Pharmacology Test 2

Front 1

List four ways to treat cancer

Back 1

Surgery
Radiation
Chemotherapy
Biologic therapy

Front 2

In order to decrease recurrence of cancer and prolong survival this type of therapy begins with radiation or surgery used to remove the macroscopic disease followed with chemotherapy to destroy microscopic malignant cells

Back 2

Adjuvant therapy

Front 3

In order to lower risk to the patient in this type of therapy chemotherapy is given prior to surgery to shrink the tumor size

Back 3

Neoadjuvant therapy

Front 4

What are the goals of palliative therapy?

Back 4

-increase quality of life
-relieve symptoms
-prolong survival

Front 5

What labs are assessed before dosing chemotherapy

Back 5

WBC count
Hgb/Hct
Platelet count
Creatinine clearance

Front 6

Most chemotherapy dosing is based on the patient's ____________.

Back 6

Body Surface Area (BSA)

Front 7

What are the basis for selecting chemotherapy regimes (5)?

Back 7

-Single agent activity against a specific tumor
-Different mechanisms of action
-No overlapping toxicities
-Optimal dose and schedule
-Different patterns of resistance

Front 8

What is the acronym for selecting chemotherapy regimes?

Back 8

S- Single/specific agent/tumor
M- Mechanism of action differ
O- Overlapping toxicities avoided
O- Optimum dosing and schedule
R- Resistance patters differ

Front 9

List three ways chemotherapy kills cancer cells.

Back 9

1. Damaging DNA
2. Interferes with DNA synthesis
3. Inhibits cell divsion

Front 10

List five chemotherapy precautions.

Back 10

1. Pregnancy
2. Myelosuppression
3. Alopecia
4. Nausea and vomiting
5. Drug interactions

Front 11

Adverse effects of these chemotherapy agents include myelosuppression, extreme nausea and vomiting and hemorrhagic cystitis

Back 11

Alkylating agents

Front 12

These two compounds cause hemorrhagic cystitis

Back 12

cyclophosphamide and ifosfamide

Front 13

With these agents cytotoxicity of the cancer cells results from inhibition of DNA replication beacuse interlinked strands do not seperate

Back 13

Alkylating agents

Front 14

Busulfan, cyclophosphamide, ifosfamide, carmustine, lomustine, dacarbazine, temozolomide, procarbazine, thiotepa

Back 14

Alkylating agents

Front 15

These chemotherapy agents act as a decoy to prevent the cells from carrying out vital functions such as cell replication for growth and division yet cannot be used by the body in a productive manner

Back 15

Antimetabolites

Front 16

List the three types of antimetabolites.

Back 16

Folate antagonists
Purine antagonists
Pyrimidine antagonists

Front 17

Methotrexate
Pemetrexed

Back 17

Antimetabolite
Folate antagonist

Front 18

6-Mercaptopurine
6-Thioguanine
Fludarabine
Cladribine

Back 18

Antimetabolite
Purine antagonists

Front 19

Fluorouracil
Cytarbabine
Gemcitabine
Capecitabine

Back 19

Antimetabolite
Pyrimidine antagonists

Front 20

Adverse effects of this type of chemotherapy include myelosuppresion (neutropenia, anemia, thrombocytopenia), nausea, vomiting and diarrhea, mucositis, hepatotoxicity, neurotoxicity, and Hand in Foot syndrome

Back 20

Antimetabolites

Front 21

List drugs that may block tubular secretion of methotrexate.

Back 21

Probenecid
salicylates
penicillin
ketoprofen

Front 22

What can be given with high doses of methotrexate to minimize adverse effects?

Back 22

Leucovorin (folinic acid) rescue

Front 23

High doses of this chemotherapy agent may cause damage to this organ.

Back 23

Methotrexate
Folate antagonist
Antimetabolite

Front 24

T/F Methotrexate is removed from the body via the liver.

Back 24

False. Approximately 60-100% of methotrexate is removed from the body by the kidneys as unchanged drug.

