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PLAB Pharmacology > Pharmacokinetics and Autonomic Drugs > Flashcards

Pharmacokinetics and Autonomic Drugs Flashcards

1
Q

what is bioavailability?

A
  • bioavailability (F) = % of administered drug reaching systemic circulation unchanged
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2
Q

when is bioavailability usually 100%?

A

F=100% for an IV dose

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3
Q

why is bioavailability usually less than 100% for an oral drug?

A

due to incomplete absorption and first pass metabolism

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4
Q

what is volume of distribution (Vd)?

A
  • amount of drug in the body / [drug] in the plasma
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5
Q

compartment and drug types when low volume of distribution

A
  • compartment: blood
  • drug types: large/charged molecules; plasma protein bound
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6
Q

compartment and drug types when medium volume of distribution

A
  • compartment: ECF
  • drug type: small hydrophilic molecules
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7
Q

compartment and drug types when high volume of distribution

A
  • compartment: all tissues including fat
  • drug type: small lipophilic mcs, especially if bound to tissue protein
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8
Q

what is the equation for half life for a first order elimination?

A

t1/2=0.693 x Vd / CL

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9
Q

what is clearance (CL)?

A
  • volume of plasma cleared of drug per unit time
  • may be impaired with defects in cardiac, hepatic, or renal function
  • CL=(rate of elimination of drug / plasma drug concentration) = Vd x Ke
    • ​Ke= elimination constant
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10
Q

what is loading dose?

A

loading dose = Cp x Vd / F

Cp = target plasma concentration at steady state

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11
Q

what is maintenance dose?

A

maintenance dose = Cp x CL x t / F

Cp = target plasma concentration at steady state

t = dosage interval (time b/w doses), if not administered continuously

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12
Q

maintenance dose and loading dose in renal or liver disease

A
  • maintenance dose decreases
  • loading dose is usually unchanged
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13
Q

what does the time to steady state depend on?

A
  • half life
  • independent of dose and dosing frequency
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14
Q

what is the difference between zero order elimination and first order elimination?

A
  • zero order–rate of elimination is constant regardless of Cp
    • constant amount of drug eliminated per unit time
    • Cp dec linearly with time
  • first order–rate of elimination is directly proportional to drug concentration
    • constant fraction of drug elminated per unit time
    • Cp dec exponentially with time
    • applies to most drugs
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15
Q

which drugs are zero order?

A
  • PEA–a pea is round shaped like the “0” in zero order
    • ​Phenytoin
    • Ethanol
    • Aspirin
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16
Q

what are weak acid drugs?

where do they get trapped?

how do you treat overdose?

A
  • phenobarbital, methotrexate, aspirin
  • trapped in basic environments
  • treat overdose with bicarbonate
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17
Q

what are weak base drugs?

where do they get trapped?

how do you treat overdose?

A
  • amphetamines
  • trapped in acidic environments
  • treat overdose with ammonium chloride
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18
Q

what are phase 1 types of drug metabolism?

what enzyme do they require?

what do they yield?

what occurs in geriatric patients?

A
  • reduction, oxidation, hydrolysis
  • require cytochrome P 450
  • yield slightly polar, water soluble metabolites
  • geratric patients lose phase I first
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19
Q

what are phase 2 type of drug metabolism?

what do they yield?

A
  • conjugation–Methylation, Glucuronidation, Acetylation, Sulfation
    • geriatric patients have More GAS (phase 2)
  • yields very polar, inactive metabolites (renally excreted)
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20
Q

what occurs in patients who are slow acetylators?

A
  • have increased side effects from certain drugs b/c of decreased rate of metabolism
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21
Q

effect of competitive antagonist on receptor binding

A
  • shifts curve right (decreased potency)
  • no change in efficacy
  • can be overcome by increasing the concentration of agonist substrate
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22
Q

effect of noncompetitive antagonist on receptor binding

A
  • shift curve down (decrease efficacy)
  • cannot be overcome by inc agonist substrate concentration
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23
Q

effect of partial agonist (alone) on receptor binding

A
  • acts at same site as full agonist, but with lower maximal effect (dec efficacy)
  • potency is an independent variable
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24
Q

what is the therapeutic index?

