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Advanced Pharmacology > Adv Pharm Test 3 Study Questions > Flashcards

Adv Pharm Test 3 Study Questions Flashcards

1
Q

Which H2 receptor agonist is least potent?

A

Cimetidine

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2
Q

Which H2 RA causes confusion in elderly?

A

Ranitidine (Zantac)

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3
Q

Which H2 RA is most potent?

A

Famotidine (Pepcid)

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4
Q

Best H2 RA for elderly

A

Famotidine (Pepcid)

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5
Q

Adverse effects unique to cimetidine

A

gynecomastia, impotence, galactorrhea

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6
Q

Which H2 RA is a CYP450 inhibitor?

A

Cimetidine

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7
Q

How long can pts use PPIs?

A

3-6 months; longer requires careful monitoring

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8
Q

PPI adverse effects

A

vitamin b deficiency
Hip fractures
Risk for infection
gastric tumors

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9
Q

How long does it take for PPI to work?

A

3-4 days

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10
Q

PPI MoA

A

binds to H+/K+ ATPase pump and irreversibly inactivates enzyme

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11
Q

Are PPIs prodrugs?

A

yes

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12
Q

When to take PPI?

A

30-60 minutes before food

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13
Q

Bulk forming meds MoA

A

absorbs water and forms bulky compound that distends colon and stimulates peristalsis

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14
Q

Bulk meds AE

A

Abdominal pain, bloating, flatulence 


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15
Q

Bulk meds drug interactions

A

absorb drugs take 2 hours before or after

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16
Q

Surfactant dosing

A

once to twice a day

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17
Q

Surfactant full onset

A

1-3 days

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18
Q

Sufactants combined w/?

A

stimulants

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19
Q

Stimulants used often used with which pts?

A

those on chronic opiod therapy

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20
Q

Stimulant dosing

A

once daily

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21
Q

Stimulant full onset

A

6-12 hours

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22
Q

Stimulant used in combo with?

A

docusate

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23
Q

Stimulant AE

A

Griping, cathartic colon (years of use) 


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24
Q

Which drug classes are used for motion sickness?

A

Histamine 1 antagonists, antimuscarniic and promethazine

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25
Q

Ondasteron indication

A

postoperative and chemotherapy-induced N/V

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26
Q

Ondasteron MOA

A

Blocks 5-HT3 receptor in CNS, chemoreceptor trigger zone, and GI tract

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27
Q

Ondasteron AE

A

Headache, QTc prolongation

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28
Q

Which Histamine1 antagonists treats vertigo?

A

Meclizine (Dramamine)

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29
Q

Side effects of motion sickness drugs?

A

drowsiness, xerostomia

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30
Q

What population to avoid with phenergan?

A

children under 2 (resp dep)

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31
Q

Phenergan routes of admin

A

oral, IV, suppository

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32
Q

Phenergan indications

A

motion sickness and drug induced NV

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33
Q

Phenergan MoA

A

Anticholinergic properties within the chemoreceptor trigger zone 


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34
Q

Scopalamine route

A

transdermal patch

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35
Q

Phenergan dosing

A

Short acting, dosed 3 to 4 times a day 


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36
Q

Glucocorticoid steroid MoA

A


inhibiting production of inflammatory cytokines and chemokines 


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37
Q

What IBD med is used for remission?

A

Methotrexate

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38
Q

Which glucocorticoid acts locally on GI tract and has less side effects?

A

Budesonide

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39
Q

Glucocorticoid indication

A

During active stage of disease

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40
Q

Which glucorticoid is most commonly used to induce remission?

A

Prednisone

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41
Q

Hydrocortisone routes

A

Tablet, injection, suppositories, foam, enema

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42
Q

Glucocorticoid AE

A

Immunodeficiency – Hyperglycemia
 – Adrenal insufficiency – Excitatory effects (insomnia)
 – Increased appetite / weight gain

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43
Q

Methotrexate MoA

A

Suppresses immune system

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44
Q

Can methotrexate be taken during pregnancy?

