MBBS Y2 Pathology Tutorials

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MEDI2011!!
Pathology!!
Tutorials!!
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GUIDE TO EXAMINATION OF SPECIMENS DEMONSTRATING COMMON PATHOLOGICAL CONDITIONS
1. WHAT AM I LOOKING AT?

Note any given information including age, sex and clinical history
Identify any normal structure and the aspect it presents, e.g. the specimen may be
a spleen
part of a lung sectioned vertically
portion of a heart, sectioned to show left ventricle and left atrium
2. LOOK FOR NORMAL TISSUE AND ADJACENT ABNORMAL TISSUE
When mounting autopsy specimens an attempt is made to show normal adjacent tissue. This may not be
possible with specimens excised surgically.
3. DESCRIBE THE ABNORMALITIES IN TERMS OF FORM, TEXTURE AND COLOUR

Form
size
shape
number (single, multiple)
symmetry or asymmetry
Texture
smooth, rough
fine, coarse, spongy
glossy, dull
opaque, translucent, transparent
Colour - colour of specimens may be modified by fixation
form of each area of colour including margins and central parts
light, dark
homogeneous or patchy
showing patterns or resemblance to familiar things
4. LOOK AT ALL PARTS OF THE SPECIMEN

Front, back, sides, top and bottom
Anatomical structures, for example
Heart – inspect:
pericardium
myocardium
endocardium
each chamber
each valve
coronary arteries
Lung – inspect:
pleura and pleural surface of lung
cut surface of lung
air passages from hilum to periphery
blood vessels from hilum to periphery
hilar lymph nodes
Integrated Pathology Learning Centre 8.03.2013
GUIDE TO EXAMINATION OF SPECIMENS DEMONSTRATING COMMON PATHOLOGICAL CONDITIONS
5. MAKE A DIAGNOSIS
Specify:
the anatomical part/parts affected
the possible pathological process/processes involved
the possible primary cause/causes
the physiological or biochemical changes that may have occurred e.g. endocrine tumours may/may
not be hormonally active
IN ALL CASES CONSIDER THE FOLLOWING POINTS:

If multiple lesions are present try to relate them causally.
When a major lesion is identified, look for evidence of its causes as well as evidence of its possible
complications.
Try to assess the stage in the evolution of the pathological process/processes shown by the
specimen.
Multiple lesions in a specimen may be unrelated causally.
Integrated Pathology Learning Centre 8.03.2013

Pathology of lymphoma 2013
Page 1
MBBS2 Tutorial – Pathology of Lymphoma
Learning objectives:
Understand lymphoma, common types

Pathology of spleen and thymus
Lymphoid neoplasms
General points:
1. Gene mutations – either loss or gain in function
2. Oncoproteins – block normal maturation
3. Protooncogenes – often activated in lymphoid cells during antigen stimulation of germinal centres
leading to tumours of germinal center cell origin
4. Inherited factors – Downs Syndrome has increased risk of developing leukaemia
5. Viruses – HTLV1, EBV and KSV are associated with specific types of lymphoma
6. Chronic immune system stimulation – H pylori and MALT lymphoma
7. Iatrogenic – radiation treatment
8. Social factors – smokers have increased risk of AML
Definitions : Leukaemia
Lymphoma
Histology review – lymph node (histology and function)
Normal lymph node

architecture.
Leukaemia – To be discussed in next tutorial
WHO classification of lymphoma
Hogkins
lymphoma
Lymphoma
B cell ) further classified

NHL ) on degree of
T cell ) differentiation
Origin of lymphoid malignancy - B cell neoplasms – bone marrow and lymph nodes
- T cell noeplasma – thymus and lymph nodes
Page 2
Reproduced from Robbins

& Cotran Pathologic
Basis of Disease 7th Ed.
2005
Diagnosis of lymphoma requires histology.

Reactive lymphadenopathy leads to a polyclonal lymphoid proliferation whereas lymphomas lead to a
monoclonal lymphoid proliferation. Antigen receptor gene analysis uses this to differentiate reactive from
malignant condition.
80-85% of lymphomas are of B cell origin
Immunohistochemistry – B and T cell markers
Lymph node stained with B

cell marker (left) and T cell
marker (right)
B cells are in the germinal
centres while T cells are in the
peri follicular mantle zone.
Flow cytometry
Two broad groups – Hodgkins and NHL (clinically important as treatment different)
- highlight differences esp spread and staging
NHL
Discuss common types
Page 3
Hodgkins lymphoma
Types
B symptoms
Importance of staging
Spleen
Histology
Splenomegaly
Infarcts
Rupture
Neoplasia
Thymus
Histology
Neonatal thymus showing the

cortex and medulla.
Hyperplasia
Thymoma
Page 4
PATHOLOGY OF LYMPHOMA
Demonstration pots
Royal Brisbane Clinical School
Abdominal swelling from M/61 yrs

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Abdominal mass F/55 yrs

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Page 5
Abdominal mass M/46yrs

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46 yrs F Spleen
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49 yrs/M with chronic valvular heart disease. Spleen

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Page 6
Incidental finding in the intestine M/44yrs

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Mediastinal organ (Normal) from baby 6 weeks old

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Demonstration Pots
PA/Mater Clinical School
Small intestine & Mesentery mass

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Mediastinal mass
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Splenomegaly
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Page 8
46 yrs/M with Abdominal pain & shoulder pain 6 days

following a road traffic accident
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Patient with cirrhosis. Removed spleen

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33 yrs/M with Splenomegaly (Storage disease)

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Demonstration Pots
Ipswich Clinical School
Small intestine & Mesentery mass

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Lesion in the spleen.

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69 yrs/F axillary swelling.

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Page 10
Normal spleen from an adult woman.

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Splenomegaly
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M/75 yrs, Mediastinal mass.

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Pathology of bone marrow/metabolic disease 2013
Page 1
MBBS2 Tutorial Outline – Pathology of Bone Marrow and Metabolic Bone Disease
Learning Objectives:
Bone marrow diseases
Bone and calcium metabolism and related diseases
Types of Marrow: Yellow (inactive)

Red (active)
Ways to examine bone marrow – aspirate, trephine
Normal bone marrow trephine

biopsy.
Constituents of bone marrow : RBC, WBC, PLT and CT (collagen, fibrous tissue)
What can happen in to marrow : aplasia

Hyperplasia
SOL - primary, metastatic
Aplastic Anaemia
Aetiology– idiopathic, drugs, chemicals, irradiation and viruses

Page 2
Bone Marrow: aplastic

anemia
Hyperplastic marrow
B12 and iron deficiency.
Space occupying lesions:

Leukaemia
types – acute and chronic
acute – ALL, AML
chronic – CLL, CML
Myeloproliferative disorders
Normal control mechanisms for governing the cell lines involved are no longer active, mutated
tyrosine kinases lead to growth factor independent proliferation. This does not impair
differentiation and causes clonal proliferation of one or more haemopoietic cell lineages.
Common features of myeloproliferative disorders:

1. Increased proliferative drive in bone marrow
2. Extramedullary haematopoiesis
3. Variable transformation to myelofibrosis
4. Variable transformation to acute leukaemia
Specific examples:
PRV – RBC overproduction
Essential thrombocytosis - increased megakaryocytes
Primary myelofibrosis – overproduction of collagen or fibrous tissue
CML – overproduction of granulocytes, Philadelphia chromosome
Leukemia
Page 3
Myelodysplastic disorders
Group of disorders characterized by clonal stem cell abnormality, leading to maturation defects
associated with ineffective haematopoiesis. This results in morphological abnormalities in blood
cells and an increased risk of transformation to acute myelogenous leukaemia.
Hallmark is cellular bone marrow with clonal progeny of mutant stem cell, which has the ability
to differentiate into RBC, WBC and platelets but in an ineffective and disordered fashion
(cytopenias in peripheral blood). Usually occurs in elderly and main complications are anaemia
and infection.
Multiple myeloma
Most common plama cell neoplasm.

Disease of elderly 65 – 70 years old.
Secrete monoclonal immunoglobulin.
BJ proteins in urine
Multifocal destructive bone lesions esp. axial skeleton.
X-ray – osteolytic lesions
Complications – hypercalcaemia (TNF increases osteoclastic activity), amyloidosis, pathological
fracture, infection, plasma cell leukaemia, myeloma kidney
(Left)Spine from a man aged 62

with multiple myeloma. Bone
marrow aspirate (Right) showed
marrow replacement by plasma
cells
Page 4
Skull from a woman

aged 62
Metabolic bone diseases
Affects entire skeleton.
Main conditions hyperparathyroidism, rickets, osteomalacia and osteoporosis.
Hyperparathyroidism - primary, secondary and tertiary

- skeletal changes
- osteitis fibrosa cystica
Vit D
Maintains plasma Ca and Phosphorus levels.
Decrease - Ricketts (children)
- osteomalacia (adults)
Source of Vit D
Pathogenesis
Osteoporosis
Increased porosity of the skeleton, due to decrease in bone mass.
Primary - senile, post-menopausal, idiopathic

Secondary - endocrine – hyperPTH
- neoplasia – multiple myeloma
- malnutrition
- drugs – steroids
Page 5
Renal osteodystrophy
Term used to describe all skeletal changes of chronic renal failure.
phosphate
retention
⁭ calcium
CRF ⁭ PTH (secondary
Hyperparathyroidism)
↓active vitamin D ↓calcium

Page 6
PATHOLOGY OF BONE MARROW/METABOLIC BONE DISEASE

Demonstration Pots
Dissection of the neck (patient died of chronic renal

failure)
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Parathyroid mass
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Femur from a patient with parathyroid adenoma.

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Page 7
Lesion in the spine

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58 yrs /M with anaemia and raised

platelet count for 6 years before death.
The spleen was very large, and
histologically showed extensive
extramedullary haemopoiesis and
numerous megakaryocytes.
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Rib lesion 41yrs/F with a parathyroid adenoma. Serum

calcium late in her illness was 3.87 mmol/l.
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Page 8
Spine 47yrs/M
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Spleen from 77 yrs/M. It weighed 850g. The

results of haematological investigations performed
just before death were as follows: blood
haemoglobin concentration, 4g/dl; white cell
9
count, 20x10 /l of which 70% were myeloblasts;
9
platelet count, 5x10 /l.
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Page 9

Demonstration Pots
femoral marrow in a woman with iron deficiency

anaemia.
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Bones from a 58 yrs/M. The patient

suffered from anaemia for 6 years before
death. Blood platelet counts ranged up to
1,000 x 109/l, and large megakaryocyte
fragments were present in the
circulation. The spleen was very large,
and contained numerous myeloid and
erythroid precursors and
megakaryocytes.
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Page 10
Skull 49 yrs/M
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Spine 62 yrs/F 15 month history of bone pain.

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Femur:
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Page 11
Spleen 6 Kgs:
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Spine 47 yrs/M
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Page 12

Demonstration Pots
Skull:
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Spleen:
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X316E.
X316E. Spleen:
Spleen: chronic
chronic
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myelocytic
myelocytic leukaemia
leukaemia
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Spine 70 yrs/F
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Page 13
Parathyroid removed from patient

with chronic renal failure
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Femur 67yrs/F died due to intracerebral

haemorrhage.
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Femur 49yrs/M
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Pathology of skin tumours 2013
Page 1
MBBS2 PATHOLOGY TUTORIAL

PATHOLOGY OF SKIN TUMOURS
Learning objectives:
Tumours of melanocyte, tumours of keratinocytes

Major macroscopic and microscopic features of skin neoplasia
Understand the role of skin biopsy
Tumours of skin divided into two groups, tumours from melanocytes and tumours from
keratinocytes
General
Skin pathology encompasses a wide variety of pathological conditions.

