. pyogenes since secondary infection often exacerbates
eczema

o Control of pruritus is essential for treatment since atopic dermatitis often represents
‘an itch that rashes’.
o Antihistamines are useful to control the pruritus.
o Treatment with systemic steroids should be limited to severe exacerbations
unresponsive to conservative topical therapy.
o In the patient with chronic atopic dermatitis therapy with systemic steroids will
generally clear the skin only briefly but cessation of the systemic therapy will
invariably be accompanied by return, if not worsening, of the dermatitis.
Contact Dermatitis
• Is an inflammatory process in skin caused by an exogenous agent or agents that directly
or indirectly injure the skin.
• Common sensitizers include preservatives in topical preparations, nickel sulfate,
potassium dichromate, thimerosal in ocular preparations, neomycin sulfate, fragrances,
formaldehyde and rubber-curing agents.
• This injury may be caused by an inherent characteristic of a compound irritant contact
dermatitis.
• An example of irritant contact dermatitis would be dermatitis induced by a concentrated
acid or base.
• Agents that cause allergic contact dermatitis induce an antigen-specific immune response.
• The clinical lesions of contact dermatitis may be acute (wet and oedematous) or chronic
(dry, thickened, and scaly) depending on the persistence of the insult.
• The most common presentation of contact dermatitis is hand eczema and it is frequently
related to occupational exposures.
• Occupation related contact dermatitis represents a significant proportion of occupation
induced injury.
• Irritant contact dermatitis is generally strictly demarcated and often localized to areas of
thin skin (eyelids, intertriginous areas) or to areas where the irritant was occluded.
• Lesions may range from
o Minimal skin erythema to areas of marked edema
o Vesicles and ulcers
• Chronic low-grade irritant dermatitis is the most common type of irritant contact
dermatitis and the most common area of involvement is the hands.
• The most common irritants encountered are
o Chronic wet work
o Soaps
o Detergents
• Treatment should be directed to avoidance of irritants and use of protective gloves or
clothing.
• Allergic contact dermatitis is a manifestation of delayed type hypersensitivity mediated
by memory T lymphocytes in the skin.
• The most common cause of allergic contact dermatitis is exposure to plants.
• Poison ivy, poison oak, and poison sumac from plants cause allergic reaction marked by
erythema, vesiculation, and severe pruritus.
• The eruption is often linear, corresponding to areas where plants have touched the skin.
• These irritants may adhere to skin, clothing, tools, pets and cause dermatitis.

Treatment of Contact Dermatitis
• If allergic contact dermatitis is suspected and an offending agent is identified and
removed the eruption will resolve.
• High potency fluorinated topical steroids are enough to relieve symptoms while the
allergic contact dermatitis runs its course.
• For those patients who require systemic therapy a tapering course over 2 to 3 weeks given
as single morning doses is the preferred method.
• They should be questioned carefully regarding occupational exposures, topical
medicaments and oral medications.
• For those patients who require systemic therapy a tapering course over 2 to 3 weeks given
as single morning doses is the preferred method.
• They should be questioned carefully regarding occupational exposures, topical
medicaments and oral medications.
Lichen Simplex Chronicus

• Is chronicus may represent the end stage of a variety of pruritic and eczematous disorders.
• It consists of a well-circumscribed plaque or plaques with lichenified or thickened skin
due to chronic scratching or rubbing.
• Common areas involved include the posterior nuchal region, dorsum of the feet, or ankles
• Treatment of lichen simplex chronicus is centered around breaking the cycle of chronic
itching and scratching which often occur during sleep
• High potency topical steroids are helpful in alleviating pruritus in most cases but in
recalcitrant cases application of topical steroids under occlusion or intralesional injection
of steroids may be required.
• Patients need to be counseled regarding driving or operating heavy equipment after taking
these medications due to their potentially potent sedative activity.
Seborrheic Dermatitis
• Seborrheic dermatitis is a common chronic disorder characterized by greasy scales
overlying erythematous patches or plaques.
• The most common location is in the scalp where it may be recognized as severe dandruff
• On the face seborrheic dermatitis affects the
o Eyebrows
o Eyelids
o Glabella
o Nasolabial fold, or ears
• Scaling within the external ear is often mistaken for a chronic fungal infection
(otomycosis), and postauricular dermatitis often becomes macerated and tender.
• Additionally seborrheic dermatitis may develop in the central chest, axilla, groin,
submammary folds and gluteal cleft.
• Rarely may cause a widespread generalized dermatitis.
• Seborrheic dermatitis is usually symptomatic with patients complaining of itching or
burning.
• Seborrheic dermatitis may be evident within the first few weeks of life and tends to occur
in the scalp (‘cradle cap’), face or groin.
• It is rarely seen in children beyond infancy but becomes evident again during adult life.
• Although it is frequently seen in patients with parkinson's disease in those who have had
cerebrovascular accidents and in those with human immunodeficiency virus (HIV)

infection the overwhelming majority of individuals with seborrheic dermatitis have no
underlying disorder.
Treatment of Seborrheic Dermatitis

• Treatment with low potency topical steroids in conjunction with shampoos containing
coal tar and/or salicylic acid is generally sufficient to control this disorder.
• High potency topical steroids solutions (betamethasone or fluocinonide) are effective for
control of scalp involvement if severe
• Fluorinated topical steroids should not be used on the face since this is often associated
with the development of rebound worsening and steroid induced rosacea or atrophy.

Handout 6.3: Pictures on Angioedema, Urticaria, Morbilliform Drug
Rash, Stevens Johnson Syndrome and Toxic Epidermal Necrolysis
(TEN)
Angioedema
Source: Integrative Health and Wellness Resource for Angioedema (2010)
Urticaria
Source: Skin sight (2010)
Morbiliform drug rash
DermAtlas 2010

Toxic Epidermal Necrolysis (TEN)
DermAtras (2010)
Steven Johnson Syndrome
DermAtras 2010

CMT 05211 Internal Medicine 2 NTA Level 5 Semester 2 Facilitator Guide
Session 7: Diabetes Mellitus 92
Session 7: Diabetes Mellitus
Prerequisites
•None
Learning Objectives
•Describe diabetes mellitus
•Classify diabetes mellitus
•Describe clinical features and investigations of diabetes mellitus
•Outline management of diabetes mellitus
•Describe complications of diabetes mellitus
Resources Needed
•Flip charts, marker pens, and masking tape
•Black/white board and chalk/whiteboard markers
•Handout 7.1: Aetiological, Classifications, Epidemiology and Pathogenesis of Diabetes
Mellitus
SESSION OVERVIEW
Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Objectives
2 10 minutes Presentation Definition

Presentation,
3 20 minutes Classification of Diabetes Mellitus
Buzz
4 15 minutes Presentation Clinical Features and Investigations
25 minutes Presentation Treatment

5
Presentation,
6 30 minutes Complications
Group Discussion
SESSION CONTENT


Step 2: Definition (10 minutes)
• Diabetes mellitus (DM) comprises a group of common metabolic disorders that present
with hyperglycemia (elevated blood glucose).
• Defect in body energy regulation and utilization leading to multi-organ complications and
early mortality.
• Hyperglycemia is a cardinal manifestation due to insulin deficiency or insulin resistance.
• Several distinct types of DM exist and are caused by a complex interaction of genetics,
environmental factors and life-style choices.
• Depending on the etiology of DM, factors contributing to hyperglycemia may include
o Reduced insulin secretion
o Decreased glucose usage, and
o Increased glucose production
• The metabolic dysregulation associated with DM causes secondary pathophysiologic
changes in multiple organ systems that impose a tremendous burden on the individual
with diabetes and on the health care system.
Step 3: Classification of Diabetes Mellitus (20 minutes)
ASK students to outline classifications of diabetes mellitus.
INVITE few pairs to give their responses and others to contribute.
RECORD the responses on board or flipchart.
• Recent changes in classification reflect an effort to classify DM on the basis of the

pathogenic process that leads to hyperglycemia, as opposed to criteria such as age of
onset or type of therapy.
• Two broad categories of DM are designated type 1(A & B) and type 2.
• Type 1A DM results from autoimmune beta cell destruction which usually leads to
insulin deficiency.
• Type 1B DM is also characterized by insulin deficiency as well as a tendency to develop
ketosis. The mechanisms leading to beta cell destruction in these patients are unknown.
• Type 2 DM is a heterogeneous group of disorders usually characterized by variable
degrees of insulin resistance, impaired insulin secretion, and increased glucose
production.
• The terms insulin-dependent diabetes mellitus (IDDM) and noninsulin-dependent
diabetes mellitus (NIDDM) are outdated because many individuals with type 2 DM
eventually require insulin treatment for control of glycemia, the use of the latter term
generated considerable confusion.

Risk Factors for Type 2 Diabetes Mellitus
• Family history of diabetes (i.e. parent or sibling with type 2 diabetes)
• Obesity i.e. body mass index (BMI) >27kg/m2
• Age >45 years
• History of gestational diabetes mellitus
• Hypertension
• High density lipoprotein (HDL) cholesterol <0.90 mmol/l (35mg/dl)
• In HIV patients, the HAART therapy can increase risk of diabetes
Other Types of Diabetes Mellitus

• Other etiologies for DM include specific genetic defects in insulin secretion or action,
metabolic abnormalities that impair insulin secretion, and a host of conditions that impair
glucose tolerance.
Gestational Diabetes Mellitus (GDM)

• Glucose intolerance may develop and first become recognized during pregnancy.
Refer students to Handout 7.1: Aetiology, Epidemiology and Pathogenesis of

Diabetes Mellitus
Step 4: Clinical Features and Investigations (15 minutes)
Clinical Features
• Possible clinical features of DM depend on the severity of disease and its complications.
These are listed below
o Polyuria
o Polydipsia
o Polyphagia
o Hyperglycaemia
o Glycosuria
o Ketosis, Acidosis
o Coma
o Weight loss
o Fatigue
o Weakness
o Blurred vision
o Frequent superficial infections e.g. vaginitis, fungal skin infections
o Slow healing of skin lesions after minor trauma
• Metabolic derangements relate mostly to hyperglycemia (osmotic diuresis, reduced
glucose entry into muscle) and to the catabolic state of the patient (urinary loss of glucose
and calories, muscle breakdown due to protein degradation and decreased protein
synthesis).
• Blurred vision results from changes in the water content of the lens and resolves as the
hyperglycemia is controlled.

Investigations
• At primary health care facilities, the following can be done to patients suspected of
having DM.
o Fasting blood sugar
o Urine for sugar
o Random blood sugar
o This can be done using simple devices e.g. glucometers and urine dipsticks. When
DM is diagnosed, patients should be referred to hospitals for further investigations to
rule out complications and for initiation of the right medications.
Criteria for Diagnosis of Diabetes Mellitus

• Symptoms of diabetes plus random blood glucose concentration equal or greater than
11.1 mmol/L (200 mg/dl) or
• Fasting plasma glucose equal or greater than7.0 mmol/L (126 mg/dl)
• In the absence of unequivocal hyperglycemia and acute metabolic decompensation, these
criteria should be confirmed by repeat testing on a different day.
• Random is defined as without regard to time since last meal
• Fasting is defined as no caloric intake for at least 8 hours
• Glucose tolerance is classified into three categories based on the Fasting Plasma Glucose
(FPG)
o FPG < 6.1 mmol/l (110 mg/dL) is considered normal
o FPG 6.1 mmol/l (110 mg/dl) but < 7.0 mmol/l (126 mg/dl) is defined as impaired
Fasting Glucose (IFG)
o FPG 7.0 mmol/l (126 mg/dl) warrants the diagnosis of DM
Step 5: Treatment (25 minutes)
• Treatment of DM should be initiated at hospital levels after thorough evaluation

including that of the complications. Thereafter, when patients are stable, follow up may
be done at health centres.
Overall Principles
• The goals of therapy for type 1 or type 2 DM are to
o Eliminate symptoms related to hyperglycemia
o Reduce or eliminate the long-term microvascular and macrovascular complications of
DM
o Allow the patient to achieve as normal a life-style as possible
o The care of an individual with either type 1 or type 2 DM requires a multidisciplinary
team
o Central to the success of this team are the patient's participation, input and enthusiasm
all of which are essential for optimal diabetes management
Education for Patient with Diabetes Mellitus on Nutrition and Exercise

• Patient participation is an essential component of comprehensive diabetes care
• The patient with type 1 or type 2 DM should receive education about nutrition, exercise,
care of diabetes during illness and medications to lower the plasma glucose.
• Nutrition education should focus on balanced healthy eating (avoidance of alcohol, high
sugar foods such as desserts).

• Regular daily exercise is important, recommendation is 20-30 minutes of exercise daily
(this can be walking).
• Patients should also be educated as to the long term consequences of uncontrolled
diabetes (renal impairment, higher risk of ocular damage, increased risk of heart attack,
and neuropathy).
• Along with improved compliance patient education allows individuals with DM to
assume greater responsibility for their care.
• Patient education should be viewed as a continuing process with regular visits for
reinforcement; it should not be a process that is completed after one or two visits to a
nurse educator or nutritionist.
Monitoring Level of Glycemic Control

• Optimal monitoring of glycemic control involves plasma glucose measurements by the
patient and an assessment of long-term control by the physician measurement of
glycosylated haemoglobin (GHb ) and review of the patient's self-measurements of
plasma glucose.
• These measurements are complementary; the patient's measurements provide a picture of
short-term glycemic control whereas the GHb reflects average glycemic control over the
previous 2 to 3 months.
• Integration of both measurements provides an accurate assessment of the glycemic
control achieved.
Type I Diabetes Mellitus
Insulin Regimens
• In all regimens long-acting insulin (lente, ultralente, or glargine insulin) supply basal
insulin whereas prandial insulin is provided by either regular or lispro insulin.
• Lispro should be injected just before a meal.
• Regular insulin is given 30 to 45 min prior to a meal.
• No insulin regimen reproduces the precise insulin secretory pattern of the pancreatic islet.
• In general individuals with type 1 DM require 0.5 to 1.0 Unit/kg per day of insulin
divided into multiple doses.
• Initial insulin-dosing regimens should be conservative approximately 40 to 50% of the
insulin should be given as basal insulin to avoid hypoglycemia (which can be a serious
side effect of treatment of diabetes).
• A single daily injection of insulin is not appropriate therapy in type 1 DM.
• One commonly used regimen consists of twice-daily (2/3) injections of an intermediate
insulin (NPH or lente) mixed with a short-acting insulin before the morning and evening
meal.
• Such regimens usually prescribe two-thirds of the total daily insulin dose in the morning
(with about two-thirds given as intermediate-acting insulin and one-third as short-acting)
and one-third before the evening meal (with approximately one-half given as
intermediate-acting insulin and one-half as short-acting).
Type 2 Diabetes Mellitus
General Aspects
• The goals of therapy for type 2 DM are similar to those in type 1.

• While glycemic control tends to dominate the management of type 1 DM, the care of
individuals with type 2 DM must also include attention to the treatment of conditions
associated with type 2 DM (obesity, hypertension, dyslipidemia, cardiovascular disease)
and detection/management of DM-related complications.
• DM-specific complications may be present in up to 20 to 50% of individuals with newly
diagnosed type 2 DM.
• Reduction in cardiovascular risk is of paramount importance as this is the leading cause
of mortality in these individuals.
Glucose Lowering Agents

• Based on their mechanisms of action, oral glucose-lowering agents are subdivided into
agents that
o Increase insulin secretion
o Reduce glucose production or
o Increase insulin sensitivity
• Oral glucose-lowering agents (with the exception of alpha-glucosidase inhibitors) are
ineffective in type 1 DM and should not be used for glucose management of severely ill
individuals with type 2 DM.
• Insulin is sometimes the initial glucose-lowering agent even in type 2 DM.
Oral Glucose Lowering Agents

• Insulin secretagogues
o First generation sulfonylurea
o Second generation sulfonylurea
• Biguanides (metformin)- this is usually the first drug of choice if available for type 2
diabetes as long as there are no contraindications (e.g., in renal failure).
• Thiazolidinediones - these are less favored for treatment given their recent complications
and side effects.
• Alpha-glucosidase inhibitors - also less effective as initial therapy.
Step 6: Complications (30 minutes)
DIVIDE students into small manageable groups
ASK students to describe complications of diabetes mellitus and record them on piece of
paper.
INVITE one group to share their responses.
ALLOW other groups to add up what the first group did not cover.
Acute Complications
• Diabetic ketoacidosis (DKA) nonketotic hyperosmolar state (NKHS), Hypoglycemia are
acute complications of diabetes.

• DKA is seen primarily in individuals with type 1 DM, and NKHS is seen in individuals
with type 2 DM.
• Both disorders are associated with absolute or relative insulin deficiency, volume
depletion, and altered mental status.
• DKA and NKHS exist along a continuum of hyperglycemia, with or without ketosis.
• Both disorders are associated with potentially serious complications if not promptly
diagnosed and treated.
• Diabetic ketoacidosis is a medical emergency and if suspected needs immediate
intervention and transfer to the hospital
Chronic Complications of Diabetes Mellitus

• DM and its complications produce a wide range of symptoms and signs.
• Those secondary to acute hyperglycemia may occur at any stage of the disease.
• Those related to chronic complications begin to appear during the second decade of
hyperglycemia.
• Individuals with previously undetected type 2 DM may present with chronic
complications of DM at the time of diagnosis.
• The history and physical examination should assess for symptoms or signs of acute
hyperglycemia and should screen for the chronic complications and conditions associated
with DM.
• Chronic complications of DM affect many organ systems and are responsible for the
majority of morbidity and mortality associated with the disease.
• Chronic complications can be divided into vascular and nonvascular complications.
• The vascular complications of DM are further subdivided into
o Microvascular
Retinopathy
Neuropathy
Nephropathy
o Macrovascular Complications
Coronary Artery Disease
Peripheral Vascular disease leading to diabetic foot
Cerebrovascular disease
• Nonvascular complications include problems such as
o Gastroparesis
o Sexual dysfunction
o Skin changes
• This division is rather arbitrary since it is likely that multiple pathogenic processes are
involved in all forms of complications.
• The risk of chronic complications increases as a function of the duration of
hyperglycemia.
• They usually become apparent in the second decade of hyperglycemia.
• Since type 2 DM may have a long asymptomatic period of hyperglycemia, many
individuals with type 2 DM have complications at the time of diagnosis.

• Diabetes mellitus is primarily due to insulin deficiency or resistance.

• Hyperglycemia is a cardinal manifestation of diabetes mellitus.
• Depending on the etiology of the DM, factors contributing to hyperglycemia may include
o Reduced insulin secretion
o Decreased glucose usage and
o Increased glucose production
• Diabetic ketoacidosis (DKA) nonketotic hyperosmolar state (NKHS) and hypoglycemia
are acute complications of diabetes.
• Explain the clinical features of DM.

• Describe the treatment of diabetes mellitus.
• Mention chronic complications of diabetes mellitus.
• Explain the importance of health education regarding the patient of diabetes mellitus.
References
McGraw Hill.
• Cumming A.D. (2003). Davidson’s Principles and Practice of Medicine. Oxford:
Edinburgh.
Saunders.
• Zimmerman, B. (1998). Medical Management of Type 2 Diabetes. Retrieved May 10th
2010 from http://cgi.ebay.com/Medical-Management-Type-2-Diabetes-Bruce-
Zimmerman-Paperback-1998-/341618422000.

Handout 7.1: Aetiological, Classifications, Pathogenesis and
Epidemiology of Diabetes Mellitus
Aetiological Classification of Diabetes Mellitus

• Type 1 diabetes (β-cell destruction, usually leading to absolute insulin deficiency)
o Immune-mediated
o Idiopathic
• Type 2 diabetes (may range from predominantly insulin resistance with relative insulin
deficiency to a predominantly insulin secretory defect with insulin resistance)
• Other specific causes of diabetes
o Genetic defects of β-cell function
o Genetic defects in insulin action
o Diseases of the exocrine pancreas, pancreatitis, pancreatectomy, neoplasia, cystic
fibrosis, hemochromatosis, fibrocalculous pancreatopathy.
o Endocrinopathies, acromegaly, cushing's syndrome, glucagonoma,
pheochromocytoma, hyperthyroidism, somatostatinoma, aldosteronoma
o Drug- or chemical-induced, pentamidine, nicotinic acid, glucocorticoids, thyroid
hormone, diazoxide, β-adrenergic agonists, thiazides, phenytoin, protease inhibitors,
clozapine, beta blockers.
o Infections, congenital rubella, cytomegalovirus, coxsackie.
o Uncommon forms of immune-mediated diabetes’stiff-man’ syndrome, anti-insulin
receptor antibodies.
o Other genetic syndromes sometimes associated with diabetes
Down's syndrome
Klinefelter's syndrome
Turner's syndrome
Wolfram's syndrome
Friedreich's ataxia
Huntington's chorea
o Gestational diabetes mellitus (GDM)
Epidemiology of Diabetes Mellitus

• The worldwide prevalence of DM has risen dramatically over the past two decades.
• It is projected that the number of individuals with DM will continue to increase in the
near future.
• There is considerable geographic variation in the incidence of both type 1 and type 2
DM.
• The prevalence of type 2 DM and its harbinger, impaired glucose tolerance (IGT), is
highest in certain Pacific islands, intermediate in countries such as India and the United
States, and relatively low in Russia and China.
• This variability is likely due to both genetic and environmental factors. There is also
considerable variation in DM prevalence among different ethnic populations within a
given country.

