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CVPR Unit 2 > Lecture review 2 > Flashcards

Lecture review 2 Flashcards

1
Q

Most common cause of ACS?

- one other?

A

By far: atherosclerotic plaque rupture with thrombus

other: cocaine abuse→ ↑s sympathetic tone by blocking NE reuptake + enhance catecholamines → vasospasms and ↓ myocardial O2 supply

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2
Q

Most common cause of ACS?

A

By far: atherosclerotic plaque rupture with thrombus

other: cocaine abuse→ ↑s sympathetic tone by blocking NE reuptake + enhance catecholamines → vasospasms and ↓ myocardial O2 supply

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3
Q

Systemic signs of subsequent catecholamine release

A

diaphoresis (sweating)
tachycardia
cool/clammy skin

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4
Q

When does Troponin

  • begin
  • peak
  • last until
A
  • begin: 3-4 hours
  • peak: 18-36 hours
  • last until: up to 10 days
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5
Q

When does CKMB

  • begin
  • peak
  • last until
A
  • begin: 3-4 hours
  • peak: 24 hours
  • last until: 2-4 days
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6
Q

Anticoagulants

A 
Enoxaparin (LMWH)
UF Heparin (long one)
Fondaparinux
Bivalirudin
Thrombolytics
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7
Q

Antiplatelets

A

Aspirin

Clopidogrel
Prasugrel
Ticagrelor

GPIIb/IIIa inhibitors

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8
Q

Anticoagulants

A 
Enoxaparin (LMWH)
UF Heparin (long one)
Fondaparinux
Bivalirudin
Thrombolytics
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9
Q

name their targets
Enoxaparin (LMWH)
DX-9065a

A

Factor Xa

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10
Q

name their targets
UF Heparin (long one)
Fondaparinux

A

AT III directly

and thrombin indirectly

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11
Q

Anticoagulants

A 
Enoxaparin (LMWH)
UF Heparin (long one)
Fondaparinux
Bivalirudin
Thrombolytics
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12
Q

Antiplatelets

A

Aspirin

Clopidogrel
Prasugrel
Ticagrelor

GPIIb/IIIa inhibitors

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13
Q

Name their targets
Bivalirudin
Thrombolytics

A

Bivalirudin: direct thrombin inhib

Thrombolytics: fibrin

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14
Q

Name their targets
Aspirin

Clopidogrel
Prasugrel
Ticagrelor

A

Aspirin: irreversibly inhibits cox 1 preventing the formation of thromboxane A2.

Clopidogrel
Prasugrel
Ticagrelor
- blocks P2Y12: inhibiting ADP binding

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15
Q

Name their targets
Aspirin

Clopidogrel
Prasugrel
Ticagrelor

A

Aspirin: irreversibly inhibits cox 1 preventing the formation of thromboxane A2.

Clopidogrel
Prasugrel
Ticagrelor
- all blocks P2Y12: inhibiting ADP binding

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16
Q

Contraindications for Exercise Treadmill Test (ETT):

A 
Unstable angina
untreated arrythmias
advanced AV block
HF
acute myocarditis, pericarditis
aortic stenosis
uncontrolled HTN
HOCM
acute illness
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17
Q

When is B-Type most helpful?

A

Actually most helpful when it is normal: good at excluding HF as cause of symptoms

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18
Q

Atherosclerosis is a category under the big group ______

name other categories in that group

A

Arteriosclerosis

  1. atherosclerosis
  2. Monckeberg’s medial calcific sclerosis
  3. arteriosclerosis of small arteries/arterioles
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19
Q

Aortic dissection primarily occurs in individuals with _____

A

HTN (>90%) of cases

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20
Q

Known ischemic heart disease syndromes

A
  1. angina pectoris (most common)
  2. MI
  3. Chronic ischemic HD → congestive HF
  4. sudden cardiac death
21
Q

What is the time frame when an infarcted heart is susceptible to rupture?

