Index
1- Neurology …….... 1
2- Cardiology …....... 6
3- Respiratory ....... 12
4- Asthma ……....... 18
5- GIT ….………..... 20
6- Hepatology …..... 26
7- Endocrinology .... 28
8- Nephrology ........ 30
9- Hematology ........ 34
10- Rheumatology .. 38
11- Neonatology .... 00
12- Growth ……..... 00
13- Nutrition …...... 00
14- Infec. & Vacc ... 00
10- Genetics …....... 00
16- Emergencies ..... 00
 Neurology
Hydrocephalus Cerebral Palsy
Non progressive – Non fatal – Non curable Motor disability
Obstructive Non-Obstructive affecting Developing brain (1st year).
(non-Communicating) (Communicating)
Etiology
Separate ventricular cyst Inter-ventricular space not separated from
from sub-arachnoid space sub-arachnoid
Prenatal (2C) Perinatal (2H) Postnatal
Hypoxia & Hge.
Congenital (2A) Cerebral malformation Hypoxic ischemic injury Infection
Congenital (Duct)
Agenesis of villi (Most common) (Meningitis, encephalitis)
Duct of sylvius (Most Common)
Arnold Chiari Congenital infection Hyper Na
Duct of Luschka and Magendie
(Hydrocephalus + Meningomyelocele) (TORCH) Hge (ICH) Hypoglycemia
Acquired
Acquired Kernicterus
Traumatic: Intra Ventricular Hge
Traumatic: Sub arachnoid Hge.
Inflammatory: Post meningitis
Neoplastic: medulloblastoma
Inflammatory: post meningitis Early feature
Neoplastic: choroid plexus papilloma Motor delay, Microcephaly, Persistence reflexes, Feeding difficulty, Floppy infant.

Duct of sylvius stenosis Types

Congenital - Traumatic - Inflammatory (Toxoplasma)
Spastic 70 Dyskinetic 10 Ataxic 10 Ataxic 10
Clinical Picture
Pyramidal tract Basal ganglia Cerebellum Both
<2years >2years UMNL
Hypotonia
(Head – Back – Skin) Hypertonia
Abnormal movement
Hypotonia Hypotonia
Hyperreflexia coordination Hyperreflexia
Volume Emotional
+ve babinski
widened separated sutures and fontanelles.
Prominent veins
ICT Paresis
Sunset appearance
UMNL Quadri Hemi Di Mono
Squint – Optic atrophy
Both Sides One side
Both LL One limb (Arm)
Investigations (CT - Cranial US - MRI - fundus examination) pseudo bulbar Arm > Leg

Treatment Investigations (CT – MRI – EEG – TORCH)

Ventriculo-peritoneal shunt (VP shunt)
Treatment (Physiotherapy – Rehabituation)
Ventriculo-Atrial shunt (VA shunt) (Obsolete dt risk of Infective endocarditis)
 Neuro muscular disorders

Ant. Horn cells (First year) Peripheral nerves Muscle (First 5 years)
(Werding Hoffmann) (Guillain barre) (Duchenne) ‫طفل الساللم‬

The most common cause of The most common cause of The Most common & Most serious
floppy infant acute paralysis in children Muscular dystrophy

Autosomal recessive Ch. No.5
Etiology Apoptosis of Ant. Horn cells “motor”
Post-infection polyneuritis
X-linked recessive
Ab. Attached to nerve >> Demyelination >>
Dystrophin gene mutations >>
Conduction >> Paralysis
Dystrophic Ptn >> Ca & Creatine influx
(motor, sensory, autonomic)
Infection then paralysis (Resp. & GIT)

Diminished fetal movements Atrophy & Pseudo hypertory

Bilateral symmetrical ascending paralysis
Floppy infant Hypotonia
Hyporeflexia
C/P Hypotonia & Hyporeflexia (pelvic girdle, Shoulder& Trunk Ms.)
Paresthesia
Bulbar Palsy Cardiomyopathy & cardioMegaly
Change in BP & HR
Tongue Fasciculations Pes cavus sclerosis
Facial & Bulbar Palsy
Death from Resp. failure

Clinical
Investiga EMG CSF >> Ptn +
Serum CPK
Genetic Cytoalbuminous dissociation
tions Complications
EMG
(post infectious)
Biopsy (Characteristic)
EMG >> Nerve conduction velocity
(Diagnostic)

Gradual complete recovery Physiotherapy

Physiotherapy Plasmapheresis Rehab
TTT
Rehab Physiotherapy Corticosteroids
IV. Ig 400mg/kg/day for 5 days Die 15 – 25y
 Meningitis Encephalitis

Bacterial
Viral:
• First 2 months: B Hemolytic strept – E coli – Listeria
• HSV (most common)(temporal lobe)
• 2 m – 12 y: Capsulated bacteria
Etiology Viral Enterovirus – Epstein bar virus
• Enterovirus
• Epstein bar virus
T.B Fungal
• Arbovirus
Source: Direct – Blood spread

General: Poor feeding - Purpura fulminans – Septicemia – Vomiting – DIC

Shock
Viremia >> ICT – Convulsion – Coma
ICT: Bulging & Tense fontanelle – Separated sutures – Persistent
Cerebrum >> Coma – Convulsion – Motor deficit
C/P Headache – Projectile vomiting – Papilledema – Hypertension
Cerebellum >> Ataxia – Tremors
Bradycardia
Brain stem >> Cranial nerves
Meningeal irritation: Neck pain & rigidity – Brudzinski – Kernig’s
Cortex (3Cs): Confusion – Coma – Convulsions

Early:
• Brain: Effusion >> Convulsion >> Abscess
• Blood: Septicemia & Shock >> DIC & ADH
Complicati
Late:
ons • Hydrocephalus – epilepsy – MR
• Empyema >> ICT >> Herniation >> Late CP
• Deafness

CSF Normal Bacterial Viral TB

Color Clear Turbid Clear Yellow CSF – Serology (For viral Ab)
Investigati CT
Cell Lymphocyte Polymorph Lymphocyte Lymphocyte
ons Ptn 20-40 Mild
MRI (Foci of demyelination) (Temporal lobe demyelination in herpes encephalitis)
EEG (Diffuse bilateral slowing of background activity)
Glucose 40-80 Mild
Supportive:
I.V fluid 70% - Anticonvulsant – Ventilation
Specific:
Supportive: ABC
Antibiotic I.V
Anticonvulsant
Treatment < 2 months >> Cefotaxim
Dehydration measures
> 2 months >> Cefotaxim + vancomycin
ICU >> Antiviral
Steroid under cover of antibiotic
(Supra renal affection – H.influenza – ICT)
Follow up

Prevention HIB vaccine – Polysaccharide vaccine – Rifampicin

 Intellectual disability
Epilepsy
(Mental retardation)
Etiology Etiology
Hereditary (progressive) Idiopathic 80% – Secondary 20% (As CP ) – Reflex – Epilepsy $
• Chromosomal abnormalities (Down – Fragile x)
• Genetic Microcephaly
•
•
Metabolic (Phenylketonuria – Homocystinuria)
Neurodegenerative
Acute symptomatic seizure
Acquired: Pre, Peri, Post-natal (as CP)
Etiology
Unknown (25%)
CNS infection – Metabolic – Trauma – Brain edema – Poisons & Toxins
Grades (IQ = mental age/chronological Age x 100)
Classification
Mild Mod. Severe profound
school MR
Generalized Focal Unknown
Absence
IQ 50 – 75% 35 – 50% 20 – 35% < 20%
5-20 sec Tonic Clonic Myoclonic Atonic 3-8 months
Educable Trainable Non-trainable Non-trainable ‫فاصل ونواصل‬
Triggered by
Investigations Hyperventilation
Pre-ictal Headache &
Sensory
flashes of light Sudden Loss of
Karyotyping – TORCH – Metabolic – T3, T4 & TSH Motor Repeated attacks
CT – MRI Ictal Sudden loss of jerky Postural
No post-ictal
EEG consciousness & falling movement tone
Focal >> ttt: Corticosteroid,
Post-ictal Paralysis
Good prognosis 2ry General ACTH
Treatment Deep sleep
Dietary EEG: EEG:
Physiotherapy 3spikes/sec wave hypsarrhythmia
Speech therapy (character) (character)
Drugs
Clinical evaluation
History Examination
Seizure before – Character – Etiology – Treatment General – CNS – Abdomen

Investigations (CBC – Electrolyte – CSF - TORCH – Metabolism – EEG – CT – MRI)

Treatment
Generalized: Sodium valproate Absence: Ethosuximide
Focal: Carbamazepine Neonate: Phenobarbitone
Infantile: Steroid – ACTH – Clonazepam
Status Epilepticus < 30 min Floppy infant Poliomyelitis
Epileptic patient – Prolonged convulsions – CSF infection Sever persistent hypotonia at birth or in early infancy Almost eradicated
ICH – Hypoxic ischemic injury – Metabolic Viral infection of Ant. Horn cells
Etiology
Complications Etiology
Central (Atonic CP – Cortical malformation) Oral & droplet
CNS: Ischemia – Edema – Hge Peripheral (Werdnig Hoffmann – Neuropathy – Neonatal Man is the only reservoir
CVS: Shock – Failure – Arrest Myasthenia – Myopathy)
Respiratory: Apnea – Obstruction – Edema
Metabolic: Temp. – (PH, Glucose, Na)
Genetic (Down – Prader willi $) Immunity
Trans placental: passive – 6 m.
C/P (‫ رجله‬- ‫ ظهره‬- ‫)راسه‬ Vaccination: Active – Lifelong
Treatment
Head lag – Curved trunk – Frog leg position
First aid (ABC) C/P
First line drug (diazepam, phenytoin) – ICU Unilateral – Bilateral Asymmetrical
LMNL
Motor affection
Febrile Convulsion 5% (5) Acute Paralysis Bulbar & Resp. paralysis

Due to rapid rise of body Temp. Types

5m – 5y Genetic susceptibility Unapparent – Abortive – Non paralytic – Paralytic
Etiology (Spinal cord) – Encephalitic (Brain)
Simple 80 Complex 20
5-15 m >15 m Cerebral (stroke)
Prevention Polio vaccine
Generalized Focal Spinal cord (Trauma – Transverse myelitis)
Not recurrent Recurrent Ant. Horn cells (Poliomyelitis >> Asymmetric Ascending) Treatment
Normal after attack neurological Nerves (Guillain barre >> Symmetric ascending
Gradual incomplete recovery
Post-diphtheric >> Symmetric descending)
Treatment First aid ABC Isolation – Physiotherapy – Orthopedic.
Neuromuscular (Botulism >> Symmetric descending)
Temperature >> Paracetamol & tape water
Anti convulsion – Cause

Acute Disseminated
Progressive motor weakness Encephalomyelitis
Brain abscess
4 – 8years. Staph. – Strept.
Demyelination disease occurring at any age
Etiology CNNS + muscle Post infection – Post vaccination. Site: Frontal – Parietal – Temporal. (Single or Multiple)
Cerebral (Tumor & cyst – Degenerative)
Nerve (Neuropathy) C/P: Meningeal irritation – Encephalopathy C/P: Toxemia – ICT – Convulsions – Coma.
Neuromuscular (Myasthenia)
Spinal cord (Tumor – Degenerative) Investigations: CT – MRI – EEG – CSF Investigations: CT – MRI.
Muscular (Duchenne) (Most common)
Treatment: IV Steroid – IV IG Treatment: Combination of antibiotics.
 Peripheral resistance determine our pressure.
valves keep blood inside pulmonary and aorta.
Mitral valve closes at 5mmhg ( early systole ).
S2 = aortic and pulmonary valves closure ( splitted ).
Tricuspid valve closes at 3mmhg ( early systole ).
S1 = mitral and tricuspid closure.