Other important factors when assessing skin lesions:
Two major layers of skin : epidermis and dermis – derived from different embryonic
components therefore morphologically different.
Epidermis is stratified, cellular , avascular, lacks nerves and sits on a basement
membrane. Adnexae eg. Hair follicles extend from epidermis into the dermis.
Histology of Skin
Epidermis – 5 layers, sweat glands, hair follicles, sebaceous glands
Dermis is divided into papillary and reticular dermis.
Subcutaneous fat.
Microscopic definitions:
Hyperkeratosis
Parakeratosis
Hypergranulosis
Acanthosis
Acantholysis
Spongiosis
Exocytosis
Page 2
The clinical sign is related to the underlying pathology.

Eg. Scaling – hyperkeratosis, parakeratosis
Blister – spongiosis
Pigmented skin lesions
Melanocytes
– migrate from neural crest to dermo-epidermal junction
Lesions without proliferation of melanocytes – freckles, melasma
Lesions with proliferation of melanocytes – Lentigo, Melanocytic naevi, Dysplastic naevi
Intradermal naevus.
Dysplastic naevi.
Malignant melanoma
Pathogenesis
Clinocopathological features
Clinical changes
Tumour progression
Main 4 types
Histopathology – Breslow thickness, Clarke’s levels, completeness of excision
Clinical course – metastases, sentinel node biopsy
Page 3
Epithelial Tumours
Skin tag (fibroepithelial polyp)
Seborrhoeic keratosis
Keratoacanthoma
Solar keratosis – pathogenesis
Intraepidermal carcinoma
BCC
SCC
Solar keratosis. A solar keratosis

excised from the face.
Carcinoma in situ.
BCC
Page 4
SCC.
BCC
Page 5
Melanoma
*The following conditions will be discussed if there is time*
Inflammatory Dermatoses
Acute and Chronic
Acute – lasts days to weeks, characterized by inflammation, oedema and epidermal,

vascular or subcutaneous injury. Examples: urticaria, acute eczematous dermatitis,
erythema multiforme,
Chronic – last months to years, often show altered epidermal growth eg hyperplasia.
Examples: psoriasis, seborrhoeic dermatitis, lichen planus.
Bullous disorders:
Blistering dermatoses are characterized by fluid filled spaces with the skin. The level at
which the vesicle or bullous occur is important for histological diagnosis.
Examples:
Subcorneal: impetigo
Page 6
Reproduced from Robbins &

Cotran Pathologic Basis of
Disease 7th Ed. 2005
Suprabasal: pemphigus vulgaris

Subepidermal: bullous pemphigoid

Clinically the more superficial the vesicle or bullous the more likely it is to rupture and
hence the lesions will be “weepy”.
Page 7

Demonstration Pots
spine 42yrs/M.
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92yrs/F Skin fore-arm

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Page 8
42 yrs/M scaly lesions face

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66 yrs/M
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51 yrs /M
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Page 9

Demonstration Pots
76 yrs/F: Pigmented lesion from back with

itchiness
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54 yrs/F pigmented lesion leg

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Page 10
Amputated toe
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Amputated hand
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68 yrs/M lesion from the site of a chronic

varicose ulcer, which has been present on
the leg for 15 years.
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Page 11

Demonstration Pots
Amputated specimen hand

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Spine 29 yrs /M
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Ulcerated haemangioma of the foot in

a man aged 64. Operative surgical
specimen.
Page 12
Amputated hand
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Multiple pigmented coin like lesions with “stuck

on” appearance
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57/F lower leg.

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Page 13
Skin eyelids. Tumour invading

eylids and orbit.
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Cardiovascular I: Ischemic and hypertensive heart disease 2013
Page 1
MBBS2 Tutorial – Cardiovascular I Tutorial
Ischemic and Hypertensive Heart Disease
Learning objectives
Pathogenesis of ischemia
Morphological changes and complications of infarction
Pathogenesis and complications of hypertensive heart disease
Anatomy and blood supply of the heart
Definition of Ischemia – imbalance between supply (perfusion) and demand for oxygenated
blood.
This may come about by impaired blood supply (90% of cases of ischemia are due to
atherosclerotic coronary arterial obstruction) or the myocardium becomes hypertrophic
resulting in a greater demand on the blood supply.
The myocardium may hypertrophy as an adaptive response eg. in systemic hypertension or
idiopathic e.g. cardiomyopathy.
Myocardium is very active and 30% of the muscle fibres are made up of mitochondria
therefore aerobic metabolism is essential.
Compensatory mechanisms;
1. Autoregulatory mechanism controls blood flow through the coronary vascular bed.
When obstruction occurs in a major coronary vessel, the peripheral resistance distal
to the obstruction is reduced so that blood flow is maintained.
2. If obstruction occurs over a period of time collateral circulation develops.
In order for ischemia to develop at least 75% of the lumen must be obstructed.
Pathogenesis of atherosclerosis
Page 2
(Reproduced from Robbins & Cotran Pathologic Basis of Disease 7th Ed. 2005)
Sequential progression of lesion in coronary artery causing the four clinical manifestations
of IHD
Clinical manisfestation of IHD, four syndromes:
1. Angina pectoris
2. Myocardial infarction – types (transmural, subendocardial)
- role of plaque change
- light microscope changes
4 – 12 hours
1 – 3 days
Page 3
4 – 9 days: Macrophages being phagocytosis, development of granulation tissue.
10 days onwards:
Weeks to months
- consequences and complications

3. Chronic ischaemic heart disease
4. Sudden cardiac death.
Hypertensive Heart Disease

Definition and pathogenesis (adaptive response to pressure overload)
Criteria for diagnosis
Specimen from 62 yrs/M
Morphology of hypertensive heart disease

Complications
Page 4
CVI – PATHOLOGY OF ISCHAEMIC HEART DISEASE & HYPERTENSION

Demonstration Pots
Heart of a 20 year old woman

who was killed in a motor
vehicle accident.
A 60 year old woman experienced the

sudden onset of severe pain in the chest
and left arm.
Sudden onset of severe chest pain

since two weeks in a hypertensive
woman aged 42.
Chest pain in a man aged 58 with a history of

hypertension and of having smoked 20 cigarettes a day.
Page 5
A 58 year old man

with severe chest pain
and dyspnea.
60 yrs male with old

H/O IHD
Man aged 72 with a past history

of MI underwent CABG
(coronary artery bypass graft)
and died after 3 weeks
Page 6
Patient with acute myocardial

infarction (AMI) developing
pansystolic murmur 4 days later
1
2

Page 7

Demonstration Pots
70 year old man with h/o severe

breathlessness.
Autopsy specimen 5
days after chest pain.
Patient with acute myocardial infarction

(AMI) developed pansystolic murmur 5
days later.
1
2

Page 8
Autopsy specimen from a 68 year

old hypertensive and diabetic man.
A 65 year old man with a

long H/O hypertension.
A 67 year old man with prolonged

H/O hypertension and severe
dyspnea.
Page 9

Demonstration Pots
A patient who died 5 days after onset of

severe chest pain.
A 70 year old man with H/O

IHD, hypertension and dyspnea
An autopsy specimen of a patient

following trauma to the anterior chest
wall.
Page 10
A 55 year old man with H/O severe

hypertension.
A 78 year old man with chest pain.
Woman aged 77 was found to have

blood stained fluid in the pericardial
cavity at autopsy.
Cardiovascular II: Congestive cardiac failure, pulmonary hypertension, cor pulmonale, pericardial disease, and tumours 2013
Page No. 1
MBBS2 Tutorial – Cardiovascular System II

Congestive cardiac failure, pulmonary hypertension, cor pulmonale, pericardial disease,
and tumours.
To understand the pathogenesis of congestive cardiac failure and cor pulmonale.

Know and understand other cardiac disorders including cardiomyopathy, myocarditis,
pericardial disease and tumours.
CCF
Occurs when CO does not equal demand. Common endpoint for many myocardial,
valvular, congenital and some extracardiac diseases and results in hypertrophy/dilatation.
You need to consider why the heart has failed:

1. failure of pump - MI
2. obstruction to flow – AS
3. regurgitant flow – AR
4. disorders of conduction – arrhythmia
5. disruption of circulatory system – gunshot wound, # femur – blood loss
Compensation:
1. Frank-Starling : increased preload dilation leads to increased contraction
2. hypertrophy
3. increased heart rate via neurotransmitters eg adrenaline
When exceeded = CCF
Page No. 2
X1194N. 76 year old man with polyostotic Paget's

disease of bone. Blood pressure normal. No evidence
of ischaemic heart disease.
Clinicopathological features – left sided heart failure - pathogenesis and relevant

morphological changes
1. dyspnoea and lung pathology

2. kidney – fluid retention, renin angiotensin aldosterone system
3. brain – hypoxia in severe failure
(right sided heart failure considered under cor pulmonale)
Pulmonary hypertension
Pulmonary circulation – low resistance, one eighth systemic pressure

Pulmonary hypertension = when pulmonary pressure reaches one quarter
May be Primary – cause unknown

Secondary – most frequent
- increased blood flow or pressure – mitral stenosis
- increased pulm vascular resistance – emboli
- left heart resistance to blood flow – systemic sclerosis
Cor pulmonale
RV hypertrophy and/or dilatation due to pulmonary hypertension (due to lung or

pulmonary vasculature disease)
Definition excludes dilatation caused by congenital heart disease or by diseases of left
side of heart.
May be acute or chronic.

Depends on suddenness : acute – massive pulm embolus (dilatation)
chronic – due to prolonged pressure overload
Morphology differs, in chronic have hypertrophy, acute only dilation.
Page No. 3
Predisposing disorders :
1. lung parenchyma – cystic fibrosis, diffuse interstitial pulm fibrosis
2. pulmonary vasculature – extensive thromboembolism
3. disorders affecting chest wall movement – kyphoscoliosis
4. pulmonary arterial constriction – hypoxia, metabolic acidosis
Clinicopathological features – right sided heart failure - pathogenesis and relevant

morphological changes
1. hepatomegaly – passive congestion
2. splenomegaly – elevated pressure in portal vein
3. peripheral oedema
4. pleural effusions
Myocardial disease
Cardiomyopathy
Brief description of types, include pathogenesis and morphology.
Use of endomyocardial biopsies.
Myocarditis
Definition
Major causes – elaborate on common ones
lymphocytic infiltration hypersensitivity myocarditis,

inflammatory infiltrate mainly eosinophils
giant cell myocarditis
Page No. 4
Pericardial disease
Pericardial effusion and haemopericardium

Pericarditis – acute vs chronic
- causes
- morphology
Cardiac tumours
Primary and Metastatic

Most common primary tumours are benign. Important ones include-
- Myxoma
- Rhabdomyoma
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Effects of non-cardiac neoplasms on the CVS eg SVC syndrome
Page No. 5
CVII – CONGESTIVE CARDIAC FAILURE, PULMONARY HYPERTENSION,

COR PULMONALE, PERICARDIAL DISEASE AND TUMOURS
Demonstration Pots
Man aged 59 years.
Female aged 17 years. The patient

collapsed at a disco, and died 2 hours
later.
This patient presented with signs of

heart failure 6 months before death.
Page No. 6
X265B.
Woman aged 72 with long-standing heart

failure. Death was due to coincidental
perforation of a chronic duodenal ulcer.
Man aged 64. He had smoked 60 cigarettes a day

for 40 years, but had given them up in the terminal
stages of his illness. At the time of his final
admission to hospital, the pH of his arterial blood
was 7.16.
Page No. 7
Previously healthy man aged 33 who died

suddenly. The heart weighed 550 g
Page No. 8

COR PULMONALE, PERICARDIAL DISEASE, AND TUMOURS
Demonstration Pots
Patient had a history of chronic renal

failure.
76 year old man with polyostotic Paget's

disease of bone. Blood pressure normal.
No evidence of ischaemic heart disease.
Page No. 9
Patient had a history of atrial fibrillation.
What might be the clinical effects of this

lesion?
Young woman. She died soon

after admission to hospital in a
profoundly shocked state.
Page No. 10
What am I? Clinical features of

congestive cardiac failure may be
found in this condition.
Page No. 11

COR PULMONALE, PERICARDIAL DISEASE, AND TUMOURS
Demonstration Pots
The myocardial discoloration is an

artefact.
An incidental finding in a
woman aged 40 killed in a
motor vehicle accident.
Page No. 12
Man aged 53. Smoker.
Woman aged 61 with chronic renal

failure and long-standing
hypertension. Two days before
death her blood urea was 206mg.%.
60 year old female patient

2013 - CVSIII – Thrombosis & Embolism; Pathology of arteries & veins
Page 1
MBBS2 Tutorial – Cardiovascular III
Thrombosis and Embolism; Pathology of arteries and veins
Know and understand predisposing factors to thrombosis and embolism
Outcome and complications of thrombi and emboli
Pathology of aneurysms
Classification of vasculitis
Template
Anatomy of blood vessels
Artery thicker than vein as need to withstand a higher pressure.

