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Pharm II > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

what about the structure of LAs increases their lipophilicity?

A

longer hydrocarbon chain and interconnecting chain

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2
Q

how do ester and amide LA metabolism differ?

A

esters - metabolized by plasma and liver pseudocholinesterases
amides - metabolized by liver P450s

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3
Q

how does LA change on either side of the cell membrane?

A

outside - uncharged

inside - becomes charged (this is what blocks the channel)

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4
Q

which drugs are used for topical anesthesia

A

benzocaine and cocaine

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5
Q

procaine and lidocaine can both be used for which 3 forms of LA?

A

infiltration (injection), epidural, spinal

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6
Q

why does LA getting to the brain cause convulsions?

A

d/t blockade of the GABA-A receptors (causes decr inhibition)

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7
Q

how is cocaine the exception when it comes to LAs having adverse cardio effects?

A

causes tachycardia, vasoconstriction, HTN

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8
Q

how does Epi affect the action of LAs?

A

it incr the LA action by 50%

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9
Q

how does diazepam aid in the tox caused by LAs?

A

treats convulsions d/t systemic absorption by activating the GABA-A receptors in the CNS

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10
Q

how is clonidine used as an adjunct in LA admin?

A

decr substance P and glutamate release (decr pain transmission)

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11
Q

which routes of LA admin is clonidine used in?

A

epidural and spinal

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12
Q

what are the protective components of the stomach?

A

mucous, bicarbonate, PGE

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13
Q

why do you need to be careful with cimetidine?

A

it is metabolized by CYPs so can interact with warfarin and phenytoin

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14
Q

which patients need a dose adjustment for H2 blockers?

A

renal insufficiency

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15
Q

how long does one dose of omeprazole work for?

A

t1/2 = 1.5hrs, however decr acid secretion for 2-3 days

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16
Q

rare side effects of omeprazole

A

nausea, diarrhea, dizziness

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17
Q

how do PPIs affect the bones with longterm use?

A

decr acidity decr the amount of Ca absorbed so bones more fragile

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18
Q

what is the first choice treatment in Zollinger-Ellison syndrome?

A

omeprazole

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19
Q

what indication is omeprazole less than ideal for?

A

occasional heartburn

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20
Q

which upper GI drugs can you develop a tolerance to?

A

H2 blockers

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21
Q

when can antacids be taken?

A

after a meal when there is acid present

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22
Q

what AE does Mg(OH)2 have if given alone?

A

diarrhea

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23
Q

what AE does Al(OH)3 or CaCO3 have if either are given alone?

A

constipation

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24
Q

how can antacids affect the urine?

A

they can increase the pH and alter the elimination of acidic and basic drugs

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25
Q

which drugs do Al(OH)3 and CaCO3 alter the absorption of?

A

tetracycline, INH, ketoconazole

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26
Q

which drug must be admin 2 hours after tetracycline, phenytoin, and digoxin and why?

A

sucralfate b/c it can absorb other drugs

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27
Q

when must sucralfate be admin?

A

before a meal

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28
Q

what strange AE does bismuth cause?

A

blackened tongue and stool

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29
Q

why can’t bismuth be used in children?

A

salicylate acid causes Reye’s syndrome

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30
Q

what is bismuth esp good for and why?

A

H. pylori infection d/t antimicrobial feature

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31
Q

what is misoprostol CI in?

A

pregnancy (d/t induction of contractions)

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32
Q

which drugs is B12 malabsorption associated with? why?

A

PPIs

d/t the fact that B12 absorption needs an acidic environment

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33
Q

where is the majority of 5-HT produced?

A

guts

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34
Q

how does metoclopramide affect the LES and pyloric sphincters?

A

incr LES tone to prevent backup

relaxes pyloric sphincter tone to incr gastric emptying

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35
Q

how do the MOAs for metoclopramide and ondansetron differ?

A

metoclopramide - D2 & 5-HT3 antagonist; 5-HT4 agonist

ondansetron - 5-HT3 receptor antagonist

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36
Q

how can ondansetron effectiveness be incr?