A

No

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45
Q

What supplement should you take with methotrexate?

A

Folate

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46
Q

How often is methotrexate administered?

A

Once a week

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47
Q

Carbonic Anhydrase Inhibitor indications

A

– Glaucoma
 – Urinary alkalinization
 – Metabolic alkalosis
 – Acute mountain sickness

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48
Q

Which class of diuretics is not useful for HTN or dieresis?

A

Carbonic Anhydrase inhibitors

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49
Q

What are loop diuretics most effective for?

A

Fluid elimination, not HTN

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50
Q

Loops routes

A

Oral and IV

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51
Q

Loops MoA

A

– Inhibits sodium reabsorption in the ascending limb of Loop of Henle – Promotes up to 25% sodium and water excretion – Increases urinary excretion of other end

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52
Q

What is the most notable AE of loops?

A

Hypokalemia

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53
Q

What AE is unique to loops

A

Hypocalcemia

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54
Q

Loops AE

A

– Hypotension
 – Hyponatremia
 – Hypochloremia
 – Hypokalemia
 – Hypomagnesemia – Hypocalcemia – Ototoxicity
 – Azotemia = renal injury

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55
Q

Which diuretics have ceiling effect?

A

Loops

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56
Q

How are loops excreted?

A

Renally

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57
Q

Should we give more or less loops to kidney patients?

A

More

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58
Q

Which loop has lowest oral bioavailbility?

A

Furosemide

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59
Q

Thiazides MoA

A

– Inhibits sodium reabsorption in the distal tubule – Promotes up to 5% sodium and water excretion – Increase urinary excretion of other electrolytes

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60
Q

When is the effectiveness of thiazides diminished?

A

When CrCl falls below 30 mL/min

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61
Q

1st line diuretic for HTN

A

Thiazides

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62
Q

How long for max effect on blood pressure with thiazides?

A

2-4 weeks

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63
Q

Thiazides AE

A

– Hypotension – Hyponatremia – Hypokalemia – Hypomagnesemia – Hypercalcemia
 – Increased uric acid
 – Increased plasma glucose levels – Azotemia

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64
Q

Are thiazides used extensively for edema?

A

No

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65
Q

how do loops and thiazides work together?

A

blocks Na+ reabsorption in distal nephron segments

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66
Q

Potassium-Sparing Diuretics MoA

A

– Acts at collecting duct to inhibit sodium reabsorption
– Promotes up to 2% sodium and water excretion
– Blocks effects of aldosterone in kidney

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67
Q

Potassium-Sparing Diuretics AE

A

– Hypotension
– Nausea and vomiting, constipation, diarrhea – Hypercalcemia
– Hyperkalemia
– Gynecomastia (spironolactone)

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68
Q

Beta blockers MoA

A

– Block β1 receptors in cardiac muscle
Decrease heart rate (negative chronotropic effects)
Decrease cardiac output (negative inotropic effects)
– Inhibit the release of renin from the kidneys
– Some agents inhibit activity of the sympathetic nervous system
– Some agents directly decrease peripheral vascular resistance

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69
Q

Beta Blockers AE

A

o Hypotension

o Bronchospasm – relates to β1 selectivity!!

o Bradycardia

o Fatigue, exercise intolerance
o Depression, confusion, agitation, psychosis

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70
Q

Beta blockers indication

A 
Hypertension
– Angina pectoris
– Myocardial infarction
– Heart failure
– Ventricular arrhythmia – Migraine prophylaxis – Hyperthyroidism
– Glaucoma
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71
Q

Which beta blockers have beta selectivity?

A

Atenolol, metprolol

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72
Q

Which beta blockers have alpha blockade?

A

carvedilol

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73
Q

What does alpha blockade acheive?

A

decreased sympahtetic stim causing vasodilation

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74
Q

Decreased beta selectivity can affect which organ?

