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MS3 - general > Histopathology > Flashcards

Histopathology Flashcards

1
Q

Difference between aetiology and pathogenesis?

A

Cause vs mechanism

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2
Q

Types of biopsy?

A
  1. core/needle: for deep organ lesions eg breast/liver, etc
  2. punch: for superficial organ lesions (smaller needle)
  3. incisional (wedges): if ulcerated, you want to have a look at central parts as well as the peripheral parts
  4. excisional: if small enough
  5. removal of entire organ (esp in sarcoma)
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3
Q

3 Stages of histopathology?

How long does the process take?

A
  1. Biopsy
  2. Fixation
    - preserve the structures in 10% formalin (can last for years)
    - this denatures the proteins but maintains morphology
  3. Processing
    - section cutting
    - staining
    - mounting
    - etc
  • minimum 7 days
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4
Q

2 cytopathology techniques?

Advantages vs disadvantages?

A
  1. FNAC:
    - fine needle aspiration cytology
  2. Exofoliative cytology (sample attained by rubbing or shedding of the cells):
    I. cervical
    II. Non-cervical
    - urine
    - sputum, BAL (broncho-alveolar lavage) and brushing
    - Bile duct
    - Serous fluid

Adv:
- quick (min 10 min) and low cost (£5 per sample vs 125 histopathology biopsy analysis)
Disadv:
- cant differentiate between in-situ and invasive malignancy

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5
Q

4 Benign disorders of liver?

A
  1. Haemangioma
    - vascular tomour
  2. Liver cell adenoma
    - more in women (ass with oral contraceptives)
    - some may become malignant
  3. Bile duct malformation
  4. Focal nodular hyperplasia
    - central scar
    - more in women
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6
Q

3 Malignant disorders of liver?

A
  1. Hepatocellular carcinoma
  2. Angiosarcoma
  3. Cholangiocarcinoma
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7
Q

Hepatocellular carcinoma (HCC)

  1. epi
  2. causes 3
  3. a specific type
  4. how to distinguish on histology slide?
A
  1. more in men
    • cirrhosis
    • Hep B/C
    • autoimmune hepatitis/chronic biliary disease
  3. Fibrolammelar HCC
    - affects younger ppl
    - no background of cirrhosis
    - histology: blue fibrotic tissue
  4. Bile within the duct
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8
Q

Liver Angiosarcoma

  1. def
  2. causes 4
  3. epi
A
  1. connective tissue tumour affecting liver
  2. arsenic, thorotrolast, steroids, vinyl chloride
  3. more in old men
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9
Q

Cholangiocarcinoma

  1. def
  2. ass with?
A
  1. cancer of epithelial cells of bile duct

2. chronic inflammation of bile duct (PSC,PBC)

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10
Q

Viral hepatitis

I. Hep A

  1. transmission
  2. Sx

II. Hep B

  1. transmission
  2. Sx

III. Hep C

  1. transmission
  2. Sx

IV. Delta virus

  1. transmission
  2. Sx

V. Hep E

  1. transmission
  2. Sx
  3. More severe in?
A

I. Hep A

  1. faeco-ral
  2. can be mild or can lead to liver failure

II. Hep B

  1. body fluid
  2. can lead to cirrhosis and HCC

III. Hep C

  1. blood
  2. can lead to cirrhosis and HCC

IV. Delta virus

  1. super/co infection with hep B
  2. can lead to fulminant hepatitis (acute liver failure and encephalopathy)

V. Hep E

  1. Food/water
  2. Acute/fulminant
  3. pregnant/children
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11
Q

(non) alcoholic fatty liver disease causes?

A
  • alcohol
  • obesity
  • diabetes
  • drugs
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12
Q

Autoimmune hepatitis

  1. Ix? 3
  2. Sx
  3. Mx
A
    • High alanine aminotransferase(ALT),
    • High IgG
    • ANA positive
  2. can lead to cirrhosis and HCC
  3. Steroids/immunosuppression
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13
Q

Chronic biliary disease

I. Primary sclerosing cholangitis (PSC)

  1. def
  2. Ix
  3. epi

II. Primary biliary cirrhosis

  1. def
  2. Ix
  3. epi
A

I. Primary sclerosing cholangitis (PSC)

  1. autoimmune affects large bile ducts
    • AMA -ive
    • maybe p-ANCA +ive
  3. young middle age men

II. Primary biliary cirrhosis

  1. autoimmune affects small bile ducts
    • AMA -ive
    • IgM +ive
    • High alkaline phosphatase
  3. middle age men
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14
Q

Inherited disorders of liver

I. Wilson’s disease

  1. def
  2. Sx
  3. Genetics

II. Haemochromatosis

  1. def
  2. Sx
  3. Genetics

III. Alpha-1 antityripsin deficiency

  1. def
  2. Sx
  3. Genetics
A

I. Wilson’s disease

  1. abnormal storage of copper in liver (iris, etc)
  2. liver failure
  3. autosomal recessive, chromosme 13

II. Haemochromatosis

  1. increased iron absorption/storage in liver
  2. cirrhosis/HCC
  3. autosomal recessive, chromosme 6, HFE gene

III. Alpha-1 antityripsin deficiency

  1. abnormal protein accumulation in liver
  2. fibrosis-> cirrhosis –> HCC
  3. chromosme 14
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15
Q

Main problem/pathology of Cirrhosis

A
  1. Recurrent damage/ regeneration of hepatocytes around the blood vessels
  2. Leads to scarring (fibrosis) around the vessel, and increased cellular thickness (up to 40 instead of max 2 layers of cells around vessel)
  3. Hepatocytes cant take part in exchange with blood (too far away from it): blood passes through liver like it would through a shunt, nothing changes in terms of its content
  4. can lead to necrosis or further regeneration
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16
Q

3 centres of immune system?

A
  1. primary
    - bone marrow and thymus
  2. secondary
    - lymphoid follicles and T zone, spleen, GI
  3. Tertiary
    - genital tract, skin
    - T cells patrol the surfaces
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17
Q

Various blood cell development from stem cells?

A

Stem cell–> Myeloid and lymphoid stem cells

I. Myeloid Pathway

Myeloid stem cell to

  1. Red blood cells
  2. Platelets
  3. Myeloblasts –> granulocytes (eosoniphil, neutrophil, basophil)

II. Lymphoid pathway

Lymphoid stem cell--> lymphoblast 
Lymphoblast to 
1. B-cells
2. T-cells
3. Natural killer cells
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18
Q

For each state the place for formation and maturation:

  1. B cell
  2. T cell
A
  1. formed and matured in bone marrow

2. formed in bone marrow, matures in thymuus

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19
Q

B lymphoid follicles

  1. 3 layers?
  2. process of activation of naive mature B cells?
A 
1. 
I. germinal cell:
- B-cells get activated here
II. Mantle zone:
- naive B-cells reside, ready to enter germinal centre
III. Marginal zone
- memory B cells reside here

2.
I. naive cells are presented antigens by antigen presenting cells (eg T cell or dendritic cells)
II. They enter the dark zone of germinal centre, and undergo somatic hyper mutation (SHM), presenting different immunoglobulins on their surface (become centroblasts)
III. The defective ones are selected against and undergo apoptosis, others differentiate into either:
- Memory B-cells: resides in marginal zone
- Plasma cells: produce antibodies against that antigen

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20
Q

Mucosa associated lymphoid tissue (MALT)

  1. def
  2. Describe the series of events happening when an antigen is presented to gut?
A
  1. it is a site for local immunity, has a well developed marginal zone

2.
I. M-cells on the epithelium uptake the antigen
II. dendritic cells pick that up and present it to T-cells
III. T-cells activate B-cells
IV. B cells migrate to mesentric lymph node
V. plasma cells go back to the tissue through endothelial venules and secrete IgA

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21
Q

Difference between leukaemia and lymphoma?

A

Leukaemia:
- tumour more in blood/bone marrow than lymph nodes
Lymphoma:
- tumour more in lymph nodes than blood/bone marrow

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22
Q

Grade vs stage of a tumour?

