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SBM > Pharm > Flashcards

Pharm Flashcards

1
Q

quantal dose-response

A

all or nothing- you are either protected or you are not

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2
Q

ED50

A

where 50% of animals are protected

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3
Q

LD50

A

kills 50% of animals

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4
Q

chemical vs physical form

A

same drug cannot be in different chemical forms, but can be in different physical forms

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5
Q

Therapeutic Index

A

LD50/ED50

ideally 10

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6
Q

margin of safety

A

LD1/ED99

comparing extremes of the dose response curves to indicate any over lap

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7
Q

Protective Index

A

=ED50 (undesireable)/ED50 (desireable)

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8
Q

chronicity index

A

=(1-dose of LD50)/(90-doseLD50)
has to do with clearance
1 is best (total clearance) vs 90 (virtually no clearance)

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9
Q

Threshold dose

A

apparent all or none phenomenon at a specific threshold dose

–may not be a REAL threshold but an apparent threshold

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10
Q

potency

A

relative dose required to produce a given effect
(should not be equated with therapeutic superiority)
affinity is one component, but not the whole thing

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11
Q

intrinsic activity

A

often referred to as efficacy in intact patient; magnitude of maximal response (highest dose)
efficacy is one component, but not whole thing

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12
Q

affinity

A

K1/K2

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13
Q

efficacy

A

K3

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14
Q

Chemical antagonism

A

direct interaction of the agonist and antagonist

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15
Q

functional antagonism

A

two agonists act independently but lead to opposite biological effects, so kinda cancel each other out (or one takes over)

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16
Q

competitive antagonism

A

the antagonist binds to the receptor, but elicits no response (affinity, but no efficacy)- however, competes with agonist for binding sites
–eq and non-eq

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17
Q

Eq antagonism

A

competitive
reversible
can be overcome if dose of against is increase enough

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18
Q

non-eq antagonsim

A

competitive
irreversible-perm block of agonist binding and receptor function
cannot be overcome by increasing dose ofagonist

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19
Q

non-comp antagonist

A

antagonist acts at a site other than the site of agonist binding but affects the same process

could also bind to another site on same receptor and alter the ability of the receptor to interact with agonist–“allosteric effect”

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20
Q

inverse antagonist

A

shifts eq towards inactive

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21
Q

synergy

A

need more than one to make–>additive

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22
Q

potentiation

A

the effect of one drug makes another work better

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23
Q

rate of absorption

A

movement of drug from site of administration to the blood

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24
Q

rate of distribution

A

delivery of drug from blood to tissues and target sites

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25
Q

bioavailability

A

amount of drug that actually reaches the target site in a pharmacologically active and bioavailable form

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26
Q

only bioavailable drug

A

drugs that are not bound to albumin

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27
Q

passive diffusion

A

down a concentration gradient in non-ionized form; dependent on partition coefficient

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28
Q

filtration

A

down a pressure gradient

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29
Q

bulk flow

A

across a cap wall (small molecules)

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30
Q

mechanisms of drug transport across membranes

A

1) active transport
2) facilitated transport
3) ion pair transport-
4) endocytosis

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31
Q

oral is good for drugs with

A

high partition coefficient and favorable pKa

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32
Q

stomach only absorps

A

weak acts

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33
Q

small intestine uses

A

passive diffusion

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34
Q

5 factors affecting GI absoprtion

A 
gastric emptying time
intestinal motility
food and food consumption
formulations of drugs
metabolism & digestion
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35
Q

high partition coefficient means it is

A

lipophilic

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36
Q

what crosses very readily in lung?