A

lungs

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75
Q

ACEI MoA

A

Inhibit RAAS by preventing conversion of
angiotensin I to angiotensin II → decreased systemic vascular resistance → decreased blood pressure
– Inhibit degradation of bradykinin and increase synthesis of vasodilating prostaglandins

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76
Q

ACEI indications

A

HTN
– Heart failure
– Left ventricular dysfunction – Diabetic nephropathy
– Acute myocardial infarction – Chronic kidney disease

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77
Q

How are most common ACEIs eliminated?

A

renally

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78
Q

ACEI AE

A

– Hypotension
– Hyperkalemia
– Acute renal failure – Cough
– Angioedema

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79
Q

ACEI interactions

A

Potassium supplements or potassium sparing

diuretics

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80
Q

ACEI contraindications

A

– Pregnancy, aortic stenosis, renal artery stenosis

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81
Q

ARB MoA

A

Selectively block the vasoconstrictive effects of angiotensin II by blocking binding of angiotensin II to its receptor
– Used in patients that can’t tolerate ACEI due to cough – Should probably not be use if angioedema on ACEI

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82
Q

ARB AE

A

– Hypotension
– Hyperkalemia
– Acute renal failure
– Angioedema (very rare)

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83
Q

ARB drug interactions

A

Potassium supplements or potassium sparing

diuretics

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84
Q

ARB contraindications

A

Pregnancy, aortic stenosis, renal artery stenosis

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85
Q

Do ACE and ARB affect cardiac outpout and blood volume?

A

no

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86
Q

Calcium channel blocker MOA

A

– Blocking calcium entry into smooth muscle – Results in vasodilation
– Can also affect cardiac conduction

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87
Q

Difference b/x DHP and non DHP CCBs

A

Non DHP lower cardiac output; not used for HTN

88
Q

Non-DHP CCBs

A

verapamil and diltiazem

89
Q

Which DHP CCB is also given IV

A

Nicardipine

90
Q

CCB indications

A

HTN
– Angina pectoris
– Peripheral vascular disease
– Migraine prophylaxis (non-DHP) – Arrhythmia (non-DHP)

91
Q

CCB AE

A

– Relative to DHP
Hypotension Headache and flushing Peripheral edema
– Relative to non-DHP Bradycardia
Hypotension Constipation (verapamil)

92
Q

a1 receptor agonists MoA

A

– Decrease sympathetic stimulation causing vasodilation and thus reducing blood pressure

93
Q

a1 receptor agonists AE

A

Adverse effects
– First dose phenomenon → decreased blood pressure
– Chronic administration → water and sodium
accumulation
Used as a last-line agent in the treatment of hypertension

94
Q

a2 receptor agonists MoA

A

2 Receptor Agonists Mechanism of action

– Decrease sympathetic stimulation to cause vasodilation and thus reduce blood pressure

95
Q

Which a2 receptor is avail as oral, IV and patch?

96
Q

a2 receptor agonists AE

A

– Sedation and headache
– Abrupt discontinuation may result in rebound
hypertension
Used as a last-line agent in the treatment of hypertension

97
Q

direct vasodilators MoA

A

– Causes artery relaxation (vasodilation) resulting in decreased blood pressure

98
Q

direct vasodilators adherence issue

A

TID very poor adherence

99
Q

direct vasodilators AE

A

– Hydralazine → Tachycardia and fluid retention – Minoxidil → hirsutism

100
Q

direct vasodilators indications

A

severe HTN

101
Q

HTN med choices for patients with DM–hyperalbuminuria

A

ACEI or ARBs

102
Q

HTN med choices for patients with CKD

A

ACEI or ARBs (if ACEI isn’t tolerated)

103
Q

Sodium Nitroprusside MoA

A

Converts to nitric oxide (NO)
Decreases preload (venodilation) and afterload (arterial dilation) to a similar degree
Reduces cardiac output and increases heart rate

104
Q

How is sodium nitroprusside administered?

A

continuous infusion (half life < 10 minutes)

105
Q

Sodium Nitroprusside AE

A

generates cyanide

tachycardia

106
Q

When is there a risk of toxicity with sodium nitroprusside?