A

Grade:

  • describes appearance under microscope
  • Low: slow growth rate, difficult to cure, resembles the local architecture
  • High: fast growth rate, easier to cure, does not resemble the local architecture- undifferentiated

Stage:

  • whether it stays in the same place or not
  • 0: in-situ
  • stage 4: metastasis
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23
Q

4 Viruses and their associated lymphomas?

A
  1. Epstein-Barr virus:
    - burkit, hodgkin, post-transplant, AIDs related
  2. HTLV 1:
    - T-cell non-hodgkin lymphoma (NHL)
  3. Human Herpes virus 8
    - aka kaposi sarcoma
    - plasma cell malignancy
  4. Hep C:
    - B-cell NHL
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24
Q

B cell neoplasm classification?

A

I. central

  • B lymphoblastic lymphoma/leukaemia

II. peripheral

a. pre-germinal centre (GC) neoplasm:
- mantle cell lymphoma
b. GC neoplasm:
- follicular lymphoma
- hodgkin lymphoma
- Burkit lymphoma
c. Post-GC:
- marginal zone & MALT lymphoma
- lymphoplasmocytic lymphoma
- plasma cell myeloma

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25
Q

T cell neoplasm classification?

A

I. T-lymphoblastic lymphoma/leukaemia

II. Peripheral (mature) T cell/ natural killer cell lymphoma/leukaemia

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26
Q

T cell pathway of maturation?

A

Stage 1:
Immature T cells –>
a. Natural killer cell
b. Subcapsular cortical thymocyte (in thymus)

Stage2:
Subcapsular cortical thymocyte (in thymus):
I. γδ T-cell
II. αβ T-cell

Stage 3:
αβ T-cell –> naive medullary thymocytes:
1. CD4+ –antigen–> T-blast –> Effector or memory T cell
2. CD8+ –antigen–> T-blast –> Effector or memory T cell

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27
Q

Difference between CD4 and CD8 T-cell?

A

CD4:
- responds to MHC-II (found on antigen presenting cells such as dendritic cells)
- help B-cells produce antibodies
CD8:
- responds to MHC-I (found on all cells, presenting normal cell proteins)
- kills the foreign cell

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28
Q

Hodgkin lymphoma

  1. def
  2. epi
  3. ass with which virus?
  4. what cells seen under microscope?
  5. malignant cells aka?
  6. 3 features of malignant cells under microscope?
A
  1. nodal enlargement + B symptoms
  2. bimodal: very young and very old
  3. ass with EBV in 35%
  4. 1-5% malignant cells with the rest being inflammatory infiltrates
  5. Reed sternberg
  6. large atypical, binucleated cells with prominent red nucleolus
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29
Q

Diagnostic tools for lymphomas?

A
  1. morphology
  2. Immunohistochemistry
    - fixed dead tissue
    - chi 67 dye stains proliferating cells
    - CD20 dye stains B-cells
  3. Flow cytometry
    - live cells put through machine
    - antigens added adn shaun a lazer at them
    - protein expression of different lymphomas differentiated
  4. PCR
    - see if colonal or polycolonal by comparing length of the fragments
  5. FISH (fluorescent in-situ hybridisation)
    - fluorescent probes inserted either end of gene
    - if expressed in different places separately, mean translocated differently (suggestive of some lymphomas with MIC oncogenic)
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30
Q

Which areas of heart are supplied by the following?

  1. Left anterior descending
  2. left circumflex
  3. right coronary artery
A
  1. apex
    anterior wall of L ventricle
    2/3 ventricular septum
  2. lateral wall of L ventricle
  3. posterior 1/3 of ventricular septum
    R ventricle
    posterior-basal wall of L ventricle
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31
Q

Transmural vs subendocardial MI?

A

Transmural:

  • necrosis involves (nearly) full thickness of ventricular wall
  • limited to a single coronary area of supply

Subendocardial:

  • limited to inner 1/3
  • can extend beyond areas of supply of 1 artery
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32
Q

Lab tests for MI?

A
  1. Troponin T and I
  2. lactate dehyrdogenase
  3. creatine kinase MB isoenzyme
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33
Q

Valvular disease

I. degenerative

  1. name 3 types?
  2. what do they increase the risk of?
  3. what condition ass with one of them?

II. rheumatic related

  1. def
  2. pathogen
  3. main complication
  4. chronic effect on valve?
A

I.
- calcification of aortic valve (due to wear and tear)

  • calcification of mitral valve: increases the risk of IE, PE, and DVT
  • myoxomatous degeneration of mitral valve (mitral valve prolapse) : this is ass with Marfans syndrome

II.
1. acute, systemic autoimmune inflammatro disoreder

  1. a few weeks post group A (β-haemolytic) streptococal pharyngitis
  2. inflammatory deformity of valve (esp mitral)
    • leaflet thickening
    • commisure fusion
    • shortening, thickening, and fusion of chordae tendinae
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34
Q

Hashimato’s thyroiditis

  1. def
  2. F:M
  3. Sx
A
  1. hypothyroidism, autoimune, antithyroid antibodies, lymphocytic destruction of thyroid gland
  2. F:M 10:1
3.
Myxoedema : slowing of mind and body
 Weight gain, constipation
 Cold intolerance
 Tiredness, depression
 Big tongue, deep voice (deposition of matrix substances in viscera and skin)
 Thin hair
 Weak heartbeat
 Slow reflexes
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35
Q

4 causes of hyperthyroidism?

A 
 Graves’ disease: 85% of cases
 Hyperfunctional multinodular goitre
(MNG is usually euthyroid)
 Hyperfunctional adenoma (benign follicular tumour) - rarely
 carcinoma
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36
Q

Grave’s disease (diffuse toxic goitre)

  1. def
  2. Sx
A
  1. autoimmune thyroid stimulating antibodies

2.

  • symmetrical enlargement of thyroid gland
  • exopthalmus (deposition of connective tissue behind eye lid)
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37
Q

Hyperfunctional multinodular goitre (HMG)

  1. leads to?
  2. Sx?
A
  1. hyperthyroidism
  2. Usually euthyroid (normal function of thyroid gland)
    Large goitre may lad to tracheal compression or dysphagia
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38
Q 
Neoplasms of thyroid gland
I. Follicular adenoma of thyroid
1. what? Sx?
2. Mx?
II. Carcinoma
1. 4 types
2. what are Psammoma bodies 
3. which one causes calcitonin
A

I.

  1. benign euthyroid
  2. Mx; thyroid lobectomy

II.
Papillary:
- most common
- get psammoma (epithelial cells, with pale empty nuclei)
Follicular
Anaplastic:
- elderly prone, aggressive, no response to treatment, fatal
Medullary:
- c-cells of thyroid, secreting calctonin
- amyloid stroma

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39
Q

Ix for thyroid gland hyper/hypothyroidism?

A

 Hyper/Hypothyroidism - thyroid function tests, autoantibodies
 Thyroid enlargement/nodules – ultrasound
 Thyroid nodules:
- FNA cytology
- Excision, if indicated: thyroid lobectomy or total thyroidectomy - for histology

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40
Q

Hyperparathyroidism

I. primary
1. causes

II. Secondary
1. cause

III.Sx?
IV. Ix?

A 
I. 
1.
- Adenoma (1 lobe big, 3 lobes small or normal)
- Hyperplasia (4 lobes big)
 - Carcinoma (very high Ca, >35)

II. chronic renal failure (due to compensation for hypercalaemia

III. high PTH–> hypercalcaemia

IV. 
 Ultrasound +/- Sestamibi scan
 Excision of one or more parathyroid
glands for histology
 Use of intra-operative frozen section – to confirm tissue is parathyroid (not thyroid, lymph node or brown fat)
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41
Q

Sestamibi scan:

A

Uses radioactive technetium-99
Highlights hyperactive P/T glands 1 = tumour
Results variable in
hyperplasia

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42
Q

Primary adrenal insufficiency (addison’s)

  1. causes
  2. cause of Sx?
  3. Sx
  4. cause of hyperpigmentation
  5. acute adrenal crisis?
A 
1. 
MOST COMMON: Autoimmune destruction 
 Tuberculosis
 Removal
 Metastatic cancer
 AIDS (CMV, Mycobacterium, Kaposi’s)  Congenital hypoplasia
  1. Symptoms due to low levels of glucocorticoids and mineralocorticoids
  2.  Weakness, tiredness
     GI disturbance: nausea, vomiting, wt loss,
    diarrhoea
     Hyperpigmentation of skin
     Potassium retention and sodium loss; hypotension
  3. due to pro-opiomelanocortin from pituitary – a precursor of ACTH and melanocyte stimulating hormone
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43
Q