Pediatric hypertension Acute congestive heart failure

Stages: Etiology:
• Normal < (90th percentile). • Preload (VR): Lt to Rt shunt.
• Pre HTN (90th : 95th). • Contractility: ischemic heart – infarction – myopathy.
• Stage 1 (95th : 99th). • Afterload (TPR): HTN – AS – coarcitation.
• Arrythmia.
• Stage 2 > 99th.

Etiology: Grading:
• Kidney: renal diseases - renal artery stenosis. • Grade I: HF only (3Ts) tachycardia – tachypnea – tender liver.
• Grade II: HF + respiratory failure (chest) hypoxia – cyanosis – crepitations – congestion.
RBF << Renin << Angiotensin << Na & Water retention.
• Grade III: HF + circulatory failure (shock) hypotension – hypoperfusion – MOSF.
• Heart: Coarcitation of aorta = UL BP LL BP.
• Hormones: (Cortisol – Aldosterone – Catecholamines). Investigations:
• Brain: ICT – Pain.
• Essential HTN. • CXR – ECG – Echo.
• ABG – Cardiac marker (troponin).
C/P:
• Increase ICT : 3Ps (persistent headache – papilledema – projectile vomiting).
Treatment:
• Hypertensive retinopathy. • Supportive (semi setting – fluid restriction 70% - oxygen).
• Coma and convulsions. • Preload (Diuretics).
• Heart failure. • Contractility (Digoxin).
• Afterload (ACE-I).
Investigations:
• KFT - urine analysis - renal doppler.
• Electrolyte - lipid profile - FBS.
• Sonar - Echo.

Treatment:
Cause + lifestyle modification.
Antihypertensive drugs (Diuretics - BB - ACEI - CCB).
 Acyanotic heart diseases
(Lt to Rt shunt) (Increase pulmonary blood flow)
ASD
VSD PDA
Secundum 80 Primum 20
Interventricular septum
High defect Lower interatrial
Defect Membranous 80 Distal to origin of subclavian artery
Less serious more serious
Muscular 20

LV << RV << Lung Aorta << Pulmonary << Lung LA << RA << RV << Lung
Haemo-
Lung congestion Lung congestion Lung congestion
dynamics Biventricular enlargement LV enlargement RV enlargement Biventricular

Large VSD
Onset: 2nd week 3rd or 4th decade Infancy
Small VSD Difficult feeding Small PDA Large PDA Asymptomatic HF
History Asymptomatic Dyspnea Asymptomatic As VSD Dysnea Dysnea
FTT Chest infection Chest infection
Recurrent chest infection

General FTT As VSD +

Normal Normal Recurrent chest infection
examination Recurrent chest infection Water hummer pulse

Biventricular enlargement LV enlargement RV enlargement Biventricular

Cardiac Pan-systolic
Systolic thrill Systolic thrill
Accentuated S2 Continuous murmur Accentuated S2 Wide fixed splitted S2
examination murmur
Pan-systolic harsh Continuous machinery No murmur (ejection systolic if PS)
murmur murmur

Investigations CXR – ECG - Echo CXR – ECG - Echo CXR – ECG – Echo - Catheter

HF – recurrent chest infection – FTT HF – recurrent chest infection – FTT

HF – recurrent chest infection
Complications Infective endocarditis Infective endocarditis
Arrythmia
Eisenmenger $ Eisenmenger $ of lower limb

Medical
Surgical Medical ( anti PG )
Treatment • Pulmonary A. Banding Surgical or catheter closure
Surgical or catheter closure

• Heart – lung transplantation

 Acyanotic heart diseases
(Obstructive lesions)
Coarcitation of aorta Aortic stenosis Pulmonary stenosis

Valvular Valvular
Defect Distal to origin of subclavian artery (PDA?!)
Supra & sub valvular (rare) Supra & sub valvular (rare)

Haemo- Pressure gradient across aorta Pressure gradient across aortic valve
Pressure gradient across pulmonary valve
UL BP LLBP collaterals BP
dynamics LV enlargement LV enlargement
RV enlargement

Mild: asymptomatic
Mild: asymptomatic Mild: asymptomatic
History Severe: ICT HF Severe: CO Lt side HF
Severe: CO Rt side HF
+ cyanosis

General UL BP LLBP Systolic BP

examination Weak, absent or delayed femoral pulse Pulse volume

LV enlargement LV enlargement RV enlargement

Cardiac No thrill Systolic thrill Systolic thrill
examination Accentuated S2 Muffled S2 Muffled S2
Systolic harsh murmur Systolic ejection click murmur Systolic ejection harsh murmur

Investigation CXR – ECG – Echo CXR – ECG – Echo CXR – ECG – Echo
s Spiral CT or angiography Post stenotic prominent aorta Post stenotic prominent pulmonary

Complication HF – Infective endocarditis HF – Infective endocarditis

HF – Infective endocarditis
s Intracranial Hge

Medical
Pressure gradient > 50 mmhg
Surgical (coarcetectomy)
Ballon valvuloplasty Balloon valvuloplasty
Treatment Catheter
Valve repair valvotomy
• Balloon angioplasty
Valve replacement
• Stent insertion
 Cyanotic heart diseases
Tetralogy of Fallot Transposition of Great Arteries
( PBF) ( PBF)
Pulmonary stenosis
Aorta arises from RV
Overriding Aorta
Defect Large VSD
Pulmonary arises from LV
**Communication is a must**
RV Hypertrophy
Pulmonary (Stenotic) << PBF
RV LV << Pulmonary << Lung << LV
Aorta (Overriding) << Cyanosis 2 parallel
Haemo-dynamics Mild RV hypertrophy circulations
RV << Aorta << Body (Cyanosis) << RV
**ASD, VSD or PDA is essential**
No shunt across VSD
Cyanosis Delayed gradual narrowing of infundibulum & closure of PDA Cyanosis Early not relieved by 100% Oxygen
Dyspnea Dyspnea
History Hype cyanotic spell Recurrent chest infection
Squatting HF

General
FTT – Central cyanosis - Clubbing FTT – Central cyanosis - Clubbing
examination
RV Hypertrophy
RV Hypertrophy
Cardiac Aortic enlargement so higher sound
Single S2 (Due to Anterior displacement of aorta)
Single S2 Pulmonary stenosis so lower sound)
examination Systolic thrill (PS)
No murmur (Only murmur of mixing defect)
Harsh ejection systolic murmur
CBC: Hb - HCV
CBC: Hb - HCV
ECG – Echo
Investigations CXR: Boot shape
ECG – Echo
CXR: Egg on side – Lung plethora
Catheterization

Thrombosis – Infective endocarditis – Brain abscess Thrombosis – Infective endocarditis – Brain abscess
Complications Iron deficiency anemia Recurrent chest infection

Medical: Propranolol – Iron – Hyper cyanotic spell - IE Medical: PG

Surgical: Surgical:
Treatment • Blalock taussing • Balloon atrial septostomy
• Total correction • Arterial switch
 Rheumatic Fever
*Auto-immune *Following Upper Respiratory tract infection
*Peak at 5 – 15 years *Streptococci *M/C cause of acquired heart disease in children
Mechanism: Investigation:
Cross reactivity & Genetic susceptibility CBC: Leukocytosis – ESR – CRP
CXR – ECG – Echo
Diagnosis:
2 Major or 1 Major + 2 Minor Management:
1) Prevention:
*Major criteria of JONES: -Primary: Good housing – Tonsillectomy
1) Joints (Polyarthritis) in 70%: IM Benzathine Penicillin 1.200.000 IO
- Inflammatory swelling, Redness, Hotness, Tenderness & Oral Penicillin V
Limitation of movement Oral Amoxicillin
- Migratory fleeting – Asymmetrical Oral Erythromycin
- Dramatic response to Salicylate -Secondary for recurrence:
2) Carditis in 50% it is the most serious & the most fatal Benzathine Penicillin every 2 – 3 weeks for 10 years
- Endocarditis: (M A T P): LT < RT Mitral < Aortic after last attack or 21 years old (which is longer)
Acute << Swelling << Regurge (Carey Coombs Murmur) 2) Treatment:
Chronic << Fibrosis (Double mitral) -Antibiotics:
- Myocarditis: BF << Tachycardia IM Benzathine Penicillin 600.000 – 1.200.000 IO
Muffled heart sound -Supportive:
Cardiomegaly & HF Decrease salt and water in diet - Rest
- Pericarditis: Stitching pain – Rub – Effusion -Specific:
3) Nodules: Subcutaneous – Painless – Hard – over bony prominence Arthritis << Aspirin
4) Erythema Marginatum: Not pruritic – Progressive margin – Carditis << Cortisone
Central fading Chorea << Phenobarbitone
5) Sydenham Chorea: F < M – Darting tongue – Boat shaped hand -Treatment of complications:
Antibodies cross to brain (Basal ganglia) << Abnormal – Irregular HF – Arrythmia (Early)
– Sudden – Jerky movement – Increase by stress – Decrease by rest RHD – Recurrence – IE (Late)

*Minor criteria (F R A P P):

Fever – Raised ESR & CRP – Arthralgia – Prolonged PR
– Previous Rhematic fever
 Infective Endocarditis

