Pharm Flashcards

1
Q

risk factors for drug interactions

A
multiple medications
female gender
extremes of age
major organ dysfunction
genetic polymorphisms
metabolic and endocrine dysfunction
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2
Q

pharmacokinetics

A

what body does to drug

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3
Q

pharmacodynamics

A

what drug does to body

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4
Q

additive

A

alcohol and benzo

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5
Q

antagonist

A

diazepam and flumazenil

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6
Q

caution with tobramycin

A

worsens respiratory depression in surgery
decrease Ach and interacts with succinylcholine
reverse with neostigmine

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7
Q

antacids

A

prevent absorption

interacts with tetracycline

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8
Q

cholestyramine

A

interacts with digoxin and warfarin

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9
Q

mycophenolate mofetil

A

interacts with ferrous sulfate, Ca, Mg, or Al
physical complex prevents absorption
not due to pH effect

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10
Q

shift in peak but not bioavailability

A

due to changes in GI motility

just changes rate of absorption

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11
Q

decreased gastric motility

A

decreased rate of absorption

amitriptyline, morphine

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12
Q

increases gastric motility

A

greater peak effect

metoclopramide

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13
Q

raises gastric pH

A

H2 antagonists and PPI

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14
Q

H2 antagonists decrease

A

ktoconazole and itraconazole

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15
Q

PPI decreases

A

atazanavir, itraconazole, and ketoconazole

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16
Q

p-glycoprotein

A

ATP dependent molecular transport

protects from harmful substances-out of brain, into gut, lumen, bile and urine

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17
Q

inhibitors p-glycoprotein

A

ketoconazole, erythromycin, grapefruit juice, clarithromycin

some are inhibitors of CYP3A

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18
Q

OCP and antibiotics

A

greater failure if taken with erythromycin

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19
Q

warfarin and SMX-TMP

A

warfarin usually 99% bound

SMX-TMP increase INR>6

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20
Q

cytochrome p450

A

present in ER

primarily phase I metabolism

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21
Q

inhibition p450

A

ketoconazole, cimetidine, erythromycin, grapefruit juice (furanocoumarins and naringin), and clarithromycin

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22
Q

induction p450

A

phenytoin, rifampin, carbamazepine, St. John Wort

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23
Q

CYP1A2-theophylline

A

induced by phenobarbital

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24
Q

CYP2C9-warfarin

A

induced by rifampin

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25
Q

inducer CYP3A4

A

phenytoin

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26
Q

inhibitor CYP3A4

A

erythromycin, ketoconazole

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27
Q

tamoxifen CYP2D6

A

less formation of active metabolite in slow metabolizers

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28
Q

CYP2C19 and clopidogrel

A

less effective in slow metabolizers

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29
Q

renal tubular secretion

A

drug compete for same transport
probenecid and penicillins
sulfa and MTX (increase MTX levels in blood)

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30
Q

altered tubular reabsorption

A

trimethoprim inhibits sodium channel in distal tubule results in increased K reabsorption (higher dose in pneumocystis)
lithium and diuretics leads to decreased lithium clearance

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31
Q

digoxin and quinidine

A

less digoxin renal excretion

p glycoprotein inhibitor

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32
Q

alterations in urine pH

A

non-ionized are reabsorbed
high pH causes basic to be unionized
low pH causes acidic to be unionized

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33
Q

acetazolamide and quinidine/amphetamines

A

increase urine pH

higher unionized quinidine-higher reabsorption

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34
Q

aspirin and acetazolamide

A

increase ASA toxicity
metabolic acidosis increase unionized ASA into brain
increase ASA filtered and reabsorbed by kidney

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35
Q

high potential macrolides

A

erythromycin and clarithromycin

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36
Q

high potential H2 blockers

A

cimetidine

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37
Q

high statins

A

lovastatin (prodrug) and atorvastatin

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38
Q

lethal dose

A

lower LD is more toxic

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39
Q

mechanism of carbon monoxide toxicity

A

binds ferrous iron to form carboxyHb
reduction in O2 carrying capacity
toxicity from anoxia

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40
Q

target of carbon monoxide

A

globus pallidus in cerebellum

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41
Q

mechanism of cyanide toxicity

A

mitochondrial toxin that inhibits ETC

binds ferric iron-inhibit electron transport between a and a3

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42
Q

symptoms cyanide toxicity

A

rapid progression
nausea, lightheadedness, hyperventilation, feelings of suffocation, convulsions, coma
increased HR followed by decreased
death from respiratory failure, brain damage in recovered

