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Pharmacology > EXAM #2: REVIEW > Flashcards

EXAM #2: REVIEW Flashcards

1
Q

What drug is used to prevent the adverse effects of high dose methotrexate?

A

Leucovorin

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2
Q

What are the unique adverse effects associated with Methotrexate?

A

Nephrotoxicity

Interstitial pneumonitis

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3
Q

What enzyme does 5-FU inhibit?

A

Thymidylate Synthase

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4
Q

What are the unique adverse effects associated with 5-FU?

A

Oral and GI ulcers

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5
Q

What is Capecitabine?

A

Oral 5-FU

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6
Q

What is disease is Cytarabine primarily used as a chemotheraputic agent for?

A

AML

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7
Q

What enzyme does Cytarabine require to be activated?

A

Deoxycytidine Kinase

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8
Q

What enzyme inactivates Cytatabine?

A

Cytidine Deaminase

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9
Q

What is the unique syndrome seen with Cytarabine? What are the symptoms?

A

Cerebellar Syndrome

  • Ataxia
  • Dysarthria
  • Nystagmus
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10
Q

What enzyme activates Gemcitabine into its active form?

A

Deoxycytidine Kinase

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11
Q

What enzyme does Gemcitabine specifically inhibit?

A

Ribonucleotide Reductase

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12
Q

What enzyme do 6-Mercaptopurine and 6-Thioguanine require for activation?

A

HGPRT

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13
Q

What enzyme inactivates 6-Mercaptopurine?

A

Thiopurine Methyltransferase (TPMT)

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14
Q

What diseases are 6-MU and 6-TG commonly used to treat?

A

AML and ALL

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15
Q

What disease is Fludarabine used to treat?

A

CLL

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16
Q

What enzyme activates Fludarabine?

A

Deoxycytidine Kinase

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17
Q

What enzymes does Fludarabine specifically inhibit?

A

Ribonucleotide Reductase
DNA polymerase

Also inhibits mRNA translation

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18
Q

What disease is Cladrabine used to treat?

A

Hairy Cell Leukemia

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19
Q

What enzyme does Cladrabine specifically inhibit?

A

Ribonucleotide Reductase

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20
Q

What is the mechanism of action of Cyclophosphamine?

A

Nitrogen mustard DNA alkylating agent

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21
Q

What is the metabolite of Cyclophosphamine that is particularly harmful? What does it cause?

A

Acrolein–>Hemmorhagic cystitis

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22
Q

What drug is used to prevent Hemorrhagic cystitis in Cyclophosphamine administration?

A

MENSA

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23
Q

What is the mechanism of action of Carmustine? What is it used to treat?

A

Nitrosurea alkylating agent that is highly lipophilic –> Brain cancer

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24
Q

What two enzymes reduce the efficacy of the DNA alkylating agents?

A

Glutathione

MGMT

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25
Q

List the three Platinum compounds. What is their mechanism of action?

A

Cisplastin
Carbiplatin
Oxiplatin

These drugs are all non-classical DNA alkylating agents

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26
Q

What are the unique adverse effects associated with Cisplatin?

A

Nephrotoxicity
Peripheral Neuropathy
Anaphylaxis

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27
Q

How is the neprotoxicity associated with Cisplastin prevented?

A

Co-administration with IV saline

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28
Q

What adverse effect is seen with Carbiplatin?

A

Anaphylaxis only

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29
Q

What is the mechanism of action of Procarbazine? What is it used to treat?

A

Non-classical alkylating agent used to treat Hodgkins’ Disease

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30
Q

What is the mechanism of action of Dacarbazine? What is it used to treat?

A

Non-classical alkylating agent used to treat Melamona and Sarcoma

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31
Q

What is the mechanism of action of Temozolamide? What is it used to treat?

A

Non-classical alkylating agent used to treat Glioblastoma and Melanoma

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32
Q

List the Anti-microtubule drugs. What phase of the cell cycle do these agents perturb?

A

Vinblastine
Vincristine
Paclitaxel
Docetaxel

M-phase

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33
Q

Which of the anti-microtubule drugs inhibit microtubule polymerization?

A

Vinblastine and Vincristine

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34
Q

Which of the anti-microtubule drugs inhibit microtubule depolymerization?

