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Pharmacology > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

ACE Inhibitor Suffix

A

-pril

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2
Q

ARB Suffix

A

-sartan

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3
Q

Calcium Channel Blockers (DHPs) Suffix

A

-dipine

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4
Q

Beta-Blocker Suffix

A

-olol

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5
Q

Statins Suffix

A

-statin

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6
Q

A chronic, dry, non-productive cough is most likely to be observed with what medication?

A

ACE Inhibitors

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7
Q

What is the mechanism of action for ACE Inhibitors?

A

Stops the production of angiotensin II

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8
Q

What compound does ACE breakdown and what does it cause?

A

Bradykinin, causing it to last in the body for longer

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9
Q

What drug classes are used in the treatment of hypertension?

A

• ACE Inhibitors
• ARBs
• Calcium Channel Blockers
• Beta Blockers
• Diuretics

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10
Q

What heart failure patients should get ACE Inhibitors?

A

ALL patients with an ejection fraction ≤ 40%

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11
Q

ACE Inhibitors are particularly useful for the treatment of hypertension in patients with what other conditions?

A

Diabetes, diabetic nephropathy, post-MI, or high risk of coronary artery disease

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12
Q

Side Effects of ACE Inhibitors

A

• Hypotension & Dizziness
• Cough - dry, constant
• Angioedema - vasodilation in lungs
• Renal Dysfunction (↓ kidney function)
• Hyperkalemia (↑Potassium)

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13
Q

How do ACE Inhibitors impact blood pressure & potassium levels?

A

• ↑ Potassium
• ↓ BP

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14
Q

ACE Inhibitor Warnings & Drug Interactions

A

• do not use during pregnancy (fetal HTN)
• do not use with bilateral renal artery stenosis

Drug Interactions

• K+ supplements - ACE retains too much K+
• NSAIDs - can lead to acute renal failure
• constrict afferent while ACE constrict efferent
• Cyclosporine - ↑ risk of heart failure

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15
Q

ACE Inhibitor Drugs

A

• Benazepril
• Enalapril
• Lisinopril
• Ramipril

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16
Q

What is the mechanism of action of ARBs?

A

allows for production of angiotensin II but does NOT allow binding of Angiotensin II to the receptor

BLOCKS THE ANGIOTENSIN II RECEPTOR

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17
Q

Side Effects of ARBs

A

• LESS cough & angioedema (than ACE inhibitors)
• Hypotension & dizziness
• Renal Dysfunction (↓ kidney function)
• Hyperkalemia (↑ K+)

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18
Q

Similarities & Differences in ACE Inhibitors & ARBs

A

• Similar morbidity & mortality
• Similar in efficacy in HF (ACE inhibitors are better)

• ARBs have less cough & angioedema

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19
Q

ARB Drug Names

A

• Irbesartan
• Losartan
• Olmesartan
• Valsartan

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20
Q

Calcium Channel Blockers: what do they do and what do they cause?

A

• Block Ca+ from entering the cardiac muscle

CAUSE:
• ↓ HR
• Vasodilation (relax smooth muscles of blood vessels)

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21
Q

What do Dihydropyridines (DHPs) work on?

A

• only affect vasculature (NOT the heart muscle)
• Strong vasodilation

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22
Q

Which calcium channel blockers are the strongest vasodilators?

A

dihydropyridines

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23
Q

Calcium Channel Blocker Drugs - Non-DHPs

A

• Dilitiazem
• Verapamil

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24
Q

What do Non-DHP Calcium Channel Blockers do?

A

• ↓ HR
• Work in the heart & vessels
• Makes the heart beat with less force

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25
Q

What drugs are Non-DHP Calcium Channel Blockers & what do they do?

A

• Dilitiazem & Verapamil

• ↓ HR
• Work on the heart & vessels
• Heart beats with less force

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26
Q

Dihydropyridine (DHP) Calcium Channel Blocker Drugs

A

• Amlodipine
• Nifedipine

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27
Q

Common Adverse Effects of DHPs & Non-DHP Calcium Channel Blockers

A

DHPs
• Headache
• Flushing
• Pedal Edema
• Hypotension
• Reflex Tachycardia (↑ HR due to ↓ BP)

Non-DHPs
• Constipation
• Hypotension
• Bradycardia
• AV Block
• CHF

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28
Q

Common Adverse Side Effects of Non-DHP Calcium Channel Blockers

A

• Hypotension
• Constipation
• Bradycardia
• AV Block
• CHF

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29
Q

Common Adverse Effects of DHP Calcium Channel Blockers

A

• Hypotension
• Headache
• Flushing
• Pedal Edema
• Reflex Tachycardia (↑ HR due to ↓ BP)

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30
Q

Drug Interactions of Non-DHP Calcium Channel Blockers

A

Verapamil & Diltiazem

• can CAUSE many drug interactions
• SLOW the breakdown of other drugs
•change metabolism and/or transport of drugs

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31
Q

Drug Interactions of DHP Calcium Channel Blockers

A

Amlodepine

• Subject of many drug interactions
• Sensitive to changes caused by other drugs

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32
Q

What happens when B1 is activated by norepinephrine?

A

• ↑ HR
• ↑ Contractility
• ↑ Renin Release

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33
Q

What happens when B2 is activated by norepinephrine?

A

• Relaxation of vascular, bronchial, & uterine smooth muscle

• ↑ insulin release
• ↑ tremor
• ↑ glycogenolysis
• glycogen to glucose-1-phosphate & glucose

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34
Q

What happens when B3 is activated by norepinephrine?

A

• ↑ lipolysis
• ↑ urinary bladder relaxation

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35
Q

What happens when a1 is activated by norepinephrine?

