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Spring Pharm Block 4 > FR Review 3 - Cardiac Drugs > Flashcards

FR Review 3 - Cardiac Drugs Flashcards

1
Q

Classify the four Ca channel blockers by their myocardial and vascular effects.

A

Verapamil: 95% heart and 5% vasculature (1st CCB)
Diltiazem: 50% heart and 50% vasculature
Nifedipine: 5% heart and 95% vasculature
Amlodipine: 1% heart and 99% vasculature

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2
Q

What is the primary use of verapamil and diltiazem?

A

Rate control in atrial fibrillation –> no use in CHF

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3
Q

What is the primary use of nifedipine and amlodipine?

A

Anti-hypertensives and safe in CHF

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4
Q

What is the most significant adverse effect of nifedipine and amlodipine and how is it managed?

A

Non-cardiogenic peripheral edema. Treat with a low dose diuretic if it bothers the patient.

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5
Q

Other than HTN, list and define a potential use for nifedipine.

A

Achalasia –> lower esophageal tone is too high

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6
Q

Other than the primary AE, what is another rare AE associated with nifedipine?

A

gingival hyperplasia

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7
Q

Differentiate selective from non-selective beta blockers.

A

Selective: block only beta-1
Non-selective: block both beta-1 and beta-2
-Goal is to block B-1 –> blocking B-2 is baggage

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8
Q

What is ISA in relation to beta blockers?

A

ISA = intrinsic sympathomimetic activity. Some beta blockers have some mild beta agonist properties. They still have more beta antagonist effects but the are less potent beta antagonists.

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9
Q

What is the benefit of beta blockers that also have alpha-1 antagonism and give some examples.

A

More potent beta blockers s/p vasodilation - useful in cocaine OD. Exs: carvbedilol, labetalol

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10
Q

Give three examples of commonly used beta-1 selective beta blockers.

A

atenolol, metoprolol, esmolol

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11
Q

Explain why patients on beta blockers must have them withdrawn slowly over a relatively long period of time.

A

While on beta blockers, the heart upregulates beta 1 receptors and increases their sensitivity. Sudden withdrawal of the medication can lead to tachycardia and hypertension.

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12
Q

What is unique about the pharmacokinetics of esmolol?

A

It is eliminated via plasma esterases (in blood), meaning the drug will have a short 1/2 life and can only be given IV.

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13
Q

What 3 beta blockers are used for CHF?

A

Carvedilol, Metoprolol XL, Bisoprolol

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14
Q

What are the indications for use of propranolol?

A

Tremor, anxiety/stage fright, aggression, thyroid storm

DOC for portal HTN

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15
Q

If a patient with asthma or COPD history has to be on a beta-blocker, which ones are safest?

A

Selective BBs –> asthma/COPD patients should not have drugs that block B-2

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16
Q

Describe the efect of beta blockers in patients that are prescribed an epi-pen.

A

BBs decrease the efficacy of epi-pens –> pateints should carry two epi-pens if they are on BBs.

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17
Q

Name 3 alpha-1 blockers and state the caution with these medications?

A

Doxazosin, Prazosin, Terazosin. They are very potent vasodilators that cause postural HypoTN and falls.

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18
Q

List three selective (bladder specific) alpha-1 blockers and describe their use.

A

Afluzosin, Silodosin, Tamsulosin. Blockade of alpha-1 in the bladder promotes urination - used in BPH.

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19
Q

What is the mechanism of action of clonidine?

A

Centrally acting alpha-2 agonist –> dec release of epi and norepi from the synapse and decreases BP

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20
Q

What are the indications for use of clonidine?

A

Last line as an anti-hypertensive

Other: ADD/ADHD, epidurals, smoke cessation

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21
Q

What are three actions of angiotensin II?

A
  • potent vasoconstriction
  • secretion of aldosterone retaining renal Na and H2O
  • stimulates cardiac and vascular smooth muscle proliferation –> hypertrophy and dec efficiency
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22
Q

What is the mechanism of action of ACE Inhibitors (ACEi) and angiotensin receptor blockers (ARB)?

A

ACEi prevents conversion of angiotensin I to angiotensin II. ARB prevents angiotensin II from binding to receptors.

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23
Q

All ACEi drugs end in what suffix? List examples.

A

“pril” - elanapril, captopril, lisinopril, quinapril

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24
Q

What action of ACEi drugs may cause a dry, hacking cough?

A

Inhibition of kinase which increase bradykinin in lungs. Bradykinin is a vasodilator and promotes production of other vasodilators. Inc bradykinin in the lungs can also cause a cough.

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25
Q

How is a cough caused by an ACEi treated?