Acute adrenal criss

  1. precipitated by?
  2. leads to?
  3. Mx
A

 Precipitated by infection, trauma, surgical procedures
 Causes vomiting, abdo pain, hypotension, coma
 Rapidly fatal unless treated promptly with corticosteroids

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44
Q

Secondary adrenal insufficiency

  1. causes
  2. mx?
A
  1. Disorders of hypothalamus or pituitary – reduced output of ACTH
  2. Treatment with steroids, long term
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45
Q

Cushing’s syndrome

  1. Sx?
  2. commonest cause?
A
  1.  Central obesity, abdo striae, moon facies
     Thin skin, easy bruising, hypertension
     Glucose intolerance
  2. Most commonly iatrogenic due to glucocorticoid administration
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46
Q

Multiple endocrine neoplasm

  1. def
  2. what type of lesions
  3. types?
A
  1. Genetically inherited diseases: autosomal dominant
    - involves multiple endocrine organs
  2. Proliferative lesions (hyperplasia, adenoma or carcinoma)
  3. Types 1 and 2: 2A, 2B, FMTC (familial medullary thyroid carcinoma- only affects thyroid and nothing else)
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47
Q

MEN 1

  1. how common
  2. mutation
  3. which glands affected
A
  1. 1:35000
  2. MEN1 gene on chromosome 11q13 , is a tumour suppressing gene and mutations leads to hyperplasia
    • parathyroid
    • pituitary
    • pancreas
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48
Q

MEN 2

I. MEN2a
1. how common
2. which glands affected?
II. MEN2b
1. how common 
2. which glands affected?

III. mutations in what?

A

I. MEN2a
1. 1:40000
2. PTH hyperplasia, medullary carcinoma, phaeochromocytoma
II. MEN2b
1. 1:1,000,000
2. PTH hyperplasia, medullary carcinoma, phaeochromocytoma
+
 Marfanoid body habitus in 80%
 Mucosal neuroma in up to 100% (lips, tongue, mouth, bowel)

III. MEN 2A , 2B and FMTC : mutations in RET oncogene, on chromosome 10. Specific mutations in each of the 3 variants

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49
Q

Cyst vs abscess vs empyema

A 
Cyst:
- filled with fluid
- lined with epithelial cells
Abscess:
- filled with pus
- lined with granulation tissue (repaired tissue, includes both new blood vessels and fibroblasts)
Empyema:
- pus collection in a body cavity 
- eg pleural cavity or gall bladder
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50
Q

Granuloma

A
  • localised collection of modified macrophages
  • (central necrosis)
  • represents chronic inflammation
  • causes: TB, sarcoid, leprosy, fungal infection
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51
Q

Pneumonia vs pneumonitis?

A

Pneumonia:
- inflammation + consolidation of bronchus
Pneumonitis:
- just inflammation

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52
Q

Lobar vs bronchopneumonia

  1. age
  2. Sx
  3. pathogen
  4. morphology
  5. prognosis
A
  1. young, healthy vs bimodal (extreme) age distribution; children and elderly
  2. high grade fever, cough, sputum vs either asymptomatic or flu-like sx
  3. strong (eg strepto pneumonia) vs weak (eg influenza and staphyl)
  4. both alveoli filled with neutrophilic exudate, but affecting different parts
  5. good (healthy individuals) vs poor
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53
Q

Complications of pneumonia

A
  1. Abscess formation (Type 3 pneumococci
    and klebsiella)
  2. Empyema
  3. Organisation of the exudate with fibrosis
  4. Bacteremic dissemination to other organs
    e.g. heart valves causing metastatic
    abscess.
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54
Q

Pulmonary TB

  1. Pathogens
  2. types
  3. Ix
  4. morphology
  5. Tx
  6. disinfection
A
  1. Caused by M Tuberculosis
    •Mycobacterium T Hominis: typical: human-human spread
    •Mycobacterium T Bovis: atypical: cattle to human (rare due to pasteuriasation of milk)
  2. I. primary: acute inflammation–>neutrophils cant destroy–>macrophages phagocytose–> chronic–> granuloma
    II. secondary: re-entry or immunosuppression leads to recurrence
    III. Miliary
    - can be both primary or secondary
    - very weak immune system, multiple colony formation in lungs or elsewhere
  3. I. Acid-fast bacili (AFB) staining and culture
    II. heaf test
    III. Raised ESR
  4. multinucleated giant cells, granuloma, collection of modified macrophages
  5. combination abx for at least 6 months
  6. UV light (not responsive to heat or disinfectants)
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55
Q

What type of white blood cell seen in :

  1. acute inflammation
  2. chronic inflammation
A
  1. neutrophils

2. mononuclear cells

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56
Q

Bronchogenic carcinoma

  1. 5 year survival
  2. Rfs
  3. classification
  4. Sx
A
  1. Overall 5 year survival rate is 4 – 7%.
    • smoking
    • asbestos
    • radiation
    • oncogenes (c-myc: small cell carcinoma, K-ras: adenocarcinoma)
3. 
I. Squamous cell carcinoma
II. Adenocarcinoma
III. Bronchioloalveolar carcinoma
IV. Large cell undifferentiated carcinoma
V. Neuroendocrine tumours
- Carcinoid
- Atypical carcinoid
- Small cell carcinoma
- Large cell neuroendocrine carcinoma
  1. •Weight loss, cough and haemoptysis
    • metastasis and common to sites include lymph node, bone, brain, liver and
    adrenals.
    • Paraneoplastic effects are common and are due to ectopic hormones.
    - ACTH and ADH from small cell carcinoma
    - PTH from squamous cell carcinoma
    • Finger-clubbing and hypertrophic pulmonary
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57
Q

Pleura pathologies

A 
• PLEURITIS (pleurisy)
• PNEUMOTHORAX
• EFFUSIONS
- HYDRO-THORAX
- HEMO-THORAX
- CHYLO-THORAX ( It results from lymph formed in the digestive system called chyle accumulating in the pleural cavity due to either disruption or obstruction of the thoracic duct)
• MESOTHELIOMAS
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58
Q

Acid fast bacili (AFB) staining and culture?

A

Staining:

  • Initially, Carbol Fuchsin stains every cell.
  • When they are destained with acid-alcohol, only non-acid-fast bacteria get destained since they do not have a thick, waxy lipid layer like acid-fast bacteria.
  • When counter stain is applied, non-acid-fast bacteria pick it up and become blue when viewed under the microscope.
  • Acid-fast bacteria retain Carbol Fuchsin so they appear red.

Culture:
takes 4-5 weeks to grow

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59
Q

Anatomy of breast tissue

2 cell layers of ductal-lobular sytem

A
  • Histologically breast consist of glandular
    (parenchymal) and supporting (connective) tissue.
  • Glandular element is divided into branching duct system and terminal duct lobular units (TDLU).
  • The TDLU is formed by the lobule and terminal ductule and represents the secretory portion of the gland.
  • The TDLU connects with the subsegmental duct, which in turn leads to a
    segmental duct and this to a
    collecting/lactiferous duct which
    empties into the nipple

The entire ductal-lobular system of the breast is lined by two cell types.

