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Pharmacology > Final Exam > Flashcards

Final Exam Flashcards

1
Q

principal endogenous estrogen

A

estradiol

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2
Q

principal progestational hormone

A

progesterone

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3
Q

days 1-14 of cycle

A

follicular phase, dominated by estrogen

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4
Q

days 14-28 of cycle

A

luteal phase, dominated by progesterone

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5
Q

raloxifene effects on bone density, breast cancer, CV, & uterine cancer

A

raloxifene- SERM
positive effects on bone density and breast cancer risk
increases risk of CV events
does not increase risk of uterine cancer

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6
Q

estrogen/bazedoxifine

A

combined estrogen and estrogen receptor agonist/antagonist
prescribed for vasomotor symptoms, osteoporosis prevention
PROTECTS ENDOMETRIUM

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7
Q

effects of adding progestin to HRT

A

protects against endometrial cancer
stimulates breast cancer risk
depression
breast tenderness

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8
Q

Women who still have a uterus must have what added to their estrogen HRT therapy?

A

progestin

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9
Q

chlorphiramine

A

first gen antihistamine

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10
Q

clemastine

A

first gen antihistamine

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11
Q

fexofenadine (allegra)

A

second generation antihistamine

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12
Q

cetirizine

A

second generation antihistamine

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13
Q

budesonide

A

glucocorticoid drug for asthma

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14
Q

fluticasone

A

glucocorticoid drug for asthma

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15
Q

adverse effects of inhaled glucocorticoid therapy for asthma

A

dysphonia and oropharyngeal candidiasis

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16
Q

Montelukast

A

leukotriene modifier for asthma

oral administration

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17
Q

cromolyn

A

used for prophylaxis of asthma symptoms. Suppresses inflammation.

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18
Q

principal bronchodilators in asthma treatment

A

Beta 2 adrenergic agonists-

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19
Q

salmeterol

A

longer-acting beta agonist for asthma treatment. Not effective for immediate rescue therapy.

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20
Q

adverse effects of beta2 adrenergic agonists

A

tachycardia, angina, tremor— dose dependent, should not occur unless pt is overdosing on inhaler.

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21
Q

fluticasone/salmeterol and budesonide

A

glucocorticoid/LABA combinations for long-term asthma maintenance in adults and children who have failed treatment with SABA. LABA should never be taken alone- should always be taken with glucocorticoid

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22
Q

How long to wait between 2 puffs of beta agonist? How much to wait between SABA and glucocorticoid?

A

1 minute between puffs of albuterol

5 minutes between SABA and glucocorticoid

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23
Q

Therapy of severe asthma exacerbations

A

oxygen
systemic, IV glucocorticoid
nebulized high-dose SABA
nebulized ipratropium (anticholinergic med) to reduce airflow obstruction

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24
Q

ipratropium

A

anticholinergic receptor that further reduces bronchoconstriction in acute asthma exacerbations
Adverse effects: dry mouth, irritation of pharynx, increase in eye pressure in those with glaucoma, and rare possible CV events.

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25
Q

What drugs are used to treat H. pylori with ulcer?

A

Antibiotics and antisecretory agents (H2 blockers, prilosec)

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26
Q

Antibiotics for PUD and H. pylori

A 
Amoxicillin
Clarithromycin
Bismuth compounds
Tetracycline
Metronidazole (flagyl)

Use a minimum of 2 antibiotics, up to 3

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27
Q

Cimetidine

A

H2-receptor antagonist for PUD
May cross BBB and cause CNS side effects
Cannot be taken within 1 hour of an antacid, best on an empty stomach.
Antiadrogenic effects.
IV bolus: can cause hypotension and dysrhythmias.

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28
Q

Ranitidine

A

H2-receptor antagonist for PUD

Newer generation— few side effects and fewer interactions

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29
Q

Famotidine

A

H2-receptor antagonist for PUD

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30
Q

H2-receptor antagonists

A

First-choice drugs for treating gastric and duodenal ulcers. Suppress secretion of gastric acid

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31
Q

What should not be ingested while taking Metronidazole (Flagyl)

A

alcohol

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32
Q

sucralfate (Carafate)

A

Sucralfate creates a protective, mucous like barrier for up to six hours. It does nothing to acid secretions and is not absorbed and thus has minimal side effects. Constipation occurs in about 2% of patients. Because it is not absorbed, systemic effects are absent.