Pathogenesis of DM
Type 1 DM
• Type 1A DM develops as a result of the synergistic effects of genetic, environmental, and
immunologic factors that ultimately destroy the pancreatic beta cells.
TYPE 2 DM
• Type 2 DM is a heterogeneous disorder with a complex etiology that develops in
response to genetic and environmental influences.
• Central to the development of type 2 DM are insulin resistance and abnormal insulin
secretion. Although controversy remains regarding the primary defect, most studies
support the view that insulin resistance precedes insulin secretory defects.
• Type 2 DM has a strong genetic component.
• Although the major genes that predispose to this disorder have yet to be identified, it is
clear that the disease is polygenic and multifactorial.
• The concordance of type 2 DM in identical twins is between 70 and 90%.
• Individuals with a parent with type 2 DM have an increased risk of diabetes if both
parents have type 2 DM the risk in offspring may reach 40%.
• Insulin resistance as demonstrated by reduced glucose utilization in skeletal muscle is
present in many non diabetic first-degree relatives of individuals with type 2 DM.
• However definition of the genetic abnormalities of type 2 DM remains a challenge
because the genetic defect in insulin secretion or action may not manifest itself unless an
environmental event or another genetic defect such as obesity is superimposed.
Metabolic Abnormalities Associated with Diabetes Mellitus

• Insulin Resistance
• Impaired Insulin Secretion
• Increased Hepatic Glucose Production
Insulin Preparations
• Current insulin preparations are generated by recombinant DNA technology and consist
of the amino acid sequence of human insulin.
• Animal insulin (beef or pork) is no longer used.
• Basal insulin requirements are provided by intermediate (NPH or lente) or long-acting
(ultra-lente or glargine) insulin formulations.
• These are usually combined with short-acting insulin in an attempt to mimic physiologic
insulin release with meals.
Insulin Secretagogues
• Categorized into
o First generation sulfonylurea
o Second generation sulfonylurea
• At maximum doses first-generation sulfonylureas are similar in potency to second-

generation agents but have a longer half-life, a greater incidence of hypoglycemia and
more frequent drug interactions
o Thus second-generation sulfonylureas are generally preferred
o Sulfonylureas reduce both fasting and postprandial glucose and should be initiated at
low doses and increased at 1- to 2-week intervals.

• In general sulfonylureas increase insulin acutely and thus should be taken shortly before a
meal with chronic therapy though insulin release is more sustained.
• Insulin secretagogues are well tolerated in general.
Figure 1: Characteristics of Sulfonylureas

Generic Name Approved Daily Duration of
Dosage Range, mg Action in hours Clearance
First generation
Chlorpropamide 100-500 daily >48 Renal
Tolazamide 100-1000 12-24 Hepatic, renal
Tolbutamide 500-3000 6-12 Hepatic
Second generation
Glimepiride 1-8 24 Hepatic, renal
Glipizide 2.5-40 12-18 Hepatic
Glipizide (extended 5-10 24 Hepatic
release)
Glyburide 1.25-20 12-24 Hepatic, renal
Glyburide (micronized) 0.75-12 12-24 Hepatic, renal
Meglitinides
Repaglinide 0.5-16 2-6 Hepatic
Source: Zimmerman, 1998
Biguanides
• Metformin is representative of this class of agents
• It reduces hepatic glucose production through an undefined mechanism and may improve
peripheral glucose utilization slightly
• Metformin reduces fasting plasma glucose and insulin levels, improves the lipid profile
and promotes modest weight loss
• The initial starting dose of 500 mg once or twice a day can be increased to 850 mg tid or
1000 mg bid
• The major toxicity of metformin is lactic acidosis
• Though well tolerated in general, some individuals develop gastrointestinal side effects
(diarrhea, anorexia, nausea, and metallic taste}
• Metformin should not be used in patients with
o Renal insufficiency
o Any form of acidosis
o Congestive heart failure
o Liver disease or
o Severe hypoxia
Figure 2: Drugs for Management of Type 2 Diabetes Mellitus

Class Mechanism of Action
Sulfonylureas Increase insulin secretion
Biguanides Decrease gluconeogenesis
Thiazolidinediones Reduce insulin resistance
A-glucosidaase inhibitors Slow GIT absorption of glucose
Source: Zimmerman, 1998

Insulin Therapy in Type 2 DM
• Modest doses of insulin are quite efficacious in controlling hyperglycemia in newly
diagnosed type 2 DM.
• Insulin should be considered as the initial therapy in type 2 DM.
o Particularly in lean individuals or those with severe weight loss.
o In individuals with underlying renal or hepatic disease that precludes oral glucose-
lowering agents.
o In individuals who are hospitalized or acutely ill.
• Insulin therapy is ultimately required by a substantial number of individuals with type 2
DM because of the progressive nature of the disorder and the relative insulin deficiency
that develops in patients with long-standing diabetes.
• Because endogenous insulin secretion continues and is capable of providing some
coverage of mealtime caloric intake, insulin is usually initiated in a single dose of
intermediate-acting insulin (0.3 to 0.4 U/kg per day), given either before breakfast or just
before bedtime (or ultralente at bedtime).
• Since fasting hyperglycemia and increased hepatic glucose production are prominent
features of type 2 DM, bedtime insulin is more effective in clinical trials than a single
dose of morning insulin.
• Some physicians prefer a relatively low, fixed starting dose of intermediate-acting insulin
(~15 to 20 units in the morning and 5 to 10 units at bedtime) to avoid hypoglycemia.
• Both morning and bedtime intermediate insulin may be used in combination with oral
glucose-lowering agents (biguanides, a-glucosidase inhibitors, or thiazolidinediones).

Session 8: HIV Care at First Level Health Facilities
Prerequisites
• CMT 05109 Pharmacology and Therapeutics
Learning Objectives
• Describe IMAI approach in HIV care
• List goals and benefits of ART
• Describe the criteria for initiating ART in Tanzania
• Describe the requirements for starting ART for PLHIV
• Describe the first line ART regimens in Tanzania
• Explain how to monitor and follow-up a patient on ART
• List reasons for stopping or changing ART regimen
Resources Needed
• Handout 8.1: When to Refer Patients to Higher Level Facilities for ART
• Handout 8.2: Using the 5 A’s to Ensure Patient Readiness
• Worksheet 8.1: Practice with CTC Forms
SESSION OVERVIEW
Step Time Activity/Method Content
2 25 minutes Presentation Acute and Chronic Conditions and their Care

Presentation, Group First Visit to care and Treatment Clinic
3 30 minutes
Activity (CTC)
Presentation, Goals of ART and Requirements for Starting
4 15 minutes
Brainstorm ART
Patients who Should not Start ART at First
Level Health Facility
First Line Regimens in Tanzania, Initiating
and Follow up of Patients on ART

Session 8: HIV Care at First Level Health Facilities 105
SESSIION CON
NTENT
Step 1:
1 Presenttation of Session
S Tiitle and Learning
L O
Objective
es (5 minu
utes)
READ or ASK thee students too read the leearning objeectives, andd clarify.
ASK sttudents if thhey have anyy questions before conttinuing.
Step 2:
2 Acute and
a Chron
nic Condiitions and
d their Caare (25 miinutes)
• A patient is deffined as havving chronicc illness if she/he

s continues to be iill for more than
one month. Exxample of chhronic diseaases includee
o Leprosy
o Tuberculossis
o HIV and AIDSA
o Sickle cell disease (SC CD)
o Diabetes
o Hypertensioon
• Exaamples of accute condition include
o Common bacterial
b infeections
o Malaria
o Neurologiccal and menttal health prroblems
• Care of PLHIV V by Integraated Manageement of Ad dult and Addolescent Illlness (IMAII)
apprroach consiiders acute, chronic andd palliative care.
Figure 1: Integratioon of Acutee, Palliative and Chroniic Care
Source: WHO
W 2009
• Chrronic care byy IMAI appproach is baased on 10 principles

p off Good Chroonic Care which
w
are discussed inn the figuree below.

M 2 NTA Level 5 Semester 2 Facilitattor Guide
Session 8:
8 HIV Care at
a First Level Health
H Facilitiies 106
Figure 2:
2 General Principles
P o Good Chrronic Care by
of b IMAI Appproach
Source: MOHSW
M 20055
Step 3:
3 First Viisit to Carre and Trreatment Clinic [CTC] (30 m
minutes)
• Thee first visit is very impoortant for thhe PLHIV beecause a lott is needed tto be done and
a
empphasized thrrough the seequence desscribed in th he figure below.

Session 8:
8 HIV Care at
H Facilitiies 107
Figure 3: Sequence of Care after Positive HIV Test
Source: MOHSW 2005

Filling CTC 1 and CTC 2
Activity: Small Group Activity (5 minutes)
If time is limited students can just do this on their own rather than dividing into small groups,
and then can report back to the larger group once they are all done.
TELL students they practice how to fill CTC 1 and CTC 2 forms.
REFER students to Worksheet 8.1: Practice with CTC Forms.
TELL each group to have one person reading the patient scenario. Then each group work
together to fill out CTC 1 and CTC 2 forms as completely as possible based on the
information provided in the patient scenario.
RECONVENE the groups after 5 minutes
ASK students to explain how they filled out the forms and review the correct answers
SUMARIZE by highlighting the most important parts of the card such as the patient
identification number which is unique.
ASK students if they have any questions before proceeding.
Step 4: Goals of ART and Requirements for Starting ART (15 minutes)
• The primary goals of antiretroviral therapy are to

o Maximal and durable suppression of viral load
o Restoration and/or preservation of immunologic function
o Improvement of quality of life
Reduction of HIV-related morbidity and mortality
• Secondary goals are to
o Decrease the incidence of HIV
o Increased uptake of voluntary testing and counseling with more people knowing their
status and practicing safer sex
o The reduction of transmission of HIV in discordant couples
o Reducing the risks of HIV transmission from mother to child
Medical Eligibility for ART in Adults

• Before considering ART to a patient there must be a written communication for his/her
HIV status (positive results)
• Then determine eligibility for ART as indicated here below
o If CD4 testing is available
All patients with CD4 < 200cells/ml regardless of symptoms
All patients with WHO clinical stage 4 no matter of CD4 count
All patients with WHO clinical stage 3 with CD4 count <350 cells/ml

o If CD4 testing not available
All patients with WHO clinical stage 3 & 4
When is the Adults Patient Considered Ready to Start ART

ASK students when is a patient ready to start ART?
ALLOW few students to respond and record on the flip chart/board.
SUMARIZE the discussion by using the content below.

• Patient understands ARV therapy
• Patient ready to adhere to lifelong treatment
• Patient actively involved in his own care
• Family and/or social support available
• Treatment supporter if possible
• Adhered to previous visits and medication
• Barriers to adherence have been addressed
• The patient is ready and meets medical criteria for initiating ART
Refer Students to
Handout 8.1: When to Refer Patients to Higher Level Facilities for ART
Handout 8.2: Using 5A’s to Ensure Patient Readiness
Step 5: Patients who should not Start ART at First Level Health Facility
(5 minutes)
• Patients with the following conditions should not be started ART at first level health
facility but should be referred to hospitals for initiation.
o Severe illness (e.g. Anaemia) or WHO clinical stage 4 condition
o Currently TB treatment
o Peripheral neuropathy
o Jaundice or known liver disease
o Chronic disease like diabetes mellitus or heart disease
o Paediatric patient
o History of previous use of ART
Step 6: First Line Regimens in Tanzania, Initiating and Follow up of

Patients on ART (25 minutes)
• Recommended First line ARV drugs in Tanzania

o Zidovudine (AZT)
o Stavudine (d4T)
o Lamivudine (3TC)
o Emtricitabine (FTC)
o Tenofovir (TDF)
o Nevirapine (NVP)
o Efavirenz (EFV)

• The following drug combinations can be made out of these drugs for adults and
adolescents and should be used according to indications and contraindications that govern
the use of ARVs to minimize side effects and drugs interactions.
o AZT+ 3TC+EFV
This is the default first regimen
o AZT+3TC+NVP
When EFV is contraindicated e.g. first trimester pregnancy or serious psychiatric
disorder or seizures.
NVP challenge dosing is required
o d4T+3TC+NVP
When there is significant anaemia and EFV is also contraindicated
NVP challenge dosing is required. Do not use if pt has peripheral neuropathy
o d4T+3TC+EFV
o When AZT is contraindicated, e.g., anaemia
o TDF+FTC+EFV
o TDF+FTC +NVP
o TDF+3TC+EFV
o TDF+3TC+NVP
TDF is used when both d4T and AZT are contraindicated
FTC works just as 3TC although it can be given once a day
Do not use if patient has renal insufficiency
• Side effects of first line ARV drugs may be divided into
o Very Common
o Potentially serious
o Those occurring later during treatment
• Very common side effects usually occurs when treatment begin and improve within 2-4
weeks.
o It is important to warn the patient about them and give them some simple advice on
what to do if they occur.
o Nausea and diarrhoea can occur in almost all ARVs
o AZT commonly causes
Headache
Feeling tired (fatigue)
Muscle pain (myositis)
o Efavirenz commonly causes
Strange dreams (nightmares)
Difficulty sleeping (somnolence or drowsiness)
Mood changes
Dizziness
Loss of concentration or memory
• Potentially serious side effects require emergency consultation/referral to hospital for
management.
o The main serious side effect of AZT is anaemia that may present with severe pallor or
low haemoglobin.
o NVP and EFV causes
Yellow eyes (jaundice) due to liver damage (hepatitis). This is more common with
NVP than EFV.
Hypersensitivity reaction (more common with NVP than EFV). This may present
as a skin rash or Steven Johnson’s syndrome.

o d4T causes
Severe abdominal pain due to pancreas damage (pancreatitis).
Numbness and tingling in hands and feet (peripheral neuropathy).
Lactic acidosis that presents with shortness of breath/fast breathing with
prominent fatigue.
• Side effects occurring later during treatment.
o Severe abnomimal distribution of the body fat commonly occur with d4T.
o Fat gain on the belly, breast, shoulders and neck with
o Fat loss from legs, arms, buttocks and face
• Management of ARV side effects include the following
o Explaining to the patient about very common possible side effects before the person
starts.
o Giving advice on how to manage these very common side effects.
o Informing the patient to give immediate attention to side effects by accessing to the
clinic physically or by phone.
o Initiating discussion about side effects even if the patient does not volunteer
them spontaneously refer patients to high facility level.
Figure 4: Adult ART Laboratory Tests for Monitoring Patients on First Line Regimen
Regimens Monitoring Tests Frequency Rationale
d4T/3TC/NVP CD4 Staging, 6-monthly ART monitoring
ALT Baseline, week 2, 4 Contains NVP
and 8, thereafter 6-
monthly
AZT/3TC/NVP CD4 Staging, 6-monthly ART monitoring
ALT Baseline, week 2, 4 Contains NVP and
and 8, thereafter 6- AZT
monthly and
whenever
symptomatic
FBP Baseline, week 4 and Contains AZT
8, thereafter 6-
monthly
d4T/3TC/EFV CD4 Staging, 6-monthly ART monitoring
ALT 6-monthly or Contains EFV
symptomatic
AZT/3TC/EFV CD4 Staging, 6-monthly ART monitoring
ALT 6-monthly or Contains EFV
symptomatic
FBP Baseline, week 4 and Contains AZT
8, thereafter 6-
monthly
TDF containing Urinalysis Baseline, and 3 TDF can be
regimen Serum monthly nephrotoxic
Creatinine Baseline, and once
yearly
Source: MOHSW 2009

• A patient is defined as having chronic illness if she/he continues to be ill for more than
one month.
• Secondary goals (benefits) of ARV therapy include improve quality of life, increasing
immunity and reduce mother to child transmission.
• ART to a patient should be considered when she/he is HIV positive with written
documentation and meets the medical eligibility.
• The ARV drug regimens used are according to the available guideline and should base on
the indications and contraindications.
• Explain the principles chronic care

• What are the medical eligibilities for ART?
• Mention the first line ARV drugs
• Mention potentially serious side effects of first line ARV drugs
References
• MOHSW (2005). General Principles of Good Chronic Care: IMAI, Guidelines for Health
Workers Dispensaries and Health Centres in Tanzania. Dar es Salaam, Tanzania:
Ministry of Health and Social Welfare.
• MOHSW (2007). Basic Training Course for Comprehensive Management of HIV/AIDS.
Dar es Salaam, Tanzania: Ministry of Health and Social Welfare.
• MOHSW (2009). National Guidelines for the Management of HIV and AIDS. Dar es
Salaam, Tanzania: Ministry of Health and Social Welfare.

Worksheet 8.1:
8 Practiice with CTC
C Form
ms
Instrucctions
Read thhe followingg case studyy, and fill ouut CTC form
ms 1 and 2 on
o followingg pages as
complettely as you can for thiss patient.
Scenario
The pattient's namee is David B. B He was born
b in July about 27 yeears ago. Thhis is his firrst visit
to the Dareda
D clinic. The facillity code is 2456.
2 His unique
u CTCC ID numbeer is 245602 200.
There iss no health facility file number. He H is married to Lydia and a has no cchildren. He H lives
in Babaati district, Dareda.
D Alii Juma is the hamlet chhairman for Dareda. Thhe ten cell leader
for Davvid’s cell is Omar Chrisstopher. Daavid’s teleph hone numbeer is 123.4556.789. He shows a
written confirmatioon of his HIIV test from m May 30, laast year. He H has had nno prior AR RT but
comes nown on his own (self-reefer), becauuse he heard d that this heealth centree has ART
availablle. Lydia will
w be his trreatment suppporter and has the sam me address. Her mobile
numberr is 234.567.891. He has never needed home--based care.. His wife iis HIV+ butt has not
enrolledd in HIV caare yet. Shee is 26 yearss old. They do not havee children. He has no drug d
allergiees and at thiss visit, he has no symptoms of HIV V or TB. HisH weight iss 70 kg. He is
workingg and deliveers mail. Hee has thrushh, so his clin nical stage iss 3. There is no CD4 av vailable
at the health centree. David is started
s on cootrimoxazole, and is reeferred for nnutritional support.
He is too return in 2 weeks.
CTC 1 Form

Session 8:
8 HIV Care at
H Facilitiies 114
CTC 2 Form
Source: MOHSW, 2009

Handout 8.1: When to Refer Patients to Higher Level Facilities
for ART
Patients to Refer to a Higher Level Facility

• Patients who require urgent referrals must be referred to a higher level facility.
• Patients with the following conditions or circumstances must be referred to a higher level
facility.
Anaemia
• There are several causes of anemia and these patients need to be referred to hospital
where appropriate investigations can be done to determine the cause and start the right
regimen.
• Measuring HB is very important because patients who are anaemic cannot take one of the
first line ARVs (i.e. AZT containing regimen).
• Anaemia might be very severe and require transfusion which is only available at
hospitals.
Jaundice or a Known Liver Problem

• Patients with suspected liver disease present with yellow eyes (jaundice) and right upper
abdominal pain; these patients need to be referred to a higher level to investigate liver
disease and for a decision on when to start treatment and which regimen to use.
• Patients with suspected liver disease should have their liver function tested so as to
determine the extent of the liver damage (how raised their liver enzymes are).
Chronic Illnesses
• Patients with chronic illnesses (e.g. diabetes mellitus, hypertension and other heart
diseases) may be using other drugs that can interact with ARVs and therefore they should
be referred to a higher level as the conditions may require more specialized care than is
not available at a first level facility.
Paediatric Patients
• Children with HIV should be referred to a higher level as care for children can be difficult
and challenging (drugs need to be matched to age, body weight and/or body surface area,
some drugs are not used at some ages, drugs need to be continually matched by changes
in their weight and age)
• Children should be started on ARVs by the district clinician then can be monitored at the
first level health facility.
Current or Past Intravenous Drug Use

• Patients suspected of using IV drugs should be referred to a higher level for management
of HIV, investigation for OIs associated with intravenous drug use (Hepatitis B and C),
management of their addiction, and thorough adherence counseling
• Specialized centers for treatment of drug addiction may only be available at referral
hospitals

Past Use of ARVs
• Patients who have used ARVs (except those who have used NVP for PMTCT) may
already be resistant to first-line ARVs and need to be referred to a higher level for further
evaluation.
Patients with Tuberculosis

• Patients with tuberculosis require special consideration.
• The following TB patients should be referred to a higher level facility
o Patients on ART who develop TB
o Patients on TB treatment for pulmonary TB who experience weight loss while on
treatment, develop signs of a WHO stage 4 conditions, or develop thrush,
pyomyositis, recurrent pneumonia, persistent diarrhea, or new prolonged fever
o HIV-positive patients with extra pulmonary TB who are on treatment
o TB patients with CD4 less than 350
• The following patients can be managed at the first level facility
o Smear-positive pulmonary TB patients who are doing well on treatment
o Patients who have completed TB treatment for either pulmonary or extra pulmonary
TB
o TB patients with a CD4 count more than 350
Patients with Peripheral Neuropathy

• Patients with peripheral neuropathy require a specific ART regimen
o Patients with peripheral neuropathy should be prescribed AZT + 3TC + NVP
o They should not be given d4T because it will worsen the neuropathy
o A patient with both anemia and peripheral neuropathy who can neither use AZT nor
D4T should be referred to another level for the appropriate management

Handout 8.2: Using the 5 A’s to Ensure Patient Readiness
Health care providers should use the 5 A’s to assess patient readiness for ART. These 5As
stand for Assess, Advise, Agree, Assist and Arrange
Assess the Patient

• Understanding of HIV, ART, and goals
• Interest on ART
Advice the Patient on

• HIV and AIDS
• Condom use
• Benefits of ART
• Course of HIV disease
• Opportunistic infections and how to prevent them
• Nutrition
Agree with the patient on

• Treatment plan prior to ART initiation and ensure patient is ready and motivated
Assist the Patient

• Develop resources
• Support
• Arrangements for adherence
• Provide information materials and plan a home visit if desired by patient
Arrange
• Follow-up visit after ART initiation
• Discussion at clinical team meeting
• Home visit, as appropriate and feasible

Session 9: Tuberculosis and HIV Co-Infection
Prerequisites
• CMT 04104 Microbiology, Parasitology and Medical Entomology
• CMT 04207 Communicable Diseases
Learning Objectives
By the end of this session, students are expected to be able to:
• Describe relationship between HIV and TB
• Describe clinical presentation of TB in TB/HIV co-infected patients
• Explain TB/HIV collaborative activities
• To describe strategies for reducing TB burden in PLHIV and HIV in TB patients
• Explain diagnostic approaches for TB/HIV co-infection
• Outline management of TB/HIV co-infected patients
• Describe measure to prevent TB/HIV co-infection
Resources Needed
• Handout 9.1: Review of TB Status
• Handout 9.2: Regimens for TB/HIV Co-infected Patients
• Handout 9.3:TB Screening Tool
SESSION OVERVIEW
Step Time Activity/Method Content

Presentation,
2 25 minutes TB/HIV Interaction
Group Discussion
Clinical Presentation of TB in HIV Negative
and Positive Patients
Diagnosis and Differential Diagnosis of
TB/HIV
5 20 minutes Presentation Treatment of TB/HIV Patients
6 15 minutes Presentation Collaborative TB/HIV Activities
7 15 minutes Presentation Measures to Prevent TB/HIV Co-infection

Session 9: Tuberculosis and HIV Co-Infection 119
SESSION CONTENT

Step 2: TB/HIV Interaction (25 minutes)
ASK students to describe points of interaction between TB and HIV.
ALLOW 5 minutes for students to discuss and record their answers on the board/ flipchart.
RECONVENE the groups.
INVITE one group to volunteer and present their responses.
• An increasing number of people have both HIV and TB. HIV and AIDS is the number
one infectious cause of death in the world.
• Many people with HIV and AIDS become ill with TB and die of TB.
• In many countries including Tanzania, the TB and HIV pandemics are fuelling each
other. As a result, the global community has adopted the ‘Two Diseases, One Person’
motto for addressing care.
• Increased TB cases among HIV-infected people poses increased risk of TB transmission
to the general community.
• The prevalence of HIV among persons with TB is high. In Tanzania, National TB and
Leprosy Program (NTLP) estimate 50% of TB patients to be co-infected with HIV.
• There is also a high prevalence of TB among persons living with HIV. It is estimated
that 5-10% of HIV patients are co-infected with TB.
• Because of the interaction between these two diseases, it is important that health care
providers work together to treat patients effectively.