  • the inner epithelial cells
  • the outer myoepithelial cells
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60
Q

Myoepithelisl cells markers

A

SMM,
p63
ck5/6

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61
Q

Diseases of Breast Classification

A 
I. INFLAMMATORY
• Acute mastitis
• Chronic mastitis
• Mammary duct ectasia (dilation)
• Fat necrosis
II. PROLIFERATIVE
• Fibrocystic change
• Radial Scar
III. NEOPLASTIC
---Benign
• Adenoma
• Fibroadenoma
• Papilloma
---Malignant
• Carcinoma
• Sarcoma
• Paget’s disease
• Phylloides tumour
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62
Q

Breast Lumps

I. diffuse
II. discrete
III. Mobile
IV. Tethered

A 
I. Diffuse Fibrosis/fibrocystic change
II. Discrete Neoplasm/ cyst / abscess /
hamartoma
III. Mobile Benign neoplasm
IV. Tethered Carcinoma
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63
Q

Interpretation of nipple sx
I. discharge
II. retraction
III. erythema

A 
NIPPLE
I. Discharge
•Milky: Pregnancy
•Bloody: duct papilloma /
carcinoma
II. Retraction: Invasive carcinoma
III. Erythema: Pagets disease or eczema
& scaling
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64
Q

Fibrocytic changes in breast tissue

  1. pathogenesis
  2. age
  3. microscopic changes?
A
  1. cycle->E2 secretion->proliferation of breast epithelium->keep getting bigger->burst->inflammation->fibrocytic change
  2. Common in 25 - 45 yrs age group
3. Microscopic picture
• cysts
• fibrosis
• Apocrine metaplasia (change of 1 cell to another)
• epithelial hyperplasia 
• calcification
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65
Q

Fibroadenoma

  1. age
  2. size changes with pregnancy or age?
  3. types of cells involved
  4. malignant or benign
  5. Mx
A
  1. B/W the ages of 20-35yrs
  2. Increases in size during pregnancy, Decrease in size with age
  3. composed of both proliferating ducts and connective tissue stroma.
  4. benign
  5. nothing
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66
Q

Phylloides tumour

  1. age
  2. types of cells
  3. malignant or benign
  4. which component is malignant?
  5. Mx
A 
1. Usually occurs in 4th and 5th decade
of life.
2. M/s it is composed of epithelial and
mesenchymal elements
3. either
4. the mesenchymal component 
5. Treatment is wide local excision.
67
Q

Risk factors for breast carcinoma?

A
  1. Female sex and age
  2. reproductive history
    • early menarche
    • late menopause
    • nulliparous women
    • 1st pregnancy after 30yrs of age
  3. obesity
  4. family history in 1st degree relative
    • 1.5-2x if 1 relative
    • 4-6x if two affected relatives
  5. geography
  6. atypical hyperplasia
68
Q

Genes ass with breast carcinoma

A
  • BRCA 1, ch 17, ovary and breast

* BRCA 2, ch 13

69
Q

Breast carcinoma classification

A 
1. Insitu carcinoma
•Ductal carcinoma in situ
- - mx: excision
•Lobular carcinoma in situ
- - mx: bilateral mastectomy
- - may get invasive
2. Invasive carcinoma
•Invasive ductal carcinoma NST (75-85%)
•Invasive lobular carcinoma (10%)
- - multifocal 
- - MRI needed
- - recurrance after 15 yr
•Others (5%)
70
Q

Breast screening program

A

• All women aged between 50-64 years
(now up to 69 years) are invited for mammographic examination.
•Every three years

71
Q

Complications of reflux oesophagitis?

A

STRICTURE
BARRETT’S
NEOPLASIA

72
Q

Achalasia

  1. aetiology
  2. pathogenesis
  3. long term complication
A
  1. autoimmune?
    • inflammatory destruction of myenteric ganglion cells (regulate peristalsis)
    • lower oseophagus sphincter doesnt close
  3. squamous cell carcinoma
73
Q

Infection of oesophagus

  1. 3 pathogens
  2. chagas disease
    I. pathogen
    II. transmission
A
    • candida
    • herpes simplex virus
    • trypanosomiasis
  2. I. Trypanosoma cruzi
    II. Transmitted in faeces of ‘blood sucking’ reduviid bug – via its bite.
74
Q

Barret’s metaplasia

  1. def
  2. aetiology
  3. Barrets segment
A
  1. Metaplastic replacement of oesophageal lining (stratified squamous) by glandular mucosa
  2. Reflux of gastric (acid) and duodenal (bile) contents into the oesophagus
  3. segment between squamous columnar junction (SCJ) and gastro-oesophageal junction (GOJ)
75
Q

Oesophageal neoplasia

A
  1. Squamous cell carcinoma
    - 20%
    - M:F = 3:1
    - lower > upper > middle
    - China, Japan, Iran, South Africa
    - prognosis poor: DXT +/- surgery
  2. Adenocarcinoma
    - 80%
    - prognosis good only if early
  3. Other neoplasms are rare:
    - Mesenchymal neoplasms (e.g. leiomyoma)
    - Lymphoma
76
Q

TNM staging?

A

T (tumour): Depth of invasion through
oesophageal wall

((((T1: Tumour invades submucosa
T2: Tumour invades muscularis propria
T3: Tumour invades through the muscularis propria into the
subserosa, or into the pericolic or perirectal tissues
T4: Tumour directly invades other organs or structures,
and/or perforates visceral peritoneum
))))

N (nodes): Involvement of lymph nodes by
carcinoma
(((
N0: No regional lymph node metastasis
N1: Metastasis in 1 to 3 regional lymph nodes
N2: Metastasis in 4 or more regional lymph nodes
)))

M (metastases): Presence of metastases
(((
M0: No distant metastasis
M1: Distant metastasis present
)))
77
Q

Sequence of events leading to adenocarcinoma of oesophagus?

A

normal squamous –> Barret’s (columnar) –> dysplasia –> adenocarcinoma

78
Q 
ABC classification of gastritis
For each, mention:
I. type
II. cause
III. synonyms 
IV. pathology
A 
A
I. for auto-immune
(or atrophic)
II. auto-immune 
III. Chronic atrophic gastritis
IV. Chronic atrophic gastritis with IM
B
I. for bacterial
II. bacterial 
III. Chronic superficial gastritis
IV. Chronic active gastritis
C
I. for chemical
II. Chemical, bile reflux, drugs
III. Reflux gastritis, reactive gastritis
IV. 
Foveolar hyperplasia,
oedema,
telangiectasia 
lack of inflammatory cells
79
Q

Helicobactor pylori?

  1. Diseases caused by it?
  2. pathogenesis
  3. direction of HP progress?
  4. how does it lead to carcinoma?
A

1.
• GASTRITIS
• ULCER
• MALT lymphoma (mucosa associated lymphoid tissue)
• CARCINOMA
2. normal lumen pH=2, foveal cell produce mucous pH= 7, attaches there and causes inflammation
3. moves proximally, starts in antrum, moves towards gastric body
4.
superficial gastritis -> atrophic gastritis ->intestinal metaplasia -> dysplasia -> carcinoma

80
Q

Treatment of MALT

A

Eradication of HP with proton pump inhibitor,

antibiotics +/- bismuth

81
Q

4 types of Gastric Neoplasia

A

Adenocarcinoma
Lymphoma
Neuro-endocrine tumour (including ‘carcinoid’)
GIST (gastrointestinal stromal tumour)

82
Q

Adenocarcinoma of the stomach

  1. M:F
  2. RFs?
  3. prognosis
A 
1. M:F = 3:1
2.
- diet (high salt, low diary products)
- Helicobacter
- intestinal metaplasia
  1. Poor prognosis if advanced (<20% 5 yr survival)
    Good prognosis if early gastric cancer (90% 5 yr surv)
83
Q

GIST (gastrointestinal stromal tumour)

  1. mutation in?
  2. Mx?
A
  1. Mutations in tyrosine kinase genes (KIT)
  2. Surgery
    +/- TKI inhibitors (e.g. imatinib)
84
Q

Coeliac disease

  1. cause
  2. Mx
  3. Histological changes
A 
Malabsorption (e.g. anaemia, low
albumin)
1. Auto-immune disease with an abnormal
immunological reaction to gluten
2. Improvement on gluten-free diet
3. 
- Flat mucosa
- Reduction in the normal villous
height to crypt depth ratio from 5:1 to
<3:1
- Crypt hyperplasia
- Increased intraepithelial lymphocytes
- Infiltration of the lamina propria
by plasma cells and lymphocytes
85
Q

GIARDIASIS

  1. pathogen
  2. transmission
  3. more likely in?
A
  1. Giardia lamblia
  2. Contaminated water (person-to-person
    spreading by faecal-oral transmission)
  3. Immunocompromised patients more likely to be infected e.g.AIDS and
    common variable immunodeficiency (Ig
    deficiency).
86
Q

Neuro endocrine tumour (NET)

  1. subtypes
  2. prognosis
A 
1. 
I. carcinoid 
- grade 1, 2
- not curable, but slow progression
II. small cell carcinoma 
- grade 3 
- lethat- poor prognosis
87
Q

