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pharm drugs > CV drugs (8) > Flashcards

CV drugs (8) Flashcards

1
Q

What drugs are used to treat Angina?

A

Calcium channel blockers, Nitrates, Beta blockers

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2
Q

Nitrates MOA

A

relaxation of smooth muscle whin blood vessels, resulting in the desired vasodilatory effect

decrease preload and afterload reduce workload of heart reduce O2 demand

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3
Q

How do you store Nitrates?

A

Limit light expossure by keeping in brown glass bottle

Short shelf life (6 months, 3 months)

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4
Q

How do you know if Nitrates is working?

A

Tingling sensation as drug dissolves

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5
Q

What is the dosage for Nitrates?

A

After 1st dose relief should occur within 1-2 minutes
2nd dose if symptoms still present after 5 minutes ( up to 3 doses in 15 min)
No relief  possible MI

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6
Q

Nitrates AE

A

reflex tachycardia, dizziness, OH (orthostasis), weakness, severed headache

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7
Q

What do you do when suspecting cardiac event?

A

chew 325 mg non-enteric coated aspirin.

Up to 3 doses of NG can be administered over 15 minutes
IV nitroglycerin may be started in ED

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8
Q

Antithrombotic Classes

A

Antiplatelets, Anticoagulants, Fibrinolytics

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9
Q

What is the difference between Antiplanets and Anticoagulants?

A

Antiplatelets- preventing the thrombus

Anticoagulants-use when some one developed a clot and prevent it from worsening

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10
Q

What drugs class are Antiplatelets?

A

Aspirin, ADP receptor inhibitors

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11
Q

ADP Receptor drugs?

A

Clopidogrel (Plavix)

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12
Q

MOA ADP Receptor Inhibitors (Irreversible)

A

block ADP binding to receptor thus decrease platelet aggregation

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13
Q

How long does Clopidogrel (Plavix) last?

A

platelet aggregation (for lifespan of platelet, 7-10 days)

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14
Q

What is the biggest concern for clopidogrel (Plavix)?

A

Bleed is biggest concern- monitor symptoms and labs (Hgb/Hct)

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15
Q

How is ADP Receptor Inhibitors metabolized?

A

CPY

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16
Q

What are some uses for ADP Receptor Inhibitors?

A

Used after ACS (acute coronary syndrome) with PCI (stent placement), stroke (Plavix only)

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17
Q

Heparin MOA

A

inactivates thrombin and FIXa, FXa, FXIa, FXIIa = prevents conversion of fibrinogen to fibrin

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18
Q

How long does it take for Warfarin to have an effect

A

Does not have immediate effect- usually 3-5 days for full effect and longer to stabilize dose

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19
Q

When do you use nitrates?

A

Sublingual nitrates drug of choice for acute attacks to provide immediate symptom relief

also be administered before activity to prevent symptoms

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20
Q

What are the Nitrate drugs?

A

Nitroglycerin

Isosorbide mononitrate

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21
Q

What is the role of Thrombin?

A

Converts fibrinogen to fibrin

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22
Q

What are the box warnings for ADP Receptor Inhibitors (Irreversible)?

A

↓ efficacy in some genetic variants that make them CYP2C19 poor metabolizers (present in 50% of Asians, 30% African-Americans, 25% Caucasians)

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23
Q

What are the Parenteral and PO Anticoagulant class?

A

Parenteral- Heparin, LMWH

PO: Vitamin K antagonist, Direct thrombin inhibitor, Factor SX inhibitors

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24
Q

Reversal Agent for Heparin

A

protamine sulfate

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25
Q

What is HIT?

How do you treat HIT?

A

When antibodies which bind to heparin thus is activates platelets and increase clotting

Treat with direct thrombin inhibitors or Factor Xa inhibitors

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26
Q

What is a LMWH drug?

A

enoxaparin (Lovenox)

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27
Q

How is LMWH different than Heparin?

A

LMWH has greater effect on inhibiting FXa than thrombin

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28
Q

Why is LMWH preferred over Heparin?

A

simple dosing, no monitoring requires, decrease HIT

29
Q

What is the new reversal agent for LMWH?

A

andexanet alfa (Andexxa)

30
Q

What is drug is Vitamin K Antagonist?

A

warfarin (Coumadin)

31
Q

Vitamin K Antagonist MOA?

A

depletes Vitamin K thus synthesis of factors VII, IX, X and II, and protein C and S

32
Q

If INR is low, what is the patient at risk for?

A

more risk of clotting

33
Q

If INR is high, what is the patient at risk for?

A

More risk for a bleed

34
Q

What are INR levels for Atrial fibulation or venous thrombus embolism

A

AF: 2-3
VTE: 2.5-3.5

35
Q

What CV drugs have genetic variants for CYP?

A

Warfarin and Clopidogrel (Plavix)

36
Q

What happens to INR when there is an increase consumption of vitamin K foods/

A

Decrease INR

37
Q

Direct Thrombin Inhibitor MOA

A

binds directly and reversibly to thrombin with high selectivity  inhibits conversion of fibrinogen to fibrin

38
Q

What to lookout for when taking Direct Thrombin Inhibitor?