Figure 1: TB/HIV Interaction
Source: MOHSW 2009
• HIV has a great impact on TB as outlined here below

o HIV is the highest known risk factor for developing TB.
o It promotes progression to active TB in people with both recently acquired and latent
M. Tuberculosis infection.
o HIV increases risk of recurrent TB through relapse (because of persistence of M.
Tuberculosis) and re-infection (due to new infection with M. Tuberculosis).
o HIV affects the clinical presentation of TB.
o PLHIV more often present with atypical presentation of pulmonary disease or extra-
pulmonary manifestations.
o It affects the diagnosis of TB because there are more smear negative cases (low
bacterial load) and HIV positive persons are more likely to have a negative TB skin
test due to skin test anergy (especially if CD4 is low).
o HIV affects TB treatment as side effects overlap (ART and TB treatment) more often,
high pill burden affects adherence, relapse and re-infection after treatment more
common, and immune reconstitution affects initiation of ART.
o Before HIV and AIDS, TB drugs were well tolerated with cutaneous reactions
occurring in less than 5% of patients. With HIV, reactions occur in 15-20% of
patients.
• TB also impacts HIV as follows
o It is the most common opportunistic infection (OI) in HIV infected people.
o TB increases the risk of progression from HIV to AIDS and is the leading cause of
death among PLHIV.
Step 3: Clinical Presentation of TB in HIV Negative and Positive Patients

(15 minutes)
Clinical Presentation of TB in HIV Negative Patients

• In HIV-negative patients 80 to 85 percent of TB cases are pulmonary while 15 percent are
extra pulmonary.
• Clinical presentation of TB in these patients includes
o Fever
o Chronic cough with sputum production
o Haemoptysis
o Weight loss
o Night sweat

• Radiological presentation includes
o Upper lobe involvement
o Cavitations
o Fibrosis
Clinical Presentation of TB in HIV Positive Patients

• Clinical presentation of TB in HIV infected patients differs to some degree from that in
HIV negative TB patients as outlined in the figure below.
• There are more extrapulmonary manifestations compared to HIV negative patients.
Figure 2: Typical Presentation of TB in HIV Positive Patients

TB Related Conditions % of PLHIV who Develop TB Condition
Pulmonary disease 75%
Hilar or mediastinal adenopathy 20% - 59%
Pleural effusions 12% - 28%
Miliary pattern 7% - 18%
Normal CXR, positive sputum culture 12%
Source: MOHSW 2009
• CD4 levels in HIV positive patients may determine how pulmonary TB presents. Those
with high CD4 count may present more or less the same as in HIV negative TB patients.
Figure 3: Pulmonary TB Presentation in HIV Positive Patients

High CD4 Low CD4
Clinical Haemoptysis High fever
Chronic cough Dyspnoea
Night Sweat Weight loss
Weight loss
Smear Often positive (80%-90%) Often negative
X-Ray Cavitary lesions Lower lobe infitrates
Upper lobe infiltrates Intra-thoracic LN
Bilateral infiltrates No cavitation
No abnormalities
Source: MOHSW 2009
Step 4: Diagnosis and Differential Diagnosis of TB/HIV (10 minutes)
Diagnosis
• These are tools that help quickly assess patients and make decisions.
• Reaching to a diagnosis starts with history taking and thorough physical examination of
the patient.
• It also involves conducting a laboratory examination
o Sputum or aspirate microscopy for AFB (Ziehl–Neelsen stain). This includes
examination of the cerebrospinal fluid (CSF) in TB meningitis.
o Culture of sputum in pulmonary TB and aspirates for extra pulmonary tuberculosis
o Histological examination tissue biopsy in some extrapulmonary TB conditions for
example TB adenitis.
• Chest X-ray (CXR).

o X-ray alone is not reliable because there is no single x-ray appearance typical for
pulmonary tuberculosis (PTB).
o CXR may be very useful in the case of smear negative suspects, especially in patients
with HIV or other conditions and acutely or severely ill patients.
o All persons with chest radiographic findings suggestive of TB should have sputum
specimens submitted for microbiological examination if they haven’t done so already.
o An x-ray should only be done in TB diagnosis if the above criteria are met.
o However, an x-ray may have another use as an indicator of TB treatment progress
(e.g. before discharge from TB treatment to confirm patient’s response to treatment).
o Sputum smears are still the preferred method.
• Other tests
o Tuberculin Skin Test
Refer students to Handout 9.1: Review of TB Status
Differential Diagnosis for PTB Suspects

• Pneumocystis carinii pneumonia (PCP)
• Bacterial pneumonia
• Fungal pneumonia
Step 5: Treatment of TB/HIV Patients (20 minutes)
• Treatment of TB in HIV positive patients is almost the same as in HIV negative patients
o Case definition are the same
o Treatment categories are the same
o The same drugs are used
o The treatment phases are the same (i.e., induction phase and continuation phase)
o Duration of treatment is the same
• The difference exists when one considers of starting ARV drugs on top of anti-TB drugs.
This actually affects the choice of which ARV drugs to use (especially the NNRTIs and
PIs).
o It is not advisable to start ARVs and anti-TB drugs at the same time. This reduces the
risk of immune reconstitution inflammatory syndrome (IRIS).
o Nevirapine (NVP) and most of the protease inhibitors (PIs) are not recommended
when rifampicin is used (use Efavirenz instead). This is to avoid harmful drug
interaction between NVP, PIs and rifampicin.
o If Efavirenz is also contraindicated e.g. in pregnancy or severe mental disturbance,
triple nucleoside reverse transcriptase inhibitors (triple nukes) can be used for
example Zidovudine + Lamivudine + Abacavir. This requires expertise from
experienced clinicians.
o There are guiding indications on starting ART to TB/HIV co-infected patients as
shown in the figure 4 below.

Figure 4: Indications for ART initiation in TB/HIV
CD4>350 Treat TB first, re-assess for ART after
completion of TB treatment
CD4 200-350 Treat TB first for 2 months before starting ART
CD4< 200 or Begin ART as early as 2 weeks after TB
CD4<15% or WHO treatment initiation
HIV stage 4
Source: MOHSW 2008
o The timing of ART initiation depends on the patient’s CD4 count because delaying.
o ART until after the initiation of TB treatment can reduce the risk of IRIS.
o In patients with lower CD4 counts, ART can be lifesaving if initiated as soon as
possible.
o Drug interactions are also a major concern for treatment of patients with TB-HIV
co-infection
• Follow the national guidelines when prescribing ART for patients on anti-TB regimen
Refer students to Handout 9.2: Regimens for TB/HIV Co-infected Patients
Note: Patients with TB/HIV co-infection should be referred to hospitals for initiation of
co-treatment. Alternatively, experienced clinicians may be consulted on the treatment plan of
the patient.
Step 6: Collaborative TB/HIV Activities (15 minutes)
Rationale for TB/HIV Collaborative Activities

• Given the relationship between TB and HIV means that implementing joint TB/HIV
interventions is essential.
o All patients with HIV infection should be screened for TB and managed
appropriately.
o All patients with TB should be screened for HIV and managed accordingly if they
turn to be positive.
• The National AIDS Control Program (NACP) and National Tuberculosis and Leprosy
Program (NTLP) are now working together on this issue, since TB is the most common
OI and therefore the most common killer disease among PLHIV.
• Due to the high burden of TB globally and nationally TB/HIV collaborative activities are
essential.
Overview of Collaborative TB/HIV Activities

• In order to control TB/HIV co-infection, WHO and MOHSW recommend a unified
approach: ‘one person, two diseases’. This describes a holistic approach to the care of TB
and HIV patients. This means that TB patients should be screened for HIV and HIV-
positive patients should be screened for TB.
• Controlling TB and HIV should be the priority of health care workers at all levels. For
this reason, there is a need for collaboration between TB and HIV programs,
collaboration at the health facility level, and enhanced training of health workers to
manage both diseases.

• Coordinating mechanisms should be established between TB and HIV programmes.
Referrals and linkages between these programmes should be strengthened for continuum
of care.
• There are three objectives of collaborative TB/HIV activities
o To establish the mechanisms for collaboration
o To decrease the burden of TB in PLHIV
o To decrease the burden of HIV in TB patients
Establish Mechanisms for Collaboration

• Recommended activities for this objective include
o Set up coordinating body for TB/HIV activities that are effective at all levels
o Establishing positions of collaborative TB/HIV coordinators and officers at all levels
o Conducting surveillance of HIV prevalence among TB patients
o Conducting joint TB/HIV planning
o Conducting monitoring & evaluation, and
o Facilitating partnership development and coordination.
Decrease TB Burden among PLHIV

• Recommended activities to meet this objective include
o Establishing intensified TB case-finding. A successful TB programme should target
at detecting at least 70% of new smear positive cases.
o Introducing isoniazid (INH) preventive therapy (after first ruling out active TB).
Using INH before excluding active TB means using mono-therapy that will lead to
resistance.
o Use infection control strategies in the clinic and hospitals to reduce risk of
transmission
Refer students to Handout 9.3: TB Screening Tool
o Ensuring TB infection control in health care and congregate settings (places where
large numbers of people come together).
o Introducing ART, patient education, and ensure that patients with active TB complete
their treatment. A successful TB program should target at curing 85% of smear
positive TB cases and that completion of a full course of therapy is required.
Decrease the Burden of HIV in TB Patients

• Main Recommended activities to meet this objective include
o Providing HIV counseling and testing
o Introducing HIV prevention methods
o Introducing cotrimoxazole preventive therapy (CPT)
o Ensuring care and support
o Providing ARV therapy.
Step 7: Measures to Prevent TB/HIV Co-infection (15 minutes)
• Isoniazid preventive therapy (IPT)

o Should be part of package of care for people living with HIV.
o The exclusion of active TB is vitally important and the inability to exclude active TB
may limit use of IPT.

o IPT is effective in HIV-infected people who have high TB risk and have been
screened to exclude active TB.
o The dose for adults is Isoniazid 300 mg daily for 6 to8 months, and the dose for
children is 5mg/kg body weight daily for 6 – 8 months. This should be given with
vitamin B6 (pyridoxine) to reduce the risk of neuropathy.
o The program should ensure appropriate monitoring and follow up.
o Information about TB, including preventive therapy, should be made available to
PLHIV.
o All health care providers for patients with TB should ensure that, persons (especially
children under 5 years of age and persons with HIV infection) who are in close
contact with smear positive TB patients, are evaluated for latent and active and
managed in line with international recommendations.
• Patient education
o Educate patients to
Cover their mouths when coughing (cough into clothing or cloth-not into hands)
Use sputum cups with lids
Avoid coughing directly at the other patients.
Wash hands often
Do not share clothing or cloths that have been coughed into
o Provide information about TB infection/disease and treatment
• Environmental control measures for TB
o These measures are the second line of defence for preventing spread of TB in health
care settings. These include
Opening doors and windows
Designing waiting areas and exam rooms to have maximum natural ventilation
(and use of fans if they are available)
Collecting sputum outside and away from others.
o It is also important to ensure TB infection control in health care settings, laboratory
settings, and congregate settings (e.g. prisons, schools, refugee camps, army camps)
o If possible, it is important to position a fan behind you so air blows from you to the
patient to outside (figure 9.5). If no fan is available, be sure to position yourself up
wind from TB patient, preferably by an open window or other well ventilated area.
Figure 5: Proper Air Flow in Relation to Patient and Health Worker
Source: MOHSW 2009
o Provide HIV counselling and testing

o HIV testing and counseling should be offered to all TB patients.
o TB programmes should mainstream provision of HIV counseling and testing or
establish a referral linkage with HIV and AIDS programmes.

• Introduce HIV prevention methods
o Implement comprehensive HIV prevention strategies, including screening TB patients
for STIs and referring pregnant TB patients to PMTCT.
o Providers should also reduce heterosexual transmission of HIV by
Promoting HIV testing and counselling
Creating and maintaining supportive social environment
Reducing stigma and discrimination
Encouraging disclosure of patients HIV status to significant others
Promote male circumcision
Encouraging sexual abstinence or delayed onset of sex (especially for
adolescents), faithfulness, safer sex practices including consistent and correct use
of condoms
Practicing better recognition and management of STIs/RTIs (sexually transmitted
infections and reproductive tract infections).
• Prevent other opportunistic infections (OIs)
o Cotrimoxazole preventive therapy (CPT) should be provided to TB patients
co-infected with HIV.
o All TB/HIV co-infected patients are eligible for CPT, but it can be stopped when the
patient’s immune system has significantly improved (CD4 >350 for 6 months)
o TB patients should start CPT as soon as they are identified to be infected with HIV, as
it prevents a lot of OIs.
• Protection of health workers

o Increases awareness of TB infection in health care workers
o Increase and enhance access to both provider initiated counselling and testing (PITC)
and voluntary counselling and testing (VCT) to hence care workers
o Improve TB diagnostic services for health care workers
o Advocate personal respiratory protection in special situations
o Reassure all health care workers of the maintained confidentiality to all services
• TB incidence is on the rise due to HIV.

• When TB and HIV interact, they make each other worse.
• TB/HIV co-infection leads to several challenges in the areas of prevention, diagnosis, and
treatment.
• With severe HIV disease, TB is more likely to present as extrapulmonary disease.
• Multidrug therapy is recommended when treating TB in HIV positive patient just as in
HIV negative patients.
• Monitoring patients for side effects if treating HIV and TB is very important
• TB/HIV co-infection requires a coordinated response which includes establishing
mechanisms for collaboration.
• What are the challenges of HIV/TB treatment?

• Describe the importance of TB/HIV collaborative activities.
• Which measures should be taken to prevent TB in HIV patients?
• Outline the management of TBHIV co-infected patient based on CD4 levels.

References
• Cumming, A.D. (2006). Davidson’s Principles and Practice of Medicine.Oxford
• Kumar, P. & Clark, M. (2007). Clinical Medicine. Edinburgh: Elsevier Saunders,
• WHO (1999). Tuberculosis Infection Control in the Era of Expanding HIV Care and
Treatment: Guidelines for the Prevention of Tuberculosis in Health Care Facilities in
Resource-Limited Settings. Retrieved June 22nd, 2010 from http://www.who.int/tb/
publications/2006/tbhiv_infectioncontrol_addendum.pdf.

Handout 9.1: Review of TB Status

Handout 9.2: TB Screening Tool
Source: MOHSW, 2008

Handout 9.3: Regimens for TB/HIV Co-Infected Patients
TB/HIV Patient with CD4 < 200 or CD4 < 15% or WHO HIV stage 4
Week Week 3-8 Months 2-6 Month 7 on
1-2
Morning Fixed dose combination FDC of AZT + 3TC in FDC of AZT + 3TC in
(FDC) of AZT + 3TC in adults or separate adults or separate
adults or separate tabs/syrups for children tabs/syrups for children
tabs/syrups for children
FDC of FDC of RHZE FDC of RH

RHZE
Evening FDC of AZT + 3TC in FDC of AZT + 3TC in FDC of AZT + 3TC in
adults or separate adults or separate adults or separate
tabs/syrups for children + tabs/syrups for children tabs/syrups for children
EFV + EFV + EFV
TB/HIV Patient with CD4 200-350

Week 1-2 Week 3-8 Months 2-6 Month 7 on
Morning FDC of AZT + 3TC in FDC of AZT + 3TC
adults or separate in adults or separate
tabs/syrups for children tabs/syrups for
children
FDC of FDC of FDC of RH
RHZE RHZE
Evening FDC of AZT + 3TC in FDC of AZT + 3TC

adults or separate in adults or separate
tabs/syrups for children + tabs/syrups for
EFV children + EFV
TB/HIV Patient with CD4 >350

Week 1-2 Week 3-8 Months 2-6 Month 7 on
Morning
FDC of RHZE FDC of RHZE FDC of RH Reassess for ART
Evening

Session 10: Diagnosis and Management of Opportunistic
Infections
Prerequisites
• CMT 04207 Communicable Diseases
Learning Objectives
• Define opportunistic infections
• Outline common opportunistic infections
• Describe investigations of common opportunistic infections
• Describe treatment of common opportunistic infections
• Describe prevention of common opportunistic infections
• Explain the role of prophylaxis in the prevention of opportunistic infections
Resources Needed
• Handout 10.1: Kaposi’s Sarcoma
SESSION OVERVIEW
Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction and Learning Objectives
2 05 minutes Presentation Definition of Opportunistic Infections (OIs)

Presentation,
3 25 minutes Common Opportunistic Infections (OIs)
Group Discussion
Clinical Features of Common OIs affecting
the Respiratory System
Clinical Features of Common OIs affecting the
CNS
Clinical Features of Common OIs affecting
the GIT & Skin
Investigations & Treatment of Common OIs
affecting the Respiratory System
affecting the CNS
affecting GIT & Skin
Prophylaxis of Common OIs & Prevention of
OIs

Session 10: Diagnosis and Management of Opportunistic Infections 133
SESSION CONTENT

Step 2: Definition of Opportunistic Infection [OIs] (5 minutes)
• Opportunistic infection: An infection caused by an organism that does not usually cause
disease in a healthy person with a normal immune system.
• When the immune system is compromised such as through HIV infection, this creates an
‘opportunity’ for the pathogen to infect.
• OIs are important HIV indicator diseases and may be the trigger for an HIV diagnosis
• The natural history of HIV involves a progressive loss of CD4 T lymphocytes
• As CD4 level declines, risk of contracting OIs increases.
• OIs may be bacterial, viral, fungal, or parasitic.
• Any body organs/systems can be affected.
Step 3: Common Opportunistic Infections (25 minutes)

ASK each group to list down common opportunistic infections affecting various systems of
the body.
ALLOW 5 minutes for them to discuss and record their answers on a flipchart.
INVITE one group to report out what they have discussed for 5 minutes.
SUMMARIZE the discussion by using content below.
HIV-Related Respiratory Illnesses

• Common OIs affecting the respiratory system include
o Bacterial Pneumonia
o Pneumocystis jirovecii pneumonia (PCP)
o Tuberculosis
• Other OIs affecting the respiratory system include
o Atypical bacteria (chlamydia and mycoplasma)
o Toxoplasmosis, cytomegalovirus (CMV) and Mycobacterium avium complex
(MAC)
o Cryptococcosis

Opportunistic Infections Affecting Central Nervous System (CNS)
• There are many Opportunistic infections that can affect the CNS, the commonest being
o Bacterial meningitis
o Cryptococcal meningitis
o Tuberculous meningitis
o Toxoplasmosis
• Other infections that may affect the CNS include
o CMV (encephalitis)
o HSV (encephalitis)
o JC virus (progressive multifocal leukoencephalopathy)
Opportunistic Infections Affecting Gastrointestinal Tract

• Oro-oesophageal diseases
• Candidiasis ‘thrush’
• Herpes simplex virus (HSV)
• Aphthous ulcers
• CMV ulcers
• Kaposi sarcoma
• Diarrhoeal illness
OIs Affecting Skin

• Viral infections such as herpes zoster, Molluscum contagiosum, genital warts
• Parasitic e.g. Scabies
• Fungal infection such as candida, tinea infection of the body
• Bacterial skin infection e.g. impetigo, recurrent and multiple abscesses
• Malignancies e.g Kaposi’s sarcoma (KS)
Non OIs HIV Related Diseases

• Drug reactions e.g. Steven Johnson syndrome
• Immunologic disorders/allergic conditions e.g. Psoriasis, Papular Pruritic Eruptions
Seborrhoeic dermatitis
Infections of Importance
• Syphilis
o Syphilis is an STI and is found in relatively large number of HIV infected persons due
to fact that the means of transmission are similar and GUDs are a risk factor for HIV
acquisition and transmission
Step 4: Clinical Features of Common OIs Affecting Respiratory System

(10 minutes)
Bacterial Pneumonia
• Common symptoms
o Fever, chills
o Cough
o Shortness of breath
o Purulent sputum
o Abrupt start
o Can occur at any CD4 count

