Pharmacology Flashcards
(424 cards)
1
Q
Thiazide diuretics, ACE inhibitors, angiotensin
II receptor blockers (ARBs), dihydropyridine
Ca2+ channel blockers are all what type of treatment?
A
Primary (essential)
hypertension treatment.
2
Q
- Diuretics, ACE inhibitors/ARBs, β-blockers for compensated HF, aldosterone antagonists may be used in the treatment of what?
- β-blockers must be used cautiously in
decompensated HF and are contraindicated in
cardiogenic shock in the treatment of what? - In HF, ARBs may be combined with the
neprilysin inhibitor sacubitril, in the treatment of what?
A
Hypertension with
heart failure
3
Q
- ACE inhibitors/ARBs, Ca2+ channel blockers,
thiazide diuretics, β-blockers are used in the treatment of what? - ACE inhibitors/ARBs are protective against
diabetic nephropathy in the treatment of what?
A
Hypertension with
diabetes mellitus
4
Q
- ARBs, Ca2+ channel blockers, thiazide diuretics,
selective β-blockers are used in the treatment of what? - Avoid nonselective β-blockers to prevent
β2-receptor–induced bronchoconstriction in what treatment? - Avoid ACE inhibitors to prevent confusion
between drug or asthma-related cough in what treatment?
A
Hypertension in
asthma
5
Q
Hydralazine, labetalol, methyldopa, nifedipine are used in what treatment?
(He Likes My Neonate)
A
Hypertension in
pregnancy
6
Q
Amlodipine, clevidipine, nicardipine, nifedipine, nimodipine (dihydropyridines, act on vascular
smooth muscle); diltiazem, verapamil (non-dihydropyridines, act on heart) are all types of ____?
A
Calcium channel blockers
7
Q
- Block voltage-dependent L-type calcium channels of cardiac and smooth muscle leading to decrease in muscle contractility is an MoA for what type of drug?
- Vascular smooth muscle—amlodipine = nifedipine > diltiazem > verapamil.
Heart—verapamil > diltiazem > amlodipine = nifedipine (verapamil = ventricle) is an MoA for what type of drug?
A
Calcium channel blockers
8
Q
Increase in cGMP leading to smooth muscle relaxation. Vasodilates arterioles > veins; afterload reduction is an MoA for which type of drug?
A
Hydralazine
9
Q
For what circumstances do you Treat with clevidipine, fenoldopam, labetalol, nicardipine, or nitroprusside?
A
Hypertensive
emergency
10
Q
- What drug is Short acting; increases cGMP via direct release of NO?
- Can cause cyanide toxicity (releases cyanide)?
A
Nitroprusside
11
Q
What drug is Dopamine D1 receptor agonist—coronary, peripheral, renal, and splanchnic vasodilation. DECREASES BP,
and INCREASES
natriuresis?
2. Also used postoperatively as an antihypertensive.
3. Can cause hypotension and tachycardia.
A
Fenoldopam
12
Q
Nitroglycerin, isosorbide dinitrate, isosorbide mononitrate are what type of drugs?
A
Nitrates
13
Q
Vasodilate by INCREASING NO in vascular smooth muscle LEADING TO INCREASE in cGMP and smooth muscle relaxation.
Dilate veins»_space; arteries. DECREASES preload, are MoAs of ___?
A
Nitrates
14
Q
What treatment has the Goal of reduction of myocardial O2 consumption (MVO2) by DECREASING 1 or more of the determinants of
MVO2: end-diastolic volume, BP, HR, contractility.
A
Antianginal therapy
15
Q
What effects do nitrates and β-BLOCKERS have on End-diastolic volume?
A
- Decreases nitrates
- No effect or increases β-BLOCKERS
- No effect or increases both.
16
Q
What effects do nitrates and β-BLOCKERS have on blood pressure?
A
- Decreases nitrates
- Decreases β-BLOCKERS
17
Q
What effects do nitrates and β-BLOCKERS have on Contractility?
A
- No effect on nitrates
- Decreases β-BLOCKERS
- Little/No effect on both
18
Q
What effects do Nitrates and β-BLOCKERS have on Heart Rate?
A
- Increases nitrates (reflex response)
- Decreases β-BLOCKERS
- No effect/ Decreases both
19
Q
What effects do Nitrates and β-BLOCKERS have on Ejection Time?
A
- Decreases Nitrates
- Increases β-BLOCKERS
- Little/No effect on both
20
Q
what effects do Nitrates and β-BLOCKERS have on MVO2?
A
- Decreases nitrates
- Decreases β-BLOCKERS
21
Q
Verapamil use effects is similar to what other class of drugs?
A
β-BLOCKERS
22
Q
Pindolol and acebutolol are partial β-agonists that should be used with caution with which kind of patients?
A
Patients with Angina
23
Q
The Inhibition of the late phase of sodium current thereby reducing diastolic wall tension and oxygen
consumption.
2. Does not affect heart rate or contractility, are the MoA of what kind of drugs?
A
Ranolazine
24
Q
Selective PDE-3 inhibitor. In cardiomyocytes: INCREASING cAMP accumulation LEADING TO INCREASE IN Ca2+ infux LEADING TO INCREASE IN inotropy and chronotropy. In vascular smooth muscle: INCREASE IN cAMP accumulation LEADING TO inhibition of MLCK activity LEADING TO general vasodilation, are all MoAs of which kind of drug?
A
Milrinone
25
1.Lovastatin,
2. Pravastatin have what kind of effects on LDL, HDL, and Triglycerides?
1. Decreases LDL (x3)
2. Increases HDL
3. Decreases Triglycerides
26
Which drug's MoA
1. Inhibits conversion of HMG-CoA to mevalonate, a
cholesterol precursor;
2. DECREASE
mortality in CAD patients?
HMG-CoA reductase
inhibitors
(eg, lovastatin,
pravastatin)
27
Which Lipid Lowering Agents inhibits HMG-CoA reductase?
Lovastatin ,Pravastatin
28
Which Lipid Lowering Agents are Bile Acid Resins?
Cholestyramine,
Colestipol,
Colesevelam
29
Which Lipid Lowering Agent's MoA prevents cholesterol absorption
at small intestine brush
border?
Ezetimibe
30
Which Lipid Lowering Agents are Fibrates?
Gemfbrozil,
Bezafbrate,
Fenofbrate
31
Which Lipid Lowering Agent's MoA Inhibits lipolysis (hormonesensitive lipase) in adipose
tissue; reduces hepatic VLDL
synthesis?
Niacin (vitamin B3)
32
Which Lipid Lowering Agents are PCSK9 inhibitors?
Alirocumab,
Evolocumab
33
What effects do 1.Cholestyramine,
2.Colestipol,
3.Colesevelam have on LDL, HDL and TRI?
1. Decreases LDL (x2)
2. Slightly increases HDL
3. Slightly increases Triglycerides.
34
What effect does Ezetimibe have on LDL, HDL and TRI?
1. Decreases LDL (x2)
2. Increases/ Has no effect on HDL
3. Decreases/ Has no effect on TRI
35
What effect does
1. Gemfbrozil,
2. Bezafbrate,
3. Fenofbrate
have on LDL, HDL and TRI?
1. Decreases LDL
2. Increases HDL
3. Decreases TRI (x3)
36
What effect does Niacin (vitamin B3) have on LDL, HDL and TRI?
1. Decreases LDL (x2)
2. Increases HDL (x2)
3. Decreases TRI
37
What effect does
1. Alirocumab,
2.Evolocumab
have on LDL, HDL and TRI?
1. Decreases LDL (x3)
2. Increases HDL
3. Decreases TRI
38
Which Lipid Lowering Agent's MoA
1. Upregulate LPL LEADING TO INCREASE in TG
clearance?
2. Activates PPAR-α to induce
HDL synthesis?
1. Gemfbrozil,
2. Bezafbrate,
3. Fenofbrate
(FIBRATES)
39
Which Lipid Lowering Agent's MoA
1. Inhibits lipolysis (hormonesensitive lipase) in adipose
tissue;
2. Reduces hepatic VLDL
synthesis?
Niacin (vitamin B3)
40
Which Lipid Lowering Agent's MoA leads to
1. Inactivation of LDL-receptor
degradation,
2. Increasing
amount of LDL removed
from bloodstream?
1. Alirocumab,
2.Evolocumab
(PCSK9 inhibitors)
41
Digoxin is what type of drug?
Cardiac glycosides
42
Which drug's MoA
1. Directs inhibition of Na+/K+ ATPase
which LEADS TO
indirect inhibition of Na+/Ca2+ exchanger.
2. INCREASES
[Ca2+]I LEADING TO positive inotropy.
3. Stimulates vagus
nerve LEADING TO DECREASE in HR?
Dioxigin.
43
Which class of drugs
1. Slows or blocks (DECREASE) conduction (especially in depolarized cells).
2. DECREASE slope of phase 0 depolarization.
3. Are
state dependent (selectively depress tissue that is frequently depolarized [eg, tachycardia]).
Antiarrhythmics—
sodium channel
blockers (class I)
44
Quinidine, Procainamide, Disopyramide are all a part of what class of drugs?