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43
Q

treatment cyanide toxicity

A

nitrite to converte hemoglobin to HbFe3

administer thiosulfate

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44
Q

mechanism of toxicity organophosphates

A

inhibit AchE

increase Ach levels and exaggerate effects of cholinergic

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45
Q

treatment for organophosphates

A

atropine and 2PAM

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46
Q

carbamates mechanism of toxicity

A

inhibits AchE but reactivates faster (half life 1 hr)

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47
Q

treatment for carbamate

A

atropine only

do not use 2PAM

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48
Q

symptoms paraquat

A

inhaled-acute irritation, pulmonary fibrosis
oral-irritation and ulceration of mucous membranes
dermal-erythema, ulceration, cataract formation

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49
Q

treatment paraquat

A

gastric lavage
kaolin-limited use
hemodialysis or hemoperfusion

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50
Q

qualitative test

A

paraquat

sodium dithionite in 2N sodium hydroxide forms blue color

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51
Q

acute toxicity benzene

A

CNS depression and/or pulmonary irritation/edema

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52
Q

chronic toxicity benzene

A

anemia, leukemia, lymphomas

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53
Q

acute toluene and xylene toxicity

A

CNS depression

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54
Q

standardized supplements

A

certain concentration is consistent between batches

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55
Q

NF

A

meets standard for purity, strength of marker compound and labeling

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56
Q

effects of garlic

A

lowers cholesterol

inhibits platelet aggregation

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57
Q

ingredients of garlic responsible for platelet aggregation

A

ajoene (allicin) and diallyl trisulfide

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58
Q

non-refrigerator chopped garlic

A

risk of c. diff if stored at room temperature

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59
Q

activity in horse chesnut

A

escin (good) and asesculin (adverse)

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60
Q

effect of escin in horse chesnut

A

reduces leg pain and swelling

decreases vascular permeability of venous capillaries

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61
Q

effect of aesculin

A

similar to warfarin

bleeding gums, nose

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62
Q

contraindications horse chesnut

A

anticoagulants, NSAIDs-enhance bleeding
pregnancy
breast feeding

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63
Q

standardized ginko

A

for quercetin, kaempferol, and isorhamnetine

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64
Q

effects kaempferol from ginko

A

anti-oxidant

improves ATP and glucose utilization

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65
Q

effects of kaempferol and apigenin

A

inhibitors of MAO-A and MAO-B

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66
Q

adverse effects of ginko

A

major bleeding
drug interactions-aspirin, NSAIDs, warfarin, heparin, clopidogrel
seizures and ingestion from lethal ingestion

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67
Q

interferes with amino acid metabolism

A

antivitamin B6

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68
Q

standardized St. John Wort

A

hypericin and hyperforin

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69
Q

serotonin re-uptake inhibitor

A

dependent on hyperforin content

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70
Q

MAO inhibition

A

hypericin and hyperforin

SSRI>MAOI

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71
Q

side effects St. John Wort

A

HA, loss of appetite
should not be taken with MAOI or SSRI
induces P450 cyp3A4

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72
Q

increase dose when on St. John Wort

A

OCP, theophylline, warfarin

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73
Q

active ingredient Valerian

A

valerenic acid, valtrate

glutamine

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74
Q

neural effects of valerian

A

bind GABA A open Cl

hyperpolarization

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75
Q

use echinacea

A

lessens symptoms of colds, flu, infections

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76
Q

e purpura

A

only aerial

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77
Q

e pallida

A

aerial and root active

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78
Q

e angustifolia

A

root

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79
Q

arabinogalactan

A

releases IL-1 TNFa

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80
Q

heteroxylan

A

stimulates PMN phagocytosis

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81
Q

side effects for echinacea

A

avoid if allergic to plants in daisy or ragweed

avoid with immunosuppressants

82
Q

actions saw palmetto

A

inhibitor of 5alpha reductase

may block translocation of cytosol androgen receptor to nucleus

83
Q

marketed uses ginseng

A

antioxidant
anti-aging
anticancer
adaptogen

84
Q

active ingredient ginseng

A

gensenosides

85
Q

effect ginseng

A
lipid lowering and increase HDL
panax inhibits platelet aggregation
stimulate NO
adaptogen-reduces cortisol and NT during stress
improves chemotaxis of PMN
improves glycemic control in diabetics
86
Q

anti-cancer ginseng

A

lowers stomach and colon cancer

87
Q

adverse effects ginseng

A

nervousness, insomnia-avoid use with caffeine

88
Q

uses KAVA

A

sedation and relaxation

interaction with GABA

89
Q

side effects KAVA

A

hepatic toxicity
sedation do not mix with alcohol
yellow pigment to skin and nails