As arteries become narrower the wall thickness diminishes.
Wall – endothelial cells

- smooth muscle
- extracellular matrix – collagen, elastin etc..
3 concentric layers - intima, media, adventitia
Intima – endothelial cells, minimal subendothelial CT
- internal elastic lamina separates it from the media
Media – smooth muscle
- vasa vasorum (vessels of vessels)
- external elastic lamina separates it from the adventitial
Adventitia – CT, nerves, vasa vasorum
Main Pathology of vessels:
Thrombosis
Embolism
Arteriosclerosis
Anuerysm
Vasculitis
Thrombosis
Definition of thrombus
Pathogenesis of thrombi – Virchow triad
Page 2
Morphology of thrombi
Arterial (white) thrombus (arrow)

comprising mainly platelets and
fibrin.
Outcome and complications of thrombi
(Left). Occlusive venous thrombus. Note

coralline thrombus with alternating
layers of platelets and fibrin (arrowhead)
and consecutive clot (arrow) that forms
after vessel occlusion.
(Right). Organizing thrombus. Note
ingrowth of vessels and fibroblasts (blue
arrows) into lumenal thrombus (black
arrows). Some collagen deposition has
occurred.
Page 3
Organized thrombus (arrows) in

femoral vein. Note how the
fibrous bands interfere with the
functional integrity of valves,
thus producing deep venous
insufficiency.
Embolus
Definition of embolus
Types of emboli
X3015C. Brain in fatal fat

embolism syndrome.
(Left). Symetrically round, (empty)

pulmonary vessels (arrows) in fat
embolism.
(Right). Oil Red O stain on frozen
lung tissue demonstrating fat
(arrows) in pulmonary vessels.
1
2

Page 4
Massive pulmonary
embolism.
Outcomes and complications
Ateriosclerosis:
Arterial wall thickening and loss of elasticity (literally means hardening of arteries.
3 patterns
1. Atherosclerosis
2. Monckeberg medial calcific sclerosis
3. Arteriolosclerosis (assoc primarily with hypertension)
Pathogenesis of Atherosclerosis
Risk factors
Lipid streaks (arrows) in the

aorta of a male aged 21 years.
These are the earliest
manifestation of
atherosclerosis.
Page 5
Lipid (fatty) streak. Note

subendothelial collection of
'foam' cells (F). The cells appear
to be empty because the lipid has
been dissolved out in the
processing of the tissue.
(Left) Aorta: atheroma. Fibro-fatty

plaques (arrows).The next stage in
the development of atherosclerosis.
(Right) Fibrofatty plaque. Note
fibrous cap (black arrow) and
underlying lipid in form of
cholesterol crystals (blue arrows).
(Left). Close-up of fibrofatty plaque.

Page 6
Male aged 74 Complicated atheroma

of aorta
(Left) Atheromatous aorta with thrombosis.

Man aged 64.
(Right) Atheroma of the arch of the aorta and
branches with thrombosis of the right internal
carotid artery in a man aged 69. Autopsy
disclosed old and recent infarction of the right
cerebral hemisphere. This is one cause of
cerebral infarction (stroke)
Marked atheromatous stenosis of

orifice of right renal artery (blue
arrow) with advanced ischaemic
atrophy of right kidney. B.P. 180/105.
Blood urea 8.6 mmol/l. Male aged 84.
Renal artery stenosis is one cause of
hypertension.
Complications of atherosclerosis
Monckeberg medial calcific sclerosis
Arterioslcerosis
Role of hypertension – benign vs malignant
Anuerysms
Definition
True vs false
Page 7
(Left) Complicated atheroma with aneurysm of

the lower abdominal aorta. Woman aged 81 with
chronic renal failure and hypertension. Note
thrombus (blue arrow) within aneurysm (red
arrow).
(Right) Atheromatous aneurysm of the abdominal
aorta with thrombosis. Note lines of Zahn on its
surface (arrows)
Sudden rupture of an abdominal aneurysm causes
death, but the rupture may occur slowly as a
continuous leak that presents as abdominal pain.
Abdominal aneurysms can be repaired surgically
and this is a common operative procedure.
(Left) Aortic dissection in a hypertensive male of

71. A large amount of blood clot was found in the
pericardial sac at autopsy. Note the myocardial
hypertrophy and the aortic intimal tear (arrow).
(Right) Aortic dissection: note compression of
lumen of innominate artery (arrow), best seen from
the top of the pot. Hypertensive left ventricular
hypertrophy.
Outcomes of aneurysm
Vasculitis
Classification according to size of vessel.
(Left) Polyarteritis nodosa. Male aged 12 years.

Note the beaded appearance (arrows) of the
coronary arteries. The inflamed wall bulges
forming an aneurysm seen as nodules
(Right) Polyarteritis nodosa. There is segmental
necrosis (arrow) of the walls of small and medium
sized muscular arteries and perivascular
inflammation.
Page 8
CARDIOVASCULAR III
Demonstration pots
A man aged 93 with gangrene of

the left hallux and ulceration of the
left lower leg.
A 70 year old man had severe

abdominal pain and was in
shock on arrival to
emergency.
A man aged 86 with dementia,

cardiac failure and lower limb
venous thrombosis.
1
2

Page 9
A man aged 62 treated successfully

with penicillin for acute bacterial
endocarditis of the aortic valve 5
months before death.
A 60 year old man with

syphilis was in hypovolemic
shock during admission.
Aorta of a 69 year old

hypertensive & diabetic
man.
Page 10
Aorta of a 75 year old woman

who died of acute myocardial
infarction.
A man with long standing diabetes

mellitus complained of pain in lower
limbs.
1
2

Page 11
CARDIOVASCULAR III
Demonstration Pots
Patient had metastatic carcinoma

with pancreatic deposits.
The patient suffered from

ulceration of the legs and had large
collateral veins of abdominal wall.
Patient with high cholesterol

levels died of acute myocardial
infarction.
Page 12
A 68 year chronic smoker with

signs & symptoms of systemic
thromboembolism.
A 78 year old hypertensive man

presented with abdominal pain
& shock.
A 72 year old man

presented with feeble pulses
and BP of 70/40.
A woman aged 66 who died 10 days after

developing a myocardial infarct.
Page 13
A man aged 56 had

myocardial infarction, heart
failure and left atrial
thrombosis.
A 65 year old man with syphilis.

Page 14
CARDIOVASCULAR III
Demonstration Pots
Thoracic and abdominal aorta in

an old hypertensive man.
A 78 year old diabetic woman with

atrial fibrillation and left atrial
thrombosis.
A 65 year old hypertensive male

experienced the sudden onset of severe
central chest pain that radiated to the
back and legs four days before death.
Man aged 84 who died suddenly one

month after repair of a ruptured
abdominal aortic aneurysm.
Page 15
A man aged 50 with carcinoma of the

pancreas with swollen leg.
A 50 year old woman had

severe chest pain and died
after a short while.
2013 - Cardiovascular IV – Valvular heart disease, infective endocarditis & congenital heart disease
Page 1
MBBS 2 Tutorial – Cardiovascular IV
Valvular heart disease, infective endocarditis & congenital heart disease
Learning Objectives :
Understand types of valvular defects
Pathogenesis and outcome of rheumatic heart disease and infectious endocarditis
Know pathology of congenital heart disease
Review normal valve anatomy and function
Valvular heart diseases
Types :
Regurgitation – failure of valve to close causing reversed blood flow

Stenosis – failure of valve to open completely, impeding forward flow
Pure or mixed disease

Isolated (one valve) or combined (more than one)
Stenosis is almost always due to a primary valve disease, whereas regurgitation may be due to valve
disease or fuctional.
Functional regurgitation – valve incompetent due to 1. dilation of the ventricle or 2. dilation of aortic or
pulmonary artery
Clinical consequence depends on – degree of abnormality

- rate of development
- rate and quality of compensatory mechanism
Discuss:
Mitral incompetence – floppy mitral valve
Floppy mitral valve (arrows) in a man

aged 56 who died suddenly and
unexpectedly. There was a past history
of syncopal attacks. Microscopy
showed an increase in myxoid ground
substance in the valve leaflets.
Mitral stenosis
Aortic incompetence
Aortic stenosis esp. calcific aortic valve disease, bicuspid aortic valve
Page 2
Stenosed, calcified, bicuspid aortic valve. Woman

aged 66. Heart weighed 610 g.
This condition can be found incidentally without
any history of rheumatic fever.
Approach to Valve vegetations
1. RHD – small, warty
2. IE – large, bulky, irregular
3. NBTE – bland
4. Libman Sacks – small to medium, both sides of valve
Rheumatic Heart Disease

Pathogenesis
Clinical diagnosis
Page 3
Active rheumatic carditis in a girl aged 11. There was a 4

year history of recurrent attacks of rheumatic fever and of
persistent mitral and aortic incompetence with severe heart
failure. Death occurred suddenly. Note the thickening of the
mitral (blue arrows) and aortic cusps (black arrows) with
rows of vegetations near their edges, the fibrosis of the left
atrial endocardium, the dilatation and hypertrophy of all
cardiac chambers, and the chronic obliterative pericarditis.
Tiny vegetations were also present on the atrial surface of the
tricuspid valve.
Discuss histology
Histology - Rheumatic myocarditis. The

classical Aschoff body is seen here. The cells
are located in the perivascular region within the
myocardium. The ‘Anitschkow’ cells are plump
activated macrophages (arrowed in B), and these
are admixed with other inflammatory cells. The
‘Anitchkow’ cells have chromatin arranged in a
central ribbon and this has been likened to the
appearance of a caterpillar (hence "caterpillar
cells"). [Aschoff was from Freiburg and
Anitchkow was from St. Petersburg.]
Discuss complications and outcomes
Chronic rheumatic heart disease with involvement

of aortic, mitral (arrows) and tricuspid valves in a
woman of 61. She had had four attacks of acute
rheumatic fever at the ages of 4, 14, 18 and 30
years. Exertional dyspnoea was first noted when
she was 30: Nocturnal dyspnoea and ankle
swelling began at the age of 50. She died of heart
failure at 61.
The first symptoms of the presence of rheumatic
heart disease are often seen during pregnancy.
Page 4
Infectious Endocarditis
Pathogenesis
Infective endocarditis due to Streptococcus

viridans in a woman aged 35. Note the
multiple vegetations (arrows). S. viridans is
probably the commonest organism to cause
infective endocarditis. It has a low degree of
virulence. Formerly this form of endocarditis
was called sub acute bacterial endocarditis.
A.B. Infective endocarditis. Features to

note are the thickened fibrotic valve
leaflet (black arrow), the vegetation
(blue arrows) containing pink fibrin and
platelets, and the dark blue colonies of
bacteria (red arrow), better seen in the
higher power photomicrograph in B.
A B
Discuss complications
Page 5
Perforation (arrow) of mitral

cusp due to Staphylococcus
aureus endocarditis.
Other valvular heart disease – SLE, marantic vegetations
Valve Prosthesis
Types
Complications
Mitral and aortic valve prostheses (arrow) inserted in a
man aged 49 with heart failure due to chronic valve
disease following rheumatic fever at the age of 3 years.
During the 1960’s definitive surgery for damaged heart
valves was introduced. Many different types of valve
were tested. Some of them caused immunological
rejection but ultimately the valves were made of inert
material. Calf valves were used with good lasting
qualities in some centres.
The spouses of some patients were worried by the noise
Congenital heart disease