A

3-7 days

22
Q

PARENTERAL anticoagulant agents

A 
Heparin (UF)
Enoxaparin (LMWH)
Fondaparinux
Lepiruden
Bivaliruden
23
Q

ORAL anticoagulant agents

A

Warfarin
Non-vit K Oral Anticoagulants (NOAC)
Dabigatran
Rivaroxaban

24
Q
  • Parins
  • Oxaban:
  • ruden:
  • grels
A
  • Parins are indirect that act through antithrombin III (ATIII) and inhibit Xa
  • Oxaban: direct Xa inhibitors
  • ruden: direct Thrombin inhibitors
  • grels, you know its an ADP antagonist
25
Q

How do you monitor heparin? LMWH? Warfarin?

A

Heparin: aPTT
LMWH: not needed
Warfarin:

26
Q

Overdose treatment for UFH/LMWH

A

protamine

27
Q

Which one is first order renal elimination kinetics and which one is xero order dose dependent kinetics?

A

LMWH: first order

UFH: zero order (dose dependent)

28
Q

When is NOAC preferred over warfarin?

A

Nonvalvular A Fib

29
Q

Medical treatment to prevent recurrent Ischemic episodes

A
  • Three classes:
    1. Organic nitrates - venodilators (and arterial)
    2. β-adrenergic blockers
    3. Calcium channel blockers

Goal: ↓ cardiac workload, ↑ myocardial perfusion

30
Q

increased LVEDP (choose one) increases/decreases coronary blood flow

A

decreases

31
Q

Which anti-anginal agents increase HR? (bad)

  • BBs
  • Nitrates
  • Nifedipine
  • Verapamil
  • Diltiazem
A
  • Nitrates

- Nifedipine

32
Q

Which anti-anginal agents increase HR? (bad)

  • BBs
  • Nitrates
  • Nifedipine
  • Verapamil
  • Diltiazem
A
  • Nitrates

- Nifedipine

33
Q

Which anti-anginal agents increase LV volume? (bad)

  • BBs
  • Nitrates
  • Nifedipine
  • Verapamil
  • Diltiazem
A

BBs

34
Q

Which drugs decrease demand?

  • BBs
  • Nitrates
  • CCBs
  • Antithrombotics
A
  • BBs
  • Nitrates
  • CCBs
35
Q

Which drugs reduce thrombosis?

  • BBs
  • Nitrates
  • CCBs
  • Antithrombotics
A

antithrombotics

36
Q

Which drugs prevent vasospasm?

  • BBs
  • Nitrates
  • CCBs
  • Antithrombotics
A
  • Nitrates

- CCBs

37
Q

Which nitrate would you use for acute and longer acting angina prevention?

A

Nitroglycerin: acute attacks

Isosorbide: longer acting prevention

*note: - Nitrates are purely for symptomatic relief, not improve survival

38
Q

Will BBs prevent vasospasms? Why/why not?

A

No, bc they are not vasodilators

  • want to use nitrates/CCBs to prevent vasospasms that cut supply
39
Q

Nitrates result in an (choose one) increase/ decrease in LVEDP and systemic vascular resistance

A

decrease

40
Q

1st line use of CCBs

A
  1. rate control of a fib/ a flutter
  2. coronary vasospasm or raynauds
  3. HOCM
41
Q

2nd line uses of CCBs

A

HTN

Stable angina

42
Q

CCBs:

Dihydropyridines

A

Nifedipine,

Amlodipine

43
Q

CCBs:

Nondyhydropyridines

A

Verapamil

Diltiazem

44
Q

CCBs:
Dihydropyridines
- do they act on nodal cells?

A

Nifedipine,
Amlodipine

No, verapamil and diltiazem do

45
Q

CCBs:
Nondyhydropyridines
- do they act on nodal cells?

A

Verapamil
Diltiazem

Yes

46
Q

What happens to myocardial perfusion if you block B2?

A

Like other beta-adrenergic agonists, they cause smooth muscle relaxation

If you block B2, youll block the vasodilatory effect → constrict → increase LV volume → decrease myocardial blood perfusion

47
Q

HTN is the no 1 risk factor for what?

A

HF

48
Q

T/F aspirin reduces CVD events in type II diabetes

T/F raising HDL or lowering TG reduces CVD events

A

False

False

CVPR Unit 2 (6 decks)

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