“The Queen Proclaims Diso’s pyramid.”
Class IA
45
Which drug's MoA
1. INCREASES AP duration,
2. INCREASES effective refractory period
(ERP) in ventricular action potential,
3. INCREASES QT
interval, some potassium channel blocking
effects.
1. Quinidine,
2. Procainamide,
3. Disopyramide
46
Lidocaine, MexileTine are all part of which class of drugs?
(“I’d Buy Liddy’s Mexican Tacos.”)
Class IB
47
Which drug's MOA
1. DECREASES AP duration. 2. Preferentially affect ischemic or
depolarized Purkinje and ventricular tissue.
3. Phenytoin can also fall into the IB category.
1. Lidocaine
2. MexileTine.
48
Flecainide, Propafenone are which class of drugs?
(“Can I have Fries, Please.”)
Class IC
49
Which drug's MOA
1. Signifcantly prolongs ERP in AV node and
accessory bypass tracts.
2. HAS No effect on ERP in
Purkinje and ventricular tissue.
3. HAS Minimal effect on AP duration.
1. Flecainide
2. Propafenone.
50
1. Metoprolol,
2. Propranolol,
3. Esmolol,
3. Atenolol,
4. Timolol,
5. Carvedilol are which kind of drugs?
Antiarrhythmics—
β-blockers (class II)
51
Which drug's MOA
1. Decreases SA and AV nodal activity by *DECREASING cAMP,
* DECREASING Ca2+ currents.
2. Suppress abnormal pacemakers by
DECREASING
slope of phase 4.
3. AV node particularly sensitive—INCREASE PR interval.
4. Esmolol very short acting.
Metoprolol,
2. Propranolol, e
3. Esmolol, a
4. Atenolol, timolol, carvedilol.
52
1.Amiodarone,
2.Ibutilide,
3.Dofetilide,
4.Sotalol are what class of drugs? (AIDS)
Antiarrhythmics—
potassium channel
blockers (class III)
53
Which drugs' MOA
1. INCREASES AP duration,
2. INCREASES ERP, and 3.INCREASES QT interval?
1.Amiodarone,
2.Ibutilide,
3.Dofetilide,
4.Sotalo
54
1. Verapamil,
2. Diltiazem are which class of drugs?
Antiarrhythmics—
calcium channel
blockers (class IV)
55
Which drugs MOA 1.DECREASES conduction velocity,
2.INCREASES ERP,
3.INCREASES PR interval?
1. Verapamil,
2. Diltiazem.
56
Which drug INCREASES K+ out of cells, LEADING TO hyperpolarizing the cell and REDUCING ICa, decreasing AV node conduction.
2. Drug of choice in diagnosing/terminating certain forms of SVT. Very short acting (~ 15 sec). 3.Effects blunted by theophylline and caffeine (both are adenosine receptor antagonists). 4.Adverse effects
include fushing, hypotension, chest pain, sense of impending doom, bronchospasm.
Adenosine
57
Which drug is Effective in torsades de pointes and digoxin toxicity?
Mg2+
58
Which drug's MOA is 1.Selective inhibition of funny sodium channels (If
), prolonging slow depolarization phase (phase 4).
2.REDUCTION of
SA node fring; negative chronotropic effect without inotropy.
3. Reduces cardiac O2 requirement.
Ivabradine
59
What treatment should be given to patients with Diabetes Mellitus?
They should receive education on diet, exercise, blood glucose
monitoring, and complication management. (Treatment differs based on the type of diabetes)
60
Treatment for Type 1 DM?
Insulin replacement
61
Treatment for Type 2 DM?
Oral agents (metformin is frst line), non-insulin injectables, insulin replacement;
weight loss particularly helpful in lowering blood glucose.
62
Treatment for Gestational DM?
Insulin replacement if nutrition therapy and exercise alone fail
Regular (short-acting) insulin is preferred for DKA (IV), hyperkalemia (+ glucose), stress
hyperglycemia.
63
Bind insulin receptor (tyrosine kinase activity).
1. Liver: INCREASES glucose stored as glycogen.
2. Muscle: INCREASES glycogen, protein synthesis.
3. Fat: INCREASES TG storage.
4. Cell membrane: INCREASES K+ uptake.
All of these are MOAs of which class of drugs?
Insulin preparations
Rapid acting (1-hr
peak): Lispro, Aspart,
Glulisine (no LAG)
Short acting (2–3 hr
peak): regular
Intermediate acting
(4–10 hr peak): NPH
Long acting (no real
peak): detemir,
glargine.
64
1. DECREASE in
glucagon release,
2. DECREASE in gastric emptying,
3. INCREASE in satiety are all MOAs of which kind of drugs?
Amylin analogs
Pramlintide
65
1. DECREASE in glucagon release,
2. DECREASE in gastric emptying,
3. INCREASE in
glucose-dependent insulin release,
4. INCREASE in satiety, are all MOAs of which kind of drugs?
GLP-1 analogs
Exenatide, liraglutide
66
1. Inhibit hepatic gluconeogenesis and the action
of glucagon, by inhibiting mGPD.
2. INCREASE in glycolysis, peripheral glucose uptake (INCREASE in insulin sensitivity), are all MOAs of which kind of drugs?
Biguanides
Metformin
67
Close K+ channel in pancreatic β cell
membrane LEADING TO cell depolarizes LEADING TO insulin release via INCREASE IN Ca2+ influx, is the MOA of which kind of drug?
1st generation:
1. Chlorpropamide,
2. Tolbutamide
2nd generation:
1. Glimepiride,
2. Glipizide,
3. Glyburide
68
Close K+ channel in pancreatic β cell
membrane LEADS TO cell depolarizes LEADS TO insulin
release via INCREASE IN Ca2+ influx (binding site differs
from sulfonylureas) is the MOA of which kind of drug?
1.Nateglinide,
2. Repaglinide
69
Which drug's MOA
1. Inhibits DPP-4 enzyme that deactivates GLP-1.
2. DECREASESglucagon release, gastric emptying.
3. INCREASES glucose-dependent insulin release, satiety?
1. Linagliptin,
2. Saxagliptin,
3. Sitagliptin
70
Which drug's MOA Blocks reabsorption of glucose in proximal
convoluted tubule.
1. Canaglifozin,
2. Dapaglifozin,
3. Empaglifozin
70
Which drug's MOA
1. Binds to PPAR-γ nuclear transcription
regulator which
2.LEADS TO INCREASE IN insulin sensitivity and levels
of adiponectin pregulation of glucose
metabolism and fatty acid storage?
1. Pioglitazone,
2. Rosiglitazone
70
Propylthiouracil and methimazole are what drugs?
Thioamides
71
Which drug's MOA
1. Inhibits intestinal brush-border α-glucosidases which
2. LEADS TO delayed carbohydrate hydrolysis and glucose
absorption which
3. LEADS TO DECREASE in postprandial hyperglycemia?
1. Acarbose,
2. Miglitol
72
Which drug's MOA
1. Blocks thyroid peroxidase, inhibiting the oxidation of iodide and the organifcation and coupling of
iodine which
2. LEADS TO inhibition of thyroid hormone synthesis. PTU also blocks 5′-deiodinase which
3. LEADS TO DECREASE IN peripheral
conversion of T4 to T3.
1. Propylthiouracil,
2. Methimazole.
73
Thyroid hormone replacement is the MOA of which kind of drug?
1.Levothyroxine (T4), 2.Liothyronine (T3)
74
Which drug's MOA is SIADH, blocks action of ADH at V2-receptor?
ADH antagonists
(conivaptan,
tolvaptan)
75
Which drug's MOA is ADH antagonist (member of tetracycline family)?
Demeclocycline
76
Which drug's MOA is the Synthetic analog of aldosterone with little glucocorticoid effects?
Fludrocortisone
77
Which drug's MOA Sensitizes Ca2+-sensing receptor (CaSR) in parathyroid gland to circulating Ca2+ LEADING TO DECREASE IN PTH?
Cinacalcet
78
Which drug's MOA is a Nonabsorbable phosphate binder that prevents phosphate absorption from the GI tract?
Sevelamer
79
1. Cimetidine,
2. Ranitidine,
3. Famotidine,
4. Nizatidine are which drugs?
Histamine-2 blockers
80
Which drug's MOA is a Reversible block of histamine H2-receptors which LEADS TO DECREASE in H+ secretion by parietal cells.
1. Cimetidine,
2. Ranitidine,
3. Famotidine,
4. Nizatidine
81
1. Omeprazole,
2. Lansoprazole, 3.Esomeprazole, 4.Pantoprazole, 4.Dexlansoprazole are which kind of drugs?
Proton Pump Inhibitors
82
Which drug's MOA Irreversibly inhibits H+/K+ ATPase in stomach parietal cells?
1. Omeprazole,
2. Lansoprazole, 3.Esomeprazole, 4.Pantoprazole, 4.Dexlansoprazole
83
Which kind of drugs
1. Can affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and
urinary pH or by delaying gastric emptying.
2. All can cause hypokalemia.
Antacids
84
Constipation and hypophosphatemia; proximal
muscle weakness, osteodystrophy, seizures can be caused by the overuse of which drug?
