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Phase 2a > Pathology > Flashcards

Pathology Flashcards

1
Q

Define a granuloma

A

an aggregate of epithelioid histocytes with or without giant cells

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2
Q

What cells are involved in acute inflammation?

A

neutrophil polymorphs

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3
Q

What cells are involved in chronic inflammation?

A

epithelioid histiocytes

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4
Q

What do epithelioid histiocytes secrete?

A

ACE (can therefore be used as a serum marker for granulomatous disease)

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5
Q

Give some examples of granulomatous diseases?

A

TB, sarcoidosis, Leprosy, Crohn’s, GPA

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6
Q

What cells are seen in TB?

A

Langhans giant cells

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7
Q

How can granulomas be classified?

A

Caseating (necrosis) or non-caseating (no necrosis often fibrous scar tissue)

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8
Q

After an injury what two things can happen to a tissue?

A
  1. regeneration (complete resolution of lost structures)

2. scar tissue formation

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9
Q

What is granulation tissue?

A

tissue that forms on a raw surface or open wound in the process of healing. Consists of angiogenesis surrounded by collagen (secreted by fibroblasts)

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10
Q

Which cells produce collagen to fill the gap after an injury?

A

Fibroblasts

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11
Q

Describe the two types of healing?

A

1st intention

2nd intention

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12
Q

Why can healing and repair go wrong?

A
  1. poor blood supply
  2. poor nutrition
  3. wound infection
  4. immunosuppression (HIV, DM or immunosuppressants)
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13
Q

Which two types of irregular scars are there?

A
  1. Hypertrophic- excess collagen, raised slightly

2. Keloid- excess granulation tissue, expands beyond wound edges

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14
Q

Define atrophy…

A

decrease in size due to decrease in number or size of cells

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15
Q

Define hypertrophy….

A

increase in size due to increase size of cells (skeletal muscle)

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16
Q

Define hyperplasia…

A

increase in size due increase in number of cells (smooth muscle)

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17
Q

Define dysplasia…

A

alteration of size/shape/organisation of adult cells

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18
Q

Define metaplasia…

A

full differentiation from one type of cell to another

e.g. = barretts oesophagus (simple squamous&raquo_space; columnar)

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19
Q

Define apoptosis…

A

genetically regulated cell death

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20
Q

Define necrosis…

A

death of many adjacent cells due to an extrinsic factor

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21
Q

When is metaplasia seen?

A

Barretts Oesophagus (simple squamous&raquo_space; columnar)

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22
Q

In foetal development what can turn on and off apoptosis?

A

homeobox genes

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23
Q

Define apoptosis…

A

programmed cell death

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24
Q

Name the different types of necrosis…

A

Coagulative (sticky) = infarction
Liquefactive (liquid)= bacterial or fungal
Caseous = TB
Fibrinoid= immune vasculitis e.g. polyarteritis nodosa
Fat = acute pancreatitis, breast injury
Gangrenous = gangrene

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25
Q

Give some examples of necrosis in a human…

A

Avascular necrosis of bone

Spider venom&raquo_space; necrosis of skin

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26
Q

Define a neoplasm…

A

A neoplasm is a lesion resulting from the autonomous, new and abnormal growth that persists after the initiating stimuli is removed.

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27
Q

What type of mutations can cause a neoplasm?

A

Somatic or germline
Somatic = can arise spontaneously in any cell except germ cells at any time in patients life (cannot be passed onto child)
Germline mutations- can be passed onto future generations e.g. BRCA 1

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28
Q

Define carcinogenesis…

A

The process that results in the transitioning of morphologically and genetically normal cells into neoplastic cells due to permanent genetic mutations

29
Q

What type of neoplasms does carcinogenesis apply to?