A
  • measurement of drug safety
  • Therapeutic Index = TD50/ED50 = median toxic dose / median effective dose
    • TITE
  • safer drugs have higher TI values
    • drugs with lower TI values frequently require monitoring
  • therapeutic window–dosage range that can safely and effectively treat dz
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25
Q

alpha 1 receptor:

type of receptor

G protein class

major functions

A
  • sympathetic
  • q
  • functions:
    • inc vascular smooth muscle contraction
    • inc pupillary dilator muscle contraction (mydriasis)
    • inc intestinal and bladder sphincter muscle contraction
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26
Q

alpha 2 receptor:

type of receptor

G protein class

major functions

A
  • sympathetic
  • i
  • functions:
    • dec sympathetic (adrenergic) outflow
    • decrease insulin release
    • dec lipolysis
    • inc platelet aggregation
    • dec aqueous humor product
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27
Q

beta 1 receptor

type of receptor

G protein class

major functions

A
  • sympathetic
  • s
  • functions:
    • inc heart rate
    • inc contractility
    • inc renin release
    • inc lipolysis
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28
Q

beta 2 receptor:

type of receptor

G protein class

major functions

A
  • sympathetic
  • s
  • functions:
    • vasodilation
    • bronchodilation
    • inc lipolysis
    • inc insulin release
    • dec uterine tone (tocolysis)
    • ciliary muscle relaxation
    • inc aqeuous humor production
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29
Q

beta 3 receptor:

type of receptor

G protein class

major functions

A
  • sympathetic
  • s
  • functions:
    • inc lipoysis
    • inc thermogenesis in skeletal muscle
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30
Q

M1 receptor

type of receptor

G protein class

major functions

A
  • parasympathetic
  • q
  • functions:
    • CNS
    • enteric nervous system
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31
Q

M2 receptor

type of receptor

G protein class

major functions

A
  • parasympathetic
  • i
  • functions:
    • dec heart rate
    • dec contractility of atria
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32
Q

M3 receptor

type of receptor

G protein class

major functions

A
  • parasympathetic
  • q
  • functions:
    • inc exocrine gland secretions
      • lacrimal, sweat, salivary, gastric acid
    • inc gut peristalsis
    • inc bladder contraction
    • bronchoconstriction
    • inc pupillary sphincter muscle contraction (miosis)
    • ciliary muscle contraction (accommodation)
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33
Q

D1 receptor

type of receptor

G protein class

major functions

A
  • dopamine
  • s
  • functions:
    • relaxes vascular smooth muscle
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34
Q

D2 receptor:

type of receptor

G protein class

major functions

A
  • dopamine
  • i
  • functions:
    • modulate transmitter release, especially in brain
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35
Q

H1 receptor:

type of receptor

G protein class

major functions

A
  • histamine
  • q
  • functions:
    • inc nasal and bronchial mucus production
    • inc vascular permeability
    • contraction of bronchioles
    • pruritus
    • pain
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36
Q

H2 receptor:

type of receptor

G protein class

major functions

A
  • histamine
  • s
  • functions:
    • increase gastric secretion
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37
Q

V1 receptor:

type of receptor

G protein class

major functions

A
  • vasopressin
  • q
  • functions:
    • inc vascular smooth muscle contraction
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38
Q

V2 receptor:

type of receptor

G protein class

major functions

A
  • vasopressin
  • s
  • functions:
    • inc water permeability and reabsorption in collecting tubules of kidney
      • “V<strong>2</strong> is found in 2 kidneys”
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39
Q

how to remember G protein linked 2nd messengers

A

“After qisses (kisses), you get a qiq (kick) out of siq (sick) sqs (super kinky sex).

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40
Q

tyramine–mechanism

A
  • normally degraded by monoamine oxidase (MAO)
  • levels inc in patients taking MAO inhibitors who ingest tyramine rich foods (ie. cheese, wine)
  • excess tyramine enters presynaptic vesicles and displaces other neurotransmitters (ie. NE) –> inc active presynaptic neurotransmitters –> inc diffusion of neurotransmitters into synaptic cleft –> inc sympathetic stimulation
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41
Q

what does tyramine classically cause?

