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Block 5 > Pharm > Flashcards

Pharm Flashcards

1
Q

What is the equation to determine pharmokinetic binding?

A

k2 = [L] x [R]; and k2 = KD

k1 [LR] k1

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2
Q

How is Kd determined for pharmokinetics?

A

[LR] = RT x [L]

KD + [L]

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3
Q

What is the major determinant of k2 in pharmokinetics?

A

Van Der Waals interactions

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4
Q

How is maximal effect measured?

A

Occurs when all receptors are occupied

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5
Q

Do all the receptors have to be bound to get maximal effect?

A

no, because full effect can be attained with significantly less

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6
Q

What is intrinsic activity

A

How much a particular agonist functions as an agonist as opposed to an antagonist

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7
Q

What are the purpose of spare recetpros on cells?

A

Allows a larger response with the same concentration of effeector

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8
Q

What are teh different type of antagonists?

A

chemical: combine with the agaonist
physiological: activate opposing physiological inputs
Pharmacological: blocks the effect of an agonist of a receptor

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9
Q

PHenoxybenzamine is what?

A

An irreversible inhibitor of the alpha adrenergic receptor. Used to treat hypertensive effects of pheochromocytoma

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10
Q

What is potency?

A

The relationship of the amount of drug administered and its effect

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11
Q

What are determinants of potency?

A

Affinity for site of action and ability to reach the site of action

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12
Q

How is ED50 related to potency?

A

Inversely related to potency, potency is the position of the cuve on the x-axis

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13
Q

What is efficacy and how is it determined?

A

Maximal effect prduced by drug
include a receptor ligand, intrinsic activity
charactersitics of the effector
limitations on amt of drug that can be administered

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14
Q

What are some reasons for variation in response among individuals?

A

differences in pharmokinetics such as caused by smoking
variation in amount of endogenous agonsit
changes in number or function of target
differences in component distal to the darget

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15
Q

What is P-glycoprotein?

A

An ABC carrier. Primarily binds lipophilic drugs and mediates their efflux from cells. ATP used. Multidrug resistant gees

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16
Q

What is bioavalability?

A

Fraction of administered dose of drug that reaches circulation, defined as F. IV drugs IV=1

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17
Q

What is the first pass effect for orally adminstered drugs?

A

Drug is metabolized or excreted in first pass through liver, and bioavalability can be considerably reduced.

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18
Q

Bioequivalence between preparation means?

A

Same drug
Same route of admin
same amnt of drug enters circulation
drug enters circulation at same rate

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19
Q

Where is the majority of drug absorbed in the GI tract?

A

Upper intestines

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20
Q

How does gastric emptying impact drug absorption?

A

Increased gastric emptying will increase the rate of drug absorption

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21
Q

How does dissolution of solid drug preparation affect rate of absorption?

A

It’s affected by formulation and the easier the drug will be absorbed

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22
Q

How is controlled release preparation prepared?

A

Coating active drug with hard to dissolve agents

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23
Q

What is a drawback for controlled release preparation?

A

Greater variability among patients and dose may be toxic if released all at once

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24
Q

Enteric coatings do what?

A

Protect the drug from stomach acid and stomach from drug. Gives better taste.

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25
Q

Why are drugs given buccally or sublingualy?

A

Blood drains into the superior vena cava(avoids liver on first pass)
Small surface area, so drugs need to be lipophilic, readily pass through membranes

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26
Q

Why are drugs administered rectally?

A

Useful if patient can’t or won’t swallow
50% less first pass than orally admin agent
disadvantage: variable absorption, incomplete, irritating to mucosa

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27
Q

What type of drugs are administered by transdermal patch?

A

Lipohphilic drugs only

Best if hydrated (using occlusive, water tight dressing)

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28
Q

What are parenteral injections?

A

Without intestine ( IV, Subcut, and Intramusc)

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29
Q

How do proteins injected by IV enter the circulation system?

A

Enter slowly via the lymphatic system.

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30
Q

Parenterally administered drugs distribute where first?

A 
Occurs at lungs before liver
metabolic enzymes can transform the drug
filters particulate
volatile agents can diffuse
lipophilic agents can accumulate
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31
Q

How can subcutaneous treatment be delayed?

A

Absorption can be delayed by vasoconstrictors

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32
Q

How can intramuscular treatment be variable?

A

Dependent on blood flow to the muscle.

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33
Q

Novel methods of drug delivery include?

A

Targetig of drugs using antibodies
drug eluting stents
activation of drugs at site of action

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34
Q

Drug delivery depends on blood flow how?