Etiology: Investigation:
Organisms: Viridant $ - Staph – Enterococci – HACEK Blood culture
High risk: LT < RT – Regurge < Stenosis – IV Drug – History CBC – ESR – CRP
Predisposing: Dental – Adeno-Tonsillectomy – GIT - GU CXR – ECG
ECHO (Transesophageal echo is better than transthoracic)
Pathophysiology:
Turbulence << Endothelial damage << Subendothelial C.T. Management:
exposure << Thrombus << Bacterial growth << Vegetations: 1) Prevention:
• Valve destruction -Pure oral hygiene
• Embolization -Oral or IV Amoxicillin single dose 1h before oral, respiratory or
• Immune complex deposition << Rash dental procedure
-IV Ampicillin & Gentamycin 30 mg before GIT or GU procedure
C/P: and Amoxicillin 6h after.
Infection: Fever – Headache – Malaise – Anorexia -In allergic patients: Azithromycin or Clindamycin
Embolization: Subconj. & Retinal Hge – ICH – Jenway lesion
Immune complex: Glomerulonephritis << Hematuria 2) Treatment:
Splinter He – Osler's nodules – Roth spots -Empiric:
Against staph: Methicillin or Vancomycin + Gentamycin
Criteria: (2 Major or 1 Major + 3Minor or 5 Minor) -According to culture:
Major criteria: Staph: Methicillin or Vancomycin + Gentamycin
• 2 Positive cultures of 3 – Typical organism Strept, Enterococci, HACEK: Penicillin or Ampicillin or
• Evidence of Endocarditis on ECHO Ceftriaxone + Gentamycin
(Vegetations – Abscess – Regurge) Fungus: Amphotericin B
-Surgical
Major criteria:
• Predisposing factors
• Single positive blood culture
• Fever
• Embolic manifestation
• Immune complex deposition
Symptoms of chest:
• Cough
• Dyspnea
• Expectoration
• Hemoptysis
Alveoli:
• Chest pain
• Type I alveolar cells >> mucus secretion
• Noisy chest
• Type II alveolar cells >> surfactant
• Cyanosis
• During expiration >> two layers of alveoli adhere together due to
Anatomy mucus but in the presence of Surfactant mucus is absorbed by
URT >> Nose – Nasopharynx – Larynx. surfactant and prevent collapse
LRT >> Medium & Small Sized Bronchi – Terminal – Alveoli.
Connectors >> Trachea – Main Bronchus (No narrowing or
In pneumonia:
dilatation) – Surrounded By Cartilage.
Mucus secretion increase so surfactant cannot absorb all mucus so
collapse may occur but ‫ سبحان هللا‬during full Expiration >>
During inspiration >> URT narrow & LRT wide
Expiratory spasm of adductors of vocal cord occurs (Grunting) >>
During expiration >> URT wide & LRT narrow
no full expiration >> no collapse
Noisy respiration >> Partial airway obstruction
Connectors if have secretion >> noise respiration (Ratling) ‫صوت‬
• URT >> Noisy Inspiration. LRT >> Noisy Expiration
‫البلغم مع النفس‬
• Noise due to Nose and Nasopharynx >> Snoring
• Noise due to Larynx >> Stridor
• Noise due to Medium and Small Bronchus >> Wheeze Respiratory distress:
• Noise due to alveoli >> Grunting >> Pneumonia Grade I >> Tachypnea + Working ala nasi
Grunting >> Reflex spasm of Adductors of vocal cord Grade II >> Intercostal and Subcostal retraction (LRT).
Airway >> Bronchitis – Bronchiolitis – Asthma Supra sternal and supra clavicular retraction (URT)
Alveoli + BV >> Pneumonia Grade III >> Grunting
Alveoli + BV + Airway >> Broncho-Pneumonia Grade IV >> Cyanosis
 Upper Respiratory Tract Infection (URTI)
Common cold Acute Tonsilitis
Otitis media
(Nasopharyngitis) (Pharyngitis)
Common above 2 years Common complication of acute
The commonest infection in children
Peak 4 - 7 years nasopharyngitis (6m – 6y)
Mostly viral >> Rhinovirus Streptococcus – diphtheria Mostly bacterial >> G + & G –
Organism Bacterial >> H. influenza Viral Strept. pneumonia – H. inf.
Fever >> Low grade – Irritability –
Strept.
Sneezing (subside within 2 days) Viral (mild)
High fever
If High grade >> suspect O.M Mild fever Fever – Earache – irritability
C|P Nasal discharge >> watery then
Severe sore throat
Moderate sore Drum perforation >> Discharge
Abd. Pain
mucoid (subside within week) throat
Vomiting
Feeding difficulty
Diffuse redness
Mild erythema
Follicular or
Small ulcer
membranous
Examinati in soft palate
tonsilitis Congested bulging drum
on Tender ant.
Follicular tonsilitis
Coryza – Cough -
Cervical
Conjunctivitis
lymphadenitis
Spread >> Sinusitis – O.M Ear Bone Brain
LRTI >> Bronchiolitis – Bronchitis - Early >> Quinsy Perforate. Mastoid. Meningitis
Complicat Suppurate. Petrous. Encephalitis
Pneumonia Late >> RF –
ions Prodroma of measles & W Cough PSGN Secretion Lower facial
Asthma attack deafness palsy
Antihistamine Oral Penicillin v Paracetamol for
Oral Broad Spectrum
Saline nasal drop Or Amoxicillin pain
Treatment Nasal decongestant Or Erythromycin No use for
Amoxicillin or Amoxicillin clavulanate
or 3rd gen. Cephalosporin
Avoid Aspirin >> Rey's $ For 10 days Antibiotic
 Lower Respiratory Tract Infection (LRTI)

Bronchitis Whooping Cough (Pertussis) Bronchiolitis

Prolonged cough leads to:
Large airway Chest pressure >> Pneumonia & Pneumothorax Small airway Infants < 2years
Abd. Pressure >> Hernia & Malnutrition
Commonest Cause of Acute Cough ICP >> ICH – Convulsion – Subconjunctival hge.
Commonest Cause RD & Wheeze

Mostly Viral follow Nasopharyngitis Droplet infection Bordetella Pertussis

Bacterial >> pneumonia – strept. – DPT: Compulsory vaccine
Mostly Viral >> RSV – Para influenza
Etiology staph – H. Influenza
– Adenovirus
Specific >> Measles – Pertussis – At any age as no trans placental immunity
Diphtheria against pertussis as IgM not cross placenta.

Catarrhal stage (1-2 w): Nasopharyngitis –

H/O Nasopharyngitis Fever – Cough
Gradual with dry cough Increase gradually – More at Night
Bacterial >> High fever – Prolonged Paroxysmal stage (2-4 w): Paroxysmal Prodroma >> mild URTI
Cough – Toxic manifestation attack of severe spasmodic 5-10 cough RD >> tachypnea + retraction
C/P • Early >> Dry sever brassy cough during one expiration ends with sudden Expiratory wheeze (LRT)
• Productive >> Less severe, forceful inspiratory whoop and followed Rapid recovery
Rattling, Rhonchi, Crepitation by vomiting and cyanosis
• Convalescent >> Cough Convalescent stage (1-2 w): Paroxysm
decrease and vomiting become less frequent

Leukocytosis with absolute lymphocytosis CXR >> Hyperinflation

Investiga
Rapid antigen detection ABG >> Acidosis
tion Culture From Nasal swap Antigen detection of RSV

Viral >> Spontaneous recovery Mild distress Moderate

Erythromycin >> Duration & infectivity
TTT Avoid cough suppressants
(Not curable)
Observe O2 – IV fluid
Antibiotic if bacterial Avoid aspiration bronchodilators
 Pneumonia
Parenchyma = Alveoli + BV = Restrictive Types of pneumonia:
Etiology Lobar Bronchopneumonia Interstitial
Infectious Non–Infectious Unilateral One or
Bilateral Bilateral
Bacterial: G+ G- TB Aspiration TEF – GER more lobes
Viral RSV–Adenovirus Bacterial Bacterial or viral Viral
Parasitic: Loffler $ Hypostatic CP Lobar
Patchy infiltration Para hilar shadow
Mycotic: Aspergillosis consolidation
Atypical: Mycoplasma P. Chemical kerosene
Age related pneumonia: Cystic fibrosis (Mucoviscidosis) (life threatening)
Neonates: Vertical – G B streptococci
Autosomal recessive – CFTR gene – Affects: Resp + GIT + FTT
Infant: Viral RSV – pneumococci – H. influenza Normal: Cl & water secretion >> Thin mucus
5> years: Atypical – Streptococci – H. influenza Mutation of CFTR gene >> thick mucus
• Most common >> Pneumococci
• Most serious >> Staph aureus > Pus > Infective Endocarditis Symptoms
Skin >> Salty tasting skin (1st symptom)
C/P Lung >> Clog airway >> Recurrent infection
General: Poor general condition – Poor feeding – FTT – FAHM GIT >> Clog pancreatic duct >> Enzymes >> Steatorrhea
Chest:
Infant Child
• Lobar >> Bronchial breathing – Dullness
(lung + GIT + FTT) (lung + GIT)
• Bronchopneumonia >> Crepitation
Lung >> Pneumothorax –
• Interstitial >> Severe Spasmodic Cough
Lung >> Recurrent infection Hemoptysis
Complication GIT >> Meconium ileus + GIT >> Intestinal Obst. –
Resp. failure – Pleural eff. – Abscess – Pneumatocele – Acute HF Cholestasis clog biliary duct Biliary Cirrhosis – Portal HTN
Investigations FTT – DM clog Panc. Duct
CXR – CBC – Culture Sterility >> Psychological
Bronchoscope – ABG
Investigations: Sweat chloride test > 60mmol/L
Treatment Treatment: Supportive – Not curable
Hospital if (Severe RD + < 6m.) >> IV Ampicillin + Gentamycin
Respiratory: Anti-inflammatory – Antibiotic – Mucolytic –
Home >> Oral Amoxicillin
Physiotherapy – Bronchodilator
Atypical >> Macrolide
Nutritional and psychological support – Gene therapy
 Suppurative Lung Syndrome (SLS)
Empyema Lung Abscess Bronchiectasis
Destruction of parenchyma >> Dilatation of Bronchi + Inflammatory
Definition Pus in pleural sac Cavity containing Pus destruction of bronchial & peri-bronchial tissue
+ Pus in dependent bronchi.
‫ جوة‬Complication of pneumonia & lung
Congenital Acquired
abscess AABP
Aspiration
‫ برة‬Chest Trauma & surgery Amebic lung abscess Genetic: CF – Immotile cilia –
Maldevelop
Etiology Bronchiectasis & TB Immunodeficiency
ment of
‫ تحت‬Rupture of sub diaphragmatic Pneumonia Inflammatory: Asthma
bronchi
abscess Metabolic lung abscess Infection: Abscess
Obstructive: F.B – enlarged LN
‫ نص‬Mediastinitis.
Symptoms
Dyspnea – chest pain – fever
Air entry >> Dyspnea Fever – Anorexia – Poor weight gain.
Hemoptysis
Infection >> Fever Expectoration of copious fetid mucopurulent
Copious amount of foul smelling or
Chest pain >> pleurisy Hemoptysis
purulent sputum (Fetid sputum)
Child lies on affected side Lies Hunching forward
Child lies on healthy side

Diminished movement of affected side Bronchial breathing

RD
Diminished breath sounds Persistent dyspnea
Signs Dullness on percussion
Diminished air entry
Clubbing of fingers
Localized bronchial breathing (Cavitation)
Trachea pushed to opposite side Delayed growth
Empyema or pneumothorax
Broncho-Pleural fistula Pulmonary HTN (Cor pulmonale)
Complications Pleural fibrosis
Bronchiectasis
Resp. failure
Spread
CXR – CT >> Cavity
Chest x-ray: Homogenous opacity CXR: soap bubble appearance
Investigations Thoracocentesis
Culture & Sensitivity
CT
Bronchoscopy
ABCD
Drainage Prolonged Antibiotic therapy (6w) Antibiotic
Treatment Systemic Antibiotics Bronchoscopy >> remove F.B Bronchodilator
Surgical decortication Resection of affected lobe Case local >> lobar resection
Drainage
 Tuberculosis