A

hypertensive crisis

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42
Q

name the 4 direct cholinomemetic agonists

A
  • bethanechol
  • carbachol
  • methacholine
  • pilocarpine
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43
Q

bethanechol–mechanism

A
  • activates bowel and bladder smooth muscle
  • resistant to AChE
    • “Bethany call (bethanchol) me to activate your bowels and bladder.”
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44
Q

bethanechol–use

A
  • postoperative ileus
  • neurogenic ileus
  • urinary retention
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45
Q

carbachol–mechanism

A
  • carbon copy of acetylcholine
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46
Q

carbachol–use

A
  • constricts pupil and relieves intraocular pressure in open angle glaucoma
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47
Q

methacholine–mechanism

A
  • stimulates muscarinic receptors in airway when inhaled
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48
Q

methacholine–use

A
  • challenge test for diagnosis of asthma
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49
Q

pilocarpine–mechanism

A
  • contracts ciliary muscle of eye–open angle glaucoma
  • pupillary sphincter–closed angle glucoma
  • resistant to AChE
    • “You cry, drool, and sweat on your pilow”
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50
Q

pilocarpine–use

A
  • potent stimulator of sweat, tears, saliva
  • open angle and closed angle glaucoma
  • xerostomia–Sjorgren syndrome
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51
Q

name the 7 indirect cholinomimetic agents (anticholinesterases)

A
  • donepezil
  • galantamine
  • rivastigmine
  • edrophonium
  • neostigmine
  • physostigmine
  • pyridostigmine
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52
Q

donepezil, galantamine, rivastigmine–mechanism

A
  • inc ACh
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53
Q

donepezil, galantamine, rivastigmine–use

A
  • Alzheimer disease
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54
Q

edrophonium–mechanism

A
  • inc ACh
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55
Q

edrophonium–use

A
  • historically, diagnosis of myasthenia gravis–extremely short acting
    • myasthenia now diagnosed by anti AChR Ab (anti acetylcholine receptor antibody) test
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56
Q

neostigmine–mechansm

A
  • inc ACh
    • “Neo CNS = No CNS penetration (quaternary amine)
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57
Q

neostigmine–use

A
  • postoperative and neurogenic ileus and urinary retention
  • myasthenia gravis
  • reversal of neuromuscular junction blockade–postoperative
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58
Q

physostigmine–mechanism

A
  • inc ACh
    • “Physostigmine ‘phyxes’ atropine overdose”
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59
Q

physostigmine–use

A
  • anticholinergic toxicity
  • crosses blood brain barrier –> CNS (tertiary amine)
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60
Q

pyridostigmine–mechanism

A
  • inc ACh
  • inc muscle strength
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61
Q

pyridostigmine–use

A
  • myasthenia gravis (long acting)
    • “Pyridostigmine gets rid of myasthenia gravis”
  • does not penetrate CNS–quaternary amine
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62
Q

what is important to watch for when administering any cholinomimetic agents?

A
  • exacerbation of COPD
  • asthma
  • peptic ulcers
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63
Q

what causes cholinesterase inhibitor poisoning?

A
  • often due to organophosphates, such as parathion, that irreversibly inhibit AChE
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64
Q

in which population is cholinesterase inhibitor poisoning usually seen and why?

A
  • farmers b/c organophosphates are often components of insecticides
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65
Q

what does cholinesterase inhibitor poisoning cause?

A
  • Diarrhea
  • Urination
  • Miosis
  • Bronchospasm
  • Bradycardia
  • Excitation of skeletal muscle and CNS
  • Lacrimation
  • Sweating
  • Salivation
    • “DUMBBELSS”
  • may lead ot respiratory failure if untreated
66
Q

what is the antidote for cholinesterase inhibitor poisoning?

A
  • atropine (competitive inhibitor) + pralidoxime (regenerates AChE if given early)
67
Q

name the muscarinic antagonists

A
  • atropine, homatropine, tropicamide
  • benztropine
  • glycopyrrolate
  • hyoscyamine, dicyclomine
  • ipratropium, tiotropium
  • oxybutynin, solifenacin, tolterodine
  • scopolamine
68
Q

atropine, homatropine, tropicamide–organ system and use

A
  • eye
    • produce mydriasis
    • produce cyclopegia
69
Q

benztropine–organ system and use

A
  • CNS
    • Parkinson dz
      • “park my Benz”
    • acute dystonia
70
Q

glycopyrrolate–organ system and use

A
  • GI
    • drooling
    • peptic ulcer
  • respiratory
    • preoperative use to reduce airway secretions
71
Q