A

Two phase of drug delivery dependence:
first phase highly pefused organs receive most of drug; equilibration is rapid
second phase: more poorly perfused organs; equilibration is very slow

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35
Q

Tissues ca accumulate drugs what does this act as?

A

slowly releasing resevoirs
Lipophilic drugs can be stored for long periods in fat
tetracycline adn heavy metals accumulate in bone

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36
Q

THe time to peak concentration for a drug is what?

A

The lag time

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37
Q

Area under the curve for drug absorption is what value?

A

It is the extent of absorption

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38
Q

How does one determine the apparent volume of distribution/

A

Amount of drug in body (aka dose)=Volume of distrubtion*conc

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39
Q

What values do you use to calculate the concentration of the drug in the body for volume of distribution?

A

You use C at time 0, which is extrapolated from the graph of the drug elimination phase

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40
Q

What is the relevance of bioavailability with respect to determining drug dose?

A

Needs to be taken into account, especially for oral dosing. F=bioavailability
DF=VdCo

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41
Q

Clearance from different mechanisms is related to the total clearance how?

A

additive, Cltotal=Clrenal+Clliver

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42
Q

Slope of elimination is simplified as what?

A

first order, Slope of elimination is=-kel/2.3

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43
Q

How is half life time determined?

A

T1/2=0.69/kel

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44
Q

What are the two phases for deterimining IV drug concentration?

A

alpha phase and beta phase, alpha phase is distribution of the IV drug, and beta phase is the elimination phase

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45
Q

What drugs follow zero order kinetics?

A

Mechanisms of clearance can be saturated in this istuation; ethanol, aspirin and phenytoin, drug can accumulate

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46
Q

What is the rate of clearance-volume of blood cleared of drug per unit time?

A

CL=Kel*Vd

Cl=0.69*Vd/halflife

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47
Q

What equation is the equation for steady state dosing of a drug?

A

Rate of drug in=rate of drug out
FDose/dosing interval=CLCss
Css=conc plasma drug at steady state

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48
Q

What is the equation to achieve steady state with an initial maximal dose?

A

Loading D=Vd*Css/F

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49
Q

What is an example of steroid hormone?

A

Cortisol, and binds to corticosteroid-binding globulin, enters cell where it binds glucoroticoid receptor which exists as an inactive complex in cytosol

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50
Q

What is an examples of ion channel linked receptor?

A

Receptors for acetycholine, GABA, serotonin, glycine, and glutamate

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51
Q

Nictotinic Acetycholine receptor is what type of receptor?

A

Ion channel, that allows influx of cations when bound to acetycholine

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52
Q

What type of receptor is the GABA receptor?

A

Ion channel receptor that allows influx of Cl- leading to hyperpolarization and inhibition of resposne

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53
Q

The alpha subunit of a heterotrimeric G protein coupled receptor is active when what is bound?

A

GTP

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54
Q

What are the three types of Galpha subunits?

A

GalphaS–>stimulates adenylyl cyclase
Galphai–>inhibits adenylyl cyclase
Galphaq–>activates phospholipase C

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55
Q

What are monomeric G protein such as RAS activated by?

A

Interaction with a GEF

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56
Q

What is GEF?

A

ie SOS, is the gaunine nucleotide exchange factors

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57
Q

What is an example of an important monomeric G protein?

A

MAP Kinase signaling cascade. (mitogen activating protein)

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58
Q

Ras-GTP activates what?

A

Raf which is MAPKKK

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59
Q

What does RAF phospohrylate?

A

Raf phosphorylates MKK1, MKK1 is Map kinase kinase

60
Q

What does MKK1 phosphorylate?

A

ERK which is a MAP Kinase

61
Q

GPCR can be desensitized upon phospohrylateion of the recceptor by what?

A

Beta adrenergic kinase, which allows beta-arrestin to bind it

62
Q

What are phase 1 drug elimination enzymes?

A

oxidation, reduction, dealkylation or hydrolysis;

introduce or reveal a functional group

63
Q

What are phase 2 drug eliminiation enzymes?

A

Conjugation of a drug or drug metabolite to an endogenous substrate molecule

64
Q

Where are drug metabolizing enzymes located?

A

Located in all tissues to some degree.

Liver is the highest overall but GI tract, kidney and lungs all have significant amounts

65
Q

What are some type of PHase 1 enzymes?