A

• Vasoconstriction
• mydriasis
• piloerection
• ↑ glycogenolysis

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36
Q

What happens when a2 is activated by norepinephrine?

A

• ↓ neuronal transmitter release
• ↑ platelet aggregation
• ↓ lypolysis
• ↓ insulin release

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37
Q

What is the job of beta-blockers?

A

block the activation of beta receptors

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38
Q

What do beta blockers do for patients with heart failure?

A

↓ heart rate & ↓ cardiac output, ultimately making patients feel worse at first

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39
Q

What happens when B1 & B2 receptors are antagonized (blocked)?

A

• ↓ heart rate
• ↓ contractility
• ↓ renin release (↓ angiotensin II)

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40
Q

What conditions are beta blockers used to treat?

A

• Hypertension
• Anxiety
• Tremors
• Arrhythmias
• Heart Failure

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41
Q

Mechanisms of Beta Blockers

A

• Restore HR (variability)

• Prevent arrhythmia

• Prevent / slow remodeling process

• special dose (“start low, go slow” & “target dose”)

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42
Q

Common Adverse Effects of Beta Blockers

A

• Bronchospasm
• blocking B2 causes smooth muscle contraction
• AVOID in patients with COPD, asthma, etc.

• Heart failure

• Bradycardia / bradyarrhythmias

• Vasospasm (B2)

• Metabolic Abnormalities
• ↓ HDL
• Hyperglycemia / ↓ insulin sensitivity

• Depression

• Withdrawal syndrome

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43
Q

Beta Blocker Drugs

A

• Metoprolol
• Atenolol
• Propranolol
• Carvedilol
• Labetolol
• Nebivolol

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44
Q

What are the 3 different Beta-Blocker Drug Types?

A

• Selective Agents (metoprolol & atenolol)
• Non-Selective Agents (Propranolol)
• Vasodilating Agents (Carvedilol, Labetolol, Nebivolol)

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45
Q

What Beta Blockers are Selective Agents?

A

• Metoprolol
• Atenolol

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46
Q

What Beta Blockers are Non-Selective Agents

A

• Propranolol

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47
Q

What Beta Blockers are Vasodilating Agents?

A

• Carvedilol
• Labetolol
• Nebivolol

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48
Q

What are the 3 classes of Diuretics?

A

• Loops - Furosemide

• Thiazide & Thiazide-like - Hydrochlorothiazide

• Potassium-Sparing - triamterene

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49
Q

What are Diuretics used to treat?

A

Hypertension (thiazides)

Heart Failure & Fluid overload (loops)

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50
Q

Thiazides are mainly used to treat what condition?

A

Hypertension
• morbidity & mortality benefits

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51
Q

Loop diuretics are mainly used to treat what condition?

A

Heart Failure & Fluid Overload
• symptomatic improvement only (no ↑ survival)

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52
Q

Common Adverse Effects of Diuretics

A

• Hypovolemia - low intravascular volume

• Hyperglycemia (↑ blood sugar)

• ↑ Cholesterol & Triglycerides

• ↑ Ca+ with Thiazides & ↓ Ca+ with Loops

• ↓ Potassium (K+)

• ↓ Magnesium

• Hyperuricemia (↑ uric acid)

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53
Q

What is the key difference in common adverse side effects associated with thiazides vs. loop diuretics?

A

Thiazides ↑ Calcium

Loops ↓ Calcium

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54
Q

Diuretics, ADEs, & Other Drug Problems

A

• Impotence

• Potential problems with diuretics
• diuretic resistance
• thiazide sensitivity to renal function

DRUG INTERACTIONS
• Digoxin
• Lithium
• NSAIDs
• ACE Inhibitors or K+ supplements

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55
Q

Drug Interactions associated with Diuretics (ADEs & Other Drugs)

A

• Digoxin
• Lithium
• NSAIDs
• ACE Inhibitors or K+ Supplements

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56
Q

Diuretic Drugs

A

• Chlorthalidone
• Hydrochlorothiazide
• Triamterene
• Spironolactone
• Furosemide

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57
Q

Which diuretic is required for advanced heart failure and why?

A

Spironolactone because it blocks aldosterone

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58
Q

Statin Drugs

A

• Atorvastatin
• Lovastatin
• Pravastatin
• Rosuvastatin
• Simvastatin

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59
Q

What are Statins (HMG CoA Reductase Inhibitors) used to treat?

A

lower cholesterol, specifically LDLs

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60
Q

Mechanism of Action for HMG CoA Reductase Inhibitors (Statins)

A

Blocks synthesis of HMG CoA forcing bile to be made by synthesizing cholesterol from LDL in the blood

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61
Q

Key Concepts about Statins

A

1.) GOLD STANDARD for reducing LDL
• not good for isolated high triglycerides
• may even be beneficial if “normal” LDL

2.) Relatively flat dose-response curve
• only 5-6% more LDL lowering for double dose
• start with dose close to expected need

3.) Doses should be given in the evening or at bedtime
• because statins have a short half-life

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62
Q

Adverse Side Effects of Statins (Major & Minor)

A

MAJOR
• Myalgia (muscle pain)
• Myopathy
• Rhabodomyolysis (muscle tissue breakdown)

MINOR
• Dyspepsia / heartburn
• Headache
• Taste disturbances
• Diabetes (?)

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63
Q

What are the Major Adverse Side Effects of Statins?

A

• Myalgias (muscle pain)
• Myopathy
• Rhabdomyolysis (muscle tissue breakdown)

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64
Q

What are the Minor Adverse Side Effects of Statins?