Front 25

These chemotherapy agents inhibit mitosis by disrupting the microtubule functions which are most active during the M phase of the cell cycle

Back 25

Antimicrotubules

Front 26

Adverse effects of this type of chemotherapy agent include peripheral neuropathy though nausea and vomiting are less than with other agents

Back 26

Antimicrotubules

Front 27

These chemotherapy agents cause constipation

Back 27

Vinca alkaloids

Front 28

These M phase chemotherapy agents cause mylosuppression

Back 28

Taxanes

Front 29

This type of chemotherapy agents has many drug interactions with CYP3A4

Back 29

Antimicrotubles

Front 30

Docetaxel
Paclitaxel

Back 30

Taxanes
Antimicrotubules

Front 31

Vinblastine
Vincristine
Vinorelbine

Back 31

Vinca alkaloids
antimicrotubules

Front 32

These chemotherapy agents are FATAL if given within the subarachnoid or subdural space.

Back 32

Vinca alkaloids
antimicrotubles

Front 33

Due to the binding action of these chemotherapy agents DNA can still uncoil for replication but will not be able to reform into double helix due to DNA strand breaks

Back 33

Topoisomerease inhibitors

Front 34

List the three topoisomerase inhibitors.

Back 34

Camptothecins
Epipolophyllotoxins
Anthracyclines

Front 35

Irinotecan
Topotecan

Back 35

Camptothecins
tropoisomerase inhibitors

Front 36

Etoposide (VP-16)
Teniposide

Back 36

Epipolophyllotoxins
topoisomerase inhibitors

Front 37

These chemotherapy agents combine with oxygen to form superoxide, a free radical, which can make hydrogen peroxide

Back 37

Anthracyclines
topoisomerase inhibitors

Front 38

These chemotherapy agents cause cardiac damage and extravasation (CHF and cardiomyopathy symptomotology)

Back 38

Anthracyclines
topoisomerase inhibitors

Front 39

Daunorubicin
Doxorubicin
Epirubicin
Idarubicin
Mitoxantrone

Back 39

Anthracyclines
topoisomerase inhibitors

Front 40

This chemotherapy drug requires aggressive antiemetic regimens and proper hydration to prevent nephrotoxicity and electrolyte abnormalities

Back 40

Cisplatin
Platinum drug

Front 41

If a patient is not tolerating cisplatin you could consider this similar drug.

Back 41

Carboplatin

Front 42

This chemotherapy drug causes a cold induced neuropathy.

Back 42

Oxaliplatin

Front 43

This chemotherapy drug is associated with pulmonary toxicity.

Back 43

Bleomycin

Front 44

These immune therapy agents enhance the immune systems attack on cancer cells, decrease blood vessel formation and augment expression of antigen on tumor cell surfaces

Back 44

Interferons

Front 45

This immune therapy agents causes flu-like symptoms.

Back 45

Interferons

Front 46

This immune therapy agent promotes B and T cell proliferation and triggers a cytokine cascade to attack tumors.

Back 46

Aldesleukin (Interleukin-2)

Front 47

Denileukin Difitox

Back 47

Immune therapy

Front 48

These antibodies are produced against a specific antigen.

Back 48

Monoclonal antibodies

Front 49

the "-mabs"

Back 49

Monoclonal antibodies

Front 50

Syllable source indicator for monoclonal antibodies (U)

Back 50

U = human
alemtuzumab

Front 51

Syllable source indicator for monoclonal antibodies (O)

Back 51

o = mouse
tositumomab

Front 52

Syllable source indicator for monoclonal antibodies (A)

Back 52

a = rat

Front 53

Syllable source indicator for monoclonal antibodies (E)

Back 53

e = hamster

Front 54

Syllable source indicator for monoclonal antibodies (I)

Back 54

i = primate

Front 55

Syllable source indicator for monoclonal antibodies (Xi)

Back 55

Xi = cross between human and animal source
ceftuximab

Front 56

What might you pretreat a patient with before giving monoclonal antibodies?

Back 56

Acetaminophen and diphenhydramine to prevent or minimize allergic reactions

Front 57

Adverse effects of these types of chemotherapy agents include myelosuppresion, severe diarrhea, nause and vomiting, mucositis and secondary leukemia.

Back 57

topoisomerase inhibitors

Front 58

This chemotherapy drug is associated with secondary leukemia

Back 58

etoposide
topoisomerase inhibitor

Front 59

What are the JNC 7 diagnostic lab values for chronic kidney disease?