False +ve False -ve

Site: Lung – Tonsils – Intestine – Skin
Doctor: SC inj.
Require: Aerobic media – Low immunity BCG
Patient: immunodeficiency
Immunosuppressive
Atypical leprosy
Antiviral vaccine
NB: Lung apex is the M/C site Tuberculin: outdate
Gohn’s Focus >> Small caseating TB below pleura 0.5 – 1 cm
Good immunity >> Fibrosis & Calcification Prevention:
Low immunity >> Spread General: Good housing – Nutrition
Primary complex: Gohn's focus – lymphadenitis – lymphangitis Elimination of TB in cattle
Early diagnosis & TTT
C/P: 90% asymptomatic Examination % radiography for whom deal with children
General: 2 Loss (Weight & Appetite) – 2 Night (Sweeting & Fever) BCG: live attenuated vaccine
Chest: Chronic Cough (Main) – Localized Wheeze – Recurrent Cheapest and Most effective
Chest infection and failure of antibiotic TTT for long time 0.1 ml Intradermally 1st month
Booster at 6 years
Investigations: Chemoprophylaxis: INH to whom live near TB contact
CBC: Lymphocytosis – ESR
Culture: direct by Z-N stain – Lowenstein Jensen (4w) – BACTEC Treatment: 6-9 months
(10d) Drug S/E dose
QuantiFERON – LN Biopsy – ELISA – PCR
INH Vit B6 + Liver failure
Tuberculin test: 0.1 ml PPD Intradermally >> Read reaction
Rifampin Red urine 20 mg |kg |d
after 2-3 days
Pyrazamide Oral
Induration: < 5mms = Negative
ethambutol Optic neuropathy
5 – 9 = Repeat
Streptomycin
>10mms = Positive (Vacc. or Infection) Deafness + nephrotoxic
Ethionamide
>15mms = Infection
Corticosteroid: TB Serositis – Miliary TB affect supra renal
 M/C – Chronic – Diffuse – Obstructive airway disease Affects 18% of Population & 10% of School children
Polygenic Multifactorial 80% have their first symptoms before 5 years
B2 >> Bronchodilator Vagal >> Bronchoconstriction Before puberty Male : Female = 2:1 After = Equal

Pathophysiology:
Airway obstruction due to Airway obstruction Lead to Mild Moderate Severe Life
Bronchoconstriction
Area of hyperinflation RD Grade I II IV IV
Mucosal edema
Hypersecretion of mucus
Segmental atelectasis Resp. rate Normal Greatly Gasping| fall
Cellular infiltration
Ventilation perfusion mismatch
Alveolar hypoventilation
Accessory ms Absent Mild Moderate
More sever during expiration Cyanosis normal pallor Cyanosis cyanosis

Asthma triggers: HR Normal Greatly Fall

Expiratory &
Allergic Non allergic Wheeze Mild Expiratory
inspiratory
Silent
Penicillin Emotion – Exercise - Exposure to cold SPO2 >95% 92-95 <92 <90
Fish – Egg – Chocolate Infection – Smoke
Dust – Pollen Drugs aspirin – NSAID PaCO2 <38 38-42 >42 >42
PEF >80% 60-80 <60
Diagnosis:
Symptoms: Wheeze – Cough – Shortness of breath Management:
History Paroxysmal - At night – Vary over time – Triggered – • Acute attack
Relieved with Bronchodilators Goals: Adequate O2 saturation – Bronchodilatation – Corticosteroid decrease inflammation +
Examination Vesicular breathing with prolonged expiration + Expiratory wheezes Monitor response to TTT
Peak flow volume| sec.
Investigations Residual capacity • Preventive ttt in-between attacks
Skin prick test – Serum IgE – CXR – Peripheral blood Eosinophilia
• Avoid triggering
DD: Avoid exposure to allergen – Respiratory Infection – Dust – Cold air – Smoke – Certain food
Single wheeze Recurrent wheezes
• Patient and family education
Aspiration – FB inhalation Not exposed to smoke during pregnancy and after birth – vaginal delivery and breast feeding
Bronchiolitis
Bronchial asthma is advised – Avoid broad spectrum antibiotic during 1st year
Bronchopneumonia
Bronchiectasis
FB unilateral
Chronic infection
HF
Congenital anomalies
OP poisoning
CHD – Ciliary dyskinesia
 Management of Asthma
• Epinephrin (Alpha and Beta receptors)
Alpha >> VC of BV >> Mucosal edema >> Secretion. Beta >> Activate adenyl cyclase (ATP >> CAMP Bronchodilator)
• Selective B2 agonist >> Bronchodilator only
If Inhaled + Saline >> Bronchodilatation + Mucus (Saline >> Mucolytic effect)
• Parasympathomimetic (Ipratropium) >> Bronchodilatation + Mucus secretion
• Aminophylline >> Suppress Phosphodiesterase >> CAMP >> bronchodilator
• Corticosteroid >> Anti-inflammatory >> Antigen antibody reaction >> Release of mediators
Acute attack
Mild & Mod. Severe Life threatening
SABA ICU – IV fluid – O2
As Mild +
Ipratropium SABA (Nebulized – IV) – IV methyl prednisone
IV steroid
Controlled O2 – IV magnesium sulphate – IV aminophylline
IV magnesium
Oral steroid
IV aminophylline
NB: If deterioration continue, treat as severe Mechanical ventilation if PaCO2 > 55mmhg

NB: Measure lung function one hour after initial TTT:

PEF 60-80% or Symptoms improved >> Moderate >> Discharge planning
PEF < 60% or Lack of response >> Severe >> Continue TTT and Reassess
In-between attack: (ICS & LTRA the Most effective)
• Inhaled glucocorticoid
• Systemic glucocorticoid
• Leukotriene receptor antagonist
• Long acting beta agonist
• Long acting anti cholinergic
• Anti IgE

Stepwise to control symptoms in infant and children

Step 1 Step 2 Step 3 Step 4 Step 5
Intermittent Uncontrolled Sever persistent

0-5 Preferred Low dose ICS Double low dose ICS Refer to specialist
SABA as needed
years Alternative LTRA Low dose ICS + LTRA
Add LTRA
Frequency of ICS

Low dose ICS + LABA or Medium dose ICS  anti IgE

6 - 11 Preferred SABA as needed Low dose ICS
Medium dose ICS Refer to specialist Phenotypic assessment
years LTRA or High dose ICS + LABA 
Alternative Low dose ICS  SABA Low dose ICS + LTRA  anti IL5  low dose oral CS
Low dose ICS + LABA tiotropium  LTRA
 Dysphagia Corrosive FB
Difficult swallowing = Dysphagia Below cricopharyngeal sphincter at upper end of
Alkalies: NaoH – KoH
esophagus
Painful = Odynophagia Acids: Sulphuric acid
Site of constriction
Asymptomatic
Congenital Burning pain – Vomiting – Dysphagia
Dysphagia
Cleft palate Regurgitation
Traumatic C/P Dyspnea – Stridor (laryngeal edema) – Cyanosis
Pain
Radiotherapy (A coin may remains latent for weeks or even
Oral lesions
months)
Oro- Corrosives
Inflammatory Perforation
pharyngeal
Pharyngitis Complicat Aspiration Smooth (Perforation)
Malnutrition Sharp (Perforation – Laceration)
Suppurations
Neoplastic
ions Esophageal stricture Corrosive (Perforation – Injury)
Shock (neurogenic – hypovolemic)
Cancer tongue Emesis
Pharyngeal Cancer Stomach wash
C/I Neutralization
Lumen Activated charcoal
F.B Investigat Endoscopy (Esophagoscopy) Esophagescopy
Wall Barium swallow Barium swallow

Atresia ions Chest X-ray X-ray

Esophageal TEF
IV fluid + Immediate demulcent
Esophagitis
Antibiotic if infection
GER
Steroid (Prevent edema and fibrosis Esophagoscopy and removal
Outside wall TTT and risk of stricture)
Vascular compression Endoscopic dilatation
Mediastinal lesion Surgical reconstruction (gastrotomy – colon bypass)
 CHPS GER Atresia Achalasia
Dilatation of lower 2/3 of
50% of infants
Male : female Most common congenital anomaly of esophagus
Lower part of esophagus below diaphragm >>
4:1 Esophagus ~ 8 years (Uncommon before
more collapse than upper part due to IAPR
school age)
Gradual hypertrophy of pyloric
Failure of mesenchymal separation of Failure of relaxation of LES
Pathology Muscle (2-7 w) >> gastric outlet IAPR >> GER
esophagus and trachea Loss of peristalsis
obstruction
Gatric distension VACTERL association Antibody to Auerbach plexus
Etiology Multifactorial Short intra abdominal part of esophagus Esophageal atresia 8% Degenerative
Transient relaxation of LES Atresia with distal TEF 85% Infection
Since birth
Asymptomatic Dysphagia for liquid more than
Projectile – Progressive – Non bilious Except H-shaped (may be narrow)
Regurgitation >> vomiting >> FTT and wight solid
Symptoms vomiting >> Weight loss &
loss
H/O polyhydramnios
Regurgitation >> Esophagitis >>
Dehydration >> Hungry Excessive salivation
Regurgitation >> pain and irritability Under nutrition
3C: cough-chocking-cyanosis
Olive shaped mass at Rt side of
umbilicus
Signs Visible Palpable Peristalsis from Lt
to Rt
Esophagitis – Stricture – Anemia
Complicat Apnea >> Aspiration >> Pneumonia

ions
SIDS
Sandifer $
Vomit HCL/KCL
Investigat CL K Acidosis
Esophageal PH: Diagnostic and Asses severity Failure to pass catheter into stomach Barium: Parrot beak
Barium (Coiling of Ryle on X-ray) X-ray
ions
Abd. US
Endoscopy Barium >> risk of aspiration Manometry: Most sensitive
Barium meal (‫)بطلناه‬
-Medical: CCB – PDE.I
Correct fluid – Electrolyte – acid base Mild: Reassure + Position + Feeding Stabilization-resp. support
-Endoscopic Pneumatic
Anti Regurgitation Formula (BebelacAR) Primary anastomosis
Treatment Pyloromyotomy (not pylorotomy >> Severe: Drugs (Prokinetic – PPI) Gastric pull up >> hiatus hernia – GER
dilatation (of choice)
-Cardio myotomy (heller)
Sinus >> Peritonitis) + Feed next day Surgical: Fundoplication Colon graft
-Botulinum toxin
 Diarrhea Frequency > 4times Fluidity Vomiting
Acute Chronic Persistent Forceful expulsion = Vomiting
< 2weeks > 2-3weeks > 2weeks (5-20% of acute GE) Non forceful = Regurgitation
Infective Non (APD) Lactose intolerance (Disaccharide)
GE >> Disaccharidase >> Lactose malabsorption >>
Bacterial Infection
Watery acidic stool
Neonatal vomiting
Campylobacter
TTT: lactose free formula
(60%) Malabsorption (3Cs)
Cow milk protein allergy Well baby sick
E coli Antibiotic Celiac
Normally: GIT is impermeable to cow milk protein Amniotic gastritis Medical Surgical
Salmonella shigella (drug induced) Cystic fibrosis
In GE: Damage mucosa >> Intestinal allergy & Blood swallow CHPS
Viral Parenteral Cholestasis Infection
Inflammation when exposed to cow milk ptn Feeding problem Atresia
Rotavirus Dietetic ICT
>> Mucous & blood in stool GER TEF
Adenovirus Other Metabolic
TTT: A.A based or Soya ptn based Hemorrhagic disease Obst.
Parasitic Short bowel
Bacterial Overgrowth
Entamoeba Immunodeficiency
Giardia
GE >> Colonic bacteria invade upper S.I >> Damage Infant & Childhood vomiting
mucosa
Medical Surgical
Pathophysiology Infection
(GIT – UTI – CNS –Resp) Intussusception
Entertoxigenic Enteroinvasive
Organism adheres >> No penetration (intact cells) >> Secrete Organism invades >> Mucosal penetration >> Inflammation
Dietetic Volvulus
toxin >> CL & H2O Absorption >> Secretion >> Watery & Exudation & CL & H2O absorption >> Bloody diarrhea
diarrhea & FAHM
Metabolic Strangulated hernia
E coli – cholera – staph E coli – salmonella – shigella – campylobacter
(Vit D – DKA – CKD)

