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CSIM > Pathology > Flashcards

Pathology Flashcards

1
Q

What are Koch’s postulates?

A

Criteria to establish a causative relationship between microbe and disease

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2
Q

What are some controllable and uncontrollable risk factors for atherosclerosis?

A

Uncontrollable - age, family history, being male

Controllable - hyperlipidaemia, hypertension, smoking, diabetes

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3
Q

Which HLA genes cause:

a) ankylosing spondylitis
b) Graves’ disease
c) coeliac disease
d) insulin-dependent diabetes
e) rheumatoid disease

A

a) B27
b) DR3
c) DR3
d) DR3/DR4
e) DR4

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4
Q

Name 3 microscopic features of cell damage

A

swollen ER and mitochondria

Chromatin clumps

Membrane blebs

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5
Q

Which enzyme triggers apoptosis?

A

Caspase 3

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6
Q

What is the difference between intrinsic and extrinsic apoptosis?

A

Intrinsic - due to cell damage cell dies it should die

Extrinsic - cell recognised that cells around it are dying so it probably should too

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7
Q

What is:

  1. Atrophy
  2. Hypertrophic
  3. Hyperplasia
  4. Metaplasia
A
  1. Decrease in cell size or number of cells
  2. Increase in cell size
  3. Increase in cell number
  4. One adult cell type changes to another
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8
Q

What are the two types of pathological calcification?

A

Dystrophic - associated with necrosis, serum Ca2+ is normal

Metastatic - associates with hypercalcaemia, no tissue damage but increased bone destruction e.g. due to paraneoplastic syndrome

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9
Q

Give some features of benign neoplasms.

A 
Slow growth rate
Few mitotic figures
Well differentiated
Often normal nuclei
Circumscribed / encapsulated
Do not invade
Do not metastasise
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10
Q

Give some features of malignant neoplasms.

A 
Rapid growth rate
Numerous mitotic figures
Variable differentiation
Hyperchromic - dark nucleus
Pleomorphic nuclei -variation in size and shape
No capsule, often ill-defined border
Invasive
Frequently metastasise
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11
Q

What is a benign neoplasm of cartilage called?

A

Chondroma

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12
Q

What is a malignant neoplasms of blood vessels called?

A

Angiosarcoma

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13
Q

What is a malignant striated muscle tumor called?

A

Rhabdomyosarcoma

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14
Q

What is a seminoma?

A

Malignant testicular neoplasm

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15
Q

What is a teratoma?

Difference between the two types.

A

Germ cell neoplasm.

Testes - malignant and do not differentiate.

Ovary - benign and differentiate a lot.

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16
Q

Name an infectious cause of Hodgkin’s lymphoma

A

Epstein-Barr virus

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17
Q

Which type of cancer tends to spread through lymphatics?

And which ones through haematogenous routes?

A

Lymphatic - carcinoma not sarcoma

Haematogenous - sarcomas AND carcinomas

18
Q

Which immunohistochemical stains are used to test for

  1. Intermediate epithelial filaments
  2. Neural crest markers
A
  1. Cytokeratin

2. S100

19
Q

Difference between grade and stage of tumour?

A

Grade - degree of differentiation, done by histological assessment

Stage - extend of spread, done by clinical/radiological assessment and lymph node histopathology

20
Q

What are the stages of CIN?

A

CIN1 - mild dysplasia, confined to basal 1/3 of epithelium
CIN2 - moderate dysplasia confined to basal 2/3 of the epithelium.
CIN3 - severe dysplasia with undifferentiated neoplastic cells spanning more than 2/3 of the epithelium. May also involve carcinoma in situ.

21
Q

What is the difference between an oncogene, a proto-oncogene and a tumour suppressor gene?

A

Oncogene - mutated/activated gene which contributes positively to neoplasia. Dominant acting.

Proto-oncogene - aka cellular oncogene, is the unaltered non-mutated cellular counterpart of an oncogene

Tumour suppressor gene - a gene which normally functions in a manner which inhibits neoplasia. Recessively acting.

22
Q

Which fungal toxin is found in some peanuts and what cancer does it predispose to?

A

Aflatoxin

Liver cancer - hepatocellular carcinoma

23
Q

Which carcinogen is found in fossil fuels, animal fat and tobacco?
How does its pathophysiology explain why some smokers never get cancer?