A

• Dyspepsia / Heartburn
• Headache
• Taste Disturbances
• Diabetes

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65
Q

Mechanism of Action for Fibrates

A

Primary focus is on LDLs due to risk of heart disease

EFFECTS ON LIPIDS
• ↓ Total Cholesterol
• ↓ LDLs
• ↑↑ HDLs
• ↓↓↓ Triglycerides

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66
Q

Common Adverse Effects of Fibrates

A

• Nausea
• Diarrhea
• Cholelithiasis (gallstones)
• Phototoxicity

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67
Q

Drug Interactions of Fibrates

A

• ↑ risk of hepatotoxicity and/or myalgias with concurrent statins and/or niacin
* DO NOT USE WITH STATINS *

• Protein binding displacement (Warfarin) = ↑ rhabdo risk

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68
Q

Fibrate Drugs

A

• Ezetimibe (Zetia) - blocks absorption fo LDL
• Gemfibrozil
• Fenofibrate

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69
Q

Mechanism of Action for Ezetimibe (Zetia) - Fibrate

A

• Blocks absorption of LDL (cholesterol absorption inhibitor)

• Modestly lowers LDL

• Increases HDL

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70
Q

Which Fibrate drug interacts and cannot be taken with Statins?

A

Gemfibrozil

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71
Q

What is unique about Ezetimibe (Zetia)?

A

It is a fibrate drug that is made to be used WITH statins

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72
Q

What are Omega-3 Fatty Acids used for and what are they made up of?

A

• ↑ HDL
• ↓ Triglycerides
• can slightly increase LDL

Ratio of EPA to DHA varies based on the drug

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73
Q

What are adverse side effects associated with the use of Omega-3 Fatty Acids?

A

• Prolonged bleeding / impaired platelet function

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74
Q

What are anti-arrhythmics used to treat?

A

arrhythmias / abnormal heartbeats (A-Fib, V-Fib)

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75
Q

What are the different classes of Anti-Arrhythmics and what do they each work on?

A

• Class I – Na+ channels (blockade)

• Class II – Beta Receptors (blockade)

• Class III – K+ Channels (prolonged repolarization)

• Class IV – Ca+ Channels (blockade)

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76
Q

What is Amiodarone and what is unique about it?

A

Anti-Arrhythmic

Technically Class III (K+ channels; ↑ repolarization), but it works across all classes

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77
Q

What are adverse side effects of Amiodarone?

A

MOST SEVERE
• Pulmonary Fibrosis (irreversible)
• Thyroid Toxicity (hyperthyroid & hypothyroid)

OTHER
• Pneumonitis
• Cardiotoxicity (bradycardia, hypotension)
• Liver toxicity
• Ophthalmic toxicities
• Dermatologic toxicity (blue/gray skin color)
• Drug interactions

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78
Q

What is the most common arrhythmia caused by Class I anti-arrhythmics (think of the Amiodarone drug study)?

A

Torsades de Pointes (TdP) - difficult to treat, can be fatal

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79
Q

Although Amiodarone has a long list of adverse side effects, what does it have a low risk of causing?

A

Torsades de Pointes (TdP)

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80
Q

Anti-Arrhythmic Drugs

A

• Amiodarone (Class III)
• Flecainide (Class IC - 1C)

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81
Q

What is the most common Anti-Arrhythmic used today?

A

Amiodarone

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82
Q

What do all anti-arrhythmics have a risk of causing?

A

Torsades de Pointes (TdP)

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83
Q

What is Flecainide used for?

A

treatment of A-Fib in patients WITHOUT structural heart issues

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84
Q

Common Adverse Effects of Flecainide

A

• Dizziness
• Visual disturbances
• Dyspnea
• Prolonged QT waves / TdP

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85
Q

Mechanism of Action in Antiepileptic Drugs (AEDs)

A

Impair activation of CNS Neurons
• suppress Na+ influx
• suppress Ca+ influx (↓ transmitter release)
• promote K+ efflux
• antagonize glutamate (block excitatory NT)
• enhance GABA (enhance inhibitory NT)

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86
Q

Side Effects of Antiepileptic Drugs

A

CNS Side Effects
• Impaired cognition (speech, concentration, etc.)
• Dizziness
• Drowsiness
• Diplopia
• Ataxia
• Incoordination
• Weakness

Suicide Risk
• AEDs increase risk 2x (↑ w/ topiramate, lamotrigine)

Pregnancy Risks

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87
Q

What are the CNS Side Effects of Antiepileptic Drugs?

A

• Ataxia
• Dizziness
• Diplopia
• Drowsiness
• Impaired Cognition (speech, concentration, etc.)
• Incoordination
• Weakness

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88
Q

What are the 2 classes of antiepileptic drugs?

A

Older (made prior to 1970s) & Newer (1990s & after)

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89
Q

What is unique about older antiepileptic drugs?

A

• Complicated pharmacokinetics (body gets used to drug, may have to increase dose)

• High drug interaction risk

• More adverse side effects
• most w/ CNS depressant effects
• possible negative effects on learning / cognition

• Greater experience…more effective?
• effective even when “new class” does NOT work

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90
Q

Older Antiepileptic Drugs

A

• Carbamazepine
• Valproic acid / Divalproex

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91
Q

Adverse Side Effects Associated with Carbamazepine

A

• May cause severe skin rash (Stevens-Johnsons Syndrome)

• Asians have it worse, need genetic testing

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92
Q

What is unique about Newer Antiepileptic Drugs?

A

• Straightforward pharmacokinetics

• Generally few drug interactions

• Fewer adverse effects
• less significant CNS depressant effects
• safer / lower risk in pregnancy

• Less experience (because they’re newer)

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93
Q

Which class of antiepileptic drugs are better to use in pregnancy due to them having a lower risk / being safer?