Crohn’s disease

  1. age
  2. what is affected
  3. colonoscopy finding?
  4. macroscopic examination
  5. histopathology
  6. complications
  7. Mx
A
  1. Maximal incidence in young adults 15-30
    yrs
  2. Any portion of the GI tract can be affected , involvement of both terminal ileum and caecum in 40-50%
  3. skip lesions
  4. I. Involved bowel portions and associated
    mesentery thickened and oedematous
    II. Mucosal lesion typically begins as a
    superficial ulcer
    III. As disease advances ulcers enlarge, deepen, giving “cobblestone” appearance
  5. I. Transmural inflammation
    II. Non-necrotising granulomas (40-60%)
    III. Crypt abscesses
    IV. Ulcers may penetrate deeply forming fissures in the muscularis propria, leading to abscess and fistula formation
    V. Healing of these penetrating lesions is
    responsible for fibrosis and stricture formations
    • Inflammatory adhesions,
    • perforation,
    • perirectal
      disease (perianal fistulas and abscesses),
    • malabsorption,
    • small bowel adenocarcinoma
    • 5-Aminosalycilic acid,
    • steroids,
    • immunosuppressive drugs,
    • monoclonal antibodies against TNF-α (Infliximab),
    • surgery
88
Q

Ulcerative colitis

  1. age
  2. histology
  3. complication
  4. Mx
A
  1. bimodal: 20-50, 60-70
    • Crypt abscesses with neutrophils within the crypt, in the crypt wall and in the lamina propria
    • Crypt architectural distortion, with gland
      branching, shortening and loss of the normal parallel arrangement of glands
      3.
    • Toxic megacolon
    • perforation,
    • massive haemorrhage,
    • colon cancer (correlation with colonic involvement and duration of disease)
    • 5-ASA,
    • steroids,
    • immunosuppressive drugs,
    • surgery
89
Q

Toxic megacolon

  1. sx
  2. cause
  3. complication of?
A 
1.
- High fever
- Tachycardia
- Diarrhoea
2. Paralysis of the motor function of the
transverse colon
3. ulcerative colitis
90
Q

Define:

  1. hyperplasia
  2. hypertrophy
  3. dysplasia
A 
1. increase in cell number by
mitosis
2. increase in cell size without
cell division
3. abnormal growth and differentiation of a
tissue often pre-malignant
91
Q

Colorectal polyps classification?

A 
1. INFLAMMATORY: pseudopolyps,
benign lymphoid polyps
2. HAMARTOMATOUS: juvenile polyp,
Peutz-Jegher
3. NEOPLASTIC: adenoma, adenocarcinoma
4. OTHERS: hyperplastic,
lipoma, leiomyoma
92
Q

INFLAMMATORY PSEUDOPOLYPS

  1. seen in which condition?
  2. macroscopic features?
  3. microscopic features?
A 
•Seen in ulcerative colitis and Crohn’s
disease
•Macroscopically: can look like
adenomas
•Microscopically: inflammatory tissue,
hyperplastic mucosa
93
Q

Hamartoma def

A
  • Benign tumour-like lesion

* Two or more differentiated tissue elements, normally present in the organ

94
Q

Juvenile polyps

  1. what are they
  2. mutation in
  3. age
  4. Sx
A 
1.
Cystic glands with normal or inflamed epithelium
2.
- SMAD4 mutation
(18q21-22) (25-30%)
3. 
•Children mean age 8
4. 
•80% in the rectum
•Clinical manifestations: bleeding
(up to 95%), prolapse
95
Q

Peutz-Jegher polyps (PJP)

  1. Sx
  2. genetics
  3. where in GI?
  4. complication
A 
1. pigmentations of oral mucosa, lips, palms,
genitalia
2. Autosomal dominant
3. 
- Occur throughout the GI tract
- Small bowel more common than
large bowel
4. Intussusception and partial or
complete obstruction
96
Q

Polyps?

  1. def
  2. what cell
  3. benign or malignant?
A
  1. protruding growth
  2. mostly epithelial, some mesenchymal
  3. either
97
Q

Neoplastic polyps

  1. def
  2. adenoma classification
  3. what 3 things make them more likely to be malignant
A
    • dysplastic, disregulated proliferation
    • Failure to fully differentiate, premalignant
  2. •Tubular
    •Tubulovillous
    •Villous
    • Fat/depressed adenoma (ass with familial colon cancer)
  3. •Villosity (25-85% of villous
    adenomas may contain cancer)
    •Size (30% of villous adenomas > 5cm
    may contain cancer)
    •Degree of dysplasia (severe)
98
Q

hyperplastic polyp

A 
Commonest in adults
•Asymptomatic, any age but
increase in 60s and 70s, mostly
rectosigmoid
•< 5 mm, sessile nodule
•Benign, no malignant potential
unless they are mixed (hyperplasticadenomatous
polyps, Serrated
Adenomas)
99
Q

Leimyomatous polyp

  1. where
  2. which part of colon wall affected
  3. sx
A
  1. Rectum, as well as jejunum, ileum
  2. Muscularis mucosae
  3. Symptoms : anaemia, bleeding due to
    ulceration, epigastric pain
100
Q

Colorectal cancer

  1. where more common in men
  2. where more common in women
  3. RFs? 3
  4. Ix?
A
  1. rectum
  2. colon
  3. Westernised lifestyle & diet
    Reduced stool bulk
    Increased fat intake
  4. •Colonoscopy:
    UC
    FAP/HNPCC
    Adenomatous Polyps
    •Faecal occult bloods (false positives)
    •Flexible sigmoidoscopy
    •Genetic testing
101
Q

Familial colorectal cancer syndrome (HNPCC)

  1. genetic
  2. right or left side?
  3. which gene affected?
  4. Amsterdam criteria
A
  1. Dominant
  2. Right sided
  3. abnormalities in 4 mismatch repair
    genes (microsatellite instability)
  4. all criteria must be met
    •Three or more family members with colorectal cancer, at
    least two of which must be first-degree relatives (e.g.
    parent, sibling or child)
    •The disease affects family members from at least two successive generations
    •One of the colorectal cancers must occur prior to age 50
    •Familial Adenomatous Polyposis excluded
102
Q

Familial adenomatous polyposis (FAP)

A 
• Without intervention virtually all
people with this condition will
develop colon cancer
•Characterised by multiple polyps
throughout the entire colon (up to
thousands)
• The polyps are not present at birth
but develop over time
103
Q

2 parts of kidney anatomy

A

cortex ( filters blood)

medulla ( stores urine)

104
Q

Nephrotic vs nephritic syndrome?

  1. chronicity
  2. change in urine components?
  3. change in blood components
  4. systemic changes?
A 
I. Nephrotic syndrome:
1. Chronic
2.Massive proteinuria (selective: albumin)
3. 
Hypoalbuminemia
Hyperlipidemia/-uria
4. Oedema
II. Nephritic syndrome
1. Acute
2.
- Varible proteinuria (not selective)
- Haematuria
3. Azotemia (high nitrogen)
4. 
- Mild oedema
- Oliguria (small amount of urine production)
- Hypertension
105
Q

Nephrotic syndrome

  1. pathophysiology
  2. protein level
  3. 3 different types
A
  1. Damage to the filtration barrier of
    the glomerulus not accompanied by inflammation or proliferative response –> Loss of foot processes
  2. protein level >3.5g/day
  3. I. minimal change disease,
    - Commonest cause of nephrotic syndrome in childhood.
    - gives oedema
    - fused foot processes in electron microscope

II. focal segmental glomerulosclerosis,

  • Primary or secondary
  • Some (focal) glomeruli show partial (segmental) hyalinization
  • Poor prognosis

III. Membranous glomerulonephritis
- Commonest cause of nephrotic
syndrome in adults.
- Deposition of anti-glomerular basal membrane antibodies
- Thickened GBM and subepithelial deposits/spikes
- 85% idiopathic, 15%- association with malignant tumours, SLE, drugs, chronic
infection

106
Q

3 different types of glomerular diseases

A

I. minimal change disease,

  • Commonest cause of nephrotic syndrome in childhood.
  • gives oedema
  • fused foot processes in electron microscope

