Adv Pharm Test 3 Study Questions Flashcards
(216 cards)
1
Q
Which H2 receptor agonist is least potent?
A
Cimetidine
2
Q
Which H2 RA causes confusion in elderly?
A
Ranitidine (Zantac)
3
Q
Which H2 RA is most potent?
A
Famotidine (Pepcid)
4
Q
Best H2 RA for elderly
A
Famotidine (Pepcid)
5
Q
Adverse effects unique to cimetidine
A
gynecomastia, impotence, galactorrhea
6
Q
Which H2 RA is a CYP450 inhibitor?
A
Cimetidine
7
Q
How long can pts use PPIs?
A
3-6 months; longer requires careful monitoring
8
Q
PPI adverse effects
A
vitamin b deficiency
Hip fractures
Risk for infection
gastric tumors
9
Q
How long does it take for PPI to work?
A
3-4 days
10
Q
PPI MoA
A
binds to H+/K+ ATPase pump and irreversibly inactivates enzyme
11
Q
Are PPIs prodrugs?
A
yes
12
Q
When to take PPI?
A
30-60 minutes before food
13
Q
Bulk forming meds MoA
A
absorbs water and forms bulky compound that distends colon and stimulates peristalsis
14
Q
Bulk meds AE
A
Abdominal pain, bloating, flatulence
15
Q
Bulk meds drug interactions
A
absorb drugs take 2 hours before or after
16
Q
Surfactant dosing
A
once to twice a day
17
Q
Surfactant full onset
A
1-3 days
18
Q
Sufactants combined w/?
A
stimulants
19
Q
Stimulants used often used with which pts?
A
those on chronic opiod therapy
20
Q
Stimulant dosing
A
once daily
21
Q
Stimulant full onset
A
6-12 hours
22
Q
Stimulant used in combo with?
A
docusate
23
Q
Stimulant AE
A
Griping, cathartic colon (years of use)
24
Q
Which drug classes are used for motion sickness?
A
Histamine 1 antagonists, antimuscarniic and promethazine
25
Ondasteron indication
postoperative and chemotherapy-induced N/V
26
Ondasteron MOA
Blocks 5-HT3 receptor in CNS, chemoreceptor trigger zone, and GI tract
27
Ondasteron AE
Headache, QTc prolongation
28
Which Histamine1 antagonists treats vertigo?
Meclizine (Dramamine)
29
Side effects of motion sickness drugs?
drowsiness, xerostomia
30
What population to avoid with phenergan?
children under 2 (resp dep)
31
Phenergan routes of admin
oral, IV, suppository
32
Phenergan indications
motion sickness and drug induced NV
33
Phenergan MoA
Anticholinergic properties within the chemoreceptor trigger zone
34
Scopalamine route
transdermal patch
35
Phenergan dosing
Short acting, dosed 3 to 4 times a day
36
Glucocorticoid steroid MoA
inhibiting production of inflammatory cytokines and chemokines
37
What IBD med is used for remission?
Methotrexate
38
Which glucocorticoid acts locally on GI tract and has less side effects?
Budesonide
39
Glucocorticoid indication
During active stage of disease
40
Which glucorticoid is most commonly used to induce remission?
Prednisone
41
Hydrocortisone routes
Tablet, injection, suppositories, foam, enema
42
Glucocorticoid AE
Immunodeficiency – Hyperglycemia
– Adrenal insufficiency – Excitatory effects (insomnia)
– Increased appetite / weight gain
43
Methotrexate MoA
Suppresses immune system
44
Can methotrexate be taken during pregnancy?
No
45
What supplement should you take with methotrexate?
Folate
46
How often is methotrexate administered?
Once a week
47
Carbonic Anhydrase Inhibitor indications
– Glaucoma
– Urinary alkalinization
– Metabolic alkalosis
– Acute mountain sickness
48
Which class of diuretics is not useful for HTN or dieresis?
Carbonic Anhydrase inhibitors
49
What are loop diuretics most effective for?