hyoscyamine, dicyclomine–organ system and use

A
  • GI
    • antispasmodics for irritable bowel syndrome
72
Q

ipratropium, tiotropium–organ system

A
  • respiratory
    • COPD
    • asthma
      • “I pray I can breathe soon”
73
Q

oxybutynin, solifenacin, tolterodine–organ system and use

A
  • genitourinary
    • reduce bladder spasms
    • urge urinary incontinence
      • overactive bladder
74
Q

scopolamine–organ system and use

A
  • CNS
    • motion sickness
75
Q

atropine–drug class and use

A
  • muscarinic antagonist
  • used to treat bradycardia and for ophthalmic applications
76
Q

what is the action of atropine on the eyes?

A
  • increase pupil dilation
  • cycloplegia
77
Q

what is the action of atropine on the airway?

A
  • decreased secretions
78
Q

what is the action of atropine on the stomach?

A
  • decreased acid secretion
79
Q

what is the action of atropine on the gut?

A
  • decrease motility
80
Q

what is the action of atropine on the bladder?

A
  • decreased urgency in cystitis
81
Q

atropine and cholinesterase inhibitor poisoning

A
  • blocks DUMBBeLSS in cholinesterase inhibitor poisoning
    • diarrhea
    • urination
    • miosis
    • bronchospasm
    • bradycardia
    • lacrimation
    • sweating
    • salivation
  • DOES NOT block excitation of skeletal muscle and CNS
    • mediated by nicotinic receptors
82
Q

atropine–toxicity

A
  • incresed body temperature–due to dec sweating
  • rapid pulse
  • dry mouth
  • dry, flushed skin
  • cycloplegia
  • constipation
  • disorientation
    • ​“Hot as a hare”
    • “Dry as a bone”
    • “Red as a beet”
    • “Blind as a bat”
    • “Mad as a hatter”
  • can cause acute angle closure glaucoma in elderly due to mydriasis
  • can cause urinary retention in men with prostatic hyperplasia
  • can cause hyperthemia in infants
83
Q

name the direct sympathomimetics

A
  • albuterol, salmeterol
  • dobutamine
  • dopamine
  • epinephrine
  • fenoldopam
  • isoproterenol
  • midocrine
  • norepinephrine
  • phenylephrine
84
Q

albuterol, salmeterol–mechanism

A
  • beta 2 > beta 1
85
Q

albuterol, salmeterol–use

A
  • albuterol for acute asthma or COPD
  • salmeterol for long term asthma or COPD control
86
Q

dobutamine–mechanism

A
  • beta 1 > beta 2, alpha
87
Q

dobutamine–use

A
  • heart failure (HF) – inotropic > chronotropic
  • cardiac stress testing
88
Q

dopamine–mechanism

A
  • D1 = D2 > beta > alpha
89
Q

dopamine–use

A
  • unstable bradycardia
  • HF
  • shock
  • inotropic and chronotropic effects at lower doses due to beta effects
  • vasoconstriction at high doses to alpha effects
90
Q

epinephrine–mechanism

A
  • beta > alpha
91
Q

epinephrine–use

A
  • anaphylaxis
  • asthma
  • open angle glaucoma
  • alpha effects predominate at high doses
  • significantly stronger effect at beta2 receptors than norepinephrine
92
Q

fenoldopam–mechanism

A
  • D1
93
Q

fenoldopam–use

A
  • postoperative hypertension
  • hypertensive crisis
  • vasodilator–coronary, peripheral, renal, splanchnic
  • promotes natriuresis
94
Q

fenoldopam–toxicity

A
  • hypotension
  • tachycardia
95
Q

isoproterenol–mechanism

A
  • beta1 > beta2
96
Q

isoproterenol–use

A
  • electrophysiologic evaluation of tachyarrhythmias
  • can worsen ischemia
97
Q

midodrine–mechanism

A
  • alpha1
98
Q

midodrine–use

A
  • autonomic insufficiency
  • postural hypotension
99
Q

midodrine–toxicity

A
  • may exacerbate supine hypertension
100
Q

norepinephrine–mechanism

A
  • alpha1 > alpha2 > beta1
101
Q

norepinephrine–use

A
  • hypotension
  • septic shock
102
Q

phenylephrine–mechanism

A
  • alpha1 > alpha2
103
Q

phenylephrine–use

A
  • hypotension (vasoconstrictor)
  • ocular procedures (mydriatic)
  • rhinitis (decongestant)
104
Q