Back 59

GFR <60ml/sec
Serum Creatinine >1.3mg/dl in women
Serum Creatinine >1.5mg/dl in men
Albuminuria

Front 60

Name three drugs that cause HTN.

Back 60

Oral contraceptives
NSAIDs
Nasal decongestants
Steroids
Appetite suppressants
Venaflaxine (Effexor)
Cyclosporine

Front 61

First line treatment of patients in heart failure? Second line treatment? Third Line treatment?

Back 61

1 = ACEi + diuretic
2 = BB
3 = ARB or aldosterone agonist

Front 62

First line treatment of patients post MI? Second line treatment? Third Line treatment?

Back 62

1 = BB + ACEi
2 = aldosterone antagonist

Front 63

First line treatment of patients with DMII? Second line treatment? Third Line treatment?

Back 63

1 = ACEi or ARB
2 = Diuretic
3 = BB or CCB

Front 64

First line treatment of patients with high CVD risk? Second line treatment? Third Line treatment?

Back 64

1 = BB
2 = ACEi, CCB or diuretic

Front 65

First line treatment of patients with CKD? Second line treatment? Third Line treatment?

Back 65

1 = ACEi or ARB

Front 66

First line treatment of patients needing recurrent stroke prevention? Second line treatment? Third Line treatment?

Back 66

1 = Diuretic + ACEi

Front 67

List factors indicating high CVD risk.

Back 67

Hypertension
Cigarette smoking
Obesity (BMI ≥ 30)
Physical inactivity
Dyslipidemia
Diabetes mellitus
Microalbuminuria or CrCl < 60 mL/min
Age >55 years for men or >65 years for women
Family history of premature CVD (<55 years for men or <65 years for women)

Front 68

List the classes of diuretics.

Back 68

Carbonic anhydrase inhibitors
Thiazides
Loop
Potassium-sparing
Aldosterone antagonists

Front 69

Hydrochlorothiazide

Back 69

Thiazide

Front 70

Patient has CrCl of 20ml/min. Will HCTZ be effective?

Back 70

HCTZ is ineffective in patients with CrCl < 30ml/min such as in CKD.

Front 71

A patient on HCTZ complains of muscle fatigue and a 'funny' heartbeat. What might be the cause?

Back 71

HCTZ can cause hypokalemia

Front 72

List two signs of hypokalemia.

Back 72

Muscle fatigue
Arrhythmias

Front 73

Patient on HCTZ complains of joint pain. What could be the problem.

Back 73

HCTZ can cause hyperuricemia leading to gout.

Front 74

T/F Hyperglycemia and hyperlipidemia in a patient taking an HCTZ is of little concern.

Back 74

True - HCTZ leads to transient and inconsequential hyperglycemia and hyperlipidemia

Front 75

Your patient suffers from a bi-polar disorder. What drug might you be concerned about when prescribing HCTZ?

Back 75

HCTZ can lead to lithium toxicity

Front 76

What would you prescribe in a patient needing a diuretic but with a CrCl = 20mL/min?

Back 76

Loop diuretics are kidney sparing whereas HCTZ is contraindicated in pts with CKD.

Front 77

A patient complains of difficulty breathing and a rash shortly after taking Lasix. What may be happening?

Back 77

Hypersensitivity reaction to the 'sulfa' that is in all loop diuretics.
Exception: ethacrynic acid

Front 78

Why should you monitor the levels of loop diuretics carefully?

Back 78

Ototoxicity

Front 79

Unlike HCTZ which can be a treatment for osteoperosis loop diuretics can cause problems with bones because of this ADE.

Back 79

hypocalcemia

Front 80

Check potassium levels in patients using these drugs and consider potassium supplementation.

Back 80

HCTZ and loop diuretics

Front 81

List three contraindications for HCTZ or loops.

Back 81

1. Anuria
2. Severe renal or hepatic disease
3. Sulfa or thiazide sensitivity

Front 82

List three drug interactions with HCTZ or loops.