A

Newer Antiepileptic Drugs

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94
Q

Newer Antiepileptic Drugs

A

• Gabapentin

• Lamotrigine (Lamictal)

• Levetiracetam (Keppra)

• Oxcarbazepine (Trileptal)

• Pregabalin (Lyrica)

• Topiramate (Topamax)

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95
Q

Side Effects & Other Considerations of Newer Antiepileptic Drugs

A

Gabapentin
• drowsiness & nystagmus

Lamotrigine (Lamictal)
• rash is relatively common…serious in <1%

Levetiracetam (Keppra)
• IV & PO (route drug can be given)
• CNS effects (drowsiness, aggression, psychosis)
• ↑ BP

Oxcarbazepine (Trileptal)
• CNS effects (drowsiness, dizziness, ataxia)
• Nausea & Vomiting

Pregabalin
• Weight gain
• Angioedema
• Euphoria (considered a schedule V (5) drug)

Topiramate
• Metabolic acidosis
• Kidney stones

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96
Q

Side Effects of Oxcarbazepine & Carbamazepine

A

CNS Effects
• drowsiness
• dizziness
• ataxia

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97
Q

Side Effects of Gabapentin

A

• drowsiness
• nystagmus

  • Not a good seizure med; mainly used for nerve pain*
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98
Q

Adverse Side Effects Lamotrigine (Lamictal)

A

Rash is relatively common
• serious in <1%

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99
Q

Adverse Side Effects of Levetiracetam (Keppra)

A

CNS Effects
• drowsiness
• aggression
• psychosis

↑ BP

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100
Q

Adverse Side Effects of Topiramate

A

• Metabolic Acidosis
• Kidney Stones

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101
Q

Other Issues with Antiepileptic Drugs

A

• Status epilepticus (acute ongoing seizure)

• Therapeutic Drug Monitoring

• Stopping therapy (avoid stopping cold turkey)

• Pregnancy
• some risk with all, but usually woman remain on med

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102
Q

Treatment Goals Diabetic Drugs

A

• Achieve & maintain HbA1C of < 7%

• Reduce microvascular & microvascular complications
• micro = neuropathy, retinopathy, amputation
• macro = heart attack, stroke, etc.

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103
Q

How does better control of A1C affect microvascular & microvascular events?

A

• ↓ microvascular events
• neuropathy, retinopathy, vision loss, amputate

• NO ↓ in macrovascular events (stroke, MI, etc.)

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104
Q

Clinical Actions of Insulin

A

• ↑ glucose, amino acid, fatty acids, & K+ uptake

• ↑ glycogen, protein, & triglyceride synthesis

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105
Q

Long-Acting Insulin Agents

A

• Detemir (Levemir) & Glargine (Lantus) are associated with LOWER risk of hypoglycemia than NPH

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106
Q

Long-Acting Insulin Drugs

A

• Detemir (Levemir)
• Glargine (Lantus)
• Degludec (Tresiba)

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107
Q

Shorter-Acting Insulin Agents

A

• Rapid-acting products preferred to regular insulin due to their faster onset of action & a lower risk of hypoglycemia

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108
Q

Short / Rapid Acting Insulin

A

• Lispro (humalog)
• Aspart (novolog)

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109
Q

What is the order of Insulin Agents used to lower the risk of hypoglycemia?

A

1.) Rapid / short-acting
2.) Regular / long-acting
3.) NPH

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110
Q

How does insulin affect potassium?

A

Insulin ↓ Potassium (K+)

111
Q

What type of Insulin can be given via IV or mixed with other insulins?

A

short-acting

112
Q

Adverse Effects of Insulin

A

• HYPOGLYCEMIA

• Lipodystrophies (bumps if you inject at same site)

• Hypokalemia (↓ K+ can lead to DKA)

113
Q

Non-Insulin Drug Therapies for Diabetes

A

• Glucose-lowering potency is generally similar among oral anti-diabetic drugs
- non-insulin drug ↓ A1C by about 1%
- insulin ↓ A1C by about 2%

• Duration of Glucose Control differs by drug
- not indefinite…3-6 years for most
- decline in β-cell function; disease progression

114
Q

Non Insulin Drugs

A

Metformin (glucophage)

115
Q

Mechanism of Action for Metformin

A

• ↓ hepatic glucose production & intestinal glucose absorption

• sensitizes target cells to insulin (insulin works better)
- does NOT lower glucose, helps body respond better

• ↓ risk of hypoglycemia

• pumped into bile & renal tubule

• good effects on weight, lipids, CV disease, & diabetes

116
Q

Adverse Side Effects of Metformin

A

• Lactic Acidosis
• Diarrhea
• Anorexia
• Dyspepsia / heartburn
• B12 Deficiency (longer term use)

117
Q

Patients with what condition should not take metformin?

A

Renal Dysfunciton

118
Q

Sulfonylureas Mechanism of Action

A

BIND TO PANCREAS FORCING IT TO MAKE ↑ INSULIN

• Promote insulin release
- inhibit ATP-sensitive K+ channels

119
Q

Risks associated with Sulfonylureas

A

• Hypoglycemia
• Impaired β-cell function
• Cardiovascular toxicity

↑ risk of heart disease
↑ weight
• bad effects on lipids

120
Q

Risks associated with Sulfonylureas

A

• Hypoglycemia
• Impaired β-cell function
• Cardiovascular toxicity (↑ heart disease)
• ↑ weight

121
Q

Sulfonylurea Suffix

A

-ide

122
Q

Sulfonylurea Drugs

A

• Glipizide
- stimulates release of insulin from pancreas

• Glimepiride
- ↑ amount of insulin released

123
Q

How do Glipizide & Glimepiride work? (Sulfonylureas)

A

GLIPIZIDE: stimulates release of insulin from pancreas

GLIMEPIRIDE: ↑ amount of insulin released

124
Q

Sodium-Glucose Cotransporter 2 (SGLT2) Inhibitor Drugs

A

• Empagliflozin (Jardiance)

125
Q

Sodium-Glucose Cotransport 2 (SGLT2) Inhibitor Mechanism of Action

A

↑ urinary excretion of glucose

• blocks kidneys' ability to absorb filtered glucose
126
Q

Sodium-Glucose Cotransporter 2 (SGLT2) Inhibitor Side Effects

A

• ↑ risk of urinary/genital tract infection (↑ UTI)

• Hypotension (↓ BP)

• Volume contraction

• Dizziness

127
Q

Sodium-Glucose Cotransporter 2 (SGLT2) Inhibitors are not recommended for patients with _________-.