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33
Q

Proton pump inhibitors

A

most effective drugs for suppressing secretion of gastric acid
Increase the risk of fracture, pneumonia, acid rebound, and C. diff infection.

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34
Q

Omeprazole (prilosec)

A

Proton pump inhibitor- inhibits gastric secretion
Irreversible proton pump inhibitor- effects last several days
Short half life
Should be used short term

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35
Q

misoprostol

A

used to treat gastric ulcers caused by NSAIDs
side effect: dose-related diarrhea
pregnancy test necessary

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36
Q

Anatacids (calcium, magnesium, aluminum compounds)

A

React with gastric acid to produce neutral salts

Use with caution in pts with renal impairment

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37
Q

contraindications for laxative use

A

abdominal pain, nausea, cramps, guarding
acute surgical abdomen- rebound, etc- workup needed before laxative
fecal impaction, bowel obstruction
habitual use
Use with caution in pregnancy and lactation

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38
Q

psyllium (metamucil and citrucel)

A

bulk-forming laxative
Functions similarly to dietary fiber
preferred treatment for temporary treatment of constipation

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39
Q

docusate sodium (colace)

A

surfactant laxative—commonly used for pts on opiates

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40
Q

bisacodyl (dulcolax)

A

stimulant laxative
stimulate intestinal motility
increase quantities of water and electrolytes in the intestinal lumen
good for opioid-induced constipation

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41
Q

milk of magnesia and polyethylene glycol (miralax)

A

osmotic laxatives
poorly absorbed salts that draw water into the intestinal lumen
low doses- work in 6-12 hours
high dose- results in 2-6 hours (cathartic effect)
cause substantial water loss and dehydration, renal toxicity
may cause sodium retention and exacerbate HF, HTN, edema (sodium phosphate compounds are worst for this)

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42
Q

Bowel-cleansing products for colonscopy

A

Sodium phosphate- hypertonic
Polyethylene glycol plus electrolytes (GoLYTELY)— isotonic with body fluids, no major loss of electrolytes, but requires large volume of bad-tasting liquid.

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43
Q

Which laxatives are commonly used long-term use and seem safe in children?

A

???

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44
Q

Which laxative is preferred to prevent opioid-induced constipation?

A

Bisacodyl (dulcolax)

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45
Q

Penicillin

A

narrow-spectrum penicillin that is effective only on gram-positive bacteria. It works on strep that can’t make the enzyme penicillinase. Penicillin can produce a mild allergic reaction or even a life-threatening anaphylactic reaction.

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46
Q

Ampicillin

A

a broad-spectrum penicillin that is effective on some gram negative bacteria as well as gram positive.
Adverse effects include rash (common side effect) and diarrhea (common side effect).

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47
Q

2 main gram positive bacteria

A

strep and staph

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48
Q

1 drug for group A strep

A

penicillin

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49
Q

nafcillin

A

narrow spectrum penicillin

pencilinase-resistant- works against staph aureus drugs that make penicilinase

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50
Q

ticarcillin

A

extended-spectrum
effective against pseudomonas
still will not kill MRSA
risk of sodium overload (given as a salt)

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51
Q

penicillin G (benzylpenicillin)

A

effective against gram positive organisms
least toxic of all antibiotics
most common cause of drug allergy

52
Q

nafcillin, oxacillin, and dicloxacillin- what are they useful for?

A

useful against most staph aureus

NOT USEFUL AGAINST MRSA

53
Q

ampicillin and amoxicillin

A

cover gram negative and gram positive organisms
may help for an infection like an ear or urinary infection with multiple organisms

SE: rash or diarrhea- common rxn

54
Q

clavulanic acid

A

beta-lactamase inhibitor- blocks penicillinase.

55
Q

ampicillin/sulbactam and amoxicillin/clavulanic acid

A

extends antimicrobial spectrum when combined with penicillinase-sensitive antibiotics

56
Q

how to prescribe for pt with penicillin allergy hx

A

if mild rxn hx: consider cephalosporin

if severe rxn hx: avoid administration of penicillin or cephalosporins

57
Q

symptoms of penicillin allergy severe rxn

A

laryngeal edema
bronchoconstriction, wheezing
severe hypotension
urticaria

58
Q

What happens when penicillins and aminoglycoside antibiotics (gentamicin, amikacin) are mixed in IV solution? How should these drugs be administered if both are ordered for your patient?

A

Penicillins can inactivate aminoglycosides. Therefore, penicillins and aminoglycosides should never be mixed in the same IV solution. They should be administered separately.

59
Q

How do the cephalosporins work?

