Cardio Unit 2

Question 1

What does heparin have to bind to in order to work as an anti-coagulant?

Answer 1

Antithrombin (aka ATIII aka antithrombin 3)

Question 2

What parts of the coag cascade does the heparin-ATIII work on?

Answer 2

Thrombin (2a)

Factor Xa

Question 3

-parin

Signifies what for a pharmaceutical?

Answer 3

It works indirectly through ATIII

Question 4

-xaban

Signifies what for a pharmaceutical?

Answer 4

Directly Xa inhibitors

Xaban = ban the Xa :)

Question 5

What are the oral anticoag drugs?

Answer 5

Warfarin (Coumadin)
Dabigatran
Rivaroxaban
Apixaban
Edoxaban

Question 6

-rudin

Signifies what for a pharmaceutical?

Answer 6

Direct thrombin (2a) inhibitor (comes from hirudin, which is what leeches secrete as an anticoag)

Question 7

What test do you use to monitor heparin?

Answer 7

aPTT

zero-order dose-dependent kinetics; usually given as continuous infusion

Question 8

What test do you use to monitor LMWH?

Answer 8

Not needed. Dosed mg/kg

first-order renal elimination kinetics

Question 9

How do you treat an overdose of heparin or LMWH?

Answer 9

Protamine

Question 10

When are heparin & LMWH used?

Answer 10

(1) Treatment of coronary occlusion in unstable angina or acute MI (ACS)
(2) Prevent state of hypercoag following vascular injury/venous stasis
(3) Prophylaxis/treatment of DVT
(4) Prevention of cerebral thrombosis in evolving stroke

Question 11

How do you decide whether to use heparin or LMWH?

Answer 11

LMWH generally preferred:

• less variability (no monitoring)
• less thrombocytopenia

However, heparin effect is more rapidly & completely reversed by protamine - safer in pts with renal impairment (LMWH renally excreted)

Question 12

What is the mechanism of action of Warfarin?

Answer 12

Acts in liver to prevent synthesis of 2, 7, 9, 10 clotting factors

Question 13

What is the mechanism of Dabigatran?

Answer 13

Acts in the plasma to directly inhibit the action of thrombin (2a)

Question 14

What is the mechanism of rivaroxaban/apixaban?

Answer 14

Acts in the plasma to directly inhibit 10a

Question 15

When should Warfarin be used?

Answer 15

A-fib with valvular problems (mechanical/bioprosthetic valve, prior MVR or MVS)
Also pts with CKD

Question 16

What type of anticoagulant is preferred in non-valvular a-fib?

Answer 16

NOAC

Non-Vit K Oral Anticoags = Dabigatran, Rivaroxaban, Apixaban, Edoxaban

Question 17

-grel (-grel-)

Signifies what for a pharmaceutical?

Answer 17

ADP receptor antagonist (antiplatelet)

Question 18

What is the major drug used to decreased cardiac oxygen demand in pts with stable angina?

Answer 18

β-blockers!

Question 19

What is the big difference between β-blockers and nitrates + CCBs?

Answer 19

β-blockers are not vasodilators

Question 20

What is the mechanism of action of nitrates?

Answer 20

They are converted to NO –> ↑ GTP to cGMP –> vasodilation in vascular SM –> ↓ in systolic pressure –> ↓ in preload/LVEDP
Primary effect: ↓ wall tension, so ↓ myocardial O2 demand
Secondary effect: improves perfusion of myocardium

Question 21

What is the negative effect of nitrates and why does this happen?

Answer 21

They cause an ↑ in heart rate. Because vasodilation –> BP goes down –> reflex tachycardia

Question 22

Why do β-blockers cause an ↑ in LV volume?

Answer 22

They block β2 dilation in vascular SM on venous side –> increase tone –> more blood back –> ventricles filled more

Question 23

What is variant (Prinzmetal) angina?

Answer 23

Intense vasospasm. Not related to plaques.

Question 24

In stable angina, what drugs do you give? (demand increases)

Answer 24

You want to ↓ demand: β-blockers, nitrates, CCBs

these also marginally ↑ supply

Question 25

In unstable angina, what drugs do you give? (↓ in supply)

Answer 25

You want to reduce thrombosis, ↓ demand, ↑ supply: antiplatelet/anticoags, β-blockers, nitrates, CCBs

Question 26

In variant angina, what drugs do you give? (vasoconstriction)

Answer 26

Prevent vasospasm: nitrates, CCBs

Question 27

-dipine

Signifies what for a pharmaceutical?

Answer 27

Calcium channel blockers - specifically, DHPs

Question 28

What are the two CCBs we learned about that don’t follow the nomenclature rule?

Answer 28

Verapamil and Diltiazem (non-DHP)

Question 29

When are CCBs typically not used as much?

Answer 29

Unstable angina

Question 30

What is the full, detailed MOA of CCBs in vascular SM?

Answer 30

Block L-type Ca channels –> prevent Ca-calmodulin complex –> prevent the activation of myosin light chain kinase –> MLCK leads to SM contraction via phosphorylation of myosin heads

Question 31

Where do nifedipine and amlodipine (CCBs) have their strongest dilatory effect?

Answer 31

Vessels (not heart)

Question 32

Where does verapamil (CCB) have its strongest dilatory effect?

Answer 32

SA/AV conduction (phase 0) –> anti-arrhythmic effects (↓ HR, ↓ contractility)

Question 33

Where does diltiazem have its strongest dilatory effect?

Answer 33

SA/AV conduction (phase 0) and contraction (phase 2) (↓ HR, ↓ contractility)

Question 34

Are Class I and Class III drugs more rate-controllers or rhythm-controllers?

Answer 34

Rhythm-controllers (more dangerous)

Question 35

What are the major uses of CCBs?

Answer 35

#1 - ANGINA. Long-lasting ↓ in PVR
- reduced heart O2 requirement, reduced coronary arterial tone 

Otherwise, arrhythmias, HTN, subarachnoid hemorrhage, inhibition of premature labor

Question 36

What could happen to a pt if you give them a high initial dose of metoprolol?

Answer 36

Metoprolol is β1 (cardiac) selective, but only at lower doses. If you give someone a higher dose, could also work on β2 receptors (lungs/blood vessels) - BAD. (Could cause bronchospasm in an asthmatic pt!)

Question 37

What are β-blockers used for in angina?

Answer 37

Useful in STABLE ANGINA - ↓ oxygen requirements (↓ HR, BP, & contractility).

Can block reflex tachycardia in nitrates

NOT vasodilators, thus not useful in variant angina