A

severe renal dysfunction

128
Q

What are Incretins?

A

a group of hormones produced by the GI system that stimulate the release of insulin from the pancreas & help preserve β-cells

  • only works when glucose is ↑ *
129
Q

Drugs Acting via Incretins

A

• stimulate insulin release in a glucose-dependent manner

• ↑ satiety & ↓ food intake

• Preserve β-cells

• Glucose will move from the food into the blood at a slower rate to avoid postprandial hyperglycemia

130
Q

GLP-1 Analogs (antagonists)

Potency & Side Effects

A

More potent (powerful) than DPP-IV inhibitors
- better at lowering glucose, more side effects

Side Effects

• Acute Pancreatitis
• Diarrhea
• Nausea & Vomiting
• Thyroid C-cell tumors

131
Q

GLP-1 Receptor Agonist Drugs

A

Liraglutide (Victoza)

132
Q

DPP-IV Inhibitors

A

• Less potent than GLP-1 analogs

• Oral

• Generally well-tolerated, less side effects

133
Q

DPP-IV Inhibitor Drug

A

Sitagliptin (Januvia)

  • also co-packaged with Metformin
134
Q

Which drug class for diabetes is considered to be a last resort?

A

Thiazolidinediones (TZDs)

135
Q

Thiazolidinedione (TZDs) Drugs

A

Pioglitazone (actos)

136
Q

Mechanism of Action of Thiazolidinediones (TZDs)

A

↓ insulin resistance
- ↑ sensitivity of insulin receptors

137
Q

Adverse Side Effects of Thiazolidinediones (TZDs)

A

• Weight gain
• Fluid retention
• Edema
• ↑ BP
• MI, HF, CV death, & Bladder cancer

138
Q

Short / Rapid Acting Insulin

A

• Lispro (humalog)
• Aspart (novolog)

139
Q

H2-Receptor Antagonist (blocker) Mechanism of Action

A

• Bind to histamine receptor (H2RA - H2 receptor)

- prevents histamine from stimulating parietal cells
- ↓ acid (H+ ions) production = ↑ pH
140
Q

How do H2 Receptor Antagonists impact acid production & pH?

A

↓ acid production (H+ ions)

↑ pH

141
Q

H2RA Drugs (H2 Receptor Antagonists)

A

• Ranitidine (zantac = off market)

• Ramotidine (pepcid)

142
Q

Proton Pump Inhibitor (PPI) Mechanism of Action

A

Activated by the acidic inside of the parietal cell and bind to the inside of the proton pumps which blocks acid (H+ ions) from being released into the stomach.

143
Q

Proton Pump Inhibitor Suffix

A

-prazole

144
Q

Proton Pump Inhibitor (PPI) Suffix

A

-prazole

145
Q

Proton Pump Inhibitor Drugs

A

• Esomeprazole

• Lansoprazole (prevacid)

• Omeprazole

• Pantoprazole (protonix)

146
Q

Side Effects of PPIs (proton pump inhibitors)

A

• Headache
• Nausea
• Diarrhea
• Abdominal pain
• ↑ fracture risk
• Vitamin / mineral malabsorption

•↑ chance of aspiration pneumonia in non-ambulatory pts

147
Q

Which class of acid suppressants is more powerful?

A

Proton Pump Inhibitors

148
Q

Antacid Mechanism of Action

A

Neutralize secreted acid

• work quickly but only short-term

149
Q

Common Side Effects of Antacids

A

• Constipation

• Diarrhea

• Neurotoxicity

• Hypophosphatemia
- ↓ phosphate levels in blood

• Acid rebound
- body makes ↑ acid to combat pH change

• Drug Interactions

• Chelation
- antacids bind other meds making them inactive

150
Q

Sucralfate Mechanism of Action

A

Sucrose Sulfate (sucrose + sulfated aluminum chloride) binds positively charged proteins in base of ulcers

  • Binds to ulcers forming a protective barrier *
151
Q

Side Effects of Sucralfate

A

** Constipation **
** Drug Interactions **
• Neurotoxicity (Al3+ accumulation)
• Bezoar formation
• Hypophosphatemia
- ↓ phosphate levels in blood

152
Q

What is Hypophosphatemia?