A

high partition coefficient anesthetics

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37
Q

albumin has

A

positive and negative charged binding sites

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38
Q

lung receives

A

100% CO

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39
Q

kidney receives

A

25%CO

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40
Q

what can cross the BBB

A

high partition, non-ionized, free drugs can cross

inflammation can increase permeability

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41
Q

half-life

A

t=0.693/Kel

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42
Q

Volume of distribution

A

Vd=D/Co (L/Kg)

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43
Q

Clearance

A

Clp=KelxVd (L/hr/kg)

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44
Q

oral fraction

A

Foral=AUCoral/AUCiv

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45
Q

Loading Dose

A

D*=Css x Vd (mg)

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46
Q

Maintenance Dose

A

MD=Css x Vd x Kel (mg/hr or mg/min)

=Css x Clp (x time interval)

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47
Q

rate of eliminaton

A

x=xe^(-kt)

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48
Q

if route of elimination is saturated,

A

drug follows0 order onnects

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49
Q

Vd: 3-5 L

A

no penetration from plasma

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50
Q

Vd: 12-15 L

A

no penetration into cells from interstitium

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51
Q

Vd: 30-40L

A

distributed throughout body water

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52
Q

> 50 L

A

accumulated in body tissues (e.g. lipophilic)

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53
Q

ares of concern in dosing

A

time to peak concentration (tmax) in blood
Maximum attained concentration (cmax)
area under curve (AUC)

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54
Q

steady state

A

independent of dose and depends only on rate of elimination (Kel), so to avoid delay use a loading dose

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55
Q

pro-drug

A

more active than parent compound

mitomycin C, cyclophosphamide, codeine

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56
Q

Pro-toxin

A

when metabolized drug turns toxic

aflatoxin B1, benzoapyrene

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57
Q

goal of phase 1 metabolism

A

make lipophilic drugs more hydrophilic

CYP liver enzymes add groups, oxidate, reduce

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58
Q

phase 2 metabolism

A

conjugation
take phase 1 metabolite and bind to large, polar glucoronic acid so can be readily excreted from body
occurs predominantly from UDP-GT

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59
Q

neonatal hyperbilirubinemia

A

inability of newborn babies to metabolize bill to bill fluuronide conjugate–>leads to CNS damage

60
Q

chloramphenicol (antibiotic)

A

deficinecy in UDP-GT leads to excessive free drug in blood and tissue and drug-associateed toxicities
gray baby syndrome

61
Q

crigler-naijar syndrome

A

almost total genetic deficiency in hepatic UDP-GT

babies highly jaundiced–>death occurs in early childhood

62
Q

B-glucuronidsae

A

releases drug
present in mucosa of small intestine
entero-hepatic circulation for drug (re-abs by GI)

63
Q

n-acyetyl conjugation

A

catalyzed by n-acetyltransferases in population
fast and slow acetylators in population
important for isonizaid, sulfamethazine, paninosaliyclic acid, hydralazine

64
Q

overdosing on acetaminophen

A

generates reactive metabolites that attack tissues and lead to liver toxicity and failure

65
Q

acute alocohol

A

inhibits drug metabolism, prolonging and intensifying effects of drugs (esp CNS depressant), though competitive inhibition of metabolism

66
Q

chronic alcohol

A

increases drug metabolism and clearance through induction of P450 and other enzymes

67
Q

induce drug metabolism because induce P450

A

green things, brussel sprouts cabbage, cauliflower

68
Q

grape fruit juice

A

contains furanocoumarins that inhibit CYP3A4 metabolism

also inhibit Pgp- mediated durg efflus in intestine and liver

–>both mechanisms increase bioavailability and toxicity of a large group of CYP3A4 substrate drugs

69
Q

charcoal broiled beef diet

A

xenobioti metabolizing enzymes induced higher in beef eaters so they have lower phenacetin plasma levels

70
Q

ABC transport proteins

A

Pglycoprotein: transport large and functionally unrelated molecules

MRP: phase II conjugates of drugs and metabolites
large and diverse group of molecules out of cells

71
Q

Sympathetic Neruons

A

T1-L3 short–>ACH to ganglia -long–>target organs (NE)

72
Q

Parasympathetic Neruons

A

cervical and sacral areas-long—>ACH at ganglia near target organ-short—>target organ (ach)

73
Q

pressor center is in

A

medulla

74
Q

how to cholinergic neurons make Ach

A

acetyl coa + choline–< acetylcoline–>put in vesicles–>exocytosed

75
Q

M1 Ach R

A

nerve endings
Gqcoupled–>increase IP3 & DAG
myenteric plexus

76
Q

M2 Ach R

A

heart, some nerve endings
Gi–>decrease cAMP, activate K+ channels
slow SA node

77
Q

M3 Ach R

A

smooth muscle glands
Gq coupled–>inc IP3, DAG
contract detruser muscle, increase salivation