Fluid elimination, not HTN
50
Loops routes
Oral and IV
51
Loops MoA
– 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
52
What is the most notable AE of loops?
Hypokalemia
53
What AE is unique to loops
Hypocalcemia
54
Loops AE
– Hypotension
– Hyponatremia
– Hypochloremia
– Hypokalemia
– Hypomagnesemia – Hypocalcemia – Ototoxicity
– Azotemia = renal injury
55
Which diuretics have ceiling effect?
Loops
56
How are loops excreted?
Renally
57
Should we give more or less loops to kidney patients?
More
58
Which loop has lowest oral bioavailbility?
Furosemide
59
Thiazides MoA
– Inhibits sodium reabsorption in the distal tubule – Promotes up to 5% sodium and water excretion – Increase urinary excretion of other electrolytes
60
When is the effectiveness of thiazides diminished?
When CrCl falls below 30 mL/min
61
1st line diuretic for HTN
Thiazides
62
How long for max effect on blood pressure with thiazides?
2-4 weeks
63
Thiazides AE
– Hypotension – Hyponatremia – Hypokalemia – Hypomagnesemia – Hypercalcemia
– Increased uric acid
– Increased plasma glucose levels – Azotemia
64
Are thiazides used extensively for edema?
No
65
how do loops and thiazides work together?
blocks Na+ reabsorption in distal nephron segments
66
Potassium-Sparing Diuretics MoA
– Acts at collecting duct to inhibit sodium reabsorption
– Promotes up to 2% sodium and water excretion
– Blocks effects of aldosterone in kidney
67
Potassium-Sparing Diuretics AE
– Hypotension
– Nausea and vomiting, constipation, diarrhea – Hypercalcemia
– Hyperkalemia
– Gynecomastia (spironolactone)
68
Beta blockers MoA
– 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
69
Beta Blockers AE
o Hypotension
o Bronchospasm – relates to β1 selectivity!!
o Bradycardia
o Fatigue, exercise intolerance
o Depression, confusion, agitation, psychosis
70
Beta blockers indication
```
Hypertension
– Angina pectoris
– Myocardial infarction
– Heart failure
– Ventricular arrhythmia – Migraine prophylaxis – Hyperthyroidism
– Glaucoma
```
71
Which beta blockers have beta selectivity?
Atenolol, metprolol
72
Which beta blockers have alpha blockade?
carvedilol
73
What does alpha blockade acheive?
decreased sympahtetic stim causing vasodilation
74
Decreased beta selectivity can affect which organ?
lungs
75
ACEI MoA
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
76
ACEI indications
HTN
– Heart failure
– Left ventricular dysfunction – Diabetic nephropathy
– Acute myocardial infarction – Chronic kidney disease
77
How are most common ACEIs eliminated?
renally
78
ACEI AE
– Hypotension
– Hyperkalemia
– Acute renal failure – Cough
– Angioedema
79
ACEI interactions
Potassium supplements or potassium sparing
| diuretics
80
ACEI contraindications
– Pregnancy, aortic stenosis, renal artery stenosis
81
ARB MoA
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
82
ARB AE
– Hypotension
– Hyperkalemia
– Acute renal failure
– Angioedema (very rare)
83
ARB drug interactions
Potassium supplements or potassium sparing
| diuretics
84
ARB contraindications
Pregnancy, aortic stenosis, renal artery stenosis
85
Do ACE and ARB affect cardiac outpout and blood volume?
