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Circulation Part 2 > Pharmacology- Lecture > Flashcards

Pharmacology- Lecture Flashcards

1
Q

Categories of drugs to treat acute coronary syndrome (ACS)

A
  1. Beta blockers
  2. Anti-platelet medications
  3. Statins
  4. Thrombolytics (not always used)
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2
Q

We use beta blockers to reduce cardiac demand in the setting of ACS because of their _ and _ effects

A

We use beta blockers to reduce cardiac demand in the setting of ACS because of their chronotropic and ionotropic effects

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3
Q

Statins have three roles:

A

Statins have three roles:
1. Decrease LDL
2. Inhibit thrombosis
3. Inhibit inflammation

Statins are prescribed in the setting of ACS due to their anti-thrombosis and anti-inflammatory effects on the heart

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4
Q

Two drugs that stimulate B1 are _ and _

A

Two drugs that stimulate B1 are dobutamine and isoproterenol

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5
Q

Two drugs that inhibit B1 are _ and _

A

Two drugs that inhibit B1 are metoprolol and carvedilol

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6
Q

Name three indications for giving a beta blocker

A

Name three indications for giving a beta blocker: hypertension, angina, ACS
* Beta blockers are able to slow the heart rate, decrease contractility, and also decrease renin secretion which decreases blood pressure

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7
Q

If the drug ends in “-olol” it means that the drug is _

A

If the drug ends in “-olol” it means that the drug is selective for B1 or B1/B2
* If the drug starts with A-N: it is cardioselective (B1 only)
* If the drug starts with N-Z: it is nonselective (B1/B2)

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8
Q

If the drug ends in “-ilol” , “-alol” it means that the drug is _

A

If the drug ends in “-ilol” , “-alol” it means that the drug is combined alpha and beta blocker
* Affects a1, B1, B2

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9
Q

B2 is responsible for _ , so drugs that non-selectively block B1 and B2 can cause _ off-target toxicity

A

B2 is responsible for vascular smooth muscle relaxation (lungs) , so drugs that non-selectively block B1 and B2 can cause bronchospasm off-target toxicity

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10
Q

Beta-blocker use for HTN may cause _ mechanism-based toxicity

A

Beta-blocker use for HTN may cause bradycardia mechanism-based toxicity

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11
Q

Aspirin and ibuprofen have _ mechanism in the setting of ACS

A

Aspirin and ibuprofen block platelet activation
* COX inhibitor
* Blocks TXA2

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12
Q

Clopidogrel, prasugrel, ticagrelor, cangrelor all work by _

A

Clopidogrel, prasugrel, ticagrelor, cangrelor all work by P2Y12 inhibition
* Block ADP binding
* Block activation

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13
Q

Why do we not use warfarin in the setting of ACS?

A

ACS takes 7 days to work as an anticoagulant
* In the beginning, it causes a transient hypercoagulative state –> dangerous in ACS

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14
Q

Recall that heparins work by activating anti-thrombin ; Unfractionated heparin stimulates AT to work on factors _
Fondaparinux and Enoxaparin stimulates AT to work on factors _

A

Recall that heparins work by activating anti-thrombin ; Unfractionated heparin stimulates AT to work on factors thrombin & Xa
Fondaparinux and Enoxaparin stimulates AT to work on factor Xa only

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15
Q

The first generation thrombolytic drugs include _ and _ ; these drugs are _

A

The first generation thrombolytic drugs include streptokinase and urokinase ; these drugs are not-fibrin specific

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16
Q

2nd generation thrombolytic drugs include _ ; which is _

A

2nd generation thrombolytic drugs include alteplase ; which is fibrin-specific

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17
Q

3rd generation thrombolytic drugs include _ and _ ; these are _

A

3rd generation thrombolytic drugs include tenecteplase and reteplase ; these are even more fibrin-specific

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18
Q

All thrombolytic, “clot-busters” are _

A

All thrombolytic, “clot-busters” are plasminogen activators
* They are all enzymes

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19
Q

Atorvastatin and simvastatin work via _ mechanism

A

Atorvastatin and simvastatin work via inhibiting HMG-CoA reductase
* Simvastatin- short acting
* Atorvastatin- long acting

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20
Q

What are the effects of statins on LDL, HDL, TGs?

A

Statins- atorvastatin, simvastatin
* LDL: majorly decreased
* HDL: increased
* TGs: decreased

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21
Q

Drugs that begin with “Cole” like colestipol, cholestyramine, and colesevelam work via _

A

Drugs that begin with “Cole-“ like colestipol, cholestyramine, and colesevelam work via bile acid sequestration

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22
Q

The “cole” drugs, aka bile acid sequestrants have what effect on LDL, HDL, TGs?