A

Paclitaxel

Docetaxel

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35
Q

What is the unique adverse effect seen with Vincristine?

A

Neurotoxicity

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36
Q

What is the unique adverse effect seen with Paclitaxel?

A

Peripheral Neuropathy
Anaphylaxis
Myelosuppression

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37
Q

What drugs are used to prevent the anaphylaxis seen with Paclitaxel?

A

Diphenhydramine

Dexamethasone

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38
Q

What drug is given to counteract the myelosuppression seen with Paclitaxel?

A

Filgrastim, a G-CSF drug

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39
Q

List the Topoisomerase I inhibitors.

A

Topotecan

Irinotecan

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40
Q

List the Topoisomerase II inhibitor.

A

Etoposide

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41
Q

What is the mechanism of action of Doxorubicin?

A

This is an antibiotic that:

  • Topoisomerase II inhibitor
  • Intercalates DNA
  • Inhibits DNA polymerase
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42
Q

What is the unique adverse effect seen with Doxorubicin?

A

Irreversible cardiomyopathy

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43
Q

How is the cardiomyopathy seen with Doxorubicin prevented?

A

Dexrazoxane

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44
Q

What is the mechanism of action of Bleomycin?

A

Small peptide that cause single and double strand DNA breaks in G2

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45
Q

What unique adverse effect is seen with Bleomycin?

A

Pulmonary toxicity

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46
Q

What is the mechanism of action of Tamoxifen?

A

Estrogen receptor antagonist

*****Treats estrogen receptor positive breast cancer

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47
Q

What is the mechanism of action of Anastrazole?

A

Inhibits aromatase to prevent conversion of Testosterone to estrogen in post-menopausal women with estrogen receptor positive breast cancer

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48
Q

What is the mechanism of action of Leuprolide and Goserelin?

A

These are GnRH AGONISTS used to treat prostate cancer

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49
Q

What is the mechanism of action of Degarelix?

A

GnRH ANTAGONIST used to treat prostate cancer

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50
Q

What is the mechanism of action of Trastuzumab?

A

HER-2 receptor antagonist

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51
Q

What is the unique side effect seen with Trastuzumab?

A

Cardiotoxicity

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52
Q

What is the mechanism of action of Cetuximab?

A

EGFR antagonist used to treat COLON CANCER

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53
Q

Activating mutation of what proto-oncogene limits the efficacy of Cetuximab?

A

Ras

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54
Q

What is the mechanism of action of Bevacizumab?

A

VEGF inhibitor

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55
Q

What is the mechanism of action of Lapinotab?

A

EGFR and HER-2blocker (downstream target) used for REFRACTORY BREAST CANCER

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56
Q

What is the mechanism of action of Erlotinib?

A

EGFR receptor blocker used for NON SMALL CELL LUNG CANCER

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57
Q

What is the unique side effect associated with Asparaginase?

A

Anaphylaxis

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58
Q

What is the mechanism of action of Bortezomib?

A

Proteasome inhibitor that increases p53

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59
Q

What is the unique adverse effect associated with Bortezomib?

A

Peripheral neuropathy

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60
Q

What is the mechanism of action of Temsirolimus?

A

mTOR1 inhibitor

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61
Q

What are the unique adverse effects seen with Temsirolimus?

A

Hyperglycemia

Triglyceridemia

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62
Q

Which antineoplastic agents are nephrotoxic?

A

Cisplastin

Methotrexate

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63
Q

Which antineoplastic agents are neurotoxic?

A 
Vincristine 
Cytarabine
Cisplastin
Bortezomib 
Paclitaxel
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64
Q

Which antineoplastic agents are cardiotoxic?

A

Doxorubicin

Trastuzumab

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65
Q

Which antineoplastic agents cause bladder toxicity?

A

Cyclophosmphamide

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66
Q

Which antineoplastic agents cause hypersensitivity reactions/ anaphylaxis?

A

Asparaginase

Paclitaxel

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67
Q

List the ADP receptor antagonists/ P2Y12 antagonists.

A

Clopidegril
Prasugrel
Ticagrelor
Cangrelor

68
Q

Which ADP receptor antagonists are irreversible?

A

Clopidegril

Prasugel

69
Q

Which ADP receptor antagonists are reversible?

