Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

DT3 Exam 2 > Pharm > Flashcards

Pharm Flashcards

1
Q

multidrug-resistant TB

A

TB resistant to INH and RIF
high risk for treatment failure and further acquired drug resistance
refer them to ID specialists and state health departments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

extensive drug resistant TB

A

MDR (INH and RIF) plus resistance to FQN and at least one other injectable (amikacin, kanamycin, capreomycin)
relatively rare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

cell wall comparison

A

inner leaflet of outer membrane composed of arabinogalactan and mycolic acids
outer leaflet is composed of extractable phospholipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

principles for TB treatment

A

use multiple drugs
prolonged treatment required for successful eradication
patients must be followed closely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

therapeutic failure

A

positive sputum cultures after 4 months compliant therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

goals of TB treatment

A

convert sputum cultures to negative
prevent the emergence of resistance
assure a complete cure without relapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

MOA rifampin

A

inhibits DNA dependent RNAP
suppression of initiation of chain formation in RNA synthesis
bactericidal-kills within macrophages and in caseating granulomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

synergism for rifampin

A

isoniazid

shortens course of therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

distribution of rifampin

A

widely distributed

excellent tissue distribution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

metabolism of rifampin

A

metabolized by deacetylation

autoinduction of metabolism occurs-maximum at 6 doses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

adverse effects of rifampin

A

transient elevation in serum transaminases
hepatotoxicity (higher risk in alcoholics)
GI upset
hypersensitivity
discoloration of bodily fluids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

drug interactions for rifampin

A 
increase in P450
increased metabolism of 
warfarin
theophylline
narcotics
oral hypoglycemics
steroids (oral contraceptives)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

place of rifampin in therapy

A

treatment of active TB

2nd line for preventative therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

mechanism of action isoniazid

A

inhibits synthesis of mycolic acid
transported into bacterium-kills actively growing in extracellular, inhibits dormant organisms in macrophages and caseating granulomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

metabolism isoniazid

A

primarily by acetylation

monoacetyl hydrazine-important metabolite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

source of hepatotoxic effects in isoniazid

A

hydroxylated to an electrophilic intermediate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

rates of acetylation of isoniazid

A

slow or rapid acetylators
slow-higher chance of adverse reactions
Egyptians-slow
Eskimos and Japanese-rapid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

elimination of isoniazid

A

elimination dependent on acetylator phenotype

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

adverse effects of isoniazid

A

transient elevation in serum transaminases
hepatotoxicity
neurotoxicity
hypersensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

avoiding neurotoxicity from isoniazid

A

pyridoxine (B6) to reduce incidence

particularly important in alcoholics, children, malnourished, slow acetylators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

use of isoniazid in therapy

A

treatment of active TB

preventative therapy for patients with +PPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

mechanism of action for pyrazinamide

A

not documented

bactericidal toward dormant organisms in acidic environment within macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

metabolism of pyrazinamide

A

hydrolyzed in liver to active pyrazinoic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

elimination of pyrazinamide

A

5-hydroxypyrazinoic acid excreted by kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

adverse effects of pyrazinamide

A

hepatotoxicity
hyperuricemia (decreased renal excretion)
GI upset
hypersensitivity (photosensitivity, rash)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

mechanism of action for ethambutol

A

bacteriostatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

elimination of ethambutol

A

elimination of parent compound+inactive metabolite excreted in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

adverse effects ethambutol

A

optic neuritis (decreased red-green acuity)
monitor every 4-6 weeks
use caution in young children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

mechanism of action for streptomycin

A

aminoglycoside antibiotic
bactericidal through protein inhibition
inactive against intracellular organism
alternative to ethambutol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

absorption of streptomycin

A

poorly absorbed in GI tract

administer IV or IM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

adverse effects for streptomycin

A

nephrotoxicity (less than other aminoglycosides)
impairment of 8th cranial nerve function (vertigo>hearing)
pain on injection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

second line agents

A 
para-aminosalicylate
ethionamide
cycloserine
capreomycin
kanamycin
amikacin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

rifabutin

A

rifamycin derivative
used in TB patients who have experienced intolerance to rifampin or experiencing interactions
more active against MAC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

adverse reactions to rifabutin

A 
rash
GI
arthralgias
myalgias
discoloration of urine/sweat/tears 
neutropenia 
hepatotoxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

requirements for rifapentine

A

with INH in continuation phase
must be HIV negative
must have non-cavitary, drug susceptible pulmonary TB with negative sputum smears at completion of initial phase of treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

mechanism of action clofazamine

A

causes inhibition of transcription

used as an antileprosy agent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

clofazamine adverse reactions

A

GI upset
severe and life threatening abdominal pain and organ damage from crystal deposition
discoloration of skin and eyes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

macrolides in TB

A

unlikely to be effective against TB

clarithromycin and azithromycin against MAC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

quinolones in TB

A

ciprofloxacin and ofloxacin effective against TB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

