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Pathology Flashcards

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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
What is laminar flow
Cells travel in the centre of arterial vessels and don't touch endothelial walls
26
deep venous thrombous DVT: massive constituents usually forms in legs can fragment to DV emboli often pulmonary PE: pulmonory embolism
27
What are the 3 stages of thrombosis?
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
28
Describe the intrinsic pathway of coag cascade incl common pathwaay
12->11->9->8->10-> 2->1 (2->1 via 5) 10-> 2->1 (2->1 via 5) = common pathway
29
Describe the extrinsic pathway of coag cascade
3->7->10-> 2->1 (2->1 via 5)
30
What are the 3 factors that can initiate thrombosis.
virchows triad: 1. Change in vessel wall; endothelial injury 2. Change in blood flow; decr. bloodflow 3. Change in blood consitiuents; hypercoaguability:
31
Name the factors that result in components of virchows triad
1. endothelial injury (trauma, surgury, MI, smoking) 2. decr. bloodflow (AF, immobility) 3. hypercoaguability: sepsis, malignancy, concp. + pregnancy, arthersclorosis
32
Name the two types of thrombosis
arterial venous
33
cause of arterial thrombosis and associated conditions
atherogenesis (clot forming in arteries- process of plaque accumalation) MI, ischemic stroke, peripheral vascular disease
34
cause of venous thrombosis and associated conditions
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
treatment of venous thrombosis
anticoagulants (DOACs and warfarin)
36
treatment of arterial thrombosis
antiplatelets (aspirin)
37
how patients present w venous thrombosis
red, lots of pain, tender, swollen
38
how patients present w arterial thrombosis
cold, pale, clammy
39
3 possibe outcomes from thrombosis
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
2 types of emboli
arterial emboli- from arterial thrombosis (eg from MI and causes ischemic stroke) venous emboli- DVT lodges in pulmonary -> PE
41
What is likely to occur if an emboli enters the arterial system?
Can travel and lodge anywhere prior to its change into the venous system
42
What is likely to occur if embolus enters the venous system
- Will enter RHS heart -> vena cava will lodge in the pulmonary arteries - lung capillary size is 1rbc wide- pevents entering arterial circulation
43
What is ischemia?
A reduction of blood flow to tissue w no other implications
44
What is infarction?
Reduction of blood flo to tissue which results in cell death Usually due to arterial thrombosis
45
Which organs are less susceptible to infarction and why?
Liver, lung, brain around circle of willis Due to dual arterial supply so in result of thrombus organ still has blood supply
46
Can repaired tissue regenerate?
No
47
What is resolution?
Forming undamaged tissue which can regenerate
48
What is repair and examples of tissue repair
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
Which cells regenerate?
Osteocytes Hepatocytes Pneumocytes All blood cells Gut and skin epithelium
50
Which cells don't regenerate?
myocardial cells neurones
51
Define hypertropy
The increase in tissue size through the increase in cell size
52
Give an example of hypertrophy
Increase in skeletal cell size in athletes and bodybuilders
53
Define hyperplasia
Increase in tissue size through the increase in number of cells
54
Give an example of hyperplasia
Prostatic hyperplasia Endometrial hyperplasia
55
What is the difference between hypertrophy and hyperplasia
Hypertrophy is the increase in cell size where hyperplasia is the increase in cell numbers
56
Give an example where hyperplasia and hypertrophy occur simultaneously
Smooth muscle in th euterus during pregnancy
57
Define atrophy with an example
The decrease in tissue size through the decrease in cell size or cell number eg cerebral atrophy in dementia
58
Define metaplasia
The change in cell differentiation from 1 fully differentiated cell type to another fully differentiated cell type
59
Give an example of metaplasia
Smoking damage: bronchi ciliated columnar EP -> non-ciliated squamous EP from reserve cells
60
Define dysplasia
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
Define apoptosis
Single cell, programmed, non-inflammatory cell death
62
Define necrosis
Death of a large number of cells (tissue/ organ) due to external factor eg injury, disease, infarction Inflammatory and traumatic
63
What causes cells to apoptose?
Protein p53 detects cell DNA damage Causes enzyme caspase to shrink and therefore kill cell
64
What causes cells to apoptose?
Protein p53 detects cell DNA damage Causes enzyme caspase to shrink and therefore kill cell
65
Give a use of apoptosis in health
Normal cell turnover - aids in development
66
Give function of apoptosis in disease
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
Give examples of necrosis
Infarction- myocardial/ cerebral Pancreatitis TB Gangrene Frost bite Toxic venom from insects and reptiles
68
Define carcinogenesis
It is the transformation of normal cells to neoplastic through genetic alteration or permenant mutation
69
Which tumours form as a result of carcinogenesis?
malignant neoplasms
70
Define oncogenesis
The formation of benign or malignant tumours
71
Define tumour and what is included in this name
Any abnormal swelling Neoplasms, hyperplasia, hypertrophy, inflammation
72
What are neoplasms?
Autonomous, abnormal, persistent new growths Only from nucleated cells Can be benign or malignant
73
Can RBC from neoplasms?
No, as they don't have nucleuses
74
What are carcinogens?
Any agent that is known or suspected to cause cancer through altering DNA
75
What are the 5 classes of carcinogens?
1. chemical 2. viral (DNA + RNA) 3. biological agents (hormones, mycotoxins, parasites) 4. non/ionising radiation 5. misc

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