Clinical diagnosis of GE
Treatment
Severity Symptoms Complications >> Loss of Metoclopramide S/E : (Extrapyramidal reaction)
High fever (Bacteria infection) H2O >> Dehydration >> Shock >> Renal Failure
Domperidoe S/E : (Ventricular arrythmia)
Mild: 4 – 6 motions / day Vomiting may be: >> Acidosis
Moderate: 6 - 10 / day Absent (Parasitic) K+ & Ca2+ >> Convulsions Ondansetrone S/E : (Diarrhea)
Severe: >10 / day Mild (Bacteria) Vit K >> Bleeding
Severe (Viral) Persistent diarrhea & Malnutrition

Investigations
For the Cause >> Stool analysis & Culture – CBC – CRP – ESR – Blood culture

For Complications >> KFTs – electrolyte – ABG – bleeding profile

 Mild
Dehydration
Moderate Severe
(N)
Weight Home management Hospital management if:
3-5% 6-10% >10%
loss ORS – feeding – symptoms – specific Severe Dehydration
Mental 1) ORS
Sever persistent Vomiting
Conscious Irritable Coma Severe Electrolyte disturbance
CIC Complications
Composition
4 Vitals: Cations = Anions = Glucose = 100
N + ++ or -- 1) Shock therapy over 30 m
HR Na + K = Cl + Citrate = Glucose = 110
pulse N Weak Very 90 + 20 = 80 + 30 = 110 = 110 Lactate ringer 10-20ml/Kg

RR N Rapid Rapid deep

Glucose facilitated Na absorption 2) Deficit therapy over 6-8h
Amount
Glucose 5% & saline 1:1 + 20mEq/l K+
BP N - -- No dehydration >> 50 - 100ml
4 Fluids: Mild >> 50 - 80ml/Kg Mild >> 50ml/Kg
N prolong prolong Mod >> 80 - 10ml/Kg Mod >> 80ml/Kg
Refill Not in severe dehydration Severe >> 100ml/Kg
Tears N - --
Oral Regular Spoon every 1 – 2 m 3) Maintenance therapy over 16-18h
UOP N oliguria anuria

Fluid 2) Feeding Glucose 5% & saline 4:1

40 ml/Kg 80 120
loss as early as possible First 10Kg >> 100ml/Kg
11:20Kg >> 50ml/Kg
Fontan. N Depressed Marked 3) Symptomatic Above 20Kg >> 20ml/Kg
Eye N Sunken marked
Antiemetic – Antipyretic Correct dehydration then resume oral
Skin N Recoil<2S >2S
No Antidiarrhea or Antimotility Hypernatremic: Deficit + Maintenance
Tongue N Dry Very
4) Specific slow correction with Glu : Saline 2:1
Types (to avoid brain edema)
Entamoeba >> metronidazole 50mg/Kg/d
Isotonic 75% Hyper 15% Hypo 10% Giardia >> metronidazole 25mg/Kg/d Hyponatremic: Deficit + Maintenance
H2O loss = elect. loss Water < Elect. Water > Elect.
No fluid shift Cell >> ECF ECF >> cell Cholera >> tetracycline slow correction with Glu : Saline 1:1
Etiology: Sweat-vomit- (to avoid Neurological complication)
‫غلطة دكتور‬ Salmonella & shigella >> ampicillin or 3rd gen cephalosporin
Acute GE DKA
Poor recoil Fair Very poor
Depressed font Mild Marked
Sunken eye Mild Marked
Dry tongue Very dry Moist
 Constipation Celiac Disease
Infrequent Hard stool Gluten sensitive enteropathy
Mainly in proximal SI (jejunum)
Soft stool every 3 days = Normal
Mucosal damage – Villous atrophy – Crypt hyperplasia – Lymphocytic infiltration
Hard stool every 3 days = Constipation
C/P
Etiology
Onset: weaning 6m – 2y
Functional after Organic Diarrhea – Abdominal distension – FTT
Pale loose offensive stool
Neonatal period (AADD4M)
Autoimmune >> Associated disorder (DM – thyroiditis – Addison)
Anatomical
Investigations
Painful defecation >> Voluntary Anorexia nervosa
withholding Defect in spinal cord (NTD) Antibody against intestine (Tissue transglutaminase – anti-Endomysial)
Drugs (Anticholinergic – Narcotic) Jejunal biopsy
Dilated rectum with large vol. of stool Megacolon
Malabsorption (3Cs) Treatment
Encopresis (Fecal soiling) Myopathy Gluten free diet
Metabolic (Hypo K – Hypothyroid– Hyper Ca)

Hirschsprung Disease
Absence of ganglion cell in myenteric & submucosal plexus of rectum & colon
>> Failure of relaxation
Male : female = 4 : 1 Sporadic

C/P
Delayed passage of meconium - Intestinal obstruction
Chronic constipation

Investigations
Barium enema – Anorectal manometry
Suction rectal biopsy (Gold Standard)

PR examination
Empty rectum – Narrow segment – Gush of liquid stool

Treatment: Surgical may be laparoscopic

 Acute Abdominal Pain Chronic Abdominal Pain
Medical Surgical Dysfunctional Organic
Infection
Medical conditions > 90% < 10%
(Most Common)
GE Acute appendicitis (Most Common) PCDDD
Vasculopathy 4S
Hepatitis Meckel's diverticulum Parasitic
HSP
Pancreatitis
Sickle cell
Strangulated inguinal hernia Predisposing Social
Chronic Constipation
Cholecystitis Volvulus School phobia
Appendicitis
Chemical irritations
Intussusception
Factors Sympathy
Dietetic
Drugs Drug
Pyelonephritis Impacted fecal mass Simulation
DKA Disaccharide intolerance
Peritonitis
Lead
Pharyngitis Periumbilical
Away from umbilicus
Intussusception Pain Dull aching
Variable
Severe
Not severe
variable
Proximal bowel into Distal Ilio-Cecal Most common < 20m

3 m : 3 y >> Due to Loose – Long – Lax Mesentery Appearance Healthy Toxic

Congestion >> Bleeding >> Necrosis (Ischemia)
Diarrhea – Constipation –
C/P Vomiting – Jaundice –
Association No
Dysuria – Drugs –
Sudden severe colicky pain
Pain recurs at frequent interval Hematuria...
Red currant jelly stool
Sausage shaped mass in right upper quadrant Focal tenderness
Mucous & blood in PR examination Abd. exam Normal Organomegaly
Shock like state, abdominal distension & bilious vomiting masses

Investigations investigation Normal According to cause

Abd. US – X ray abdomen – Barium enema

treatment Reassaurance Cause
Treatment
Pneumatic (hydro) reduction or surgical reduction
Resection anastomosis
 RBCs Hemolysis <> Bilirubin (Unconjugated) (Fat-soluble) >< Conjugation in liver (Water soluble) <> Intestine << Stercobilinogen.
Cause of jaundice: Production >> Uptake >> Conjugation >> Excretion (Cholestasis) >> Enterohepatic circulation.

Cholestasis Portal HTN

Bile flow >> Excretion >> Conjugated (No Kernicterus) Splenomegaly + Ascites + Hematemesis

Etiology
Idiopathic Neonatal Hepatitis (The Most Common) + (IUGR)
Infections: Bacterial – Viral – Protozoal infection
Choledochal cyst: Dilatation of the common bile duct
Metabolic: CHO – AA – Lipid – A1 Antitrypsin deficiency
Extrahepatic biliary atresia (2nd most common)
Familial Cholestatic $: Alagille – Progressive familial intrahepatic cholestasis – Paucity of IHPD
# Alagille $: Cholestasis + CHD + Paucity of intrahepatic bile duct + Corneal anomalies
# Alpha 1 antitrypsin deficiency: Cholestasis + Wheezes Bilirubin + Bile acid + Bile salt
> > Fat digestion – Fat soluble vit absorption – Pale Stool
Splenic + Mesenteric >> Portal Vein >> Portal tract > Bile canaliculi > Hepatic vein >> IVC
Etiology
Pre-hepatic: Portal V. thrombosis – Congenital obstruction.
Hepatic: Portal tract – Cirrhosis – Central V. thrombosis.
Post-hepatic: Budd Chiari $ - Constrictive Pericarditis.
Pathophysiology
Splenomegaly + Collaterals >> Esophageal varices – Piles – Caput medusae.

C/P C/P
Excretion: Fat malabsorption – Vit KEDA – Pale stool Hematemesis >> First presentation
Retention: Jaundice – Pruritis – Bradycardia – Liver damage Abd. >> Caput – Ascites
Complications: FTT – Cirrhosis – Portal HTN – Liver cell failure Organomegaly >> Spleen & Liver according to cause

Investigations: 2x4 (Liver Function Test) Investigations

- Direct & total bilirubin (> 20% Direct) Liver Function test (2x4)
- AST & ALT Upper GI Endoscopy (Diagnostic & Therapeutic)
- Alkaline phosphatase & GGT Abd. U/S & Doppler
-Albumin & Prothrombin CT Angiography – MR Venography.
Idiopathic EHBA
Biopsy Giant cells No Giant cells
HIDA Dye Pass No Pass
Treatment
U/S - Absent Gall bladder Emergency: ICU – IV. Fluids – Blood transfusion – Correction of coagulopathy - Drugs
Stool Periods of Normal Persistent Pale Correction of coagulopathy: Vit. K – Fresh plasma – PLT
Drugs: H2 receptor blocker – Vasospasm
NG tube for Monitoring & Wash
Treatment: Endoscopy After stop of bleeding
Vit. K Emergency shunt
EHBA: Kasai – Liver transplantation Prevent rebleeding: Avoid Aspirin – Band ligation – Propranolol
Treat the cause * (Propranolol also used in tetralogy of Fallot)
 Non-hepatotropic viruses: EBV – CMV – HSV. Hepatotropic viruses:
HAV RNA Feco-oral Vaccine 2-6 w No chronicity
HBC
Viral DNA Blood borne Vaccine 2-6 m Yes
HCV RNA Blood borne No Vaccine 1-5 m Yes
Hepatitis HDV RNA Blood borne Vaccine 3-6 w Yes
HEV RNA Feco-oral Vaccine 2-9 w No chronicity