RIPE or RIPS

A

use if >4% resistance

6 months for general TB treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

avoid in renal failure

A

avoid streptomycin, kanamycin, and capreomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

avoid in children

A

avoid ethambutol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

suspected treatment failure

A

add >2 new TB agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

lepromatous leprosy

A

loss of specific cell mediated immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

tuberculoid leprosy

A

strong cell mediated immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

diagnosis of leprosy

A

acid-fast stain and cytologic examination of skin

response to lepromin skin test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

treatment of leprosy

A

dapsone/rifampin/clofazimine

duration for 3-5 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

mechanism of action dapsone

A

competitive inhibitor of folic acid synthesis
inhibition of dihydropteroate synthase which prevents utilization of PABA
bacteriostatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

adverse reactions to dapsone

A

hemolytic anemia

hypersensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

MAI

A

symptoms usually when CD4 <100
prophylaxis at <50
fever, night sweats, weight loss, anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

macrolides in MAC

A

clarithromycin better than azithromycin

usually one with ethambutol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

inflammatory mechanism of asthma

A

increase mast cells, eosinophils, Th2 cells

increase histamine, D4, D2 in airway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

inflammatory mechanism of COPD

A

increase neutrophils, macrophages, CD8T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

role of space chamber

A

increase proportion of drug entering airway

used to decrease oropharyngeal deposition of inhaled corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

albuterol, levalbuterol

A

B2 agonist with quick onset

used to reverse asthma/bronchospasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

adverse effects of albuterol, levalbuterol

A

overuse indicates worsening asthma
airway tolerance
tremor, restlessness, tachycardia, hypokalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

epinephrine MOA

A

A1, A2, B1, B2 agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

adverse effects of epinephrine

A

palpitations, pale complexion, sweating, tremor, anxiety

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

adverse effects isoproterenol

A

cardiac stimulation

non-selective B agonist not used in US

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

salmeterol, formoterol, indacterol

A

long acting B2 agonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

uses for LABA

A

prophylaxis
not used in acute asthma attack
have to be given with inhaled corticosteroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

combination inhalers

A

more effective than corticosteroids or LABA alone

increase B2 receptor numbers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

ipratropium, tiotropium

A

muscarinic receptor antagonists
do not cross BBB (quaternary amines)
ipra 4x, tio 2x

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

adverse effects ipratropium, tiotropium

A 
bitter taste
dry mouth
glaucoma
urinary retention
paradoxical bronchospasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

methacholine

A

agonist that is used to diagnose bronchial airway hyperactivity in patients that have asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

theophylline

A

weak inhibitor of PDE isoforms, bronchodilator, anti-inflammatory activity, inhibits A1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

metabolism of theophylline

A

metabolized by p450

large variations in clearance (intra and inter-individual variability)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

toxicity of theophylline

A

headache, nausea, vomiting and restlessness at low dose toxicity
high concentration-cardiac arrhythmias (PDE3), seizurs (A1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

beclomethasone, flunisolide, fluticasone, mometasone, triaminolone

A

maximal benefit may take weeks

front line therapy for asthma

70
Q

local effects of corticosteroids

A

dysphonia, cough, oropharyngeal candidiasis

spacer decreases local adverse effects

71
Q

leukotriene inhibitors

A

cysteinyl leukotrienes are produced during asthma

72
Q

zafirlukast, montelukast, pranlukast

A

selective leukotriene receptor antagonist (C4/D4/E4)

73
Q

zileuton

A

inhibits 5-lipoxygenase (rate limiting enzyme in leukotriene biosynthesis)

74
Q

use of leukotriene inhibitors

A

reduce occurrence of bronchospasm in response to allergens, cold air, and exercise

75
Q

timing of leukotriene antagonists

A

monte 1x

zafir 2x

76
Q

frequency for zileuton

77
Q

adverse effects leukotriene inhibitors

A

hepatic toxicity
HA in zafirlukast
fever and chills in Zileuton

78
Q

MOA cromolyn and nedocromil

A

mast cell stabilizers

inhibit mast cell degranulation and histamine release

79
Q

use of cromolyn

A

asthma and allergic rhinitis

80
Q

MOA omalizumab

A

anti-IgE

inhibits binding of IgE to IgE receptors on mast cells

81
Q

adverse effects omalizumab

A

anaphylaxis

82
Q

use omalizumab

A

severe asthma not controlled by corticosteroids

83
Q

use alpha-1-proteinase inhibitor

A

used to inhibit the activity of elastase (due to alpha-1-antitrypsin deficiency)
leads to early onset emphysema