Back 82

1. NSAIDs
2. Lithium
3. Potassium losing meds (digoxin and corticosteroids)

Front 83

triamterene (Thiazide)

Back 83

Potassium sparing diuretic

Front 84

What are some signs of hyperkalemia?

Back 84

Muscle cramps
Rash
Dizziness

Front 85

What are compelling indications for the development of hyperkalemia?

Back 85

CKD
DMII
ACEi or ARB
NSAIDs
potassium supplements

Front 86

spironolactone (Aldactone)

Back 86

Aldosterone antagonist

Front 87

What class of diuretic would you consider for patients in whom the risk of hypokalemia would pose a significant clinical risk.

Back 87

Aldosterone antagonists
(spironolactone)

Front 88

Other than hyperkalemia, list the possible ADEs associated with aldosterone antagonists.

Back 88

Antiandrgen effects
-gynecomastia
-decreased libido
-impotents
-menstrual irregularities
-hair growth in women

Front 89

"-pril"

Back 89

ACEi
Captopril
Lisinopril
Ramipril

Front 90

Captopril
Lisinopril
Ramipril

Back 90

ACEi

Front 91

telmisartan (Micardis)
valsartan (Diovan)

Back 91

ARBs

Front 92

List the compelling indications for CVD that would indicate the need for an ACEi.

Back 92

- HF
- post MI
- CKD
- DM
- recurrent stroke prevention

Front 93

If patients have stage 1 HTN and thiazide monotherapy is unsuccessful what is the next step?

Back 93

ACEi or ARB

Front 94

T/F Compelling indications for CVD NOT indicated for ARBs include?

Back 94

- post MI
- recurrent stroke therapy

Front 95

T/F ACEi should not be used in patients with renal disease.

Back 95

False - ACEi are renal protective

Front 96

In addition to hyperkalemia, neutropenia, proteinuria and angioedema what ADE is most likely to present in patiens taking an ACEi?

Back 96

dry cough

Front 97

ACEi and ARBs are contraindicated in the following (2)...

Back 97

-pregnancy
-angioedema

Front 98

List the mechanism(s) of action for beta blockers.

Back 98

1. block andrenergic receptors in the heart which decrease heart rate
2. block renin which limits the RAAS system and leads to decreased blood volume

Front 99

Where are beta-1 receptors located primarily.

Back 99

Heart and kidneys

Front 100

Where are beta-1 AND beta-2 receptors located?

Back 100

Heart
Kidneys
Lungs
Pancreas
Arteriolar smooth muscle

Front 101

Atenolol
Metoprolol (Lopressor)

Back 101

Cardioselective BB

Front 102

Propranolol

Back 102

Noncardioselective BB

Front 103

Propronaolol has been associated with this disease.

Back 103

glaucoma

Front 104

You patient is experiencing syncope after you prescribed atenolol. What might you consider as an alternate therapy?

Back 104

A BB with intrinsic sympathomemetic activity (ISA) prevents bradycardia

Front 105

Mixed alpha and beta blocker?

Back 105

carvedilol (Coreg)
labetolol

Front 106

What would you prescribe for a patient with Stage 2 HTN?

Back 106

HCTZ and BB as initial therapy.

Front 107

Your patient has concomitant heart failure and is taking a loop and ACEi. What might you consider adding if HTN is still not controlled?

Back 107

BB

Front 108

Patient with DM has HTN that is not responding to ACEi and HCTZ. What might you consider adding?

Back 108

BB or CCB

Front 109

This beta blocker is most lipophilic ____________ whereas ___________ is least lipophilic.

Back 109

propranolol / atenolol

Front 110

A patient taking this medication for HTN could experience CNS problems because the drug is lipophilic.

Back 110

propranolol (BB)

Front 111

These two beta blockers undergo extensive first pass metabolism.

Back 111

propranolol and metoprolol

Front 112

List ADEs with BB

Back 112

- bradycardia
- acute exacerbation of bronchospasms
- masking hypoglycemia
- ED

Front 113

T/F If a patient with COPD begins experiencing breathing problems after several months of therapy with a high dose beta block you should d/c the drug immediately.

Back 113

False - beta blockers should be tapered when d/c to avoid rebound hypertension.

Front 114

CCB mechanism of action is to inhibit passage of calcium through voltage-gated L-type calcium channels at these two sites.