A
  • CYP 450s
  • Flavin-containing monooxygenases
    dehydrogenases
    hydrolases
    esterases
    amidases
66
Q

What are the three families of cytochrome p450s involved in drug metabolis?

A

CYP1, CYP2, CYP3

67
Q

What are the three isoforoms of CYP450s that are involved in 90% of drug metabolism?

A

CYP3A~50%
CYP2D6~25%
CYP2C9~15%

68
Q

Flavin-containing monooxygenase(FMO) do what?

A

Monooxygenase reactions, with substrates that are soft nucleophiles. Excludes non-substrates rather than selectively binding substrates; products usually more polar less toxic

69
Q

FMO3 exist where?

A

Liver, brain, kidney and is 2-3% of hepatic protien

70
Q

FMO2 is present in what group?

A

26% of african americans in the lung and non functional in caucasians

71
Q

What enzyme is responsible for glucuronidation?

A

UDP-glucuronosyl transferase

72
Q

What enzyme is responsible for acetylation?

A

N-acetyltransferases

73
Q

What enzyme is responsible for sulfation?

A

sulfotransferases

74
Q

What enzyme is rsponsible for glutathione conjugation?

A

glutathione S-transferases

75
Q

What is TMPT?

A

Thiopurine methyltransferase

76
Q

What is ethanol an inducer of ?

A

CYP2E1

77
Q

What CYP is not as inducible as the others?

A

CYP2D6

78
Q

What are some inducers of UGTs and GSTs?

A

tobacco smoke, phenobarbital, polycyclic aromatic hydrocarbons, benzopyrene

79
Q

What are the major cause of CYP-related drug interactions?

A

Competitive substrates/inhibitors for P450

80
Q

Several inhibitors of CYP2D6 can reduce its activity to nearly 0 some examples?

A

chloroquine, quinide, fluoxetine

81
Q

How does grapefruit juice work as an inhibitor?

A

Inhibits only CYP3A by furanocoumarin, in the intestine but increases amnt that reaches circulation CYP3A handles 50%

82
Q

How are FMOs inhibited and induced?

A

Neigher significantly induced or inhibited; less susceptible to to competitive substrate inhibition
less potential for metabolic drug-drug interactions

83
Q

Women require half the dose of what drug?

A

zolpidem; even though CYP3A present at similar levels

84
Q

What is the NAT-2 polymorphism?

A

Slow inactivators lead to increased neurological side effects from teh drug
isoniazid
can check for with caffeine metabolism

85
Q

CYP2d6 polymorphism are present in what percentage of population; what causes ultrafast metabolism?

A

genotypic frequency 30%; phenotype frequency between 2 and 10 % dependent on ethnicity
ultrafast is caused by multiple coppies of normal allele

86
Q

What type of drugs are effected by CYP2d6 metabolism?

A 
Antidepressants** esp tricyclics
beta-blockers[metropolol, propanolol, timolol, carvedilol]
antiarrythmatics[encainide, flecainide]
neurleptics
codeine
dextromorphan
87
Q

What is the prevalence of CYP2C19 are poor metabolizers

A

3-20%

88
Q

What classes of drugs are effected by CYP2C19 polymorphism

A 
Proton Pump inhibitors [omeprazole]
anticonvulsants [phenytoin]
anti-depressants
anti-cancer
horomones [progesterone]
anti-platelet [clopidogrel]
89
Q

What classes of drugs are effected by CYP2C9 polymorphism?

A

anticoagulant[warfarin]
anticonvulsant
type 2 diabetes [tolbutamide]

90
Q

Psuedocholinesterase polymorphism can lead to what?

A

multiple reduced variance can lead to apnea and paralysis for 2-3 hours from succinylcholine as well as cocaine and insectide toxicity

91
Q

How does one test for atypical cholinesterase activity?

A

in vitro diagnostic test using dibucaine, which inhibits normal cholinesterase activity better than atypical

92
Q

TPMT polymorphism leads to what?

A

life-threatening bone marrow suppression in 6-mercaptopurine trerated patients

93
Q

Nicotinic Receptors are involved in what?

A

Striated muscles, motor neurons utilize acetycholine

94
Q

Parasmpathetic receptors utilize what type of recetors?

A

Musarinic receptors

95
Q

What type of receptors are utilized by sympathetic glands?

A

Alpha/Beta adrenergic receptors

except for sweat glands (musarinic receptors)

96
Q

Nicotinic Receptors are involved in what?

A

Striated muscles, motor neurons utilize acetycholine

97
Q

Parasmpathetic receptors utilize what type of recetors?

