Exam 1 Flashcards
1
Q
what about the structure of LAs increases their lipophilicity?
A
longer hydrocarbon chain and interconnecting chain
2
Q
how do ester and amide LA metabolism differ?
A
esters - metabolized by plasma and liver pseudocholinesterases
amides - metabolized by liver P450s
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)
4
Q
which drugs are used for topical anesthesia
A
benzocaine and cocaine
5
Q
procaine and lidocaine can both be used for which 3 forms of LA?
A
infiltration (injection), epidural, spinal
6
Q
why does LA getting to the brain cause convulsions?
A
d/t blockade of the GABA-A receptors (causes decr inhibition)
7
Q
how is cocaine the exception when it comes to LAs having adverse cardio effects?
A
causes tachycardia, vasoconstriction, HTN
8
Q
how does Epi affect the action of LAs?
A
it incr the LA action by 50%
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
10
Q
how is clonidine used as an adjunct in LA admin?
A
decr substance P and glutamate release (decr pain transmission)
11
Q
which routes of LA admin is clonidine used in?
A
epidural and spinal
12
Q
what are the protective components of the stomach?
A
mucous, bicarbonate, PGE
13
Q
why do you need to be careful with cimetidine?
A
it is metabolized by CYPs so can interact with warfarin and phenytoin
14
Q
which patients need a dose adjustment for H2 blockers?
A
renal insufficiency
15
Q
how long does one dose of omeprazole work for?
A
t1/2 = 1.5hrs, however decr acid secretion for 2-3 days
16
Q
rare side effects of omeprazole
A
nausea, diarrhea, dizziness
17
Q
how do PPIs affect the bones with longterm use?
A
decr acidity decr the amount of Ca absorbed so bones more fragile
18
Q
what is the first choice treatment in Zollinger-Ellison syndrome?
A
omeprazole
19
Q
what indication is omeprazole less than ideal for?
A
occasional heartburn
20
Q
which upper GI drugs can you develop a tolerance to?
A
H2 blockers
21
Q
when can antacids be taken?
A
after a meal when there is acid present
22
Q
what AE does Mg(OH)2 have if given alone?
A
diarrhea
23
Q
what AE does Al(OH)3 or CaCO3 have if either are given alone?
A
constipation
24
Q
how can antacids affect the urine?
A
they can increase the pH and alter the elimination of acidic and basic drugs
25
which drugs do Al(OH)3 and CaCO3 alter the absorption of?
tetracycline, INH, ketoconazole
26
which drug must be admin 2 hours after tetracycline, phenytoin, and digoxin and why?
sucralfate b/c it can absorb other drugs
27
when must sucralfate be admin?
before a meal
28
what strange AE does bismuth cause?
blackened tongue and stool
29
why can't bismuth be used in children?
salicylate acid causes Reye's syndrome
30
what is bismuth esp good for and why?
H. pylori infection d/t antimicrobial feature
31
what is misoprostol CI in?
pregnancy (d/t induction of contractions)
32
which drugs is B12 malabsorption associated with? why?
PPIs
| d/t the fact that B12 absorption needs an acidic environment
33
where is the majority of 5-HT produced?
guts
34
how does metoclopramide affect the LES and pyloric sphincters?
incr LES tone to prevent backup
| relaxes pyloric sphincter tone to incr gastric emptying
35
how do the MOAs for metoclopramide and ondansetron differ?
metoclopramide - D2 & 5-HT3 antagonist; 5-HT4 agonist
| ondansetron - 5-HT3 receptor antagonist
36
how can ondansetron effectiveness be incr?
adding dexamethasone or aprepitant
37
metoclopramide AEs
parkinsonism like sx, tardive dyskinesia
38
ondansetron AEs
constipation and headache/GI sx
39
why can't linaclotide be used in children
reports of mortality d/t dehydration in mice
40
how do linaclotide and lubiprostone MOAs differ?
Linaclotide - activates CFTR via cGMP
| Lubiprostone - directly activates ClC2 Cl channel
41
what type of solution is Mg(OH)2 as an osmotic laxative and how does this affect its MOA?
admin as hypertonic solution which incr osmotic pressure and causes accumulation of fluids in GI tract
42
what are the indications for saline laxative (MgOH2)?
colonoscopy prep
| IBS-C
43
how do steroids help IBD?
reduce ulceration and cause initial remission
44
what are the GI prodrugs?
omeprazole, sulfasalazine, azathioprine
45
adverse effects of 5-ASA
diarrhea, nausea, headaches, hypersensitivity, bone marrow suppression
46
AE of infliximab
infections (d/t immunosuppression)
47
what is azathioprine good for?
IBD long term treatment (response could take weeks-months)
48
which drugs are substrates for P450 enzymes and therefore can have their metabolism affected by ethanol
TCAs, H1 antihistamines, narcotics, anticonvulsants, BZs
49
lethal dose of alcohol
> 500mg/dL
50
at what dose of alcohol does impaired driving occur?