name the indirect sympathomimetics

A
  • amphetamine
  • cocaine
  • ephedrine
105
Q

amphetamine–mechanism

A
  • indirect general agonist
  • reuptake inhibitor
  • releases stored catecholamines
106
Q

amphetamine–use

A
  • narcolepsy
  • obesity
  • ADHD
107
Q

cocaine–mechanism

A
  • indirect general agonist
  • reuptake inhibitor
108
Q

cocaine–use

A
  • causes vasoconstriction and local anesthesia
109
Q

what to remember about cocaine intoxication?

A
  • never give beta blockers
    • can lead to unopposed alpha1 activation and extreme hypertension
110
Q

ephedrine–mechanism

A
  • indirect general agonist
  • releases stored catecholamines
111
Q

ephedrine–use

A
  • nasal decongestion
  • urinary incontinence
  • hypotension
112
Q

norepinephrine vs. isoproterenol

A
  • norepinephrine inc systolic and diastolic pressures as a result of alpha1 mediated vasoconstriction –> inc mean arterial pressure –> reflex bradycardia
  • isoproterenol–not commonly used anymore
    • has little alpha effect but causes beta2 mediated vasodilation –> dec mean arterial pressure and inc heart rate thru beta1 and reflex activity
113
Q

name the sympatholytics alpha2 agonists

A
  • clonidine, guanfacine
  • alpha methyldopa
114
Q

clonidine, guanfacine–use

A
  • hypertensive urgency (limited situations)
  • ADHD
  • tourette syndrome
115
Q

clonidine, guanfacine–toxicity

A
  • CNS depression
  • bradycardia
  • hypotension
  • respiratory depression
  • miosis
116
Q

alpha methyldopa–use

A
  • hypertension during pregnancy
117
Q

alpha methyldopa–toxicity

A
  • direct Coombs + hemolysis
  • SLE like syndrome
118
Q

name the non-selective alpha blockers

A
  • phenoxybenzamine (irreversible)
  • phentolamine (reversible)
119
Q

phenoxybenzamine–use

A
  • pheochromocytoma (used preoperatively) to prevent catecholamine (hypertensive) crisis
120
Q

phenoxybenzamine–toxicity

A
  • orthostatic hypotension
  • reflex tachycardia
121
Q

phentolamine–use

A
  • give to patients on MAO inhibitors who eat tyramine containing foods
122
Q

phentolamine–toxicity

A
  • orthostatic hypotension
  • reflex tachycardia
123
Q

name the alpha1 selective alpha blockers

A
  • -osin ending
    • Prazosin, terazosin, doxazosin
    • tamsulosin
124
Q

Prazosin, terazosin, doxazosin–use

A
  • urinary symptoms of BPH
  • PTSD–prazosin
  • hypertension
125
Q

Prazosin, terazosin, doxazosin–toxicity

A
  • 1st dose orthostatic hypotension
  • dizziness
  • headache
126
Q

tamsulosin–use

A
  • urinary symptoms of BPH
127
Q

tamsulosin–toxicity

A
  • 1st dose orthostatic hypotension
  • dizziness
  • headache
128
Q

name the alpha2 selective alpha blockers

A
  • mirtazapine
129
Q

mirtazapine–use

A
  • depression
130
Q

mirtazapine–toxicity

A
  • sedation
  • inc serum cholesterol
  • inc appetite
131
Q

alpha blockade of epinephrine vs. phenylephrine

A
  • effects of an alpha blocker like phentolamine on blood pressure responses to epinephrine and phenylephrine
    • epinephrine response exhibits reversal of the mean blood pressure change, from a net inc (alpha response) to a net decrease (beta 2 response)
    • the response to phenylephrine is suppressed but not reversed b/c phenylephrine is a “pure” alpha agonist w/o beta action
132
Q

name the beta blockers

A
  • acebutolol
  • atenolol
  • betaxolol
  • carvedilol
  • esmolol
  • labetalol
  • metoprolol
  • nadolol
  • nebivolol
  • pindolol
  • propranolol
  • timolol
133
Q

beta blockers–use

A
  • angina pectoris
  • MI
  • SVT (metoprolol, esmolol)
  • hypertension
  • HF
  • glaucoma (timolol)
  • variceal bleeding (nadolol, propranolol)
134
Q

how do beta blockers work for angina pectoris?