A

↓ levels of phosphate in the blood

153
Q

Bronchial constriction is a concern in patients with asthma or COPD with which drugs?

 a.) Angiotensin Receptor Blockers
 b.) ACE Inhibitors
 c.) Dihydropyridine calcium channel blockers
 d.) Beta-Blockers
A

d.) Beta-blockers

154
Q

Which of the drug classes is most likely to cause bradycardia?

 a.) All classes listed here have a similar risk
 b.) ACE Inhibitors
 c.) Dihydropyridine calcium channel blockers
 d.) Beta-Blockers
A

d.) Beta-Blockers

155
Q

Which of these drugs can cause hyperkalemia, meaning the patient’s serum potassium may need to be monitored closely?

 a.) Dihydropyridine calcium channel blockers
 b.) ACE Inhibitors
 c.) Beta-Blockers
 d.) Angiotensin Receptor Blockers
A

d.) Angiotensin Receptor Blockers (ARBs)

156
Q

pendent edema is a common side effect of which drugs?

 a.) Beta-blockers 
 b.) Angiotensin Receptor Blockers (ARBs)
 c.) Non-Dihydropyridine Ca+ channel blockers
 d) Dihydropyridine Ca+ channel blockers
A

d.) Dihydropyridine calcium channel blockers

157
Q

Which drugs have a high risk of causing adverse metabolic effects like an increase in glucose and new-onset diabetes?

 a.) ACE Inhibitors
 b.) Beta-Blockers
 c.) DHP Calcium Channel Blockers
 d.) Non-DHP Calcium Channel Blockers
A

b.) Beta-Blockers

158
Q

Metoprolol (Lopressor) is a member of what drug class?

a.) Dihydropyridine calcium channel blockers
b.) Beta-blockers
c.) Non-Dihydropyridine calcium channel blockers
d.) ACE Inhibitors
A

b.) Beta-blockers

159
Q

A chronic, dry, non-productive cough is a relatively common side effect of which drugs?

a.) Non-DHP calcium channel blockers
b.) ACE Inhibitors
c.) Angiotensin Receptor Blockers (ARBs)
d.) Beta-Blockers
A

b.) ACE Inhibitors

160
Q

Amlodipine (Norvasc) is what type of drug?

 a.) Non-DHP Calcium Channel Blockers
 b.) ACE Inhibitor
 c.) DHP Calcium Channel Blockers
 d.) Angiotensin Receptor Blockers (ARBs)
A

c.) DHP Calcium Channel Blocker

161
Q

Benzapril (Lotensin) is a member of what drug class?

 a.) DHP Calcium Channel Blockers
 b.) ACE Inhibitors
 c.) Angiotensin Receptor Blockers (ARBs)
 d.) Beta-Blockers
A

b.) ACE Inhibitors

162
Q

Which of these diuretic classes is most potent at removing fluid (increasing urine output)?

 a.) Potassium-Sparing
 b.) Loops
 c.) All are equally potent
 d.) Thiazide & Thiazide-like
A

b.) Loops

163
Q

Which of these drugs act as both a diuretic and an aldosterone antagonist, giving it unique actions in treating heart failure?

 a.) Furosemide (Lasix)
 b.) Hydrochlorothiazide
 c.) Ezetimibe (Zetia)
 d.) Spironolactone
A

d.) Spironolactone

164
Q

Muscle toxicity (myalgia, myopathy, rhabdomyolysis) is a concern with what drugs?

 a.) HMG-CoA Reductive Inhibitors ("Statins")
 b.) Anti-arrhythmics
 c.) Loop diuretics
 d.) Omega-3 fatty acids
A

a.) HMG-CoA Reductase Inhibitors (Statins)

165
Q

Which diuretics have a relatively flat dose-response curve, increase serum calcium concentrations, and are less effective in patients with severe renal dysfunction?

 a.) Loop diuretics
 b.) Thiazide diuretics
 c.) Potassium-sparing diuretics
 d.) That describes all diuretics
A

b.) Thiazide diuretics

166
Q

Which of these drug classes that can substantially reduce serum triglyceride concentrations also have the potential to impair platelet function, leading to an increased risk of bleeding or bruising and possible interaction concerns when used with other antiplatelet agents or anticoagulants?

 a.) Ezetimibe
 b.) Fibrates
 c.) HMG-CoA Reductase Inhibitors ("Statins")
 d.) Omega-3 fatty acids
A

d.) Omega-3 fatty acids

167
Q

Which of these is a diuretic?

 a.) Rosuvastatin (Crestor)
 b.) Gemfibrozil (Lopid)
 c.) Flecainide (Tambocor)
 d.) Chlorthalidone (Hygroton)
A

d.) Chlorthalidone (hygroton)

168
Q

Hyperthyroidism & Hypothyroidism are both possible side effects of what drug?

 a.) Atorvastatin (Lipitor)
 b.) Flecainide (Tambocor)
 c.) Gemfibrozil (Lopid)
 d.) Amiodarone (Cordarone)
A

d.) Amiodarone

169
Q

Close monitoring of the QT Interval is required with the use of which of these drugs?

 a.) Fenofibrate (Tricor)
 b.) Flecainide (Tambocor)
 c.) Simvastatin (Zocor)
 d.) Furosemide (Lasix)
A

b.) Flecainide

170
Q

What drug class is most likely to cause bradycardia?

A

Beta-Blockers

171
Q

A dry, chronic, non-productive cough is most likely to be observed with which class of medications?

A

ACE Inhibitors

172
Q

Dependent edema is a relatively common side effect of which drugs?

A

Dihydropyridine (DHP) Calcium Channel Blockers

173
Q

What medication class is most closely associated with adverse metabolic effects, including increased hemoglobin A1C concentrations & new-onset diabetes?

A

Beta-Blockers

174
Q

Bronchial constriction, leading to a risk of adverse pulmonary effects that may be a concern for patients with ashtma or COPD, is most likely associated with what drug?

A

Propranolol

175
Q

What drug has the highest risk of causing hyperkalemia?

A

Lisinopril

176
Q

Metoprolol (Lopressor) is what type of drug?

A

Beta-Blocker

177
Q

What drug class is Benazepril (Lotensin) a member of?

A

ACE Inhibitor

178
Q

Losartan (Cozier) is a member of what drug class?

A

Angiotensin Receptor Blockers

179
Q

Which drug category is most likely to cause hypokalemia, hypomagnesemia, and other electrolyte abnormalities?