no
86
Calcium channel blocker MOA
– Blocking calcium entry into smooth muscle – Results in vasodilation
– Can also affect cardiac conduction
87
Difference b/x DHP and non DHP CCBs
Non DHP lower cardiac output; not used for HTN
88
Non-DHP CCBs
verapamil and diltiazem
89
Which DHP CCB is also given IV
Nicardipine
90
CCB indications
HTN
– Angina pectoris
– Peripheral vascular disease
– Migraine prophylaxis (non-DHP) – Arrhythmia (non-DHP)
91
CCB AE
– Relative to DHP
Hypotension Headache and flushing Peripheral edema
– Relative to non-DHP Bradycardia
Hypotension Constipation (verapamil)
92
a1 receptor agonists MoA
– Decrease sympathetic stimulation causing vasodilation and thus reducing blood pressure
93
a1 receptor agonists AE
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
a2 receptor agonists MoA
2 Receptor Agonists Mechanism of action
| – Decrease sympathetic stimulation to cause vasodilation and thus reduce blood pressure
95
Which a2 receptor is avail as oral, IV and patch?
clonidine
96
a2 receptor agonists AE
– Sedation and headache
– Abrupt discontinuation may result in rebound
hypertension
Used as a last-line agent in the treatment of hypertension
97
direct vasodilators MoA
– Causes artery relaxation (vasodilation) resulting in decreased blood pressure
98
direct vasodilators adherence issue
TID very poor adherence
99
direct vasodilators AE
– Hydralazine → Tachycardia and fluid retention – Minoxidil → hirsutism
100
direct vasodilators indications
severe HTN
101
HTN med choices for patients with DM--hyperalbuminuria
ACEI or ARBs
102
HTN med choices for patients with CKD
ACEI or ARBs (if ACEI isn't tolerated)
103
Sodium Nitroprusside MoA
Converts to nitric oxide (NO)
Decreases preload (venodilation) and afterload (arterial dilation) to a similar degree
Reduces cardiac output and increases heart rate
104
How is sodium nitroprusside administered?
continuous infusion (half life < 10 minutes)
105
Sodium Nitroprusside AE
generates cyanide
| tachycardia
106
When is there a risk of toxicity with sodium nitroprusside?
- with doses > 2 micrograms/kg/min
- prolong admin
- renal or hepatic insufficiency
107
Sodium nitroprusside is NOT indicated for
ACS
Aortic dissection
increased ICP
108
Nitroglycerin MoA
relxes venous smooth muscle (combine with sulf groups that mimic NO)
109
Which is more potent for lowering BP: sodium ntiroprusside or nitroglycerin?
sodium nitroprusside
110
Which vasodilator is used for acute heart failure or ACS?
nitroglycerin
111
How is nitrogrlycerin administered?
continuous IV; half likfe 2-3 mintues
112
Disadvantages of nitroglycerin
tachyphylaxis; you need a nitrate free interval
113
Nitroglycerin AE
– Hypotension
– Headache
– Reflex tachycardia
114
Nitroglycerin interactions
– Phosphodiesterase-5 inhibitors (i.e. sildenafil)
115
What IV CCB is used for HTN emergency?
Nicardipine
116
How is nicardipine administered?
1-15 mg/hr continuous
117
Unique issue with nicardipine
tri-phasic elimination; watch for accumulation
118
Loop diuretics short term benefit
Decreased jugular venous distension, pulmonary congestion, and peripheral edema
119
Loop diuretics intermediate benefits
Decreased daily symptoms, improved cardiac function increased exercise tolerance
120
Do loop diuretics affect mortality rates?
no
121
What cocktail is recommended for HFrEF
ACEI/ARB/ARNI + beta blocker + aldosterone antagonist
122
How long to space out ARNI and ACEI?
36 hours
123
What to monitor on ACEI/ARB/ARNI?
renal function
potassium
Hypotension
124
beta blockers for HF
carvedilol
metoprolol
Bisoprolol
125
Which GI drug class has a FDA warning about its use with clopidogrel? Why?
PPI’s inhibit the metabolism of clopidogrel, which is a prodrug, and can lead to decreased efficacy.