90
Q

ingredients feverfew

A

sesquiterpene, lactones, parthenolide

91
Q

mechanism of action feverfew

A

inhibits PLA2

inhibits platelet serotonin release

92
Q

adverse effects feverfew

A

joint pain, muscle aches, insomnia
causes uterine contraction
menstrual irregularities and heavier blood flow

93
Q

herbs to avoid prior to surgery

A
garlic
horse chesnut
ginko biloba
St. John wort
feverfew
94
Q

herbs to avoid when taking MAOI and SSRI

A

St. John Wort

valerian

95
Q

herbs to avoid with alcohol

A

valerian

kava

96
Q

risks from metasl

A

accumulate because not metabolized

bind to proteins, enzymes via S, O, N

97
Q

properties of ideal chelating agent

A

less toxic than metal
enhance excretion
chelate at physiological pH
not metabolized readily
hydrophilic-distribution similar to metals
greater affinity for metals than calcium or iron in body

98
Q

calcium disodium EDTA

A

administer IM or IV for lead and cadmium

metal displaces Ca in center of molecule

99
Q

contraindications calcium disodium EDTA

A

renal disease

100
Q

disodium EDTA

A

used for hypercalcemia

101
Q

succimer

A

sulfhydryl groups bind metal
administer orally for lead toxicity
low compliance due to taste

102
Q

dimercaprol

A

SH bind to metal

used for lead, arsenic, inorganic mercury

103
Q

contraindication dimercaprol

A

peanut allergy

104
Q

contraindication BAL dimercaprol

A

liver disease

105
Q

drug of choice Wilson disease

A

Penicillamine

106
Q

adverse effect penicillamine

A

agranulocytosis

107
Q

contraindication penicillamine

A

renal disease

108
Q

distribution of lead in body

A

liver, kidney, RBC
RBC>95% of lead bound to Hb
redistributes to bone replacing Ca-form tertiary lead phosphate

109
Q

signs of lead poisoning

A
microcytic anemia, basophilic stipling and hemolysis
lead colic (chronic)
lead palsy (chronic)
110
Q

signs of lead encephalopathy

A

convulsions, cerebral edema and death

111
Q

lead interaction with neurological tissue

A

peripheral, axon degeneration

in brain interferes with Ca dependent reactions

112
Q

lead interactions with blood

A

inhibits heme synthesis
basophilic stipling due to RNA
decrease life span and heme synthesis

113
Q

lead inhibition of heme enzymes

A

alpha aminolevulinate dehydratase (cytosolic) and ferrochelatase (mitochondrial)

114
Q

blood and urine indicators lead

A

increase levels of alpha aminoleuvulinic acid and coporphyrin III
whole blood sensitive indicator

115
Q

chelation for low levels of lead

A

succimer and penicillamine

116
Q

chelation for high levels of lead

A

calcium disodium EDTA and dimercaprol

117
Q

mercury through inhalation

A

elemental

118
Q

mercury through inhalation or oral

A

inorganic

119
Q

most toxic mercury

A

organomercurial

120
Q

mechanism of mercury toxicity

A

bind to sulfhydryl groups and inactivate proteins and enzymes

121
Q

damage from elemental mercury

A

converted from valence to +2 by catalase in RBC

122
Q

uncharged mercury causing damage

A

charged BBB

123
Q

signs of mercury toxicity

A

tremor, irritability, erethism

124
Q

inorganic mercury causing gray color

A

bind to SH protein in mouth and esophagus

125
Q

chronic inorganic mercury

A

photophobia and acrodynia (reddening of face and chest)

126
Q

most toxic form of mercury

A

organomercurials-targets nervous system

127
Q

minamata disease

A

methylmercury causing weakness, visual field constriction, ataxia, and numbness
inorganic mercury released into environment taken up by algae-methylmercury into fish that ate algae