A

Diuretics

180
Q

Myalgia, myopathy, and rhabdomyolysis are closely associated with which drug class?

A

Statins

181
Q

Which drug is expected to cause an increase in serum calcium concentrations?

A

Chlorthalidone (Hygroton) = thiazide diuretic

182
Q

What drug would be used to lower serum triglyceride concentrations and is associated with a risk for gallstones, phytotoxicity, and a serious drug interaction with statins?

A

Gemfibrozil (Lopid) = fibrate

183
Q

Which drug class is the most potent diuretic, displaying a “high ceiling” and a linear dose-response curve?

A

Loop Diuretics

184
Q

Gynecomastia is a side effect closely related with what drug?

A

Spironolactone

185
Q

Antiplatelet effects, leading to a risk of bleeding or bruising, are most commonly associated with what drug?

A

Omega-3 Fatty Acids

186
Q

What drug is a potassium-sparing diuretic?

A

Triamterene

187
Q

What medications end with “-olol”?

A

Beta-Blockers

188
Q

What medications end with “-pril”?

A

ACE Inhibitors

189
Q

Which medications end in “-sartan”?

A

ARBs (angiotensin receptor blocker)

190
Q

Hyperkalmeia is caused by which drug class?

A

ACE Inhibitors

191
Q

ACE Inhibitor MOA

A

inhibits the production of Angiotensin II & breaks down bradykinin

192
Q

List ACE Inhibitor Drugs

A

• Benazepril
• Enalapril
• Lisinopril
• Ramipril

193
Q

Benefits of ARBs over ACE Inhibitors

A

does not produce cough

 -could be due to the fact that ARBs do not affect bradykinin
194
Q

List Angiotensin Receptor Blocker (ARB) Drugs

A

• Irbesartan
• Losartan
• Olmesartan
• Valsartan

195
Q

What do ACE Inhibitors do to bradykinin?

A

Increase bradykinin levels (cough?)

196
Q

What is the difference in DHP & Non-DHP Calcium Channel Blockers?

A

DHP Calcium Channel Blockers do NOT affect HR

Non-DHP Calcium Channel Blockers affect HR

197
Q

List Non-Dihydropyridine (Non-DHP) Calcium Channel Blockers

A

• Diltiazam
• Verapamil

 - can cause a lot of drug interactions because they're metabolized in the liver
198
Q

Which Calcium Channel Blocker is more vascular selective?

A

Dihydropyridines - they cause vasoDILATION

199
Q

Which Calcium Channel Blocker is more heart selective?

A

Non-Dihydropyridines

200
Q

Which drug class causes an increase in potassium?

A

ACE Inhibitors (lisinopril)
- sometimes potassium-sparing diuretics

201
Q

Pharmakokinetics

A

What the body does to the drug

202
Q

Pharmacodynamics

A

What the drug does to the body

203
Q

Which drug class do Amlodepine & Nifedipine belong to?

A

Dihydropyridine (DHP) Calcium Channel Blockers

204
Q

Which drug class do Verapamil & Diltiazem belong to?

A

Non-Dihydropyridie (Non-DHP) Calcium Channel Blockers

205
Q

What is the primary side effect of Dihydropyridines (DHPs)?

A

edema

206
Q

What is the primary side effect of non-DHPs?

A

bradycardia

207
Q

Which drug is best at vasodilation?

A

DHP Calcium Channel Blockers

208
Q

List Selective Beta Blocker Drugs

A

• Metoprolol
• Atenolol

209
Q

List Non-Selective Beta Blocker Drugs

A

• Propranolol

210
Q

List Vasodilating Beta Blocker Drugs

A

• Carvedilol
• Labetalol
• Nebivolol

211
Q

List the adverse side effects of beta-blockers

A

• Bradycardia
• Bronchospasm
• Hyperglycemia (diabetes)
• ↓ insulin sensitivity
• Depression
• ↑ A1C

212
Q

What is the drug class of choice for the treatment of tremors?

A

Beta Blockers

213
Q

Patients with what condition(s) should not be put on Beta Blockers?

A

Asthma or respiratory issues

214
Q

What drug class is the preferred INITIAL agent for the treatment of hypertension?

A

diuretics

215
Q

How do loop diuretics affect calcium?

A

↓ Calcium

216
Q

How do Thiazide diuretics affect calcium?

A

↑ Calcium

217
Q

List Potassium-sparing diuretic drugs

A

• Spironolactone
• Amiloride
• Triamterene

218
Q

Which class of diuretics is the most powerful?

A

Loop Diuretics

219
Q

Common Adverse Side Effects of Diuretics

A

• ↓ K+
• ↓ Magnesium
• Hyperglycemia
• Hypovolemia
• Electrolyte imbalance

220
Q

Which class of diuretics has an increased sensitivity to renal function?

A

Thiazide Diuretics

221
Q

Which class of diuretics has a linear response curve?

A

Loop diuretics

222
Q

Which class of diuretics has a low dose response curve?

A

Thiazide diuretics

223
Q

Side Effects of Antiepileptic Drugs

A

• Impaired cognition
• Drowsiness
• ↑ suicide risk
• Pregnancy Risks

224
Q

Suicide is higher with which antiepileptic drugs?

A

• Topirimate
• Lamotrigene

225
Q

List Older Antiepileptic Drugs

A

• Carbamazepine
• Valproic Acid / Divalproex

226
Q

Side Effects / Risks associated with Carbamazepine

A

• Severe skin reaction
- worse in asians; need genetic tessting

227
Q

List Newer Antiepileptic Drugs

A

• Gabapentin
• Lamotrigene
• Levetracetam
• Oxcarbazepine
• Pregabalin
• Topiramate

228
Q

Side Effects associated with Lamotrigine (Lamictal)

A

Rash

229
Q

Common use for Gabapentin

A

nerve pain

230
Q

Which drug class is associated with a risk for myalgia, myopathy, & rhabdomyolysis?