A

Bind to penicillin binding proteins thereby disrupting cell wall synthesis and activate enzymes that damage the cell wall causing it to lyse.

60
Q

Third Generation Cephalosporins

A

Highly active against gram-negative organisms
More resistant to beta-lactamase
Able to penetrate CSF / BBB → treatment for encephalitis, meningitis

61
Q

Fourth Generation

A

Highly resistant to beta-lactamase
Extensive gram-negative coverage
Pseudomonas coverage (found in immunocompromised hosts)

62
Q

ceftaroline

A

Fifth generation Cephalosporin

active against MRSA!

63
Q

cefotetan (what side effects?)

A

Cephalosporin
Do not take with alcohol,
Interferes with vitamin K- can cause bleeding. Should not be used with warfarin, aspirin, etc.

64
Q

first and second generation cephalosporins

A

used for prophylaxis and against gram positives

rarely used for active infections

65
Q

Imipenem

A

carbapenem
not effective against MRSA
extremely broad spectrum with low toxicity
might give to very sick pt with multiple organisms—chemo or similar situation

66
Q

vancomycin

A

effective against MRSA
good drug if serious infection and very penicillin allergic
Good for C. diff is metronidazole was ineffective, or for severe cases.
typically given IV, but sometimes given orally through NG tube.
toxicity: ear (careful with aminoglycosides, loop diuretics). red man syndrome- infuse slowly (1 hr) to prevent, renal toxicity

67
Q

food/drug/tetracycline interactions

A 
Absorption of tetracyclines is decreased if given with
Milk products
Calcium supplements
Iron supplements
Magnesium-containing laxatives
Most antacids
68
Q

What is the principle limiting adverse effect of erythromycin? What is different about azithromycin?

A

Erythromycin’s most common adverse effect is GI pain → nausea, gastric pain, diarrhea, vomiting. Azithromycin does not produce this adverse effect.

69
Q

Who should not take tetracyclines and why?

A

Due to the risk of discoloration of teeth in children, pregnant women and children under the age of 8 should not use tetracyclines. Specifically, tetracycline & demeclocycline are eliminated in the urine and should not be used in a patient with renal compromise. If patient needs to be on a tetracycline, doxycycline or minocycline are better choices as they are eliminated by the liver.

70
Q

What happens when erythromycin is combined with an -azole antifungal?

A

-azole antifungal drugs can inhibit erythromycin metabolism → raising plasma erythromycin levels which can cause QT prolongation & sudden cardiac death. Also be careful with cardiac pts

Erythromycin is a P450 inhibitor and can raise the plasma levels of other drugs: theophylline (used for asthma), carbamazepine (used for seizures and BPD), and warfarin.

71
Q

erythromycin

A

broad spectrum macrolide antibiotics

severe GI side effects

72
Q

azithromycin & clarithromycin

A

does not cause severe GI effects.

73
Q

clindamycin

A

broad spectrum, treats anaerobic infections outside the CNS—often GI bugs
associated with C. diff!

74
Q

which -mycin is assoiated with C. diff?

A

clindamycin

75
Q

linezolid (zyvoxx)

A 
new class of antibiotics called oxazolidinones
Active against VRE: vancomycin resistant enterococci & MRSA
76
Q

Why is the drug chloramphenicol rarely used? Be familiar with a dangerous toxicity that occurs in infants.

A 
It is rarely used due to lack of safety and is only used for life-threatening infections.  It can produce “Gray Syndrome” where they infant takes on a grey pallor and has a protruding abdomen.  It is also associated with:
Reversible bone marrow depression
Fatal aplastic anemia
GI effects
Peripheral neuropathy
77
Q

Tetracycline and doxycycline. How do these drugs work? What is their spectrum of action?

A

Tetracycline & doxycycline are in the “tetracycline” family of drugs which are broad-spectrum antibiotics for systemic therapy. They suppress bacterial growth by inhibiting protein synthesis. They are bacteriostatic → preventing growth, not necessarily killing bacteria. Because they can suppress growth of healthy bacteria as well, they can cause a “superinfection” or the proliferation of fungus in the patient.

78
Q

a common immunization-preventable infection for which erythromycin is the first-line drug

A

Bordetella pertussis → Whooping cough

79
Q

aminoglycocides

A

gentamicin, tobramycin and amikacin
narrow spectrum bactericidal antibiotics. They are used to kill aerobic, gram-negative bacilli
Must be given IV or parenterally

80
Q

Which aminoglycocide drug will be used in your hospital, or are they all the same?