Acute Hepatitis Acute Liver Cell Failure

Bad prognosis & high mortality
Etiology: 4I + $
Icteric (M/C) Anicteric Cholestatic Fulminant Infections Inborn error of metabolism Iatrogenic (drugs & toxins) Immune Rey $
Pre: (2 - 6 days)
FAHM – Abd. Pain – No Jaundice C/P: 3
vomiting – Dark urine (1) Metabolic function (APCDE)
Edema of Biliary
Icteric: (2 - 4 W) Only GI -- Coagulation factors >> Bleeding tendency
system >> Acute liver failure
Jaundice – Bilirubin > 5 Manifestation: -- Albumin >> Edema & Ascites
Decrease Bile flow
– Enlarged tender liver Anorexia – Vomiting – Ptn (A.A) Retention >> Hepatic Encephalopathy
Convalescent: liver size Diarrhea – Colic Dysfunction neutrophils >> 2ry Bacterial infection
– Pale stool – Dark urine. Electrolyte disturbance >> -- (Na – K – Glu)
Investigations: (2) Excretion (B B)
LFT (2x4) Ammonia ++ Bilirubin >> Jaundice
Acidosis (Na – K – Glu). ++ Bile salt >> Renal failure (Hepato-Renal $) + Pruritis
Serum Albumin (Normal if Acute – Decreased if Chronic) (3) Detoxification
Viral markers: ++ Ammonia >> Vomiting – Brain edema – Encephalopathy
HAV: Anti-HAV IgM (Acute) – Anti-HAV IgG (Recovery)
HBV:
Chronic Hepatitis > 6m
HBsAg & Anti-HBc IgM (Acute) Etiology: (6I)
Anti-HBsAg (Immunity) 4 as Fulminant + IBD + Idiopathic Neonatal hepatitis
HBsAg & Anti-HBc IgG (Chronic)
HBeAg (Infectious)
HCV: PCR >> HCV RNA antigen
C/P:
Asymptomatic Hepatosplenomegaly
Jaundice – Bleeding – Ascites – Spider nevi – Palmer Erythema
Prevention: Symptoms of the Cause
HAV (food borne): Isolation 7d – Strict hand wash – Inactivated HA vaccine
HBV – HCV (blood borne): Strict screening – Sterilization – HB vaccine (0, 1, 6)
Breast milk doesn’t contain HBV
Complications: Cirrhosis – HCC – Portal HTN – Liver failure.
Newborn of HBV mother >> vaccination & Ig
HAV close contacts >> Ig. Investigations: LFT US – Doppler – Endoscopy – Biopsy
For the Etiology:
Wilson: Ceruloplasmin – Serum CU – Keyser ring
Autoimmune: ANA – Hypergammaglobulinemia

Treatment: Of the cause – Supportive – Liver Transplantation

 Hypothyroidism
Thyroid hormone action C/P
• Metabolism
• Growth and Development Congenital Acquired
Early in life >> Irreversible brain damage and MR Neonate Infant & Child
• Stimulate (Cardiac function – GIT motility – RBC synthesis) At birth
• Carotene >> Vit A
(Asymptomatic)

Etiology Later on (3P 2C)

Sympto Prolonged gestation Motor, Mental &
No MR
Primary Secondary School under activeness
ms period Physical Retardation
(Glandular cause) (pituitary cause) Prolonged jaundice
Poor activity & Feed
Congenital Acquired Constipation
Gland (Aplastic – Hypo Cry is Weak
Hashimoto
– Ectopic) 75%
(Antibody against • Head: Ant fontanelle
Hormone
thyroid + Pancreas) TSH Deficiency open – Wrinkled
(Dyshormonogenesis)
• Ant Hair line: Low
Iodine (Deficiency)
Surgical removal • Eyelids: Puffy
Drug (Anti thyroid)
• Mouth: Open – ( 3D, , )
Investigations (4 Thyroid – 3 ‫(صور‬ Large tongue – Delayed bone age
(FFTT)
Lip pallor – Decelerated growth
Thyroid (Profile – US – Scan – Screen neonates 3rd:7th day) (Profile: T4 – TSH) Fontanelle open
Delayed dentation Delayed Puberty
X-ray (Delayed Bone age + Open Post. Fontanelle) – CT (Tumor) – CBC (Anemia) Signs FTT
• Neck: Short + Goiter Metabolism
Hypothermia
Treatment Hypotonia
• Skin: Pale – Dry – (Cold intolerance)
Yellow Activity (Brady –
Eltroxin – L-thyroxin for life
• Abdomen: Constipation)
First symptom improve >> Body temp then Activity Distended +
Umbilical hernia
Follow up by Bone age – Growth – Hormonal profile
• Limbs: Short
+ Broad hand
 DM DKA
Polygenic (Environmental Infection – Autoimmune – Genetic down-twin)
Predisposing factors
Type 1 DM: 90% Type 2 DM: 10%
Infection >> Cortisol (Anti-Insulin)
Insulin >> The only hypoglycemic hormone – Anabolic
Anti-Insulin >> Catabolic Insulin under dosage >> Glucose
So, Insulin >> Anabolism & Catabolism Trauma >> Stress >> Anti-Insulin Hormones

Pathophysiology Insulin Anti-Insulin >> Glucose >> Glucosuria + Fluid loss

Glucose uptake by cells: >> Fat >> Ketone >> Acidosis + Ketonuria
Fat >> Lipolysis << FFA + Ketone bodies << Ketonemia << Ketoacidosis + Ketonuria
Protein >> Synthesis + Catabolism << Wasting + Growth failure
C/P (Classic as DM + Early + Late)
CHO >> Glycogenolysis + Gluconeogenesis + Glu Utilization << Hyperglycemia << • Early: Vomiting – Abdominal pain (Ketone irritant)
Glucosuria (Osmotic) >> Polyuria + Electrolyte loss >> Stimulate thirst center >> Polydipsia
• Late: Circulatory – Respiratory – Cardio – Neuro
C/P (Classic + Acute and Chronic Complications) Vomiting and polyuria >> Dehydration >> Shock
•Classic (3 Poly ‫)ويخس‬ Acidosis >> Deep rapid breathing – Acetone odor
Polyuria – Polydipsia – Polyphagia + Weight loss
Acidosis >> Shift K extracellular and H intra >> Hyper K >> Arrythmia
Polyuria >> 2ry Nocturnal Enuresis >> Infection
20-40% 1st presentation is DKA & Coma Cerebral depression and Coma

•Acute complication (‫)سكر‬ Investigations

DKA – Hypoglycemia – Infection (UTI & Fungal most common)
Blood glucose (Hyperglycemia < 200 mg/dl) – ABG (Acidosis) – Urine (Glucose – Ketone)
•Chronic complications (vasculopathy)
DD
Retinopathy – Neuropathy – Nephropathy Treatment (Fluid – Insulin – Acidosis – Myocardial – Antibiotic)
Ischemic HD Nocturnal enuresis
Diabetic foot – Delayed puberty Shock 10 ml/kg saline or ringer over 30 m repeated 3 times
DKA
Associated autoimmune (Celiac – Thyroiditis)
Deficit = % Dehydration * BW (kg)
Investigations Chronic RF Deficit + Maintenance = 1st 10 kg (100 ml/kg/24h) – 2nd 10 kg (50)
Maintenance Above 20kg (20) (Gradual over 48h / If rapid << Brain Edema )
•RBS > 200 mg/dl + Symptoms (Stress hyperglycemia no symptoms) Add K+ After passage urine
•FBS > 126 mg/dl (Normal: 70:100) Insulin after 1 h from fluid (Low dose IV infusion 0.1 unit/kg/h)
•PP2h > 200 mg/dl (Normal: <140)
NaHco3 only in severe Acidosis (Na >> Brain hge & Arrythmia) (Ketone >> NaHco3)
•HbA1c > 6.5%
NB: K+ is C/I in oliguria
 Introduction Ptnuria Hematuria

Function of kidney Abnormal amount of Ptn in urine > 5 RBC/HPF

• Regulation of (fluid – electrolytes – acid base – BP) Normally Etiology

• Vit D activation < 4 mg/m2/h
Or Ptn/creatinine ratio < 0.2 Glomerular
• Erythropoiesis Due to shredding of mucoprotein that cover cells of tubule (Dysmorphic – RBC cast – Dark – Ptnuria – HTN ) (3N 2H)
• Excretion of waste products
• Nephrotic (most common)
Heavy Ptnuria x10
Filtration barrier > 40 mg/m2/h
• Nephritic
Or Ptn/creatinine ratio > 2 • Nephropathy IgA
Endothelial cells of capillaries (fenestration)
• Collagen IV (Alport $ with deafness)
GBM have –ve charge glycoprotein Classification according to • HSP
• Duration (Transient and persistent) • HUS
Podocytes Pedicles Slits
• Origin (Glomerular and non) • SLE
• Molecules < 1.8nm << Freely filtered
• Molecules > 3.6nm << Not filtered Postural Ptnuria Non Glomerular
Persistent disappear in supine position (first morning (Fresh Bright Red)
So, serum Ptn (-ve charge) ~3.5nm cannot be filtered sample is free)
Compression of Lt renal V. • UTI (most common)
Starling forces of filtration • Stones
Selective • Sickle cell
Hydrostatic and Oncotic pressure
Non selective • Cytic kidney
NFP = HPgc – HPcs – Pgc = (60–15–30=15mmhg) Ptnuria • Exercise
• Trauma – Tumor
LMW Ptn in urine LMW + HMW
Red brown urine without RBC
BM sialoPtn
Distruction of GBM Hb – Myoglobin – Drug – Dye
dysfunction
GFR depends on Gross Microscopic
MCN$
• NFP (Net Filtration Pressure) Glomerular Non
Congenital N$ Symptomatic Asymptomatic
• Kf (Filtration Coefficient) (Surface area available for
filtration and permeability)