A

adding dexamethasone or aprepitant

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37
Q

metoclopramide AEs

A

parkinsonism like sx, tardive dyskinesia

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38
Q

ondansetron AEs

A

constipation and headache/GI sx

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39
Q

why can’t linaclotide be used in children

A

reports of mortality d/t dehydration in mice

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40
Q

how do linaclotide and lubiprostone MOAs differ?

A

Linaclotide - activates CFTR via cGMP

Lubiprostone - directly activates ClC2 Cl channel

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41
Q

what type of solution is Mg(OH)2 as an osmotic laxative and how does this affect its MOA?

A

admin as hypertonic solution which incr osmotic pressure and causes accumulation of fluids in GI tract

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42
Q

what are the indications for saline laxative (MgOH2)?

A

colonoscopy prep

IBS-C

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43
Q

how do steroids help IBD?

A

reduce ulceration and cause initial remission

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44
Q

what are the GI prodrugs?

A

omeprazole, sulfasalazine, azathioprine

45
Q

adverse effects of 5-ASA

A

diarrhea, nausea, headaches, hypersensitivity, bone marrow suppression

46
Q

AE of infliximab

A

infections (d/t immunosuppression)

47
Q

what is azathioprine good for?

A

IBD long term treatment (response could take weeks-months)

48
Q

which drugs are substrates for P450 enzymes and therefore can have their metabolism affected by ethanol

A

TCAs, H1 antihistamines, narcotics, anticonvulsants, BZs

49
Q

lethal dose of alcohol

A

> 500mg/dL

50
Q

at what dose of alcohol does impaired driving occur?

A

50-80 mg/dL

51
Q

alcohol’s affect on GABA

A

at high conc, it will incr the inhibitory effect of GABA

52
Q

what is the mechanism behind alcohol induced vomiting

A

alcohol excites the 5-HT3 receptors which leads to emesis

53
Q

why can’t acetaminophen be used with alcohol?

A

it coverts acetaminophen to a hepatotoxic metabolite

54
Q

what are the 3 endocrine effects of alcohol use?

A

gynecomastia, testicular atrophy, salt retention

55
Q

tx for alcohol w/d syndrome

A

long acting BZs (diazepam, chlordiazepoxide), clonidine, propranolol

56
Q

what does chronic EtOH use incr (neurologically)

A

incr synaptic concentration of dopamine, serotonin, endogenous opioids

57
Q

how do functional tolerance and metabolic tolerance differ?

A

metabolic tolerance - d/t induction of MEOS enzymes
functional tolerance - reduction of CNS sensitivity to alcohol d/t down regulation of GABA receptors, up regulation of NMDA (glutamate) receptors, up regulation of Ca channels

58
Q

how is naltrexone used for alcoholism?

A

anti-craving b/c it reduces the reward assoc w/alcohol consumption

59
Q

which population do you need to be careful with in prescribing naltrexone? why?

A

opioid dependent patients b/c it can lead to severe w/d

60
Q

other than naltrexone, which medications are used for used for their anti-craving effect?

A

acamprosate and topiramate

61
Q

what is NAC?

A

N-acetylcysteine

used to tx chronic alcoholics suspected of acetaminophen poisoning which could lead to irreversible liver damage

62
Q

what is fomepizole used for?

A

antidote to methanol and ethylene glycol toxicity

63
Q

how does one get ethylene glycol poisoning?

A

industrial exposure or drinking antifreeze

64
Q

what is oxalic acid?

A

what ethylene glycol is metabolized to

can cause severe acidosis and renal damage

65
Q

what is used to prevent the results of ethylene glycol toxicity?

A

ethanol (will compete for oxidation by ADH)

66
Q

what is the Narcan test

A

used if you suspect recovering alcoholic is abusing opioids

67
Q

what is methanol metabolized into and what can it cause?

A

formaldehyde which can cause severe acidosis, blindness, and retinal damage

68
Q

how can methanol intoxication be reversed?

A

IV ethanol (will compete for ADH and prevent the oxidation of methanol)

69
Q

how do clonidine and propranolol each decr sympathetic outflow?

A

clonidine - activates alpha2 adrenergic receptors in the CNS
propranolol - block beta adrenergic receptors in the CNS

70
Q

more lipid soluble an anesthetic the more ______ it is

A

potent

71
Q

how is anesthetic uptake calculated

A

gas solubility in the blood x cardiac output x gradient between alveolar and blood anesthetic partial pressures

72
Q

why is it beneficial that inhaled anesthetics decr CO?