Pneumocystis Pneumonia
• Occurs in patient with
o CD4 count < 200
o WHO stage 4 condition
• Common symptoms
o Fever
o Dry cough
o Slow evolution
o Progressive dyspnea
Tuberculosis
• Presentation may be a combination of cough, fever and sputum production
• Presentation may be atypical with dry cough, or no cough with fever only
• Excessive night sweats
• Loss of weight
• Chest pain
• Breathlessness
Step 5: Clinical Features of Common OIs Affecting the CNS (10 minutes)
Cryptococcal Meningitis
• Sub-acute onset of fever, headache, altered mental status
• Neck stiffness might be there or not at all
• The respiratory system may also be affected by Cryptococcus neoformans and present
with pulmonary symptoms e.g. cough and chest pain
• Often occurs in patients with CD4 count less than 50 cells/ml.
Note that, other conditions may cause altered mental state. These include
o Cerebral malaria
o Dehydration
o Meningitis (TB/crypto/bacterial)
o Toxoplasmosis
o HIV encephalopathy
o Psychosis
Cerebral Toxoplasmosis
• Generally occurs with CD4 count of less than 100 cells/ml
• Patients present with progressive focal neurological deficit
• There may also be convulsions, confusion and headache
• Alteration of mental state is rare
Peripheral Neuropathy
• This is a common HIV complication
• Usually symmetrical with stocking-glove distribution
• May be caused by
o HIV itself
o Drugs used in the treatment of HIV mainly Stavudine (d4T), didanosine (ddI) and
anti-TB drugs e.g. INH
o Alcoholism
o Diabetes

Step 6: Clinical Features of Common OIs Affecting the GIT & Skin
(10 minutes)
Common OIs Affecting the GIT

• Oral Candidiasis (Oral thrush)
o Occurs increasingly at CD4 < 300.
o Presents with white painless plaques on the buccal, pharyngeal mucosa or tongue
surface that can easily be scraped off
• Oro-Oesophageal candidiasis
o Caused by Candida albicans
o Occurs in WHO stage 4
o May presents with difficult/painful swallowing and retrosternal pain. Other causes of
painful swallowing may include CMV and/or HSV lesions in the oesophagus.
• Diagnosis of oesophageal thrush is based on presentation and response to empiric
treatment.
• Treatment for thrush includes Nystatin mouthwash (dissolved in half glass water),
clotrimazole lozenges, and Fluconazole if oesophagitis or intractable oral thrush
Common OIs Affecting the Skin

• Herpes Simplex Virus (HSV)
o Painful shallow ulcers/vesicles that can occur around the mouth or genital regions, but
can present anywhere on the body
o Occur at any stage of CD4 count but increasingly as CD4 falls
o HSV I and II occur at any CD4
o Chronic HSV is seen when CD4 < 100
• HSV type 1 (oral herpes)
o Cold sores around mouth and lips, but usually not the tongue
o About 96% of people have antibodies to HSV type 1, though flare-ups are much more
common in HIV disease
• HSV type 2 (genital herpes)
o Very painful sores around the genitals
• Kaposi’s Sarcoma-caused by human herpes virus type 8 (HHV – 8)
Refer students to Handout 10.1: Kaposi’s Sarcoma
• Papular Pruritic Eruptions (PPE)

• Molluscum Contagiosum
• Seborrheic Dermatitis
Step 7: Investigations & Treatment of Common OIs Affecting the

Respiratory System (10 minutes)
Bacterial Pneumonia
• Investigations
o Chest X-ray
o Full blood picture
o Gram stain and AFB stain of sputum if available
o Most common pathogens

Streptococcus pneumonia
o Hemophilus influenza
o Staphylococcus aureus
• Treatment
o Amoxicillin or Amoxicillin + Clavulanic Acid
o Follow-up
See the patient in 3-5 days
PCP
• Investigations
o Clinical examination and history is most helpful to reach a diagnosis
o CXR may be done but can be normal or have generalized nodular opacities
o Increased Serum Lactate Dehydrogenase enzyme in severe cases
o Blood gas analysis
o Pulse-oximetry to detectthe level of hypoxia
o Induced sputum if available with silver staining to look for PCP
Note: Most of the investigations are not available in the primary health care facilities hence
referral is unavoidable after the pre-referral management.
Treatment
• High dose Cotrimoxazole at a dose of 12-15mg/kg body weight a day based on
trimethoprim component
• (The drug for a day should be in 3-4 divided doses)
• The dosage should also be for 21 days (3 weeks)
• Oxygen therapy
• Steroids e.g., Prednisolone may be used if there is severe hypoxia
Note: Patients suspected of having PCP should be referred to hospitals for proper
management and support for hypoxia. Pre referral management should always be done before
the patient is referred.
Tuberculosis
• Investigations
o Laboratory examinations
AFB microscopy for sputum and aspirates
Culture of sputum or aspirates for EPTB
Histological examination - Biopsy tissue
o Chest X-ray (CXR) alone is not reliable as there is no X-ray appearance typical for
pulmonary tuberculosis (PTB)
Treatment
• Effective treatment requires the prescription of adequate chemotherapy including
o Appropriate drug combinations
o Drugs that are taken regularly
o Drugs that are taken for a sufficient period of time
o Beware of interactions with ART (e.g. Nevirapine and Protease Inhibitors with
rifampicin)

Step 8: Investigations and Treatment of Common OIs Affecting the CNS
(10 minutes)
Cryptococcal Meningitis
• Suspected meningitis should be referred to hospital for proper investigations.
Investigations
• Lumbar puncture (LP)
o Increased opening pressure
o India ink staining may detect the yeast
o In more advanced hospitals serum or cerebrospinal fluid cryptococcal antigen
(CRAG) may be done
Treatment
• Treatment needs to be done at hospital level.
• Cryptococcal Meningitis may be treated with:
o Amphotericin B 0.7 mg/kg/day IV with or without Flucytosine 100mg/kg/day (in
divided doses) x 14 days during the induction stage
o This is then followed by Fluconazole 400mg/day for 8 weeks in the maintenance
phase
o Thereafter oral Fluconazole 200mg daily) until patient has sustained CD4 increase
greater than 200 for more than 6 months in the suppressive phase
o In most resource limited countries, Amphotericin B and Flucytosine are not readily
available.
o Alternatively, give intravenous (IV) Fluconazole 400mg/day x 10 days until patient
can take orally.
o Then continue with the same dose for ten weeks.
o Thereafter maintain 200mg daily.
Toxoplasmosis
• Investigations
o The diagnosis is mostly clinical (though not very accurate)
o Diagnostic investigations are done at hospital levels, therefore patients need to be
referred
o Lumbar puncture which is usually normal excludes other causes of the clinical
presentations
o In more advanced and well equipped hospitals serum toxoplasma antibodies may be
performed
o Respond to treatment in 7-10 days
o Differential diagnosis
Tuberculoma
Cerebral lymphoma
Cryptococcoma
• Treatment
o Patients should be referred for proper evaluation and initiation of treatment
o In acute cerebral toxoplasmosis treat with
Sulphadiazine 100-200mg/kg/day up to 1 gram in divided doses and
Pyrimethamine 50mg once daily (give 100 mg in the first day) and
Folinic acid 10mg daily as long as pyrimethamine is being given

o For maintenance therapy, give
Sulphadiazine 1 gm two times a day
Pyremithamine 25 mg daily and folic acid 10 mg daily
o In resource limited settings, the above mentioned drugs are usually not readily
available. Alternative treatment may include use of high dose cotrimoxazole or a
combination of sulfadoxine and pyrimethamine (SP).
Peripheral Neuropathy
• Treatment
o Analgesic
o Vitamin B (pyridoxine)
o Consider amitriptyline or carbamazepine if pain is unresolved by the use of ordinary
analgesics
o Usually improves with ART but avoid stavudine and didanosine as they may
aggrevate the condition as part of their side effects.
Step 9: Treatment of Common OIs Affecting the GI Tract & Skin (10
minutes)
Candidiasis
• Treatment
o Nystatin mouthwash dissolved in half glass water
o Clotrimazole lozenges
o Fluconazole if oesophagitis or intractable oral thrush at a dose of 150mg/day or
200mg/day for 2-3 weeks
Herpes Simplex Virus (HSV)

• Treatment
o Acyclovir shortens healing time
o Given at a dosage of 400 mg 3 times/day for 10 days
Step 10: Prophylaxis and Prevention of Common OIs (10 minutes)
Cotrimoxazole in Adults
• Very effective in preventing PCP, toxoplasmosis, other pneumonias and diarrheal
diseases
• Is used for
o All HIV-infected patients in WHO stage 2, 3, or 4
o Asymptomatic HIV infected individuals with CD4 counts of < 350 cells/mm3
o All patients with previous PCP and their CD4 count is still less than 350 cells/mm3
• Adult dose is 960mg (160mg Trimethoprim/800mg Sulphamethaxazole) daily given as 2
tablets of single strength of 480mg (80mg trimethoprim/400mg sulphamethaxazole) or 1
tablet of double strength 960mg when available
• Duration
o Ongoing for patients not on ARVs
o Stop when CD4 >350 for patients taking ARVs

Isoniazid Preventive Therapy (IPT)
• IPT is preventive therapy for TB
• It should be part of package for care people living with HIV
• Exclusion of active TB is vitally important
• Inability to exclude active TB may limit use of IPT
• Effective in HIV-infected people
• Can be given to people with HIV having high TB risk and have been screened to exclude
active TB disease
Prevention of Opportunistic Infections (OIs)

• Avoid unpasteurized dairy products, raw or undercooked eggs, meat, poultry, or fish to
avoid salmonella/shigella infections
• Avoid undercooked or raw meat for toxoplasmosis
• Family should be advised to boil drinking water to avoid diarrhoea diseases
• Avoid contact with bird droppings for cryptococcosis
• OIs are a significant cause of morbidity and mortality for PLHIV in Tanzania.
• OIs are treatable and sometimes preventable.
• Incidence of OIs decreases with the use of ART.
• It is important to perform comprehensive history and physical examination to screen for
these important conditions, and follow up after treatment.
• Patients with severe OIs are highest priority for ART initiation.
• Mention common opportunistic diseases according to body systems

• Describe clinical features of Pneumocystis pneumonia
• How can OIs be prevented?
References
• Kumar, P. & Clark, M. (2007). Clinical Medicine: Edinburgh: Elsevier Saunders.
• Cumming, A.D. (2006). Davidson’s Principles and Practice of Medicine: Oxford
Salaam, Tanzania: Ministry of Health and Social Welfare

Handout 10.1: Kaposis Sarcoma
• Common cancer in PLHIV aetiologically linked to Human Herpes Virus (HHV) type 8
but KS can also occur in HIV negative patients
• Can occur at any CD4 level
Diagnosis and Management

• Diagnosis made by observing characteristic lesions
• Lesions can be cutaneous, mucosal, or visceral involvement
• Confirmation requires examination of biopsy of the lesion
Management
• Less extensive disease responds to ART
• Refer patients with severe disease to a hospital especially if pulmonary disease is
suspected
• Radiotherapy and/or Chemotherapy is indicated for patients with rapidly progressive
disease

Session 10: Diagnosis and Management of Opportunistic Infecti 142
Session 11: Introduction to Psychiatry and Mental Health
Prerequisites
• CMT 04213 Clinical skills
• CMT 04210 Basic patient care
Learning Objectives
• Define health, mental health and mental illness
• Describe basis of mental health
• Classify mental illnesses
• Describe general causes of mental illnesses
• Describe history taking in psychiatry
• Describe mental state examination for formulation of psychiatric diagnosis
Resources Needed
• Worksheet 11.1: Role Play Information
SESSION OVERVIEW
Activity/
Step Time Content
Method
Definition of Health, Mental Health and Mental
Illness
Introduction to Mental Health (Psychiatry),
Presentation,
3 20 minutes Classification and General Causes of Mental
Brainstorm
Health
4 30 minutes Presentation History Taking in Psychiatric
Presentation,
5 40 minutes Mental Status Examination
Role Play

Session 11: Introduction to Psychiatry and Mental Health 143
Step 2: Definition of Health, Mental Health and Mental Illness
(10 minutes)
Health
• A condition in which all functions of the body and mind are normally active
• In other words health involves finding balance in all aspects of your life
o Physically
o Mentally
o Emotionally and
o Spiritually
• The World Health Organization defines health as a state of complete physical, mental, or
social well-being and not merely the absence of disease or infirmity.
Mental Health
• A state of well-being in which the individual realizes his or her own abilities, can cope
with the normal stresses of life, can work productively and fruitfully, and is able to make
a contribution to his or her community.
• Psychological adjustment to one’s circumstances or environment.
• The ability to cope with or make the best of changing stresses and stimuli.
Mental Illness
• Any of various conditions characterized by impairment of an individual's normal
cognitive, emotional, or behavioural functioning, and caused by social, psychological,
biochemical, genetic, or other factors, such as infection or head trauma.
Step 3: Introduction to Mental Health (Psychiatry), Classification and

General Causes of Mental Illness (20 minutes)
Introduction
• Psychiatry is the branch of medicine that deals with the cause, diagnosis, treatment and
prevention of mental illness; as well as promotion of mental health.
• Mental illness abnormalities can be seen in a number of ways
o Significant deviation from normal thoughts and feelings
o Significant deviation from normal behaviors
o Perceived subjective distress
Classifications
• The classification of mental disorders (also known as psychiatric nosology or taxonomy)
is a key aspect of psychiatry.
• It is an important issue for consumers and providers of mental health services.
• There are currently two widely established systems for classifying mental illness.
• Chapter V of the International Classification Of Diseases (ICD-10) produced by the
World Health Organization (WHO) and the
• Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) produced by the
American Psychiatric Association (APA)
• Both list categories of disorders thought to be distinct types, and have deliberately
converged their codes in recent revisions so that the manuals are often broadly
comparable, although significant differences remain.

• The International Classification of Diseases (ICD) is an international standard diagnostic
classification for a wide variety of health conditions. Chapter V focuses on ‘mental and
behavioural disorders’ and consists of 10 main groups:
o F0: Organic, including symptomatic, mental disorders
o F1: Mental and behavioural disorders due to use of psychoactive substances
o F2: Schizophrenia, schizotypal and delusional disorders
o F3: Mood [affective] disorders
o F4: Neurotic, stress-related and somatoform disorders
o F5: Behavioural syndromes associated with physiological disturbances and physical
factors
o F6: Disorders of personality and behaviour in adult persons
o F7: Mental retardation
o F8: Disorders of psychological development
o F9: Behavioural and emotional disorders with onset usually occurring in childhood
and adolescence
o In addition, a group of ‘unspecified mental disorders’.
• Within each group there are more specific subcategories. The ICD includes personality
disorders on the same domain as other mental disorders, unlike the DSM.
• The ICD-10 state that mental disorder is ‘not an exact term’, although is generally used
‘to imply the existence of a clinically recognizable set of symptoms or behaviours
associated in most cases with distress and with interference with personal functions.
• The DSM-IV characterizes mental disorder as a clinically significant behavioral or
psychological syndrome or pattern that occurs in an individual and that
o Is associated with present distress, or disability, or with a significant increased risk of
suffering.
o No definition adequately specifies precise boundaries for the concept of 'mental
disorder'.
o Different situations call for different definitions.
• The DSM also states that ‘there is no assumption that each category of mental disorder is
a completely discrete entity with absolute boundaries dividing it from other mental
disorders or from no mental disorder.’
• The DSM-IV consists of five axis (domains) on which disorder can be assessed. The five
axis are:
o Axis I: Clinical Disorders (all mental disorders except Personality Disorders and
Mental Retardation)
o Axis II: Personality Disorders and Mental Retardation
o Axis III: General Medical Conditions (must be connected to a Mental Disorder)
o Axis IV: Psychosocial and Environmental Problems (for example limited social
support network)
o Axis V: Global assessment of functioning (psychological, social and job-related
functions are evaluated on a continuum between mental health and extreme mental
disorder)

General Causes of Mental Illness (5 minutes)
Activity: Brainstorming (5 minutes)
ASK students to mention the general causes of mental illnesses.
RECORD their responses on a flip chart/ board.
Predisposing Factors
• Genetics
• Teratogenic effects
Precipitating Factors
• Childhood abuse
• Family disputes
• Orphanage
• Cannabis or other illicit drug use
• Alcohol
• Bad social influence
Perpetuating Factors
• Family disharmony
• Poverty
• Chronic illness
• Cannabis use
• Bad social influence
Step 4: History Taking in Psychiatric (30 minutes)
Particulars of the Patients and Rapport Building

• Identification Data
o Name, age, sex, marital status, education, occupation, religion socio-economic
background
Presenting Complaints from the Patient and/or Relatives
Activity: Exercise
• Mr Jones is a 74 year old man seen at outpatient clinic with his wife because of memory
loss
• It is important to take history primarily from the patient and not from relative or next of
kin unless if the patient is uncooperative or is mute secondary to his illness.
• But in case of memory loss the history from the family member is also very important. As
patients with memory loss do not remember what happened
• Confidentiality must be observed.

History of the Presenting Chief Complaints
• Onset of symptoms chronologically
• Duration
• Course/progression
• Complication or problems the symptoms has caused
• Then cover any associated symptoms like problem with sleep, appetite and energy
• Ask about their mood and motivation for activities they normally enjoy
• Try to use the patient’s own words
• Include important negatives here as well
• This has to cover everything that is of relevance to the presentation and diagnosis
Past Psychiatric History

• Very often linked to the history of the presenting complaints which include
o Diagnosis
o Previous admissions
o Previous contact with psychiatrist
o Previous contact with other professionals
o Previous antipsychotic treatment
o Previous response to treatments
Past Medical History

• Ask about surgical operations
• Ask about medical conditions such as endocrine disease, cardiovascular, and infectious
• Ask about other conditions like head injuries, effects of post anaesthesia and spinal cord
injuries.
• Ask about obstetric conditions such as puerperal psychosis, eclampsia.
Review of Other Systems Chronologically

• Start with the affected systems
Drug History
y Prescribed medications
y Over the counter use
y Herbal medicines
y Liquids and injections
y Illicit drug use-including indigenous substances
Family History
y Family structure (inheritable diseases)
y Deaths in the family and their causes
y Psychiatric illness in the family
y Social economic status in the family
y Education and employment within the family members
y Family harmony prescribed
y Alcohol use problems
y Sub-clinical traits (personality traits)

Personal History
• A narrative from birth to recent
• Start with
o Pregnancy (normal, complicated, unintended)
o Birth
o Childhood
o Relationships with family/friends
o Schooling and age at leaving
o Menstrual and obstetric (in females)
o Sexual and marital issues
o Jobs performed
Social History
y What sort of place they live at
y Who are they living with
y Any help
y Drug and alcohol (if not done already)
y Smoking
Premorbid Personality
y People can have many different reactions to different situations.
y Ask what they use to engage in for activities and what are they able to do now.
y Ask about what gives them support, such as family, friends and spiritual/religion.
Forensic History
y Violence /anger
y Trouble with police
y Arrests
y Convictions
y Times in prison
y Current situation e.g. probation
• Refer to Session 2: General Examination in CMT 05101 Internal Medicine 1
Step 5: Mental Status Examination (40 minutes)
• Psychiatric examination is covered systematically as follows
General Appearance and Behavior

• May be uncooperative or mute patients
o Terms might include
Tidy, unkempt, anxious, agitated, threatening, tearful, eye contact (good/poor)
pacing, gestures, restless.
Gait and posture
Motor activity (excitement, stupor, catatonic, restlessness)

Speech
y Need to include descriptions of
o Rate of speech
o Volume
o Content of speech
Mood/Affect
• Rate as low/high
• Anxious
• Talks about subjective patient experiences
• Might also want to include associated features of mood disturbance include sociality
• Changes minute to minute
• Rate as blunted or
• Reduced or
• Flat (absence of emotional expression) or
• Inappropriate or
• Labile
• Apathy, ambivalence, euphoria
Thought
• Progression or sequence of thoughts
o Flight of ideas
o Retardation of thought
o Preservation of thoughts
o Circumstaciality
o Thought block
• Content of thoughts
o Obsessions
o Delusions – these are false, fixed and unbreakable beliefs that falls outside the
person’s social, cultural or religious background) e.g.
Delusions of grandeur – a person believes that she/he is some one of great
importance
Delusions of persecution - a person believes that he has been selected for attack or
is being plotted against
Nihilist Delusions – a person believes that either he does not exist or that some
portions of himself are not existing
Delusions of self accusation- A person believes that he/she has sinned that is why
she/he is diseased
Erotomanic delusions - a person believes that he/she is loved intensely by ‘the
loved object’ who is usually married , of high socioeconomic status (public figure)
Perception
y Types include
o Hallucinations and Illusions
y Illusion
o A misperception of an object
o Occurs in
Normal people
Delirium
Dementia

y Hallucinations
o A perceptioon without an
a object
o Obvious onnes include
Auditorry
Visual anda tactile
Cognitiion
• Connsciousness (rate as norrmal, clouded, stupor or o coma)
• Orieentation (time, place, person)
p
• Atteention (digitt span test, give 5 digitt not all even and not alll odd and let him repeat
imm
mediately)
• Conncentration (count seriaal 7 from 1000 or serial 3 from 20 backward)
b
• Judggment (abillity to distinnguish or to decide bad from good and vise veerse)
o Rate as good/g intactt/ normal orr poor/ imp paired/ abnoormal
• Reaasoning (abiility to distinnguish betwween two id dentical item
ms)
• Mem mory (shorrt and long term )
• Inteelligence (uuse simple arithmetic
a teest)
Insightt
• Com mplete deniaal of illnesss
• Sligght awarenness
• Inteellectual insight
• Afteer a detailedd history annd examinatiion, investig
gations are carried out based on th
he
diaggnostic and etiological formulationns
• Psychiatric assessment andd descriptivve formulatiion is made before listing differenttial
diaggnosis.
Activityy: Role Plaay (20 minu

utes)
EXPLA AIN to studdents that theere will be a role play between

b a patient
p and a health carre
provideer. Two studdents will be volunteer, one to play y role of health care prrovider and another
will plaay a role of a patient.
ASK sttudents to voolunteer to be role playyers.

R
Refer the volunteer
v too Worksheeet 11. 1: Ro
ole Play Infformation sso that he/sh
he can
read thee descriptionn regardingg the role plaay.
EXPLA AIN that thee patient wiill interact with

w the heaalth care proovider and pprovide answ wers to
the heallth care provvider’s questions (theree are no right or wrongg answers – the patient just
needs too provide reesponses whhile keepingg in mind th he informatiion about thhe patient on
n this
scenarioo)
EMPH HASIZE beffore beginniing the role play that thhe health care provider should con ncentrate
on the presenting
p c
complaint orr the reasonn why the paatient has coome to seekk care when
n taking
the histoory.
Activity contiinued on neext page.