A

Ticagrelor

Cangrelor

70
Q

Which ADP receptor antagonists have been shown to be more efficacious? What is their drawback?

A

Prasugrel
Ticagrelor

Despite being more efficacious, also associated with more bleeding

71
Q

What CYP enzyme metabolizes Clopidegril?

72
Q

What is the clinical significance of CYP2C19?

A
  • Highly polymorphic

- Inhibited by omeprazole i.e. omeprazole increases the efficacy of Clopidegril

73
Q

List the GPIIb/IIIa antagonists. Which of these are a Fab antibody, peptide, and non-peptide small molecule?

A 
Abciximab - Fab antibody 
Integrelin 
Eptifabitide- peptide
Tirofiban- non-peptide small molecule 
Lamifiban
74
Q

What are the adverse effects seen with GPIIb/IIIa administration?

A

Thrombocytopenia

Bleeding

75
Q

What is the mechanism of action of Voraxapar?

A

PARR antagonist

76
Q

What is the adverse effect associated with Voraxapar?

A

Intracranial bleeding

**Note that this drug is contraindicated in patients with a history of intracranial bleeding

77
Q

What is dual anti-platelet therapy? Triple?

A 
Dual= ASA and clopidegril 
Triple= + Warfarin
78
Q

List the indirect thrombin/ Factor X inhibitors. What is the difference between these three drugs?

A

Heparin
Enoxaparin - LMWH
Fondapainaux - Pentasaccharide

79
Q

What are the adverse effects associated with Heparin?

A

Bleeding
Osteoporosis
HIT

80
Q

What drug reverses Heparin?

81
Q

List the direct thrombin inhibitors.

A

Lepirudin
Bivalrudin
Argatraban
Dabigatran (oral)

82
Q

Which of the direct thrombin inhibitors is divalent? What does this mean?

A

“rudins” –> block the active site and E1 site on Thrombin

83
Q

Which of the direct thrombin inhibitors is monovalent? What does this mean?

A

“an’s” –>block only the active site

84
Q

List the direct Factor Xa inhibitors.

A

Rivaroxaban

Apixaban

85
Q

What enzyme metabolizes Warfarin?

86
Q

List the fibrinolytic drugs.

A

Streptokinase
Alteplase
Reteplase
Tenectaplase

(t-PA)

87
Q

What are the unique adverse effects seen with Streptokinase administration?

A

Tolerance

Hypersensitivity reaction

88
Q

What drugs can reverse fibrinolytic therapy?

A

Aminocaproic acid

Tranexamic acid

89
Q

Draw the general pathway of cholesterol metabolism.

90
Q

What drug blocks NPC1L1?

91
Q

What is the function of Apo C-II?

A

Activation of LPL

92
Q

What is the transporter that get cholesterol from the periphery into HDL?

93
Q

What disorder is characterized by decreased LPL expression or function?

A

Primary Chylomicronemia

94
Q

What is the manifestation of Primary Chylomicronemia?

A

Increased chylomicrons and VLDL

95
Q

Which drugs are best at treating Primary Chylomicronemia?

A

Fibrates and Niacin

96
Q

What disease is characterized by decreased Apo E function of expression?

A

Dysbetalipoproteinemia

97
Q

What is the manifestation of Dysbetalipoproteinemia?

A

Increased IDL and chylomicron remnants

98
Q

What is the best therapy for Dysbetalipoproteinemia?

A

Fibrates and Niacin

99
Q

What disease is characterized by decreased apo C-II function or expression?

A

Familial Hypertriglyceridemia

100
Q

What is the manifestation of Familial Hypertriglyceridemia ?

A

Increased Chylomicrons and VLDL

101
Q

What is the best therapy for Familial Hypertriglyceridemia ?

A

Fibrates and Niacin

102
Q

What disease is characterized by decreased LDLR function or expression?

A

Familial Hypercholesterolemia

103
Q

What is the manifestation of Familial Hypercholesterolemia?

A

Increased LDL

104
Q

What is the best therapy for Familial Hypercholesterolemia?

A

Statins
Ezetimibe
Bile acid binding resins
Niacin

105
Q

What is the effect of decreased Apo-B 100 function of expression?

A

Increased LDL

106
Q

What is the best treatment for an ApoB-100 defect?