84
Q

opioids for cough

A

bind mu, suppress in medullary cough center to suppress cough

85
Q

adverse effects from opioids

A

sedation, constipation, opioid-induced respiratory depression could be troublesome in asthma

86
Q

dextromethorphan MOA

A

centrally active N-methyl-D-aspartate antagonist

acts in medullary cough center to suppress cough

87
Q

adverse effects dextromethrophan

A

hallucinations at high concentrations

88
Q

MOA benzonatate

A

acts peripherally by inhibiting stretch receptors in respiratory passages and lungs to suppress cough

89
Q

adverse effects benzonatate

90
Q

MOA guaifenesin

A

increase volume and reducing viscosity of secretions in trachea and bronchi

91
Q

adverse guaifenesin

92
Q

MOA N-acetylcysteine

A

free sulfhydryl group opens disulfide bond in mucus proteins and lowers mucus viscosity

93
Q

use N-acetylcysteine

A

acetaminophen overdose

COPD, CF

94
Q

MOA dornase alpha

A

DNAse that reduces viscoelasticity of sputum in patients with CF by breaking long extracellular DNA molecules into smaller fragments

95
Q

adverse effects dornase alpha

96
Q

first generation anti-histamines

A

diphenhydramine, brompheniramine, chlorphenamine

97
Q

second generation anti-histamines

A

loratidine, cetirizine

98
Q

uses for anti-histamines

A

allergic rhinitis, sleep aid, urticaria, motion sickness

99
Q

adverse effects for anti-histamines

A

dizziness, sedation

100
Q

use of diphenhydramine

A

sleep aid and motion sickness

101
Q

nasal spray ipratropium

A

rhinorrhea, allergic rhinitis

102
Q

oxymetazoline

A

alpha1 agonist

103
Q

phenylephrine

A

selective alpha1 agonist

104
Q

pseudoephedrine

A

alpha and beta agonist that may also enhance release of norepinephrine

105
Q

indications for adrenergic agonists

A

decongestants

106
Q

adverse effects of adrenergic agonists

A

rebound nasal congestion
hypertension
ischemia, peripheral ischemia, angina

107
Q

synthesis of histamine

A

from histidine by histidine decarboxylase

108
Q

basophils with histamine

109
Q

mast cells with histamine

A

skin
intestinal mucosa
lung
around blood vessels and nerves

110
Q

non-mast cells with histamine

A

gastric enterochromaffin cells
epidermis
CNS neurons

111
Q

complex with histamine

A 
heparin
chondroitin sulfate
eosinophilic chemotactic factor 
neutrophilic factor
proteases
112
Q

metabolism of histamine

A

methylation to from N-methylhistamine
converted to N-methylimidazoleacetic acid by MAO
oxidative deamination by diamine oxidase to imidazole acetic acid

113
Q

metabolites of histamine

A

imidazole acetic acid

N-methylhistamine

114
Q

substances that release histamine from mast cells

A

curare
morphine
venoms
inflammatory mediators

115
Q

histamine from gastric ECL cells

A

released by acetylcholine and gastrin

116
Q

H1 receptor

A

smooth muscle, endothelium, brain
Gq
chlorpheniramine antagonist

117
Q

H2 receptor

A

gastric mucosa, cardiac muscle, mast cells, brain
Gs
ranitidine antagonist

118
Q

H3 receptor

A

presynaptic brain, myenteric plexus
Gi
thioperamide, clobenpropit antagonist

119
Q

H4 receptor

A

eosinophils, neutrophils, CD4 T cells
Gi
thioperamide

120
Q

result of histamine in blood vessels

A

vasodilation-flushing, decrease BP

indirect-release of NO and PGI2

121
Q

result of histamine in capillary permeability

A

increase permeability leading to edema

responsible for urticaria

122
Q

result of histamine in heart

A

increase rate and force of contraction

123
Q

result of histamine in lungs

A

bronchoconstriction

124
Q

result of histamine in gastric mucosa

A

increase acid secretion from parietal cells

125
Q

result of histamine from nerve endings

A

pruritis from epidermis

pain and itching from dermis

126
Q

result of histamine from CNS

A

increased wakefulness and suppresses appetite

127
Q

triple response

A

red spot-vasodialtion
wheal-increase capillary permeability
flare-axon reflex leading to vasodilation

