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EMS > T2 Cardiology Pathology > Flashcards

T2 Cardiology Pathology Flashcards

1
Q

What does the fibrous cap of the atheroma covering contain?

A
  • smooth muscle cells
  • macrophages
  • foam cells
  • lymphocytes
  • collagen
  • elastin
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2
Q

What does the necrotic centre of the atheroma covering contain?

A
  • cell debris
  • cholesterol crystals
  • foam cells
  • Ca
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3
Q

According to the response-to-injury hypothesis, what molecules take place in the progressive interactions following the endothelial injury?

A
  • modified lipoproteins
  • myocyte-driven macrophages
  • T-lymphocytes
  • a. wall constituents
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4
Q

What is the morphological evolution of the fatty streak? Do they always result in atherosclerosis?

A
  • lesion –> fatty-filled foamy macrophages –> multiple flat yellow spots –> fatty streak
  • no
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5
Q

What is the morphological evolution of an atherosclerotic plaque?

A

intimal thickening –> lipid accumulation –> white yellow –> red superimposed thrombus on plaque –> vessel lumen impingement

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6
Q

What is the main composition of an a thrombus vs a v thrombus?

A

a –> platelets; v –> fibrin

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7
Q

Give an example of an anti-platelet agent used to treat a thrombosis

A

clopidogrel

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8
Q

Give an example of an anti-coagulant agent used to treat v thrombosis

A

heparin

warfarin

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9
Q

What factors can cause endothelial damage? (Virchow’s triad)

A
  • endothelial dysfunction: smoking, hypertension

- endothelial damage: surgery, catheter, trauma

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10
Q

What hereditry factors can cause hypercoagulability? (Virchow’s triad)

A
  • Factor V Leiden
  • Prothrombin
  • Protein S&S deficiency
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11
Q

What acquitred factors can cause hypercoagulability? (Virchow’s triad)

A
  • cancer
  • chemo
  • OCR/HRT
  • pregnancy
  • obesity
  • HIT
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12
Q

What endothelila injury causing factors contribute to stasis? (Virchow’s triad)

A
  • immobility

- polycythemia

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13
Q

What is the sequelae of thrombosis?

A
  • occlusion of vessel
  • dissolution
  • incorporation into vessel wall
  • recanalisation
  • embolisation
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14
Q

What are the causes of systemic emboli?

A
  • sequelae of MI
  • AF
  • infective carditis
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15
Q

Difference does stable plaque differ to unsabel one?

A
  • small lipid core
  • thick fibrous cap
  • low macrophage content
  • low microvessel density
  • no intraplaque haemorhage
  • no cap rupture
  • no superimposed thrombus
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16
Q

What is the detailed mechanism of IH injury?

A
  • no OP –> less ATP
  • anaerobic –> more lactate, glycogen stores depleted
  • Na pump fails –> Na accumulation
  • memb damage –> intracellularprotein leakage –> enzymes digest cell
  • Ca pump fail –> Ca influx
  • less protein synthesis
17
Q

What intercellular proteins are produced by cardiac muscle damage?

A
  • creatine kinase

- troponins

18
Q

What intercellular proteins are produced by liver damage?

A
  • transaminases

- AK phosphate

19
Q

Whata are the causes of ischaemia?

A
  • vascular occlusion
  • vasospasm
  • vascular damage
  • extrinsic compression
  • mechanical interruption
  • hypoperfusion
20
Q

What organs have end arterial circulations, and would thus be severly affected by ischaemia?

A
  • kidneys
  • spleen
  • testies
21
Q

In a rapid restoration of blood flow, what therapeutic measures are used for 1) ischamia and 2) strokes?

A
  • PCI

- thrombolysis

22
Q

Why is an infarction less dangerous when the rate of occlusion is slow?

A

more time for collateral supplies to form

23
Q

How long does it take before the following tissues are irreversibly damaged due to ischaemia? neurone, myocyte damage, cardiac fibroblast

A
  • 3-4 mins
  • 20-30 mins
  • hrs
24
Q

What is the cause and pathophysiology of coagulative necrosis?

A
  • denaturation

- enzyme unable to break down structure –> basic outline preserved (eusinophilic) –> tissue remain firm

25
Q

What is the cause and pathophysiology of liquefactive necrosis?

A
  • enzyme digestion

- cyst formed

26
Q

What infarcts are red?

A
  • dual blood upply

- venous infarcts

27
Q

Morphology of MI

A

Look up diagram

28
Q

How does unsuccessful therapeutic intervention of ishcaemia lead to reperfusion injury?

A
  • +++ reactive O2 species
  • cytokines recruitment
  • complementary pathway activated
29
Q

What is the aetiology of hypovolaemic shock?

A
  • IVF —
  • venous return, pre-load —
  • SV —
  • CO —
30
Q

What is the compensation for hypovolaemic shock?

A
  • vasoconstriction –> +++ TPR

- tachycardia

31
Q

What is the compensation in cardiogenic shock?

A
  • vasoconstriction –> +++ TPR
32
Q

What are the four causes of cardiogenic shock?

A
  • myopathic
  • arrhythmia
  • mechanical
  • extra-cardiac
    (for specific examples for each one visit notes)
33
Q

What is the cause of disruptive shock?

A
  • SVR —

- severe vasodilation

34
Q

What is the compensation in disruptive shock?

A
  • +++ SV

- +++ CO

35
Q

What are the subtypes of disruptive shock?

A
  • anaphylactic
  • septic
  • toxic shock synfrome
  • neurogenic
36
Q

what is the disruptive component of septic shock?

A
  • inflam. & non-inflam. cascade
  • vascular permeability
  • vasodilation
37
Q

what is the hypovolaemic component of septic shock?

A
  • — oral intake
  • vomiting
  • diarrhoea
38
Q

what is the cardiogenic component of septic shock?

A

sepsis-related M dysfunction

EMS (10 decks)

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