Back 114

vascular smooth muscle
cardiac myocytes

Front 115

"-pine"

Back 115

CCB

Front 116

Amlodipine
Nifedipine

Back 116

DHP CCBs

Front 117

Diltiazem
Verapamil

Back 117

Non-DHP CCBs

Front 118

Patient presents with reflex tachycardia, dizziness, flushing and peripheral edema. Name the possible drug ADE?

Back 118

DHP CCB

Front 119

Patient presents with gingival hyperplasia. Name the possible drug ADE.

Back 119

DHP CCB

Front 120

Non DHP CCBs are contraindicated with which drug(s)?

Back 120

-simvastatin
-digoxen
-cyclosporine
-lovastatin

Front 121

Doxazosin (Cardura)

Back 121

Alpha-1 blocker

Front 122

This drug can lead to symptomatic benefits in men with BHP.

Back 122

alpha-1 blocker
"-zosin"

Front 123

According to the ALLHAT study, patients taking this drug may have higher incidence of stroke, HF and CV events.

Back 123

Alpha-1 blockers

Front 124

Patients presenting with priapism may be taking this drug.

Back 124

Alpha-1 blocker

Front 125

Avoid use of this drug in elderly patients due to increased risk of orthostatic hypotension.

Back 125

Alpha-1 blockers

Front 126

List the reactions of the first dose phenomenon in alpha-1 blockers

Back 126

- dizziness
- faintness
- palpitations
- syncope

Front 127

Clonidine (catapres)

Back 127

alpha-2 agonist

Front 128

When treating resistant HTN consider this drug.

Back 128

clonidine

Front 129

Consider this alpha-2 blocker in pregnancy but watch for this ADE.

Back 129

methyldopa/hepatitis

Front 130

Patients taking alpha-2 blockers have low adherence because of the following ADEs...?

Back 130

-sodium/water retention
-sedation
-dry mouth
-depression
-dizziness
-constipation
-urinary retention
-blurred vission
-rebound HTN when d/c

Front 131

An African American woman unresponsive to ACEi and ARB has concomitant HF?

Back 131

Diuretic + Hydralazine

Front 132

Hydralazine
Minoxidil

Back 132

Direct vasodilators

Front 133

Patient presents with lupus-like syndrome (SLE). Which drug would you d/c?

Back 133

Hydralazine

Front 134

Patient presents with SLE. What drug would you d/c and replace with?

Back 134

Hydralazine/minoxidil

Front 135

Guanadrel
Guanethidine
Reserpine

Back 135

Peripheral adrenergic antagonists

Front 136

What is the standard therapy for African Americans with HTN

Back 136

-Thiazide
-BB or CCB
-ACEi (hit-n-miss)

Front 137

T/F If monotherapy yeilds only a partial response in HTN then d/c and try a drug from another class.

Back 137

False. For partial response continue current therapy and add a drug from another class.

Front 138

List possible TOD due to HTN

Back 138

-encephalopathy
-intracranial hemorrhage
-accute LVF + pulmonary edema
-dissecting aortic aneurysm
-unstable angina
-eclampsia

Front 139

What is the difference between 'urgency' and 'emergency' in HTN?

Back 139

Both BP > 180/120
Urgency = no TOD
Emergency = TOD

Front 140

Treatment of HTN emergency?

Back 140

-sodium nitroprusside
-nicardipine (CCB)
-fenoldopam
-nitroglycerin
-enalaprilat (ACEi)
-hydralazine
-labetolol
-Esmolol

Front 141

Treatment of HTN urgency?

Back 141

-adjust current therapy
-consider clonidine (alpha-2 agonist)

Front 142

List the mechanisms of HMG-CoA reductase inhibitors.

Back 142

-lowers LDL-c
-upregulates LDL receptors in the liver

Front 143

List pleotropic effects of statins

Back 143

-anti-inflammatory
-improved endothelial function
-increased Nitric Oxide availability
-antioxidant
-stabilization of plaques
-reduction of plaque progression
-antithrombotic effects

Front 144

simvastatin
atorvastatin
rosuvastatin

Back 144

HMG-CoA reductase inhibitors

Front 145

Patient is on multiple drugs metabolized by CYP system. What statins would you avoid and what statins would you consider?