128
Q

treatment low mercury

A

penicillamine

129
Q

treatment severe mercury

A

dimercaprol

130
Q

contraindications dimercaprol

A

high brain mercury levels

increases brain levels

131
Q

mechanism arsenic toxicity

A

As3 binds sulfhydryl
As5 replaces P in ATP uncoupling oxphos
AsH3 hemolysis

132
Q

signs of arsenic toxicity

A

vasodilator, permeability of capillary, arrhythmia, rice water diarrhea, loss of albumin, cancer and hyperkeratosis, hemolysis (from gas)
garlic odor to breath and sweat

133
Q

Mee’s lines

A

horizontal lines on fingernails

134
Q

treatment arsenic poisoning

A

penicillamine
dimercaprol
treat symptoms of arsine gas

135
Q

target cadmium

A

kidney-damage to proximal tubules

lungs-emphysema

136
Q

metallothionein

A

inducible protein
induced by cadmium, mercury, arsenic exposure
high cysteine content, metal-SH binding

137
Q

accumulation Cd

A

in liver and kidney bound to metallothionein

Cd cleaved giving high tissue levels

138
Q

treatment cadmium toxicity

A

disodium EDTA

BAL contraindicated-increases renal toxicity

139
Q

monitor for cadmium

A

beta2 microglobulin

protein excretion increased following renal damage

140
Q

itai itai disease

A

accidental ingestion of cadmium in water and food

causes renal damage, osteoporosis, bone pain (from replacement of Ca by Cd)

141
Q

deaths from acute poisoning

A

cardiovascular complications

depressed respiration

142
Q

most common items for accidental ingestion in children

A

vitamins containing iron, OTC medications, cleaning supplies, pesticides

143
Q

most common poisons in adults

A

analgesic, drugs of abuse, antidepressants, sedatives, anti-anxiety agents, alcohol

144
Q

syrup of ipecac

A

stimulates CTZ in brain
direct effect on stomach
used for acetaminophen, atnihistamines, vitamins, cold remedies, benzos, pesticides

145
Q

contraindications emesis

A
corrosive agents-drain cleaner, ammonia, electric dishwasher cleaner
loss of gag reflex
comatose
sharp objects (glass)
agents associated with steroids
hydrocarbons-aspiration
146
Q

agents causing seizures

A

strychnine
tricyclic antidepressants
gamma hydroxybutyrate

147
Q

MOA activated charcoal

A

absorbs drugs then removed by lavage or through feces

148
Q

uses activated charcoal

A

acetaminophen, aspirin, amphetamines, benzos (oxazepam), digoxin, opiates, malathion, nicotine, syrup of ipecac

149
Q

contraindications activated charcoal

A

corrosive or caustic agents

ineffective for acids, alkali, most metals or petroleum distillates

150
Q

naloxone

A

opiate overdose

competitive reversible antagonist of opiate receptor

151
Q

flumazenil

A

benzodiazepine overdose

competitive reversible antagonist

152
Q

method to enhance excretion

A

sodium bicarbonate alkalinize urine to enhance excretion of acidic drugs (barbituates and aspirin)

153
Q

petroleum distillates

A

major target is aspiration into lungs

household solvents most common cause

154
Q

risk of aspiration

A

dependent on viscosity, volatility and surface tension

155
Q

best determinant of aspiration potential

A

viscosity (low viscosity SUS=high aspiration risk)

156
Q

surface tension

A

low surface tension allows rapid spreading

157
Q

volatility

A

movement from liquid to gas, displace oxygen from alveoli causing hypoxia

158
Q

death from huffing

A

hypoxia

may also cause permanent brain damage

159
Q

benzene causes

A

leukemia

160
Q

toluene causes

A

blindness and hearing loss

161
Q

huffing while pregnant

A

decreased birth weight, increased fetal death, nerve damage

162
Q

calculating iron toxicity

A

off elemental Fe content (ferrous sulfate higher than ferrous gluconate)

163
Q

first stage iron toxicity

A

vomiting, stomach pain, diarrhea

164
Q

second phase iron toxicity

A

apparent recovery-lethargy with no vomiting

6-24 hr

165
Q

third phase iron toxicity

A

organ failure of heart, liver, kidney, nervous system

12-24 hr

166
Q

fourth phase iron toxicity

A

scarring causes pyloric obstruction

4-6 wks

167
Q

treatment iron toxicity

A

emesis
lavage-bicarbonate to decrease absorption
chelation-deferoxamine

168
Q

target organ acetaminophen

A

liver and kidney

causes liver centrilobular necrosis and kidney tubular necrosis

169
Q

liver damage from acetaminophen

A

metabolized to NAPQI by p450

detoxed by glutathione-with glutathione depletion NAPQI binds proteins

170
Q

timeline acetaminophen toxicity

A

first 24 hr minor GI and nausea
24-48 hr hepatic damage appears
blood levels correlate to toxicity and time expired