A

Statins
Ezetimibe
Bile acid binding resins
Niacin

107
Q

List the Fibrates.

A

Gemfibrozil

Fenofibrate

108
Q

What is the mechanism of action of the Fibrates?

A

PPAR activation

109
Q

List the bile acid binding resins.

A

Cholestyramine
Cholesevelam
Colestipol

110
Q

What is the mechanism of action of Niacin?

A

Inhibition of adipocyte hormone sensitive lipase

111
Q

List the statins.

A 
Atorvastatin
Rouvastatin
Lovastatin
Pitastatin 
Simvastatin
Flouvastatin
112
Q

What are the indications for Quinidine?

A

Refractory:

  • A-fib/flutter
  • Life threatening ventricular arrhythmia
113
Q

What are the indications for Procainamide?

A

1) Re-entry SVT
2) A-fib
3) A-flutter with WPW
4) Life threatening ventricular arrhythmia

114
Q

What are the indications for Lidocaine?

A
  • Post MI arrhythmia

- Digitalis induced arrhythmia

115
Q

What are the indications for Propafenone?

A

1) PSVT
2) Atrial arrhythmia
3) Ventricular arrhythmia in patients WITHOUT heart disease

116
Q

What are the indications for Amiodarone?

A

1) Acute conversion of VT or VF
2) A-fib
3) AVNRT
4) WPW

117
Q

What are the indications for Verapamil?

A

1) SVT
2) A-fib with RVR
3) Angina
4) HTN

118
Q

What are the contraindications to Verapamil?

A
  • Conduction block
  • WPW + a-fib
  • Ventricular Tachycardia
119
Q

What are the adverse effects seen with Adenosine administration?

A

1) Bradycardia/ heart block
2) Flushing
3) Dyspnea
4) Hypotension (A2 mediated vasodilation)

120
Q

What are the indications for Acetazolamide?

A

1) Glaucoma
2) Acute Mountain Sickness
3) Urinary Alkalization
4) Edema

121
Q

What are the adverse effects of Acetazolamide?

A
  • Hyperchloremic metabolic acidosis
  • Renal stones
  • Renal K+ loss
122
Q

What are the contraindications for Acetazolamide?

123
Q

What are the indications for osmotic diuretics?

A

1) Prophylaxis for acute renal failure
2) Cerebral edema
3) Dialysis disequilibrium
4) Acute glaucoma

124
Q

What are the adverse effects of osmotic diuretics?

A
  • Pulmonary edema

- Hypo/hypernatremia

125
Q

List the loop diuretics.

A

Furosemide
Bumetanide
Ethacrynic acid

126
Q

What are the indications for loop diuretics?

A

1) Pulmonary edema
2) CHF
3) Acute renal failure
4) Hyperglycemia

127
Q

What are the adverse effects of the loop diuretics?

A
  • Hypokalemia, natremia, calcemia, magnesia
  • Ototoxicity
  • Hyperuricemia
128
Q

List the Thiazide diuretics?

A

Chlorathalidone
Hydrochlorothiazide
Metalazone
Indapamide

129
Q

What is unique about the Thiazide diuretics in terms of ion secretion/ absorption?

A

Stimulation of PTH causes Ca++ REABSORPTION

130
Q

What are the indications for Thiazide diuretics?

A

HTN
CHF
Hypercalciuria/ renal stones
Nephrogenic DM Insipidus

131
Q

List the K+ sparing diuretics.

A

Amiloride

Triamtrene

132
Q

What is the MOA of K+ diuretics?

A

Block epithelial Na+ channels on principal cells; thus, K+ is NOT secreted

133
Q

What are the indications for the K+ diuretics?

A
  • Hypokalemic alkalosis

- Combination therapy to prevent hypokalemia

134
Q

List the Aldosterone antagonists.

A

Spironolactone

Eplerenone

135
Q

What are the indications for Aldosterone antagonists?

A

1) Edema
2) CHF
3) HTN
4) Primary or secondary hyperaldosteronism

136
Q

What are the adverse effects of the aldosterone antagonists?

A
  • Hyperkalemia
  • Metabolic acidosis in cirrhosis
  • Hormonal effects (gynecomastia, impotence…etc.)
137
Q

What are the contraindications for ACE inhibitors?