Aluminum hydroxide
85
Which drug's MOA
1. Binds to ulcer base, providing physical protection and allowing HCO3– secretion to reestablish
pH gradient in the mucous layer.
2. Requires acidic environment; usually not given with PPIs/H2
blockers.
Bismuth,
2. Sucralfate
86
Which drug's MOA is
1. PGE1 analog.
2. INCREASES production and secretion of gastric mucous barrier,
3. DECREASES acid production?
Misoprostol
87
Which drug's MOA is
1. Long-acting somatostatin analog;
2.Inhibits secretion of various splanchnic vasodilatory hormones?
Octreotide
88
Which drug's MOA is a 1.Combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-infammatory).
2. Activated by colonic bacteria.
Sulfasalazine
89
Which drug's MOA IS
1. Agonist at μ-opioid receptors;
2. Slows gut motility.
3. Poor CNS penetration (low addictive potential)?
Loperamide
90
Which drug's MOA is
1. 5-HT3 antagonist;
2. DECREASES vagal stimulation.
3. Powerful central-acting antiemetic.
Ondansetron
91
Which drug's MOA is a
1. D2 receptor antagonist.
2. INCREASES resting tone, contractility, LES tone, motility, promotes gastric emptying.
3.Does not influence colon transport time?
Metoclopramide
92
Which drug's MOA Inhibits gastric and pancreatic lipase which LEADS TO DECREASE in breakdown and absorption of dietary fats?
Orlistat
93
1. Psyllium,
2.Methylcellulose are which kind of drugs?
Bulk-forming laxatives
94
1. Magnesium hydroxide,
2. Magnesium citrate,
3. Polyethylene glycol,
4. Lactulose are which kind of drugs?
Osmotic laxatives
95
What kind of drug is Senna?
Stimulant
96
Docusate is which kind of drug?
Emollients
97
Which drugs' MOA is Soluble fibers drawing water
into gut lumen, forming a
viscous liquid that promotes
peristalsis?
Psyllium, Methylcellulose
98
Which drug's MOA
1. Provides osmotic load to draw
water into GI lumen?
2. Lactulose also treats hepatic
encephalopathy: gut fora
degrade lactulose into
metabolites (lactic acid,
acetic acid) that promote
nitrogen excretion as NH4+?
1. Magnesium hydroxide,
2. Magnesium citrate,
3. Polyethylene glycol,
4. Lactulose
99
Which drug's MOA Enteric nerve stimulation
which LEADS TO
colonic contractions?
SENNA
100
Which drug's MOA Promotes incorporation of
water and fat into stool?
Docusate
101
Which drug's MOA is a 1.Substance P antagonist?2.Blocks NK1 (neurokinin-1) receptors in brain?
Aprepitant
102
Which drug's MOA Activates antithrombin, which DECREASES action of IIa (thrombin) and factor Xa. Short half-life?
Heparin
103
Bivalirudin (related to hirudin, the anticoagulant used by leeches), Argatroban, Dabigatran (only
oral agent in class) are all which kind of drugs?
Direct thrombin
inhibitors
104
Which drug's MOA Directly inhibits activity of free and clot-associated thrombin?
Bivalirudin (related to hirudin, the anticoagulant used by leeches), Argatroban, Dabigatran (only
oral agent in class).
105
Which drug's MOA Interferes with γ-carboxylation of vitamin K–
dependent clotting factors II, VII, IX, and X,
and proteins C and S. Metabolism affected
by polymorphisms in the gene for vitamin
K epoxide reductase complex (VKORC1).
In laboratory assay, has effect on EXtrinsic
pathway and INCREASES PT. Long half-life?
Warfarin
106
ApiXaban, RivaroXaban are which kind of drugs?
Direct factor Xa
inhibitors
107
Which drug's MOA Binds to and directly inhibit factor Xa?
ApiXaban, RivaroXaban
108
Alteplase (tPA),
Reteplase (rPA), Streptokinase,
Tenecteplase (TNK-tPA) are which kind of drugs?
Thrombolytics
109
Which drug's MOA Directly or indirectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin
clots. INCREASES PT, INCREASES PTT, no change in platelet count?
Alteplase (tPA),
Reteplase (rPA), Streptokinase,
Tenecteplase (TNK-tPA)
110
Clopidogrel,
Prasugrel,
Ticagrelor (reversible), Ticlopidine, are which kind of drugs?
ADP receptor inhibitors
111
Which drug's MOA Inhibits platelet aggregation by irreversibly blocking ADP (P2Y12) receptor. Prevents expression of
glycoproteins IIb/IIIa on platelet surface?
Clopidogrel,
Prasugrel,
Ticagrelor (reversible), Ticlopidine.
112
Which drugs' MOA are Phosphodiesterase inhibitors;
INCREASES cAMP in platelets, resulting in inhibition of platelet aggregation;
vasodilators?
Cilostazol, Dipyridamole
113
Abciximab, Eptifbatide, Tirofban are which kind of drugs?
Glycoprotein IIb/IIIa
Inhibitors
114
Which drug's MOA Binds to the glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation. Abciximab
is made from monoclonal antibody Fab fragments?
Abciximab,
Eptifbatide,
Tirofban
115
Which drug's MOA is Purine (thiol) analogs
LEADS TO DECREASE in
de novo purine synthesis?
Activated by HGPRT?
Azathioprine is metabolized
into 6-MP?
Azathioprine,
6-mercaptopurine
116
Which drug's MOA is a Purine analog which LEADS TO multiple
mechanisms (eg, inhibition
of DNA polymerase, DNA
strand breaks)?
Cladribine
117
Which drug's MOA is a Pyrimidine analog which LEADS TO DNA
chain termination. At higher
concentrations, inhibits DNA
polymerase?
Cytarabine
(arabinofuranosyl
cytidine)
118
Which drug's MOA is Pyrimidine analog bioactivated
to 5-FdUMP, which
covalently complexes with
thymidylate synthase and
folic acid? Capecitabine is a
prodrug with similar activity.
This complex inhibits
thymidylate synthase
which LEADS TO DECREASE in
dTMP and LEADS TO DECREASE in DNA
synthesis?
5-fuorouracil
119
Which drug's MOA is a Folic acid analog that
competitively inhibits
dihydrofolate reductase
which LEADS TO DECREASE in
dTMP which LEADS TO DECREASE in DNA
synthesis?
Methotrexate
120
Which drug's MOA Induces free radical formation
which LEADS TO breaks in DNA strands?
Bleomycin
121
Which drug's MOA Intercalates into DNA,
preventing RNA synthesis?
Dactinomycin
(actinomycin D)
122
Which drug's MOA Generates free radicals.
Intercalate in DNA which LEADS TO breaks in
DNA which LEADS TO DECREASE in replication.
Interferes with topoisomerase II
enzyme?
Doxorubicin,
Daunorubicin
123
Which drug's MOA Cross-links DNA?
Busulfan
124
Which drug's MOA Cross-links DNA at guanine?
Requires bioactivation by liver?
A nitrogen mustard?
Cyclophosphamide,
Ifosfamide
125
Which drug's MOA Requires bioactivation?
Cross blood-brain barrier
which LEADS TO
CNS. Cross-link DNA?
Nitrosoureas
126
Which drug's MOA is a Cell cycle phase–nonspecifc
alkylating agent, mechanism
not yet defned?
Procarbazine
127
Which drug's MOA Hyperstabilizes polymerized
microtubules in M phase so
that mitotic spindle cannot
break down (anaphase cannot occur)?
Paclitaxel, other
taxanes
128
Which drug's MOA are Vinca alkaloids that bind
β-tubulin and inhibit
its polymerization into
microtubules which LEADS TO preventing
mitotic spindle formation
(M-phase arrest)?
Vincristine, vinblastine
129
Which drug's MOA Cross-links DNA?
Cisplatin, carboplatin
130
Which drug's MOA Inhibits topoisomerase II which LEADS TO INCREASE IN DNA degradation?
Etoposide, Teniposide
131
Which drug's MOA Inhibits topoisomerase I and prevents DNA unwinding and replication?
Irinotecan, Topotecan
132
Which drug's MOA Inhibits ribonucleotide reductase which LEADS TO DECREASE in DNA Synthesis (S-phase specifc)?
Hydroxyurea
133
Which drug's MOA is a Monoclonal antibody against VEGF. Inhibits angiogenesis (BeVacizumab inhibits Blood Vessel formation)?
Bevacizumab
134
Which drug's MOA is an EGFR tyrosine kinase inhibitor?
Erlotinib
135
Which drug's MOA is a Monoclonal antibody against EGFR?
Cetuximab
136
Which drug's MOA is a Tyrosine kinase inhibitor of BCR-ABL (Philadelphia chromosome fusion gene in CML) and c-kit (common in GI stromal tumors)?
Imatinib
137
Which drug's MOA is a Monoclonal antibody against CD20, which is found on most B-cell neoplasms?
Rituximab
138
Which drugs' MOA are Proteasome inhibitors, induce arrest at G2-M phase and apoptosis?
