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Pharmacology > Mid term > Flashcards

Mid term Flashcards

1
Q

Examples of drugs that are plant derived

A

digoxin, aspirin, morphine

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2
Q

semi synthetic drugs

A

have component of both synthetic and naturally occurring molecule

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3
Q

xenobiotics

A

compound that is foreign to the body

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4
Q

types of names of drugs

A

chemical name, generic name, brand name

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5
Q

5 rights of drug administration

A

right drug, right patient, right dose, right route, right time

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6
Q

oral administration

A

most common route; drugs must be metabolized in gut wall or liver prior to reaching circulation (first pass metabolism)

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7
Q

first pass metabolism

A

metabolizing of a drug that decreases the amount of active drug absorbed; metabolism of a drug before it reaches systemic circulation (ex: PO and PR); can be metabolized by enzymes in the intestines prior to undergoing further metabolism in liver prior to systemic circulation

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8
Q

sublingual administration

A

absorbed under the tongue; lots of vasculature making it a good way to administer medication that needs to enter bloodstream rapidly

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9
Q

transdermal administration

A

slow and continuous absorption through the skin

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10
Q

interosseous administration

A

injecting into bone marrow; substitute for inability to obtain IV access

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11
Q

intramuscular administration

A

delivered into muscle; muscle mass and perfusion can affect how quickly drug is absorbed

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12
Q

subcutaneous

A

delivered into subcutaneous fatty tissue directly below skin

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13
Q

Intravenous administration

A

fastest route to administer drugs; rapidly distributed

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14
Q

intrathecal

A

delivering drugs into spinal cord to reach CNS; released into CSF

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15
Q

intraperitoneal

A

peritoneum is semi-permeable and some people on dialysis may receive drugs this way

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16
Q

bioavailability

A

rate and extent of absorption; amount that reaches circulation

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17
Q

drug chemical/physiochemical properties affecting absorption

A

drug solubility/dissolution rate, size/surface area, polymorphism/amorphism, solvates/hydrates, salt form of drug, ionization stated, pKA/lipophilicity and GI pH

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18
Q

drug formulation factors affecting absorption

A

disintegration time, manufacturing variables, nature type and dose, ingredients, product age and storage conditions

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19
Q

patient factors that affect drug absorption

A

age, gastric emptying time, intestinal transit time, disease status, blood flow at absorption site, first pass metabolism, GI content (food)

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20
Q

pharmacokinetics of medication in body

A
  1. absorbed into circulation
  2. distributed to various tissues
  3. metabolized or broken down
  4. eliminated/excreted in urine or feces
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21
Q

absorption

A

transportation of unmetabolized drug from site of administration to the body circulation system

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22
Q

area of the body with the fastest drug absorption

A

duodenal mucosa because of the villi and microvilli which proved large surface area

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23
Q

overview of how drugs work

A

bind to a receptor -> activate cascade of intracellular effects -> results in change in cellular function -> cause physiological response of the drug

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24
Q

agonist

A

enhances activity; molecule capable of binding to and activating target protein; produce the desired effects by activating receptors

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25
Q

example of agonist

A

fentanyl binds to Mu, kappa, and delta receptors of CNS and PNS, activating them to produce desired affects such as analgesia and euphoria

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26
Q

antagonist

A

molecule that binds to target and prevents other molecules from binding to active receptor site

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27
Q

example of antagonist

A

atropine which is an antimuscarinic agent blocks muscarinic receptors of heart reversing vagally stimulated bradycardia

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28
Q

what happens when there is repeated receptor activation of a drug

A

desensitization of receptor response; decreased efficacy of drug

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29
Q

efficacy of a drug

A

extent that a drug can produce a response when all receptors/binding sites are occupied

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30
Q

potency of a drug

A

amount of drug necessary to produce an effect (more potent requires lower dosage)

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31
Q

therapeutic index

A

ratio of the drug that produces toxicity in half of the population to the dose that produces clinically desired response in half the population

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32
Q

as molecular weight approaches 500 daltons

A

skin permeation approaches zero

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33
Q

chiral atoms

A

carbon atom connected to 4 different substituents; creates asymmetric carbon atom that is not superimposable

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34
Q

R enantiomer of albuterol

A

right handed; creates the bronchodilation effect of when interacting with beta receptor

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35
Q

S enantiomer of albuterol

A

left handed; blocks metabolic pathways of R enantiomer and has slower rate of elimination causing accumulation in lungs = hyperreactivity and inflammation