A

Bile acid sequestrants:
* LDL: well decreased
* HDL: increased slightly
* TGs: increased slightly

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23
Q

The main side effect of bile acid sequestrant drugs is _

A

The main side effect of bile acid sequestrant drugs is GI upset

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24
Q

The two main side effects of HMG-CoA reductase inhibitors are _

A

The two main side effects of HMG-CoA reductase inhibitors are myopathy and liver damage

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25
Q

Niacin is an anti-lipid drug that acts as a _

A

Niacin is an anti-lipid drug that acts as a lipase inhibitor

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26
Q

The main side effect of niacin is _

A

The main side effect of niacin is flushing

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27
Q

What are the effects of niacin on LDL, HDL, and TGs?

A

Niacin (lipase inhibitor):
* LDL: well decreased
* HDL: well increased
* TGs: decreased

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28
Q

Fibrates like clofibrate, fenofibrate, and gemfibrozil work via _

A

Fibrates like clofibrate, fenofibrate, and gemfibrozil work via LPL activation

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29
Q

What effects do fibrates have on LDL, HDL, and TGs?

A

Fibrates (LPL activators):
* LDL: decreased
* HDL: increased
* TGs: significantly decreased

30
Q

Ezetimibe is a drug that is a _

A

Ezetimibe is a drug that is a cholesterol absorption inhibitor
* It only decreased LDL consistently
* Side effect: diarrhea

31
Q

Alirocumab and Evolocumab are _ type drugs

A

Alirocumab and Evolocumab are PCSK9 inhibitors
* These enzymes regulate the level of LDL receptors
* Blocking this enzyme puts more LDL receptors in the membrane
* Decreases LDL

32
Q

What is the effect of the “-cumab” drugs on LDL, HDL, TGs?

A

The “-cumab” drugs (PCSK9 inhibitors)
* LDL: significantly decreased
* HDL: increased
* TGs: decreased

33
Q

The side effect of the “-cumab” drugs is _

A

The side effect of the “-cumab” drugs is flu-like symptoms

34
Q

The main side effect of fibrates is _

A

The main side effect of fibrates is dyspepsia (upset stomach)

35
Q

The most effective anti-lipid drug class for decreasing TGs is _

A

The most effective anti-lipid drug class for decreasing TGs is fibrates

36
Q

The two most effective drug classes for decreasing LDL are _ and _

A

The two most effective drug classes for decreasing LDL are statins and PCSK9 (mab) drugs

37
Q

Statin drugs block the synthesis of _ during cholesterol synthesis

A

Statin drugs block the synthesis of mevalonate during cholesterol synthesis

38
Q

Normally PCSK9 _ LDL receptors

A

Normally PCSK9 degrades LDL receptors
* We give PCSK9 inhibitors to stop this and increase number of LDL receptors on the liver
* Deprive the liver of cholesterol
* Causes the liver to pull LDL from the plasma

39
Q

Examples of drugs that might increase statin toxicities include _

A

Examples of drugs that might increase statin toxicities include CYP3A4 inhibitors
* Azoles, amiodarone, grapefruit inhibit CYP
* Impairs metabolism of statins

40
Q

Another anti-lipid drug called _ can also inhibit statin metabolism by blocking _

A

Another anti-lipid drug called Gemfibrozil (fibrate) can also inhibit statin metabolism by blocking glucuronidase

41
Q

The antiarrythmic drugs that primarily affect the cardiac myocyte AP are _ and _

A

The antiarrythmic drugs that primarily affect the cardiac myocyte AP are class I and class III
* Class I blocks Na+ influx
* Class III blocks K+ efflux

42
Q

The Class IA Na+ channel blockers also block _

A

The Class IA Na+ channel blockers also block K+ efflux

This means that both class I and class III antiarrythmics prolong the QT interval

43
Q

The most potent Na+ channel blockers are class _ and they affect the ECG by _

A

The most potent Na+ channel blockers are class IC and they affect the ECG by prolongation of QRS

44
Q

Drugs that block K+ channels have the following effects:

A

Drugs that block K+ channels…
1. Slow repolarization
2. Increase AP duration
3. Prolong QT interval
4. Increase the risk of torsades

45
Q

Any drug that _ increases the risk for torsades

A

Any drug that prolongs QT interval increases the risk for torsades

46
Q

Among the Class III drugs, _ has the lowest risk of torsades de point

A

Among the Class III drugs, amiodarone has the lowest risk of torsades de point

47
Q

Class II antiarrythmics work by _

A

Class II antiarrythmics are beta blockers and they work by reducing phase 4 slope –> slowing AV node depolarization

48
Q

Class IV antiarrythmics work by _

A

Class IV antiarrythmics work by blocking Ca2+ influx –> slow phase 0

49
Q

Only _ type calcium channel blockers are anti-arrhythmics

A

Only non-dihydropyridine calcium channel blockers are anti-arrhythmics
* Since these are able to act on AV/SA node
* Ex: Verapamil, Diltiazem

50
Q

What variables are we wanting to improve with the administration of heart failure medications?
Preload, afterload, etc

A

We want to give drugs that can help:
1. Decrease preload
2. Decrease afterload
3. Increase contractility
4. Decrease cardiac remodeling