GFR = NFP * Kf
 Nephrotic $ (minimal change nephrotic) Nephritic $ (acute post
Ptnuria – Hypo Ptnemia – streptococcal glomerulonephritis)
Hyper lipidemia – edema Hematuria – Oliguria – HTN – Edema
Clinico - Laboratory $
Clinical $
No renal impairment
Renal impairment
2 – 6 years
5 – 12 years
Male : female is 2:1 Steroid sensitive
Proliferative GN
LM: No changes or minimal mesangial proliferation
Pathology EM: Fusion of foot process of podocytes << Slits
Molecular similarity between streptococcal
and glomerular antigens << Antigen antibody complex << Deposition along GBM
Edema 1st periorbital then generalized morning night Edema: mild acute localized
Ptnuria – Hypo Ptnemia – Hyper lipidemia H/O strept infection 1-6 weeks ago
C/P No persistent HTN, Hematuria or Fever Hematuria: gross painless dark
NB: Steroids S/E: HTN Oliguria HTN in 60%
Infection: Edema (Culture media) – Ptnuria (Ig) – Steroid
3 Failure (Brain – Heart – Kidney)
Thromboembolic events: Ptnuria (hemoconcentration and Clotting
Hypertensive Encephalopathy – Intracranial Hge
Complicat factors) – hyperlipidemia
HF AKI
ions Ptnuria: Fluid shift from intravascular to Interstitium
Hyperkalemia ( RAAS << Renin & Aldosterone: K excretion)
Hypovolemia (Hemoconcentration)
Hypovolemia: Diuretics – Diarrhea
Urine – Blood – Renal
Urine – Blood – Renal
Ptnuria – Sterile pyuria
Heavy Ptnuria – Hyaline casts
Investigati Kidney Function Test: Impaired – ASOT – C3
Hypoalbuminemia < 2.5g/dl – Hyperlipidemia > 200
on KFT – C3 – C4: Normal
C4: Normal (SLE: C3 and C4)
Renal US: Swollen inflamed (echogenic bright)
Renal US and Biopsy if atypical N$
Renal biopsy if (rapidly progressive – C3 > 3m – Normal C3)
Diet – Diuretics – Dialysis – Complications
Diet – Diuretics – Steroid – Immunosuppressive – Complications
Fluid balance – Na
(Fat – Water – Na) (Ptn as kidney normal)
Diuretics in Edema and RF
Treatment Severe edema: Diuretics + Albumin
Dialysis in RF
Prednisolone (2 3 4) 2mg/kg/d in 3doses for 4weeks
CCB in HTN
If steroid resistant: Immunosuppressive
Digitalis not used if HF due to renal excretion
Congenital nephrotic $ < 3months Pathophysiology of Nephrotic $
Autosomal recessive with poor prognosis - Genetic mutation in podocyte or congenital infection TORCH - Podocyte injury of Gene mutation in its pts << Glomerular capillary permeability << Heavy
C/P: Generalized edema – Large size placenta – Hypothyroidism range ptnuria & Albumin loss << Hypoalbuminemia ( Oncotic P.) << Generalized Edema
- Lipoprotein lipase (2ry to urinary loss) << Fat destruction Hyper-
TTT: Albumin with Diuretics – ACE.I – Nephrectomy – Dialysis - Hepatic synthesis of lipoproteins (2ry to hypoalbuminemia << Fat production lipidemia
 Urinary tract infection Nocturnal enuresis
Pyelonephritis = Fever Cystitis = No Fever Male : Female 3:1 as males have long urethra
1st year = Male : Female 3:1 more in uncircumcised boys +ve Family history
>1year = Male : Female 1:10 as females have very short urethra, very close to anal orifice 5 y: 15% 10 y: 5% 15 y: 1%
E-coli the most common cause
Ascending or blood borne
Etiology
Predisposing factors Secondary
Primary 80% (APSD)
Patient Doctor 20%
Incomplete micturation - Infrequent voiding Obstructive uropathy No dry period Dry period > 6m
Poor hygeine
Antibiotics ADH decrease at night
Uncircumcised boy - vulvitis
Adenoid hypertrophy
Consipation - Neuropathic bladder Organic : UTI
Positive family history
psychologic
Sleep disorder
C/P Delayed maturation of bladder control
Neonates and infants
Older children Investigation
(septicemia)
(Cause – Xray – Urine – MRI)
Pyelonephritis cystitis
Treatment
Fever – jaundice Fever – Rigor Dysuria – incontinence
Vomiting – diarrhea Hematuria Frequency – Urgency 4:6 years >6years
Feeding difficult HTN 2ry Enuresis
Abd. pain Loin pain Supra pubic pain
(Simple measure) (Drugs)
‫قبل النوم‬
Anti cholinergic :
Investigations (Urine – Blood) Decrees fluid intake
Increase bladder capacity
Midstream – Urine bag (Risk of contamination, Good –ve test) – urination
Bladder catheterization – Suprapubic aspiration (in sick newborn) ‫النوم‬ Desmopressin : anti diuretic
Pyuria pus cells > 5/HPF – WBC cast
Wake child to void Single night dose
• Pyuria without UTI (Fever – Nephritic – Dehydration)
• UTI without pyuria (Antibiotic – Closed infection – TB) ‫بعد ما يصحي‬
Colony count > 100.000 single pathogen (Diagnostic)
Leukocytosis – ESR – CRP Reward for dry night Alarm device
U/S – DMSA Avoid punishment
Voiding cystourethrogram (diagnose VUR – PUV)

Treatment
Cystitis: Nitrofurantoin or Amoxicillin (Oral for 5 days)
Pyelonephritis: Ceftriaxone or Cefotaxime or 3rd gen Cephalosporin (Oral or parenteral 7-14 days)
 Acute kidney injury Chronic kidney disease
Rapid – Reversible – Oliguria or Anuria – Disturbance fluid electrolyte acid Progressive – Irreversible – Polyuria

Prerenal (3H) Renal (GAVI) Postrenal 5C 2S $

(Hypoperfusion) (Injury/Damage) (Obstruction) Congenital (Aplasia – Hypo – Obstruction) Cystinosis
Glomerular (AGN) Cystic kidney Chronic GN Chronic pyelonephritis
Causes Hypovolemia Acute tubular necrosis Congenital (stricture – Segmental glomerulosclerosis Stones
Hypotension Vascular (HUS) PUV) Genetic nephrotic $
Hypoxemia Interstitial nephritis Acquired (stone – tumor)
GFR > 90 = No symptoms
RIFLE stages Normal creatinine < 1 60 : 90 = Mild GFR decrease
Stages Risk (1.5) Injury (2) Failure (3) Loss of function 30 : 60 = Moderate decrease
End stage = Renal transplantation 15 : 30 = Severe decrease
<15 = Replacement therapy
Asymptomatic (symptoms appear after 60:80% of function lost)
Retention of:
Anorexia – vomiting (toxins)
Chronic unexplained anemia
Fluid: Edema – HTN – HF
Chronic unexplained HTN
C/P Acid: Metabolic acidosis (deep rapid respiration)
Growth failure and short stature
K: Hyperkalemia (arrythmia)
Delayed puberty: Suprapubic DHEA
Fluid more than Na and Ca: Dilutional hypo natremia and calcemia
Rickets: Ca Po4
Toxins (urea and creatinine): Encephalopathy and coma
Polyuria – Polydipsia – Enuresis
Impaired KFT Ca Po4 acidosis anemia
Investi Renal US: Atrophic kidney except polycystic and obstruction
KFT – ABG – electrolytes
Xray: delayed bone age – rickets
gation Renal biopsy
GFR > 15 = Conservative ( diet – drugs)
Oliguria: Exclude obstruction then asses hydration
Ptn ( or debate) impaired KF ( Ptn) Growth failure ( Ptn) ???
Hypo or normal: Fluid intake (insensible + UOP + losses) urine pass
Salt - Free intake of CHO and Fat
If no urine pass or overload: Lasix 2mg/kg then Lasix 10mg/kg
Recombinant GH (growth failure) – Erythropoietin (anemia)
TTT If no response: 2-5 microgame/kg/m + fluid balance
Vit D3 (rickets) Ca and phosphate binders CaCo3
Acidosis: NaHco3
ACE.I and Diuretics (HTN)
Hyper K: Stop source – Slow Iv Ca gluconate – Shift K intracellular – Excretion
NB: Avoid Frusemide (nephrotoxic)
Dialysis if: Oliguria with overload – Bleeding – Rapidly rising KFT
GFR < 15 = Replacement therapy (dialysis or transplantation)
Blood components Factors affecting erythropoiesis (4H) Hb composition
Plasma: 54% of blood volume *Hypoxia *Hormones *(Hum) Nutrition Iron internal Ptn on surface
RBC: 45% of blood volume = HCV *Hemopoietic growth factor (ILs) Fetal Hb: 2 alpha + 2 gamma
WBC: 1% of blood volume Adult Hb: 2 alpha +2 beta
Adult spare Hb: 2alpha + 2delta
Anemia Iron deficiency anemia
• Bioavailability of iron 10%
Decrease RBC Increase Blood • Iron is absorbed in ferrous form and distributed in ferric form
production destruction loss • Phytate and tannic acid absorption of iron
Dys-
BM failure Corpuscle Extra Etiology
hematopoietic Store: anemic mother - twin Intake: false weaning
Absorption: diarrhea - malabsorption Requirement: girls
Iron Membrane Immune Trauma
RBC aplasia
B12 Accident
Aplastic Enzymes C/P (Anemia + Iron deficiency)
Folic acid Non - Surgery
Infiltration Atrophic glossitis – Poor appetite – Pica – Spooning nails
Chronic inflam. Hb immune bleeding
Investigation (anemia + iron deficiency + cause)
Ferritin serum iron TIBC Stool analysis Endoscopy
C/P of anemia (PCDEF)
Pallor – TachyCardia – Dyspnea – Easy Fatigue - HF Prevention
Adequate supply – Avoid cow milk – Proper weaning
Investigations
Prove anemia: CBC: Hb HCV – Prophylactic iron – Powdered formula well fortified with iron

Complications of blood transfusion (APCD) Treatment

Antibody formation Polymicrobial infection oral or parenteral iron
Common problem (Venous access) Deposition of iron Successful iron therapy:
1st day: Improved Appetite 2nd day: Bone marrow hyperplasia
3rd day: CBC show reticulocytosis
 Chronic hemolytic anemia
Thalassemia (Cooleys anemia) Sickle cell Crisis
The commonest autosomal recessive Black races Autosomal recessive Sequestration
Homozygous Hetero (asymptomatic)
Major: (2gene mutation, homozygous) – Minor:(1gene mutation, hetero) Beta chain defect Large amount of blood acutely pooled in spleen
Glutamic Valine
Intermedia: (moderate severity, homozygous)
Shock – Hepatosplenomegaly – Acute abdomen
Beta thalassemia major
Pathogenesis
Hypoxia << Deoxygenated << HbS << Polymerization IV fluid – RBC transfusion – Splenectomy
HbF At age of 3months HbA but beta chain of HbA is defective leads to: << Sickle shape << Distortion of RBC & occlusion of
Amount of HbA Free alpha chain leads to hemolysis BV
Hyper hemolytic crisis
C/P: Anemia + Hemolysis + Complications C/P: anemia + hemolysis + complications Sickle cell + G6PD deficiency
Hemolysis 5 colors: (Jaundice – Dark urine on standing – Dark stool –
Acute anemia + Hb-uria
Red urine attack – Bronze discoloration) Investigation
5 Organomegaly: (Liver – Spleen – Lymph nodes – BM – Heart) Prove Anemia + Prove Hemolysis + Sickle shape Reticulocytotic