II. focal segmental glomerulosclerosis,

  • Primary or secondary
  • Some (focal) glomeruli show partial (segmental) hyalinization
  • Poor prognosis

III. Membranous glomerulonephritis
- Commonest cause of nephrotic
syndrome in adults.
- Deposition of anti-glomerular basal membrane antibodies
- Thickened GBM and subepithelial deposits/spikes
- 85% idiopathic, 15%- association with malignant tumours, SLE, drugs, chronic
infection

107
Q

Nephritic syndrome

  1. pathophysiology
  2. 2 types?
A
  1. Inflammation, vascular and epithelial damage (vs damaging the membrane only in nephrotic), plus or minus proliferation of glomerular cells
  2. I. Proliferative glomerulonephritis (POST INFECTIVE) ++++

II. Membranoproliferative (mesangiocapillary) glomerulonephritis

  • Diffuse mesangioproliferative glomerulonephritis
  • Crescentic glomerulonephritis
  • Lupus nephritis
108
Q

Glomerulonephritis

  1. 2 types of causes?
  2. aetiology?
  3. Ix
  4. prognosis in children and adults
A
  1. Primary or secondary to systemic disease.
  2. Immunological aetiology (+++ deposition of immune complex in the glomerular/capillary wall).
  3. immunohistochemistry:
    - Local deposition of circulating immune complexes
    - Anti-glomerular basal membrane antibodies
    - Antibodies against glomerular component
    • Benign outcome in children
    • Permanent compromise of renal function in adults.
109
Q

Acute tubular necrosis

  1. causes
  2. prognosis
  3. presentation
A
    • Ischaemia,
    • Toxic injury by drugs (statin), radio
      contrast dyes, radiation,
      haemoglobin, myoglobin
    • Disseminated intravascular
      coagulation
    • Urinary obstruction
  2. Tubular injury can be reversible
    and most patient recover
  3. acute renal failure
110
Q

3 causes of Tubulointersitial nephritis

A
  • Acute pyelonephritis
  • Chronic pyelonephritis & reflux nephropathy
  • Drugs and toxins- analgesic nephropathy
111
Q

Acute pyelonephritis

  1. sx?
  2. pathophysiology
A
  1. fever and elevated creatinine.

2. There is an acute inflammatory infiltrate in the interstitium and tubular lumina.

112
Q

Chronic pyelonephritis

I. 3 post-mortem features?
II. histopathological features?

A
  1. The surface of the kidney is irregularly/or geographically, depressed in the scarred
    areas with pseudo bulging of the remaining intact parenchyma.
  2. Chronic pyelonephritis can affect both kidneys simultaneously; however, the scarring is asymmetrical.
  3. The cut surface would reveal dilated, blunted, or deformed calyces.

II.

  • Many dilated “colloid” filled tubules are present.
  • This phenomenon is known as thyroidisation of the kidney.
113
Q

Hypertensive kidney disease

A
  1. Benign nephrosclerosis
    - thickening of intima of vessel, narrowing of lumen
    - Focal sclerosis of renal arterioles & small arteries> focal ischaemia >cortical scarring.
    - Some degree of nephrosclerosis is present at autopsy with ↑ age.
    - HTN and DM ↑ the severity of the
    lesion
  2. Malignant HTN & accelerated nephrosclerosis
114
Q

Cystic kidney disease

3 different types?

A

I. Malformative/congenital:
- Multicystic renal dysplasia (most common causes of abdominal mass in
newborn)
- Medullary sponge kidney

II. Acquired:

  • Acquired renal cystic disease (mostly post dialysis), can lead to carcinoma
  • Simple cysts (most common abnormality of the kidney)

III. Hereditary:
- Autosomal dominant (adult) polycystic kidney disease
(ADPKD)
- Autosomal recessive (infantile) polycystic kidney disease
- Nephronophthisis-medullary cystic kidney disease complex

115
Q

Adult polycystic disease

  1. uni or bilaeral?
  2. age of presentation
  3. sx
  4. complication
  5. mx
A
  1. Bilateral.
  2. Presents in middle age.
  3. Haematuria, UTI, abdo mass, HTN. Assoc with Cerebral aneurysms, subarachnoid haem, and cysts in other organs (liver,
    pancreas, lung)
    4.CRF: ruptured berry aneurysm
  4. Supportive, treat HTN, some will need
    dialysis/transplant
116
Q

Infantile polycystic disease

  1. one or both kidneys
  2. associated with which phenotype?
  3. complication
A 
1. Large abdominal masses (both
kidneys affected) at birth
2. Possible “Potter” phenotype: various congenital abnormalities, lower than normal amniotic fluid in ultrasound
3. Evolves into
 death shortly after birth in severe forms
 Renal failure
 Hypertension
 Portal hypertension
117
Q

Chronic kidney failure

Stages chronic kidney failure?
GFR for each stage?
Description
Symptoms?

2 important causes?

A

1 >90 Normal or increased GFR, with other
evidence of kidney damage
Asymptomatic

2 60–89 Slight decrease in GFR, with other
evidence of kidney damage
Asymptomatic

3A 45–59 Moderate decrease in GFR, with or
without other evidence of kidney
damage
Polyuria, anemia,
hypertension 
3B 30–44
4 15–29 Severe decrease in GFR, with or
without other evidence of kidney
damage
Uremia, oedema,
metabolic acidosis,
hypocalcemia

5 < 15 Established renal failure Terminal uremia

:
TWO very important causes: DIABETES and HYPERTENSION

118
Q

Acute renal failure

  1. most common cause?
  2. description
  3. 2 important physiological changes?
  4. oliguric phase vs recovery phase
A
  1. acute kidney injury
  2. Rapid reduction of in renal excretory function (within 48 hr)
    • Absolute increase in serum creatinine >/=m0.3 mg/dl serum urea, Cr,
      K with anuria/oliguria (<15ml/hr)
    • Reduction in urine output (oliguria) less than 0.5ml/kg per hour for
      more than 6 hr
  4. Oliguric phase– metabolic acidosis, increased urea
    o Recovery phase– polyuria
119
Q

NEPHROLITHIASIS

  1. def
  2. m vs f?
  3. 4 different types?
A
  1. Stone formation either in the kidney or renal tract.
  2. M>F.
  3. I. Calcium oxalate
    - Hypercalcaemia/Idiopathic hypercalciuria. 75%
    II. Triple phosphate (magnesium ammonium calcium phosphate)
    - Proteus infection which splits urea into ammonium. (Staghorn calculus). 15%.
    III. Urate
    - Hyperuricaemia (GOUT). 6%
    IV. Cystine
    In born error of metabolism. 1%
120
Q

Renal tumours

A 
I. Childhood
- Wilm’s tumour
II. Benign
- Papillary adenomas. 
- Found atautopsy (<5mm).
- Fibroma
III. Malignant 
- Renal Cell Carcinoma (80%)
- Transitional cell carcinoma (20%)
121
Q

Renal cell carcinoma (RCC)

  1. RFs?
  2. Sx?
  3. prognosis
  4. histotypes?
A
    • smoking, HTN, obesity, heavy metals.
    • Von Hippel Lindau syndrome (haemangioblastoma of cerebellum,
      retina, renal cyst, bilateral RCC)
  2. Clinical presentation:
    - Paraneoplastic conditions. Eg: polycythemia, hypercalcaemia, liver
    dysfunction, Cushing syndrome, amyloidosis.
    - Palpable mass,
    - Haematuria,
    - Backpain.
  3. Survival- 5 yrs 70% if no mets, 45% if mets.
  4. Clear cell, papillary and chromophobe.
122
Q

Bladder tumours

  1. 3 types?
  2. RFs?
  3. sx
  4. prognosis
A 
1. 
I. Benign: papilloma (1%)
II. Low malignant potential: papillary
urothelial neoplasm with low malignant
potential (PUNLMP)
III. Malignant:
- Low grade papillary urothelial
carcinoma.
- High grade urothelial carcinoma
2. 
- Smoking
- Industrial exposure to arylamines
- Previous irradiation
- Long term use of analgesic
- Cyclophosphamyde
- Schistosoma Haematobium
3. painless haematuria
4. 
- Papillomas, PUNLMP and LG Pa Carcinomas 98% of survival
at 10 years with 10% progressing toward high grade.
- HG Pa Carcioma 75% of survival at 10 years
123
Q

Cause of Perinatal Deaths

A
  1. Spontaneous preterm delivery and
    hypertensive disorders - most common
    obstetric events leading to perinatal
    deaths (28.7%) .
  2. Prematurity - main cause of early neonatal deaths (62%).
  3. Death associated with fetal abnormalities (only12%)
124
Q

Chromosomal disorders in foetus?