Refers to heart and great vessels
Main problems are either shunts or obstruction to blood flow

Shunts may be right to left or left to right
R to L:
Discuss why cyanosis occurs
Explain paradoxical embolism
Fallot’s tetralogy
Transpostition of great vessels
L to R:
ASD
VSD
PDA
Page 6
AV septal defect
Patent ductus arteriosus. Marked right

ventricular hypertrophy. Atheroma of pulmonary
artery due to severe pulmonary hypertension.
This is an example of Eisenmenger's syndrome
complicating a shunt.
Atrial septal defect in a man aged 20 who died

of a ruptured angiomatous malformation in the
cerebellum. Note the right ventricular
enlargement. No recorded cardiac symptoms.
Discuss pathogenesis of pulmonary hypertension and shunt reversal
Obstructions:
Coarctation of aorta
Congenital aortic valve stenosis
Page 7
CARDIOVASCULAR IV
Demonstration pots
Woman aged 73 who died of metastatic

gall-bladder carcinoma. There were
recent infarcts in kidney, spleen, brain
and heart. Thrombi were also present in
the femoral veins and the inferior vena
cava.
Woman aged 81 admitted with 3 week history

of rigors, fever and polyarthritis. Developed
aortic diastolic murmur 1 week later, and
escherichia coli was grown from blood and
joint aspirate. Died 2 weeks after admission
with severe heart failure. Right pelvi-ureteric
stenosis and pyonephrosis found at autopsy.
Page 8
Page 9
CARDIOVASCULAR IV
Demonstration pots
Aortic valve prosthesis inserted in 1965, and

longterm anticoagulant therapy instituted. In
October, 1973, developed subdural haematoma
after minor trauma. As a result, anticoagulant
therapy was given only intermittently, and patient
developed symptoms suggestive of multiple
episodes of cerebral embolism. At autopsy in
1974, thrombosis was found to have occurred on
the prosthesis, and there were cerebral and
renal infarcts of various ages.
Page 10
Man aged 53 with metastatic

carcinoma of the caecum.
Man of 68.
Woman aged 50; an

incidental autopsy finding.
Page 11
Woman aged 63 who died of myocardial

infarction.
Page 12
CARDIOVASCULAR IV
Demonstration pots
Woman aged 35.
Man aged 48.

Page 13
Man aged 56 who died suddenly and

unexpectedly. There was a past history of
syncopal attacks.
Woman aged 55 who died 3 days after the

onset of rigors and generalized myalgia.
Patient aged 24. The artery at the bottom left

is the femoral.
Man aged 65.

2013 - Respiratory I - Pathology of Pneumonia
Page 1
MBBS2 Tutorial – Respiratory I – Pathology of Pneumonia
***Important note: “The students are strongly advised to attend/listen to the relevant week’s pathology
lecture prior to attending the tutorials as all the conditions may not be covered in the tutorials and any
questions may be addressed in the discussion forum”
Learning Objectives
Understand and recognize the pathology and complications of pneumonia.
Understand the pathogenesis of tuberculosis.
To recognize the features of tuberculosis
Reproduced from Robbins & Cotran Pathologic

Basis of Disease 7th Ed. 2005
Histology - Normal Lung. Note

the thin alveolar septa (arrow)
containing only a single capillary
and thin investing connective
tissue support.
Pneumonia:
Types – broncho and lobar
Pathogenesis of each type
stages of lobar pneumonia
complications of pneumonia
Page 2
Acute bronchopneumonia. Small grey foci of

consolidation (blue arrows) are widely
scattered through both lungs, which are
hyperaemic. Black arrows indicate pre-
existing carbon deposition.
Acute, pneumococcal lobar pneumonia.

A young woman who died within 24
hours of admission to hospital in spite of
antibiotic therapy. Arrows indicate the
area of consolidation.
Special pneumonias
Viral and mycoplasma

Legionnaire’s
Lung infections in immune-compromised host:
1. Pneumocystis carinii
2. Cytomegalovirus
3. Aspergillus
4. Candida
5. other fungi
Chronic lung infections
Tuberculosis
-organism
- granulomatous reaction pattern
-typical histology
Fibrocaseous tuberculosis. Note

zones of caseous necrosis (N),
epithelioid macrophages (E), giant
cells (arrows).
Page 3
ZN stain
Acid fast bacilli

(arrows) (Ziehl-Neelsen
stain).
-primary, secondary, progressive (miliary)

Primary TB
- Ghon focus
- Ghon complex
Secondary TB
- location and histology
Progressive pulmonary tuberculosis
- pathogenesis of miliary TB
Lung abscess
Definition
Causes and mechanism:
1. aspiration
2. pre-existing lung infection eg pneumonia
3. immunosuppression
4. septic emobolism to lung
5. neoplasia
Page 4
Woman aged 24 with Staphylococcus aureus septicaemia. Three

weeks before death a boil on her buttock had been incised, and a few
days later she developed fever and myalgia. Her condition then
deteriorated rapidly: multiple pustules appeared in the skin, she
became dyspnoeic and deeply jaundiced, urine volume fell and there
was clouding of consciousness. White cell count was 19.6 x 109/l,
with 84% neutrophils. Terminally, there was evidence of
disseminated intravascular coagulation.
Reproduced from Robbins & Cotran

Pathologic Basis of Disease 7th Ed.
2005
Page 5
RESPIRATORY I
Demonstration pots
Normal lung from a young

adult
Man aged 41 who died 4 days after

the onset of a cough productive of
brownish sputum and of sharp left-
sided chest pain.
Woman aged 24 with Staphylococcus aureus septicaemia. Three weeks before death
a boil on her buttock had been incised, and a few days later she developed fever and
myalgia. Her condition then deteriorated rapidly: multiple pustules appeared in the
skin, she became dyspnoeic and deeply jaundiced, urine volume fell and there was
clouding of consciousness. White cell count was 19.6 x 101, with 84% neutrophils.
Terminally, there was evidence of disseminated intravascular coagulation.
Page 6
Woman aged 23 years who died 2 weeks after the onset of

symptoms of respiratory infection. She developed an
erythematous rash, peritonitis, pericarditis and shock in the
terminal stages of her illness. The organism was isolated from
sputum, pleural fluid and blood. Antibiotics to which the
organism was sensitive were used only on the last day of life.
Woman aged 32 who died 5 days after the onset of

cough, chest pain and fever. She received intensive
antibiotic therapy during the last 3 days of life.
Man aged 70 who died 2 weeks after removal of a

meningioma. He remained unconscious following
the operation, and autopsy disclosed extensive
cerebral infarction.
.
Page 7
RESPIRATORY I
Demonstration pots
Man aged 72 years.
Woman aged 32 who died 5 days after the onset of

cough, chest pain and fever. She received intensive
antibiotic therapy during the last 3 days of life.
Page 8
Woman aged 41 with renal failure due to amyloid disease.

The specimen comprises the lower lobe of the left lung.
Aged 12 months.
Page 9
RESPIRATORY I
Demonstration pots
Male alcoholic aged 61 who had been drinking heavily

and who had been sick for several weeks before death.
Man aged 76 with Parkinson’s disease..
Man aged 52 who died of staphylococcus aureus

septicaemia complicating a shoulder injury.
Abscesses were also present in the kidneys and
spleen.
Page 10
Man aged 65. There was a two month of lethargy, weight

loss, fever and dry cough.
Girl aged 4 years with fibrocystic disease of the pancreas.

2013 - Respiratory System II
Page 1
MBBS2 Tutorial - Respiratory System II
Chronic Lung Disease and Diseases of Pulmonary Vasculature
1. To understand the mechanisms leading to chronic lung disease

2. To understand the differences between obstructive and restrictive lung disease
3. Gross and histological features of the different forms of diffuse lung disease
4. Knowledge of the causes and complications of chronic lung disease
5. To know the important diseases of pulmonary vasculature
Obstructive lung disease
Includes emphysema, chronic bronchitis, asthma and bronchiectasis.
Emphysema
Definition & types
pathogenesis
morphology
Clinical course


Page 2

Severe panacinar emphysema in a man aged

85. Here the extent of tissue destruction is
greater. There is no fibrosis.
Chronic Bronchitis
Definition
pathogenesis
morphology
Clinical features
Asthma
Definition
Pathogenesis
Types – atopic, non-atopic, drug induced and occupational
Morphology
Clinical course

Left. Microscopically, the major change is

eosinophil infiltration into the wall of the bronchi.
Right. Higher magnification of the bronchial wall
showing the large number of eosinophils (arrows)
Page 3
Bronchiectasis
Definition
Pathogenesis
Morphology
X3360B. Death due to acute

bronchopneumonia in a patient
with bronchiectasis.
Restrictive or diffuse interstitial lung disease
Categories : fibrosing eg usual interstitial pneumonia (UIP), pneumoconiosis

Granulomatous eg sarcoidosis
Other eg pulmonary alveolar proteinosis
Pneumoconiosis
Important complications of chronic lung disease:
UIP: Reproduced from

Robbins & Cotran Pathologic
Pulmonary asbestosis in a man aged 50 who was exposed to

asbestos dust 16 years before death. He had marked dyspnoea and
clubbing of fingers during the last 6 years of life.
Fibrocaseous tuberculosis is also present in upper lobe (red
arrows). Note that fibrosis in asbestosis is maximal in lower zones
(black arrows).On chest X-rays the changes of tuberculosis are
seen in the upper lobes while those of asbestosis are seen in the
lower lobes.
Page 4
(Left). Asbestosis. In this low power view normal

alveoli are seen at the top of the picture (red arrows)
and interstitial fibrosis in the lower part. (black
arrows). See the enlarged air spaces which
contribute to the honeycomb appearance.
(Right). High power view shows asbestos bodies
(black arrows).
Calcified fibrous plaques in the parietal pleura of a man aged

63 who was exposed to asbestos dust 25 years before death.
These plaques do not contain asbestos bodies
Sarcoidosis: Reproduced
from Robbins & Cotran
Pathologic Basis of Disease
7th Ed. 2005
Malignant pleural mesothelioma in a man aged 63 who was

exposed to asbestos dust 25 years before death.
Page 5
Diseases of Vascular Origin
Broad classification
1. damage to vessels eg arteritis
2. obstruction eg pulmonary emboli
3. variations in intravascular pressure eg pulmonary hypertension
Cor pulmonale in a man aged 64. See the thickened right

ventricular wall (red arrows). He had been treated for
chronic obstructive pulmonary disease for 14 years before
death. He had smoked 60 cigarettes a day for 40 years. At
the time of his final admission to hospital, the pH of his
arterial blood was 7.16

2005
Page 6
RESPIRATORY SYSTEM II
Demonstration Pots
Eighteen year old man with 6 months' history Of

wheezing
80 yrs/M chronic smoker
85yrs/M
59 yrs/M cement factory worker and who suffered from

respiratory insufficiency
Page 7
73 yrs/Male complicated by right heart failure.