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36
Q

polypharmacy

A

regular use of at least 5 medications

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37
Q

BEERS criteria

A
  1. reduce older adults exposure to potentially inappropriate medications; 2. educate clinicians and patients; 3. serve as tool for quality of care, cost, and patterns of drug use in older adults
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38
Q

pharmacokinetics

A

what the body does to a drug

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39
Q

phamarcodynamics

A

what the drug does to the body

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40
Q

distribution of drug depends on

A

blood flow, capillary permeability, binding of drugs to plasma proteins, binding of drugs to tissues, lipophilicity, volume of distribution

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41
Q

main source of drug metabolism

A

liver due to the enzymes present

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42
Q

how drugs can be metabolized

A

oxidation, reduction, hydrolysis, hydration, conjugation, condensation, isomerization

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43
Q

reasons for increased half life in indviduals

A

decreased renal/hepatic blood flow, decreased extracting of drug from plasma, decreased metabolism (ex: liver cirrhosis)

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44
Q

first order kinetics

A

rate of elimination is proportional to drug concentration; more drug = faster metabolism

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45
Q

zero order kinetics

A

rate of elimination is constant

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46
Q

examples of zero order kinetics

A

warfarin, heparin, aspirin, alcohol, theophylline, tolbutamide, phenytoin, phenylbutazone, ethanol

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47
Q

purpose of drug metabolism

A

make drug more hydrophilic and more water soluble to facilitate elimination

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48
Q

drug metabolized from and to

A
  1. toxic drug to nontoxic metabolite; 2. prodrug to an active drug; 3. active drug to inactive drug
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49
Q

phase 1 metabolism

A

oxidation, reduction, and hydrolysis reactions that converts drug to more polar molecule or converts lipid soluble to water soluble

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50
Q

most important enzyme in phase 1 metabolism

A

CYP450

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51
Q

CYP450

A

microsomal superfamily of isoenzymes that catalyzes oxidation of many drugs; can be induced or inhibited

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52
Q

phase 2 metabolism

A

conversion of parent drug to more polar (water soluble) inactive metabolites; renally excreted

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53
Q

CYP450 components

A

CYP3A4 and CYP206 which metabolize 50% and 25% of drugs

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54
Q

glomerular filtration

A

drugs enter kidney through renal arteries and divide to form glomerular capillary

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55
Q

proximal tubular secretion

A

represents primary kidney mechanism for eliminating hundreds of commonly prescribed meds

56
Q

distal tubular reabsoprtion

A

passive process where drugs are reabsorbed into systemic circulation from lumen of distal tubules

57
Q

normal glomerular filtration rate

A

120mL/min/1.73m3

58
Q

pain

A

unpleasant sensory and emotional experience associated with actual or potential tissue damage

59
Q

nocioceptive pain

A

to minimize and avoid damage from intense noxious stimuli; immediate attention and withdrawal

60
Q

inflammatory pain

A

low threshold pain; tenderness discourages contact and movement reducing further risk of injury and promoting healing

61
Q

neuropathic pain

A

lesion or disease of somatosensory nervous system; low threshold

62
Q

CNS dysfunctional pain

A

no damage or inflammation; low threshold

63
Q

pain therapies to close gate

A

massage, acupuncture, electrotherapy (surface nerve stim)

64
Q

non-opioid analgesics

A

acetaminophen, ibuprofen, aspirin, anticonvulsants, antidepressants, topical agents, other NSAIDs

65
Q

acetaminophen mechanism of action

A

interaction of cyclooxygenase and cyclooxygenase receptor pathway; acts on CNS cox receptors to block them and decrease prostaglandin synthesis = analgesic effect

66
Q

acetaminophen mechanism of action (other way)

A

stimulates descending serotonergic pathway which regulates pain

67
Q

acetaminophen dosage

A

pediatrics = weight based
adults = 325-975 (max 4g in 24 hours)

68
Q

acetaminophen onset

A

30-60 minutes oral
5-10 minutes IV
peaks in about 4 hours

69
Q

acetaminophen metabolism

A

undergoes both phase 1 and phase 2

70
Q

primary metabolic pathway of acetaminophen

A

sulfation and glucuronidation leading to more water soluble metabolite to be excreted renally

71
Q

rest of metabolic pathway of acetaminophen

A

metabolized by cytochrome P450 system to N-acetyl-p-benzoquinomine (toxic metabolite) which can bind to liver cells and cause injury; quickly bound to tripeptide glutathione inactivating metabolite and becoming more water soluble to be excreted renally