A 
1. Trisomy 21
The incidence of Down syndrome is estimated at 1 per 800 to 1,000 births.
2. Trisomy 18 (Edward´s Syndrome)
3. Trisomy 13 (Patau´s Syndrome)
4. Triploidy
5. Turner’s Syndrome (45,X0)
125
Q

Babies of diabetic mothers

  1. which type is worse?
  2. Signs?
  3. Risk at delivery?
A 
1. 
Type I moms normally know of it, and have it under control. 
Type 2: is normally less controlled
2. 
- Increased somatic size (macrosomia)
- Increased incidence of Perinatal Death
- Increased frequency of malformation
- Hypertrophy of islets of Langerhans with B cell hyperplasia and hyperinsulinaemia.
  1. When born, they’re very heavy. They may have hyperinsulinaemia as they are not giving it to mom anymore, so they develop hypoglycaemia and may die.
126
Q

Pre-eclampsia

  1. def
  2. Maternal sx?
  3. perinatal sx?
A
  1. vessels are not transformed properly leading to placenta
  2. maternal high BP and protein in urine
  3. Autopsy finding: IUGR (Intrauterine growth restriction ) and asymmetrical growth restriction (if stops growing, babies need to be taken out as it means placenta is not providing nutrients anymore)
  4. increased smooth muscle around the spiral artery, means they can constrict leading to reduced supply to foetus
127
Q

Social history of mom for perinatal pathology?

A
  1. maternal drug use esp cocaine
  2. alcohol
  3. smoking
128
Q

Skin-related findings on perinatal autopsy of

A

Skin goes wrinkly (early days)

Maceration: Skin slippage post mortem in stillborn (means baby was dead for a while)

129
Q

Perinatal Autopsy, Common Pathological Findings

A
  1. Anecephaly
    absence of brain and skull vault
  2. Spina bifida
    - neural tube defect, back is open
    - if small can be stitched up
  3. Hydrops
    - generalised oedema of the fetus
    - twins: if one pumps blood into another, hydrotropic one dies, if not picked the small one dies too
  4. Atresia of the bowel
    - blunt ending tube
    - no connection to the distal part of the bowel
  5. Single palmar crease (Trisomy 21)
  6. Findings in oligohydramnios
    - wrinkled glove like skin and potter facies
    - agenesis of kidneys, no urine production, featus pressed against the uterus, abnormal facial features
    - they cannot swallow enough fluid, lungs cant be expanded, born with pulmonary hypoplasia
130
Q

Acute Choriomanionitis

  1. def
  2. complication
  3. when happens?
A
  1. acute inflammation of the fetal membranes
  2. Ascending infection (due to group B streptococci)
  3. Common after premature rupture of membranes
131
Q

Placental pathology

A
  1. infarct due to pre-eclampsia

2. Acute Choriomanionitis

132
Q

Most common childhood cancer

A 
• Leukemias (30%)
• Brain and CNS tumours (26%)
• Neuroblastoma (6%)
• Wilms tumour (5%) - nephroblast tumour
• Non Hodgkin Lymphomas and Hodgkin
Lymphomas (8%)
• Rhabdomyosarcoma (2%)
• Bone cancer (3%)
• Retinoblastoma (2%
133
Q

Hirschsprung’s disease

  1. def
  2. cause
  3. pattern
  4. presentation
  5. Mx?
A
    • Developmental disorder where neurons invade the bowel, due to absence of the ganglion cells, resulting in smooth muscle narrowing of the bowel
  • Developmental disorder with absence of
    ganglion cells in distal rectum,
  1. Due to failure of neural crest cells
    migration during development of enteric
    nervous system
  2. always starts distally and goes proximally
4. 
Commonly presents in newborn period:
- delayed meconium passage (48hrs)
- abdominal distension
- bilious vomiting
  1. Anal pull through:
    - leave the muscle ring of the rectum, but dissect the mucosa for biopsy
    - if biopsy shows ganglion cells, dissect the affected part, attach the normal part of bowel to the muscle ring
134
Q

Cystic fibrosis

  1. genetics?
  2. pathology in lungs
  3. pathology in bowel
  4. histology feature
A
  1. Autosomal recessive mutation of CTFR gene
  2. -mucus plugging of airways
    - severe suppurative lung
    disease
    - Brochiectasis
    • Bowel lumen filled with inspissated meconium (amber colour)
    • Intestinal atresia
    • Rectal prolaps
  4. Characteristically mucus extends deep
    into crypts
135
Q

Coeliac disease

  1. def
  2. higher risk in?
  3. sx
  4. long term complication
  5. assessment of severity
  6. histological changes?
A
  1. Inflammatory reaction to gliadine
  2. Seen more frequently in insulin dependent diabetes type1 and Trisomy 21
3. 
• Young children: 
failure to thrive, diarrhea, malabsorption, abdominal distention
• Older children:
- abdominal pain
  1. Long term complications
    - in adults- osteoporosis,
    - intestinal T-lymphoma
    • General correlation between antibody and
      severity
    • Anti-gliadine and Antitissue
      transglutaminase antibodies -> AGA and
      TGA raised in blood
    • Villous atrophy
    • Increased intraepithelial lymphocytes (>40/100 enterocytes, IELs)
    • Increased lamina propria inflammatory
      cells
136
Q

Polycystic kidney diseases in babies

  1. genetics
  2. what proportion stillbirth?
  3. what gene associated with it?
  4. why can’t they get a kidney transplant
A
  1. Autosomal Recessive PolycysticKidney Disease (ARPKD)
  2. Most cases result in stillbirth or
    early neonatal death (40%);
    encountered in 1:20,000 live
    births.
  3. Associated with gene PKHD1
    that maps to chr region 6p21- p12 and encodes for protein fibrocystin located in cilium
  4. adults have higher BP, and kidneys need to be adjusted for recipient BP
137
Q

Tunica vaginalis?

A

covers testes, it’s a part of peritoneum

If there is any fluid within abdominal peritoneum (ascites) and there is a connection with tunica vaginalis, fluid can enter this cavity causing hydrocele

138
Q

Direct and indirect hernias of abdomen into scrotum?

A

Direct: abdomen to scrotum
Indirect: abdomen through inguinal canal

139
Q

Testes

  1. What is the parenchyma of testes made off?
  2. 3 types of cells within testes
  3. Stages of development of sperm
A
  1. The parenchyma is divided into approximately 250 lobules, each lobule containing up to four seminiferous
    tubules.
    • The tubules contain sertoli cells (provide support) and germ cells in various stages of development
    • Interstitial cells ( aka Leydig cells,)
  3. Spermatogonium –>Primary spermatocyte -> Secondary spermatocyte -> Spermatid-> Spermatozoon (mature)
140
Q

Sperm passage

A

The rete testis, located at the hilus of the testis, receives the luminal contents of the
seminiferous tubules.
The rete testis empties into the ductuli efferentis, aggregated in the region of the head of the epididymis
The epididymis is connecting the ductuli efferentis to the vas deferens.
The vas deferens is a 30-40 cm tubular
structure, empties into the prostatic urethra at the level of the velumontanum.
The distal portion joins the excretory duct of the seminal vesicle to form the ejaculatory duct

141
Q

TESTICULAR TUMOURS

  1. peak incidence age
  2. 2 main types
A
  1. Peak incidence 15-34 years
    • Germ cell tumours (90%)
    • Sex-cord stromal tumours (sertoli and laydig cells)
142
Q

Germ cell tumours of testicles

  1. malignant or benign?
  2. what can they differentiate into?
  3. sx
  4. RFs?
A
  1. mostly malignant
  2. any embryonic or extraembryonic tissue
    • painless unilateral enlargement of testis
    • Secondary hydrocoele
    • gynaecomastia
  4. I. Cryptorchidism - higher the location greater the risk
    II. Genetic predisposition
    - Sibs have 10-fold high risk
    - Blacks in Africa have very low incidence
    III. Testicular dysgenesis
    - Testicular feminisation
    - Klinefelter syndrome
    IV. Cytogenetic changes involving chromosome 12 and 1
  5. I. In situ
    •Intratubular Germ Cell Neoplasia

II. Invasive
• Seminoma
• Non seminomatous Germ Cell Tumours
—- Embryonal Carcinoma
—- Yolk Sac tumour (if similar to yolk cell, secrete efp)
—- Choriocarcinoma (if similar to trophoblast, secrete scg)
—- Teratoma (tumour of totipotent cells, give rise to any cells)

III. Combined

143
Q

Hydrocoele?