Plasma bicarbonate 38 mmoll.
51 yrs /M smoker with Eisenmenger's syndrome

complicating atrial septal defect.
Page 8
Demonstration Pots
72 yrs /M. Culture of the bronchial exudate

grew Pseudomonas aeruginosa.
Lung from a young boy

Page 9
Parietal pleura 78 yrs/M
Pulmonary artery from a

young woman
Page 10
Demonstration Pots
25 yrs/F. She had hypertrophic pulmonary

osteoarthropathy and cor pulmonale.
67 yrs/M with a long history of repiratory insufficiency

and corpulmonale. shortly before death arterial blood
PO2 was 37mm Hg and PCO2 43mm Hg.
83 yrs/M
Page 11
2013 - Respiratory System III
Page 1
MBBS2 Tutorial – Respiratory System III
Pulmonary Tumours and Diseases of the Upper Respiratory Tract
1. Classification of pulmonary tumours (including mesothelioma).

2. Recognized appearances and complications of lung tumours
3. Understand the principal pathologies of the upper aerodigestive tract, particularly carcinoma of
the oropharynx and larynx
Pulmonary tumours
Primary or secondary
Primary:
Aetiology and Pathogenesis
Like other cancers get stepwise accumulation of genetic abnormalities that transform benign bronchial
epithelium to neoplastic tissue. Major environmental insults that inflict genetic damage are known
Precursor lesions – does not imply that progression to invasion will occur
Types – 90-95% carcinomas
- bronchial carcinoids
- mesenchymal tumours
Classification of carcinomas:
- classified according to histological appearance
- squamous cell carcinoma (25%-40%)
- adenocarcinoma (25%-40%)
- small cell (20%-25%)
- large cell (10%-15%)
Clinically classified into two groups on the basis of likelihood of metastases and response to treatment -
small cell and non-small cell
Morphology : most tend to arise centrally, adenocarcinoma tends to arise peripherally.

Others – harmatoma (coin lesion)
Complications
Paraneoplastic syndrome
Staging
Page 2
Squamous, adeno, small cell and

large cell carcinoma. Reproduced
from Robbins & Cotran Pathologic
Broncho alveolar carcinoma.

Cotran Pathologic Basis of Disease
7th Ed. 2005
Carcinoid tumour (red arrow)

with obstruction, bronchiectasis
(blue arrow) and infection.
Operative surgical specimen.
Page 3
Numerous metastases from renal cell

carcinoma. Reproduced from
Robbins & Cotran Pathologic Basis
of Disease 7th Ed. 2005
Permeation of peribronchial pulmonary lymphatics by metastatic

gastric carcinoma. This is often referred to as lymphangitis
carcinomatosa. This pattern of spread may be caused by a number
of different tumours, including carcinoma of the lung itself.
Note the peri lobular (red arrows) and peribronchial (blue arrows)
distribution.
Pleural tumours – mesothelioma
Upper Respiratory Tract
Larynx
Inflammations :
– epiglottitis
Page 4
Acute epiglottitis. Note the oedema and

congestion (arrows).
Croup (LTB)
Acute laryngo-tracheo-bronchitis in a man aged 48 with alcoholic cirrhosis

and bleeding oesophageal varices who was comatose during the last few days
of life. Note the reddening of the epiglottis and the tracheal mucosa.
Reactive nodules
Papilloma
Carcinoma of larynx:

2005
Page 5
RESPIRATORY SYSTEM III
Demonstration Pots
Operative surgical specimen of a 50 year old

man who is a chain smoker and presented
with chronic cough.
Operative surgical specimen from 66 year

old man, a chronic smoker, presented with
chronic cough with expectoration.
A 70 year old man with chronic

cough and significant weight
loss.
A female epileptic aged 57 years was eating in

bed, and suddenly moaned and fell backwards
unconscious. When an ambulance bearer
arrived she was found to be dead.
Page 6
Operative surgical specimen from

62 year old female who presented
with hoarseness of voice and
dyspnea.
Lungs of a 65 year old man who

underwent a gastrointestinal surgery
few years back.
Man aged 75 who suffered a cardiac arrest

associated with myocardial infarction 7 days
before death, and remained deeply unconscious
thereafter.
A man aged 56 presented with mental confusion caused by severe

hypercalcaemia (4.05 m mol/l). He died soon after admission.
A man aged 63 who was exposed to asbestos dust 25 years presented

with dyspnea before death.
Page 7
Demonstration Pots
A man aged 48, non smoker, with

breathlessness and cough.
Autopsy specimen from a 67 year old man who

complained of hoarseness of voice and lately
dyspnea.
4 yr old girl c/o sore throat at night. Death

occurred during the night.
Page 8
Lung of a woman aged 37 who

underwent breast surgery 3 years ago.
A 70 year old chronic smoker

presented with chronic cough & weight
loss.
A man aged 53 presented 6 months before death

with cough productive of purulent sputum and
chronic tiredness. He had smoked more than 20
cigarettes a day for over 20 years.
Operative surgical specimen from a man aged 69

who had smoked heavily for many years with
dyspnea, cough & fever.
Page 9
A man aged 63 who was exposed to asbestos dust for

25 years presented with breathlessness before death.
Page 10
Demonstration Pots
Man aged 72 with staphylococcus aureus

septicaemia and mutliple organ failure.
Male aged 66 with chronic bronchitis.

Smoked 30 cigarettes a day for many years.
Operative surgical specimen from a 41 year

old man who presented with hoarseness of
voice.
Page 11
Lung of a 69 year old man who underwent a

cutaneous surgery 4 years before death.
A man aged 48 with a history of exposure to

asbestos dust for 25 years presented with
breathlessness before death.
Lung in a man aged 53 who had smoked 30

cigarettes a day for many years. Death was
due to cerebral embolism secondary to left
ventricular mural thrombosis complicating
acute myocardial infarction.
2013 - Pathology of the Liver
Page 1
MBBS2 - Pathology of the Liver
Please note these objectives are a guide to what students are expected to understand after the
lectures, tutorials and private reading.
Learning objectives from lectures and tutorials

1. To know the different types of liver injury that can be seen in alcoholic liver disease
2. To understand the causes, pathogenesis and complications of cirrhosis
3. To know the infections that result in acute and chronic liver disease
4. To recognize the types of liver tumours
5. To be aware of the major vascular and intrahepatic biliary diseases
Review the histology of the liver and blood supply – acinar and lobular concepts. Acinar concept is
considered more useful as it explains better many of the pathophysiological disturbances in liver
disease.

7th Ed. 2005.

7th Ed. 2005.
Liver disease – Primary – alcoholic liver disease, metabolic liver disease, drug-induced liver disease,
infective liver disease, hepatocellular carcinoma
Secondary – CCF, Metastatic disease
Role of liver biopsies in pathology.
Functional reserve is huge therefore masks clinical impact of early liver disease.
So tends to be a slowly progressive pattern.
Patients usually present with chronic disease.
Patterns of hepatic injury:

Limited number of responses to injury.
Page 2
5 general responses:
- inflammation
- degeneration and intracellular accumulation
X2904B. Marked fatty change of the liver.

Man aged 45 who was found in a confused
state in a boarding house room: he was
surrounded by empty wine bottles. Death
occurred as a result of inhalation of vomitus
soon after his admission to hospital. At the
time of autopsy it would have felt very greasy.
Note the pallor of this specimen.
Fatty liver histologically shows clear spaces in

the hepatocytes. Individual cells are swollen
with the fat (it is clear because fat is removed
from the tissues during processing) and this is
the reason that fatty livers are usually enlarged
clinically. Cytoplasm and nucleus are
displaced to the periphery of the cell by the
lipid droplet.
- necrosis and apoptosis

- regeneration
- fibrosis
Discuss each response
The features and pathogenesis of:

Hepatic failure
Cirrhosis
What are the defining features of cirrhosis?

Various aetiological agents (macroscopic and often microscopic examination may not be diagnostic).
Aetiological agents:
1. Alcohol, other toxins and drugs
2. Inflammatory conditions eg. viral, autoiummune
3. Biliary disorders
4. Inherited diseases eg. Haemochromatosis
5. Vascular diseases eg. Hepatic vein thrombosis
6. Cryptogenic
Micronodular (most likely alcohol or haemochromatosis) vs macronodular

Page 3
X164B. Coarsely nodular cirrhosis in a

female aged 12 years who had suffered
from acute hepatitis 5 years before death.
The mode of evolution of the cirrhosis was
not followed by liver biopsy in this case.
See the large rounded nodules (arrows)
each surrounded by fibrous tissue.

7th Ed. 2005
Complications:
1. Portal hypertension – why does it occur with cirrhosis?
Portal hypertension

7th Ed. 2005
Page 4
X3710. Large oesophageal varices

(arrows) in a patient with chronic
portal hypertension. They have
partially collapsed in the fixed
specimen.
2. Hepatic failure
3. Hepatocellular carcinoma
Congenital liver disease
X308B. Polycystic disease of liver in

a woman aged 51 who died of
uraemia secondary to polycystic
kidneys (autosomal dominant, or
"adult", type.
Alcoholic liver disease

2005
Discuss the morphology and pathogenesis

Page 5
This photomicrograph shows Mallory’s hyaline (M),

hepatocyte swelling (H)
and neutrophil infiltration (N).
Although Mallory’s hyaline is the best known
histological feature, it may not be present in every case or
it may be difficult to find. The fibrosis is important; it
develops in response to the inflammation and begins
around the central vein. With repeated deposition it
eventually links the central veins to the portal tracts,
causes distortion and leads to cirrhosis.
Alcoholic cirrhosis. This shows parenchymal nodules

(N) surrounded by fibrous septae (F). By the time
cirrhosis has developed, the features of alcoholic liver
disease may no longer be detectable. This is particularly
the case if the patient has stopped drinking. Obviously
if fatty change and Mallory’s hyaline are seen, then
alcohol becomes a very likely aetiology.
Metabolic liver disease
NASH
Haemochromatosis – primary and secondary
Histology: Genetic haemochromatosis. This picture

shows iron as brown granular pigment (arrows) in
the hepatocytes. The portal tracts are expanded by
fibrosis (F), but the liver is not cirrhotic. In
haemochromatosis, the iron deposition occurs
primarily in the hepatocytes. This differs from
transfusional overload where the deposition is also
marked in reticuloendothelial cells (macrophages),
particularly the Kupffer cells.
Page 6
Iron is detected in the cells using

Prussian blue, or Perls’ stain,
which stains the iron blue. This is 4
+ iron deposition.
Wilsons disease
Drug-induced liver disease
At least 10% of drug reactions involve the liver, as the liver plays an important role in metabolism and
in the conjugation and elimination of toxic substances from the body.
Two types : predictable (dose-related) and unpredictable (idiosyncratic)
Two sites of damage – hepatocellular or cholestatic.
Histology:drug-induced
intrahepatic cholestasis. Note
perivenular intracanalicular
cholestasis (black arrows)
Infective liver disease