Bortezomib, Carflzomib
139
Which drug's MOA is a Selective estrogen receptor modulators (SERMs)—receptor antagonists in breast and agonists in
bone. Block the binding of estrogen to ER ⊕ cells?
Tamoxifen, Raloxifene
140
Which drug's MOA is a Monoclonal antibody against HER-2 (c-erbB2), a tyrosine kinase receptor. Helps kill cancer cells
that overexpress HER-2 through inhibition of HER-2 initiated cellular signaling and antibodydependent cytotoxicity?
Trastuzumab (Herceptin)
141
Which drug's MOA is a Small molecule inhibitor of BRAF oncogene ⊕ melanoma? VEmuRAF-enib is for V600Emutated BRAF inhibition.
Vemurafenib
142
Which drug's MOA is a Recombinant uricase that catalyzes metabolism of uric acid to allantoin?
Rasburicase
143
Which drug's MOA Reversibly inhibits cyclooxygenase, mostly in CNS. Inactivated peripherally?
Acetaminophen
144
___is a neutrophil chemotactic agent.
LTB4
145
___ inhibits platelet aggregation and promotes
vasodilation.
PGI2
(Platelet-Gathering Inhibitor)
146
Which drug's MOA is a NSAID that irreversibly inhibits cyclooxygenase (both COX-1 and COX-2) by covalent acetylation
which LEADS TO DECREASE in
synthesis of TXA2 and prostaglandins.? INCREASES bleeding time. No effect on PT, PTT. Effect lasts
until new platelets are produced?
Aspirin
147
Which drug's MOA Reversibly and selectively inhibits the cyclooxygenase (COX) isoform 2 (“Selecoxib”), which is
found in infammatory cells and vascular endothelium and mediates infammation and pain;
spares COX-1, which helps maintain gastric mucosa. Thus, does not have the corrosive effects
of other NSAIDs on the GI lining. Spares platelet function as TXA2 production is dependent on
COX-1.
Celecoxib
148
Which drug's MOA Reversibly inhibit cyclooxygenase (both COX-1 and COX-2).
Blocks prostaglandin synthesis?
Ibuprofen,
Naproxen,
Indomethacin,
Ketorolac,
Diclofenac,
Meloxicam,
Piroxicam
149
Ibuprofen, naproxen, indomethacin, ketorolac, diclofenac, meloxicam, piroxicam are all which types of drugs?
Nonsteroidal
anti-infammatory
drugs
150
Which drug's MOA Reversibly inhibits dihydroorotate dehydrogenase, preventing pyrimidine synthesis? Suppresses
T-cell proliferation?
Lefunomide
151
Alendronate, Ibandronate, Risedronate, Zoledronate are all which kind of drugs?
Bisphosphonates
152
Which drug's MOA are Pyrophosphate analogs; bind hydroxyapatite in bone, inhibiting osteoclast activity?
Alendronate,
Ibandronate,
Risedronate,
Zoledronate
153
Which drug's MOA is a Recombinant PTH analog?Qosteoblastic activity when administered in pulsatile fashion?
Teriparatide
154
Which drug's MOA Inhibits reabsorption of uric acid in proximal
convoluted tubule (also inhibits secretion of
penicillin). Can precipitate uric acid calculi?
Probenecid
155
Which drug's MOA is a Fusion protein (decoy receptor
for TNF-α + IgG1 Fc),
produced by recombinant
DNA?
Etanercept
156
Which drug's MOA is a Anti-TNF-α monoclonal
antibody?
Infiximab,
Adalimumab,
Certolizumab,
Golimumab
157
Benzodiazepines MOA?
INCREASES GABA-A action
158
Carbamazepine MOA?
Blocks Na+ channels
159
Ethosuximide MOA?
Blocks thalamic T-type Ca2+
channels
160
Gabapentin MOA?
Primarily inhibits high-voltageactivated Ca2+ channels;
designed as GABA analog
161
Lamotrigine MOA?
Blocks voltage-gated Na+
channels, inhibits the release
of glutamate
162
Levetiracetam
Unknown; may modulate
GABA and glutamate release
163
Phenobarbital
INCREASES GABA-A action
164
Which drug's MOA Blocks Na+ channels; zeroorder kinetics?
Phenytoin,
Fosphenytoin
165
Tiagabine MOA?
INCREASES GABA by inhibiting reuptake
166
Topiramate MOA?
Blocks Na+ channels, INCREASES GABA
action
167
Valproic acid MOA?
INCREASES Na+ channel inactivation,
INCREASES GABA concentration
by inhibiting GABA
transaminase
168
Vigabatrin MOA?
INCREASES GABA. Irreversible GABA transaminase inhibitor
169
Phenobarbital, Pentobarbital,
Thiopental,
Secobarbital, are all types of what kind of drug?
Barbiturates
170
Which drugs' MOA Facilitates GABA-A action by INCREASING duration of Cl− channel opening, thus DECREASING neuron firing (barbidurates
which INCREASES
duration).
Phenobarbital,
Pentobarbital,
Thiopental,
Secobarbital
171
Diazepam,
Lorazepam,
Triazolam,
Temazepam,
Oxazepam,
Midazolam, Chlordiazepoxide,
Alprazolam, are all what kind of drug?
Benzodiazepines
172
Which drugs' MOA FacilitateS GABA-A action by INCREASING frequency of
Cl− channel opening. DECREASES REM sleep. Most
have long half-lives and active metabolites
(exceptions [ATOM]: Alprazolam, Triazolam,
Oxazepam, and Midazolam are short acting
LEADING TO
higher addictive potential).
Diazepam,
Lorazepam,
Triazolam,
Temazepam,
Oxazepam,
Midazolam, Chlordiazepoxide,
Alprazolam
173
Zolpidem,
Zaleplon,
esZopiclone are all what kind of drug?
Nonbenzodiazepine
hypnotics
174
Which drug's MOA Acts via the BZ-1 subtype of the GABA receptor. Effects reversed by fumazenil. Sleep cycle less
affected as compared with benzodiazepine hypnotics?
Zolpidem,
Zaleplon,
esZopiclone
175
Suvorexant MOA?
Orexin (hypocretin) receptor antagonist.
176
Ramelteon MOA?
Melatonin receptor agonist, binds MT1 and MT2 in suprachiasmatic nucleus.
177
Sumatriptan is what kind of drug?
Triptans
178
Sumatriptan MOA?
5-HT1B/1D agonists. Inhibit trigeminal nerve
activation; prevent vasoactive peptide release;
induce vasoconstriction.
179
Bromocriptine,
Amantadine,
Levodopa (with carbidopa), Selegiline (and COMT inhibitors),
Antimuscarinics (BALSA) are all what kinds of drug?
Parkinson disease
drugs
180
Bromocriptine, Amantadine, Levodopa (with carbidopa), Selegiline (and COMT inhibitors),
Antimuscarinics (BALSA) are kinds of what drug?
Parkinson disease
drugs
181
Ergot—Bromocriptine MOA?
Dopamine agonists
182
Amantadine MOA?
INCREASE dopamine availability
183
Levodopa MOA?
INCREASE L-DOPA availability
184
Selegiline MOA?
Prevent dopamine
breakdown
185
Antimuscarinic MOA?
Curb excess cholinergic
activity
186
Levodopa/carbidopa MOA?
INCREASES level of dopamine in brain. Unlike dopamine, l-DOPA can cross blood-brain barrier and is
converted by dopa decarboxylase in the CNS to dopamine. Carbidopa, a peripheral DOPA
decarboxylase inhibitor, is given with l-DOPA to INCREASE the bioavailability of l-DOPA in the brain and
to limit peripheral side effects.
187
Which drug's MOA Selectively inhibits MAO-B?(metabolize dopamine) LEADS TO INCREASE in dopamine availability?
Selegiline,
Rasagiline
187
Which drug's MOA Inhibits vesicular monoamine transporter (VMAT) dopamine LEADING TO DECREASE in vesicle packaging and release?
Tetrabenazine,
Reserpine
188
Riluzole MOA?
DECREASES neuron glutamate excitotoxicity.
189
Memantine MOA?
NMDA receptor antagonist; helps prevent
excitotoxicity (mediated by Ca2+).
190
Which drugs' MOA are AChE inhibitors?
Donepezil,
Rivastigmine,
Galantamine
191
Desfurane,
Halothane,
Enfurane,
Isofurane,
Sevofurane,
Methoxyfurane,
N2O are all which kind of drug?
Inhaled anesthetics
192
Thiopental MOA?
Facilitate GABA-A (barbiturate).
193
Midazolam MOA?
Facilitate GABA-A
(benzodiazepine).
194
Propofol MOA?
Potentiates GABA-A.
195
Ketamine MOA?
NMDA receptor antagonist.
196
Esters—Procaine, Tetracaine, Benzocaine, Chloroprocaine.
Amides—lIdocaIne, MepIvacaIne, BupIvacaIne, RopIvacaIne, are all which kind of drug?
Local anesthetics
197
Succinylcholine MOA?
Strong ACh receptor agonist; produces sustained depolarization and prevents
muscle contraction.
198
Atracurium,
Cisatracurium, Pancuronium,
Rocuronium,
Tubocurarine,
Vecuronium are all which kind of drugs?