A

higher CO means slower induction b/c it removes the agent faster from the alveoli and thus takes longer for equilibrium to be reached between the alveoli and the brain (lower CO means less anesthetic taken to the periphery which is not the site of action)

73
Q

what is MAC?

A

minimum alveolar concentration - end tidal concentration of inhaled anesthetic needed to eliminate movement in 50% of patients stimulated by an incision

74
Q

what are BZs good for?

A

reduce anxiety, induce amnesia

75
Q

what are antihistamines good for?

A

ppx for allergic rxn, some sedation

76
Q

what are antiemetics good for?

A

prevent aspiration, decr postop N/V

77
Q

what are opioids good for?

A

provide analgesia

78
Q

what are antimuscarinics good for?

A

amnesia, prevent bradycardia and fluid secretion

79
Q

what are muscle relaxants good for?

A

facilitating intubation

80
Q

what is the big disadvantage with halothane?

A

halothane hepatitis

81
Q

what is the MC used inhaled anesthetic?

A

isoflurane

82
Q

what are the advantages with isoflurane?

A

CO maintained, systemic vessels dilate causing small decr in BP, arrhythmias are uncommon, potent coronary vasodilator

83
Q

why are sevoflurane & desflurane unique?

A

can be used for outpatient anesthesia d/t rapid recovery

84
Q

NO provides ____ but not ____

A

analgesia; anesthesia

85
Q

what are the characteristics of malignant hyperthermia?

A

sustained muscle contraction, lactate production, increased body temp

86
Q

how does dantrolene tx malignant hyperthermia?

A

reduces intracellular Ca

87
Q

what should be provided upon d/c of NO and why?

A

100% oxygen b/c hypoxia may occur

88
Q

why should NO be used w/caution in closed spaces?

A

it incr the volume of closed spaces (can cause pneumothorax or incr pressure in sinus)

89
Q

what is the milk of amnesia?

A

propofol (hypnotic and forgetful rest)

90
Q

what determines the duration of action for IV anesthetics?

A

redistribution to body groups (VRG, muscle groups, fat group, vessel poor group)

91
Q

what is the advantage of sodium thiopental?

A

little postop excitement or vomiting

92
Q

which patient population is ketamine better for and why?

A

kids

adverse effects less common

93
Q

what are the AEs of ketamine?

A

incr muscle tone causing involuntary movements

hallucinations

94
Q

what is the unique advantage of ketamine?

A

does not cause respiratory depression

may cause incr in BP

95
Q

what is the unique advantage of etomidate?

A

antagonist available

96
Q

if a drug accumulates somewhere what does that mean in terms of recovery?

A

it will be slow

97
Q

which IV agent(s) provide analgesia?

A

ketamine

98
Q

which IV agents do not provide analgesia?

A

propofol, sodium thiopental, etomidate

99
Q

which IV agent can cause a painful injection?

A

etomidate

100
Q

what type of proteins do DAAs target?

A

non-structural proteins

101
Q

what is the BBW for DAAs?

A

HBV reactivation of HCV/HBV coinfection

102
Q

what are the 3 types of DAAs?

A

protease inhibitors (PIs, NS3/4), polymerase inhibitors (NS5B), NS5A inhibitors

103
Q

How does clonidine effect the C and A fibers?

A

Activates a2 adrenergic receptors on both fiber types to decr release of glutamate and substance P

104
Q

How is clonidine used in LA admin?

A

Adjunct to epidural and spinal

105
Q

What is the diazepam mechanism of action?

A

Activate GABA in CNS

106
Q

For which drug does the isomer used matter? And why?

A

Ropivacaine - S isomer has low affinity for cardiac Na channels

107
Q

What are the antimuscarinics? And what do they do?

A

Scopolamine and atropine

Cause amnesia and prevent bradycardia and fluid secretion

108
Q

Blood:gas coefficient tells us what about the GA?

A

Onset

109
Q

MAC tells us what about the GA?

A

Potency

Pharm II (2 decks)

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