Back 145

Avoid: atorvastatin, lovastatin and simvastatin
Consider: rosuvastatin or pravastatin

Front 146

Unlike simvastatin that should be taken PM due to a short half-life, this statin has a longer half-life and can be taken in the AM.

Back 146

rosuvastatin

Front 147

Patients may have elevated liver enzymes 3x's the normal limit when taking this class of drug.

Back 147

statins

Front 148

Elderly patient with hypothyroidism complains of muscle pain. What drug would you consider d/c?

Back 148

statin

Front 149

Contraindicated drugs with BAS: cholestyramine and colestipol...

Back 149

-Take prevastatin 1 hour before or 3 hours after BAS
-Do not take fluvastatin within 4 hours of BAS

Front 150

This drug increases the risk of myopathy and rhabdomyolysis when used with many statins.

Back 150

gemfibrozil

Front 151

This drug inhibits intestinal absorption of cholesterol working at the brush border of the small intestine.

Back 151

ezetimibe (Zetia)

Front 152

Possible drug interactions with ezetimibe?

Back 152

cyclosporine
warfarin

Front 153

cholestyramine
colestipol
colesevelam

Back 153

Bile acid sequestrants (BAS)

Front 154

Describe the mechanism of action for BAS.

Back 154

BAS block the reabsorption of bile acids in the intestines leading to reduced LDL-c and upregulation of LDL receptors

Front 155

Patient complains of constipation, flatulence and steatorrhea (fatty stool). What drug might you d/c?

Back 155

BAS
colesevalem

Front 156

Patient is found to have a vitamin K deficiency leading to bleeding. What drug would you d/c?

Back 156

BAS
colesevalem

Front 157

T/F All BAS delay or reduce absorption of other drugs.

Back 157

Though cholestyramine and colestipol both in powder form affect absorption colesevalem is in pill form and does not affect absorption of other drugs

Front 158

Patient has hypertriglyceridemia?

Back 158

Fibric Acid
gemfibrozil or fenofibrate

Front 159

These drugs activate peroxisome proliferator activated receptor alpha. Activation of this receptor leads to an increase in lipolysis and elimination of triglyceride-rich particles through the activation of lipoprotein lipase and reduction in the production of apoprotein C-3.

Back 159

Fibric acid
gemfibrozil and fenofibrate

Front 160

List the mechanism of elimination for fenofibrate and gemfibrozil.

Back 160

fenofibrate - excreted in the urine as metabolites
gemfibrozil - hepatic metabolism

Front 161

What do you tell a patient that asks, "When should I take gemfibrozil?"

Back 161

Take 30 minutes before meals

Front 162

When initiating therapy with fibric acid derivatives you may see an increase in ___________.

Back 162

Serum creatinine

Front 163

Use of gemfibrozil with statins may cause...?

Back 163

Increased myopathy

Front 164

Use of gemfibrozil with ezetimibe may cause...?

Back 164

gallstones

Front 165

Use of gemfibrozil with warfarin may cause...?

Back 165

increased risk of bleeding

Front 166

Use of gemfibrozil with prandin may cause...?

Back 166

hypoglycemia

Front 167

What is the correct dosing for gemfibrozil in an adult.

Back 167

600 mg twice daily at least 30 minutes prior to morning and evening meals.

Front 168

T/F NKF recommends gemfibrozil as preferred fibrate in patients with CKF of kidney transplant.

Back 168

True

Front 169

If you want to increase a patient's HDL you would consider this drug.

Back 169

Nicotinic acid (niacin)

Front 170

What is the most common side effect of niacin and how can it be prevented?

Back 170

flushing/asprin 30-45 minutes before dose

Front 171

What mechanism causes flushing with the administration of niacin?

Back 171

release of prostaglandin D

Front 172

Consider a risk benefit analysis when prescribing this drug to patients with DM because of an increased risk of hyperglycemia.

Back 172

niacin

Front 173

Lovaza

Back 173

Prescription form of Omega-3 fatty acids

Front 174

Though this medication decreases triglycerides it may increase HDL.

Back 174

Lovaza (Omega-3 fatty acids)