78
Q

Nn ACh Receptor

A

ANS ganglia
Na-K ion channel–>Na
depolarizes postgang fiber–>evokes AP

79
Q

Nm Ach Receptor

A

neuromuscular end plate
Na-K ion channel–>Na+
depolarizes muscle cell, evokes AP and contraction

80
Q

how to make NE

A

tyrosine–>DOPA–>Dopamine–>into vesicle–>adds B-hydroxyl–>NE

81
Q

5 Ach Receptors

A

M1, M2, M3, Nn, Nm

82
Q

6 NE receptors

A

A1, A3, B2, B3, B4, DA1

83
Q

A1 NE receptor

A

smooth muscle, glands,
Gq
increase Ca2+–>contraction (vascular SM- vasoconstriction), secretion

also inhivits SA node

*STIMULATE BP**

84
Q

A2 NE receptor

A

nerve endings (some smooth muscle)
Gi
decrease transmitter release (nerve)- contract, SM

85
Q

Beta 1

A

Cardiac muscle, JGA
Gs–>increase camp
increase HR and contractility, renin release

also stimualtes SA node

86
Q

Beta 2

A

smooth muscle, liver, heart
Gs–>inc camp
relax bronchiolar SM, increase glycogenolysis, increase HR and contractility

87
Q

Beta 3

A

adipose tissue
Gs
increase lipolysis

88
Q

Da1

A

smoth muscle
Gs
relax vascular SM in renal arterioles

89
Q

sarin nerve gas

A

increases amount of Ach in body (inhibits AchE)

90
Q

5 ways SNS helps BP go up

A 
arterioles (SVR)
SA node (HR)
LV (contractility)
veins (tone)
kidneys (renin)
adrenal medulla (releases E and NE)
91
Q

PANS CNS origin

A

rostral ventrolateral medulla

92
Q

PANS origin

A

Nucleus ambiguus

93
Q

direct acting sympoatomimetic drugs

A

act on post-syn receptors

NE, EPI

94
Q

indirect acting drugs

A

keep NE in synapse longer

  • enhance release of NE at synapse
  • block reputake of NE after release at synapse
  • blocks degradation of NE
95
Q

enhances release of NE at synapse

A

amphetamine, meth MDMA

96
Q

blocks reuptake NE

A

cocaine, amitriptyline

97
Q

blocks degradation of NE

A

MAO-inhibitors

98
Q

2 alpha agonists

A

Phenyleprine (a1)

Clonidine (a2)

99
Q

mixed alpha, beta agonists (3)

A

Epinephrine
NE
Dopamine

100
Q

4 Beta agonists

A

Isoproterenol
Dobutamine
Albuterol
Mirabegron

101
Q

alpha antagonists

A

prazosin/minipress
tamsulosin/flomax
phentolamine/regitine

102
Q

beta antagonists

A

atenolol

propanolol

103
Q

Mixed a,b

A

labetolol

104
Q

nonspecific Ach agonists (2)

A

Ach

Carbachol

105
Q

3 Muscarinic Agonists

A

Methacholine
Bethanechol
Pilocarpine

106
Q

2 Nicotinic Agonists

A

Nicotine

Varenicline (Chantix)

107
Q

Short Acting cholinesterase inhibitors

A

edrophonium

108
Q

Int acting cholinesterate inhibitors

A

neostigmine

physostigmine

109
Q

long acting cholinesterase inhibitors

A 
echothiphate
parathion
malathion
sarin
soman
110
Q

presynaptic indirect cholinomimetics

A

metoclopramide

111
Q

3 places M receptors are located at

A

effector tissues innervated by PS fibers
very select postganglionic sympathetic targets (sweat glands)
endothelium (non-innervated tissue)

112
Q

Cholinomimetic overdose-cholinergic syndrome

A

muscarine poisioning

DUMBBELSS

113
Q

SLUDGE syndrome

A 
major muscarinic/nicotinic effects
salivation
lacrimation
urination
defetation
GI upset
Emesis
114
Q

Why do muscarinic receptors cause hypotension?