A
  • with doses > 2 micrograms/kg/min
  • prolong admin
  • renal or hepatic insufficiency
107
Q

Sodium nitroprusside is NOT indicated for

A

ACS
Aortic dissection
increased ICP

108
Q

Nitroglycerin MoA

A

relxes venous smooth muscle (combine with sulf groups that mimic NO)

109
Q

Which is more potent for lowering BP: sodium ntiroprusside or nitroglycerin?

A

sodium nitroprusside

110
Q

Which vasodilator is used for acute heart failure or ACS?

A

nitroglycerin

111
Q

How is nitrogrlycerin administered?

A

continuous IV; half likfe 2-3 mintues

112
Q

Disadvantages of nitroglycerin

A

tachyphylaxis; you need a nitrate free interval

113
Q

Nitroglycerin AE

A

– Hypotension
– Headache
– Reflex tachycardia

114
Q

Nitroglycerin interactions

A

– Phosphodiesterase-5 inhibitors (i.e. sildenafil)

115
Q

What IV CCB is used for HTN emergency?

A

Nicardipine

116
Q

How is nicardipine administered?

A

1-15 mg/hr continuous

117
Q

Unique issue with nicardipine

A

tri-phasic elimination; watch for accumulation

118
Q

Loop diuretics short term benefit

A

Decreased jugular venous distension, pulmonary congestion, and peripheral edema

119
Q

Loop diuretics intermediate benefits

A

Decreased daily symptoms, improved cardiac function increased exercise tolerance

120
Q

Do loop diuretics affect mortality rates?

121
Q

What cocktail is recommended for HFrEF

A

ACEI/ARB/ARNI + beta blocker + aldosterone antagonist

122
Q

How long to space out ARNI and ACEI?

123
Q

What to monitor on ACEI/ARB/ARNI?

A

renal function
potassium
Hypotension

124
Q

beta blockers for HF

A

carvedilol
metoprolol
Bisoprolol

125
Q

Which GI drug class has a FDA warning about its use with clopidogrel? Why?

A

PPI’s inhibit the metabolism of clopidogrel, which is a prodrug, and can lead to decreased efficacy.

126
Q

aldosterone blockade meds

A

spironolactone and eplerenone

127
Q

benefits of digoxin

A

improved symptoms and
exercise tolerance, decreased hospitalizations

128
Q

Digoxin place in therapy

A

in patients with symptomatic LV dysfunction despite optimal ACE inhibitor (or ARB), β-blocker, spironolactone (if appropriate), and diuretic therapy
and some arrythmias

129
Q

Digoxin MoA

A

◦ Na+K+ ATPase inhibitor → enhance Ca++ entry into
the cell
◦ Slows heart rate (chronotropic effect): good for afib
◦ Decreases central sympathetic outflow: good for HF

130
Q

Is Digoxin dialyzable?

131
Q

Does digoxin have a long half life?

132
Q

Digoxin AE

A

◦ Nausea, vomiting, diarrhea, abdominal pain ◦ Headache, visual disturbances (green/yellow
“halos”)
◦ Cardiac arrhythmias

133
Q

What’s used to treat digoxin toxicity?

134
Q

Digoxin drug interactions

A

amiodarone, antacids, verapamil

135
Q

What’s an alternative in HF patients unable to take an ACEIs or ARBs because of severe renal insufficiency, hyperkalemia,or angioedema

A

Hydralazine–isosorbide dinitrate

136
Q

Ivrabradine MoA

A

◦ Inhibits the “funny” current to slow HR

137
Q

Ivrabradine AE

A

bradycardia and visual disturbances

138
Q

When is ivrabradine used?

A

in pts with elevated HR

139
Q

Does ivrabradine reduce mortality?

140
Q

Does ivrabradine reduce hospitalizations?

141
Q

which HF meds don’t reduce mortality?

A

loops, ivrabradine

142
Q

HFpEF treatment

A

reduce tachy and BP

143
Q

Leading dose for asprin in pts with ACS?