A

fluid within tunica vaginalis

144
Q

Seminoma

  1. def
  2. subtypes
  3. tx
  4. Classical Seminoma features
  5. spermatocytic features
A
  1. remain as germ cell differentiation
  2. For therapeutic reasons divided into 2 Main sub-types:
    - classical seminoma
    - spermatocytic
  3. seminoma very sensitive to radiotherapy, others response to chemotherapy
    • Commonest sub-type
    • Peak in 4th decade
    • m/s sheets of rounded cells with clear
      cytoplasm and variable lymphocytic
      infiltrate in the stroma

5.

  • accounts for 3-5% of all seminomas
  • occurs in older age group
  • m/s mixed population of small, intermediate and giant cells with increased mitotic rate
  • prognosis is excellent
145
Q

Intra Tubular Germ Cell Neoplasia

A

o In-situ stage
o Proliferation of neoplastic germ cells within seminiferous tubules.
o

146
Q

Germ Cell Tumours: Embryonal Carcinoma (MTU)

  1. incidence age?
  2. which one worse this or seminoma?
  3. histological features?
A
  1. Mostly in 20 - 30 years age group
  2. More aggressive than seminoma
  3. M/S the cells are anaplastic and arranged in glandular, alveolar, solid or papillary growth patterns.
147
Q

Germ Cell Tumours: Yolk Sac Tumour

  1. difference between adult and children?
  2. histological feature
  3. serum AFP level
A
    • In children pure form, most common GCT in infants and children up to 3 yrs of age, good prognosis.
    • In adults associated with embryonal carcinoma
  2. Schiller-Duval bodies (central blood vessel surrounded by tumour cells formed by a perivascular layer of tumour cells.
  3. Serum levels of Alpha Foetal Protein are raised and the neoplastic cells are positive for AFP
148
Q

Germ Cell Tumours Choriocarcinoma (MTT)

  1. includes which types of cells?
  2. malignant or benign
  3. HCG serum level?
A
  • Composed of both cyto and syncitiotrophoblasts.
  • Highly malignant
  • Raised serum HCG levels
149
Q

3 ways of spread of germ cell tumours of testes

A
  1. Direct to rete testis and epididymis
  2. Via lymphatics to para-aortic lymph
    nodes and then to mediastinal lymph
    nodes.
  3. via blood to lung, liver and bone
    (teratoma).
150
Q 
Prostate
NODULAR HYPERPLASIA (BPH)
  1. cause?
  2. histological features
A
  1. caused by androgens (dihydrotestosterone
    DHT)
  2. M/s there is increase in glandular and
    stromal component in both
151
Q

CARCINOMA OF PROSTATE

  1. histological features
  2. Grading
  3. diagnosis
A
  1. M/S, adencarcinoma ie tumour forms small glandular structures lined by single layer of cells.
  2. Grading - Gleason’s score depending up to the growth patterns:
    - Stage A not palpable
    - Stage B Palpable, confined to prostate
    - Stage C Extracapsular extension
    - Stage D Metastatic
3. Diagnosis:
• Raised PSA level
• Digital PR examination
• Imaging
• Biopsy
152
Q

Two structural parts of prostate and what type of neoplasm they lead to?

A
  • Consists of five lobes
  • Inner zone (periurethral) - nodular hyperplasia
  • Outer zone (cortical) - carcinoma
153
Q

Uterus - Endometrial adenocarcinoma

  1. sx
  2. predisposing factors?
  3. 2 groups of patients that tend to get it
  4. types
  5. FIGO staging
A

 postmenopausal bleeding

    • Obese
    • Nulliparous with non-ovulatory cycles
    • Diabetes
    • Hypertension
    • Infertility
    • Perimenopausal with oestrogen excess
    • elderly with atrophic endometrium
4. 
Type I
 simple hyperplasia 
- still rounded glands 
 complex hyperplasia 
- more irregular glands
 atypical complex hyperplasia 
- increased nucleus:cytoplasmic, irregulalr neuclei
 carcinoma
Type II (endometrial atrophy)
  1.  Stage I – Confined to corpus uteri
     Stage II – Invading cervix, not beyond uterus
     Stage III – Beyond uterus, not beyond true pelvis
     Stage IV – Beyond true pelvis +/-bladder +/- rectum
154
Q

Leiomyoma vs Leiomyosarcoma of uterus

A 
Both Fibroids: 
I. Leiomyoma
 Benign tumour of smooth muscle
 Multiple
 White-grey
 Whorled, uniform
II. Leiomyosarcoma
 Malignant
 Usually single
 Necrosis
 Haemorrhage
 Frequent mitoses
155
Q

Ectopic pregnancy

  1. where most common?
  2. complication
  3. RFs?
  4. def
  5. presentation
  6. diagnosis
  7. mx
A
  1. Ovaries, abdominal cavity and uterine section of oviducts
  2. Risk of rupture and fatal haemorrhage in oviduct implantation
  3. I. Previous surgery to fellopian tube (eg sterillisation)
    II. Chronic salpingitis (inflammation of fellopian tube)
    III. Pelvic inflammatory disease (inflammation of upper genital tract, ascends from sexually transmitted disease eg chlamydia, )
  4. pregnancy outside endometrium
  5. sudden abdominal pain and severe bleeding
  6. ultrasound
  7. removal of that part or drainage
156
Q

Surface epithelial ovarian tumours

  1. cell type
  2. pattern of growth?
  3. invasiveness?
A
  1. Cell type: serous (fellopian tube), mucinous(endocervix), endometrioid (endometrium) etc.
  2. Pattern of growth: cystic, solid, surface.
     Amount of fibrous stroma
  3. Atypia and invasiveness:
    - benign,
    - borderline (atypia, behave in intermediate way between benign and malignant)
    - malignant
157
Q

Which sex do the following give rise to?
Warfian duct?
Malarian duct?

A

Warfian duct/mesonephric duct: male genitals

Malarian duct/paramesonephric duct: female genital tract

158
Q

Squamous cell carcinoma of cervix

  1. epithelium of cervix before puberty
  2. epithelium of cervix after puberty
  3. Infecting pathogens making it more likely?
  4. How do these pathogens work?
  5. mx
A
  1. Vagina: squamous
    Cervix: columnar
  2. After puberty, cervix grows, exposing it’s epithelium. Cells undergo metaplasia, adding a squamous layer over the glandular. Transition zone can lead to squamous carcinoma of cervix
3.
HPV 6-11 
- warts (low risk) 
HPV -16-18
- potentially cause dysplasia/squamous cell carcinoma
  1. P3 and retinoblastoma get bound by HPV proteins, making them less able to brake the cell cycle
  2. large excision of transitional zone may be enough, otherwise hysterectomy
159
Q

Dyskariosis vs dysplasia

A

Individual cells vs whole tissue

160
Q

Abnormally located uterine tissue

A

I. Adenomyosis:

  • presence of ectopic glandular tissue found in the myometrium uterus
  • sx: dysmenorrhea

II. Endometriosis

  • endometrial tissue outside of the uterus
  • sx: pelvic pain and infertility
161
Q

Types of ovarian tumours

A
  1. surface epithelial cells (mesothelial cells)
    - little ovarian inclusion bodies within ovum released after ovulation, these bodies may be neoplastic
  2. germ cells
  3. sex-cord stroma
  4. metastasis (bowel, or blood stream)
162
Q

Germ cell tumour of ovary vs testes

A

Ovary mostly benign, testes mostly malignant

163
Q

Dysprunia

A

pain on intercourse

MS3 - general (6 decks)

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