A

Regional resistance to certain agents has occurred. For example, in Maine, patients are started first on gentamicin and in NYC, they might first be started on amikacin.

81
Q

aminoglycoside adverse effects and interactions

A 
nephrotoxicity
ototoxicity
neuromuscular blockade
interactions:
lood diuretics, vanco (ototoxic)
nephrotoxic drugs
skeletal muscle relaxants (succinylcholine, anesthetics)- increased risk of neuromuscular blockade
82
Q

What is the treatment for aminoglycoside-induced neuromuscular blockade?

A

calcium glutamate

83
Q

gentamicin

A

narrow spectrum drug for aerobic gram negative bacilli
ototoxic
nephrotoxic

84
Q

sulfamethoxazole and trimethoprim

A

broad spectrum antibiotics
suppress bacterial growth by inhibiting tetrahydrofolic acid
inhibit the synthesis of folic acid (folate)

85
Q

sulfonamides (sulfamethoxazole and trimethoprim) adverse effects

A

hypersensitivity rxns, including SJ syndrome- blistering, sloughing, fever
hematologic effects- anemia
kernicterus- bilirubin in the CNS, bad in newborns
renal damage from crystalluria

86
Q

sulfamethoxazole and trimethoprim drug interactions

A

raises levels of oral hypoglycemic drugs, may cause hypoglycemia
displaces warfarin from albumin- increases bleeding risk

87
Q

sulfamethoxazole and trimethoprim

A

bilirubin in the CNS due to sulfonamides, may cause permanent neurological damage in newborns

88
Q

trimethoprim

A

inhibits dihydrofolate reductase for folic acid production
hematologic effects
avoid in pregnancy

89
Q

sulfamethoxazole and trimethoprim

A

inhibits 2 different steps in bacteria folic acid synthesis- much more effective than either one alone.
use for UTI, otitis media, bronchitis, shigellosis, pneumonia

90
Q

What should we consider when giving sulfonamides to African-American patients? Recall G6PD deficiency.

A

Sulfonamides can cause hemolytic anemia in patients with G6PD deficiency, most common among African Americans and people of Mediterranean origin.

91
Q

Induction phase of TB treatment

A

2 months

use four drugs

92
Q

continuation phase of TB treatment—what length, which drugs?

A

4 months

use two drugs: isoniazid and rifampin

93
Q

intermittent dosing of TB treatment

A

easier to accomplish
higher compliance
2-3 times a week

94
Q

what ppd sign is considered positive?

A

1 cm induration around the injection site in moderate risk pts

95
Q

latent TB treatment

A

INH- 9 months. treatment of choice

or isoniazid with rifapentine for 3 months

96
Q

first-line anti TB drugs

A

isoniazid and rifampin

97
Q

isoniazid (INH)

A

only used to treat TB
adverse effects:
peripheral neuropathy- paresthesias and weakness of hands and feet, pyroxidine (B6) is given to reverse
hepatotoxicity- drug should be stopped if lfts 3x baseline
optic neuritis

98
Q

rifampin

A

broad-spectrum antibiotic but mainly used for TB
SE:
hepatotoxicity
discoloration of body fluids
P450 inducer- do not use with oral contraceptives
lowers warfarin levels, HIV drug levels
increases hepatotoxicity of INH and other TB drugs

99
Q

fluoroquinolones (-floxacin)

A

broad-spectrum agents with multiple applications
disrupt DNA replication
mild side effects, can cause tendon rupture- usually effects achilles tendon- discontinue med and avoid weight bearing. this occurs more often in older pts who are taking steroids

100
Q

cipro

A

broad-spectrum- inhibits bacterial DNA gyrase and topoisomerase II
use for respiratory, UTI, GI, joints, bones, skin, soft tissue, GU
SE: GI, CNS- dizziness, confusion, headache, restlessness, confusion- especially in elderly.
interacts with calcium, zinc, magnesium, etc

101
Q

metronidazole (flagyl)

A

bactericidal for anaerobes
drug of choice for c. diff
protozoal infections- giardia, trichomonas
helicobacter pylori
adverse effects: GI upset, neurotoxicity
drug interaction: alcohol: DISULFURAM-LIKE RXN!

