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Cardio > Vasculitis and Complications of MI (Nichols) > Flashcards

Vasculitis and Complications of MI (Nichols) Flashcards

1
Q

Heterogeneous group of inflammatory blood vessel diseases that are mostly autoimmune (and a few are infectious in etiology

A

vasculitis

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2
Q

What is the most specific sign of vasculitis?

A

palpable purpura

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3
Q

Acute necrotizing inflammatory disease of arterioles, capillaries and venules, especially in the skin

A

hypersensitivity angiitis

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4
Q

What is hypersensitivity angiitis of the:
skin?
internal and generalized?

A

skin: leukocytoclastic vasculitis (10% due to meds)
internal: microscopic polyangiitis

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5
Q

T or F: hypersensitivity angiitis is necrotizing

A

True: blood vessels become necrotic)

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6
Q

What vessels does hypersensitivity angiitis affect?

A

arterioles, capillaries, and venules

  • *the smallest blood vessels
  • particularly in the skin*
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7
Q

What is leukocytoclasia and what is it assc with?

A

infiltration and breakdown of blood vessels by neutrophils with breakdown

Hypersensitivity angiitis

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8
Q

nuclear dust from leukocytoplasia

A

Hypersensitivity angiitis

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9
Q

T or F: the lesions in Hypersensitivity angiitis will all be in the same phase (i.e. if there are polys in one there will be polys in another and if lymphocytes are in one they will be in the other)

A

T

**polyareritis nodosa they will be in diff phases

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10
Q

What is the difference between the lesions in polyartitis nodosa and hypersensticiry angiitis?

A

in Hypersensitivity angiitis will all be in the same phase (i.e. if there are polys in one there will be polys in another and if lymphocytes are in one they will be in the other)

in polyareritis nodosa they will be in diff phases

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11
Q

What will a skin biopsy look like in HS angiitis?

A

clustering of blue dots (neutrophils and lymphocytes) around a blood vessel

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12
Q

What are the Tx for HS angiitis?

A

skin (Leukocytoclastic vasculitis): none (except stop drug)

internal (Microscopic polyangiitis): if major organ damage: immunosuppressive therapy

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13
Q

Granulomatous inflammatory disease of medium & large arteries, especially in the head, and (in 10%) thoracic aorta and its branches

A

temporal Arteritis (aka Giant cell Arteritis)

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14
Q

What is the epidemiology of temporal Arteritis (aka Giant cell Arteritis)?

A

elderly white females

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15
Q

segmental transmural chronic granulomatous with multi nucleated giant cells centering on internal elastic lamina
intimal thickening and stenosis

palpable and tender areas of inflammation

A

temporal Arteritis (aka Giant cell Arteritis)

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16
Q

What type of arteries does temoral arterits involve?

A

medium and large (esp in the head)

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17
Q

Where are the giant cells found in temporal Arteritis (aka Giant cell Arteritis)? How do they contribute to pathology?

A

along internal elastic lamina and destroying it –> destroy blood vessels

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18
Q

What is the most common sign/symptom of temporal arteritis?

worst complication?

A

headache

blindness

19
Q

How is temporal arteritis Dx? what is the Tx?

A

elevated ESR and positive biopsy

steroids +/- aspirin

20
Q

mucocutaneous LN syndrome

A

kawasaki disease

21
Q

What arteries does Kawasaki disease typically affect?

A

medium arteries (esp coronaries with aneurysm formation in 20%)

22
Q

What is the epidemiology of kawasaki disease?

A

1-2 yo children

asians

23
Q
  • Endothelial necrosis (+ transmural inflammation with neutrophils, lymphocytes, necrosis)
  • aneurysms and thrombosis formation
A

Kawasaki disease

24
Q

What are the complications of kawasaki disease?

A

MI (rare in 1y/o….)
arterial rupture
death (1%)

25
Q

signs and symptoms of Kawasaki disease (4)

A

persistent high fever
conjunctivitis (red eye)
mucosal/tongue and skin erythema
cervical lymphadenopathy

26
Q

What is the Tx of kawasaki disease?

A

IV Ig and aspirin (reduced risk of CV events from 20 to <5%)

27
Q

What is the #1 complication of MI?

A

cardiac arrhythmia (90% of cases)

but can get any of the other ones we learned about

28
Q

What is the 2nd most common complication of MI? What is the manifestation of this?

A

hear failure (60% of cases)

dyspnea, pulmonary rales, S3 gallup

29
Q

What is the 3rd most common complication of MI? What is the manifestation of this?

A 
mural thrombus (20% of cases) on the endocardial surface of the infract 
**stasis at site of infarct
30
Q

Where do the mural thrombi that form post MI typically embolize? When?

A

brain or kidney in 2nd or 3rd week

31
Q

Cardiogenic shock occurs when ____% if the left ventricles is infarcted

A

greater 40%

32
Q

What is the 4th most common complication of an MI? When does this typically occur?

A 
cardiac rupture (5% of cases) 
5th day (wall is not strengthened by scar yet/it is at its weakest)
33
Q

____ commonly occurs with transmural infarcts and poor collateral circulation

A

cardiac rupture

34
Q

Cardiac rupture occurring on a free wall of left ventricle will cause _____

A

cardiac temponade

35
Q

Cardiac rupture on the inter-ventricular septum will create a ______

A

sudden shunt of blood from the left ventricle to the right ventricle

36
Q

What is the 5th most common complication of an MI? When does it occur?

A

pericarditis over transmural infarcts (5% of cases) = inflammation reaches the surface of the heart
2 weeks to months after MI

37
Q

Dressler syndrome

A

???

38
Q

T or F: Nichols told a nice woman who unexpectedly lost her husband that he just “dropped over dead”

A

T

39
Q

thinned scar from transmural infarct which moves paradoxically outward in systole

A

dyskinesia

40
Q

What is the 6th most common complication fo MI?

A

ventricular aneurism/dyskinesia (thin wall)

41
Q

What is the 7th most common complication of MI?

A

ruptured papillary muscle

42
Q

Which papillary muscle usually ruptures? What does this cause?

A

posterior causing mitral regurg

43
Q

But what is the most common cause of acute mitral regurg post MI? 2nd most common?

A

heart failure > rupture of papillary muscle

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