A

Musarinic receptors

98
Q

What type of receptors are utilized by sympathetic glands?

A

Alpha/Beta adrenergic receptors

except for sweat glands (musarinic receptors)

99
Q

monoamine oxidase does what?

A

Major role in neurons to metabolize norepinephrine

100
Q

VMAT2 is what?

A

UPtakes dopamine and norepinephrine into vesicles for storage

101
Q

What is ENT?

A

Effector Neuroepinephrine transporter, uptakkes neuroepinephrine into efefctor cell

102
Q

monoamine oxidase does what?

A

Major role in neurons to metabolize norepinephrine

103
Q

What is pre-synaptic alpha2 receptors when bound by neuroepinephrine does what?

A

Inhibits adenylate cyclase when bound by neuroepinephrine, which increases Ca2+ into neuron and increases exocytosis

104
Q

What is the role of COMT?

A

transfers a methyl group to the 3-hydroxy position of a norepinephrine metabolism and deactivates it

105
Q

What is ChAT?

A

Produces aceytcholine from AcCoA and Choline;

Choline Acetyltransferase

106
Q

Where is M1 receptor located, and what G protein family is responsible?

A

Peripheral and Central nervous system; depolarization of nerves activate phospholipase
Gq

107
Q

What is M2 receptor responsible for and it’s location?

A

Gi
heart, nerves, smooth muscle
decrease electrical conduction and muscle contraction
, inhibits AC; activate potassium channels

108
Q

What is M3 receptor responsible for, location and its G protein?

A

Gq, glands smooth muscle, endothelium, increase secretion and muscle contraction
activate phospholipase C

109
Q

What is alpha2 receptor location, response and g protein?

A

Gi, nerve terminals, pancreatic Beta cells, vascular smooth muscle, decrease NE release, decrease insulin secretion, contraction, inhibit AC, downregulate cAMP, activate phospholipase

110
Q

What is M5 location, G protein and location?

A

Gq, CNS, depolarization and activate pohopholipase C

111
Q

What is alpha1 receptor location, response and g protein?

A

Gq, vascular and other smooth muscle, glands, contraction and secretion from glands, activate phospohlipase C

112
Q

What is alpha2 receptor location, response and g protein?

A

Gi, nerve terminals, pancreatic Beta cells, vascular smooth muscle, decrease NE release, decrease insulin secretion, contraction, inhibit AC, downregulate cAMP, activate phospholipase

113
Q

What is teh role of Beta1 receptor,?

A

Gs, cardiac muscle, juxtaglomerular cells, increase heart rate and renin secretion, upreg cAMP

114
Q

What is the role of Beta2 receptor?

A

Gs, vascular and other smooth muscle, skeletal muscle, liver, relaxation, glycogenolysis, activate cAMP

115
Q

Waht is teh role of beta3 receptor?

A

Gs, adipose tissue, lipolysis, activate cAMP

116
Q

All therapeutic antibodies are what type?

A

IgG

117
Q

What is the ending for nomenclature source antibodies?

A
  • umab — Human (Used against an immune target)
  • momab – Murine (mainly used against tumor)
  • -ximab – Chimeric (Used on cardiovascular system)
  • zumab – Humanized (Used against a virus)
118
Q

Neonatal Fc Receptor for IgG does what?

A

Protects IgG from degradation-prolongs serum half life.

119
Q

How does antibody play a role in anatagonism or neutralization?

A

Antibody binds and inactivates soluble antigen or acts as a competitive inhibitor of ligand to a cellular receptor

120
Q

What does Bevacizumab do?

A

Humanized IgG1 that binds and inhibits the angiogenic growth factor vascular endothelial growth factor (VEGF) from binding its receptor

121
Q

How does Cetuximab?

A

Chimeric antibody that binds to the epidermal growth factor receptor. Promotes antibody-dependent cellular cytotoxicity.

122
Q

What does abciximab do?

A

anti-coagulation
Chimeric Fab fragment taht binds the GPIIb/IIIa receptor on platelets
Competitively inhibits fibrinogen binding to platelets GPIIb/IIIa receptor
used to prevent intravascular platelet aggregation
No Fc region since this is a Fab fragment

123
Q

What does Rituximab do?

A

Chimeric IgG1 that binds CD20 on malignant B cells

ADCC of malignant B cells results- used to treat non-Hodgkin lymphoma

124
Q

What two drugs are involved in antibody bound toxin or radionuclides?

A

Ibritumomab tiuxetan, Brentuximab vedotin,

125
Q

Ibritumomab tiuxen delivers what to B cells and by what mechanism?