102
Q

daptomycin (cubicin)

A

kills virtually all gram positive bacteria, including MRSA and VRE
no significant drug interactions
adverse effects- possible muscle injury
monitor CK for muscle damage

103
Q

drugs to kill MRSA

A

daptomycin (cubicin), vancomycin, linzolid (zyvoxx)

104
Q

amphotericin B

A

broad spectrum antifungal agent
binds to ergosterol in fungal cell membrane
drug of choice for most systemic mycoses
highly toxic:
-infusion rxn- occurs 1-3 hours after starting infusion
-nephrotoxicity
-hypokalemia
-must be given IV- no oral administration

105
Q

treatment for amphotericin B infusion rxn

A

diphenhydramine, acetaminophen, meperidine

mepiridine works best for muscle jerks

106
Q

nephrotoxicity of amphotericin

A

extent related to dose
if you reach 4g, you will have some permanent kidney damage
infuse 1 L of saline on days of treatment
avoid concurrent administration of aminoglycosides- loop diuretics, antivirals, NSAIDs.
monitor serum creatinine.

107
Q

what antifungal can be given with amphotericin B to minimize toxicity?

A

flucytosine can be added to amphotericin b to reduce toxicity- a dose of the 2 drugs together can reduce toxicity by lowering amphotericin dose

108
Q

-azoles

A

broad spectrum antifungals
lower toxicity than amphotericin
can be given orally
hepatotoxic- inhibit P450 drug enzymes

109
Q

itraconazole

A

used for systemic mycoses, alternative to amphtotericin b
SE:
cardiosuppression in patients with heart failure- decrease in ventrical ejection fraction
liver damage
can inhibit drug metabolizing enzymes- levels of many drugs go up

110
Q

fluconazole

A

often given orally
given for yeast infections
GI effects common

111
Q

onychomycosis

A

nail infection- difficult to treat

3-6 months of oral treatment needed- terbinafine (lamisil) is preferred treatment

112
Q

clotrimazole

A

topical antifungal

113
Q

griseofulvin

A

oral antifungal

114
Q

terbinafine (lamisil)

A

topical and oral- preferred treatment for nails

115
Q

how long should antifungal treatment be continued

A

a week after symptoms have cleared

116
Q

nystatin (mycostatin)

A

antifungal
used only for candidiasis in skin, mouth, esophagus, and vagina
can be used orally or topically

117
Q

Acyclovir (zorivax)

A

active only against members of herpesvirus family- HSV and VZV
suppresses recurrences, shorterns duration of infection- does not eradicate virus
some resistance occurs
adverse effects:
IV: phelbitis, nephrotoxicity (administer with fluids)
oral: GI, vertigo

118
Q

oseltamivir (tamiflu)

A

must be given within 2 days of exposure, given to pts with high risk of serious illness
neuraminidase inhibitor

119
Q

What is the G0 phase of the cell cycle? Are tumors in this phase responsive to chemotherapy?

A

G0 phase is resting phase → tumors in this phase are not susceptible to chemo drugs, which are targeted at DNA synthesis, etc, aspects of cell proliferation.

Chemo often affects drugs in the synthesis (S) phase, the mitosis (M) phase, or the G1 or G2 phases

120
Q

What lab parameters must be carefully monitored during chemotherapy?

A

Neutropenia - if ANC (absolute neutrophil count) drops below 500 cells/ mm3, therapy should be stopped.
Thrombocytopenia - low platelets
Anemia - low RBC count

121
Q

What is the principal earliest sign of infection in a patient on chemotherapy?

A

fever- Be very cautious of neutropenic patients with fever, even low grade- 38°C or 100.4°F

122
Q

What does filgrastim (G-CSF) do?

A

Stimulates neutrophil production. Can be administered.

123
Q

What does erythropoietin (epoetin, Epogen) do?

A

It’s a hormone that stimulates RBC production. May stimulate cancer growth so generally only given in palliative care. Given as SubQ injection.

124
Q

How do we treat chemotherapy-induced thrombocytopenia?

A

platelet therapy

125
Q

What is hyperuricemia? Hyperuricemia commonly results from after chemotherapy for which cancers?

A

Hyperuricemia is excess uric acid in the blood → caused by the breakdown of DNA after cell death. It is most common in treatment for leukemia and lymphomas due to the massive cell death.

126
Q

allopurinol

A

prevents hyperuricemia in cancer patients by inhibiting xanthine oxidase, an enzyme involved in converting nucleic acids to uric acid.

127
Q

Vomiting/GI symptoms treatments for cancer

A

Glucocorticoid like dexamethasone and Zofran (Ondansetron) or other -setron drug

Pharmacology (13 decks)

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