A

1) Pregnancy
2) Bilateral renal artery stenosis
3) Angioedema

138
Q

Under what circumstances will ACE inhibitors have an increase in favorable effects?

A
  • Low K+ or hypokalemia
  • Pre-DM
  • Albuminuria
139
Q

Under what circumstances will ACE inhibitors have an unfavorable effects?

A
  • High K+ or hyperkalemia

- Volume depletion

140
Q

What are the adverse effects of ACE inhibitors?

A 
C= cough
A= angioedema 
P= potassium (increased) 
T= taste change 
O= hypOtension
P= pregnancy--> fetopathic 
R= rash 
i
l
141
Q

List the ACE inhibitors.

A

Lisinpril
Captopril
Fosinopril

142
Q

What are the contraindications for ARB therapy?

A

Pregnancy

Bilateral renal artery stenosis

143
Q

List the ARBs.

A

Losartan
Valsartan
Candesartan

144
Q

What is the role of DHP Ca++ blockers in HTN?

A

1) First line or add on therapy for uncomplicated

2) Add on therapy for DM and CAD

145
Q

When should DHP Ca++ blockers be avoided?

A

LV dysfunction

146
Q

List the DHP Ca++ blockers used in anti-HTN therapy.

A

Nifedipine
Amlodipine
Felodipine

147
Q

Under what circumstances can DHP Ca++ therapy have increased favorable effects?

A

1) Reynaud Syndrome
2) Elderly patient with isolated systolic HTN
3) Cyclosporine induced HTN

148
Q

Under what circumstances can DHP Ca++ therapy unfavorable effects?

A
  • Peripheral edema

- Tachycardia

149
Q

What is the role of NDPH Ca++ blockers in HTN?

A

1) First line or add on for uncomplicated HTN
2) Add on for DM
3) Alternative to Beta-blockers in CAD

These drugs will DECREASE myocardial oxygen consumption*

150
Q

When should NDHP Ca++ blockers be avoided?

A
  • AV block

- LV dysfunction

151
Q

Under what circumstances can NDHP Ca++ therapy have increased favorable effects?

A

1) Reynaud Syndrome
2) Migraine
3) Arrhythmia
4) Tachycardia

152
Q

Under what circumstances can NDHP Ca++ therapy unfavorable effects?

A
  • Peripheral edema
  • Bradycardia
  • AV block
153
Q

When are Thiazide diuretics first-line therapy in HTN?

A

1) LV dysfunction

2) S/p CVA

154
Q

When should Thiazide diuretics be avoided?

A

1) Allergy to Sulfa
2) Gout
3) Hyponatremia
4) Hypokalemia
5) Pre-DM/ elevated fasting glucose

155
Q

What comorbid conditions should Thiazide diuretics be used in, if a patient has HTN?

A
  • Osteoporosis b/c of increased Ca++ reabsorption

- Hyperkalemia b/c of K+ excretion

156
Q

When are Beta blockers first line therapy for patients with HTN?

A

CAD and LV dysfunction

157
Q

Are aldosterone antagonists first line therapy or add on therapy?

A

Add on therapy

158
Q

What situations should aldosterone antagonists be used as add on therapy?

A

Resistant HTN
CAD
LV Dysfunction

159
Q

In addition to their normal use, when is aldosterone antagonist therapy beneficial?

A

Hypokalemia

CKD

160
Q

What is the role of alpha-1 antagonists in HTN therapy?

A
  • Used in conjunction w/ diuretics

- Lower cholesterol and trigylcerides

161
Q

List the central alpha 2 agonists.

A

Clonidine

A-methyldopa

162
Q

What adverse effects are seen with alpha-methyldopa?

A

1) Hepatotoxicity

2) Positive direct coombs test

163
Q

What is the mechanism of action of Hydralazine?

A
  • Arterial vasodilation by blocking IP3 induced Ca++ release
  • Opens K+ channels to hyperpolarize vascular smooth muscle
164
Q

What is the role of Hydralazine in HTN therapy?

A
  • Add on for resistant HTN esp. in CKD

- SAFE in pregnancy

165
Q

What enzyme activates organic nitrates?

A

Mitochondiral aldehyde reductase

Pharmacology (64 decks)

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