A

Antibody binds CD20 and delivers radionuclide to kill cell

126
Q

Brentuximab vedotin delivers what to a b cell how?

A

Antibody binds CD30 and delivers the microtubule antagonist monomethyl auristatin to B cell.

127
Q

Capromab pendetide does what?

A

Antibody binds prostate specific membrane antigen and delivers 111In to detect prostate cancer.

128
Q

What is teh route of administration for muscarinic agonists Bethanechol and pilocarpine?

A

not administered IV bc will cause hypotension
orally ( bethanechol, pilocarpine)
SubCut (bethanechol)
Opthalmic (pilocarpine, acetycholine

129
Q

What are the side effects of Bethanechol and pilocarpine with systemic exposure?

A

SLUDGE: salivation, lacrimation, urination, defecation, GI upset, emesis
hypotension, bradycarida, blurred vision

130
Q

What do you treat Bethanechol and pilocarpine toxicity with?

A

Muscarinic receptor antagonist, atropine

131
Q

What pateients should you be cuatious with administering Bethanechol and pilocarpine?

A

Asthma, COPD
Urinary, GI obstruction and peptic ulcer
CV disease involving bradycardia or hypotension

132
Q

what do acetylcholinesterase inhibitors do?

A 
enhance the effect of endogenous released acetycholine, effective at any site where acetycholine is neurotransmiter
SIte of actions:
Ganglia
neuromusc junction
CNS
post-ganglionic parasympathetic junciton
133
Q

What are the two types of acetylcholinesterase inhibitors?

A

reversible and irreversible

134
Q

What are the two types of neuromuscular blocking agens?

A

Competitive and Depolarzing blockers

135
Q

What are acetylcholinesterase inhibitors?

A

Irreversiblely phosphorlate serine in substrate binding domain, and they are organophosphate acetylcholinesterase inhibitors
lipophilic and penetrate anywhere

136
Q

What are the side effects of muscarinic receptor antagonists?

A

no sweating, dry mouth, red from that combination, mydriasis, cycloplegia, drowsiness and at toxic concentrations ataxia, restlessness, excitemetn, hallucinationa dn delirium

137
Q

What pts should use muscarinic receptor antagonits with caution?

A

glaucoma pts
Benign prostatic hyperplasia
tacycardia and angina

138
Q

What are tx for muscarinic receptor antagonist poisoning?

A

limit absorption, physostigimine

139
Q

What are causes of Muscarinic receptor antagonist poisoning?

A

belladonna alkaloids, drugs block it including histamine receptor blockers, antipsychotics, tricyclic antidepressants

140
Q

What are substrate inhibitors of acetylcholinesterase inhibitors?

A

hydrolyzed by ACh slowly, carbamate derivatives, reversible Acetylcholinesterase inhibiots

141
Q

What is the result of oganophosphate toxicity?

A

SLUDGE
hypotension, bradycardia, bronchocontrction
medulla respiratory center depression and muscle paralysis due to depolarizing neuromusc
death due to respiratory failure

142
Q

What do neuromuscular blocking agents do?

A

blcok neurotransmission at neuromuscular junction porducing paralysis of skeletal muscle

143
Q

What is the mian role of neuromuscular blocking agents?

A

main clinical use is an adjuvant in surgical anesthesia to obtain relaxation of skeletal muscle to facilitatie operative manipulations

144
Q

What are the two chemical classes of competitive neuromuscular blocking agents?

A

aminosteroids

benzylisoquinolines

145
Q

What are some properties of competitive neuromuscular blocking agents?

A

copete with acetycholine for end-plate nicotinic receptor as an antagonist
no CNS pen, bc quaternary amines
variable potency, blocking ganglionic nicotinic
blockade of muscarinic effect stimulate histamine relase

146
Q

What is the mechanism of action of depolarizing neuromuscular blockers?

A

activate nicotinic receptors at junction maintaing end plate depolarization and prevents transmission of another action potential, agonist of nicotinic receptor

147
Q

What are the adverse effects and toxicity of neuromuscular blockers?

A 
Competitive:
prolonged apea
oxicity or OD can be reverswed with neostigmine or edrophonium
can also reverse decrease duration of action with acetylcholinesterase inhibitor, if they treat with athat they should treat with glycopyrrolate to minimize muscarinic actions
Depolarizing:
prolonged apnea
malignant hyperthermia
hyperkalemia
muscle pain

Block 5 (5 decks)

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