128
Q

metabolism of loratadine

129
Q

duration of anti-histamines

A

second generation longer acting
active metabolites of older drugs
prolonged duration of action and excreted unchanged

130
Q

effects of H1 antagonism

A 
reversible competitive
little effect on bronchoconstriction
vasoconstriction
no permeabiltiy
decreased HR
suppresses flare 
some relief of atopic dermatitis and contact dermatitis
131
Q

strongest muscarinic effect

A

promethazine

132
Q

muscarinic effect of second generation

133
Q

adverse reactions to antihistamines

A

CNS stimulation seen in poisoning
depression seen in first generation (potentiated by alcohol and CNS depressants)
antimuscarinic effects for 1st generation
GI for 1st generation

134
Q

uses of antihistamines

A

exudative allergy-rhinitis, urticaria, conjunctivitis
bronchial asthma
systemic anaphylaxis

135
Q

prevent motion sickness

A

promethazine

136
Q

H2 receptor antagonists

A

cimetidine
ranitidine
famotidine

137
Q

effects of H2 antagonists

A

decrease gastric acid secretion

138
Q

adverse effects of H2 antagonists

A

HA
GI
fatigue, drowsiness

139
Q

pharmacokinetics H2 antagonists

A

renal excretion

drug interactions from Cimetidine (inhibits p450)

140
Q

use H2 antagonists

A

promote healing of peptic or duodenal ulcer
uncomplicated GERD
prophylaxis of stress ulcers

141
Q

use H2 antagonists

A

promote healing of peptic or duodenal ulcer
uncomplicated GERD
prophylaxis of stress ulcers

142
Q

tidal volume

A

volume of air inspired and expired during normal quiet breathing

143
Q

inspiratory reserve volume

A

maximum amount of air that can be inahled after a normal tidal volume inspiration

144
Q

expiratory reserve volume

A

maximum amount of air that can be exhaled from the resting expiratory level

145
Q

residual volume

A

volume of air remaining in the lungs at the end of maximum expiration

146
Q

vital capacity

A

volume of air that can be exhaled from lungs after a maximum inspiration
VC=IRV+TV+ERV

147
Q

inspiratory capacity

A

maximum amount of air that can be inhaled from the end of a tidal volume
IC=IRV+TV

148
Q

functional residual capacity

A

volume of air in lungs at the end of TV expiration
elastic force of chest wall balanced by elastic force of lungs
FRC=ERV+RV

149
Q

total lung capacity

A

volume of air in lungs after maximum inspiration

TLC=IRV+TV+ERV+RV

150
Q

kussals

A

rapid shallow breathing

151
Q

emaciation cachectic

A

malignancy
TB
pulmonary cachexia syndrome

152
Q

obese

A

sleep apnea syndrome

153
Q

clubbing

A

widening of AP and lateral diameter of terminal portion of fingers
angle between the nail and skin is greater than 180
periungual skin is stretched and shiny

154
Q

causes of clubbing

A 
intrathoracic malignancy (lung, pleural, mediastinal)
suppurative lung disease (abscess, bronchiectasis, empyema)
interstitial fibrosis (alveolar capillary block syndrome)
155
Q

atelectasis shift

A

towards affected side

156
Q

plerual effusion shift

A

to unaffected side

157
Q

pneumothorax shift

A

to unaffected side

158
Q

asymmetrical chest expansion

A

abnormal side expands less

lags behind the normal side

159
Q

vocal fremitus increased

A

alveolar consolidation

160
Q

vocal fremitus decreased

A

increased distance between lung and chest wall

pneumothorax, pleural effusion

161
Q

increased dullness

A

atelectasis, alveolar filling/consolidation, pleural effusion, fibrosis

162
Q

hyperresonance

A

hyperinflation, pneumothorax

163
Q

normal inspiration:expiration ratio

164
Q

rhonchi

A

obstruction to airways

diffuse-asthma or COPD

165
Q

crackles

A

sound generated from collapsed state
chronic bronchitis, pneumonia, CHF, atelectasis
on inspiration-secretions in bronchi

166
Q

wheezes

A

correspond to degree of airway obstruction

167
Q

extrathoracic lesion stridor

A

on inspiration

laryngomalacia/vocal cord lesions/edema after extubations

168
Q

intrathoracic lesion stridor

A

on expiration

tracheomalacia/bronchomalacia/extrinsic compression

169
Q

fixed lesions stridor

A

croup
paralysis of both vocal cords
laryngeal mass or webs (like Plummer-Vinson?)

170
Q

obstructive ratio

A

decreased
DLCO may be normal
TLC and RV might be high

171
Q

restrictive ratio

A

normal

decreased DLCO

DT3 Exam 2 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions