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Cardio Block - CPR > General, Week 3 Cardio > Flashcards

General, Week 3 Cardio Flashcards

1
Q

what does thrombin do in the clotting cascade?

A

conversion of fibrinogen to fibrin

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2
Q

what is the main result of primary hemostasis?

A

formation of a platelet plug

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3
Q

what is the main result of secondary hemostasis?

A

formation of an insoluble fibrin clot (mortar for the platelet bricks)

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4
Q

what does the D-dimer tell you?

what makes/releases the D-dimer

A

if the patient is clotting or not

  • plasmin (which breaks up fibrin cross links) releases the D-dimer
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5
Q

what does factor 13 do in clotting?

A

it cross links the fibrin

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6
Q

what laboratory clotting test tests the instristic pathway?

what about the extrinsic pathway?

A

PT - extrinsic (TF and F7)

APTT - intrinsic (F12, F11, F9, F8)

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7
Q

what does antithrombin do in the body?

A

inhibits thrombin and certain coagulation factors

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8
Q

what does t-PA do?

what releases it?

A

activates plasminogen –> plasminogen + tPA activate plasmin, which breaks the fibrin clot and releases D-dimers

endothelial cells release tPA

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9
Q

what are the three ways that the body physiologically limits clot size?

A
  1. prothrombin
  2. Protein C and Protein S
  3. t-PA, plasminogen –> plasmin
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10
Q

the binding of what with thrombin activated protein c?

A

thrombomodulin (on endothelial cells)

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11
Q

what is the test of control (lab clotting times) for unfractionated heparin?

A

APTT (intrinsic pathway)

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12
Q

what are the factors that predispose thrombosis? Virchow’s triad

A
  1. endothelial injury
  2. stasis
  3. hyper coagulability (inherited or acquired)
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13
Q

with unfractionated heparin, what is the danger of giving it? (why do you need testing)

A

it binds to other proteins in plasma - don’t really know what dose you need

variable responses (can bind non -plasma protein, don’t really know how much you need)

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14
Q

with LMWH (low molecular weight heparin), why don’t you need to use the test of control?

A

much more predictable

doesn’t bind a bunch of non-anticoagulant proteins (because it is shorter), know how much you should give, less variable

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15
Q

what is the mechanism of UFH (unfractionated heparin)

A

it binds antithrombin, changing its shape and making it better able to bind F10a

ALSO, the UFH is long enough to wrap around and also bind thrombin

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16
Q

what is the mechanism of LMWH?

A

only long enough to bind to antithrombin

produces conformational change

this allows antithrombin to better bind 10a

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17
Q

what is fondaparinux?

what is its mechanism?

A

it is a synthetic analog of just the heparin binding interaction with antithrombin

it binds antithrombin –> conformational change –> better binds F10a

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18
Q

how do you give heparin? (either of the 3 forms)

A

IV or subQ

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19
Q

what can unfractionated heparin be reversed with?

what about LMWH?

A

protamine sulfate

not sufficient for LMWH or fondaparinux

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20
Q

what are the two major adverse effects of heparin?

A
  1. hemorrhage
  2. heparin induced thrombocytopenia (HIT)

HIT greater in UFH, less in other two

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21
Q

what does heparin induced thrombocytopenia - HIT -cause (2)?

A

it causes a decrease in platelet count (they are activated and consumed and going into a thrombus)

THROMBUS FORMATION because of IgG against heparin and PF4

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22
Q

how can you diagnose HIT?

A

decrease in platelet count ( > 50%)

PLATELET COUNT (and clinical circumstance, did they just undergo a major surgery?)

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23
Q

how do you manage HIT?

A
  1. cessation of heparin

2. direct thrombin inhibitor - argatroban

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24
Q

what is argatroban?

what is it used for?

A

it is a direct thrombin inhibitor

used for heparin induced thrombocytopenia

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25
Q

what is enoxaparin?

what is its mechanism?

A

low molecular weight heparin

binds to antithrombin and targets the inhibition of F10a

SUBQ

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26
Q

what is the antidote for LMWH and fondparinux?

A

there is none yet

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27
Q

what is the mechanism of warfarin?

A

competitive vitamin K antagonist, interferes with the vit K dependent synthesis of factors 2, 7, 9, 10, and protein C and S

28
Q

which is a teratogen? warfarin or heparin?

A

warfarin

heparin can’t cross the placenta

29
Q

how is warfarin metabolized?

A

cytochrome P450

30
Q

what is the test of control for warfarin?

A

PT (INR)

extrinsic

31
Q

what are the clinical indications for heparin drugs?