Nondepolarizing
neuromuscular
blocking drug
199
Which drug's MOA is competitive
with ACh for receptors?
Atracurium,
Cisatracurium,
Pancuronium,
Rocuronium,
Tubocurarine,
Vecuronium
200
Dantrolene MOA?
Prevents release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle by binding to the
ryanodine receptor.
201
Baclofen MOA?
Skeletal muscle relaxant. GABA-B receptor agonist in spinal cord.
202
Cyclobenzaprine MOA?
Skeletal muscle relaxant. Acts within CNS.
203
Opioid analgesics
Act as agonists at opioid receptors (μ = β-endorphin, δ = enkephalin, κ = dynorphin) to modulate
synaptic transmission—close presynaptic Ca2+ channel, open postsynaptic K+ channels LEADS TO DECREASE in
synaptic transmission. Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P.
204
Pentazocine MOA?
κ-opioid receptor agonist and μ-opioid receptor weak antagonist or partial agonist.
205
Butorphanol MOA?
κ-opioid receptor agonist and μ-opioid receptor partial agonist.
206
Tramadol MOA?
Very weak opioid agonist; also inhibits 5-HT receptors.
207
Which drugs DECREASE IOP via DECREASE in amount of aqueous humor (inhibit synthesis/secretion or INCREASE drainage).
Glaucoma drugs
208
Timolol, betaxolol, carteolol are examples of which kind of drugs?
β-blockers
209
Epinephrine (α1),
Apraclonidine,
Brimonidine (α2) are examples of which kind of drugs?
α-agonists
210
Acetazolamide is an example of which drug?
Diuretics
211
Bimatoprost, Latanoprost
(PGF2α) is an exhale of which kind of drug?
Prostaglandins
212
Direct: Pilocarpine, Carbachol
Indirect: Physostigmine,
Echothiophate are examples of which kind of drug?
Cholinomimetics (M3)
213
Which drug's MOA DECREASES aqueous humor synthesis
Timolol,
Betaxolol,
Carteolol
214
Which drug's MOA DECREASES
aqueous humor synthesis via
vasoconstriction ,(epinephrine)
DECREASING
aqueous humor synthesis
(apraclonidine, brimonidine)
Epinephrine (α1),
Apraclonidine,
Brimonidine (α2)
215
Acetazolamide MOA?
DECREASES aqueous humor synthesis
via inhibition of carbonic
anhydrase.
216
Which drug's MOA INCREASES outfow of aqueous humor via
DECREASING
resistance of fLow through
uveoscleral pathway?
Bimatoprost,
Latanoprost
(PGF2α)
217
Which drug's MOA INCREASES
outfow of aqueous humor via
contraction of ciliary muscle
and opening of trabecular
meshwork
Use pilocarpine in acute angle
closure glaucoma—very
effective at opening meshwork
into canal of Schlemm
Direct: pilocarpine, carbachol
Indirect: physostigmine,
echothiophate
218
Methylphenidate, Dextroamphetamine, Methamphetamine are which kind of drugs?
Central nervous system
stimulants.
219
Which drug's MOA INCREASES catecholamines in the synaptic cleft, especially norepinephrine and dopamine?
Methylphenidate, Dextroamphetamine, Methamphetamine.
220
Haloperidol,
Pimozide,
Trifuoperazine,
Fuphenazine,
Thioridazine, Chlorpromazine are which kind of drugs?
Typical antipsychotics
221
Which drugs' MOA Blocks dopamine D2 receptor (INCREASES cAMP)
Haloperidol,
Pimozide,
Trifuoperazine,
Fuphenazine,
Thioridazine,
Chlorpromazine
222
Aripiprazole,
Asenapine,
Clozapine,
Olanzapine,
Quetiapine,
Iloperidone,
Paliperidone,
Risperidone,
Lurasidone,
Ziprasidone are which kind of drugs?
Atypical
antipsychotics
223
Which drugs MOA are Not completely understood. Most are D2
antagonists; aripiprazole is D2 partial agonist.
Varied effects on 5-HT2, dopamine, and
α- and H1-receptors?
Aripiprazole,
Asenapine,
Clozapine,
Olanzapine,
Quetiapine,
Iloperidone,
Paliperidone,
Risperidone,
Lurasidone,
Ziprasidone
224
Lithium MOA?
Not established; possibly related to inhibition of
phosphoinositol cascade.
225
Buspirone MOA?
Stimulates 5-HT-1A receptors.
226
Fluoxetine,
Fuvoxamine,
Paroxetine,
Sertraline,
Escitalopram,
Citalopram are which kind of drugs?
Selective serotonin
reuptake inhibitors
227
Which drug's MOA is SSRIs inhibit 5-HT reuptake?
Fluoxetine,
Fuvoxamine,
Paroxetine,
Sertraline,
Escitalopram,
Citalopram
228
Venlafaxine,
Desvenlafaxine,
Duloxetine,
Levomilnacipran, Milnacipran are which kinds of drugs?
Serotonin-norepinephrine reuptake inhibitors
229
Which drug's MOA SNRIs inhibit 5-HT and NE reuptake?
Venlafaxine,
Desvenlafaxine,
Duloxetine,
Levomilnacipran,
Milnacipran
230
Amitriptyline,
Nortriptyline,
Imipramine,
Desipramine,
Clomipramine,
Doxepin, and
Amoxapine are which kind of drugs?
Tricyclic
antidepressants
231
Which drug's MOA are TCAs inhibit 5-HT and NE reuptake?
Amitriptyline,
Nortriptyline,
Imipramine,
Desipramine,
Clomipramine,
Doxepin, and
Amoxapine
232
Tranylcypromine, Phenelzine,
Isocarboxazid,
Selegiline (selective MAO-B inhibitor) are which kind of drugs?
Monoamine oxidase
inhibitors
233
Which drug's MOA are Nonselective MAO inhibition that INCREASES levels of amine neurotransmitters (norepinephrine, 5-HT,
dopamine).
Tranylcypromine, Phenelzine,
Isocarboxazid,
Selegiline (selective MAO-B inhibitor)
234
Bupropion MOA?
Inhibits NE and dopamine reuptake.
Also used for smoking cessation.
Toxicity: stimulant effects
(tachycardia, insomnia), headache, seizures in anorexic/bulimic patients. Favorable sexual side
effect profle.
235
Mirtazapine MOA?
α2-antagonist (INCREASES release of NE and 5-HT), potent 5-HT2 and 5-HT3 receptor antagonist and H1
antagonist. Toxicity: sedation (which may be desirable in depressed patients with insomnia),
INCREASES
appetite, weight gain (which may be desirable in elderly or anorexic patients), dry mouth.
236
Trazodone MOA?
Primarily blocks 5-HT2, α1-adrenergic, and H1 receptors; also weakly inhibits 5-HT reuptake.
Used primarily for insomnia, as high doses are needed for antidepressant effects. Toxicity: sedation,
nausea, priapism, postural hypotension.
Called traZZZobone due to sedative and male-specifc
side effects.
237
Varenicline MOA?
Nicotinic ACh receptor partial agonist.
Used for smoking cessation. Toxicity: sleep disturbance,
may depress mood. Varenicline helps nicotine cravings decline.
238
Vilazodone MOA?
Inhibits 5-HT reuptake; 5-HT1A receptor partial agonist. Used for major depressive disorder.
Toxicity: headache, diarrhea, nausea, q weight, anticholinergic effects.
May cause serotonin
syndrome if taken with other serotonergic agents.
239
Vortioxetine MOA?
Inhibits 5-HT reuptake; 5-HT1A receptor agonist and 5-HT3 receptor antagonist. Used for major
depressive disorder.
Toxicity: nausea, sexual dysfunction, sleep disturbances (abnormal dreams),
anticholinergic effects.
May cause serotonin syndrome if taken with other serotonergic agents.
240
Methadone MOA?
Long-acting oral opiate used for heroin detoxifcation or long-term maintenance therapy.
241
Buprenorphine +
naloxone MOA?
Sublingual buprenorphine (partial agonist) is absorbed and used for maintenance therapy.
Naloxone (antagonist, not orally bioavailable) is added to lower IV abuse potential.
242
Naltrexone MOA?
Long-acting opioid given IM or as nasal spray to treat acute overdose in unconscious individual.
Also used for relapse prevention once detoxifed. Use naltrexone for the long trex back to sobriety.
243
Mannitol MOA?
Osmotic diuretic. INCREASES tubular fluid osmolarity LEADING TO INCREASE IN urine flow, DECREASING intracranial/intraocular pressure.
244
Acetazolamide MOA?
Carbonic anhydrase inhibitor. Causes selflimited NaHCO3 diuresis and DECREASING total body
HCO3− stores.
245
Furosemide,
Bumetanide,
Torsemide, are which kinds of drugs?
Loop diuretics
246
Which drug's MOA is
1. Sulfonamide loop diuretics. Inhibit cotransport
system (Na+/K+/2Cl−) of thick ascending limb
of loop of Henle.
2. Abolish hypertonicity of
medulla, preventing concentration of urine.
