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haroon ICS > haroon pathology > Flashcards

haroon pathology Flashcards

1
Q

3 stages of inflammation

A
  1. increase in vessel calbire - it gets wider
  2. fluid exudate
  3. cellular exudate
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2
Q

neutrophil action in acute inflammation

A
  1. margination
  2. adhesion using selectin protein
  3. emigration + diapedisis
  4. chemotaxis - following cytokines to inflammation site
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3
Q

neutrophil action at site of acute inflmaation

A
  1. phagocytosis
  2. phagolysosome formation + bacterial killing
  3. macrophages clear debris
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4
Q

define granuloma

A

aggregate of epitheloid histocytes

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5
Q

how to detect granulomatous disease

A

high ACE because granulomas secrete ACE

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6
Q

3 stages of thrombosis

A
  1. vasospasm
  2. formation of primary platelt plug
  3. coagulation cascade
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7
Q

how is primary platelet plug formed

A

VWF binds to exposed collagen

platelts bind to VWF via gp1b

activates platelts

they go from discoid to pseudopoid

platelts bind to each other via gp2a/3b –> aggregation

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8
Q

intrinsic part of coagulation cascade

A

12
11
9
8
10

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9
Q

extrinsic part of coahulation cascade

A

3
7
10

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10
Q

common part of coagulation cascade

A

10
5
2
1

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11
Q

how do arterial thrombi present

A

cold, pale, loss of pulse

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12
Q

how do venous thrombi present

A

tender, swollen, red

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13
Q

treatment for arterial thrombi

A

antiplatelts - aspirin

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14
Q

treatment for veous thrombi

A

DOAC or warfarin

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15
Q

3 fates of thrombi

A
  1. resolution
  2. organisation
  3. embolism
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16
Q

where do arterial emboli form

A

in systemic circulation from left heart

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17
Q

where do venous embol form

A

in pulmonary circulation from right heart

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18
Q

components of atheroscloertic plauqe

A
  • lipid
  • smooth muscke
  • macrophages/foam cells
  • platelets
  • fibroblasts
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19
Q

formation of atherscloeritc plaque

A
  1. fatty streak
  2. lipid accumulation
  3. plateley aggregation
  4. fibrin mesh and rbc trapping
  5. fibrous cap
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20
Q

define apoptosis

A

non inflammatory controlled cell death

21
Q

what happens in apoptosis

A
  • cells shrink
  • organeless are retained
  • cell membrane in tact
  • chromatin unaltered so no mutation
  • easy process
22
Q

3 mechancisms of apptosis

A
  1. intrinsic
  2. extrinsic
  3. cytotoxic
23
Q

what happens in intrinsic apoptosis

A

bax protein acts on mitochondiral membrane to promote cytochrome c release

activates caspases –> apoptosis

24
Q

what happens in extrinsic apoptosis

A

FasL or TNF-L binds to CSM receptots

activates caspases –> apoptosis

25
Q

what happens in cytotoxic apoptosis

A

CD8+ binding releases granzyme B from CD8+ cell

granzyme B –> perforin –> caspases –> apoptosis

26
Q

define necrosis

A

inflmmatory traumatic cell death

27
Q

what happens in necrosis

A
  • cells burst
  • organelles splurge out
  • cell membranes damaged
  • chromatin altered so big mutation risk
28
Q

which cells can neoplasms arise from

A

nucleated cells only

cant srise from erythrocytes

29
Q

define neoplasm

A

autonomos abnormal persistent new growth

30
Q

how can benign tumours be patholgicL

A
  1. horomone secreting eg prolactinoma
  2. put pressure on local structures
  3. obtstruction
  4. transformation into malignant
31
Q

impavcts of malignant tumours

A
  • pressure on structurs
  • form secondary metastatic tumours
  • obstruction
  • from paraneoplastc sydnromes
  • blood loss
  • pain
32
Q

non glandular benign tumour

A

papilloma

33
Q

non glandular malignant tumiur

A

carcinoma

34
Q

glandular benign tumur

A

adenoma

35
Q

glandular malignant tumour

A

adenocarcinoma

36
Q

which tumour never metastatsizes

A

basal cell carcinoma

37
Q

what does teratoma mean

A

cancer of all 3 germ layers

38
Q

4 characteristucs of neoplastic cell

A
  1. autocrine growth stimulation
  2. evasion of apoptosis
  3. telomerase
  4. susatined angiogenesis and ability to invade BM
39
Q

how do neoplasms have autocrine growth stimulation

A
  • overexpression of growth hormone
  • mutation of tumour supressor genes eg p53
  • underexpression of growth inhibitors
40
Q

how does telomerase help neoplastic cells

A

prevents telomeres shorterning with each replication

41
Q

pathway of metastasis

A
  1. detachment from primary site
  2. invasion of other tissues
  3. invasion of blood vessels
  4. evasion of host defence, adherence to blood vessel wall
  5. extravasation to distant site
42
Q

3 methods of spread for metastastes

A
  1. haemategenous
  2. lymphatics
  3. transolemic - via effusion and fluid
43
Q

how do sarcomas mostly spread

A

hameatogenous

44
Q

most common method of tumur staging

A

TNM - tumour, node , metastases

except for lymphoma, lakeumea, and CNS cancers

45
Q

what kind of prevention is cancer screening

A

secondary

46
Q

which cancers are screened for in uk

A

cervical - cervical swab

breast - mammogram

colorectal - foecal occult

47
Q

what does heel prick test at birth test for

A
  • cystic fibrosis
  • sickle cell anemia
  • congential hypothyroidism
48
Q
A

haroon ICS (3 decks)

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