Complications Prophylaxis Hb transfusion

Anemic HF – Bilirubin stones – Crisis – Deposition of iron – Easy bone Full immunization – Penicillin – Folic acid
Fracture – Growth retardation – Hypersplenism – Auto splenectomy – Vaso occlusive crisis
Complications of blood transfusion Aplastic anemia
Treatment Parvovirus 19 infection
Investigations Acute crisis – Chronic problems: Severe anemia
Prove anemia: CBC (Hydroxy carbamide – BM transplantation)
Prove hemolysis: Reticulocytotic – Bilirubin Reticulocytopenia
Suspect thalassemia: Shape – Target cell – Hb electrophoresis – Gene Hereditary spherocytosis
Europe Autosomal dominant RBC transfusion
Treatment Defect in red cell membrane Ptn << Surface to vol.
Supportive: Iron – HBV vaccine – Vit D – Ca – Iron chelating –
Life long packed RBC 10-15 ml/Kg/month
Ratio and Na/water entry
Vaso occlusive crisis
Only in sickle cell
Splenectomy: Not before 4years as phagocytic cells of spleen is the only cells C/P: anemia + hemolysis + complications
that can phagocytose capsulated organism Bony pain – Acute chest – Ischemic GIT – Ischemic
Before: vaccination against capsulated organism Investigation Neuropathy – Priapism – Splenic infarction
After : penicillin Prove Anemia + Prove Hemolysis + Spherocytes

BM transplantation Gene therapy HbF synthesis Treatment Infectious crisis

Folic acid – Blood transfusion – Spleen enlargement << Infarction << Healed by fibrosis
Cholecystectomy – Splenectomy << Regress << Auto splenectomy << Infection
 Acute hemolytic anemia Aplastic anemia Acute leukemia

X – linked Pancytopenia Malignant proliferation without differentiation of WBC

Pathogenesis RBC Anemia Risk

NADP WBC Fever Genetic – Chromosomal (Fanconi) –
Platelets Purpura Chemical – Viral – Immunodeficiency
Glucose G6P Gluconate 6 P
NADPH
NADPH provides H+ which protect Hb against oxidation
Investigations Acute 95% Chronic 5%
CBC – BM aspirate & biopsy (hypocellular) According to percentage of abnormal cells
>20% blast cells 5% blast cells
In absence of G6PD: Lymphoblastic 75%
Hb << met-Hb No chronic lymphoblastic in
Acquired 2-5 years
Congenital Good prognosis
children
C/P Causes Idiopathic
Fanconi Myeloid 20% Myeloid rare
Anemia + 3 colors (Pallor – Jaundice – Red urine) 2ry >5 years Philadelphia chromosome
+ NO organomegaly Exposure to toxins Poor prognosis (t9:12)
Inheritance Autosomal recessive
Infection
Complication C/P
Acute HF Age Around 5 years Any age Infiltration of BM and other organs with blast cells
Microcephaly BM Anemia – Infection – Bleeding
Precipitating factors Microphthalmia RES Hepatosplenomegaly – Lymphadenopathy
Spontaneous onset Other Testicular – CNS infiltration
Infection – Drugs – Fava bean Absent thumb
Pallor
C/P Absent radius
Investigation Short stature
Purpura Investigation
Recurrent infection CBC: Pancytopenia
Renal malformation
Prove Anemia + Prove Hemolysis + Heinz body Pigmented skin BM examination
Lumbar puncture: Infection
Treatment Investigations + Investigations +
Chest Xray: Mediastina mass (t cell disease)
Investig Chromosomal break
Urgent packed RBC transfusion – Prevent subsequent attack
ations Skeletal survey Normal
Prognosis
Abd US chromosomal break
Age – Subtype – respond to chemotherapy –
Supportive WBC > 50000 (poor prognosis)
Mild
TTT
Supportive
(imunosupression) Treatment
BM transplantation
Severe (BM Supportive: PLTs – blood transfusion – hydration – infection
transplantation) Chemotherapy
 Purpura Hemophilia
Minute bleeding due to PLTs or vascular defect Hemophilia A (classic)
Platelets X –linked factor VIII
Life span: 7-10 days
Function (on capillaries): Seal point of bleeding – Initiate coagulation – Clot retraction C/P
Bleeding in neonatal period
ITP Extensive hematoma with minor trauma
Bleeding from orifices
Autoantibody against PLTs Acquired generalized He History of viral infection 2 ago ICH
Hemarthrosis with trauma or spontaneous (severe)
C/P: Bleeding + Anemia
Skin: Flat purple not itchy (Petechiae, Purpura, Ecchymosis)
Complication
Mucous membrane: Gum – Epistaxis – Hematuria ICH
Organ: ICH Psoas Hge (loos sheath can collect 1l of blood)
Ankylosis
Investigation
CBC: PLT < 20000 – Hb – Normal WBC
Investigation
BM: Normal number of megakaryocyte but with defective budding Phase 1 defect prolonged APTT factor VIII
Antibodies: Anti-PLTs antibody
Treatment
Treatment Cold compress
Mild: Observe – Avoid (Trauma – Aspirin – NSAIDs) Replacement (Cryoprecipitate – Purified plasma derived factor VIII conc. – Recomb. f. VIII)
Moderate: IVIG 1g/kg/d for 2d (Very expensive – Blood borne infection) Desmopressin ( Release of factor VIII)
Prednisolone 2mg/kg/d for 2w Physiotherapy
Sever: PLTs transfusion + IVIG + IV Methyl Prednisolone 2mg/kg/d Hemophilia B VW disease
Plasma phoresies – Emergency Splenectomy X-linked Autosomal dominant
VW Ptn
Factor IX PLTs adhesion
Factor VIII activity
Coagulation scheme Delayed onset
Phase1 (intrinsic) Mild bleeding
* 4 Factors: VIII IX XI XII * APTT
DIC
Phase2 (extrinsic)
Hge and thrombosis with end organ damage
* 1 Factor: VII *PT

Phase3 (common) Investigation: Prolonged PT – APTT Fibrinogen FDPS

*4 Factors: I II V X *APTT – PT – fibrinogen
Treatment: Cause – Bleeding replacement therapy
 Juvenil Idiopathic Arthritis (JIA) Systemic Lupus (JSLE)
Multi factorial. Multi systems.
Multi factorial. Clinical diagnosis.
Female predominance.
Criteria: < 16 years.  1 joint.  6 weeks.
More CNC & Renal affection than adult.
Systemic type Oligo articular Poly articular Enthesitis related
• Constitutional: FAHM
 1 joint 1-4 large joints  5 small & large joints Arthritis +
• Mucocutaneous: Malar rash – Photosensitivity –
Preceded by fever (knee) tenderness at
Discoid – Painless oral & nasal ulcer – Alopecia
2weeks daily and spiky Symmetrical insertion of tendon –
• Musculoskeletal: Non erosive arthritis– Myalgia
+  1 of: Asymmetrical ligament – capsule –
Systems:
• Maculopapular rash Female > Male fascia +  2 of:
• CNS: Psychosis – Depression – ICH – Seizures
non fixed non 50% of JIA cases • Sacroiliac joint
• Cardio: Pan carditis – Arrythmia
C/P pruritic salmon pink 2-4 & 10-14 years tenderness or
• Pulmonary: Pneumonitis – Vasculitis – HTN
related to fever Male : Female 3:1 lumbosacral pain
• GIT: Peritonitis – Pancreatitis – Hepatitis
• HSM Cervical spine – TMJ – • HLA B27 antigen
• Renal: Nephritis – Cellular cast – Ptnuria
• LN enlargement 2 - 4 years inter-phalangeal • Male > 6 years
• Heme: Pancytopenia
• Serositis • Acute ant. Uveitis
• Endocrine: Hypothyroid – DM – Delay Puberty
Complication: • Ankylosing
• Serositis: Pleuritis – Pericarditis
MAS: Macrophage spondylitis
• Antiphospholipid antibody $: Thrombosis
activation $
Type 1 Type 2
Anemia –
Investigat Young Boys RF +Ve RF -Ve CBC – ESR – CRP – KFT – LFT – Urinalysis –
Leukocytosis –
girls Ankylosing Aggressive Benign Albumin
ion Thrombocytosis
Uveitis spondylitis Deformities Uveitis ANA – Anticardiolipin Ab – Lupus anticoagulant
ESR - CRP
+Ve HLA B27 C3 & C4
ANA antigen

Diagnosis Clinical diagnosis 4 Criteria (at least 1 clinical & 1 laboratory)

• Clinical: 4 Mucocutaneus (Acute – Chronic –
TTT Ulcer – Alopecia) – Arthritis – Serositis –
Remission NSAID
3 Heme (Hemolytic anemia – Leukopenia –
Steroids: Topical (uveitis) – Intra articular (oligo) – Systemic (systemic)
Damage Thrombocytopenia) – CNC – Renal
Methotrexate: 1st line in poly articular
(Deformities) • Lab: ANA – ADNA – Antiphospholipid Ab –
Anti TNF: 2nd line in poly articular
Anti smith Ab – C3 & C4 – Coombs test
Normal Anti IL1 & IL 6: 2nd line in systemic following steroid
growth
TTT as JIA + hydroxychloroquine
 Vasculitis
HSP Kawasaki (Mucocutaneous LN $)
The Most Common vasculitis in childhood. Clinical diagnosis. The leading cause of acquired heart disease in developed countries.
Autoimmune against capillaries (Small vessels) by circulating IgA Affect Medium vessels (Coronaries)
3 - 15 years Male : Female 1.5 : 1 Boys < 5 years

Post infection (B hemolytic strept. – Viral – Mycoplasma)

Etiology Post vaccine Unknown etiology
Allergy Acute febrile phase: fever 1-2 weeks
or Deposition of IgA Subacute: Desquamation – Thrombocytosis – Coronary artery aneurysm 3weeks
Course Disorder of coagulation and activation (rapid decline in F. XIII) Convalescent: 6 - 8 weeks
Drug induce (methotrexate – anti. TNF

Fever > 38C persistent at least 5 days –Non-remitting

Schoenlein: At least 4 of 5:
Elevated purpura (not in face) – SC edema • Erythema or Edema of hand and foot or peeling of fingers and toes
Arthritis: 2\3 of cases: Self-limited – Oligo articular • Polymorphous Skin Rash
C/P Henoch: • Conjunctival Injection without exudate
GIT: 1\2 of cases: Pain – Vomiting – Diarrhea • Strawberry Tongue or erythema of lips and oral cavity
Urinary: 1\3 of cases: Nephritis – HTN – Ptnuria • Unilateral Cervical Lymphadenopathy
CNS: ICH – Headache • Other:
Coronary A. aneurysm – Hepatic affection – CNS irritability – Arthritis
CBC: normal platelets count
ESR – CRP Leukocytosis
Investig Urine and Stool analysis ESR – CRP
ation Urea – creatinine – C3 Sterile pyuria
IgA level Serum Transaminase – Plasma lipid
Abd. Xray – US – MRI - MRA
Aspirin
Anti-inflammatory: 80-100 mg| kg | 6 hs. In febrile phase
Supportive: Hydration – Electrolyte balance Antithrombotic: 3-5 mg | kg | day
Pain: Analgesics • Coronary A. abnormalities: Antithrombotic dose as long as it persists
TTT Control HTN • No coronary A. abnormalities: low dose Aspirin for 2 years
Prednisone: Sever GIT disease – Hge – Nephritis • Large coronary A. aneurysm: Anti-coagulant as Warfarin
IVIG 400mg | kg | day for 4 days
Corticosteroids in case not responsive or relapsing after 2 doses of IVIG