A

Polycyclic aromatic hydrocarbons.

Are converted into an active carcinogens by oxygenases, and genetic variation in these enzymes leads to different susceptibility.

24
Q

What are aromatic amines and azo dyes and describe their metabolism in the body, and the cancer they cause?

A

They are:
Hydroxylated in the liver which activates them, then conjugated in the liver which deactivates them.
Then they are deconjugated in the kidney which reactivates them.

This therefore causes bladder carcinomas.

25
Q

How does UV radiation cause skin cancer?

A

UV crosslinks pyramidine bases (cytosine and thymine) which is usually repaired, but excessive damage overwhelms the repair pathway leading to mutation.

Can cause melanomas, squamous cell carcinomas and basal cell carcinomas.

26
Q

What are the viral oncogenes used by Epstein Barr virus?

A

Latent membrane protein 1 and 2 - mimics cell signalling receptors and hijacks growth-promoting signalling pathways

EBNA-2 - functions as a transcription factor to upregulate growth

27
Q

What is Rb (retinoblastoma) and how does it work?

What is its role in neoplasia?

A

Rb controls E2F by binding to it and keeping it inactive.
When growth is required, cyclin D levels increase and cycin D phosphorylates Rb, hence preventing it from binding to E2F and hence driving the expression of genes and the cell cycle.

Dysregulation of this process can lead to uncontrolled cell division.

This process disrupts the G1–>S checkpoint

28
Q

What is the APC gene and how does it work?

A

It is the adenomatous polyposis coli gene. It inhibits the cell growth signalling pathway in the colon.

29
Q

What is familial adenomatous polyposis (FAP)?

What is the genetic basis of this condition?

A

A huge amount of polyps across the whole colon.
It is caused by germline APC mutations.
All patients with this condition get a prophylactic panproctocolectomy at age 25 as the polyps can become cancerous.

APC is a tumour suppressor gene but this condition acts in an autosomal dominant way as the “second hit” occurs very easily.

30
Q

What is Li Fraumenti syndrome?

A

Germline p53 mutation

31
Q

What is hereditary non-polyposis colorectal cancer syndrome? (HNPCC)

A

No polyps.
Germine defect in 1 allele then sporadic defect in second allele coding for mismatch repair proteins.

Leads to colorectal tumours, endometrial and ovarian tumours.

32
Q

What are some causes of chronic gastritis?

A

The causes are ABC
A - autoimmune e.g. autoantibodies against parietal cells which leads to destruction of the K+/H+ pump and loss of intrinsic factor which leads to perinicious anaemia.

B - bacterial - H pylori

C - chemical e.g. bile+bicarb, gallstones etc

33
Q

What are some consequences of chronic gastritis?

A

Eventually leads to atrophic gastritis.

This can lead to intestinal metaplasia due to increased acid secretion, which predisposes to adenocarcinoma.

Or a carcinoid tumour can form due to ECL cell hyperplasia.

34
Q

What is an ulcer?

A

It is a breach in the GI wall FUTHER THAN the muscularis mucosae.

35
Q

What are the two types of peptic ulcers? Explain differences between them.

A

Gastric ulcer - has normal/low acid, affects older people.

Duodenal - normal/high acid and affects younger people

36
Q

What are some causes of acute oesophagitis?

A

Candida, herpes

37
Q

What are some causes of chronic oesophagitis?

A

Main cause is reflux.

Other causes are Chron’s disease and TB.

38
Q

Name some hallmark features of Chron’s disease?

A 
Fissuring ulcers
Strictures
Discontinuous inflammation affects whole GI tract
Granulomas
Low malignancy risk
Transmural inflammation
39
Q

Name some hallmark features of ulcerative colitis?

A 
Toxic megacolon
Limited to colon
Continuous / pancolitis
Inflammation confined to mucosa
Pseudopolyps
High malignancy risk
40
Q

Describe the transmission of Hepatitis A-E

A 
A - faecal-oral, shellfish, polluted water
B - blood borne
C - blood borne
D - blood borne
E - uncooked pork products
41
Q

Name some causes of acute and chronic hepatitis?

A

Acute - hep A, hep E, CMV, EBV

Chronic - hep B, hep C, hep D

CSIM (5 decks)

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