51
Q

If we want to decrease preload, decrease afterload, and decrease cardiac remodeling we can administer _ drugs

A

If we want to decrease preload, decrease afterload, and decrease cardiac remodeling we can administer ACE inhibitor, ARBs, ARNi or b1 antagonist
* Benazepril is an ACE inhibitor
* Losartan is a ARB
* Sacubitril + valsartan is an ARNi
* Metoprolol is a b1 blocker

52
Q

ACEi, ARBs, and ARNis have neurohormonal effects of _

A

ACEi, ARBs, and ARNis have neurohormonal effects of reverse remodeling –> lowers wall stress –> decreases myocardial oxygen demand
* Ventricle gets smaller, decreased fibrosis, decreased sodium and water retention, decreased sympathetic tone

53
Q

ACEi, ARBs, and ARNis have hemodynamic effects of _

A

ACEi, ARBs, and ARNis have hemodynamic effects of reducing afterload –> decreases myocardial oxygen demand and increases stroke volume

54
Q

_ drugs are twice as effective at decreasing mortality compared to their counterparts

A

Angiotensin neprilysin inhibitors (ARNi) drugs are twice as effective at decreasing mortality compared to their counterparts

55
Q

Describe the beta blocker paradox; when should we use beta blockers and when should we avoid them?

A

SNS activation is good in acute heart failure –> we want SNS to compensate for poor perfusion to organs

Chronically, SNS activation is maladaptive so we use beta blockers in chronic settings

56
Q

On target toxicities of beta blockers include _

A

On target toxicities of beta blockers include bradycardia, heart block, inhibition of reflex tachycardia (hiding hypoglycemia)
* Therefore they are contraindicated in situations of acute decompensated HF, severe bradycardia, heart block

57
Q

Off target toxicities of beta blockers include _

A

Off target toxicities of beta blockers include bronchoconstriction via blockage of B2

58
Q

Patient with heart failure was given dapagliflozin and empagliflozin to alleviate heart failure symptoms; what is the mechanism of action?

A

Patient with heart failure was given dapagliflozin and empagliflozin –> these block sodium glucose transporter in the nephrons –> decreasing reabsorption of glucose, sodium and water

59
Q

_ is a drug that can be used to increase inotropy in heart failure patients by blocking Na/K ATPase

A

Digoxin is a drug that can be used to increase inotropy in heart failure patients by blocking Na/K ATPase

60
Q

Digoxin side effects include:

A

Digoxin side effects include: arrhythmias, confusion, somnolence, seizure, visual disturbances, nausea/vomiting
* Digoxin is not commonly used anymore due to its narrow therapeutic window

61
Q

Acute heart failure instances/ cardiogenic shock may be treated with _

A

Acute heart failure instances/ cardiogenic shock may be treated with
* Phenylephrine- alpha1 agonist
* Milrinone- PDE3 inhibitor
* Dobutamine- beta1 agonist
* Epi, NE, Dopamine
* Vasopressin

62
Q

_ and _ are examples of drugs that inhibit alpha1 and prevent vasoconstriction (may be used in hypertension)

A

Doxazosin and Prazosin are examples of drugs that inhibit alpha1 and prevent vasoconstriction (may be used in hypertension)
* They are able to lower blood pressure without directly affecting cardiac output

63
Q

Catecholamines like _ , _ , and _ are important int the context of acute HF or cardiogenic shock

A

Catecholamines like Epi , NE , and dopamine are important int the context of acute HF or cardiogenic shock

64
Q

Of the catecholamines, _ is selective for beta2

A

Of the catecholamines, Epi is selective for beta2 –> makes since because we use Epi in anaphylaxis to bronchodilate

65
Q

Dopamine is normally only selective for dopamine receptors unless _

A

Dopamine is normally only selective for dopamine receptors unless we increase concentration such that it becomes nonselective across all receptors

66
Q

Vasopressin is a hormone that is produced in the _ and secreted by the _ to help increase arterial blood pressure

A

Vasopressin is a hormone that is produced in the hypothalamus and secreted by the posterior pituitary to help increase arterial blood pressure

67
Q

Vasopressin is different from aldosterone.. how?

A

Vasopressin directly increases water reabsorption
Aldosterone indirectly increases water reabsorption via sodium reabsorption

68
Q

Via its V1 receptor, vasopressin causes _

A

Via its V1 receptor, vasopressin causes blood vessel constriction
* This is a rapid way it increases BP

69
Q

Via its V2 receptor, vasopressin causes _

A

Via its V2 receptor, vasopressin causes water reabsorption via aquaporin channels in kidney
* This is a slow way it increases BP

70
Q

Dobutamine acts on _ to _

A

Dobutamine acts on beta1 to increase heart rate and contractility

71
Q

Milrinone is a drug that is used for _ and works by _

A

Milrinone is a drug that is used for increasing contractility and works by inhibiting phosphodiesterase 3
* PDE3 inhibitor –> stops the degradation of cAMP –> leads to an increase in cAMP

Circulation Part 2 (15 decks)

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