A

Statins (HMG-CoA Reductase Inhibitors)

231
Q

Side Effects associated with Pregabalin (Lyrica)

A

• Weight gain
• Euphoria
• Angioedema

232
Q

Side Effects associated with Levetiracetam (Keppra)

A

• ↑ BP
• least CNS effects out of all antiepileptic drugs

233
Q

Side Effects associated with Topiramate

A

• Kidney Stones
• Bone Issues
• Metabolic acidosis
- stops body’s ability to reabsorb bicarbonate

234
Q

How should antiepileptic drug therapy be stopped?

A

slowly over time; no abrupt withdrawl

235
Q

How does better control of A1C affect microvascular events?

A

↓ microvascular events

236
Q

How does better control of A1C impact macrovascular events

A

does NOT impact macrovascular events

237
Q

What are microvascular events?

A

damage to small blood vessels
• neuropathy
• retinopathy
• amputation

238
Q

What are macrovascular events?

A

damage to large blood vessels
• stroke, heart attack, etc.

239
Q

List Insulin Drugs

A

• Lispro
• Aspart
• Detemir
• Glargine
• Degludec

240
Q

List Fast-Acting / Rapid-Acting Insulin Drugs

A

• Lispro
• Aspart

241
Q

Lispro & Aspart are what class of insulin drug?

A

rapid-acting

242
Q

List long-acting / slow-acting insulin drugs

A

• Detemir
• Glargine
• Degludec

243
Q

Detemir, Glargine, & Degludec are what class of insulin drug?

A

slow-acting

244
Q

Side Effects of Insulin Drugs

A

• Hypoglycemia
• Hypokalemia
• Weight gain

245
Q

What is the number 1 recommended non-insulin drug for diabetes?

A

Metformin

246
Q

Metformin MOA

A

lowers A1C

247
Q

Side Effects of Metformin

A

• Lactic acidosis
• B12 deficiency

248
Q

SGLT2 Inhibitor MOA

A

↑ glucose excretion in urine

249
Q

What do SGLT2 inhibitors have a favorable effect on?

A

weight & BP

250
Q

List an SGLT2 Inhibitor drug

A

Empagliflozin (jardiance)

251
Q

GLP1 Agonist MOA

A

stimulate the release of insulin from the pancreas

252
Q

Side Effects of GLP1 agonists

A

• Nausea
• Diarrhea
• Acute pancreatitis
• Thyroid C-cell tumors

253
Q

What do drugs acting via Incretins do?

A

• very low risk of hypoglycemia
• ↑ satiety
• ↓ food intake
• Preserve β-cells
• Control postprandial glucose

254
Q

GLP-1 Receptor Agonist Drugs

A

Liraglutide

255
Q

Are GLP-1 Agonists or DPP-IV more potent / powerful?

A

GLP-1 Agonists

256
Q

List DPP-IV Inhibitor Drugs

A

Sitagliptin (januvia)

257
Q

List Thiazolidinedione (TZD) Drugs

A

• Pioglitazone (actos)

258
Q

Thiazolidinediones (TZDs) MOA

A

↑ sensitivity of insulin receptors

259
Q

Side Effects of TZDs (Thiazolidinediones)

A

• Fluid Retention
• Edema
• Weight gain
• ↑ BP
• MI, HF, CV death, & Bladder cancer

260
Q

H2RA (Histamine 2 Receptor Antagonist) MOA

A

blocks the histamine receptor which decreases acid production & increases stomach pH (less H+ ions)

261
Q

Chelation

A

Positive ions can bind to drugs in the gut which inactivates the other drug

262
Q

List H2RA Drugs

A

• Ranitidine (zantac)
• Famotidine (pepcid)

263
Q

Proton Pump Inhibitor (PPI) MOA

A

blocks proton pumps from inside the parietal cell which blocks acid from being released into the stomach

264
Q

List of PPI Drugs

A

• Omeprazole (prilosec)
• Esomeprazole (nexium)
• Lansoprazole (prevacid)
• Pantoprazole (protonix)

265
Q

Suffix of Proton Pump Inhibitors (PPIs)

A

“-prazole”

266
Q

Common Side Effects of PPIs

A

• Headache
• Nausea
• Diarrhea
• Abdominal pain
• ↑ risk of fracture
• Malabsorption (of vitamins & minerals)

267
Q

Antacid MOA

A

neutralize secreted acid

268
Q

Common Side Effects of Antacids

A

• Constipation
• Diarrhea
• Neurotoxicity
• Hypophosphatemia
• Acid rebound (body makes ↑ acid)
• Drug interactions (/ chelation)

269
Q

What is Sucralfate used to treat?

A

ulcers

270
Q

Sucralfate MOA

A

sucrose sulfate binds positively charged proteins in the base of ulcers
* needs acidic environment *

271
Q

Side Effects of Sucralfate

A

• Constipation
• Hypophosphatemia
• Neurotoxicity

272
Q

Mnemonic for Newer Antiepileptic Drugs

A

Obese
Limping
Giants
Purchased
Little
Tyrants

273
Q

Mnemonic & Drugs for Newer Antiepileptic Drugs

A

Obese = Oxcarbazepine

Limping = Lamotrigine (Lamictal)

Giants = Gabapentin

Purchased = Pregabalin (Lyrica)

Little = Levetiracetam (Keppra)

Tyrants = Topiramate

Pharmacology (5 decks)

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