Session 11:
1 Introductiion to Psychiaatry and Mentaal Health 150
EXPLAIN to the rest of the students that their job is to observe the encounter, without
interrupting. Remind students that the health care provider’s job is to determine what the
patient’s main issues are and give a concise mental state evaluation.
Provide feedback at the end of the role play first commenting on steps done well. Advise the
health care provider if any steps were omitted and on possible improvements.
START the role play.
DE-ROLE the student who were role-playing as health care provider and as a patient, once
the role play is over.
SUMMARISE the role play, emphasizing the proper sequences of taking mental state
examination and asking for more details to explore the primary presenting complaint in more
depth.
ASK students if they have questions about the role play if any and address them before
proceed to next step.
• Mental illness changes in thinking, mood and behavior cause significant distress and
impaired functioning.
• There are predisposing, precipitating and perpetuating factors for mental illnesses
• Thorough medical and psychiatric history taking for patients with mental illnesses is of
paramount importance.
• Mental status examination/evaluation is important in reaching to the specific mental
illness (diagnosis).
• Many illnesses can present with mental health symptoms and is important to identify any
treatable/reversible conditions.
• Define health, mental health and mental illness

• List down four types of anxiety disorders
• What do you understand by insight?
References
McGraw Hill.
• Cumming, A.D. (2003). Davidson’s Principles and Practice of Medicine. Oxford:
Edinburgh.
• David M. N. (2006). The African Textbook of Clinical Psychiatry and Mental Health.
Nairobi, Kenya: AMREF
Saunders.

Worksheet 11.1: Role Play Information
Patient Information (Justin)

Justin ran away from home when he was fifteen and has lived off the streets in Dar es
Salaam for five years, surviving through begging and shoplifting. He reported many
times to the police that people over the street are after him and that they want to harm
him. He says that he is planning for a fight back. His body hygiene is deteriorating and
he feeds on refusal from the dust bin. Justin is brought to the psychiatric clinic under
police escort.
Another student to act like a health worker and conduct Mental State Examination from
Justin history using mental status examination notes from step 5 above.

Session 12: Epilepsy
Prerequisites
• CMT 04210 Basic Patient Care
Learning Objectives
• Define epilepsy
• Explain etiology of epilepsy
• Describe clinical classification of epilepsy
• Outline differential diagnosis of epilepsy
• List investigations of epilepsy
• Identify treatment of epilepsy
• Describe status epileptics
Resources Needed
• Handout 12.1: Pictorial Illustration of Partial and Generalized Epilepsy
• Handout 12.2: Drug Management for Epilepsy
• Worksheet 12.1: Diagnosis of Epilepsy
SESSION OVERVIEW
Activity/
Step Time Content
Method
2 10 minutes Presentation Definition
3 10 minutes Presentation Etiological Factors
4 10 minutes Presentation Clinical Classification
5 10 minutes Presentation Differential Diagnosis
6 10 minutes Presentation Investigations

Presentation,
7 35 minutes Treatment
Case study
Definition and Management of Status
Epilepticus

Session 12: Epilepsy 153
Step 2: Definition (10 minutes)
• Epilepsy (in Greek ‘to seize’) is a neuropsychiatric condition or brain disorder in which
clusters of nerve cells, or neurons, in the brain sometimes signal abnormally.
o Neurons normally generate electrochemical impulses that act on other neurons,
glands, and muscles to produce human thoughts, feelings, and actions.
• In epilepsy, the normal pattern of neuronal activity becomes disturbed, causing strange
sensations, emotions, and behavior, or sometimes convulsions, muscle spasms, and loss
of consciousness.
• During a seizure, neurons may fire as many as 500 times a second, much faster than
normal. In some people, this happens only occasionally; for others, it may happen up to
hundreds of times a day.
Step 3: Etiological Factors (10 minutes)
• The common causes of seizures in infants and children include:

o Congenital malformations
o Prenatal injuries or hypoxia
o Developmental neurologic disorders
o Metabolic defects
o Injuries
o Infections
• In young adults seizures are commonly caused by
o Head trauma
o Brain tumors
o Infection/high fever
o Arteriovenous malformations
• In elderly seizures may be caused by
o Cerebrovascular disease
o CNS degenerative diseases
o Brain tumors are common causes
o Genetic risk increases 2-3 times in individuals with first degree relatives suffering
epilepsy
o Head trauma
• Precipitating factors of seizures are
o Sleep deprivation
o Emotional disturbances/stress
o Flickering light like in discos, or after watching TV over many hours
o Poor drug compliance
o Medical drugs such as Chlorpromazine, Haloperidol are safer but can still cause fits in
high doses
o Alcohol and drugs like Amphetamine and Cocaine
o Hypoglycemia

Step 4: Clinical Classification (10 minutes)
• Seizures are described and distinguished by clinical pattern as

o Partial/Focal Seizures - beginning focally in one area of the brain
o Generalized Seizures - They start generalized (bilateral) in the whole brain at the
same time
Refer students to Handout 12.1: Pictorial Illustration of Partial and

Generalized Epilepsy
Types of Partial/Focal Seizures

• Simple partial seizures with motoric fits of some part of the body but no loss of
consciousness and frequently with aura
• Complex partial seizures with reduced level of consciousness and frequently with aura
• Partial seizures with secondary generalization. These begin as simple or complex partial
seizures but then spread to the rest of the brain and look like generalized tonic-clonic
seizures with movements and frequently with aura
• An aura represents the initial phase of a focal seizure
Types of Primary Generalized Seizure

• Grand Mal Tonic-Clonic Seizure
o Grand mal is a French word meaning the ‘big evil’
o The most common seizure during which the person fall to the ground
o There is sudden loss of consciousness without aura
o Tonic and clonic phase of convulsions
o Terminal sleep which lasts for minutes to one hour
o Phase of being confused, disoriented and dysphoric
• Absence Seizure
o Absence or Petit mal a French word meaning ‘small evil’
o Starts suddenly without aura
o Lasts for some seconds only
o Patient does not fall down
o Loss of awareness, patient stares , seems absent minded, stops talking or responding
o Regains consciousness suddenly without post-ictal abnormalities and continues his
activities as if nothing happened
• Other Types of Primary Generalized Seizures
o Myoclonic seizure
o Atonic seizure
Step 5: Differential Diagnosis (10 minutes)
• Pyrexia (fever)
o Convulsions occuring in children under 5 years due to high grade fever known as
febrile convulsions
o In the majority there is no recurrence
o Febrile convulsions are not usually labeled as epilepsy
• Brain tumors and abscesses
o Mass occupying lesions (SOL) in the cortex cause seizure either partial or secondary
generalized seizures

o Hydrocephalus also lowers seizures threshold
• Vascular problems
o Seizures sometimes follow cerebral infarction especially in the elderly
o There is a peak in incidence late in life
o May present with seizures and occasionally a subarachnoid bleeding
• Alcohol, drugs and drug withdrawal
o Chronic alcohol abuse is a common cause of seizures
o Occurs either while drinking heavily (rum fit) or during periods of withdrawal
o Alcohol-induced hypoglycaemia also provokes epileptiform attacks
o Antipsychotics such as phenothiazides and antidepressants (tricyclics) may sometimes
precipitate epileptic seizures
o Withdrawal of anticonvulsant drugs especially phenobarbitone and benzodiazepines
may provoke seizures
o Many medications can lower seizure threshholds (e.g. efavirenz, bupropion)
• Encephalitis and inflammatory conditions
o Seizures occur frequently as presenting features of
Viral encephalitis
Central nervous HIV manifestations
Toxoplasmosis
Cytomegalovirus
Bacterial and viral meningitis
Neurosyphilis
CNS cysticercosis (due to calcification by taenia solium cysticerci in the brain)
Cryptococcus meningitis
Cerebral malaria
• Metabolic abnormalities
o Seizures are seen with
Hypocalcaemia
Acute hypoxia
Uraemia
Hepatocellular failure
Hypo or hypernatremia
Hypoglycemia
• Degenerative brain disorders
o Seizures can occur in dementia like in alzheimer’s disease
• Psychogenic
o Seizures which are mimicking epilepsy may occur in hysteria and other dissociative
disorders
• Pueperal
o Spontaneous paroxysmal muscular contractions and relaxation in postpartum woman
may mimic epilepsy.
• Eclampsia
o Seizures may occur in third trimester pregnancy with hypertension and
glomerulonephritis.
Step 6: Investigations (10 minutes)
Investigations Done in Primary Health Care Facilities

• Blood slides for malaria parasites

• FBP (HB is necessary)
• Urinalysis (albumin is necessary)
• Sputum for AFB
• Serological test of HIV after counseling
• Blood sugar
Investigations Done in Hospitals (in Addition to those Done in Primary Health Care
Levels)
• Renal (Kidney) function test (serum creatinine or urea)
• Liver function test (serum bilirubin, transaminases)
• VDRL (serological test for syphilis)
• Serum electrolytes (Na+ K+ Ca2+ )
• Chest X-ray
• Lumbar puncture (CSF sugar, protein, gram stain, and ZN stain, Indian Ink stain)
Investigations Done in a Consultant Hospitals (in Addition to those Done in Other
Hospitals)
• Brain scan
• Electroencephalogram EEG
• Electrocardiogram
Step 7: Treatment (35 minutes)
Generalized Tonic-Clonic Seizures

• Prevent person from hurting himself or herself
o Place something soft under the head
o Loosen tight clothing
o Clear area for sharp or hard objects
• Do not force any objects into patient's mouth
• Do not restrain patient's movements
• Turn patient on his or her side to allow saliva to drain from mouth
• Stay with the patient until seizure ends naturally
• Do not pour liquids into patient's mouth or offer any food, drink or medication until
she/he is fully awake
• Give artificial respiration if patient does not resume breathing after seizure
• Provide area for patient to rest until fully awakened accompanied by responsible person
• Be reassuring and supportive when consciousness returns
• Convulsive seizure (due to epilepsy) is not usually a medical emergency but presence of
any of the following signs indicate the need for immediate medical attention
o Seizure lasting longer than 10 minutes or occurrence of second seizure
o Difficulty in rousing at 20-minute intervals
o Complaints of difficulty with vision
o Vomiting
o Persistent headache after a rest period
o Unconsciousness
o Unequal size pupils or excessively dilated
o Other co-morbid conditions (like abnormal breathing, frothing, unusual smell from
the mouth like rotten fish smell)

Pharmacotherapy
• This includes beliefs considering the traditional and customs of a particular society in the
community, some may be superstitious i.e. spirit possession, curse, contagious and
sometimes the beliefs of mistrust of hospital treatment.
• First treatment starts with education concerning epilepsy to the community.
• Since epilepsy is not cured completely but can be controlled, treatment must be
continuous and interchangeable.
Principles of Treating Epilepsy

• Treat underlying cause
• Control the seizures with Phenobarbital
• Initial dose of Phenobarbital for children is 3 - 4 mg/kg once daily or in 2 divided doses,
increase to 8 mg/kg/day if necessary
• In adults – in acute seizures, dilute the injection in 1ml of water for injection, give
10mg/kg at a rate of not more than 100mg/minute (maximum total dose is 1g).
Maintenance dose is 60-200mg per day.
Refer Student to Handout 12.2: Drug Management for Epilepsy
Activity: Case Study (15 minutes)
ASK a volunteer to read the following case study and questions in Worksheet 12.1:
Diagnosis of Epilepsy.
ALLOW students time to discuss the answers to the questions.
TELL students to note down their responses on the worksheet.
LEAD the discussion and allow few students to share their responses.
SUMMARIZE the discussion by using answers on Worksheet 12.1: Diagnosis of Epilepsy
Step 8: Definition and Management of Status Epilepticus (15 minutes)
Definition
• Status Epilepticus exist when a series of seizures occurs without the patient regaining
awareness between attacks over a period of 30 minutes.
• Most often this refers to recurrent tonic clonic seizure.
• It is a life threatening condition and therefore a medical emergency.
• Status epileptics may be precipitated by abrupt withdrawal of anticonvulsant drugs or the
presence of major structural lesion in the brain or acute metabolic disturbance
Management
• Give immediate care as it appeared in the first aid for seizure notes
General Measures
• Secure intravenous access

• Draw blood for
o Glucose
o Urea and electrolytes including calcium and magnesium
o Liver function and
o Sample for future analysis (e.g. drug misuse)
• Give diazepam 10mg IV or rectally repeat once only after 15 minutes
• If seizure still continues after 30 minutes give Phenobarbital I.V. 10mg/kg at
100mls/minute and refer immediately
Refer students to Handout 12.2: Drug Management for Epilepsy
• Epilepsy is the tendency to develop recurrent seizures

• Epilepsy requires long-term maintenance therapy so as to prevent recurrence of seizures.
• Epilepsy can be classified clinically into two major parts namely;
o Partial/focal seizures that begins focally in one area of the brain
o Generalized seizures that manifest with generalized bilateral in the whole brain at the
same time
• Drugs that can be used in epilepsy include Phenobarbital, phenytoin or carbamazepine.
• Status epilepticus is a medical emergency condition and needs diazepam to start with in
the management.
• List down 10 points you will take to help patient found in a state of acute epileptic fit
• Outline causes of epilepsy
• Explain management of status epileptic
References
• Boom, N. A., Colledge, N.R., Walker, B.R. et al. (2006). Davidson’s Principles and
Practices of Medicine. Churchill, Livingstone.
McGraw Hill.
• Cumming, A.D. (2006). Davidson’s Principles and Practice of Medicine. Oxford
• Fischer, J.H. (1994). The Epilepsy Counseling Guide. Fair Lawn: New Jersey.
• Kumar, P. & Clark, M. (2007). Clinical Medicine. Edinburgh: Elsevier Saunders.

Handdout 12.1: Pictoriall Illustratiion of Parrtial and Generalizzed
Epilep
psy
Figure 1: Illustratioon of Partiaal and Generralized Epillepsy
Source: Cumming,
C 20008

Session 12:
1 Epilepsy 160
Handout 12.2: Drug Management for Epilepsy
Principles of Treating Epilepsy

• Treat underlying cause
• Control the seizures with Phenobarbital
• Initial dose for children is 3 to 4 mg/kg once daily or in 2 divided doses, increase to 8
mg/kg/day if necessary
• In adults – in acute seizures, dilute the injection in 1ml of water for injection, give
10mg/kg at a rate of not more than 100mg/minute (maximum total dose is 1g).
Maintenance dose is 60-200mg per day.
Figure 2: Phenobarbital Dosage by Age

5 years to 15
Age 0 to 2 months 1 years to 5 years Adult
years
Weight 4kg 8kg to 15 kg 15kg to 35kg
Initial dose ½ tab x2 1 ½ tab x2 3 tab

30mg tablet
50mg tablet 1 tab x2 2 tab
100mg tablet 1 tab 1 tab
Source: Cumming, 2008
Carbamezapine (Tegretol)
Child
• Initially 5mg/kg once daily or in 2 divided doses then increase every 2 weeks up to 10 to
20 mg/kg/day in 2 to 4 divided doses
Adult
• Initially 100-200mg once daily or in 2 divided doses then increase by 100-200mg
increments every 2 weeks up to 800-1200mg per day in 2 to 4 divided doses
• Potential side effects include
o Dizziness
o Diplopia
o Aplastic anemia (rare but potentially fatal). Therefore, need to make sure that CBC
and liver functions are monitored on this medication.
Phenytoin (Epanutin)
Child
• 5 - 8mg/kg/day in 2 to 3 divided doses (max. 300mg)
Adult
• 3-4mg/kg/day or 150-300mg once or twice daily before meals, increase gradually as
necessary in 2 to 3 divided doses
• Usual adult dosing is 200-500mg (max 60mg per day)
• Side effects of medication include

o GIT disturbances
o Nervousness
o Weight loss
o Insomnia
o Unsteadiness
o Hirsutism and excessive motor activity in the adolescents
o Haematological disorders
Megaloblastic anaemia
Leucopaenia
Thrombocytopaenia
Agranulocytosis
Aplastic anaemia
o Lymphadenopathy (occasionally)
o Gingival hyperplasia
o Coarse faeces
o Acne (especially in adolescents)
o Nystagmus in combination with diplopia and ataxia
• Lethargy, confusion and irritability (these are usually severe)
• Usually check blood levels- therapeutic levels are 10-20 ug/mL (40-80 umol/L)
• There are also drug-drug interactions between phenytoin and the protease inhibitors
(in the management of HIV)

Worksheet 12.1: Diagnosis of Epilepsy
Scenario
Fatuma is 3 years old, was born at home. She was delivered by traditional birth
attendant. Since birth Fatuma had delayed milestone, with cerebral palsy. At the nearby
village dispensary Fatuma is managed with Phenobarbital 15mg twice daily for the last
two years, due to tonic-clonic (grandmal seizure). Her condition is getting worse day to
day, that is, she is getting more convulsions than before, and she looks malnourished.
The district hospital is 100 km from her home. Fatuma’s mother is a single parent who is
a peasant and cannot afford to travel long distance to get proper medical attention for her
child. You as a district mental health coordinator visiting her village dispensary and had
an opportunity to review Fatuma.
Questions
1. What do you think is wrong with Fatuma’s management?
2. How will you like to improve Fatuma’s condition?
3. Which other steps will you take to improve Fatuma’s health?
Answers
1. What do you think is wrong with Fatuma’s management?
• Under dose of Phenobarbital
• Poor medication monitoring
• Other diagnosis- look for medical conditions that could cause seizure disorders
2. How will you like to improve Fatuma’s condition?

• Nutritional counselling
• Investigate the underlying pathology
• Elevate Phenobarbital dose according to her current weight
3. Which other steps will you take to improve Fatuma’s health?

• Check haemoglobin
• Stool for oval, and urinalysis
• Medication adherence counselling to Fatuma’s mother
• Consider referral to specialist

Session 13: Non-Organic (Functional) Psychiatric
Disorders
Prerequisites
• CMT 04210 Basic patient care
Learning Objectives
• Define nonorganic psychiatric disorders, schizophrenia, mood disorders and suicide
• Describe clinical features of schizophrenia, mood disorders and paranoid disorders
• Mention differential diagnoses of schizophrenia, mania, major depressive and paranoid
disorders
• Outline risk factors for suicide
• Explain the management of schizophrenia, mania, suicide, major depressive and paranoid
disorders
Resources Needed
• Handout 13.1: Suicide Assessment
• Handout 13.2: Patient Health Questionnaire (PHQ-9)
• Worksheet 13.1: Differential Diagnosis of Psychiatric Disorders Case Study
SESSION OVERVIEW
Activity/
Step Time Content
Method
Introduction to Nonorganic (Functional)
Psychiatric Disorders
Definition and Fundamental Symptoms of
Schizophrenia
Schneider’s Ranks of Symptoms and Criteria
for Diagnosis of Schizophrenia
Presentation, Types and Differential Diagnosis of
5 15 minutes
Brainstorm Schizophrenia
6 05 minutes Presentation Management of Schizophrenia
Definition, Types, Clinical Features and
7 25 minutes Presentation Differential Diagnosis and Management of
Mood Disorders
Definition, Risk Factors and Pre-referral
Treatment of Suicide
Presentation, Definition, Clinical Features and
9 20 minutes
Group Discussion Management of Paranoid Disorders

Session 13: Non-Organic (Functional) Psychiatric Disorders 165
Step 2: Introduction to Nonorganic (Functional) Psychiatric Disorders

(5 minutes)
• Nonorganic (functional) disorder refers to conditions in which a different set of symptoms

is present and current methods of investigation have been unable to prove structural
damage of identifiable change that accounts for the condition.
• Functional usually includes the psychogenic disorder (e.g. dissociative disorders) as well
as mood disorders, schizophrenia and related disorders.
• In this session, the following are discussed
o Schizophrenia
o Mood disorders
Mania
Major depressive disorders
o Suicide
o Paranoid disorders
Step 3: Definition and Fundamental Symptoms of Schizophrenia

(5 minutes)
• Schizophrenia: A mental disorder characterized by abnormalities in the perception or

expression of reality.
• It most commonly manifests as auditory hallucinations, paranoid or bizarre delusions, or
disorganized speech and thinking with significant social or occupational dysfunction.
Fundamental Symptoms
• Onset of symptoms typically occurs in young adulthood, with around 0.4–0.6% of the
population affected.
• Depending on the individual, a person diagnosed with schizophrenia may experience
• Hallucinations (most commonly hearing voices),
• Delusions (often bizarre or persecutory in nature), and
• Disorganized thinking and speech (ranging from loss of train of thought, to sentences
only loosely connected in meaning, to incoherence known as word salad in severe cases.
• There is often an observable pattern of emotional difficulty, for example lack of
responsiveness or motivation.
• Impairment in social cognition
• Symptoms of paranoia, and
• Social isolation

• In one uncommon subtype, the person may be largely mute, remain motionless in bizarre
postures, or exhibit purposeless agitation; these are signs of catatonia.
Step 4: Schneider’s Ranks of Symptoms and Criteria for Diagnosis of

Schizophrenia (10 minutes)
Schneider’s First Rank Symptoms of Schizophrenia
• Voices commenting: hallucinatory voices commenting on one’s actions in the third
person
• Voices discussing or arguing: hallucination of two or more voices discussing or arguing
about oneself
• Audible thought: hearing one’s own thoughts aloud
• Thought insertion
• Thought withdrawal
• Thought broadcast: one’s thought being made known to others
Schneider’s Second Rank Symptoms of Schizophrenia

• Secondary delusion: false beliefs which arises from some preceding morbid experiences
• Second person auditory hallucinations
• Visual, tactile hallucinations
• Blunting affect
• Formal thought disorder
• Catatonic symptoms
Criteria for Diagnosis

• Diagnosis is based on the patient's self-reported experiences and observed behavior.
No laboratory test for schizophrenia currently exists.
• Presence of one very clear symptom makes the diagnosis for example
o The hearing of own thoughts, the feelings of thought withdrawal, thought insertion, or
thought broadcasting
The delusions of control outside manipulation and influence or the feelings of
passivity (that is made feel, act, move etc)
Hallucinated voices which are commenting permanently on the behavior of the
patient or they talk about him between themselves
Permanent delusions of different kind preferably primary, which are
inappropriate and unacceptable in given culture
Step 5: Types and Differential Diagnosis of Schizophrenia (15 minutes)