A

Possibly ASA or by removing the ACEi drug. DO NOT treat with cough suppressants.

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26
Q

Name three cough suppressants.

A

Benzonatate, codeine, dextromethorphan

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27
Q

Other than a dry cough, what other adverse effects exist with ACEi drugs?

A

HyperK, Angioedema (may also be caused by NSAIDs), avoid in pregnancy (especially 3rd trimester)

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28
Q

Describe the effect of angiotensin II and prostaglandins on the kidneys.

A

A2: keeps the efferent arteriole closed
PGs: keeps the afferent arteriole open

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29
Q

What is the caution in prescribing ACEi drugs to patients with renal disease?

A

Must r/o renal artery stenosis. RAS reduces blood flow to the kidney. Normally, the efferent arteriole constricts to compensate and maintain renal blood flow. If an ACEi is given, this compensatory mechanism will be taken away, and kidney injury may result.

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30
Q

T/F: It is sensical to have a patient on both an ACEi and an ARB.

A

False: non-sensical

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31
Q

ARB drugs end in what suffix? List some examples.

A

“sartan” - losartan, valsartan, telmisartan

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32
Q

What is the formula to determine cerebral perfusion pressure?

A

CPP = MAP - ICP

33
Q

What is the primary use of manitol?

A

Decrease cerebral edema in patients with inc ICP

34
Q

What condition is aquaretics used to treat and by what mechanism of action? What are the causes of this condition?

A
  • Syndrome of Inappropriate ADH (SIADH)
  • SIADH is caused by tumors, TBI, or brain CA
  • Aquaretics act by antagonizing ADH receptors
35
Q

What electrolyte abnormality occurs secondary to SIADH?

A

hyponatremia s/p dilution from excess body water

36
Q

What is the mechanism of action of carbonic anhydrase inhibitors? Name the most commonly used CAI.

A

Carb anhydrase is an enzyme in high concentration in the kidneys responsible for reabsorption of HCO3. Blockade causes HCO3 to stay in urine –> pulls Na and water into the urine with it. Acetazolamide is the most commonly used CAI.

37
Q

What is the main role for CAIs today and by what mechanism of action?

A

Glaucoma eye drops: Decrease aqueous humor production and decrease intraocular pressure.

38
Q

What is the second most common use of CAIs and by what mechanism?

A

altitude sickness: mild dec in serum pH causes Hgb to more easily discharge oxygen.

39
Q

In what part of the nephron do most diuretics work?

A

Distal Tubule

40
Q

What is the affect of thiazide diuretics in patients with low creatinine clearance?

A

Essentially no efficacy: thiazides will not reach the distal tubule if kidney function is decreased (CrCl < 30).

41
Q

What are the electrolyte effects of thiazides?

A

HypoK, Hyperuricemia, Hyperglycemia (very mild), HyperCa.

42
Q

What is true about the efficacy of loop diuretics?

A

High efficacy with a high ceiling –> can keep going up on the dose.

43
Q

What are the three go to loop diuretics? Which is cheapest and used most often? Which is most potent?

A

Furosemide - cheapest and used most often
Bumetanide - highest bioavailability/potency
Torsemide

44
Q

What are the electrolyte effects of loop diuretics?

A

hypoK, hypoCa, hyperuricemia, hyperglycemia

45
Q

What is an adverse effect of loop diuretics caused by rapid IV administration of the drug?

A

ototoxicity - tinnitus, mild hearing loss, imbalance

46
Q

What is the mechanism of action of aldosterone antagonists? Name the most commonly used one.

A

waste Na and retain K –> spironolactone

47
Q

What are the electrolyte effects of aldosterone antagonists?

A

hyperK (“K sparing”), no significant affect on glucose or uric acid. –> safest diuretic in gout

48
Q

What is an adverse effect of spironolactone and why?

A

painful gynecomastia: has estrogen effects - directly related to dose and duration of therapy.

49
Q

Other than CHF/HTN, list two additional uses for spironolactone.

A

Ascites caused by cirrhosis. Hirsutism.

50
Q

Compare and contrast non-steroidal potassium sparing diuretics with aldosterone antagonists.

A

Both waste Na and retain K. Non-steroidals do it independent of aldosterone (a steroid).

51
Q

What other diuretic are non-steroidal potassium sparing diuretics combined with and why?

A

HCTZ –> non-steroidals counteract the hypoK of HCTZ

52
Q

List the uses of NTG.

A

angina, CHF, acute MI, pulm HTN, HTN emerg.

53
Q

After how many NTG tabs should a Pt call 911 if they are still experiencing chest pain?