3. Stimulate PGE release (vasodilatory effect
on afferent arteriole); inhibited by NSAIDs.
4. INCREASES
Ca2+ excretion.
5. Loops Lose Ca2+?
Furosemide,
Bumetanide,
Torsemide,
247
Ethacrynic acid MOA?
Nonsulfonamide inhibitor of cotransport system
(Na+/K+/2Cl−) of thick ascending limb of loop
of Henle.
248
Hydrochlorothiazide, Chlorthalidone,
Metolazone, are which kind of drugs?
Thiazide diuretics
249
Which drugs MOA Inhibits NaCl reabsorption in early DCT
LEADS TO DECREASE IN
diluting capacity of nephron. rCa2+
excretion.
Hydrochlorothiazide, Chlorthalidone,
Metolazone
250
Spironolactone,
Eplerenone,
Amiloride,
Triamterene, are which kind of drugs?
Potassium-sparing
diuretics
251
Which drug's MOA is Spironolactone and eplerenone are competitive
aldosterone receptor antagonists in cortical
collecting tubule?Triamterene and Amiloride
act at the same part of the tubule by blocking
Na+ channels in the cortical collecting tubule?
Spironolactone,
Eplerenone,
Amiloride
252
List four types of
Angiotensin-converting
enzyme inhibitors.
Captopril,
Enalapril,
Lisinopril,
Ramipril.
253
Captopril,
Enalapril,
Lisinopril,
Ramipril MOA?
Inhibits ACE pr AT II pr GFR by preventing
constriction of efferent arterioles. qrenin due
to loss of negative feedback. Inhibition of ACE
also prevents inactivation of bradykinin, a
potent vasodilator
254
List three Angiotensin II receptor blockers.
Losartan,
Candesartan,
Valsartan
255
Losartan,
Candesartan,
Valsartan MOA?
Selectively block binding of angiotensin II to AT-1 receptor. Effects similar to ACE inhibitors, but
ARBs do not increase bradykinin.
256
Aliskiren MOA?
Direct renin inhibitor, blocks conversion of angiotensinogen to angiotensin I.
257
Leuprolide MOA?
GnRH analog with agonist properties
when used in pulsatile fashion; antagonist
properties when used in continuous fashion
(downregulates GnRH receptor in pituitary
LEADS TO DEACREASE in
FSH and DECREASES LH).
258
List three Estrogens.
Ethinyl estradiol,
DES,
Mestranol.
259
Ethinyl estradiol,
DES,
Mestranol MOA?
Bind estrogen receptors.
260
Clomiphene MOA?
Antagonist at estrogen receptors in hypothalamus. Prevents normal feedback inhibition and
INCREASES release of LH and FSH from pituitary, which stimulates ovulation.
Used to treat infertility
due to anovulation (eg, PCOS).
SERMs may cause hot fashes, ovarian enlargement, multiple
simultaneous pregnancies, visual disturbances.
261
List three Aromatase inhibitors.
Anastrozole,
Letrozole,
Exemestane.
262
Anastrozole,
Letrozole,
Exemestane MOA?
Inhibit peripheral conversion of androgens to estrogen.
263
List five Progestins.
Levonorgestrel, Medroxyprogesterone, Etonogestrel,
Norethindrone,
Megestrol, (and many others
when combined with estrogen.)
264
Levonorgestrel, Medroxyprogesterone, Etonogestrel,
Norethindrone,
Megestrol MOA?
Bind progesterone receptors, DECREASES growth and INCREASES vascularization of endometrium, thicken cervical mucus.
265
List two Antiprogestins.
Mifepristone
Ulipristal.
266
Mifepristone
Ulipristal MOA?
Competitive inhibitors of progestins at progesterone receptors.
267
Copper intrauterine device MOA?
Produces local inflammatory reaction toxic to sperm and ova, preventing fertilization and implantation; hormone free.
268
Danazol MOA?
Synthetic androgen that acts as partial agonist at androgen receptors.
269
Testosterone, Methyltestosterone MOA?
Agonists at androgen receptors.
270
Finasteride MOA?
5α-reductase inhibitor (DECREASES conversion of
testosterone to DHT). Used for BPH and
male-pattern baldness. Adverse effects:
gynecomastia and sexual dysfunction.
271
List three Phosphodiesterase
type 5 inhibitors.
Sildenafl,
Vardenafl,
Tadalafl.
272
Sildenafl,
Vardenafl,
Tadalafl MOA?
Inhibit PDE-5 LEADS TO INCREASE IN cGMP which LEADS TO prolonged
smooth muscle relaxation in response to NO which
LEADS TO INCREASE IN blood flow in corpus cavernosum of penis, which
DECREASES
pulmonary vascular resistance.
273
Minoxidil MOA?
Direct arteriolar vasodilator.
274
Histamine-1 blockers act as ___
Reversible inhibitors of H1 histamine receptors.
275
Name three first generation Histamine-1 blockers.
Diphenhydramine, Dimenhydrinate,
Chlorpheniramine.
276
Name three second generation Histamine-1 blockers.
Loratadine,
Fexofenadine,
Desloratadine,
Cetirizine.
277
Pseudoephedrine, Phenylephrine MOA?
α-adrenergic agonists, used as nasal decongestants.
278
Endothelin receptor
antagonists MOA?
Competitively antagonizes endothelin-1
receptors which LEADS TO DECREASE in pulmonary vascular resistance.
279
PDE-5 inhibitors MOA?
Inhibits PDE-5 LEADS TO INCREASE in cGMP LEADS TO prolonged
vasodilatory effect of NO.
280
Prostacyclin analogs MOA?
PGI-2 (prostacyclin) with direct vasodilatory
effects on pulmonary and systemic arterial
vascular beds.
Inhibits platelet aggregation.
281
Bronchoconstriction is mediated by which two pathways?
(1) infammatory processes (2) Parasympathetic tone
282
List three β2-agonists (asthma drugs).
1. Albuterol
2. Salmeterol
3. Formoterol
283
Albuterol MOA?
Relaxes bronchial smooth muscle (short acting β2-agonist). Used during acute
exacerbation.
284
1. Salmeterol
2. Formoterol MOA?
Long-acting agents for prophylaxis.
Adverse effects are tremor and arrhythmia.
285
List two Inhaled
corticosteroids.
Fluticasone,
Budesonide
286
Fluticasone,
Budesonide MOA?
Inhibit the synthesis of virtually all cytokines. Inactivate NF-κB, the
transcription factor that induces production of TNF-α and other inflammatory agents.
1st-line therapy for chronic asthma.
Use a spacer or rinse mouth after use to prevent oral thrush.
287
List two Muscarinic
antagonists.
Tiotropium,
Ipratropium
288
Tiotropium,
Ipratropium MOA?
Competitively block muscarinic receptors, preventing
bronchoconstriction.
Also used for COPD. Tiotropium is long acting.
289
List three Antileukotrienes.
Montelukast
Zafrlukast
Zileuton
290
Montelukast
Zafrlukast MOA?
Block leukotriene
receptors (CysLT1).
Especially good for
aspirin-induced and exercise-induced asthma.
291
Zileuton
5-lipoxygenase pathway inhibitor.
Blocks conversion of arachidonic acid to
leukotrienes. Hepatotoxic.
292
Mention one Anti-IgE monoclonal therapy.
Omalizumab
293
Omalizumab
Binds mostly unbound serum
IgE and blocks binding to FcεRI. Used in
allergic asthma with INCREASE in IgE levels resistant to
inhaled steroids and long-acting β2-agonists.
294
Mention one Methylxanthines.
Theophylline
295
Theophylline MOA?
likely causes bronchodilation
by inhibiting phosphodiesterase LEADS TO INCREASE IN cAMP
levels due to DECREASE cAMP hydrolysis. Usage is
limited because of narrow therapeutic index
(cardiotoxicity, neurotoxicity); metabolized
by cytochrome P-450. Blocks actions of
adenosine.
296
List two Mast cell stabilizers.
Cromolyn
Nedocromil
297
Cromolyn
Nedocromil MOA?
Prevent release of
inflammatory mediators from mast cells.
Used for prevention of bronchospasm, not for acute
bronchodilation.
298
Methacholine MOA?
Nonselective muscarinic receptor (M3) agonist.
Used in bronchial challenge test to help diagnose
asthma.
299
What are Immunosuppressants?
Agents that block lymphocyte activation and proliferation. Reduce acute transplant rejection by
suppressing cellular immunity (used as prophylaxis). Frequently combined to achieve greater
efficacy with DECREASES toxicity. Chronic suppression INCREASES risk of infection and malignancy.
300
Cyclosporine MOA?
Calcineurin inhibitor;
binds cyclophilin.
Blocks T-cell activation by
preventing IL-2 transcription.
301
Tacrolimus (FK506) MOA?
Calcineurin inhibitor;
binds FK506 binding
protein (FKBP).
Blocks T-cell activation
by preventing IL-2
transcription.
302
Sirolimus (Rapamycin) MOA?
mTOR inhibitor; binds
FKBP.
Blocks T-cell
activation and B-cell
differentiation by
preventing response
to IL-2.
303
Basiliximab MOA?