171
Q

treatment acetaminophen toxicity

A

emesis, lavage with activated charcoal
N-acetylcystine to provide cys for glutathione-replenish it
glutathione ineffective on its own

172
Q

combination of acetaminophen and alcohol

A

alcohol lowers glutathione and induces p450
diminishes NADPH so NAPQI damage occurs
excess NADH/NAD, less APAP glucuronidation

173
Q

first order kinetics aspirin

A

head ache dose-constant fraction

174
Q

zero order kinetics aspirin

A

arthritis-constant amount

increases half life

175
Q

mechanism for salicylate toxicity

A

hyperventilation-stimulates respiratory centers in medulla

uncouples oxidative phosphorylation-stimulates CO2 production

176
Q

symptoms salicylate toxicity

A

HA, tinnitus, sweating, hyperventilation, fever, drowsiness
fever in children
acid-base and electrolyte imbalance
respiratory alkalosis from stimulation of resp centers, respiratory acidosis over time, metabolic acidosis due to uncoupling oxphos (increase ketones)

177
Q

electrolyte and fluid imbalance with salicylates

A

increased bicarbonate excretion
dehydration-hyperventilation and sweating
low potassium levels

178
Q

treatment salicylate toxicity

A

emesis, lavage +/- charcoal
alkalinize urine-effective for aspirin and methyl salicylate
correct fluid and electrolytes

179
Q

isopropyl alcohol

A

greater toxicity than ethanol
converted to acetone in body, less affinity for enzymes than ethanol
gastric pain, ketones, ketoacidosis

180
Q

methanol toxicity

A

eye, photophobia, blindness

due to formic acid

181
Q

ethylene glycol

A

induces inebriation, nausea, renal failure

oxalate crystals deposit in lumen of kidney

182
Q

treatment for alcohols

A

emesis or lavage <3hr
treat with IV ethanol (compete for alcohol dehydrogenase)
fomepizol (inhibitor alcohol dehydrogenase)

183
Q

neonate

A

0-4 weeks

184
Q

perinatal

A

26th week gestation to 1 month postpartum

185
Q

infant

A

5-2 weeks after birth

186
Q

drug absorption in neonates

A

low muscle mass
gastric pH decreases after first 24 hr of life, delayed gastric emptying
pulmonary routes under development

187
Q

renal function in children

A

GFR neonate lower than adults

normalizes in 6-12 months

188
Q

drug metabolism in children

A

decrease p450 activity

conjugation reactions diminished

189
Q

plasma protein binding in children

A

decreased plasma protein binding causes diff affinity for acidic anionic drugs until 10-12 months
displacement of bilirubin-phenytoin and indomethacin

190
Q

furosemide in children

A

delayed response

191
Q

cause of problems in drugs in elderly

A

changes in pharmacokinetics and pharmacodynamics

192
Q

changes in cardiac and renal elderly

A

CO declines

GFR declines

193
Q

changes in absorption in elderly

A

decreased gastric acid-less absorption ferrous sulfate and ketoconazole
antacids lower absorption of cimetidine, digitalis, tetracycline, phenytoin

194
Q

Vd lipid soluble

A

increased due to increased adipose

increase half life-diazepam, amiodarone

195
Q

Vd water soluble

A

decreased causing increased serum levels

ethanol, procianamide, atendol

196
Q

Vd muscle soluble

A

decreased due to decreased lean body mass

digoxin

197
Q

plasma binding elderly

A

lower albumin increases free fraction of acidic drugs-warfarin and phenytoin
protein binding decreased by renal disease or uremia

198
Q

hepatic clearance in elderly

A

lower phase I metabolism

no change in phase II metabolism

199
Q

pharmacodynamic changes

A

changes in binding of drug to receptor, receptor number or altered translation of receptor responses
decreased effect of beta-adrenergic agonists and antagonists
increased response to opiates and benzos

200
Q

digoxin in elderly

A

lower renal elimination

201
Q

black box warning in elderly

A

atypical and typical dopamine antagonists

202
Q

long term use of analgesics

A

induce papillary necrosis