The liver may be affected by a wide range of pathogens, including viruses, bacteria, parasites, fungi
and rickettsia.
Page 7
1. Viral
Viruses, such as Hepatitis A, B, C, and others, may cause a range of changes in the liver. These
include a very mild and subclinical hepatitis, chronic hepatitis and even fulminant and rapidly fatal
hepatitis. As well as the hepatitis virus, others such as cytomegalovirus, Epstein-Barr and herpes
simplex can cause a hepatitis illness in addition to effects in other parts of the body.
A-C. Viral hepatitis. Picture A shows slight

disarray of the hepatocyte plates, an infiltrate of
lymphocytes in the lobules, and some apoptotic
bodies better seen in B (arrowed) and C.
Apoptotic cell death is the characteristic
mechanism of deletion of virally-infected cells.
Picture D shows the typical appearance of chronic

hepatitis, and the important features are portal
inflammation,(I) portal fibrosis (this does not
develop in every case) and interface hepatitis (so-
called "piecemeal necrosis"), which is arrowed. This
last change is characterised by irregularity of the
limiting plate, extension of lymphocytes into the
adjacent parenchyma and apoptotic bodies due to
hepatocyte death. With time the development of
fibrosis may evolve into cirrhosis, so chronic
hepatitis is an important lesion.
Page 8
Image E shows ground glass inclusions in hepatocytes

(arrowed). These are cytoplasmic collections of hepatitis B
surface antigen. This is how they appear in H&E stained
sections. They stain positively with immunoperoxidase stains
for Hep B antigen.
2. Bacterial
X2344A. Large multiloculated liver abscesses

(arrows) in a woman aged 57 who died 6 weeks after
cholecystectomy and exploration of the common bile
duct. Much of the pus that filled the abscess cavities
has been lost during preparation of the specimen for
mounting.
X2438. Disseminated tuberculosis of the liver in a

female aged 6 years. Circumscribed caseous nodules
(arrows) surrounded by tuberculous granulation tissue
are scattered through the parenchyma. Some are bile
stained, presumably as a result of involvement of bile
ducts by the necrotising process. Histological
examination showed that numerous tubercles were
also scattered through the liver: these are difficult to
see with the naked eye. Autopsy disclosed extensive
tuberculosis of the lungs and abdominal viscera.
3. Parasitic and helminthic

Page 9
X2175B. Hydatid disease of the liver in a woman

aged 36 who presented with colic due to the presence
of daughter cysts in the biliary passages. Partial
hepatectomy specimen. This is the larval stage of the
dog tapeworm E. granulosus.
Vascular liver disease

The liver has a dual blood supply, and this protects against infarction in many cases. Nevertheless, the
circulation may be affected in a number of ways.

Examples :
1. impaired flow to the liver eg. Portal vein thrombosis
2. intrahepatic impaired flow – chronic venous congestions of the liver causing a ‘nutmeg liver’
eg. in longstanding heart failure
3. outflow obstruction: eg. Budd-Chiari syndrome – thrombosis of the major hepatic veins causes
extreme blood retention in the liver
Neoplasia
The liver is a common site for metastatic spread. Primary liver cancers are relatively rare in Western
populations but are common in countries with a high incidence of hepatitis B. There are several factors
known to be important for increasing the rate of liver cancers eg. Hepatitis B and C, aflatoxin and
cirrhosis
Page 10
Classification of major liver tumours and tumour-like conditions:

Focal nodular hyperplasia
Haemangioma
Liver cell adenoma
Bile duct adenoma
Hepatoblastoma
Hepatocellular carcinoma
Metastatic
Intrahepatic biliary diseases

Bile stasis can occur at any level from the hepatocyte and canaliculus to the extrahepatic bile ducts.
Diseases affect the intrahepatic biliary apparatus at different levels.
1. canaliculus – drug induced cholestasis (already discussed)

2. small intrahepatic bile ducts – primary biliary cirrhosis
Primary biliary cirrhosis in a woman aged

56. Ten year history of itch. Smooth muscle
and mitochondrial antibodies present in
blood. Serum alkaline phosphatase
persistently high. Died with liver failure and
pneumonia. Extrahepatic bile ducts found to
be normal at autopsy. While the aetiology
cannot be determined macroscopically here,
biliary tract disease is suggested as the liver
has a greenish tinge due to bile stasis.
Portal inflammation and lack of

bile ducts in primary biliary
cirrhosis.
3. large intrahepatic bile ducts – primary sclerosing cholangitis
Concentric peribiliary fibrosis

(arrows) in primary sclerosing
cholangitis.
Page 11
4. neoplasia – bile duct adenoma

- cholangiocarcinoma
Clonorchis sinensis infection and

mucus-secreting cholangiocarcinoma in
a Chinese male aged 55 from Hong
Kong. There are many flukes in the
intrahepatic bile ducts. (some of the
flukes are presented in the separate
circle).
Page 12
PATHOLOGY OF THE LIVER
Demonstration Pots
X2838. Normal liver from a woman aged 37

who was killed in a motor vehicle accident.
Man aged 86 with multiple myeloma who

received many blood transfusions..
Man aged 43 known to have had a heavy alcohol

intake over many years. Also had hypertensive heart
failure.
Page 13
Woman aged 35 with history of hepatitis . At the time of death

had ascites, liver failure and bronchopneumonia. What is the
other organ present and how is it affected?
Woman aged 30 with a one month history of anorexia,

nausea, vomiting and abdominal discomfort. Three weeks
before death she noticed jaundice, dark urine and pale stools.
Man aged 47 with long standing heart

failure due to aortic valve disease.
Man aged 41. Death was due to GI

haemorrhage.
Page 14
Demonstration Pots
Normal adult liver. Because it has been necessary to

perfuse the liverwith formalin to achieve adequate
fixation, the liver tissue has become alittle paler than
that seen at operation or autopsy.
Patient had a history of jaundice as a child.
The patient had chronic myeloid leukaemia, and received many

blood transfusions for anaemia.
Page 15
History of heart failure.
An incidental autopsy finding in a man aged

53 who died of cerebral haemorrhage.
Man aged 73.

Page 16
Demonstration Pots
Man aged 67 with severe heart failure.
Man aged 38.
The pale colour suggests the condition, but a definitive diagnosis

cannot be made without histological examination. The patient was a
67 year old obese female diabetic who died of recurrent pulmonary
embolism: the diabetes was poorly controlled during her terminal
illness.
Page 17
Female aged 12 years who had suffered

from acute hepatitis 5 years before
death.
Man aged 73 with history of heavy alcohol intake until 4

years before death, which followed the development of
ascites, confusion and drowsiness. Note the small nodule
that differs from the rest – what is this?
Chinese male aged 55 from Hong Kong. There

are many flukes in the intrahepatic bile ducts.
Page 18
An incidental autopsy finding in a

woman who died of a ruptured
aneurysm of the internal carotid artery.
Woman of 39 who had had many transfusions for

anaemia over a period of 10 years. The nature of the
anaemia is uncertain: erythrocyte survival was shown
to be reduced but red cell production was also
depressed.
2013 – Upper Gastrointestinal Tract
Page 1
MBBS2 Tutorial –Upper Gastrointestinal Tract
1. To recognize that inflammation and tumours are the major diseases of the mouth, salivary
glands
2. To discuss and recognize the prinicipal infective, inflammatory and neoplastic pathologies of
the oesophagus and stomach, particularly reflux oesophagitis, peptic ulcer disease and
carcinoma
Salivary glands
Sialadenitis – inflammation of the salivary gland

May be viral eg mumps
Bacterial – secondary to dehydration or obstruction
Autoimmune – Sjogrens syndrome
Sialolithiasis
Neoplasms
Pleomorphic adenoma of the parotid in a man aged

25. Operative surgical specimen
A pleomorphic adenoma with glandular spaces lined

by cuboidal epithelial cells (arrows), groups of
smaller darker myoepithelial cells (short arrows)
and an abundant myxoid stroma.
Diseases of Oral Mucosa
Infections : viral - Herpes

Bacterial
Fungal – Candida
Inflammation : aphthous ulcers (many systemic conditions are associated with oral lesions) –
relationship to gastrointestinal disorders
Page 2
Neoplasms:
Premalignant conditions:
1. leukoplakia

2005
2. erythroplakia
Squamous cell carcinoma:

Progression of oral cancer
Page 3
Oesophagus
Congential lesions:
Atresia, usually associated with tracheo-oesophageal fistula
Acquired lesions:
1. Webs, rings and strictures
Stricture (arrows) of the lower end of the oesophagus in a

man aged 69 with a past history of hiatus hernia and
reflux oesophagitis.
2. Achalasia
Page 4
Chronic achalasia of the oesophagus in an elderly man. The

obstruction is at the bottom right of the specimen. Note the
marked dilatation of the oesophagus and the hypertrophy of
its muscle.
3. diverticula
4. Mallory-Weiss tear
Mallory-Weiss tear (arrow) at the gastro-oesophageal junction in a

male alcoholic aged 40, who died of massive gastro-intestinal
haemorrhage
5. Oesophageal varices
Oesophageal varices (arrows)
6. Hiatus hernia – two types sliding (95%) and rolling (5%), associated with reflux. Complications
include strangulation and obstruction.
7. Infections:
Viral – Herpes
Page 5
Herpes simplex. Characteristic histological features

are opaque 'ground glass' nuclei (arrows),
eosinophilic nuclear inclusion bodies and
multinucleate giant cell formation (arrowhead) in
infected squamous epithelium.
9. Gastro-oesophageal reflux
10. Barrett’s oesophagus
Barrett's oesophagus
long-standing Barrett's oesophagus with dysplasia
Malignant tumours
Squamous cell carcinoma (arrows) of the lower

oesophagus in a man aged 65: operative surgical
specimen.
Page 6
Adenocarcinoma
Adenocarcinoma (arrows) of
the cardio-oesophageal
junction.
Adenocarcinoma arising in
Barrett's oesophagus.
Stomach
Difference between erosion and ulcer.
Acute gastritis and multiple acute ulcers (arrows) in

a man aged 72 with Staphylococcus aureus
septicaemia. There was multiple organ failure, but
the immediate cause of his death appeared to be
massive haemorrhage into the stomach.
Gastritis – H. pylori
Active chronic gastritis with Helicobacter

(arrowhead). Intraepithelial neutrophils are
indicated by arrow.
Page 7
Silver stain showing Helicobacter in

superficial mucin.
Peptic ulceration
Role of H Pylori.
Chronic peptic ulcer on the lesser curvature of the

stomach with an eroded artery (arrow) in its base.
Man aged 67 who was known to have had a peptic
ulcer for 20 years. He had 3 haematemeses in the 3
days before partial gastrectomy was performed.
Page 8
complications:
Perforated gastric ulcer

(arrow).
Malignant tumours of the stomach
Primary:
1. Adenocarcinoma – aetiology, types, complications. Krukenberg tumours.
Ulcerating carcinoma of the

stomach. Operative surgical
specimen.
Page 9
Diffusely infiltrating carcinoma of the stomach

(a linitis plastica) in a woman aged 75.
Operative surgical specimen. Note the small,
thick walled stomach.
Signet ring cell type of carcinoma of stomach. This is the

common pattern seen in linitis plastica.
Page 10
GIT I – UPPER GASTROINTESTINAL TRACT
Demonstration Pots
stomach
upper oesophagus.
male alcoholic aged 40
Stomach female aged 61.

Page 11
stomach
partial gastrectomy specimen. Man aged 48 who had had symptoms of peptic
ulceration for many years
Bezoar with diverse components

removed surgically from the stomach of
a male aged 11 years.
lower oesophagus in a man aged 53.
Gastrectomy specimen. What
Carcinoma of the back 2013 – Upper Gastrointestinal Tract
effectofmight
the prednisone therapy
Page 12
Pharynx
tongue with deep central
have on an ulcer?
GIT I – UPPER GASTROINTESTINAL
ulceration. TRACT
Demonstration Pots
Deeply ulcerated gastric leiomyosarcoma
Gastrectomy
Localisedspecimen male aged
gastric mucosal 58.
thickening
due to hyperplasia of the mucus 2013 – Upper Gastrointestinal Tract
Page 13
secreting cells. This condition must
be distinguished from the rugal
thickening due to infiltrating
carcinoma.
upper oesophagus in a man aged 78.
Stomach & Colon. Female aged 60
Trichobezoar Page 14
GIT I – UPPER GASTROINTESTINAL TRACT
Demonstration Pots
Healed gastric ulcers. Small
Gastrectomy specimen: Male aged
Oesophagusleiomyoma.
partial gastrectomy male aged 67 2013 – Upper Gastrointestinal Tract
63. Page 15
2013 - GI III – Pathology of the Small Intestine & Exocrine pancreas
Page 1
MBBS2 Tutorial GIT III - Pathology of the Small Intestine
Learning Objectives
1. Know the major congenital abnormalities

2. To discuss the causes and pathology of ischaemic bowel disease
3. Recognize the pathology of the major causes of malabsorption
4. To discuss the major tumours of the small intestine
5. Understand the pathogenesis of appendicits and other pathologies of the appendix
6. To describe the causes, effects, macroscopic and microscopic features of acute pancreatitis
7. To describe the clinicopathological features of carcinoma of the pancreas
Small Intestine
Normal histology

2005
Congenital Abnormalities
Atresia and Stenosis – complete obstruction is called atresia, incomplete obstruction is stenosis.
Stenosis (black arrow) of second part of

duodenum in an infant. See the relation to the
pancreas (red arrow).The stomach is on the left.
Meckel’s diverticulum – located in ileum, result of incomplete regression of the vitello-intestinal duct.
Usually lined by small intestine mucosa. Heterotropic rests of pancreatic tissue or gastric mucosa may
be present (prone to ulceration and haemorrhage). Other complications – intussception, perforation and
incarceration.
Page 2
Meckel's diverticulum. A woman aged 62. An

incidental autopsy finding. See the diverticulum
(arrows) arising from the anti mesenteric side of the
small intestine.
Meconium Ileus – small intestine obstruction resulting from viscous meconium in patients with cystic
fibrosis.
Meconium ileus and focal small gut stricture (arrow).

Specimen excised surgically from a female aged 2 days with
cystic fibrosis. Note the dilatation of the gut which is filled
with sticky, viscous secretions. This is one way in which cystic
fibrosis presents in a neonate. The stenosis is an unrelated
condition.
Ectopic pancreas
Nodule of ectopic pancreas (arrows) in the wall of the

small gut. Operative surgical specimen.
This may be asymptomatic, or may cause external
pressure induced obstruction or be the apex of an
intussusception.
Ischaemic bowel disease
4 main causes of acute vascular compromise to the bowel:

1. major arterial occlusion: usually superior mesenteric artery by thrombosis or embolism

2005
Page 3
2. end artery occlusion: usually the result of vasculitis, producing small localized lesions, that may
perforate.
3. venous occlusion: hypercoaguable states, intraperitoneal sepsis
Haemorrhagic infarction of small intestine secondary

to venous obstruction. This shows full thickness
infarctio of the bowel wall. The red arrow indicates the
lumenal aspect, the black arrows the serosal aspect.
4. non-occlusive ischaemia: usually in the presence of atherosclerosis of the mesenteric arteries and
secondary to shock
Acute ischaemic enteropathy in a woman aged 63 with

metastatic leiomyosarcoma. She became shocked and
developed abdominal pain and tenderness with passage
of blood per rectum during the last few days of life. The
picture shows the lumenal aspect of the bowel.
Microscopy showed extensive mucosal necrosis and
ulceration, but reasonable preservation of the muscle
coats.
Chronic ischaemia:
Associated with mucosal ulceration and mural fibrosis mimicking inflammatory bowel disease and
often leads to a stricture.
Mechanical abnormalities leading to bowel obstruction

80% of bowel obstructions are due to hernias, intestinal adhesions, intussusceptions or volvulus.

2005
Malabsorption
Page 4
Coeliac disease
Discuss aetiology and morphology
Normal small intestinal mucosal

biopsy showing finger-like villi and
villus length to crypt width ratio of
4:1.
Mucosal biopsy in coeliac disease

showing partial villous atrophy (villus
height (blue arrows) to crypt (black
arrows) length ratio of 1:1). See the
blunt villi and elongated crypts.
Mucosal biopsy in coeliac disease

showing total villous atrophy, crypt
(black arrows) hyperplasia and
increased inflammatory cells in the
lamina propria.
Higher magnification of (C) showing damaged

surface epithelium (black arrows) with loss of
brush border, vacuolation (red arrows) and
irregular arrangement of surface epithelial
cells, increased lymphocytes in the epithelium
(blue arrows) and large numbers of plasma
cells in the lamina propria.
Other causes of malabsorption eg. Tropical sprue, Whipples, Disaccharidase deficiency

Page 5
Tumours
Classification:
Benign – adenomas, angiomas, lipomas, GIST
Malignant – Primary : adenocarcinoma, carcinoid, lymphoma, GIST
Metastatic
Carcinoid
Carcinoid tumour (black arrows) of the ileum in

a man aged 56: operative surgical specimen.
Small intestinal carcinoid. Note

grouping and regular appearance of
tumour cells.
Lymphoma
Diffuse malignant lymphoma (arrows) of the

small gut in a child aged 6 years. Operative
surgical specimen. Note how the tumour
extends to involve the bowel wall and the
adjacent mesentery.
Page 6
Appendix
Acute appendicitis
Pathogenesis
Severe acute appendicitis in a female aged

14 years.
Acute appendicitis in a man aged 27:

operative surgical specimen.
Mucinous lesions
Mucocoele
Desciptive term to describe and appendix that is full of mucous. Usually benign but may result from an
adenocarcinoma.
Mucocele of the appendix.
Mucinous cystadenoma
Commonest mucinous neoplasm
Mucinous cystadenocarcinoma
Page 7

Disease 7th Ed. 2005.
Pseudomyxoma peritonei
Pseudomyxoma peritonei arising from appendix. Male aged 52. This

is a condition in which the abdominal cavity is filled with mucus and
fibrosis. It results from spread to the peritoneum of an
adenocarcinoma from appendix, ovary or gut.
Carcinoid
Carcinoid tumour (arrows) at the tip of the

appendix(its commonest site) in a male aged
14 years: operative surgical specimen. Note
the characteristic yellow colour.
Pancreas
Retroperitoneal organ, the head lying within the duodenal loop, the body crossing the aorta and inferior
vena cava and the tail abutting onto the splenic hilum. It is a mixed endocrine and exocrine organ.
Pancreas from a man aged 32 who had been treated for

severe diabetes mellitus since early childhood. The
pancreas appears normal macroscopically.
Page 8
Diseases of the pancreas can be divided into those affecting the exocrine pancreas and those affecting
the endocrine pancreas.
Exocrine pancreas
The main conditions to affect the pancreas are inflammation (acute and chronic pancreatitis) and
tumours.
Pancreatitis is divided into acute and chronic and is usually associated with acinar cell injury.
Acute pancreatitis
This is inflammation of the pancreas, usually associated with necrosis of acini and intrapancreatic
adipose tissue. It can be a mild self-limited disease or a serious disorder with a high mortality. Over
80% of cases are associated with either biliary calculi or alcohol abuse. Other less common causes
include: infection, ischaemia, drugs, trauma and metabolic causes eg hypercalcaemia.
The pathogenesis varies according to the cause, eg obstruction of the pancreatic duct by a gallstone
leading to damage to the epithelium of the duct and subsequently damage to the glands, as opposed to
ischaemia causing infarction and necrosis.
Relatively mild acute pancreatitis. The pancreas

appears mildly congested and foci of calcification
(arrows) are present within the gland.
Severe acute haemorrhagic pancreatitis. Note the obvious

haemorrhage and the widespread deposits of calcium (arrows).
Pathogenesis of the widespread deposits of calcium:
The main changes occurring in pancreatitis are:

Protease digestion of pancreatic substance
Elastase digestion of blood vessels with subsequent haemorrhage
Lipases digesting the fat
Accompanying inflammatory reaction.

Page 9
Acute pancreatitis. The pre-existing

architecture has been essentially
destroyed.
Haemorrhage and necrosis of acute

pancreatitis, with some preserved pancreatic
parenchyma on the left (arrow).
Focal acute necrosis of perirenal fat in a patient who

had severe acute pancreatitis. The patient was oliguric
due to acute renal tubular necrosis of ischaemic type.
See the calcium deposition (arrows) highlighting foci of
enzymatic fat necrosis.
Carcinoma of the pancreas
Carcinoma of the pancreas generally refers to carcinoma of the exocrine pancreas. The great majority
of these arise from the ductal epithelium. The incidence of pancreatic cancer is increasing and as it
usually presents late, the prognosis is generally poor.
Carinoma (blue arrows) of the head of the pancreas with

obstruction of ducts and atrophy of the body (red arrow)
and the tail (black arrow).The dilated pancreatic duct can be
seen for the whole length of the pancreas.
Page 10
GI III – PATHOLOGY OF THE SMALL INTESTINE
Demonstration pots
Operative surgical
specimen from a man who
had severe pain in right
iliac fossa.
Surgical specimen of
ileum from a man who
presented with intestinal
obstruction.
A male aged 3.5 months came with abdominal

pain, vomiting, blood in stools following an
episode of upper respiratory tract infection.
Page 11
Operative surgical specimen of male

infant aged 2 days who had abdominal
distension & did not pass meconium after
birth.
An incidental surgical
finding in a man aged
78.
A man aged 72 presented 2 months

before death with epigastric pain, weight
loss and jaundice. Serum bilirubin was
94 mol/l and serum alkaline phosphatase
650 u/l.
Page 12
A 66 year old woman came with c/o

abdominal pain, significant weight loss & &
recurrent episodes of localized thrombosis of
the superficial veins in the limbs.
Page 13
Demonstration pots
An incidental autopsy finding.
Small gut of an adult who had

tuberculous infection presented
with abdominal pain, vomiting &
blood in stools.
Ileum of a neonate who did not pass

meconium after birth and was born with
an APGAR score of 8.
1
2

Page 14
Surgical specimen of ileum

from a man who presented with
intestinal obstruction.
Small gut from a man who was diagnosed to have

celiac disease many years ago was admitted with
abdominal pain & intestinal obstruction.
A 74-year-old man presented with an episode

of lower gastrointestinal (GI) bleeding and
progressively worsening anemia. His past
medical history includes surgical resection of
two separate cutaneous lesions on his back.
Surgical peritoneal specimen from a man who came

with an acute abdomen and on laparotomy was found
to have “jelly-belly” & a perforated appendix.
Page 15
A 60 year old chronic alcoholic

presented with sudden onset of
severe abdominal pain that radiated
to back.
A 70 year old chronic smoker c/o

weight loss, malaise, abdominal
pain & recurrent episodes of
localized thrombosis of the
superficial veins in the limbs and
trunk.
Page 16
Demonstration pots
An incidental autopsy finding in a