A

active eNOS–>makes NO–>stimulates guanlyl cyclase to turn GTP–>cGMP–>binds myosin lightt chain to vasodilate

115
Q

Why does muscarinic activation cause bradycardia?

A

activation of M receptors on SA node (vagus)

116
Q

other M clinical signs

A 
DUMBBELSS
Diarrhea
urination
Miosis 
Bronchorrhea/brnchoconstriction
Bradycardia
Emesis
Lacrimation
Salvation
Sweating
117
Q

therapeutically useful Ach agents

A

must be resistant to AchE

118
Q

modified forms of Ach

A

methacholine
bethanechol
pilocarpine (glaucoma)

119
Q

Nicotine Toxicity

A

Depolarizing-Desensitization Blockade
initial activation–>deactivation due to phosphotylation–> paradoxical flaccid paralysis due to blockade, have to wait until agonist is cleared

*Nm receptors

120
Q

Major signs of Nicotine Toxicity

A

Symp and PS stim- tachycardia, hypertension, cold sweat, nausea, vomitting, diarrhea, salivation, urinary incontinence

Nn and Nm blockade- syncopy, collapse, unconsciousness, flaccid paralysis

121
Q

All ChE inhibitors block

A

true Ache, plasma Che, and RBC Ache

plasma ChE is inhibited first

122
Q

what is the major concern of using cholinesterase inhibitors?

A

respiratory inundation
–paralysis of intercostal muscles and diaphragm via nicotinic desensitization blockade
–increased bronchial secretions and bronchoconstriction (mud)
central resp arrest

123
Q

AchE mechanism

A

anionic site binds quat ammoium cation

esteric site-catalytic hydrolyzes Ach ester bond

124
Q

short acting are

A

competitive inhibitors and do not form ester bond to AChE

125
Q

what is used to diagnose MG?

A

Edrophonium

rapid increase in muscle strength because inhibits ChE transiently and makes Ach more available

126
Q

2 Muscarinic Antagonists

A

atropine

scopolamine

127
Q

Depolarizing Nm cholinolytuc agonists

A

succinylcholine

128
Q

Nondepolarizing Nm antagonists

A

Benzylisoquinolines: d-tubocurarin, Cisatracurium

Aminosterioid: pancuronium, vercuronium, Rocuronium

129
Q

Nn specific

A

trimethaphan

130
Q

Muscarinic Atagonists act

A

block PS transmission to end organs

inverse agonists

131
Q

atropine toxicity

A 
mad as a hatter
Blind as a bat
dry as a bone
hot as a hare
red as a beet
performing the pee pee dance
132
Q

atropine basically does

A

unopposed symp acts (no ps)

133
Q

what is most dangerous effect of atropine in adults vs kid

A

delirum- self destructive acts

kids- temperature- doesn’t respond to antipyretics; need ice bat

134
Q

Scopolamine

A

motion sickness

anesthetic adjuvant

135
Q

Dicyclomine

A

irritable bowel and minor diarrhea

M3 selective antag

136
Q

Tropicamide

A

mydriatic eye drops for retinal exam

137
Q

Benzotripine

A

CNS Parkinsons DIsease

138
Q

Ipratropium**

A

Inhibits bronchoconstriction

139
Q

succinylcholine

A

Nm blocker
post-surgical procures and intubations

adverse effects- muscle fasciculations, hyperemia, histamine release, hyperthermia

140
Q

no succinylcholine if

A

family Hx of malignant hyperthermia
hyperkalemia
burns, trauma, tissue injury
heart failure

141
Q

d-tubocurarine

A

paralysis in fully conscious patient; only for anesthetized pt

142
Q

nondepol paralysis reversal

A

neostygmine

143
Q

depolarizing nicotinic blockers

A

TIME- neostygmine will cause muscurinic syndrome

144
Q

Trimethaphan

A

nondepol ganglionic Nn blocker

potent effects on BP
only use in hypertensive crises, dissecting aortic aneurysm

145
Q

Botox

A

indirect anticholinergic

light chain escapes from vesicles and cleaves SNARES so no docking

146
Q

botox applications

A

coesmetic
prevent arm pit sweating
strabismus
uncontrolled eye twitching

SBM (18 decks)

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