Vasculitis and Complications of MIs Flashcards Preview

Cardio Block > Vasculitis and Complications of MIs > Flashcards

Flashcards in Vasculitis and Complications of MIs Deck (55):
1

Two divisions of vasulitis

Infectious and non-infectious (primary)

2

Predominant fungal cause of infectious vasculitls

Aspergillus

3

Predominant bacterial cause of IV

Cytomegalovirus

4

Predominant bacterial cause

Psuedomonas

5

Pathophysiology of Primary Vasculitis

Dendritic cells int eh tunica adventitia go haywire and instead of disposing of self-recognizing immune cells they activate them. These immune cells then degrade the elastic lamina
Another mechanism.... Immune complex deposition. Inflammation mediated by complement, chemoattractants, neutrophils, lysosomal enzymes, free radicals.

6

Major signs and symptoms

palpable purpura and fever

7

Hypersensitivity angiitis

acute necrotizing inflammatory disease of the smallest vessels (arterioles, cappilaries, venuoles). Usually in the skin

8

Cutaneous hypersensitivity angiitis also referred to as?

Leukocytoclastic vasculitis

9

10% of cases of hypersensitivity angiitis due to?

drugs

10

What drugs?

Quinolones, penicillins, sulfonamides, Retinoids, etc...

11

Microscopic polyangiitis is

hypersensitivity angiitis involving internal organs

12

Pathogenesis of hypersensitivity angiitis?

immune complex deposition and complement activation 7-10 days after exposure to an antigen (drug)

13

Pathology of hypersensitivity angiitis

infiltration of vessels by neutrophils, later lymphocytes

14

Diagnosis requires?

biopsy

15

Signs

palpable purpura

16

Treatment

stop the drug, treat the infection, excise the tumor...etc...
If it infects the organs, treat with immunosuppresive therapy

17

Temporal arteritis

Giant cell arteritis, granulomatous inflammatory disease of medium and larger arteries, esp in the head

18

Temporal arteritis common

Fairly...1 in 750 over the age of 50, female predominance, more common in whites

19

Temporal arteritis autoimmune?

yep

20

Pathology of temporal arteritis

multinucleated giant cells destroy internal elastic lamina. Transmural granulomatous inflammation. Intimal thickening, cell proliferation and luminal stenosis

21

Signs and symptoms

headache, visual disturbance, jaw claudication, swollen tender artery.
Fever malaise and wt loss make blindness less likely

22

Polymyalgia rheumatica

chronic autoimmune inflammatory disease of muscle. Temporal arteritis is associated with it in 40% of cases.

23

Complcations of temporal arteritis

blindness, aortic aneurysm, arterial dissection, arterial rupture

24

Temporal arteritis is diagnosed by

ESR and biopsy

25

Treat temporal arteritis with

steroids

26

Temporal arteritis

old white women

27

Kawasaki disease

mucocutaneous lymph node syndrome...vasculitis of medium arteries, especially coronaries.

28

kawasaki predominantly effects who>

children 1-2 yrs of age, males, japanese

29

Kawasaki complications

arterial rupture, MI, death

30

Pathogenesis

An immune reaction to an RNA virus

31

Signs and symptoms

high fever, conjunctivitis, mucosal and skin erythema and edema, swollen strawberry tongue

32

Treat kawasaki with

Aspirin and IV Ig

33

Seven most common MI complications

cardiac arrhythmias, heart failure, mural thrombus formation, cardiac rupture, pericarditis, aneurysm formation, papillary muscle rupture

(A-rhhythmic heart forms murals that rupture peri form and then rupture)

34

Cardiac arrhythmias complicate MI in what % of cases?

90%

35

Most common arrhythmia

accelerated idioventricular rhythm

36

What is an idioventricular rhythm

originates in the ventricle, from yocytes outside the conduction system. Spreads more slowly than a normal rhythm so the QRS is wider than normal and funny looking.

37

If the rate of an idioventricular rhythm is in the normal range it is called

accelerated

38

Accelerated idioventricular rhytm is often a sign of what

reperfusion, which can mean its a good thing

39

supraventricular tacchycardia and sinus tacchycardia are only bad if:

they are too rapid

40

Ventricular tachycardia

occurs in around 15% of cases. Always bad...can turn into ventricular fibrillation

41

AV block is most likely when?

When the infarction is in right coronary artery territory b/c the AV node is more served by the right coronary artery than the left

42

Heart failure

complicates 60% of MI

43

Heart failure occurs when

20% or more of the LV is infarcted

44

When 40% of the LV is infarcted,

the patient is in cardiogenic shock

45

Heart failure due to MI are in four hemodynamic groups called forrester classes:

Class I patients have a preserved CO and low or normal left atrial pressure

46

Class II pts

Preserved CO but high left atrial pressure (over 18)

47

Class III

Low cardiac output and high atrial pressure (over 18)

48

Class IV

Low cardiac output and high left atrial pressure

49

Class II treatment

diuretic

50

Class III

Volume expansion

51

Why is it important to differentiate class II from class III?

treatment is completely different because in class III the cardiac output is low

52

Mural thrombus

complicates MIs in 20% of cases

53

Mural thrombi commony embolize where

brain or kidney in the 2nd or third week

54

Cardiac rupture

5% of cases. Allows blood part of the systolic output to go into the pericardium causing a hemopericardium and cardiac tamponade. Typically around the fifth day

55

Pericarditis

about 5% of cases...day 2-4 after MI or 2mths after due to Dressler syndrome.