72
Q

NSAID mechanism of action

A

works primarily on cyclooxygenase receptor

73
Q

NSAID with PPI

A

reduce GI affects by decreasing overall stomach pH as method to reduce risk of gastritis and GI bleeding

74
Q

gabapentin

A

anti-convulsant med that inhibits release of excitatory neurotransmitters; excreted unchanged through kidneys; used for seizure and neuropathic pain

75
Q

pregabalin

A

inhibits excitatory neurotransmitter release, focal onset seizures, diabetic neuropathy, herpetic neuralgia, and fibromyalgia

76
Q

amitriptyline

A

tricyclic antidepressant (TCA); inhibits norepi and serotonin reuptake into presynaptic neuron; prevents migraines headache and chronic pain

77
Q

duloxetine

A

inhibits serotonin and norepi reuptake (SNRI); only metabolized in liver; GI side effects; moderate inhibitor of CYP3A4

78
Q

opioids work how?

A

bind to specific receptors in CNS to produce effects that mimic action of endogenous peptide neurotransmitters

79
Q

receptor families

A
  1. Mu (MOP)
  2. Kappa (KOP)
  3. Delta (DOP)
  4. Nociceptin (NOP)
80
Q

naturally occurring compounds

A

morphine, codeine, thebaine, papaverine

81
Q

semi-synthetic compounds

A

diamorphine (heroin), dihydromorphone, buprenorphine, oxycodone

82
Q

synthetic compounds

A

pethidine, fentanyl, methadone, alfentanil, remifentanil, tapentadol

83
Q

morphine mechanism of action

A

analgesic affect d/t sterospecific interaction with opioid receptors on membranes of neuronal cells on CNS

84
Q

morphine actions

A

analgesia, euphoria, respiratory depression, cough reflex depression, miosis, emesis,

85
Q

morphine

A

hydrophilic, metabolizes through conjug. in liver and p-glycoprotein, active metabolites renally eliminated, abuse deterrent formulas available

86
Q

methadone

A

no active metabolites, racemic mix., metabolized by CYP450, lipophilic, can prolong QTC interval and cause torsades de pointes

87
Q

fentanyl

A

100x more potent than morphine, greater lipophilicity and CNS penetration than morphine, metabolized by CYP3A4, no active metabolites

88
Q

oxycodone

A

active metabolite is noroxycodone; metabolized by CYP2D6 and CYP3A4;less histamine and nausea; abuse deterrent fomulation available

89
Q

oxymorphone

A

longer duration of immediate release than other opioids; oral bioavailability increases with food and alcohol; administered 1-2 hours after eating

90
Q

hydromorphone

A

greater lipophilicity and CNS penetration than morphine; metabolized glucoronidation to H6G and H3G (renally excreted); abuse deterrent

91
Q

codeine

A

prodrug; metabolized by CYP2D6 to active drug morphine; moderate to mild pain use; not for renally impaired, children under 12, children tonsils removal, obese w/ sleep apnea

92
Q

hydrocodone

A

active metabolite is hydromorphone; metabolized by CYP2D6 and CYP3A4; abuse deterrent available

93
Q

meperidine

A

not firs choice; active metabolite normeperidine which can accumulate with renal impairment = toxicity; naloxone does not work and can worsen seizure activity; dont use in elderly, liver/renal impairment, or chronic pain manage

94
Q

tapentadol

A

Mu agonist and norepi reuptake inhibiter, treats nociceptive and neuropathic pain; metabolized by glucuronidation ; no CYP450 interact

95
Q

tramadol

A

metabolized by phase 1 and 2 with CYP2D6, CYP2B6, CYP3A4

96
Q

BUPRENORPHINE

A

mixed agonist-antagonist; partial agonist at mu and ORL-1 receptor, antagonist at kappa and delta receptor; long duration (very lipophilic); abuse deterrent available;

97
Q

BUPRENORPHINE and naloxone

A

incompletely reversed

98
Q

NALOXONE

A

antagonist at mu, kappa, and delta receptor (10x affinity for mu than kappa); half life 30-90 min; oral not effective

99
Q

naltrexone

A

antagonist; similar to naloxone but longer duration (blocks effects of heroin 24 hrs-30 days); oral or injection

100
Q

Benzodiazepines uses

A

CNS depressant, anxiolytic, hypnotic, anticonvulsant, amnesia, muscle spasm, withdrawal

101
Q

benzodiazepine structure

A

central carboxamide group 7 membered heterocyclic ring w/ halogen or nitrogen (7th pos.)

