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ICS > Pathology > Flashcards

Pathology Flashcards

1
Q

What is inflammation

A

Response to tissue injury or infection

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2
Q

Define acute inflam. w examples

A

response to tissue damage w sudden onset, short duration and usually resolves
eg infection, hypersensitvity, tissue necrosis

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3
Q

Main cell type involved in acute inflam

A

Neutrophils (polymorphs- multilobed nucleus)
involved in the intake of bacteria and debris through cytoplasmic lysozymes

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4
Q

Lifespan of neutrophils

A

2-3 days - often die at site of inflam.

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5
Q

Define chronic inflam w examples

A

Response to tissue injury w slow onset, long duration
potential sequal to acute inflam. may never resolve
Autoimmune- graves, MS, lupus, recurrent infections, rhyeumatoid arthritis

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6
Q

Main cell type involved in chronic inflam.

A

macrophages: phagocytosis (weeks -> months)
lymphocytes: B and T cells (yr+)

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7
Q

5 cardinal signs inflammation

A

rubor, dolor, calor, tumor (swelling), loss of function

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8
Q

Stage 1 of inflammation

A
  1. vessel callabre:
    proinflamatory cytokines (CK) eg NO, prostacyclin, bradykin, mediate vasodilation
    causing gaps in endothelial vessel wall
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9
Q

Stage 2 of inflammation

A
  1. fluid exudate:
    incr VD -> incr in hydrostatic pressure
    incr in wall gaps allows fluid to leak out
    “leaky vessel”
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10
Q

Stage 3 of inflammation

A
  1. cellular exudate:
    whole cells (rbc, wbc) begin to leave vessel.
    Neutrophils abundant in this exudate
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11
Q

What are cytokines?

A

small proteins used in cell signalling,
responsible for cardinal signs of inflammation and innnate and adaptive immune responses

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12
Q

Neutrophil response in acute inflam.

A
  • margination- NT migrate to edge of BV near injury site
  • adhesion of NT to BV wall and “rolls” against margin
  • emigration of NT out of BV (diapedesis)
  • chemotaxis: NT follow CK in conc gradient to site of inflam.
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13
Q

Response at site inflammation

A
  1. phagocytosis
  2. phagolysosome and bacteria killing
  3. macrophage to kill debris
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14
Q

Outcomes of acute inflam.

A
  1. resolution: normal recovery
  2. supporation: pus formation
  3. organisation: organisation of granulation tissue and fibroblasts.
  4. progression: chronic inflam. excessive recurrent inflammation- becomes chronic fibrotic tissue
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15
Q

What is the inflam. outcome for myocardial infarct and stroke?

A

cardiac tissue and neurones can’t resolve, at best the tissue can reorganise so never returns to orginal structure due to fibrosis and granulation tissue

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16
Q

Define granuloma?

A

“aggreates of epitheloid histiocytes” (macrophages)
around central pathogen
in chronic inflam
eg TB, leprosy, chrones disease

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17
Q

Central necrosis disease example

A

central death of a tissue = caseatug
TB

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18
Q

No central necrosis granuloma examples

A

leprosy, chrones, vasculitis

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19
Q

Likely reason for granuloma and eosinophil

A

parasite infection

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20
Q

Important bloodmarker associated with granulomas

A

ACE: secreted by granulomas.
incr. levels of serous ACE

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21
Q

Treatment for inflam.

A

Ice- prevents sphincters opening to prevent vessel fluid loss
Ibuprofen- inhibits prostaglandin syntheases (PG- chemical mediator for inflammation)
Corticosteroids- anti-inflam effects
Antihisamines for mosquito bites

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22
Q

Define thrombus

A

Solid mass of blood constituents (mostly PLT) forming in vessels

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23
Q

Define emboli

A

Fragment of thrombus which is carried in vascular system and occuludes a vessel

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24
Q

Difference between thrombi and emboli

A

Thrombus: mass of blood consituents (mostly platelets in BV (life or death)

Emboli: fragments of thrombi which can occlude vessels

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25
Q

What is laminar flow

A

Cells travel in the centre of arterial vessels and don’t touch endothelial walls

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26
Q
A

deep venous thrombous
DVT: massive constituents usually forms in legs
can fragment to DV emboli often pulmonary
PE: pulmonory embolism

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27
Q

What are the 3 stages of thrombosis?

A
  1. vasospasm: (vasoconstriction)
  2. 1’ platelet plug: PLT agregate due to VWF binding to exposed collagen-> PLT plug. PLT aggregation-> +FBL. G proteins used here
  3. coag. cascade -> formation of fibrin to make mesh network where rbc are entrapped -> thrombus
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28
Q

Describe the intrinsic pathway of coag cascade incl common pathwaay

A

12->11->9->8->10-> 2->1 (2->1 via 5)
10-> 2->1 (2->1 via 5) = common pathway

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29
Q

Describe the extrinsic pathway of coag cascade

A

3->7->10-> 2->1 (2->1 via 5)

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30
Q

What are the 3 factors that can initiate thrombosis.