A

324-325 mg

144
Q

Which ADP-receptor antagonist is taken 2x/day?

A

ticagrelor

145
Q

ADP-receptor antagonist prodrugs

A

clopidogrel and prasugrel

146
Q

Is Ticagrelor a prodrug?

147
Q

Which of the ADP-Receptor Antagonists is not to be used in patients with history of stroke or TIA?

148
Q

Which ADP-RA is more effective in diabetic and STEMI pts?

149
Q

What is the IV form of clopidogrel?

150
Q

Cangrelor metabolism

A

quick onset and offset

151
Q

Glycoprotein inhibitors AE

A

Low platelet count (thrombocytopenia)

Bleeding

152
Q

What are the 3 main indications for unfractionated heparin?

A

Prophylaxis of DVT/PE
Treatment of DVT/PE
Treatment of ACS or Afib

153
Q

UH dosing for DVT/PE prophylaxis

A

5,000 units subq 2-3/day

154
Q

UH dosing for treatment of DVT/PE

A

IV bolus of 80 units/kg followed by continuous IV infusion (18 units/kg/hour)

155
Q

UH dosing for treatment of ACS or AFib

A

IV bolus of 60 units/kg max 4,000) followed by continousinfusion 12 units/kg/hour max 1000)

156
Q

How to monitor unfractionated heparin?

A
  • aPTT: 1.5 -2.5s x control (60-80s)
  • Factor Xa levels (0.3-0.7 units/mL)
  • Signs of bleeding
  • Platelet count
157
Q

unfractionated heparin AE

A

bleeding, osteoporosis, thrombocytopenia

158
Q

What agent reverses UH?

159
Q

Protamine AE

A

Hypotension, brady, anaphylaxis

160
Q

Unfractionated heparin MoA

A

◦ Indirect thrombin inhibitor
◦ Binds to antithrombin III (AT/ATIII) → enhancing its activity ◦ ATIII binds to and inhibits factors IIa, IXa, Xa, XIa and XIIa
◦ Stops growth and propagation of a formed thrombus

161
Q

LMW heparin MoA

A

◦ Indirect thrombin inhibitor
◦ Binds to and activates antithrombin III (AT/ATIII)
 inactivation of factor Xa > factor IIa
◦ Stops growth and propagation of a formed
thrombus

162
Q

UH vs. LMWH

A

LMWH is nearly 100% predictable, long half-life, less HIT, doesn’t require monitoring, but protamine is less effective

163
Q

Factor Xa inhibitors used for DVT/PE/ACS

A

Fondaparinux

164
Q

Factor Xa inhibitors used for DVT/PE/ and Afib

A

Rivaraxaban
Apixiban
edoxaban

165
Q

Factor Xa inhibitors used for DVT prophy only

A

Betrixaban

166
Q

Which Factor Xa inhibitor is subq

A

Fondaparinux

167
Q

Direct Thrombin inhibitor MoA

A

◦ Bind directly to thrombin; no cofactor required for
activity
◦ Inhibit clot-bound thrombin in addition to circulating
thrombin

168
Q

Direct Thrombin inhibitor used for ACS/HIT

A

Bivalirudin

169
Q

Direct Thrombin inhibitor used for HIT

A

Agatroban and Desirudin

170
Q

Direct Thrombin inhibitor used in Afib and DVT/PE

A

Dabigatran

171
Q

Monitoring direct thrombin inhibitor

A

aPTT, plateltes, bleeding, INR

172
Q

Which direct thrombin inhibitor does not have a monitoring method?

A

Dabigatran

173
Q

Direct Thrombin Inhibitor AE

A

Antibody formation
bleeding
thrombocytopenia

174
Q

Direct thrombin inhibitor reversal agents

A

Idarucixumab

Andexanet

175
Q

Thrombolytic agents use

A

Acute MI, stroke, severe PE (coding)

176
Q

Warfarin MoA

A

INhibits 7,9,10
Prevents formation and propagation of new thrombi
No effect on circulating clotting factors or formed thrombi

177
Q

Warfarin use

A

DVT/PE, AFib, heart valve replacement

178
Q

Why does warfarin have so much interactions

A

CYP450 2C9, 3A4, lots of genetic variations and interpt variablity
highly protein bound

179
Q

Does warfarin work right away?