A

PE, DVT treatment and prophylaxis

32
Q

what are the major adverse effect(s) of warfarin?

A

BLEEDING

33
Q

what can you give to a patient to reverse the bleeding caused by warfarin therapy?

A

vitamin K

34
Q

what is the reversal agent for dabigatran?

A

idarucizumab

35
Q

what is dabigatran used for?

A

prevention of thrombus in people with atrial fibrillation

36
Q

what are the three direct factor 10a inhibitors?

A

rivaroxaban
apixaban
edoxaban

37
Q

The ________________ represents the sum of all of the mean electrical vectors occurring during ventricular depolarization.

A

mean electrical axis

38
Q

why do you not give warfarin in a patient with HIT?

A

it decreases the protein C and S activity

39
Q

what is the cause of coronary heart disease? (CHD)

A

coronary atherosclerosis

40
Q

what caused the increase in CHD in the 1900s to 1960s?? (4)

A
  1. longer life span because less infectious disease deaths
  2. more smoking
  3. processed diet
  4. less exercise
41
Q

what diet works for decreasing risk for coronary heart disease?

A

mediterranean diet

42
Q

a reduced fat diet, saturated fats, reduced cholesterol, etc. did what to cholesterol LDL levels? incidence of coronary heart disease?

A

it decreased LDL levels

it DID NOT CHANGE risk for CHD (MI or sudden cardiac death)

43
Q

what do statins do to cholesterol levels? what do they do for the incidence of CHD?

A

they decrease cholesterol levels

decrease incidence of MIs and cardiovascular death

44
Q

what is coronary heart disease?

A

atherosclerosis in the coronaries leading to signs/symptoms/complications

45
Q

what is a atheromatous plaque? (2 components)

A

elevated lesion involving the tunica intima with

  1. lipid core
  2. fibrous cap
46
Q

aneurysms that bulge out equally on both sides of the vessel are called ________ aneurysms

A

fusiform

47
Q

aneurysms that only bulge out on one wall of the vessel are called _______ aneurysms

A

sacular (berry)

48
Q

where do arterial aneurysms occur most commonly?

A

abdominal aorta

49
Q

How does an aneurysm occur? general, then some examples

A

weakened vessel wall

atherosclerosis, congenital, infection, vasculitis, medial degeneration

50
Q

where do aortic dissections occur most commonly?

A

the ascending aorta

51
Q

how does an aortic dissection present?

A

chest pain, rupture to pericardial sac, sudden death

52
Q

giant cell arteritis is a type of ______ vessel vasculitis. It usually affects what vessels?

A

large

cranial

53
Q

what lab test can help you diagnose giant cell arteritis?

what can be a more definitive measure to confirm it? (although 1/3 are false negatives)

A

erythrocyte sedimentation rate (ESR)

biopsy - giant cells and inflammation in vessel

54
Q

what is affected in Takayasu vasculitis?

A

aorta and its branches

become stenotic - thick wall and granulomatous inflammation (giant cells)

MEDIAL inflammation and descturction

55
Q

fibrinoid necrosis of all 3 layer of the blood vessel via immune system is ____________________.

A

polyarteritis nodosa (medium vessel vasculitis)

56
Q

what does polyarteritis nods present with?

A

organ dysfunction of whatever is downstream from the obstruction/aneurysm (kidneys, GI, lungs, muscles, CNS, skin, etc)

57
Q

what is the vasculitis that produces aneurysms that look like peas on a pod//

A

polyarteritis nodosa (medium)

58
Q

granulomatosis with polyangiitis is a _________ vessel vasculitis that usually affects what areas:

A

small

lung, kidneys (glomerulus), nasopharynx muscosa

59
Q

what is associated with anti-neutrophil cytoplasmic antibodies (ANCA)

A

granulomatosis with polyangiitis (small vessel vasculitis)

60
Q

what do you see on histo with granulomatosis with polyangiitis? (3)

A

geographic NECROSIS

vasculitis

giant cells

61
Q

what does a patient with giant cell arteritis present with?

A

headache, changes in vision (sometimes blindness), facial pain

62
Q

who does takayasu arteritis (large vessel vasculitis) present in?

A

usually asian females < 40 years

63
Q

transmural inflammation of the arterial wall with fibrinous necrosis leads you to think:

A

polyarteritis nodosa (medium vessel vasculitis)

64
Q

what does a valvular insufficiency mean?

A

synonym for regurgitation (does not close properly, leaks back)

65
Q

what is valvular regurgitation (insufficiency)

A

the valve does not close completely, blood leaks the other way

Cardio Block - CPR (6 decks)

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