126
aldosterone blockade meds
spironolactone and eplerenone
127
benefits of digoxin
improved symptoms and
exercise tolerance, decreased hospitalizations
128
Digoxin place in therapy
in patients with symptomatic LV dysfunction despite optimal ACE inhibitor (or ARB), β-blocker, spironolactone (if appropriate), and diuretic therapy
and some arrythmias
129
Digoxin MoA
◦ 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
Is Digoxin dialyzable?
no
131
Does digoxin have a long half life?
yes
132
Digoxin AE
◦ Nausea, vomiting, diarrhea, abdominal pain ◦ Headache, visual disturbances (green/yellow
“halos”)
◦ Cardiac arrhythmias
133
What's used to treat digoxin toxicity?
Digibind
134
Digoxin drug interactions
amiodarone, antacids, verapamil
135
What's an alternative in HF patients unable to take an ACEIs or ARBs because of severe renal insufficiency, hyperkalemia,or angioedema
Hydralazine–isosorbide dinitrate
136
Ivrabradine MoA
◦ Inhibits the “funny” current to slow HR
137
Ivrabradine AE
bradycardia and visual disturbances
138
When is ivrabradine used?
in pts with elevated HR
139
Does ivrabradine reduce mortality?
no
140
Does ivrabradine reduce hospitalizations?
yes
141
which HF meds don't reduce mortality?
loops, ivrabradine
142
HFpEF treatment
reduce tachy and BP
143
Leading dose for asprin in pts with ACS?
324-325 mg
144
Which ADP-receptor antagonist is taken 2x/day?
ticagrelor
145
ADP-receptor antagonist prodrugs
clopidogrel and prasugrel
146
Is Ticagrelor a prodrug?
no
147
Which of the ADP-Receptor Antagonists is not to be used in patients with history of stroke or TIA?
prasugrel
148
Which ADP-RA is more effective in diabetic and STEMI pts?
prasugrel
149
What is the IV form of clopidogrel?
Cangrelor
150
Cangrelor metabolism
quick onset and offset
151
Glycoprotein inhibitors AE
Low platelet count (thrombocytopenia)
| Bleeding
152
What are the 3 main indications for unfractionated heparin?
Prophylaxis of DVT/PE
Treatment of DVT/PE
Treatment of ACS or Afib
153
UH dosing for DVT/PE prophylaxis
5,000 units subq 2-3/day
154
UH dosing for treatment of DVT/PE
IV bolus of 80 units/kg followed by continuous IV infusion (18 units/kg/hour)
155
UH dosing for treatment of ACS or AFib
IV bolus of 60 units/kg max 4,000) followed by continousinfusion 12 units/kg/hour max 1000)
156
How to monitor unfractionated heparin?
- aPTT: 1.5 -2.5s x control (60-80s)
- Factor Xa levels (0.3-0.7 units/mL)
- Signs of bleeding
- Platelet count
157
unfractionated heparin AE
bleeding, osteoporosis, thrombocytopenia
158
What agent reverses UH?
protamine
159
Protamine AE
Hypotension, brady, anaphylaxis
160
Unfractionated heparin MoA
◦ 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
LMW heparin MoA
◦ 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
UH vs. LMWH
LMWH is nearly 100% predictable, long half-life, less HIT, doesn't require monitoring, but protamine is less effective
163
Factor Xa inhibitors used for DVT/PE/ACS
Fondaparinux
164
Factor Xa inhibitors used for DVT/PE/ and Afib
Rivaraxaban
Apixiban
edoxaban
165
Factor Xa inhibitors used for DVT prophy only
Betrixaban
166
Which Factor Xa inhibitor is subq
Fondaparinux
167
Direct Thrombin inhibitor MoA
◦ Bind directly to thrombin; no cofactor required for
activity
◦ Inhibit clot-bound thrombin in addition to circulating
thrombin
168
Direct Thrombin inhibitor used for ACS/HIT
Bivalirudin
169
Direct Thrombin inhibitor used for HIT
Agatroban and Desirudin
170
Direct Thrombin inhibitor used in Afib and DVT/PE
Dabigatran
171
Monitoring direct thrombin inhibitor
aPTT, plateltes, bleeding, INR
172
Which direct thrombin inhibitor does not have a monitoring method?