A

Less intracranial bleeding than warfarin but more GI bleeding

39
Q

What are Factor XA Inhibitor drugs?

A

rivaroxaban (Xarelto), apixaban (Eliquis)

40
Q

Factor XA Inhibitor MOA

A

selectively and reversibly binds FXa thus stops further coagulation cascade

41
Q

What is the difference between Rivaroxaban and Warfarin?

A

less intracranial bleed than warfarin; rivaroxaban has more GI bleed (also on Beers List)

Less drug interactions than warfarin

42
Q

What to look for when taking Rivarozaban?

A

It must be taken with a high fat meal

43
Q

Which Factor XA inhibitor drug is has the lowest risk for a bleed?

A

Apixaban

44
Q

What is preferred anticoagulant drug when patient is noncompliant

A

Take Warfarin b/c DOAC’s have a shorter duration of action

45
Q

How do you monitor with Antiplatelets and Antithrombotics?

A

Bleeding, Brusing, Block, tarry stools,
Seek med help if nosebleed or a cut wont stop bleeding
Seek med help if hit head during a fall b/c risk of intercranial bleeding

Clotting-Red, swollen, warm extremity, usually unilateral and in calf

46
Q

Fibrinolytics MOA and uses

A

MOA: plasmin breaks fibrin links in the thrombus

Use: start immediately after stroke, MI, PE

47
Q

What drugs to use for VTE Prophylaxis

A

LMWH or heparin used for prevention

Then bridge to PO

48
Q

What is 1st line long term VTE treatment?

A

DOAC

49
Q

Therapeutic Concerns for Antithrombotic Drugs

A

Falls could cause internal bleeding

Contraindicated PT treatments

50
Q

What drug classes are use to treat Atherosclerosis?

A

HMG-COA reductase inhibitors (Statins) and Ezetimibe (Cholesterol absorption Inhibitor)

51
Q

Statins MOA

A

block cholesterol synthesis

52
Q

Statins AE

A

myalgia (symmetrical, large proximal muscle groups), myopathy and rhabdomyolysis is rare, tendinopathy and tendon rupture

53
Q

Which population is likely to get myalgia from statins?

A

elderly female, low BMI Asian descent, excess alcohol, high levels physical activity

54
Q

Which statins are less likely to get myalgia?

A

pravastatin, rosuvastatin

55
Q

Ezetimibe MOA

A

inhibits absorption of cholesterol in small intestine

56
Q

What is the 1st and 2nd line Cholesterol drugs

A

1st line = statin

2nd line = ezetimibe added on if remain uncontrolled or can’t tolerate statin

57
Q

Therapeutic Concerns about Statins

A

Myositis and Myalgia
Muscle pain, fatigue, weakness
Creatinine kinase (CK) >10 times upper normal limits

Rhabdomyolysis
Severe muscle damage, marked CK elevation, renal
dysfunction

Grapefruit juice (perhaps pomegranate): inhibits CYP3A4

58
Q

HFpEF treatment

A

diuretics (loop), aldosterone antagonist (K+ sparing antagonist)

59
Q

Goals in HFrEF

A

decrease edema and congestion, increase contractility, ↓ preload and afterload = vasodilators (hydralazine, isosorbide dinitrate, sacubitril), ACEi, or ARB

60
Q

Baseline HFrEF

A

ACEi or ARB + beta-blocker + diuretic prn(loop

61
Q

Entresto MOA and AE

A

ACE and ARB MOA and AE

62
Q

Digoxin MOA

A

inhibits Na+/K+ ATPase pump in myocardial cells = ↑ intracellular sodium = ↑ Ca2+ from Na+/Ca2+ exchange pump = ↑ contractility

63
Q

Drug classes to treat Arrythmia?

A

B-blockers, Amiodarone

64
Q

Amiodarone MOA and uses

A

Used for ventricular arrhythmias

Basic MOA: Prolong the duration of the action potential by blocking K+, Na+, and Ca2+ channels; also some beta-blocker activity

65
Q

Amiodarone AE

A

Liver toxicity, thyroid dysfunction, pulmonary fibrosis, neuropathy, bluish discoloration on exposed areas of the skin

66
Q

How long does Amiodarone last?

A

Long 1/2 life. 50 days can prolone AE even after withdrawal

67
Q

What are some therapeutic concerns with Antidysrhythmic Agents?

A

Drugs may cause arrhythmias

Hypokalemia increases risk of arrhythmia
Be aware of dehydration (Diuretics!)

Effect on exercise tolerance: adequate warm up time
Negative inotropic effects = heart will not respond normally to demands of exercise
Exercise may cause rhythm disturbance from increased catecholamines, making drugs ineffective during exercise
Lack of “cool down” period will also contribute to rhythm disturbance

68
Q

Therapeutic Concerns about Digoxin

A

NTI
GI symptoms: nausea, vomiting, diarrhea, abdominal pain, anorexia
CNS: blurred vision, confusion, lethargy
Cardiac: arrhythmia (due to increased intracellular calcium  increased cardiac contractility)

69
Q

What happens when an individual taking Digoxin has impaired renal clearance?

A

Digoxin toxicity b/c its cleared mainly by the kidney

pharm drugs (10 decks)

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