A

virchows triad:
1. Change in vessel wall; endothelial injury
2. Change in blood flow; decr. bloodflow
3. Change in blood consitiuents; hypercoaguability:

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31
Q

Name the factors that result in components of virchows triad

A
  1. endothelial injury (trauma, surgury, MI, smoking)
  2. decr. bloodflow (AF, immobility)
  3. hypercoaguability: sepsis, malignancy, concp. + pregnancy, arthersclorosis
32
Q

Name the two types of thrombosis

A

arterial
venous

33
Q

cause of arterial thrombosis and associated conditions

A

atherogenesis (clot forming in arteries- process of plaque accumalation)
MI, ischemic stroke, peripheral vascular disease

34
Q

cause of venous thrombosis and associated conditions

A

venestasis - often in lower limb
(DVT- decr. and slow blood flow through that vein so blood accumalates around valves so become incompentent so clot forms)
can result in pulmonary embolism (most common)

35
Q

treatment of venous thrombosis

A

anticoagulants (DOACs and warfarin)

36
Q

treatment of arterial thrombosis

A

antiplatelets (aspirin)

37
Q

how patients present w venous thrombosis

A

red, lots of pain, tender, swollen

38
Q

how patients present w arterial thrombosis

A

cold, pale, clammy

39
Q

3 possibe outcomes from thrombosis

A
  1. resolution - clot degrades- normal physiogical return
  2. organisation: leaves scar tissue - cardiac and neurons best case scenario
  3. embolism: fragmentation of thrombi - wedges in distal (pulmonary) circulation
40
Q

2 types of emboli

A

arterial emboli- from arterial thrombosis (eg from MI and causes ischemic stroke)
venous emboli- DVT lodges in pulmonary -> PE

41
Q

What is likely to occur if an emboli enters the arterial system?

A

Can travel and lodge anywhere prior to its change into the venous system

42
Q

What is likely to occur if embolus enters the venous system

A
  • Will enter RHS heart -> vena cava will lodge in the pulmonary arteries
  • lung capillary size is 1rbc wide- pevents entering arterial circulation
43
Q

What is ischemia?

A

A reduction of blood flow to tissue w no other implications

44
Q

What is infarction?

A

Reduction of blood flo to tissue which results in cell death
Usually due to arterial thrombosis

45
Q

Which organs are less susceptible to infarction and why?

A

Liver, lung, brain around circle of willis
Due to dual arterial supply so in result of thrombus organ still has blood supply

46
Q

Can repaired tissue regenerate?

A

No

47
Q

What is resolution?

A

Forming undamaged tissue which can regenerate

48
Q

What is repair and examples of tissue repair

A

Replacement of damaged tissue with fibrous tissue
collagen produced by fibroblasts
Eg Heart after MI (fibrosis)
Brain after cerebral infarction (brain gliosis)
Spinal cord after trauma

49
Q

Which cells regenerate?

A

Osteocytes
Hepatocytes
Pneumocytes
All blood cells
Gut and skin epithelium

50
Q

Which cells don’t regenerate?

A

myocardial cells
neurones

51
Q

Define hypertropy

A

The increase in tissue size through the increase in cell size

52
Q

Give an example of hypertrophy

A

Increase in skeletal cell size in athletes and bodybuilders

53
Q

Define hyperplasia

A

Increase in tissue size through the increase in number of cells

54
Q

Give an example of hyperplasia

A

Prostatic hyperplasia
Endometrial hyperplasia

55
Q

What is the difference between hypertrophy and hyperplasia

A

Hypertrophy is the increase in cell size where hyperplasia is the increase in cell numbers

56
Q

Give an example where hyperplasia and hypertrophy occur simultaneously

A

Smooth muscle in th euterus during pregnancy

57
Q

Define atrophy with an example

A

The decrease in tissue size through the decrease in cell size or cell number
eg cerebral atrophy in dementia

58
Q

Define metaplasia

A

The change in cell differentiation from 1 fully differentiated cell type to another fully differentiated cell type

59
Q

Give an example of metaplasia

A

Smoking damage: bronchi ciliated columnar EP -> non-ciliated squamous EP from reserve cells

60
Q

Define dysplasia

A

Change in cell differentiation from 1 fully differentiated cell type to a poorly differentiated imprecise cell type
Seen in cells which are progressing to cancer (neoplasia)

61
Q

Define apoptosis

A

Single cell, programmed, non-inflammatory cell death

62
Q

Define necrosis

A

Death of a large number of cells (tissue/ organ) due to external factor eg injury, disease, infarction
Inflammatory and traumatic

63
Q

What causes cells to apoptose?

A

Protein p53 detects cell DNA damage
Causes enzyme caspase to shrink and therefore kill cell

64
Q

What causes cells to apoptose?

A

Protein p53 detects cell DNA damage
Causes enzyme caspase to shrink and therefore kill cell

65
Q

Give a use of apoptosis in health

A

Normal cell turnover - aids in development

66
Q

Give function of apoptosis in disease

A

Cancer- cells don’t often apoptose which increase the number of cells resulting in incr. in tumour size.
HIV can induce apoptosis in CD4 helper cells which can cause an immunodeficient state

67
Q

Give examples of necrosis

A

Infarction- myocardial/ cerebral
Pancreatitis
TB
Gangrene
Frost bite
Toxic venom from insects and reptiles

68
Q

Define carcinogenesis

A

It is the transformation of normal cells to neoplastic through genetic alteration or permenant mutation

69
Q

Which tumours form as a result of carcinogenesis?

A

malignant neoplasms

70
Q

Define oncogenesis

A

The formation of benign or malignant tumours

71
Q

Define tumour and what is included in this name

A

Any abnormal swelling
Neoplasms, hyperplasia, hypertrophy, inflammation

72
Q

What are neoplasms?

A

Autonomous, abnormal, persistent new growths
Only from nucleated cells
Can be benign or malignant

73
Q

Can RBC from neoplasms?

A

No, as they don’t have nucleuses

74
Q

What are carcinogens?

A

Any agent that is known or suspected to cause cancer through altering DNA

75
Q

What are the 5 classes of carcinogens?

A
  1. chemical
  2. viral (DNA + RNA)
  3. biological agents (hormones, mycotoxins, parasites)
  4. non/ionising radiation
  5. misc

ICS (11 decks)

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