Dabigatran
173
Direct Thrombin Inhibitor AE
Antibody formation
bleeding
thrombocytopenia
174
Direct thrombin inhibitor reversal agents
Idarucixumab
| Andexanet
175
Thrombolytic agents use
Acute MI, stroke, severe PE (coding)
176
Warfarin MoA
INhibits 7,9,10
Prevents formation and propagation of new thrombi
No effect on circulating clotting factors or formed thrombi
177
Warfarin use
DVT/PE, AFib, heart valve replacement
178
Why does warfarin have so much interactions
CYP450 2C9, 3A4, lots of genetic variations and interpt variablity
highly protein bound
179
Does warfarin work right away?
No, full effect takes 5-7 days
180
How to monitor warfarin?
INR
181
Warfarin dosing
5 mg a day (frail 2 mg)
182
Warfarin AE
◦ Bruising
◦ Bleeding
◦ Skin necrosis
◦ Teratogenic
183
Reversal of warfarin first line
Vitamin K
184
Reversal of warfarin in urgent cases
Kcentra
185
Risk with Kcentra
clot
186
Vitamin K adverse effects
could cause hypersensitivity with IV
187
Drug of choice for patients with Afib and heart failure
Amiodarone
188
Amiodarone MoA
◦ Blocks sodium, potassium, and calcium channels ◦ Antiadrenergic properties
189
Downsides of Amiodarone
lots of drug interactions (potent inhibitor)
super long half life
many adverse effects
190
Amiodarone AE
```
thyroid issues
brain
eye
liver
rash, photosensitivity
lungs
brady/hypo
```
191
SHould class 3 antiarrythmics be used in patients with HF?
no, could be toxic
192
Adenosine use
supraventicular or sinus tachy
193
Don't use adenosine
with other types of tachy
194
Adenosine AE
Cardiac → bradycardia and cardiac arrest
| ◦ Non-cardiac → flushing, bronchospasm, headache
195
Class 3 antiarrytmic contraindication
QT prolonged or lowe creatinine clearance
196
Can pt initiate class 3 antiarrythmic at home?
no
197
HMG COA reductase inhibitors MoA
Inhibits enzyme responsible for converting HMG- CoA to mevalonate (rate-limiting step in production of cholesterol)
198
Added benefit of HMG COA meds?
significantly reduces rates of death and
| recurrent MI in patients with CAD
199
Statins AE
Myopathy – muscle aches, pains, rhabdomyolysis
Increased liver enzymes, fulminant hepatic failure
New onset diabetes (high intensity)
200
Statins contraindications
Severe active liver disease
| Pregnancy
201
Increased risk of myopathy/ rhabdomyolysis when this is coadministered with statins
fibrates and niacin > 1 g/day
202
Niacinn MoA
Inhibits mobilization of free fatty acids from
peripheral adipose tissue to the liver
203
Niacin AE
```
Hyperglycemia/glucose intolerance
Hyperuricemia
GI distress
Hepatic issues
flushing
```
204
Fibrates MoA
Reduces rate of lipogenesis in the liver
205
Fibrates AE
Dyspepsia
Gallstones
Myopathy
Increased hepatic transaminases
206
Fibrates contraindications
Severe renal or hepatic disease
207
Cholesterol Absorption inhibitors MoA
inhibits cholesterol absorption by small intestine
208
Cholesterol Absorption inhibitors contraindications
active liver disease
209
Omega-3 fatty acids MoA
reduce TG synthesis
210
PCSK9 inhibitors MoA
prevents degradation of LDLR so that can clear blood of LDL
211
How much can PCSK9 inhibitors reduce LDL?
up to 60%
212
PCSK9 route
sub q injection
213
PCSK9 benefit
prevention or reduction in CV events in patietns with ASCVD
214
Loop Diuretic Agents
Furosemide
Bumetanide
Torsemide
Ehacrynic acid
215
potassium sparing diuretics
spironolactone
| triamlerene
216
non DHP calcium channel blockers
verapamil and diltiazem