A

ONLY MALIGNANT

30
Q

Name the two types of oncogenes…

A
  1. proto-oncogenes

2. tumour suppressor genes

31
Q

Describe the photo-oncogene RAS

A

RAS= codes for cell signalling proteins, mutation in this increases cell signalling and increase growth differentiation and survival. Mutations that permanently activate RAS responsible for 20-25% human tumours and 90% of pancreatic cancer

32
Q

Describe the tumour suppressor gene P53…

A

P53= ‘the gatekeeper of the genome’ it prevents any genome mutation. TP53 is the P53 gene in humans. A mutation in P53 is associated with CRC and endometrial cancer

33
Q

Describe the tumour suppressor gene APC…

A

APC gene= makes adenomas polyposis coli protein, which controls cell division, it also breaks down beta-catenin (B catenin promotes cell proliferation) so no APC protein results in more cell division, more Beta catenin and therefore more cell proliferation. This mutation is seen in familial adenomatous polyposis (93% risk of CRC by 50)

34
Q

Describe the adenoma-carcinoma sequence in colorectal cancer…

A

This is a sequence of mutations that occurs in most CRC. As we said, its multistep. APC&raquo_space; KRAS&raquo_space; p53 mutations
Germline mutations of APC = familial adenomatous polyposis

35
Q

Give some examples of carcinogens…

A

1) Lung cancers: cigarette smoking, asbestos (mesothelioma)
2) Bladder cancers: rubber dyes, schistosomiasis
3) Breast cancers: increased oestrogen
4) Stomach cancers: H.pylori infection
5) Cervical cancer: Human papilloma virus (HPV)
6) Liver cancer: Hepatitis B and C viruses

36
Q

Give the staging used in cancers…

A
  1. TNM- breast, lung, pancreatic, renal
  2. DUKES- colorectal cancer
  3. Gleasons- prostate
  4. Ann Arbour- Hodgkins lymphoma
37
Q

Describe DUKES staging…

A

A- no invasion into muscle
B1- through muscle wall but not out other side (No LN inv)
B2- through muscle wall and out the other side (No LN inv)
C1- through muscle wall but not out other side (LN inv)
C2- through muscle wall and out the other side (LN inv)
D- distant metastases

38
Q

Describe Ann Arbour staging…

A 
I-IV
1 = one lymph node
2= >1 lymph node on same side of diaphragm 
3= nodes on both sides of diaphragm
4= extra nodal development 
A= No B symptoms
B= symptoms
39
Q

For which condition would you not do screening and why?

A

Prostate cancer- due to false positives and non specificity of PSA

40
Q

Describe TNM staging…

A 
T1= <2cm, T2= 2-5cm, T3= >5cm T4= extends to skin or chest wall
T0= no evidence of primary tumour
Tis = carcinoma in situ

No lymph node involvement = N0 (LN involvement = N1-N3)

M0 = no distant metastases
M1= distant metastases
41
Q

Define haemostasis

A

the balance between keeping blood inside vessels fluid, and making the blood outside vessels clot

42
Q

Define a thrombus…

A

solid mass of blood constituents in life (if dead it is called a clot)

43
Q

Which three factors contribute to thrombosis?

A

Virchow’s Triad:

  1. Circulatory stasis: change in blood flow e.g. venous obstruction, AF, Immobility
  2. Hypercoagulable state: change in blood constituents e.g. increased oestrogen, thrombophilia, malignancy
  3. Endothelial injury: change in vessel wall e.g. atherosclerosis and trauma
44
Q

What is the difference between a venous and arterial thrombus?

A 
Arterial = high pressure, white thrombus, treated with anti-platelets e.g. aspirin/clopidpgrel
Venous = low pressure, red thrombus, treated with anti-coagulants e.g. Warfarin, Heparin, Rivaroxiban
45
Q

Which type of thrombus is more likely to embolise?

A

Venous

46
Q

Define an embolism…

A

obstruction of a blood vessel by a foreign object or part of a blood clot which plugs the vessel

47
Q

What can cause an embolism?

A

Dislodged thrombus, fat particles, air bubbles, vegetations of infective endocarditis

48
Q

When can an embolism be catastrophic?

