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Circulation Part 2 > Pharmacology- Lecture > Flashcards

Pharmacology- Lecture Flashcards

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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
Niacin is an anti-lipid drug that acts as a _
Niacin is an anti-lipid drug that acts as a **lipase inhibitor**
26
The main side effect of niacin is _
The main side effect of niacin is **flushing**
27
What are the effects of niacin on LDL, HDL, and TGs?
Niacin (lipase inhibitor): * LDL: well decreased * HDL: well increased * TGs: decreased
28
Fibrates like clofibrate, fenofibrate, and gemfibrozil work via _
Fibrates like clofibrate, fenofibrate, and gemfibrozil work via **LPL activation**
29
What effects do fibrates have on LDL, HDL, and TGs?
Fibrates (LPL activators): * LDL: decreased * HDL: increased * **TGs: significantly decreased**
30
Ezetimibe is a drug that is a _
Ezetimibe is a drug that is a **cholesterol absorption inhibitor** * It only decreased LDL consistently * Side effect: diarrhea
31
Alirocumab and Evolocumab are _ type drugs
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
What is the effect of the "-cumab" drugs on LDL, HDL, TGs?
The "-cumab" drugs (PCSK9 inhibitors) * **LDL: significantly decreased** * HDL: increased * TGs: decreased
33
The side effect of the "-cumab" drugs is _
The side effect of the "-cumab" drugs is **flu-like symptoms**
34
The main side effect of fibrates is _
The main side effect of fibrates is **dyspepsia (upset stomach)**
35
The most effective anti-lipid drug class for decreasing TGs is _
The most effective anti-lipid drug class for decreasing TGs is **fibrates**
36
The two most effective drug classes for decreasing LDL are _ and _
The two most effective drug classes for decreasing LDL are **statins** and **PCSK9 (mab) drugs**
37
Statin drugs block the synthesis of _ during cholesterol synthesis
Statin drugs block the synthesis of **mevalonate** during cholesterol synthesis
38
Normally PCSK9 _ LDL receptors
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
Examples of drugs that might increase statin toxicities include _
Examples of drugs that might increase statin toxicities include **CYP3A4 inhibitors** * Azoles, amiodarone, grapefruit inhibit CYP * Impairs metabolism of statins
40
Another anti-lipid drug called _ can also inhibit statin metabolism by blocking _
Another anti-lipid drug called **Gemfibrozil (fibrate)** can also inhibit statin metabolism by blocking **glucuronidase**
41
The antiarrythmic drugs that primarily affect the cardiac myocyte AP are _ and _
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
The Class IA Na+ channel blockers also block _
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
The most potent Na+ channel blockers are class _ and they affect the ECG by _
The most potent Na+ channel blockers are class **IC** and they affect the ECG by **prolongation of QRS**
44
Drugs that block K+ channels have the following effects:
Drugs that block K+ channels... 1. Slow repolarization 2. Increase AP duration 3. Prolong QT interval 4. **Increase the risk of torsades**
45
Any drug that _ increases the risk for torsades
Any drug that **prolongs QT interval** increases the risk for torsades
46
Among the Class III drugs, _ has the lowest risk of torsades de point
Among the Class III drugs, **amiodarone** has the lowest risk of torsades de point
47
Class II antiarrythmics work by _
Class II antiarrythmics are **beta blockers** and they work by **reducing phase 4 slope** --> slowing AV node depolarization
48
Class IV antiarrythmics work by _
Class IV antiarrythmics work by **blocking Ca2+ influx --> slow phase 0**
49
Only _ type calcium channel blockers are anti-arrhythmics
Only **non-dihydropyridine** calcium channel blockers are anti-arrhythmics * Since these are able to act on AV/SA node * Ex: Verapamil, Diltiazem
50
What variables are we wanting to improve with the administration of heart failure medications? Preload, afterload, etc
We want to give drugs that can help: 1. Decrease preload 2. Decrease afterload 3. Increase contractility 4. Decrease cardiac remodeling
51
If we want to decrease preload, decrease afterload, and decrease cardiac remodeling we can administer _ drugs
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
ACEi, ARBs, and ARNis have neurohormonal effects of _
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
ACEi, ARBs, and ARNis have hemodynamic effects of _
ACEi, ARBs, and ARNis have hemodynamic effects of **reducing afterload** --> decreases myocardial oxygen demand and increases stroke volume
54
_ drugs are twice as effective at decreasing mortality compared to their counterparts
**Angiotensin neprilysin inhibitors (ARNi)** drugs are twice as effective at decreasing mortality compared to their counterparts
55
Describe the beta blocker paradox; when should we use beta blockers and when should we avoid them?
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
On target toxicities of beta blockers include _
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
Off target toxicities of beta blockers include _
Off target toxicities of beta blockers include **bronchoconstriction via blockage of B2**
58
Patient with heart failure was given *dapagliflozin* and *empagliflozin* to alleviate heart failure symptoms; what is the mechanism of action?
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
_ is a drug that can be used to increase inotropy in heart failure patients by blocking Na/K ATPase
**Digoxin** is a drug that can be used to increase inotropy in heart failure patients by blocking Na/K ATPase
60
Digoxin side effects include:
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
Acute heart failure instances/ cardiogenic shock may be treated with _
Acute heart failure instances/ cardiogenic shock may be treated with * **Phenylephrine**- alpha1 agonist * **Milrinone**- PDE3 inhibitor * **Dobutamine**- beta1 agonist * **Epi, NE, Dopamine** * **Vasopressin**
62
_ and _ are examples of drugs that inhibit alpha1 and prevent vasoconstriction (may be used in hypertension)
**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
Catecholamines like _ , _ , and _ are important int the context of acute HF or cardiogenic shock
Catecholamines like **Epi** , **NE** , and **dopamine** are important int the context of acute HF or cardiogenic shock
64
Of the catecholamines, _ is selective for beta2
Of the catecholamines, **Epi** is selective for beta2 --> makes since because we use Epi in anaphylaxis to bronchodilate
65
Dopamine is normally only selective for dopamine receptors unless _
Dopamine is normally only selective for dopamine receptors unless **we increase concentration such that it becomes nonselective across all receptors**
66
Vasopressin is a hormone that is produced in the _ and secreted by the _ to help increase arterial blood pressure
Vasopressin is a hormone that is produced in the **hypothalamus** and secreted by the **posterior pituitary** to help increase arterial blood pressure
67
Vasopressin is different from aldosterone.. how?
**Vasopressin** directly increases water reabsorption **Aldosterone** indirectly increases water reabsorption via sodium reabsorption
68
Via its V1 receptor, vasopressin causes _
Via its V1 receptor, vasopressin causes **blood vessel constriction** * This is a rapid way it increases BP
69
Via its V2 receptor, vasopressin causes _
Via its V2 receptor, vasopressin causes **water reabsorption via aquaporin channels in kidney** * This is a slow way it increases BP
70
Dobutamine acts on _ to _
Dobutamine acts on **beta1** to **increase heart rate and contractility**
71
Milrinone is a drug that is used for _ and works by _
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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