A

No, full effect takes 5-7 days

180
Q

How to monitor warfarin?

181
Q

Warfarin dosing

A

5 mg a day (frail 2 mg)

182
Q

Warfarin AE

A

◦ Bruising
◦ Bleeding
◦ Skin necrosis
◦ Teratogenic

183
Q

Reversal of warfarin first line

184
Q

Reversal of warfarin in urgent cases

185
Q

Risk with Kcentra

186
Q

Vitamin K adverse effects

A

could cause hypersensitivity with IV

187
Q

Drug of choice for patients with Afib and heart failure

A

Amiodarone

188
Q

Amiodarone MoA

A

◦ Blocks sodium, potassium, and calcium channels ◦ Antiadrenergic properties

189
Q

Downsides of Amiodarone

A

lots of drug interactions (potent inhibitor)
super long half life
many adverse effects

190
Q

Amiodarone AE

A 
thyroid issues
brain 
eye
liver
rash, photosensitivity
lungs
brady/hypo
191
Q

SHould class 3 antiarrythmics be used in patients with HF?

A

no, could be toxic

192
Q

Adenosine use

A

supraventicular or sinus tachy

193
Q

Don’t use adenosine

A

with other types of tachy

194
Q

Adenosine AE

A

Cardiac → bradycardia and cardiac arrest

◦ Non-cardiac → flushing, bronchospasm, headache

195
Q

Class 3 antiarrytmic contraindication

A

QT prolonged or lowe creatinine clearance

196
Q

Can pt initiate class 3 antiarrythmic at home?

197
Q

HMG COA reductase inhibitors MoA

A

Inhibits enzyme responsible for converting HMG- CoA to mevalonate (rate-limiting step in production of cholesterol)

198
Q

Added benefit of HMG COA meds?

A

significantly reduces rates of death and

recurrent MI in patients with CAD

199
Q

Statins AE

A

Myopathy – muscle aches, pains, rhabdomyolysis
Increased liver enzymes, fulminant hepatic failure
New onset diabetes (high intensity)

200
Q

Statins contraindications

A

Severe active liver disease

Pregnancy

201
Q

Increased risk of myopathy/ rhabdomyolysis when this is coadministered with statins

A

fibrates and niacin > 1 g/day

202
Q

Niacinn MoA

A

Inhibits mobilization of free fatty acids from
peripheral adipose tissue to the liver

203
Q

Niacin AE

A 
Hyperglycemia/glucose intolerance
Hyperuricemia
GI distress
Hepatic issues
flushing
204
Q

Fibrates MoA

A

Reduces rate of lipogenesis in the liver

205
Q

Fibrates AE

A

Dyspepsia
Gallstones
Myopathy
Increased hepatic transaminases

206
Q

Fibrates contraindications

A

Severe renal or hepatic disease

207
Q

Cholesterol Absorption inhibitors MoA

A

inhibits cholesterol absorption by small intestine

208
Q

Cholesterol Absorption inhibitors contraindications

A

active liver disease

209
Q

Omega-3 fatty acids MoA

A

reduce TG synthesis

210
Q

PCSK9 inhibitors MoA

A

prevents degradation of LDLR so that can clear blood of LDL

211
Q

How much can PCSK9 inhibitors reduce LDL?

212
Q

PCSK9 route

A

sub q injection

213
Q

PCSK9 benefit

A

prevention or reduction in CV events in patietns with ASCVD

214
Q

Loop Diuretic Agents

A

Furosemide
Bumetanide
Torsemide
Ehacrynic acid

215
Q

potassium sparing diuretics

A

spironolactone

triamlerene

216
Q

non DHP calcium channel blockers

A

verapamil and diltiazem

Advanced Pharmacology (8 decks)

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