50-80 mg/dL
51
alcohol's affect on GABA
at high conc, it will incr the inhibitory effect of GABA
52
what is the mechanism behind alcohol induced vomiting
alcohol excites the 5-HT3 receptors which leads to emesis
53
why can't acetaminophen be used with alcohol?
it coverts acetaminophen to a hepatotoxic metabolite
54
what are the 3 endocrine effects of alcohol use?
gynecomastia, testicular atrophy, salt retention
55
tx for alcohol w/d syndrome
long acting BZs (diazepam, chlordiazepoxide), clonidine, propranolol
56
what does chronic EtOH use incr (neurologically)
incr synaptic concentration of dopamine, serotonin, endogenous opioids
57
how do functional tolerance and metabolic tolerance differ?
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
how is naltrexone used for alcoholism?
anti-craving b/c it reduces the reward assoc w/alcohol consumption
59
which population do you need to be careful with in prescribing naltrexone? why?
opioid dependent patients b/c it can lead to severe w/d
60
other than naltrexone, which medications are used for used for their anti-craving effect?
acamprosate and topiramate
61
what is NAC?
N-acetylcysteine
| used to tx chronic alcoholics suspected of acetaminophen poisoning which could lead to irreversible liver damage
62
what is fomepizole used for?
antidote to methanol and ethylene glycol toxicity
63
how does one get ethylene glycol poisoning?
industrial exposure or drinking antifreeze
64
what is oxalic acid?
what ethylene glycol is metabolized to
| can cause severe acidosis and renal damage
65
what is used to prevent the results of ethylene glycol toxicity?
ethanol (will compete for oxidation by ADH)
66
what is the Narcan test
used if you suspect recovering alcoholic is abusing opioids
67
what is methanol metabolized into and what can it cause?
formaldehyde which can cause severe acidosis, blindness, and retinal damage
68
how can methanol intoxication be reversed?
IV ethanol (will compete for ADH and prevent the oxidation of methanol)
69
how do clonidine and propranolol each decr sympathetic outflow?
clonidine - activates alpha2 adrenergic receptors in the CNS
propranolol - block beta adrenergic receptors in the CNS
70
more lipid soluble an anesthetic the more ______ it is
potent
71
how is anesthetic uptake calculated
gas solubility in the blood x cardiac output x gradient between alveolar and blood anesthetic partial pressures
72
why is it beneficial that inhaled anesthetics decr CO?
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
what is MAC?
minimum alveolar concentration - end tidal concentration of inhaled anesthetic needed to eliminate movement in 50% of patients stimulated by an incision
74
what are BZs good for?
reduce anxiety, induce amnesia
75
what are antihistamines good for?
ppx for allergic rxn, some sedation
76
what are antiemetics good for?
prevent aspiration, decr postop N/V
77
what are opioids good for?
provide analgesia
78
what are antimuscarinics good for?
amnesia, prevent bradycardia and fluid secretion
79
what are muscle relaxants good for?
facilitating intubation
80
what is the big disadvantage with halothane?
halothane hepatitis
81
what is the MC used inhaled anesthetic?
isoflurane
82
what are the advantages with isoflurane?
CO maintained, systemic vessels dilate causing small decr in BP, arrhythmias are uncommon, potent coronary vasodilator
83
why are sevoflurane & desflurane unique?
can be used for outpatient anesthesia d/t rapid recovery
84
NO provides ____ but not ____
analgesia; anesthesia
85
what are the characteristics of malignant hyperthermia?
sustained muscle contraction, lactate production, increased body temp
86
how does dantrolene tx malignant hyperthermia?
reduces intracellular Ca
87
what should be provided upon d/c of NO and why?
100% oxygen b/c hypoxia may occur
88
why should NO be used w/caution in closed spaces?
it incr the volume of closed spaces (can cause pneumothorax or incr pressure in sinus)
89
what is the milk of amnesia?
propofol (hypnotic and forgetful rest)
90
what determines the duration of action for IV anesthetics?
redistribution to body groups (VRG, muscle groups, fat group, vessel poor group)
91
what is the advantage of sodium thiopental?
little postop excitement or vomiting
92
which patient population is ketamine better for and why?
kids
| adverse effects less common
93
what are the AEs of ketamine?
incr muscle tone causing involuntary movements
| hallucinations
94
what is the unique advantage of ketamine?
does not cause respiratory depression
| may cause incr in BP
95
what is the unique advantage of etomidate?
antagonist available
96
if a drug accumulates somewhere what does that mean in terms of recovery?
it will be slow
97
which IV agent(s) provide analgesia?
ketamine
98
which IV agents do not provide analgesia?
propofol, sodium thiopental, etomidate
99
which IV agent can cause a painful injection?
etomidate
100
what type of proteins do DAAs target?
non-structural proteins
101
what is the BBW for DAAs?
HBV reactivation of HCV/HBV coinfection
102
what are the 3 types of DAAs?
protease inhibitors (PIs, NS3/4), polymerase inhibitors (NS5B), NS5A inhibitors
103
How does clonidine effect the C and A fibers?
Activates a2 adrenergic receptors on both fiber types to decr release of glutamate and substance P
104
How is clonidine used in LA admin?
Adjunct to epidural and spinal
105
What is the diazepam mechanism of action?
Activate GABA in CNS
106
For which drug does the isomer used matter? And why?
Ropivacaine - S isomer has low affinity for cardiac Na channels
107
What are the antimuscarinics? And what do they do?
Scopolamine and atropine
| Cause amnesia and prevent bradycardia and fluid secretion
108
Blood:gas coefficient tells us what about the GA?
Onset
109
MAC tells us what about the GA?
Potency