ASK students to mention the types of schizophrenia.
• The DSM-IV contains five types of schizophrenia

o Paranoid type: Where delusions and hallucinations are present but thought disorder,
disorganized behavior, and affective flattening are absent.
o Disorganized (hebephrenic) type: Where thought disorder and flat affect are present
together.
o Catatonic type: The subject may be almost immobile or exhibit agitated purposeless
movement. Symptoms can include catatonic stupor and waxy flexibility.
o Undifferentiated type: Psychotic symptoms are present but the criteria for paranoid,
disorganized, or catatonic types have not been met.
o Residual type: Where positive symptoms are present at a low intensity only.
• The ICD-10 defines two additional types.
o Post-schizophrenic depression: A depressive episode arising in the aftermath of a
schizophrenic illness where some low-level schizophrenic symptoms may still be
present.
o Simple schizophrenia: Insidious and progressive development of prominent negative
symptoms with no history of psychotic episodes.
Paranoid Schizophrenia
• Is characterized mainly by delusions of persecution, feelings of passive or active control
and feelings of interference.
• The delusions and hallucinations of different senses mostly with hearing voices.
• Disturbances of affect, volition and speech and catatonic symptoms are either absent or
relatively inconspicuous.
Catatonic Schizophrenia
• Catatonic schizophrenia is characterized mainly by motoric activity, which might be
strongly increased (hyperkinesis) or decreased (stupor) or automatic obedience and
negativism.
• We recognize two forms
o Productive form which shows catatonic excitement, extreme and often aggressive
activity.
o Stuporous form characterized by general inhibition of patient’s behavior or at least by
retardation and slowness followed often by mutism and negativism.
Disorganized (Hebephrenic) Schizophrenia

• Hebephrenic schizophrenia is characterized by disorganized thinking with blunted and
inappropriate emotions
• The behavior is often bizarre
• There could appear mannerisms, grimacing, inappropriate laugh, joking and sudden
impulsive reactions without external stimulation
• There is a tendency to social isolation
• Usually the prognosis is poor because of the rapid development of negative symptoms
particularly flattening of affect and loss of volition
• Hebephrenia should normally be diagnosed only in adolescents or young adults
Residual Schizophrenia
• Is characterized by absence of positive symptoms like
o Delusions
o Hallucinations
o Incoherence

o Catatonic features
o Grossly disturbed behaviour
• There is presence of negative symptoms like
o Social withdrawal
o Blunted
o Lack of energy
o Impaired social and occupational function
o Impaired self care, hygiene and grooming
Simple Schizophrenia
• This is characterized by very insidious and progressive course
• There is marked social withdrawal and shallow emotional response
• Living shabbily (untidily)
• Wandering aimlessly
• Delusions and hallucinations are usually absent, if present they are short lasting and
poorly systematized.
• Antisocial personality disorders
• Schizoaffective disorder
Investigations
• No laboratory investigations that confirm schizophrenia, but the following can be done as
routine and for ruling out organic causes of symptoms
o Hemoglobin
o ESR
o Widal test
o Blood slide for malaria
o Urinalysis
o Stool for oval
o HIV Test
o Syphilis test
Step 6: Management of Schizophrenia (5 minutes)
• Anti –psychotic drug treatment

o Chlorpromazine 50 – 100mg IM in acute phase followed by maintenance dose of up
to 400mg orally in divided dose per day.
o Haloperidol 5-15mg/day IM in acute phase followed by maintenance dose of up to
5-15 mg orally in divided dose per day.
o Injection Diazepam 10 – 20mg IV stat to calm the patient. It should be noted that
benzodiazepines can cause psychosis so should be used cautiously and in a hospital
setting.
• Anti-psychotics give side effects of extra pyramidal such as
o Tremors
o Tongue protrusion
o Stiffness of the neck and rigidity
• These side effects are controlled by

o Tablet Artane (trihexyphenidyl); initial dose of 1mg daily, then titrate up, increase to
a dose ranging from 5mg to 15mg daily.
Or
o Tablet Promethazine 50 mg once daily. This medication can cause tardive dyskinesia
so need to be aware of this.
• Take all vital signs like temperature, blood pressure, respiratory rate and pulse rate
• An investigation like blood slides for malaria parasites is also necessary.
• Blood test for syphilis and typhoid are optional if the patient’s history and premorbid
personality suggest the symptoms of infectious diseases.
• Testing for syphilis is highly recommended.
• HIV test is routine especially to those who present with first episode psychosis.
• Once the patient is calm under close supervision is referred to a consulting psychiatry
hospital whereby in a special secured ward, the patient is observed and given the correct
medications and dosages.
• Psychotherapy is also widely recommended and used in the treatment of schizophrenia,
although services may often be confined to pharmacotherapy because of reimbursement
problems or lack of training.
• Cognitive behavioral therapy (CBT) is used to target specific symptoms and improve
related issues such as self-esteem, social functioning, and insight.
• Another approach is cognitive remediation, a technique aimed at remediating the
neurocognitive deficits sometimes present in schizophrenia.
• Family therapy or education, which addresses the whole family system of an individual
with a diagnosis of schizophrenia, has been consistently found to be beneficial, at least if
the duration of intervention is longer-term.
• Rehabilitation is mandatory if the patient is in danger to himself or to his family or to the
community at large.
• Caveat to use of the neuroleptic medications: Need to be aware of a rare but potentially
fatal side effect of these medications known as neuroleptic malignant syndrome-
characterized by rigidity, fever, autonomic instability and elevated creatinine
phosphokinase (CPK).
Step 7: Definition, Types, Clinical Features and Differential Diagnosis and

Management of Mood Disorders (25 minutes)
• Mood which is a lasting and dominant emotional response which colours the whole
psychic life and it is internally felt symptom that tends to fluctuate between two extremes
of happiness and sadness.
• A mood disorder is the term given for a group of diagnoses where a disturbance in the
person's mood is hypothesized to be the main underlying feature.
Types of Mood Disorders

• Primary mood disorders include both depressive disorder (unipolar) and manic-depressive
disorder (bipolar). These include;
o Mania
o Major depression
o Hypomania
o Manic-depressive
o Anxiety

Clinical Features of Mania
• Persistent elevated expansive mood
• Excessive spending or gambling
• Impulsive travel
• Hyper-sexuality, promiscuity
• Low frustration tolerance with irritability and outbursts of anger
• Grandiosity-reflects inflated self esteem
• Flight of ideas-racing thoughts
• Increased goal oriented activities
• Pressured speech or increased talkativeness
• Vegetative signs
o Increased libido
o Weight loss and anorexia
o Insomnia (expressed as decreased need for sleep)
o Excessive energy
Management of Mania
• Chlorpromazine 50 – 100mg IM in acute phase followed with maintenance dose of up to
400mg orally in divided dose per day, or:
• Haloperidol 5 – 15mg/day IM in acute phase followed with maintenance dose of up to
5 – 20mg orally in divided dose per day.
• Lithium carbonate – in mania, 0.6-1.8g daily (elderly (300 – 400mg daily). In prophylaxis
of bipolar disorders and recurrent depression, 0.6-1.2g daily as a single dose or in 2
divided doses (patients <50kg and elderly, 300-900mg daily).
Major Depression Disorder

• Major depressive disorder is commonly called major depression, unipolar depression, or
clinical depression, where a person has two or more major depressive episodes.
• Depression without periods of mania is sometimes referred to as unipolar depression
because the mood remains at one emotional state or ‘pole’
Clinical Feature of Major Depression

• Depressed mood
• Loss of pleasure in almost all activities
• Significant weight loss or weight gain (change of 5% or more of body weight in a month)
• Decrease or increase of appetite
• Insomnia or hypersomnia (somnolence)
• Psychomotor agitation or retardation
• Fatigue or loss of energy
• Feelings of worthlessness or excessive or inappropriate guilt
• Diminished ability to think or concentrate
• Recurrent thoughts of death (not just fear of dying)
Diagnosis
• Five or more of the above symptoms have been present during the same 2 week period
and represent a change from previous functioning.
• At least one of the symptoms is either depressed mood, loss of interest or pleasure.

Differential Diagnosis of Mood Disorders
• Negative symptoms of schizophrenia
• Post schizophrenia depression
• Schizophreniform personality disorders
Management of Depression
• Antidepressant for depression i.e.
o Amitriptyline or Imipramine 25- 75mg in divided dose per day, or:
o Selective serotonin re-uptake inhibitors (SSRI) e.g. fluvoxamine (Luvox), paroxetine
(Paxil), fluoxetine (Prozac) and sertraline (Zoloft). These are commonly used in
elderly patients.
• Simple counseling (for those who are still able to talk/speak).
Note: Depression can be assessed by using a simple tool known as patient health
questionnaire (PHQ-9).
Refer Students to Handout 13.3: Patient Health Questionnaire (PHQ-9)
Step 8: Definition, Risk Factors and Pre-referral Treatment of Suicide

(15 minutes)
• Suicide: The act of causing one’s own death. Suicide may be direct or indirect.
• Suicide is direct when one has the intention of causing one’s own death, whether as an
end to be attained, or as a means to another end, as when a man kills himself to escape
condemnation, disgrace, and ruin.
• Suicide is indirect (and not usually called suicide) when one does not desire it as an end
or a means, but when one nevertheless commits an act which courts death, as in tending
someone with severe acute respiratory syndrome (SARS) knowing that they may well
succumb to the same illness or not seeking care for a treatable condition.
• Suicide occurs more frequently in clinical populations than in the general population e.g.
in patients with
o Schizophrenia
o Clinical depression
o Panic disorders
o Substance use disorders
o Epileptics
• One of the most common myths about suicide is that asking about suicide ‘plants the
seed’, and will cause your patient to commit suicide. This is not true. If you don't ask,
you lose an opportunity to prevent a suicide attempt. Actually, individuals who talk about
suicide are crying out for help.
• Are related to socio-demographics
• The presence of acute environmental stressors such as loss of a loved one
• The presence of psychiatric illness and substance use disorders
• Age 60 years or older
• Widowed
• Living alone

• Unemployed
• Financial difficulties
• Recent stressful life event (i.e., death of someone close)
• Perceived threat in intimate relationship
• Clinical depression
• Substance abuse
• Schizophrenia
• History of suicide attempts
• Severe anxiety
• Panic attacks
• Personality disorder
Risk Factors for Suicide

• Assessments and Screenings for Suicide Risk
o It is important for practitioners to be comfortable in screening for suicide risks
o During suicide risk assessments it is important to emphasize the following items
Suicidal intent
Presence of a suicidal plan
Presence of overt suicidal/self-destructive behavior
Risk factors
Motivation for suicide
Refer students to Handout 13.1: Suicide Assessment
• Suicidal intent refers to the level of the patient's intent to kill or harm him/herself
• Assess suicidal intent by questioning the patient and family members or observing the
patient's behaviors. The table below summarizes how intent can be rated.
Figure 1: Suicidal Intent Rating

Suicidal
Description
Intent Rating
Non-existent • No suicidal thoughts or plans exist
Mild • Some suicidal ideations are present but no specific or concrete plans
• Few risk factors are present
Moderate • Presence of suicidal ideations and a general plan exists
• The patient can articulate reasons for living
• Some risk factors are present
Severe • Suicidal thoughts are frequent and intense
• There is a specific plan and it is lethal
• The means to complete the act are available and the resources to access
help are limited
• Patient does not really ‘want’ to kill him/herself but many risk factors
are present
Extreme • Same as the ‘severe’ description however, the patient expresses a clear
intent to kill him/herself as soon as an opportunity presents itself
• Many risk factors are present

Pre-Referral Treatment
• No-Suicide Contracts
o The no-suicide contract is a popular and widely used clinical strategy for managing
at-risk suicidal patients.
o It is also referred to as the no-harm contract or suicide prevention contract.
o In a no-suicide contract the patient promises not to engage in self-injurious behaviors
if he or she experiences suicidal thoughts or impulses.
o The patient instead promises to inform the practitioner, other helping professions,
family members or friends.
o Sometimes with the no-suicide contracts, the patient agrees to eliminate any
dangerous objects and both the practitioner and patient sign the agreement to uphold
accountability.
o The practitioner needs to recognize the limitations of no-suicide contracts.
It does not replace the need to do a full-scale suicide risk assessment.
The practitioner must not assume a no-suicide contract guarantees the patient's
safety.
Step 9: Definition, Clinical Features and Management of Paranoid

Disorders (20 minutes)
• Paranoid personality disorder (also called delusional disorder): A psychiatric diagnosis

characterized by paranoia and a pervasive, long-standing suspiciousness and generalized
mistrust of others.
• Those with the condition are hypersensitive, are easily slighted, and habitually relate to
the world by vigilant scanning of the environment for clues or suggestions to validate
their prejudicial ideas or biases.
• They tend to be guarded and suspicious and have quite constricted emotional lives.
• Their incapacity for meaningful emotional involvement and the general pattern of isolated
withdrawal often lend a quality of schizoid isolation to their life experience.
Clinical Features
• Unkempt (shabby)
• Delusions and hallucinations
• Wandering around
• Withdrawal
• Paranoid schizophrenia
• Mania
• Depression
• Organic delusional disorder
Management
• Anti –psychotic drug treatment
o Chlorpromazine 50 – 100mg IM in acute phase followed with maintenance dose of up
to 400mg orally in divided dose per day, or:
o Haloperidol 5 – 15mg/day IM in acute phase followed with maintenance dose of up
to 5 – 20mg orally in divided dose per day.

o Injection diiazepam (vaalium) 10 -220 mg IV sttart to calm the patient. Be aware this can
cause psychhosis and reespiratory suuppression, may want to
t give loweer dose.
• Givve only one antipsychottic drug
Activvity: Large Group Disscussion (100 minutes)
SELE
ECT one stuudent to reaad the scenaario below.
Scenaario
Markk is a 23-yeaar-old unem
mployed whoo presents apparently
a w fatigue.. On examiination,
with
some psychotic symptoms
s a apparentt and in add
are dition he is irritable,
i witth significan
nt mood
swinggs, racing thhoughts andd paranoia, but
b no real features
f of lasting
l psycchosis.
Refer stu
udents to Worksheet
W 1
13.1: Differrential Diaggnosis of Pssychiatric
Disorrders
GIVE E students 5 minutes too discuss quuestions belo

ow and recoord on the w
worksheet fo
or
plenaary discussioon.
• List differenttial diagnoses

• List signs andd symptomss pointing too each diffeerential diaggnoses you hhave made.
ALLO
OW few stuudents to shhare their responses.
SUMMMARIZE the t discussiion by usingg Worksheeet 13.1: Diffferential D

Diagnosis off
Psych
hiatric Disoorders.
Step 10:
1 Key Pooints (5 minutes)
m
• In nonorganic
n or functionaal psychiatrric disorderss, there is no
n proven sttructural daamage of
idenntifiable chaange that acccounts for the
t conditio on.
• Schhizophrenia is a mentaal disorder characterize
c ed by abnoormalities inn the perception or
exprression of reality
r and its symptom ms are classsified accoording to Scchneider’s ranks
r of
symmptoms.
• Thee main typees of schizzophrenia are paranoid d, disorganiized (hebepphrenic), caatatonic,
unddifferentiatedd and residuual.
• Anttipsychoticss (e.g., chlorrpromazine and halopeeridol) are thhe main druugs used in thet
treaatment of fuunctional psyychiatric dissorder.
• In depression
d w
where tricyclic antideppressants (e..g., amitripttyline and im
mipramine) or
SSR RIs are usedd.
• Extrra-pyramidaal side effeccts of antipssychotics may
m be severre to the extent of requiiring
antiidotes such as Artane and
a promethhazine.
• Suiccide is the act
a of causinng one’s ow wn death and d has many risk factorss. Risk factoors for
suiccide should be assessedd by health care
c provideer in each and a every paatient’s visitt.

Session 13:
1 Non-Orgaanic (Functionnal) Psychiatriic Disorders 175
• Mention types of schizophrenia.

• What are the symptoms of depression?
• How can a patient with schizophrenia be managed?
• What are the risk factors for suicide?
References
McGraw Hill.
• Chiu, D., and Ames, D. (1994). Functional Psychiatric Disorders of the Elderly.
Cambridge University Press. Retrieved June 17th 2010 from http://books.google.
co.tz/books?id=1xSZ-FFPAxgC&printsec=frontcover&dq=Functional+Psychiatry+
Disorders&source=bl&ots=IwH8USJ-3O&sig=c6q-
CkEvQnHxVWkgUN36HzOqIBs&hl=sw&ei= v9oZTLq1MsSt4Qa-
38CdCg&sa=X&oi=book_result&ct=result&resnum=8&ved=
0CCsQ6AEwBw#v=onepage&q=Functional%20Psychiatry%20Disorders&f=false
• Li, M.M., Friedman, B., & Conwell, Y. et al (2007). Validity of the Patient Health
Questionnaire 2 (PGQ-2) in Identifying Major Depression in Older People. Journal of the
American Geriatric Society.
• Spitzer, R.L., Williams, J.B. & Kroenke, K. (1999). Patient Health Questionnaire.
Retrieved on July 19th, 2010 from http://muskie.usm.maine.edu/clinicalfusion
/DHHS/phq9.pdf

Worksheet 13.1: Differential Diagnosis of Psychiatric Disorders
Scenario
Mark is a 23-year-old unemployed who presents apparently with fatigue. On
examination, some psychotic symptoms are apparent and in addition he is irritable, with
significant mood swings, racing thoughts and paranoia, but no real features of lasting
psychosis.
Questions
• List differential diagnoses
• List signs and symptoms pointing to each differential diagnoses you have made
Answers
1. List differential diagnoses
• Mania
• Depression
• Paranoid disorder
2. List signs and symptoms pointing to each differential diagnoses you have made
• Mania due to
o Irritability
o Mood swings
o Racing thoughts
• Depression
o Fatigue
• Paranoid disorder
o Paranoia
o Suspiciousness

Handout 13.1: Suicide Assessment
• When evaluating the patient's risk of suicide or the intent, asses for
o The specificity and the lethality of the suicide plan
o The consideration of the method to be used
o The patient's social network
• When looking at the specificity of the plan, the practitioner should consider the following
questions
o How detailed is the plan?
o Has the patient thought through all the steps and details in how to execute the plan?
Lethality of the Plan

• Refers to how quickly the plan produces death.
• Since lethality is directly related to the method used, practitioners need to ask about the
patient's method (i.e., use of razors, gun, overdose) as well as availability and the way the
method will be employed.
• For example, does the patient plan to use a razor on his/her wrist or on his/her thigh?
• Does he/she plan to overdose on aspirin or cyanide?
• Individuals vary in their views about the methods used for suicide.
• Asses the patient's social network and the proximity of the network
• Does the patient have family, friends, and/or neighbors?
• What is the proximity of these various forms of social networks?
• Is the patient socially isolated? The more isolated the greater the risk.
• Listening and hearing a patient is the key ingredient in suicide assessment.
• Ask family members and friends if they have heard the patient express comments such as
o Soon you won't have to worry about me
o I would be better off dead or
o I don't want to be a burden to others
o Has the patient expressed feelings of hopelessness, commented about how life is
unbearable, or talked about how life is worthless?
Non-Verbal Cues Offer another Window to Assessing Suicide

• Practitioners can ask friends and/or family members question about whether the patient
has done things like
o Preparing a will and/or funeral arrangements
o Giving possessions away
o Accumulating and using prescription drugs or substances
o Use of alcohol excessively
o Visiting a physician or nurse practitioner frequently, and/or
o Withdrawing from others
• It is important to listen to the patient's verbal cues and observe nonverbal cues
• Practitioners need to directly ask the patient about their suicidal intent such as
o How often does suicide come to mind?
o How hopeless do you feel?
o Do you think about killing yourself or to deal with your problems?

• The patient's history needs to be taken into account
o Have suicidal behaviors occurred in the past?
o Has the patient engaged in self-mutilating behaviors?
• Risk of suicide increases if a history of suicidal attempts or ideations is present.
• The patient's subjective meanings of suicide need to be explored.
• In other words, what does suicide mean to the patient?
• When examining the meaning of suicide, religion and ethnicity should be taken into
account since attitudes toward death are impacted by these variables.
• For example, some groups consider suicide shameful or a moral offense, while others
may perceive it as honorable.
• Catholicism teaches that taking one's life is unacceptable.
• The practitioner needs to assess other psychosocial issues that are current and relevant in
the life of the patient such as
o What are recent stresses in the patient's life?
o Has the patient lost or anticipates losing a primary relationship?
o What is the patient's physiological state (i.e. physical illness, organic impairment)
All patients with mental health issues should be screened for HIV and syphilis as these are
more treatable causes of disorder.