102
Q

Benzo receptor interaction

A

act at GABA (a specifically) allosterically causing increased action of GABA receptor

103
Q

GABA receptor action

A

opens and allows Cl- ions in (hyperpolarizing) making neuron less likely to fire; results in calming effects

104
Q

benzo metabolism

A

highly lipophilic = longer metabolize (need to become more water-soluble); majority of metabolism liver and CYP450

105
Q

adverse side effects of benzos

A

dependence in high doses; drowsiness, confusion, ataxia, EtOH and of CNS depressants enhance, opioid use w/ benzo = sedation and resp. depress.

106
Q

barbituates

A

used for alcohol withdrawal and seizure management; mainly replaced by benzos; no analgesic/may exacerbate pain

107
Q

why were barbituates replaced

A

tolerance and physical dependence, lethal in OD, severe withdrawal

108
Q

long acting barbituate

A

phenobarbital (> 1day)

109
Q

short acting barbituate

A

pentobarbital (1-2 hours), secobarbital, amobarbital

110
Q

low does barbituate effect

A

sedation, calming effect, reduce excitement

111
Q

high dose barbituate

A

hypnosis, anesthesia, coma/death

112
Q

barbituate receptor interaction

A

low doses enhance GABA and open Cl- channel for longer; high dose open GABA without GABA present; can block glutamate receptor

113
Q

glutamate

A

excitatory neurotransmitter

114
Q

barbituate metabolism

A

liver and CYP450; half-life 100-140 hours

115
Q

anticonvulsant drug types

A

sodium channel blockers (carbamazepine), Ca blockers (depakote), unknown (keppra, gabapentin)

116
Q

topiramate

A

anticonvulsant that decreases effects of oral contraceptives

117
Q

CYP450 Induction

A

increase rate of hepatic metabolism

118
Q

CYP450 inhibitor

A

block metabolic activity

119
Q

stevens-johnson syndrome

A

disorder of skin and mucous membranes; usually reaction that resembles flu-like symptoms; painful rash/blisters where top layer dies and sheds; toxic epidermal necrolysis

120
Q

antidepressants

A

used to treat depression by potentiating effects of norepinephrine or serotonin

121
Q

norepinephrine

A

neurotransmitter and hormone; increases alertness, arousal, attention, constricts blood vessels, affects sleep wake cycle, mood, and memory

122
Q

serotonin

A

monoamine neurotransmitter that acts as hormone, influences learning and happiness, regulates body temp., sleep, sexual behavior, hunger

123
Q

90% of serotonin found where

A

GI tract cells

124
Q

decreased serotonin

A

thought to cause anxiety and depression (mania sometimes)

125
Q

types of antidepressants

A

monoamine oxidase inhibitors, tricyclic, tetracyclic and unicyclic, SARI’s, SSRI’s, SNRI’s

126
Q

serotonin syndrome

A

life threateining condition from use of serotonergic drugs; AMS, autonomic hyperactivity, neuromuscular abnormalities

127
Q

baclofen

A

antispasmotic that distributes to brain and spinal cord to cause muscle relaxation

128
Q

oral baclofen

A

70-85% bioavailability; excreted by kidneys mainly; half-life of 3 hours; brain and spinal cord

129
Q

intrathecal baclofen

A

allows for greater concentrations in spinal cord with lower levels in brain; half-life is about 5 hours

130
Q

baclofen receptor interaction

A

agonist of GABA B (only one available)

131
Q

GABA B

A

present in brain, ventral and dorsal horns, outside BBB, within sympathetic nervous system, some visceral tissues

132
Q

why use baclofen

A

spasms due to MS, TBI, spinal cord injury or lesions

133
Q

baclofen toxicity

A

hypothermia, bradycardia, hypotension, excess. saliv., HTN, tachycardia, depressed mental status, coma, seizures, resp. supress., N/V

134
Q

migraine preventative drugs

A

beta-blockers (metoprolol), anti-epilectics (topiramate), tricyclic antidepressants (amitriptyline)

135
Q

migraine abortive agents

A

ergot, triptans, ditans, calcitonin gene-related peptide (CGRP) receptor antagonists

136
Q

why no triptan use with history of MI

A

side effects can mimic MI which could hide real MI symptoms

137
Q

volume of distribution

A

Pharmacology (4 decks)

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