man aged 82.
Operative surgical specimen of male infant

aged 2 days who had abdominal distension
& did not pass meconium after birth.
A 67-year-old woman presented with

an episode of lower gastrointestinal (GI)
bleeding and progressively worsening
anemia. Her past medical history
includes surgical resection of two
separate cutaneous lesions on his
back.
A male aged 3.5 months came with

abdominal pain, bilious vomiting, red
currant jelly stools following an episode
of upper respiratory tract infection.
Page 17
Operative surgical specimen of a male

aged 21 years who presented with pain
in right iliac fossa.
Operative surgical specimen of

terminal ileum from a 43 year old
man causing small gut obstruction.
He also had hepatomegaly, diarrhea,
and flushing.
A 66 year old woman who was a chronic

smoker came with c/o abdominal pain,
significant weight loss & recurrent
episodes of localized thrombosis of the
superficial veins in the limbs.
Page 18
A 60 year old chronic

alcoholic presented with
sudden onset of severe
abdominal pain that radiated
to back.
2013 Case Study Questions
CASE 1
a) A 75 year old man presented with an ulcerated lesion on his leg, which he said had been present for
several months but now had increased in size and was bleeding. The lesion was surgically removed.
Specimen No. 1
Describe the lesion
What would be your differential diagnosis?
A representative section is shown (slide 288), list the features seen.
What would your diagnosis be now?
b) A 35 year old woman presents with a mole on her shoulder which has recently increased in size and
started to bleed. On examination there is a pigmented inflamed nodular lesion (diameter 1.2cm) with
irregular borders and two satellite nodules. The GP has taken a diagnostic incisional biopsy under local
anaesthetic for histology. Do you agree with the management so far?
The slide (308) is a representative section of the lesion, describe what you see.
What is the diagnosis?
From a prognostic point of view what are the important histological features?
She returns after 3 months with black urine, jaundice and convulsions. Admission to hospital is
arranged but she has a cardiac arrhythmia and a fatal cardiac arrest. An autopsy is done. How does the
findings in the brain (specimen no. 2) explain the signs and symptoms described?
CASE 2
Name the two types of bone marrow?
Specimen No. 3
What condition is caused by this lesion?

Would the calcium level be increased or decreased?
Explain the mechanism.
What other clinical manifestations may this disease present with?
A 20 year old patient presents with fatigue, loss of weight and vague abdominal pains. On examination
he is noted to be pale. These are his blood results:
Haemoglobin (g/dL) 7.0 (14-18)

Erythrocytes (x10 perL) 2.2 (4.6-6)
Haematocrit 21 (42-50)
MCV (fL) 130 (80-95)
MCHC (%) 34 (32-35)
Reticulocytes (x10 perL) 41 (20-70)
Comment
A biopsy is taken from his ileum. The following slide (274) is from this biopsy. What abnormalities
are seen?
How can we connect the biopsy findings with the blood results?
Would a peripheral blood film have helped?

CASE 3
Note: More than one answer may be correct.
The germinal centre of a lymph node:
A. Contains mainly T-lymphocytes. -

B. Contains dendritic reticulum cells. -
C. Contains cords and sinuses. -
D. Generates immunoglobulin-producing plasma cells. -
E. Is enlarged in a reactive lymph node. -
Hodgkins disease
A. Histologically characterized by the Reed-Sternberg cell. -

B. May be staged using the Ann Arbor system. -
C. Usually presents with painful lymphadenopathy. -
D. May be associated with eosinophillia. -
E. Associated with Askanazy cells. -
Burkitt’s lymphoma
A. Runs a prolonged couses if untreated. -

B. Is a tumour of T-lymphocytes. -
C. Is associated with the Ebstein-Barr virus. -
D. Has a geographical distributions which is similar to that of falciparum malaria. -
E. Rarely affects the jaw. -
Specimen No. 4
This is a specimen from a 25 year old patient who is HIV positive.

What is the likely diagnosis?
Would this be of T or B cell origin?
How aggressive is this disease likely to be?
What are B symptoms and is this patient likely to be suffering from them?
CASE 4
A 70 year old man presents to the ER with shortness of breath and feeling faint. He gives a history of
chest pain for the past few days, which he thought was indigestion. He is a known hypertensive and
smokes 10-15 cigarettes per day. On examination he has a rapid weak pulse and muted heart sounds.
Unfortunately before any further tests he dies.
A post mortem is done.
Specimen No. 5 -
Describe the pathological events that led to this outcome.
Slide # 310 is a section of myocardium, what are the pathological features seen?
How old is this infarct?
Name the two patterns of infarction which one is more common?
What determines the extent of the infarct?
If this was due to atheroma what are the sequence of events leading to occlusion of the vessel?
What is reperfusion injury and why does it occur?
List 4 complications of myocardial infarction.

CASE 5
A 27 year old female patient presents to her GP one week after a tooth extraction. She complains that
she feels tired and has been having recurrent fevers. On examination she is febrile, peripheral oedema
and her pulse is rapid and thready. On auscultation to the heart a mitral stenosis murmur is heard. She
is immediately sent to the ER.
Further history taking reveals that she had rheumatic fever as a child.
Urgent investigations are carried out including a chest Xray. Unfortunately she passes away soon after
these are taken.
Describe the slide #161, specimen No. 6 and chest Xray. Outline the disease mechanisms that have
occurred starting with the illness as a child.
• Slide #161 –
• Specimen No. 6 –
• X-ray -
What is the most common organism involved in this disease process?
The other group of valve vegetations are noninfected. Non-bacterial endocarditis falls into this
category, what is your understanding of this entity and give an example of when it may occur.
CASE 6
A 78 year old man was admitted to hospital with fever, malaise and shortness of breath. A history of
chronic alcohol abuse was noted. On examination he was pyrexial, dehydrated and had dullness in the
right upper chest on percussion. Auscultation of the chest revealed diminished breath sounds on the
rights side and a pleural friction rub. Describe the Xray findings.
What factors may have contributed to this.
Slide 105 corresponds with this condition. Comment on the appearance and stage of inflammatory
response.
List three possible complications.
Describe Specimen Nos. 7 and 8
What are the likely diagnoses? Describe the classical histological appearance of this disease.
Name the organism involved. Outline the pathways and spectrum of tuberculosis from primary to
miliary tuberculosis.
CASE 7
Describe the lesion seen in this X-ray (A). What is the most likely diagnosis and what would be the
histological appearance be?
Describe the lesion seen in Xray B and lesion seen in the specimen no. 9
What is the most likely diagnosis and why?
Describe the possible neurological complications.
Define paraneoplastic syndrome. List three that may occur in lung cancers.
CASE 8
A 68 year old male visits his GP complaining of indigestion. On examination he has epigastric
tenderness. The doctor suspects that the patient has a peptic ulcer and prescribes cimetidine and
advises the patient to stop smoking. Two weeks later the patient has an episode of haematemesis and is
admitted to hospital. His pulse on admission is 108/min and BP 100/65. What could the possible
causes of the haematemesis be?
Other findings on examination were ascites, spider naevi and mild gynaecomastia. What is the likely
explanation of the haemetemesis?
What pathological processes are responsible for the ascites, varices, spider naevi and gynaecomastia?
His condition stabilizes and a liver biopsy is suggested. What should be checked first?
Slide 112 is from the biopsy. Describe the features seen and do these findings suggest a cause.
Specimen no. 10 is demonstrative of one of the complications of this disease, describe the lesion seen
and suggest the likely diagnosis.
CASE 9
Draw and label a representative diagram of the features seen in slide 108. Is this likely to be acute or
chronic and why?
What organism is often implicated in this condition?
How do you determine whether to call a lesion an erosion or ulcer?
When do Curling and Cushing ulcers occur?
List two complications of peptic ulcer disease.
Describe the lesion seen in this specimen no. 11. What name is given to this lesion.
How do gastric adenocarcinomas spread and what is a Krukenberg tumour?

CASE 10
What condition is illustrated by slide 205?
Why is it important to diagnose this condition
Diagnose the condition illustrated by specimen no. 12.
Give a definition that describes the lesion.
What two factors are important in the pathogenesis of this condition?
Note: More than one answer may be correct.

The following are bacterial causes of intestinal infection:
A. Giardia lamblia –
B. Balantidium coli -
C. Schistosoma mansoni -
D. Escherichia coli -
E. Histoplasma capsulatum -
Hirschsprung’s disease:
A. usually affects the right side of the colon -
B. is caused by failure of migration of neural crest cells -
C. is not associated with meconium ileus -
D. the abnormality is in the dilated portion of bowel -
E. may cause constipation –
The following polyps in the large bowel are precancerous:

A. tubular adenoma -
B. inflammatory polyp -
C. metaplastic polyp -
D. lymphoid polyposis -
E. villous adenoma -

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1. WHAT AM I LOOKING AT?

2. LOOK FOR NORMAL TISSUE AND ADJACENT ABNORMAL TISSUE

3. DESCRIBE THE ABNORMALITIES IN TERMS OF FORM, TEXTURE AND COLOUR

4. LOOK AT ALL PARTS OF THE SPECIMEN

IN ALL CASES CONSIDER THE FOLLOWING POINTS:

Integrated Pathology Learning Centre 8.03.2013

Understand lymphoma, common types

Histology review – lymph node (histology and function)

Normal lymph node

Leukaemia – To be discussed in next tutorial

WHO classification of lymphoma

B cell ) further classified

Reproduced from Robbins

Diagnosis of lymphoma requires histology.

80-85% of lymphomas are of B cell origin

Immunohistochemistry – B and T cell markers

Lymph node stained with B

Neonatal thymus showing the

Abdominal swelling from M/61 yrs

Abdominal mass F/55 yrs

Abdominal mass M/46yrs

49 yrs/M with chronic valvular heart disease. Spleen

Incidental finding in the intestine M/44yrs

Mediastinal organ (Normal) from baby 6 weeks old

Small intestine & Mesentery mass

46 yrs/M with Abdominal pain & shoulder pain 6 days

Patient with cirrhosis. Removed spleen

33 yrs/M with Splenomegaly (Storage disease)

Small intestine & Mesentery mass

Lesion in the spleen.

69 yrs/F axillary swelling.

Normal spleen from an adult woman.

M/75 yrs, Mediastinal mass.

Types of Marrow: Yellow (inactive)

Ways to examine bone marrow – aspirate, trephine

Normal bone marrow trephine

What can happen in to marrow : aplasia

Aetiology– idiopathic, drugs, chemicals, irradiation and viruses

Bone Marrow: aplastic

Space occupying lesions:

Common features of myeloproliferative disorders:

Most common plama cell neoplasm.

(Left)Spine from a man aged 62

Skull from a woman

Metabolic bone diseases

Affects entire skeleton.

Main conditions hyperparathyroidism, rickets, osteomalacia and osteoporosis.

Hyperparathyroidism - primary, secondary and tertiary

Increased porosity of the skeleton, due to decrease in bone mass.

Primary - senile, post-menopausal, idiopathic

↓active vitamin D ↓calcium

PATHOLOGY OF BONE MARROW/METABOLIC BONE DISEASE

Dissection of the neck (patient died of chronic renal

Femur from a patient with parathyroid adenoma.

Lesion in the spine

58 yrs /M with anaemia and raised

Rib lesion 41yrs/F with a parathyroid adenoma. Serum

Spleen from 77 yrs/M. It weighed 850g. The

PATHOLOGY OF BONE MARROW/METABOLIC BONE DISEASE

femoral marrow in a woman with iron deficiency

Bones from a 58 yrs/M. The patient

Spine 62 yrs/F 15 month history of bone pain.

The following conditions will be discussed if there is time