Session 14: HIV and AIDS and Mental Health
Prerequisites
CMT 04213 Clinical Skills
CMT 04210 Basic Patient Care
Learning Objectives
By the end of this session, student will be able to:
Describe multiple cause of mental health problems in HIV and AIDS patients
Describe HIV neuropsychiatric conditions
Describe management of HIV neuropsychiatric conditions
List Psychosocial reactions to HIV and AIDS
Resources Needed
Flip charts, marker pens, and masking tape
Black/white board and chalk/whiteboard markers
Handout 14.1: Management of HIV and Mental Illness
Worksheet 14.1: Neuropsychiatric Diagnosis
SESSION OVERVIEW
Activity/
Step Time Content
Method
Presentation,
Causes/Relationship of Mental Health
2 30 minutes Group
Problems in HIV&AIDS
Discussion
3 10 minutes Presentation HIV&AIDS Encephalopathy
4 10 minutes Presentation Other HIV Neuropsychiatry Conditions

Presentation,
5 20 minutes Psychosocial Reaction to HIV&AIDS
Brainstorm
Presentation,
6 30 minutes Neuropsychiatric Manifestation of HIV
Case Study

Session 14: HIV and AIDS and Mental Health 181
Step 2: Causes/Relationship of Mental Health Problems in HIV&AIDS
(30 minutes)
ASK students to describe causes of mental health problems in HIV&AIDS.
LET students discuss in their small groups for 10 minutes and write down their responses on
the flip chart.
INVITE one group to present their responses.
INVITE other groups to add points that the first group did not cover.
Manifestations of mental disorders in HIV and AIDS are multiple and these may be due to the
following
o The virus (HIV) invasion of the brain resulting in acute inflammation, and
degenerative changes
o Sero-conversion from non-clinical to clinical AIDS stage
o Physical changes associated with the diseases progression
Progressive weight loss
Skin rashes
Subtle loss of functional ability in daily activities
o Opportunistic infections including
Tuberculosis
Cryptococcal infection
Toxoplasmosis
Cytomegalovirus (CMV)
Varicella zoster virus (VZV)
PML (progressive multifocal leukencephalopathy)
HIV dementia
Neurosyphilis
o Secondary spread of cancer such as Lymphoma and KS
o News of positive HIV test result
o Intoxication (alcohol or other drugs)
o Co-morbid mental health disorders such as depression, anxiety, bipolar and
schizophrenia
o Psychosocial and environmental factors such as
Stress stigma and discrimination
Unemployment
Bereavement
Family separations (single parent)
Orphanage
Social economic reasons

Mental Health Problems in HIV and AIDS
The nature of HIV physical symptoms, relentless progressive course together with the
reactions of other people explain why emotional distress is common in patients with HIV
infection.
Groups at high risk haemophilia and drug abusers may have other psychological or
neuropsychiatric problems in addition to symptoms of organic brain HIV infection thus
complicate the picture.
Neuropsychiatry problems and other psychosocial disorders may occur at any stage of the
disease progression.
Furthermore, effects of HIV infection in the family are significant where the partner and/or
children also suffer from the infection.
Social and cultural differences are both considerable because of the public fears of the
condition and stigma.
Step 3: HIV and AIDS Encephalopathy (10 minutes)
Causes
HIV invasion of the brain tissue results in acute inflammation and degenerative changes
Opportunistic infections including tuberculosis, cryptococcal and toxoplasmosis
Secondary spread of cancer such as Lymphoma and KS
Clinical Features
Vomiting
Irritability
Photophobia
Neck stiffness
Papilloedema
Variable pyrexia
Disturbance of consciousness from mild somnolence to coma
Delirium may be the main picture
Epileptic fits can occur
Management
• All HIV patients with CNS problems must be referred to hospitals for proper evaluation,
investigations and treatment.
History
Family members and friends may provide the vital information needed but carefully observe
confidentiality
Review of systems may lend insight to the nature of the process such as meningismus,
headache or focal neurological deficits
The past medical history is of particular importance
Medication list prescribed, over the counter, and illicit drugs must be obtained.
Centered on evidence of organ dysfunction and opportunistic infections.
Additional neurological findings may have dramatic clinical impact.

Laboratory Investigations
CD4 count
Renal function tests
Liver function tests
Blood culture
Sputum gram stain
ZN stain
Complete blood count
Electrolytes
CSF investigations
Stool and urine culture
Lumbar puncture is contraindicated for suspected case of increased intracranial pressure and
in brain hemorrhages.
All these investigations are done at a referral hospital or in CTC where laboratory facilities
are adequately available.
Treatment
Refer to CTC for the following therapy
First identify what the cause of the mental health status change is, then
o Anti-retroviral therapy with drugs which can penetrate into the CNS
o Treatment should aim at full viral suppression for longest time with the least toxicity
o Adequate nutrition, rest, regular exercise, stop alcohol use and refraining from other
drug use, output/input chart, vitals monitoring, catheterization and iv line
o Active manage of opportunistic infection or other problem if present
Refer students to Handout 14.1: Management of HIV and Mental Illness
Step 4: Other HIV Neuropsychiatric Conditions (10 minutes)
AIDS Dementia Complex (ADC)

Patients present with sub cortical encephalitis resulting in progressive sub-cortical dementia
without focal neurological sign
Development of sub-cortical dementia is a bad prognostic sign where death may occur within
6 months if not on ARV therapy
30% of HIV infected individual develop HIV associated dementia
The CD4 count is often below 200 cells/mm3
Clinical Features
Apathy or lethargy
Social withdrawal
Hyper-reflexia
Paraesthesias and increased muscle tone
Cognitive dysfunctions which include
o Concentration and memory deficits
o Inattention and later on mutism
Motor deficits including
o Motor inco-ordination
o Ataxia, spastic gait and later paraplegia

Management
Similar treatment as in HIV encephalopathy
HAART therapy is the management of choice for HIV dementia
HIV and AIDS Associated Delirium

Risk Factors for Developing Delirium in HIV
o Advanced stage of the HIV and AIDS
o Substance abuse intoxication and/or overdose
o Malignancies of the central nervous system
o Drug interactions in AIDS patients taking multiple medication
o High fever from any cause
o Seizures (convulsions)
Treatment
The treatment of HIV-associated delirium includes typical management of delirium in organic
psychiatric disorders and HIV management as in HIV encephalopathy.
Step 5: Psychosocial Reaction to HIV and AIDS (20 minutes)
ASK students to mention the psychosocial reactions to HIV and AIDS.
Patients with HIV have many psychosocial reactions which include

o Depression
o Anxiety disorders
o Substance abuse
Diagnostic Features of Depression

Depressed mood
Decreased interest in activities
Anhedonia (loss of the capacity to experience pleasure)
Fatigue
Weight loss
Impaired ability of mental concentration
Recurrent thoughts of death and hopelessness
Profound sense of not well disproportionate to medical condition

Diagnostic Challenges
Misconception that depression in HIV is normal.
Overlapping symptoms such as fatigue, weight loss and insomnia may be due to depression
or physical illness such as HIV.
Chronic pain and chronic physical syndromes co-morbid with mood disorders.
Medication-related depression and anxiety may pose challenges in the diagnosis.
Substance abuse may be associated with depression hence adding more challenges.
Management
• Mainstay of treatment is antidepressants like (amitriptyline 25-50 mg per day, to start
with. Then the dose can be slowly increased to 100-150mg a day.
• Start at low dose and increase slowly a dose of around 100-150mg daily
• Avoid overmedication and side effect
• Black Tanzanian patients respond well to a lower than recommended doses
• Common early side effects to amitryptiline are dry mouth, urinary retention. More severe
side effects include arrhythmias, delirium.
• Serotonin selective reuptake inhibitors (SSRIs) e.g., fluoxetine are preferable especially
in elderly patients. And for these there is also a need for starting at lower dosing that is
later on raised.
o Fluoxetine – 20mg daily
Step 6: Neuropsychiatric Manifestation of HIV (30 minutes)
ASK one student to read scenario below aloud.
Scenario
Frida is 31 years old HIV positive woman presents with weakness on the left side of the
body for 5 days. She has been complaining of fever and throbbing headache which is
intermittent for more than one month and she is not taking any medication. Physical
examination revealed sad mood, irritability, confusion, with increased muscle tone.
Paralyzed left arm and leg, herpes zoster scar on left side of the chest.
1. What could be the cause of confusion to Frida?

2. What kind of mental disorder is Frida suffering from?
3. How will you manage Frida?
INSTRUCT each group to work together and answer questions on Worksheet 14.1:
Neuropsychiatric Diagnosis.
TELL each group to record their responses on the worksheet.
ALLOW 10 minutes for the group work.


ASK one group to volunteer to report their responses and let other groups to add up.
SUMMARIZE the discussion by using Worksheet 14.1: Neuropsychiatric Manifestation.

There are a number of causes for mental disorders in HIV patients including virus invasion to
the brain resulting in acute inflammation and degenerative changes.
Vomiting, irritability, photophobia, neck stiffness, papilloedema and variable pyrexia are
manifestation of HIV and AIDS encephalopathy.
Management of HIV in patients with psychiatric disorder follows a normal trend as other
HIV patients that is referring to CTC clinic and providing psychosocial support.

Describe causes of HIV and AIDS encephalopathy
Identify diagnostic challenges of depression in HIV and AIDS patients
Identify factors which prevents HIV and AIDS infection
References
McGraw Hill.
• David, M. N. (2006). The African Textbook of Clinical Psychiatry and Mental Health.
Nairobi. Kenya: AMREF.

Handout 14.1: Management of HIV and Mental Illness
• Adherence to medications (ARVs, antidepressant, antipsychotics) for a person who is

suffering from mental illness is difficult to achieve
• Mentally ill patients may have no or poor insight or are incapacitated
• Family, friends, social workers need to accompany patients to CTC and psychiatry units
• Adherence plan should be followed
• Antidepressants e.g. Amitriptyline, Imipramine, dose of 25- 75 mg per day interacts with
Lopinavir and Ritonavir
• These ARVs increase antidepressant levels in serum
• Antidepressant are used in treating
o Depression
o Phobias
o Anxiety
• Serotonin specific re-uptake inhibitors e.g. Fluoxetine dose of 10- 20 mg per day is
recommended in patients on ARVs.
• Nevirapine decreases antidepressant levels
• Antidepressant increase levels of Efavirenz, Indinavir, Lopinavir and Ritonavir
• Efavirenz can cause CNS side effects such as
o Vivid dreams
o Nightmares
o Vertigo
o Confusion
o Severe side effects can be acute psychosis and would avoid use of efavirenz in a
patient with serious mental health issues (such as bipolar or schizophrenia)
• These symptoms are often mild and transient.
• Patients may benefit from assurance, but if the patient is not able to understand and has
marked elevation of psychiatric symptoms that CTC counselor, will change Efavirenz to
Nevirapine.
• Anti epileptic (anticonvlsions) medication Tegretol i.e. carbamezapine, and
antipsychotics such phenothiazides i.e. largatil, haloperidol, may cause liver toxicity
(hepatotoxicity).
• These may interact with ARVs retinovir which is also potentially hepatotoxic.
• Liver function test are necessary in these condition and immediate changing of drugs is
recommended.
• Drug abusers and alcohol dependants can have liver function test (hepatic enzymes
transaminase) elevations.
• Drug addicts may also have been suffering from residual Hepatitis B antibodies due to
sharing of intravenous needles.
• ARVs that may interact or cause hepatotoxicity to drug addicts who show symptoms of
hepato-biliary tract, should be shifted to less toxic ARVs if available or monitor very
carefully for toxicity.
Adverse Effects of Efavirenz (EFV)

• CNC Toxicity
o Very frequent (52%) usually lasts 2-4 weeks

o Dizziness, headache, insomnia, depression, impaired concentration, agitation, strange
dreams or nightmares, somnolence
• Only 2% serious psychiatric symptoms

o Depression
o Delusion
o Mania
o Suicidal thoughts
• Higher risk if history of mental illness/substance abuse
• Avoid in patients with psychiatric disorders
Efavirenz Central Nervous System Toxicity Management

• Inform patients very well and reassure
• Bedtime dosing
• Avoid driving the car in beginning
• Avoid alcohol
• Use agenda, inform friends to remember appointments
• Expose to pleasant activity before sleeping to reduce nightmares
• If serious psychiatric symptoms refer to higher level for possible replacement of EFV
with NVP

Worksheet 14.1: Neuropsychiatric Diagnosis
Scenario
Frida is 31 years old HIV positive woman presents with weakness on the left side of the body
for 5 days. She has been complaining of fever and throbbing headache which is intermittent
for more than one month and she is not taking any medication. Physical examination
revealed sad mood, irritability, confusion, with increased muscle tone. Paralyzed left arm
and leg, herpes zoster scar on left side of the chest.

Answers
• HIV and AIDS Encephalophathy
• Brain tissue damage due to stroke or infection such as (Toxoplasmosis, cryptococcosis,
TB meningitis, PML)

• AIDS dementia complex
• Depression
• Delirium (confusion)
Management
History
• Family members and friends may provide the vital information needed while carefully
observing confidentiality
• Review of systems my lend insight to the nature of the process (meningismus, headache
or focal neurological deficits)
• The past medical history is of particular importance
• Medication list prescribed, over the counter, and illicit drugs must be obtained
• Centered on evidence of organ dysfunction and opportunistic infections.
• Additional neurological findings may have dramatic clinical impact.
Laboratory Investigation
• CD4 count
• Renal function tests
• Liver function tests
• Blood culture
• Sputum gram stain (if available)

• ZN stain
• Complete blood count
• Electrolytes
• CSF investigations
• Lumbar puncture is contraindicated for suspected case of increased intracranial pressure
and in brain hemorrhages
• All these investigations are done at a referral hospital or in CTC where laboratory
facilities are adequately available
Treatment
• Refer to CTC for farther evaluation and initiation of treatment
• Need to identify underlying cause of her paralysis before initiation of any HIV specific
medications. If acute bacterial meningitis is suspected- give appropriate IV antibiotics
first before transfer.
• Anti-retroviral therapy with drugs which can penetrate into the CNS when able to take
them
o Treatment should aim at full viral suppression for the longest time with the least
toxicity
o Adequate nutrition, rest, regular exercise, stop alcohol use and refraining from other
drug use, output/input chart, vitals monitoring, catheterization and IV line
o Manage opportunistic infection

Session 15: Drug and Alcohol Abuse
Prerequisites
• CMT 04213 Clinical Skills
• CMT 04210 Basic Patient Care
Learning Objectives
• Define drugs, drug abuse and dependence
• Describe alcohol use disorders
• Describe cannabis use disorders
• Describe cocaine use disorder
• Describe management of each of the drug use disorders
Resources Needed
• Worksheet 15.1: Diagnosis of Alcohol Use Disorders Case Study
• Handout 15.1: Other Drugs of Abuse
SESSION OVERVIEW
Activity/
Step Time Content
Method
Presentation,
2 15 minutes Definition of Drug and Drug Abuse
Brainstorm
3 20 minutes Presentation Alcohol Use Disorders
Presentation,
4 30 minutes Management of Alcohol Use Disorder
Case Study
5 15 minutes Presentation Cannabis Use Disorders
6 05 minutes Presentation Management of Cannabis Use Disorder
7 15 minutes Presentation Other Drugs of Abuse

Session 15: Drug and Alcohol Abuse 193
Step 2: Definition of Drug and Drug Abuse (15 minutes)

• A drug is defined by WHO as any substance that when taken into the living organism
may modify one or more of its functions.
ASK students to define drug abuse.
ALLOW few students to give their responses.
• Drugs of abuse are generally defined as substances that when taken alter mood, cognition
(thoughts) and behavior.
• There are four important patterns of drug use disorders, which may overlap with each
other
o Acute Intoxication
This is a transient condition following administration of a drug resulting in
psycho-physiological disturbances
o Withdrawal Syndrome
Develops on total or partial withdrawal of drugs, usually after repeated and/ or
high dose use
The withdrawal symptoms last after a few hours to few days
o Dependence/Tolerance
Characterized by tolerance i.e. craving needs for higher dose of drug to get the
same benefit as previous
Known pharmacologic effect of many medications including opiates,
benzodiazepines
This may not mean addiction but need to carefully assess the situation
o Abuse/Addiction
Continue use despite awareness of harmful medical/ social effects
Addiction craving need for a drug that one cannot do without it.
Common Drugs of Abuse Found in our Society

• Alcohol
• Cannabis
• Heroin
• Cocaine
• Sedatives and hypnotics e.g. barbiturates, benzodiazepines
• Inhalants e.g. volatile solvents
• Opiates

Step 3: Alcohol Use Disorders (20 minutes)
• Excessive consumption of alcohol

• Alcohol abuse refers to excessive use of alcohol causing mental, physical or social harm
to the individual.
• Alcohol Dependence describes ‘a pattern of repeated self-administration of alcohol that
usually results in tolerance, withdrawal and compulsive alcohol-taking behavior. The
essential element of which is the continued use of the substance (alcohol) despite of its
related problems.
Clinical Features of Alcohol Intoxication

• Psychomotor impairment
• Exaggerated emotional responses
• Impaired judgment
• Ataxia
• Slurred speech
• Decreased concentration
• Labile mood
Alcohol Withdrawal Symptoms

• Usually occurs 6–24 hours after last drink and the symptoms are progressive
• Tremor
• Anxiety and agitation
• Sweating
• Nausea and vomiting
• Headache
• Sensory disturbances e.g. hallucinations or illusions
• Convulsions (seizures)
• Delirium tremens (DTs)
o Clouding of consciousness with disorientation in time and place
o Tremors
o Visual hallucination
o Psychomotor agitation and ataxia
o Insomnia
o Dehydration
• Alcohol withdrawal seizures may be of tonic clonic type and is of single episode most
likely. Sometimes status epilepticus may be precipitated. Thereafter, delirium tremens
may follow.
• Alcohol withdrawal is a medical emergency and should prompt referral to hospital for
further management.
Step 4: Management of Alcohol Use Disorder (30 minutes)
Investigations
• Hemoglobin
• ESR
• Widal test
• Mean corpuscular volume (MCV)

• Gamma glutamyl transferase (GGT)
• Liver function test
• Urinalysis
• Stool for oval
• HIV Test
Treatment
• The goal of treatment is to prevent medical and social adverse effects during period of
intoxication.
• The treatment may be non-pharmacological and pharmacological. Non-pharmacological
measure includes
o Providing safe environment and reassurance
o General medical support with iv fluids and respiratory assistance
• Pharmacologically, no antagonist (antidote) available
Treatment of Alcohol Withdrawal

• Stop alcohol use then manage withdrawal symptomatically by using
o Diazepam 30-40mg per day in divided doses (i.e. 10 mg three times daily) reducing to
0 by the end of day 5. This needs to be done in a controlled environment such as the
hospital and not as an outpatient therapy.
o Thiamine & multivitamins- because oral thiamine is poorly absorbed in patients with
a pattern of chronic alcohol consumption, high doses ideally parenterally 100 mg
intramuscularly should be considered in the first instance
o Thiamine ≥100 mg daily
o Antiemetic
o Analgesia such as paracetamol
o Any electrolytes imbalance should be corrected
o Fluid balance needs to be maintained. Patient may need IV fluid hydration with
isotonic solution such as normal saline
• Behavioral therapy, psychotherapy and group therapy is adjuvant therapy and it is
conducted in a specialized psychiatric unit by clinical psychologist.
Treatment of Alcohol Dependence

• Pre-Referral Treatment
o Treat alcohol withdrawal as explained above then refer the patient to a specialized
hospital

SELECT one student to read the scenario below aloud.
Scenario
Meg, a 47-years-old woman, always has alcohol on her breath and frequently falls. She
moved into the suburb a few months ago and is well known at the local liquor shop and hotel.
She denied alcohol use until a recent fracture and hospital admission. Since her discharge, she
has started drinking again habitually, mostly spirits.
She presents to you late one afternoon with the tremor, sweating profusely and vomiting.

Refer students to Worksheet 15..1: Diagnossis of Alcoh
hol Use Disorders Casse
Study
TELL students to answer the following questions

q an
nd record thhe responsess on their
worksheets.
What iss the possiblle diagnosiss?

List diffferential diaagnosis?
How arre you goingg to managee Meg?
GIVE students
s 10 minutes to discuss.
SELEC
CT few studdents to resppond.
RECOR
RD the respponses on thhe board/flipp chart.
SUMM MARIZE thee discussionn by using Worksheet

W 15.1: Diagn
nosis of Alccohol Use
Disordeers Case Sttudy.
Step 5:
5 Cannab
bis Use Diisorders (15
( minutes)
• Cannnabis is derrived from herb

h plant called
c Cannabis sativa
• Cannnibis is a drrug widely used in somme subculturres and is thhought to caause physical
dependence.
• When smoked,, the drug seeems to exaaggerate the pre-existing mood, be it depressio on,
euphhoria or anxxiety.
• Theere is no deffinite withdrrawal syndrrome.
• While cannabiss use can result be charracterized byb acute anxxiety, depresssion or
halllucinations, there is no convincingg data that a persisting psychosis
p can result.
• Howwever, theree is evidence that cannaabis smokin ng increasess the risk off developing
g
schiizophrenia in
i individuaals so predissposed, andd may aggravvate the conndition oncee it has
mannifested it.
Clinicaal Effects off Cannabis Use

• Acuute Effects ofo cannabis include
o Pain percepption is reduuced
o Anti-nauseaate and antii-emetic effe fects
o Increased appetite
a
o Anticonvullsant effectss
• CNS S depressannt effects off cannabis innclude
o Drowsinesss
o Reduced allertness
o Impairmentt of short teerm memoryy,
o Slowed reaactions
o Reduced acccuracy of psychomoto
p or task perfo
ormance
o Reduced motorm coordiination and muscle tonee
o Dysphoria, increased anxiety
a and panic reacttions especially in inexxperienced users
u
o Sensory disstortions, haallucinationns

Session 15:
1 Drug and Alcohol
A Abusse 197
• Cardiovascular effects
o Tachycardia
o High Cardiac Output
o High Myocardial Oxygen need
• Effects of cannabis in the respiratory system include
o Bronchodilation leading to reduced airway resistance in acute phase
o Bronchial irritation due to particulate fraction of cannabis smoke in chronic phase
o Cannabis smoke similar to tobacco smoke
• In the eye, cannabis leads to reduced intraocular (IOP) at doses that produce CNS effects
• Effects of cannabis in the immune system is unclear but there are chronic inflammatory
chest disease as well as precancerous changes
Step 6: Management of Cannabis Use Disorder (5 minutes)
Investigations
• Urine test for cannabinoid done at government chemistry laboratory
Treatment
• No specific pharmacotherapies are available yet for managing cannabis withdrawal or
relapse
• Motivational interviewing technique available at specialized hospital
Step 7: Other Drugs of Abuse (15 minutes)
• There are many other drugs that are used for abuse, these drugs include
o Cocaine
o Heroine
o Barbiturates
o Benzodiazepines
o Volatile substances
Refer students to Handout 15.1: Other Drugs of Abuse
Cocaine Abuse
• Cocaine is an alkaloid derived from the coca bush erythroxylum coca
• Cocaine is a central stimulant which inhibits the re-uptake of dopamine along with that of
nor-epinerphrine and serotonin
Clinical Features of Cocaine Use Disorder

• Pupillary dilatation
• Tachycardia
• Hypertension
• Nausea and vomiting
• Increased psychomotor activity
• Elation of mood
• Pressure of speech
• Impaired judgment with social or occupational dullness
• It can precipitate a myocardial infarction

Other Clinical Features
• Severe anxiety
• Paranoia (fear/obsession)
• Psychosis
• Irritability
• Confusion
• Desire to isolate
• Memory impairment
• Inability to concentrate
• Loss of control
• Aggressiveness
Complications of Chronic Cocaine Use

• Tactile hallucinations
• Cardiac arrhythmias
• Lung damage
• Foetal hypoxia
• Perforation of nasal septum
Cocaine Use Withdrawal Syndrome

• Withdrawal tends to peak 2–4 days following cessation of use
• Dysphoria rather than depression which may persist up to 10 weeks plus at least two of
the following
o Fatigue
o Insomnia/hypersomnia
o Psychomotor agitation
o Craving
o Increased appetite
o Vivid unpleasant dreams
Treatment of Cocaine Withdrawal

• To date, no effective pharmacotherapy for withdrawal management
• Prescribed medications
o Short-term use of benzodiazepines for
Anxiety
Agitation
Promotion of sleep
o Note: Benzodiazepines need to be used cautiously as they can cause delirium and
make things worse
• Psychotherapy

• Drugs of abuse are generally substances that when taken alter mood, cognition (thoughts)
and behavior.
• There are four important patterns of drug use disorders namely intoxication, withdrawal,
dependence and abuse.
• Complications of drug abuse are many and difficult to treat.