Monoclonal antibody;
blocks IL-2R.
304
Azathioprine MOA?
Antimetabolite
precursor of
6-mercaptopurine.
Inhibits lymphocyte
proliferation by
blocking nucleotide
synthesis.
305
Mycophenolate
Mofetil MOA?
Reversibly inhibits
IMP dehydrogenase,
preventing purine
synthesis of B and T
cells.
306
Glucocorticoids MOA?
Inhibit NF-κB.
Suppress both B- and
T-cell function by
DECREASES
transcription of
many cytokines.
Induce T cell apoptosis.
307
Epoetin alfa (EPO analog) MOA?
Erythropoietin (a bone marrow stimulant) used for Anemias (especially in renal failure.
308
Filgrastim (G-CSF), Sargramostim (GM-CSF) MOA?
Colony stimulating
factors (a bone marrow stimulant) used for Leukopenia; recovery of granulocyte and
monocyte counts.
309
Romiplostim (TPO analog), Eltrombopag (TPO
Receptor agonist) MOA?
Thrombopoietin (a bone marrow stimulant) used for Autoimmune thrombocytopenia.
310
Aldesleukin MOA?
(Immunotherapy) Interleukin-2 used for Renal cell carcinoma, metastatic melanoma.
311
IFN-α MOA?
(Immunotherapy) Interferon used for Chronic hepatitis C (not preferred) and B, renal cell carcinoma.
312
Which Immunotherapy is used for Multiple sclerosis?
IFN-β
313
Which immunotherapy is used for Chronic granulomatous disease?
IFN-γ
314
Alemtuzumab MOA?
CD52, used for CLL, MS.
NB: “Alymtuzumab”—chronic
lymphocytic leukemia.
315
Bevacizumab MOA?
VEGF, used for Colorectal cancer, renal cell
carcinoma, non-small cell
lung cancer.
NB: Also used for neovascular agerelated macular degeneration, proliferative diabetic retinopathy, and macular edema.
316
Cetuximab MOA?
EGFR, used for Stage IV colorectal cancer,
head and neck cancer.
317
Rituximab MOA?
CD20, used for B-cell non-Hodgkin
lymphoma, CLL, rheumatoid
arthritis, ITP, multiple
sclerosis
318
Trastuzumab MOA?
HER2, used for Breast cancer, gastric cancer.
NB: HER2—“tras2zumab”
319
Adalimumab,
certolizumab,
golimumab,
infiximab MOA?
Soluble TNF-α.
Used for IBD, rheumatoid arthritis,
ankylosing spondylitis,
psoriasis
NB: Etanercept is a decoy
TNF-α receptor and not a
monoclonal antibody
320
Daclizumab MOA?
CD25 (part of IL-2 receptor) Used for Relapsing multiple sclerosis.
321
Eculizumab MOA?
α4-integrin.
Used for Multiple sclerosis, Crohn disease
NB: α4-integrin: WBC adhesion
Risk of PML in patients with
JC virus.
322
Ustekinumab MOA?
IL-12/IL-23.
Used for Psoriasis, psoriatic arthritis.
323
Abciximab MOA?
Platelet glycoproteins IIb/IIIa Used for Antiplatelet agent for prevention of ischemic
complications in patients
undergoing percutaneous
coronary intervention
NB: IIb times IIIa equals
“absiximab”
324
Denosumab MOA?
RANKL
Used for Osteoporosis; inhibits osteoclast
maturation (mimics
osteoprotegerin)
NB: Denosumab affects osteoclasts
325
Digoxin immune Fab MOA?
Digoxin
Used as Antidote for digoxin toxicity.
326
Omalizumab MOA?
IgE
Used for Refractory allergic asthma;
prevents IgE binding to FcεRI
327
Palivizumab MOA?
RSV F protein
Used for RSV prophylaxis for high-risk
infants
NB: PaliVIzumab—VIrus
328
List 4 Penicillin G, V
Penicillin G (IV and IM form), penicillin V (oral).
Prototype β-lactam antibiotics.
329
Penicillin G (IV and IM form), penicillin V (oral).
Prototype β-lactam antibiotics MOA?
D-Ala-D-Ala structural analog. Bind penicillin-binding proteins (transpeptidases).
Block transpeptidase cross-linking of peptidoglycan in cell wall.
Activate autolytic enzymes.
330
List 3 Penicillinase-sensitive
penicillins
Amoxicillin,
Ampicillin;
Aminopenicillins
331
Amoxicillin,
Ampicillin;
Aminopenicillins MOA?
Same as penicillin. Wider spectrum;
penicillinase sensitive. Also combine with
clavulanic acid to protect against destruction
by β-lactamase.
332
List 3 Penicillinase-resistant
penicillins
Dicloxacillin,
Nafcillin,
Oxacillin.
333
Dicloxacillin,
Nafcillin,
Oxacillin MOA?
Same as penicillin. Narrow spectrum;
penicillinase resistant because bulky R group blocks access of β-lactamase to β-lactam ring.
334
List 2 Antipseudomonal
penicillins.
Piperacillin,
Ticarcillin.
335
Piperacillin,
Ticarcillin MOA?
Same as penicillin. Extended spectrum. Penicillinase sensitive; use with β-lactamase inhibitors.
336
List four β-lactamase inhibitors
Clavulanic acid,
Avibactam,
Sulbactam,
Tazobactam.
(Often added to penicillin antibiotics to protect the antibiotic from destruction by β-lactamase (penicillinase))
337
Clavulanic acid,
Avibactam,
Sulbactam,
Tazobactam MOA?
β-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases. Bactericidal.
338
List four Carbapenems
Doripenem,
Imipenem,
Meropenem,
Ertapenem
(DIME antibiotics are given when there is a 10/10 [life-threatening] infection).
339
Doripenem,
Imipenem,
Meropenem,
Ertapenem MOA?
Imipenem is a broad-spectrum, β-lactamase–
resistant carbapenem. Always administered
with cilastatin (inhibitor of renal
dehydropeptidase I) to DECREASE inactivation of drug
in renal tubules.
340
Name one Monobactams
Aztreonam
341
Aztreonam MOA?
Less susceptible to β-lactamases. Prevents peptidoglycan cross-linking by binding to penicillin-binding protein 3. Synergistic with aminoglycosides. No cross-allergenicity with penicillins.
342
Vancomycin MOA?
Inhibits cell wall peptidoglycan formation by binding D-Ala-D-Ala portion of cell wall precursors.
Bactericidal against most bacteria (bacteriostatic against C diffcile). Not susceptible to β-lactamases.
343
List tow 30S inhibitors
Aminoglycosides
Tetracyclines
344
List four 50S inhibitors
Chloramphenicol,
Clindamycin
Erythromycin (macrolides)
Linezolid
345
Protein synthesis inhibitors MOA
Specifcally target smaller bacterial ribosome (70S, made of 30S and 50S subunits), leaving human ribosome (80S) unaffected.
All are bacteriostatic, except aminoglycosides (bactericidal) and linezolid (variable).
346
List five Aminoglycosides
Gentamicin,
Neomycin,
Amikacin,
Tobramycin,
Streptomycin.
347
Gentamicin,
Neomycin,
Amikacin,
Tobramycin,
Streptomycin MOA?
Bactericidal; irreversible inhibition of initiation complex through binding of the 30S subunit.
Can cause misreading of mRNA. Also block translocation. Require O2 for uptake; therefore ineffective against anaerobes.
348
List three Tetracyclines
Tetracycline,
Doxycycline,
Minocycline.
349
Tetracycline,
Doxycycline,
Minocycline MOA?
Bacteriostatic; bind to 30S and prevent attachment of aminoacyl-tRNA.
Limited CNS penetration.
Doxycycline is fecally eliminated and can be used in patients with renal failure.
Do not take tetracyclines with milk (Ca2+), antacids (Ca2+ or Mg2+), or iron-containing preparations because
divalent cations inhibit drugs’ absorption in the gut.
350
Name one Glycylcycline
Tigecycline.
351
Tigecycline MOA?
Tetracycline derivative. Binds to 30S, inhibiting protein synthesis. Generally bacteriostatic.
352
Chloramphenicol MOA?
Blocks peptidyltransferase at 50S ribosomal subunit. Bacteriostatic.
353
Clindamycin MOA?
Blocks peptide transfer (translocation) at 50S ribosomal subunit. Bacteriostatic.
354
Name one Oxazolidinone.
Linezolid.
355
Linezolid MOA?
Inhibit protein synthesis by binding to 50S subunit and preventing formation of the initiation complex.
356
List three Macrolides
Azithromycin,
Clarithromycin,
Erythromycin.
357
Azithromycin,
Clarithromycin,
Erythromycin MOA?
Inhibit protein synthesis by blocking translocation (“macroslides”); bind to the 23S rRNA of the
50S ribosomal subunit. Bacteriostatic.
358
List two Polymyxins.
Colistin (polymyxin E),
Polymyxin B.
359
Colistin (polymyxin E),
Polymyxin B MOA?
Cation polypeptides that bind to phospholipids on cell membrane of gram ⊝ bacteria. Disrupt cell
membrane integrity LEADING TO leakage of cellular components LEADING TO cell death.