A
  1. DVT&raquo_space; pulmonary embolism
  2. Thrombus formed in RA in AF&raquo_space; embolic ischemic stroke or TIA
  3. Retinal embolism&raquo_space; PAINLESS sudden blindness
49
Q

Define atherosclerosis…

A

focal elevated lesions formed in the intima (furring of the arteries)

50
Q

Which vessels does atherosclerosis affect?

A

Medium and large (does not affect capillaries)

51
Q

Name 5 risk factors for atherosclerosis (how can they be categorised?)

A

Modifiable: Smoking, hypertension, hypercholesterolemia hyperlipidaemia, diabetes

Non-modifiable: Age, male sex, post menopausal, family history

52
Q

Which risk factor is most important in developing atherosclerosis?

A

Hypercholestermia

53
Q

How is an atheroma formed? Long description

A
  1. endothelial damage
  2. LDL begins to accumulate in arterial wall
  3. macrophages attracted and take up lipid to form foam cells
  4. fatty streak formed
  5. macrophages activated and release cytokines and growth factors
  6. Smooth muscle proliferation around lipid core
  7. formation of a fibrous cap (collagen)
54
Q

Give two complications of a thrombus formation…

A

Embolism: if thrombus dislodged
Aneurysm: plaques can weaken walls of arteries (AAA: males >55yrs)

55
Q

What is the difference between ischaemia and infarction?

A

Infarction = tissue DEATH due to lack of blood supply

Ischaemia= lack of O2 to tissues

56
Q

How is an atheroma formed simple steps…

A 
foam cells
fatty streak
lesion
atheroma
fibrous plaque
plaque rupture/fissure and thrombosis
57
Q

Describe the process of ageing…

A
  1. dermal elastosis: UVB light&raquo_space; protein cross-linking
  2. Osteoporosis: increased bone resorption and decreased bone formation (lack of oestrogen)
  3. cataracts: UVB light&raquo_space; protein cross linking
  4. senile dementia: neuronal loss, plaque formation
  5. sarcopenia: loss of skeletal muscle mass and strength
  6. deafness: loss of hair cells in ear
58
Q

Difference between proto-oncogenes and tumour suppressor genes?

A

proto-oncogenes, produces protein products that normally enhance cell division or inhibit normal cell death. The mutated forms of these genes are called oncogenes. The second group, called tumor suppressors, makes proteins that normally prevent cell division or cause cell death.

59
Q

Which gene mutation is seen in familial adenomatous polyposis?

A

APC gene= makes adenomas polyposis coli protein, which controls cell division, it also breaks down beta-catenin (B catenin promotes cell proliferation) so no APC protein results in more cell division, more Beta catenin and therefore more cell proliferation. This mutation is seen in familial adenomatous polyposis (93% risk of CRC by 50)

60
Q

Which mutation is associated with 90% of pancreatic cancers?

A

RAS

61
Q

Give an example of a photo-oncogene and tumour suppressor gene…

A

Proto-oncogene = RAS

Tumour suppressor gene = P53 APC

62
Q

In colorectal cancer what is the sequence of mutations?

A

adenoma-carcinoma sequence: APC&raquo_space; K-RAS&raquo_space; P-53

63
Q

Give some examples of carcinogens…

A

Lung cancers: cigarette smoking, asbestos (mesothelioma)
Bladder cancers: rubber dyes, schistosomiasis
Breast cancers: increased oestrogen
Stomach cancers: H.pylori infection
Cervical cancer: Human papilloma virus (HPV)
Liver cancer: Hepatitis B and C viruses

64
Q

Define a carcinogen…

A

A substance capable of causing malignancy in a living tissue

65
Q

How do carcinomas invade the basement membrane?

A
  • Proteases - matrix metalloproteinases
  • Collagenase
  • Cathepsin d
  • Urokinase-type plasminogen activator
  • Cell motility
66
Q

What is a carcinoma in situ?

A

Cancers start off contained - E.g. in a duct in breast tissue

67
Q

Where do kidney cancers tend to metastasise to?

A

liver

68
Q

Which cancers commonly metastasise to the liver?

A

GI: colon, stomach, pancreas, carcinoid tumours of the intestine

Phase 2a (7 decks)

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