A

3

54
Q

How does one know the NTG tab they took is working?

A

It will sting

55
Q

What are some other routes of administration of NTG other than IV and SL?

A

buccal tabs, ointment, transdermal (patch)

56
Q

T/F: NTG is available in a sustained release (SR) formulation.

A

True: can be used for HTN (rarely used)

57
Q

What type of drug is digoxin and what plant is it derived from? What is its mechanism of action?

A

Cardiac glycoside derived from the foxglove plant. Causes positive inotropy and negative chronotropy.

58
Q

What is the mechanism of action of warfarin?

A

Inhibits 2 key enzymes that form vitamin K. Vitamin K needed for the liver to make clotting factors II, VII, IX, and X. Also inhibits protein C and S.

59
Q

What is the action of protein C and S and how does this affect the action of warfarin? How is this effect mitigated?

A

C and S are anti-coagulants. Warfarin causes inc coagulation early after its admin. Give heparin when starting warfarin.

60
Q

Describe dosing of warfarin among different patients.

A

Very individualized - different patients likely to require different doses to achieve affect. Must be patient and check INR when starting patient on warfarin.

61
Q

How does diet affect warfarin?

A

Vegetarians take in more vitamin K requiring more warfarin. Meat eaters may require less warfarin.

62
Q

How does diarrhea affect warfarin dosing?

A

Diarrhea impairs absorption of fat soluble vitamins like vitamin K. Less vitamin K = decreased warfarin dose.

63
Q

What does INR stand for and why is it measured to titrate warfarin rather than PT?

A

INR = International Normalized Ratio (higher INR = prolonged bleeding time)
PT is variable in different labs, INR is consistent.

64
Q

What are the pros and cons of the novel oral anticoagulants?

A

pros: dose specific for everyone and no INR monitoring is needed (effects predictable)
cons: high cost, tough to reverse, and can’t monitor therapy (problematic in patients that may not remember how much they took)

65
Q

Name four ADP receptor inhibitors and descrie broadly their mechanism of action.

A

Ticlopidine, Clopidogrel, Prasugrel, Ticagrelor

They are anti-platelet agents

66
Q

Discuss the major potential adverse event related to heparin use and how it is mitigated.

A

HIT - heparin induced thrombocytopenia. Heparin acts as a haptin and binds to platelets. Sometimes the immune system does not recognize this complex and attacks the heparin-bound platelets. Must monitor platelet levels in a Pt on heparin.

67
Q

What is the advantage of using low molecular weight heparin?

A

Less likely to cause HIT

68
Q

Why is dopamine not used to treat parkinson’s disease?

A

It does not cross the blood-brain barrier

69
Q

What are the effects of dopamine at different dose ranges?

A

2-5 mcg/kg/min: renal artery dilation
5-10 mcg/kg/min: beta-1 agonist
> 10 mcg/kg/min: alpha-1 agonist

70
Q

What is dobutamine’s mechanism of action? How is it administered and what is its indication?

A

It is a beta-1 agonist. It is an IV only drug that is used in CHF.

71
Q

Describe the mechanism of action of glycoprotein (GP) IIB and IIIA antagonists.

A

Mediates platelet aggregation by blocking the final common pathway of platelet aggregation.

72
Q

What is the difference between plasminogen activators (tPA) and other anticoagulants?

A

Plasminogen activators eliminate existing clots where other anticoagulants only prevent new clots from forming.

73
Q

What are the absolute contraindications of tPA use?

A

ICH, intercranial trauma, brain tumors, major surgeries, GI bleeding, uncontrolled HTN

74
Q

Differentiate among class 1A, 1B, and 1C anti-arrhythmics and state the most commonly used agent in each class.

A

1A: Intermediate Na channel blockers –> procainamide
1B: Fast Na channel blockers –> lidocaine
1C: Slow Na channel blockers –> limited use s/p increased CV morbidity and mortality.

75
Q

What is the mechanism of action of class 2 anti-arrhythmics?

A

Beta-blockers

76
Q

What is the mechanism of action of class 3 anti-arrhythmics?

A

Potassium channel blockers

77
Q

What is the most commonly used class 3 anti-arrhythmic and what is special about its use?

A

Amiodarone –> anti-arrhythmic that produces the least amount of negative inotropy so it is useful in CHF

78
Q

What must be monitored when a patient is on amiodarone?

A

TSH, LFTs, ophthalmic and neurologic exams before and after administration, CXR s/p pulmonary fibrosis risk

79
Q

What is the mechanism of action of class 4 anti-arrhythmics?

A

Calcium channel blockers

Spring Pharm Block 4 (17 decks)

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