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Cardiovascular > Pathology > Flashcards

Pathology Flashcards

1
Q

What does vascular injury do to us?

A

injured endothelial cells lead to smooth muscle recruitment, replicate and elaborate extracellular matrix, leading to thicker intima and narrowed lumen

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2
Q

How does arteriolosclerosis appear on histology?

A

hyaline

hyperplastic onion skinning

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3
Q

What is an atheroma?

A

it is an atherosclerotic plaque. fibrous cap covers necrotic center

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4
Q

How to plaques form?

A
  1. chronic endothelial injury
  2. endothelial dysfunction recruits leukocytes and monocytes
  3. macrophages come and recruit smooth muscle
  4. they engulf lipids
  5. smooth muscle proliferates and matrix deposits
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5
Q

What is the earliest tissue change in atherosclerosis?

A

fatty yellow streak

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6
Q

Consequences of atherosclerosis?

A

MI
CVA
Gangrene

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7
Q

True aneurysm vs. false aneurysm:

A

Ture: intact attenuated (thin) arterial wall (berry)
False: defect in vascular wall leads to hematoma and extravasation of blood

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8
Q

What causes cystic medial degeneration?

A

marfans

elastic tissue isnt lines up and contractile, get tears in aorta and blood dissects out

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9
Q

Where is thoracic dissection pain felt?

A

tearing or stabbing pain in anterior chest radiating to the back

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10
Q

Most common vasculitis of elderly in developed countries

A

temporal (giant cell) arteritis)

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11
Q

What ANCA for Wegener’s?

A

c-ANCA

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12
Q

Raynaud phenomenon

A

exaggerated vasoconstriction in fingers and toes

red white and blue proximal to distal

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13
Q

Raynaud phenomenon can be secondary to

A

SLE, scleroderma, buerger disease, atherosclerosis

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14
Q

Hyperemia:

A

arteriolar dilation caused by inflammation or exercise

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15
Q

Congestion

A

reduced outflow of blood from venous obstruction or cardiac failure

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16
Q

Edema

A

abnormal increase in intersitial fluid within tissues caused by transudate (protein poor) fluid

17
Q

5 ways to swell

A
  1. increased hydrostatic pressure
  2. reduced plasma osmotic pressure
  3. lymphatic obstruction
  4. sodium retention
  5. inflammation
18
Q

Reasons for reduced albumin synthesis

A

reduced albumin (cirrhosis, malnutrition, nephrotic syndrome)

19
Q

What does stasis and turbulence do to us?

A

brings platelets into contact with endothelium and prevents dilution of activated clotting factors by fresh blood

20
Q

cardiogenic shock

A

low cardiac output, MI, ventricular arrhythmias, extrinsic compression and outflow obstruction

21
Q

hypovolemic shock

A

low CO due to loss of blood or plasma
massive hemorrhage
fluid loss from severe burn

22
Q

septic shock

A

vasodilation and peripheral pooling of blood

immune reaction to bacterial infection

23
Q

What are the top two reasons our heart breaks?

A
  1. failure of the pump

2. conduction disorder

24
Q

How does the heart compensate in CHF?

A
  1. increased blood volume
  2. leads to increased stretch/dilation or myocardium
  3. long fibers contract harder to increase the force needed to pump blood out
25
Q

What happens in decompensated CHF?

A

norepinephrine
NaCl and H2O retention
hypertrophy

26
Q

Common pathology in systolic heart failure

A

thin, weak heart muscle

greater and greater dilation can thin the heart

27
Q

Common pathology in diastolic heart failure

A

thick, stiff heart muscle

28
Q

Most common type of heart failure

A

systolic

29
Q

How does R side heart failure result from L side heart failure?

A

Systemic HTN > LV dilation > mitral insufficiency and LA enlargement > lung congestion and edema > R heart backup and failure > systemic congestion and edema

30
Q

What kind of heart failure will result in systemic congestion and edema?

A

R side

31
Q

What’s the most common way a plaque causes an MI?

A

ruptures, erodes, hemorrhages, and occludes vessel

32
Q

Most common location of MI

A

first few cm of LAD/LCA

Entire RCA

33
Q

How much occlusion do you need for symptomatic MI?

A

> 70%

34
Q

What is the time course of acute MI

A

by 2hrs, zone of necrosis starts to form

by 3-6 to 24 hours, you get major zone of necrosis

35
Q

Which enzymes peak early and which peak later in an acute MI?

A

Early: CK-MB
Later: TnI + TnT

36
Q

Valvular stenosis vs. insufficiency

A

Stenosis- wont open fully

insufficiency- wont close fully- regurg

37
Q

Subacute vs. Acute infective endocarditis

A

Subacute: previously diseased valve gets low virulence strain usually after dentist, just give abx

acute: normal valve get high virulence strain like staph, commonly IVDA on tricupsid (WORSE)

38
Q

What is most common type of cardiomyopathy?

A

dilated

Cardiovascular (2 decks)

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