• Control of drug abuse is very important so as to reduce their effects in individuals and
society as a whole.
• What are the common drugs of abuse?

• What are the symptoms and signs of alcohol intoxication?
• Mention four pattern of drug abuse
• Describe the management of cocaine intoxication
References
McGraw Hill.
• Cape, G. et al (2002). Management of Alcohol and Drug Problems. Oxford University:
South Melbourne.
• Clarke, C. et al. (2002). Alcohol Training Resource. Department of Human Services.
Melbourne.
• Cumming, A.D. (2008). Davidson’s Principles and Practice of Medicine. Churchill
Livingstong.
• DeCrespigny, C. & Cusack, L. (2003). Alcohol, Tobacco & Other Drugs Guidelines for
Nurses and Midwives: Flinders University and Drug and Alcohol Services Council.
• Hamilton, M., & Cape, G. (2002). History of Drug Use and Drug Policy Responses.
• Hulse, G. et al. (2002). Management of Alcohol and Drug Problems. South Melbourne.
Australia: Oxford University.
• Victoria Police (2002). Medical Management of People in Custody with Alcohol and
Drug Problems: Custodial Medicine Unit. Mornington, Victoria: Victoria Police.

Worksheet 15.1: Diagnosis of Alcohol Use Disorders Case Study
Scenario
Meg, a 47-years-old woman, always has alcohol on her breath and frequently falls. She
moved into the suburb a few months ago and is well known at the local liquor shop and hotel.
She denied alcohol use until a recent fracture and hospital admission. Since her discharge, she
has started drinking again habitually, mostly spirits.
She presents to you late one afternoon with the tremor, sweating profusely and vomiting.
1. What is the possible diagnosis?

2. List differential diagnosis?
3. How are you going to manage Meg?
Answers
1. Possible diagnosis
• Alcohol withdrawal syndrome
2. Differential diagnoses
• Alcohol abuse
• Alcohol dependence
3. Management
• Treat withdrawal using diazepam protocol and injection thiamine
• Refer for specialized care

Handout 15.1: Other Drugs of Abuse
Heroin Abuse
• Semi synthetic
• Heroin is prepared by reacting morphine with acetic anhydride or acetyl chloride
Uses
• By injection
• By sniffed/snorted, smoked
Heroin Overdose
• Clinical trial of respiratory depression, CNS depression and miosis
• Drowsiness, ‘nodding off’
• Slurred, drawling speech
• Pinpoint pupils
• Ataxia, emotional liability
• Respiratory rate is less than12 per minute
• Bradycardia, hypotension
• May progress to coma
Short Term Effects

• Soon after injection or inhalation heroin crosses the blood brain barrier
• In the brain heroin is converted to morphine and binds to opioid receptors (mu, kappa and
delta)
• Users report feeling a ‘rush’: accompanied by warm flushing of the skin, dry mouth and
heavy feeling in the extremities
• May also experience nausea, vomiting and severe itching
• Cardiac function slows
• Breathing severely slowed which may progress to death
Long Term Effects

• Tolerance and physical dependence
• Tolerance to analgesic effects develops slowly but tolerance to psychoactive effects
develops rapidly
• Addiction
• Medical complications
• Viral infections like hepatitis B, hepatitis C and HIV
• Scarred/collapsed veins
• Bacterial infections such as abscesses and endocarditis
Symptoms of Heroin Withdrawal

• Intense anxiety and dysphoria
• Craving for heroin
• Insomnia, fatigue
• Myalgias, chills
• Nausea, abdominal cramps, diarrhea
Treatment of Heroin Overdose/Intoxication

• Naloxone (opioid antagonist)
• Duration of action of naloxone is much shorter than that of opioid agonists
• Its peak effects is 5-15minutes and duration of action is only 60 minutes
• Patients who respond to naloxone must not be discharged until opioid effects have
completely worn off
Treatment of Withdrawal
Pharmacological Treatment
• Detoxification
• Usually an inpatient admission with methadone as a substitute which is prescribed in
special psychiatric hospital
Symptomatic Treatment
• Such as loperamide 2mg bid for treating withdrawal diarrhea
• Diazepam short course for treating withdrawal insomnia, but be cautious using
benzodiazepines in this situation as they may worsen the condition.
• Pharmacological treatment Options work best when combined with counseling and
structured relapse prevention programs
Barbiturates Abuse
Symptoms of Barbiturate Intoxication

• Sluggishness
• In coordination
• Difficulty in thinking
• Slowness of speech
• Faulty judgment
• Drowsiness or coma
• Shallow breathing
• Staggering
Barbiturate Dependence
• Barbiturates are a type of depressant drug that causes relaxation and sleepiness
• In relatively low doses barbiturates and alcohol have very similar clinical syndromes of
intoxication
• Excessive and prolonged dosages of barbiturate drugs such as phenobarbital, may
produce the following chronic symptoms
o Memory loss, irritability, changes in alertness, and decreased interpersonal
functioning
o Barbiturates may also cause an acute overdose syndrome which is life-threatening
Treatment of Barbiturate Intoxication

• There is no direct antidote to barbiturates or alcohol overdose
• In such overdoses respiration must be maintained by artificial means until the drugs are
removed from the body.
• Ensure breathing and circulation as well.
• Ensure adequate fluid hydration

Treatment of Barbiturate Dependence
• Is done by gradual withdrawal in stepwise manner such as reduction of 10% of the dose
every day.
• After detoxification phase follow up supportive counselling is essential to prevent
relapses.
• Benzodiazepines Abuse
• Is class of psychoactive drugs typically prescribed to treat conditions such as anxiety and
insomnia.
• They have a tranquilizing effect on the central nervous system.
Benzodiazepine Dependence
• Especially when they exhibit at least 3 of the following behaviours within a 12 month
period.
o Tolerance to the medication to the extent that the patient needs to take more to
achieve the same effects.
o Withdrawal symptoms when the medication is discontinued and taking other drugs to
relieve symptoms.
o Taking higher and higher dosages against the doctor's prescription and when they
aren't needed.
o An inability to stop.
Treatment of Benzodiazepine Dependence

• As in barbiturate dependence
• True benzodiazepine withdrawal can be life threatening (similar to alcohol) and needs to
be treated in hospital with slow taper of benzodiazepine over several days
Volatile Substances Abuse

• Commonly referred to as inhalants, solvents or solvent based products
• 4 categories of inhalants
o Solvents
o Aerosols
o Gases
o Nitrites
Clinical Features of Volatile Substance Abuse

• Red, watery eyes
• Sneezing & coughing (URTI-like symptoms)
• Chemical smell or odour on breath
• Glue, solvent, or paint stains on clothing, fingers, nose, or mouth
• Apparent intoxication/altered behaviour/risk taking
• Incoherence, confusion
• Poor coordination
• Excessive sweating
• Unusual spots, marks, rashes and sores around nose and mouth
• Excessive nasal secretions, constantly sniffing
Treatment of Volatile Intoxication

• Ensure fresh air and breathing
• Be calm and calming

• Persuade to cease sniffing if patient can communicate
• Take person to a safe environment
• Don’t attempt to counsel while intoxicated, drowsy or heavily intoxicated
• Consider the best environment for the individual and monitor physical and mental health
• Need to make patients aware that some side effects of these substances can cause
permanent changes.

Session 16: Cerebrovascular Accident/Stroke
Prerequisites
None
Learning Objectives
•Define cerebral vascular accident
•Describe causes and risk factors of cerebrovascular accident
•Outline clinical features of cerebrovascular accident
•Identify investigations and treatment of cerebrovascular accident
•Describe preventive measures for cerebrovascular accident
Resources Needed
•Flip charts, marker pens, and masking tape
•Black/white board and chalk/whiteboard markers
SESSION OVERVIEW
Activity/
Step Time Content
Method
Definition and Types of CVA
Presentation,
3 30 minutes Causes and Risk Factors for CVA
Brainstorm
Presentation,
4 20 minutes Clinical Features of CVA
Buzz
Management of CVA
6 10 minutes Presentation Prevention of CVA
SESSION CONTENT


Session 16: Cerebrovascular Accident/Stroke 207
Step 2: Definition and Types of CVA (15 minutes)
• Cerebrovascular accident (CVA): A sudden death of some brain cells due to lack of
oxygen when the blood flow to the brain is impaired by blockage or rupture of an artery
to the brain
• CVA is also known as stroke
Types of Cerebrovascular Accident
• There are two types of cerebral cardiovascular accidents/ stroke

o Ischemic
o Haemorrhagic
Ischemic Stroke/CVA
• Ischemic stroke is the most common type of stroke (~ 80%) usually due to a blocked
artery often by a blood clot
• Usually this type of stroke results from clogged arteries, a condition called atherosclerosis
• Fat, cholesterol, and other substances collect on the wall of the arteries forming a sticky
substance called plaque. Over time the plaque builds up
• This often makes it hard for blood to flow properly which can cause the blood to clot
There are two types of clots
o A clot that stays in place in the brain is called a cerebral thrombus
o A clot that breaks loose and moves through the blood to the brain is called a cerebral
embolism
• Transient ischemic attacks (TIAs) are often an early warning sign of an impending
ischaemic stroke
• They are caused by a brief interruption of the blood supply to part of the brain
• Because the blood supply is restored quickly, brain tissue may not die, as it does in a
stroke.
Hemorrhagic Stroke
• Rupture of an artery to the brain causing blood to leak into the brain
Step 3: Causes and Risk Factors for CVA (30 minutes)
ASK students to list risk factors and causes of CVA.
Risk Factors
• Atherosclerosis (narrowing or blockage of arteries by patchy deposits of fatty material in
the walls of arteries)

• High blood cholesterol levels
• High blood pressure
• Diabetes
• Smoking
• Family history of stroke
• Old age
• Too much alcohol
• Cocaine or amphetamines consumption
• Abnormal heart rhythm (atria fibrillation)
• Inflamed blood vessels (vasculitis)
Causes
• An artery to the brain may be blocked by a clot (thrombosis) which typically occurs in a
blood vessel that has previously been narrowed due to atherosclerosis
• A blood clot can form in a chamber of the heart when the heart beats irregularly, as in
atria fibrillation
• A cerebral hemorrhage (bleeding in the brain), as from an aneurysm.
Step 4: Clinical Features (20 minutes)
ASK students to outline the clinical features of CVA.
GIVE students 2 minutes to discuss in pairs.
INVITE few pairs to give their responses and record their answers on a flip chart/chalk
board.
• Strokes usually damage only one side of the brain

• Because nerves in the brain cross over to the other side of the body sign appear on the
side of the body opposite the damaged side of the brain
• Signs and symptoms depend on the area of the brain affected
o Change in alertness (consciousness)
o Coma
o Lethargy
o Drowsiness
o Stupor
• Difficulty speaking or understanding others
• Difficulty swallowing
• Difficulty writing or reading
• Headache
o Starts suddenly

o Occurs when lying flat
o Gets worse when changing positions or when bending, strain, or cough
• Loss of coordination
• Loss of balance
• Movement changes usually on only one side of the body
o Difficulty moving any body part
o Loss of fine motor skills
• Nausea or vomiting
• Seizures
• Sensation changes usually on only one side of the body
o Decreased sensation
o Numbness or tingling
• Sudden onset of confusion
• Vision changes
o Decreased vision
o Loss of all or part of vision
• Weakness or paralysis of one side of the body
Step 5: Management of CVA (20 minutes)

• Patients clinically suspected of having CVA (history and examination) must be referred to
hospital for investigation and treatment.
• Take blood pressure to rule out hypertension although sometimes blood pressure tends to
normalize after stroke.
• At primary health care facilities, pre-referral management must be done before patients
are referred (i.e. ensuring airway is open, patient is breathing and circulation is proper)
Investigations
• Diagnosis is based on medical history and symptoms but imaging and blood tests are also
done
• The blood sugar level is measured immediately because a low blood sugar level
(hypoglycemia) can cause symptoms similar to those of stroke
• Other tests at higher centers
o Computed tomography (CT scan) or Magnetic Resonance Imaging (MRI) of the brain
o Complete blood count (CBC)
o Electrocardiogram (ECG) to diagnose underlying heart disorders
o Echocardiogram if the stroke may have been caused by a blood clot from the heart
o Serum cholesterol
Treatment
• Definitive management of patients with CVA must be done in the hospital and therefore
referral is a must.
• Treatments designed to reverse or lessen the amount of tissue infarction fall within the
following categories
o Medical support
o Thrombolysis
o Anticoagulation (e.g. low molecular heparin)
o Antiplatelet agents (e.g. Aspirin)

Ischemic Stroke
• When cerebral infarction occurs the immediate goal is to optimize cerebral perfusion in
the surrounding ischemic area.
• Attention is also directed toward preventing the common complications of bedridden
patients
o Infections
Pneumonia
Urinary tract
Skin
o Deep venous thrombosis (DVT)
o Pulmonary embolism
• If treatment can be started within 3 hours of the first symptom then thrombolytic therapy
(‘clot breaking drug’) may be considered as an option
• Low doses of intravenous heparin is sometimes an option
• Supportive measures may be considered as an option
• Blood pressure is cautiously controlled. Lowering blood pressure too much may cause
another stroke to occur
Hemorrhagic Stroke
• Supportive measures only
• All blood thinning medications will make a stroke worse and therefore need to be avoided
• Correct any bleeding problems
• Blood pressure is controlled very cautiously
• Treatment of blood pressure that is too high or too low may be necessary
o Lowering elevated blood pressure into the normal range is no longer recommended
during the first few days following a stroke (current recommendation is to have BP
between 140-160 systolic in setting of acute stroke)
o If the blood pressure is low, raising it is advisable using intravenous fluids
• Pain killers may be given to control severe headache but avoid respiratory depression
• The blood sugar (glucose) in diabetics is often quite high after a stroke
• Controlling the glucose level may minimize the size of a stroke
• Oxygen is given as needed
Rehabilitation
• The goal of long-term treatment is to help the patient recover as much function as
possible and prevent future strokes
• Depending on the symptoms rehabilitation may include
o Occupational therapy
o Physical therapy
o Speech therapy
Step 6: Prevention of CVA (10 minutes)
General Principles
• A number of medical and surgical interventions as well as life-style modifications are
available for preventing stroke.
• Some of these can be widely applied because of their low cost and minimal risk.
• Others are expensive and carry substantial risk but may be valuable for selected high-risk
patients.
• One of the most important interventions to prevent stroke is to identify HTN early and
initiate proper treatment.
• If the patient has atrial fibrillation, warfarin is recommended, secondary option aspirin.
• Cholesterol levels should be brought to normal level.
• Diabetes mellitus should be controlled.
• Alcohol consumption should be limited.
• Exercising regularly and if overweight, losing weight helps people control high blood
pressure, diabetes, and high cholesterol levels.
• Having regular checkups enables a doctor to identify risk factors for stroke so that they
can be managed quickly.
• Stop smoking - this is probably the second most important intervention after HTN control
• Low dose aspirin 75 mg daily should be instituted in those at high risk for stroke with
risk factors (e.g. persons with previous stroke or TIA, diabetics, those with known
cardiac disease, or atherosclerosis). Do not use if contraindications for aspirin exist.
• Stroke occurs when an artery to the brain becomes blocked or ruptures, resulting into
death of an area of brain tissue (cerebral infarction) and causing sudden symptoms.
• Most strokes are ischemic usually due to blockage of an artery, but some are hemorrhagic
due to rupture of an artery.
• Transient ischemic attacks resemble ischemic strokes except the symptoms resolve within
short time.
• Diagnosis is based on history and symptoms, but imaging and blood tests are also done.
• Recovery after a stroke depends on many factors such as the location and extent of
damage, patient’s age and presence of other disorders.
• Controlling high blood pressure, high cholesterol levels, and high blood sugar levels and
not smoking help prevent strokes.
• Control of HTN may prevent strokes.
• What do you understand the term CVA?

• What are the risk factors for CVA?
• What are the clinical features of CVA?
• How can CVA be prevented?
References
McGraw Hill.
• Cumming, A.D. (2008). Davidson’s Principles and Practice of Medicine. Churchill
Livingstong.
• Goldstein, L.B. (2007). Braunwald's Heart Disease. Edinburgh: Oxford.
• Zivin, J.A. (2007). Hemorrhagic Cerebrovascular Disease. Cecil Medicine. Philadelphia:
Saunders Elsevier.
The development of these training materials was supported through funding from the President’s Emergency Plan for AIDS Relief
(PEPFAR) through the U.S. Department of Health and Human Services, Health Resources and Services Administration (HRSA)
Cooperative Agreement No. 6 U91 HA 06801, in collaboration with the U.S. Centers for Disease Control and Prevention’s Global AIDS
Programme (CDC/GAP) Tanzania. Its contents are solely the responsibility of the authors and do not necessarily represent the official
views of HRSA or CDC.

Internal Medicine 2 Module

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Internal Medicine 2 Module

Uploaded by

Copyright:

Available Formats

UNITED REPUBLIC OF TANZANIA

CMT 05211 Internal

CMT 05211 Internal Medicine II NTA Level 5 Semester 2 Facilitator Guide

CMT 05211 Internal Medicine II NTA Level 5 Semester 2 Facilitator Guide

In September 2009, MOHSW embarked on an innovative approach of developing the

CMT 05211 Internal Medicine II NTA Level 5 Semester 2 Facilitator Guide

These participants are listed with our gratitude below:

CMT 05211 Internal Medicine II NTA Level 5 Semester 2 Facilitator Guide

CMT 05211 Internal Medicine II NTA Level 5 Semester 2 Facilitator Guide

Editorial Review Team

Librarians and Secretaries

CMT 05211 Internal Medicine II NTA Level 5 Semester 2 Facilitator Guide

Dr. Gilbert Mliga

CMT 05211 Internal Medicine II NTA Level 5 Semester 2 Facilitator Guide

Who is the Module For?

How is the Module Organized?

CMT 05211 Internal Medicine II NTA Level 5 Semester 2 Facilitator Guide

What Should the Facilitators Do?

What You Need to Do Before Teaching with Handouts and Worksheets

How to Use the Students Manual

CMT 05211 Internal Medicine II NTA Level 5 Semester 2 Facilitator Guide

CMT 052211 Internal Medicine

CMT 05211 Internal Medicine II NTA Level 5 Semester 2 Facilitator Guide

CMT 05211 Internal Medicine II NTA Level 5 Semester 2 Facilitator Guide

9 05 minutes Presentation Evaluation

CMT 05211 Internal Medicine II NTA Level 5 Semester 1 Facilitator Guide

Step 1: Presentation of Session Title and Learning Objectives (5 minutes)

ASK students if they have any questions before continuing.

Step 2: Causes and Clinical Features of Status Asthmaticus (20 minutes)

Causes of Status Asthmaticus

Clinical Features of Status Asthmaticus

CMT 05211 Internal Medicine II NTA Level 5 Semester 1 Facilitator Guide

Step 3: Differential Diagnoses, Investigations, Treatment and

Activity: Brainstorm (5 minutes)

ASK students to mention differential diagnoses of status asthmaticus.

INVITE few students to give their responses.

RECORD the responses on the board/ flip chart.

SUMMARIZE the discussion by using the content below.

CMT 05211 Internal Medicine II NTA Level 5 Semester 1 Facilitator Guide

Treatment of Status Asthmaticus

Refer students to Handout 1.1: Drugs for Treatment of Status Asthmaticus

Step 4: Epidemiology, Causes, Pathophysiology and Clinical Features of

CMT 05211 Internal Medicine II NTA Level 5 Semester 1 Facilitator Guide

CMT 05211 Internal Medicine II NTA Level 5 Semester 1 Facilitator Guide

CMT 05211 Internal Medicine II NTA Level 5 Semester 1 Facilitator Guide

CMT 05211 Internal Medicine II NTA Level 5 Semester 1 Facilitator Guide

Step 5: Differential Diagnosis, Investigations and Treatment of Respiratory

CMT 05211 Internal Medicine II NTA Level 5 Semester 1 Facilitator Guide

CMT 05211 Internal Medicine II NTA Level 5 Semester 1 Facilitator Guide

Refer students to Handout 1.3: Complications of Respiratory Obstruction

Step 6: Classification and Clinical Features of Pulmonary Oedema

Classification of Pulmonary Oedema

Clinical Features of Pulmonary Oedema

CMT 05211 Internal Medicine II NTA Level 5 Semester 1 Facilitator Guide

Step 7: Differential Diagnosis, Investigations and Treatment of Pulmonary

CMT 05211 Internal Medicine II NTA Level 5 Semester 1 Facilitator Guide

Treatment of Pulmonary Oedema

Step 8: Key Points (5 minutes)

Step 9: Evaluation (5 minutes)

CMT 05211 Internal Medicine II NTA Level 5 Semester 1 Facilitator Guide

CMT 05211 Internal Medicine II NTA Level 5 Semester 1 Facilitator Guide

Beta Adrenergic Agonists Bronchodilators

Mast Cell Stabilizers