360
List three Sulfonamides.
Sulfamethoxazole (SMX), Sulfsoxazole,
Sulfadiazine.
361
Sulfamethoxazole (SMX), Sulfsoxazole,
Sulfadiazine MOA?
Inhibit dihydropteroate synthase, thus inhibiting folate synthesis. Bacteriostatic (bactericidal
when combined with trimethoprim).
362
Dapsone MOA?
Similar to sulfonamides, but structurally distinct agent.
363
Trimethoprim MOA?
Inhibits bacterial dihydrofolate reductase.
Bacteriostatic.
364
List six Fluoroquinolones.
Ciprofoxacin,
Enoxacin,
Norfoxacin,
Ofoxacin; respiratory fuoroquinolones—gemifoxacin,
Levofoxacin, Mmoxifoxacin.
365
Ciprofoxacin,
Enoxacin,
Norfoxacin,
Ofoxacin; respiratory fuoroquinolones—gemifoxacin,
Levofoxacin, Mmoxifoxacin MOA?
Inhibit prokaryotic enzymes topoisomerase II (DNA gyrase) and topoisomerase IV.
Bactericidal. Must not be taken with antacids
366
Daptomycin MOA?
Lipopeptide that disrupts cell membranes of gram ⊕ cocci by creating transmembrane channels.
367
Metronidazole MOA?
Forms toxic free radical metabolites in the bacterial cell that damage DNA. Bactericidal, antiprotozoal.
368
M tuberculosis Treatment?
Isoniazid
Rifampin, Isoniazid, Pyrazinamide,
Ethambutol (RIPE for treatment)
369
M avium–intracellulare Treatment?
Azithromycin, rifabutin
More drug resistant than M tuberculosis.
Azithromycin or clarithromycin + ethambutol.
Can add rifabutin or ciprofoxacin.
370
M leprae
N/A
Long-term treatment with dapsone and rifampin for tuberculoid form. Add clofazimine for lepromatous form.
371
List two Rifamycins.
Rifampin,
Rifabutin.
372
Rifampin,
Rifabutin MOA?
Inhibit DNA-dependent RNA polymerase.
373
Isoniazid MOA?
DECREASES synthesis of mycolic acids. Bacterial catalaseperoxidase (encoded by KatG) needed to
convert INH to active metabolite.
374
Pyrazinamide MOA?
Mechanism uncertain. Pyrazinamide is a prodrug that is converted to the active compound pyrazinoic acid. Works best at acidic pH (eg, in host phagolysosomes).
375
Ethambutol MOA?
DECREASES carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase.
376
Streptomycin MOA?
Interferes with 30S component of ribosome.
377
High risk for endocarditis and undergoing
surgical or dental procedures-MEDICATION?
Amoxicillin
378
Exposure to gonorrhea-MEDICATION?
Ceftriaxone
379
History of recurrent UTIs
TMP-SMX
380
Exposure to meningococcal infection
Ceftriaxone,
Ciprofoxacin, or
Rifampin
381
Pregnant woman carrying group B strep
Intrapartum penicillin G or ampicillin
382
Prevention of gonococcal conjunctivitis in newborn
Erythromycin ointment on eyes
383
Prevention of postsurgical infection due to S aureus
Cefazolin
384
Prophylaxis of strep pharyngitis in child with prior rheumatic fever
Benzathine penicillin G or oral penicillin V
385
Exposure to syphilis
Benzathine penicillin G
386
Amphotericin B MOA?
Binds ergosterol (unique to fungi); forms membrane pores that allow leakage of electrolytes.
387
Nystatin MOA?
Same as amphotericin B. Topical use only as too toxic for systemic use.
388
Flucytosine MOA?
Inhibits DNA and RNA biosynthesis by conversion to 5-fuorouracil by cytosine deaminase.
389
List seven Azoles.
Clotrimazole,
Fuconazole,
Isavuconazole,
Itraconazole,
Ketoconazole,
Miconazole,
Voriconazole.
390
Clotrimazole,
Fuconazole,
Isavuconazole,
Itraconazole,
Ketoconazole,
Miconazole,
Voriconazole MOA?
Inhibit fungal sterol (ergosterol) synthesis by inhibiting the cytochrome P-450 enzyme that converts lanosterol to ergosterol.
391
Terbinafne MOA?
Inhibits the fungal enzyme squalene epoxidase.
392
List three Echinocandins.
Anidulafungin,
Caspofungin,
Micafungin.
393
Anidulafungin,
Caspofungin,
Micafungin MOA?
Inhibit cell wall synthesis by inhibiting synthesis of β-glucan.
394
Griseofulvin MOA?
Interferes with microtubule function; disrupts mitosis. Deposits in keratin-containing tissues (eg, nails).
395
List four Antiprotozoal therapies.
Pyrimethamine (toxoplasmosis), Suramin and Melarsoprol (Trypanosoma brucei),
Nifurtimox (T cruzi),
Sodium stibogluconate (leishmaniasis).
396
Anti-mite/louse therapy
Permethrin (inhibits Na+ channel deactivation
LEADS TO
neuronal membrane depolarization),
malathion (acetylcholinesterase inhibitor),
lindane (blocks GABA channels
LEADS TO
neurotoxicity). Used to treat scabies
(Sarcoptes scabiei) and lice (Pediculus and
Pthirus).
397
Chloroquine MOA?
Blocks detoxifcation of heme into hemozoin. Heme accumulates and is toxic to plasmodia.
398
Antihelminthic therapy
Pyrantel pamoate,
Ivermectin,
Mebendazole (microtubule inhibitor), Praziquantel,
Diethylcarbamazine.
399
Oseltamivir,
Zanamivir MOA?
Inhibit infuenza neuraminidase LEADS TO DECREASING release of progeny virus.
400
Acyclovir,
Famciclovir,
Valacyclovir MOA?
Guanosine analogs. Monophosphorylated by HSV/VZV thymidine kinase and not phosphorylated in uninfected cells LEADS TO few adverse effects. Triphosphate formed by cellular enzymes. Preferentially
inhibit viral DNA polymerase by chain termination.
401
Ganciclovir MOA?
5′-monophosphate formed by a CMV viral kinase.
Guanosine analog.
Triphosphate formed by
cellular kinases.
Preferentially inhibits viral DNA polymerase.
402
Foscarnet MOA?
Viral DNA/RNA polymerase inhibitor and HIV reverse transcriptase inhibitor.
Binds to pyrophosphate-binding site of enzyme.
Does not require any kinase activation.
403
Cidofovir MOA?
Preferentially inhibits viral DNA polymerase.
Does not require phosphorylation by viral kinase
404
HIV therapy
Highly active antiretroviral therapy (HAART): often initiated at the time of HIV diagnosis.
Strongest indication for patients presenting with AIDS-defning illness, low CD4+ cell counts
(< 500 cells/mm3), or high viral load. Regimen consists of 3 drugs to prevent resistance:
2 NRTIs and preferably an integrase inhibitor.
405
Abacavir (ABC)
Didanosine (ddI)
Emtricitabine (FTC)
Lamivudine (3TC)
Stavudine (d4T)
Tenofovir (TDF)
Zidovudine (ZDV,
formerly AZT) MOA?
Competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3′ OH group).
Tenofovir is a nucleoTide; the others are nucleosides.
All need to be phosphorylated to be active.
ZDV can be used for general prophylaxis and during pregnancy to DECREASE risk of fetal transmission.
406
Delavirdine
Efavirenz
Nevirapine MOA?
Bind to reverse transcriptase at site different from NRTIs.
Do not require phosphorylation
to be active or compete with nucleotides.
407
Atazanavir
Darunavir
Fosamprenavir
Indinavir
Lopinavir
Ritonavir
Saquinavir MOA?
Inhibits HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase.
408
Enfuvirtide MOA?
Binds CCR-5 on surface of T cells/monocytes, inhibiting interaction with gp120.
409
Interferons MOA?
Glycoproteins normally synthesized by virus-infected cells, exhibiting a wide range of antiviral and
antitumoral properties.
410
Ledipasvir MOA?
Viral phosphoprotein (NS5A) inhibitor; NS5A plays important role in replication.
411
Ribavirin MOA?
Inhibits synthesis of guanine nucleotides by competitively inhibiting inosine monophosphate dehydrogenase.
412
Simeprevir MOA?
HCV protease (NS3/4A); prevents viral
replication.
413
Sofosbuvir MOA?
Inhibits HCV RNA-dependent RNA polymerase (NS5B) acting as a chain terminator.
414
What is the adverse effect of Kernicterus?
Sulfonamides
415
What is the adverse effect of Ototoxicity?
Aminoglycosides
416
What is the adverse effect of Cartilage damage?
Fluoroquinolones
417
What is the adverse effect of Embryotoxic?
Clarithromycin
418
What is the adverse effect of Discolored teeth, inhibition of bone growth?
Tetracyclines
419
What is the adverse effect of Teratogenic?
Ribavirin
420
What is the adverse effect of Teratogenic?
Griseofulvin
421
What is the adverse effect of Gray baby syndrome?
Chloramphenicol