A
  • dec heart rate and contractility
    • results in dec O2 consumption
135
Q

how do beta blockers work for MI?

A
  • dec mortality
136
Q

how do beta blockers work for SVT?

A
  • only metoprolol, esmolol
  • dec AV conduction velocity
    • class II antiarrhythmic
137
Q

how beta blockers work for hypertension?

A
  • dec cardiac output
  • dec renin secretion
    • due to beta1 receptor blockade on JGA cells
138
Q

how do beta blockers work for HF?

A
  • dec mortality
    • with bisoprolol, carvedilol, metoprolol
139
Q

how do beta blockers work for glaucoma?

A
  • only timolol
    • dec secretion of aqueous humor
140
Q

how do beta blockers work for variceal bleeding?

A
  • only nadolol, propranolol
    • dec hepatic venous pressure gradient and portal hypertension
141
Q

beta blockers–toxicity

A
  • erectile dysfunction
  • cardiovascular adverse effects–bradycardia, AV block, HF
  • CNS adverse effects–seizures, sedation, sleep alterations
  • dyslipidemia
    • with metoprolol
  • asthma/COPD exacerbations
142
Q

beta blockers and cocaine users

A
  • use with caution in cocaine users due to risk of unopposed alpha-adrenergic receptor agonist activity
143
Q

beta blockers and diabetics

A
  • despite theoretical concern of masking hypoglycemia in diabetics, benefits likely outweight the risks
    • NOT contraindicated
144
Q

name the beta1 selective antagonists (beta1 > beta2)

A
  • acebutolol–partial agonist
  • atenolol
  • betaxolol
  • esmolol
  • metoprolol
    • “selective antagonists mostly go from A to M–beta<strong>1</strong> with 1st half of alphabet”
145
Q

name the non selective antagonists (Beta1 = beta2)

A
  • Nadolol
  • Pindolol–partial agonist
  • Propranolol
  • Timolol
    • Nonselective antagonists mostly go from N to Z–beta<strong>2</strong> with 2nd half of alphabet
146
Q

name the nonselective alpha and beta antagonists

A
  • carvedilol
  • labetalol
    • both have modifed suffixes–instead of “-olol”
147
Q

nebivolol–selectivity

A
  • combines cardiac selective beta1 adrenergic blockade with stimulation of beta3 receptors which activate nitric oxide synthase in the vasculature
148
Q

name the 3 ingested seafood toxins

A
  • tetrodotoxin
  • ciguatoxin
  • histamine–scombroid poisoning
149
Q

tetrodotoxin–source

A
  • pufferfish
150
Q

tetrodotoxin–mechanism

A
  • highly potent toxin
  • binds fast voltage gated Na channels in cardiac/nerve tissue
    • prevents depolarization
151
Q

tetrodotoxin–symptoms

A
  • nausea
  • diarrhea
  • paresthesias
  • weakness
  • dizziness
  • loss of reflexes
152
Q

tetrodotoxin–treatment

A

mostly supportive

153
Q

ciguatoxin–source

A
  • reef fish such as barracuda, snapper, moray eel
154
Q

ciguatoxin–mechanism

A
  • opens Na channels which causes depolarization
155
Q

ciguatoxin–symptoms

A
  • symptoms mimic cholinergic poisoning
156
Q

ciguatoxin–treatment

A

primarily supportive

157
Q

histamine (scombroid poisoning)–source

A
  • spoiled dark meat fish such as tuna, mahi mahi, mackerel, bonito
158
Q

histamine (scombroid poisoning)–mechanism

A
  • bacterial histidine decarboxylase converts histidine to histamine
  • frequently misdiagnosed as a fish allergy
159
Q

histamine (scombroid poisoning)–symptoms

A
  • mimics anaphylaxis:
    • acute burning sensation of mouth
    • flushing of face
    • erythema
    • urticaria
    • itching
    • may progress to:
      • bronchospasm
      • angioedema
      • hypotension
160
Q

histamine (scombroid poisoning)–treatment

A
  • antihistamines
  • albuteral and epinephrine if needed

PLAB Pharmacology (17 decks)

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