Pharm Exam 1

Front 1

any substance that brings about change in biologicfuncFon through its chemical acFons; used for the treatment,cure, prevenFon or diagnosis of specific diseases or clinicalcondiFons

Back 1

drug

Front 2

an inactive form of a drug that is converted to anactive form in the body

Back 2

prodrug

Front 3

any chemical that is considered foreign to abiological system (e.g. a drug in a patient); can be a naturalcompound if it is not expected to be present but usually refersto drugs, pollutants or other toxic compounds that get into thebody

Back 3

xenobiotic

Front 4

qualitative description of how the bodyhandles the drug; includes how the drug is absorbed, where it isdistributed, how it’s metabolized, and how it’s eliminated fromthe body (ADME)

Back 4

drug disposition

Front 5

quantitative description of drug disposition

Back 5

pharmacokinetics

Front 6

the actions of the drug on teh body; usually mediated through drug actions on specific cellular receptor proteins

Back 6

pharmacodynamics

Front 7

the study of drugs

Back 7

pharmacoloty

Front 8

the preparation of dispensation of medications

Back 8

pharmacy

Front 9

the study of the harmful effects of chemicals including drugs

Back 9

toxicology

Front 10

what are the three main routes of drug administration?

Back 10

enteral (through the GI tract)

paraenteral (into the body by any route other than the GI tract, initially bypasses the liver)

topical

Front 11

what are the three forms of enteral drug administration?

Back 11

sublingual, oral, rectal

Front 12

for oral drug administration, teh drug must first disolve in __

Back 12

GI fluids

Front 13

what is the major site of oral drug absorption?

Back 13

small intestine

Front 14

how are rectal drugs administered?

Back 14

suppository preparations

Front 15

what are the three kinds of paraenteral drug admnistration?

Back 15

injection, inhalation, intranasal

Front 16

what are the 4 kinds of injection drug administration?

Back 16

subcutaneous, intramuscular, intravenous, intrathecal

Front 17

kind of injection that has instantaneous delivery to systemic circulation

Back 17

intravenous

Front 18

kind of injection that bypasses the blood brain barrier

Back 18

intrathecal

Front 19

volitile anethetics, aerosols, and dry (micronized powders) are all methods of __ drug administration

Back 19

inhalation

Front 20

drugs that have a local action on nasal mucosa (decongestant, anti-allergy); vaccines are administered via __

Back 20

intranasal

Front 21

what are the two kinds of topical drug administration?

Back 21

ophthalmic, dermal

Front 22

drug administration route that uses the instillation of drops into the eye for a local effect

Back 22

ophthalmic

Front 23

topical drug administration route that has a local action, and a possible systemic action via transdermal patches applied for a prolonged effect

Back 23

dermal

Front 24

the __ affects time to onset of the therapeutic effect

Back 24

rate of absorption

Front 25

the rate of absorption of intravenous drugs

Back 25

30-60 seconds

Front 26

rate of absorption of inhalation

Back 26

2-3 min

Front 27

rate of absorption for sublingual

Back 27

3-5

Front 28

rate of absorption for intramuscular

Back 28

10-20 min

Front 29

rate of absorption for subcutaneous

Back 29

15-30 min

Front 30

rate of absorption for rectal

Back 30

5-30 min

Front 31

rate of absorption for ingestion

Back 31

30-90 min

Front 32

rate of absorptoin for trasdermal

Back 32

variable (min-hr)

Front 33

the process of getting a drug from teh point of administration into teh systemic circulation

Back 33

drug absorption

Front 34

getting drugs into the body

Back 34

absorption

Front 35

moving drugs witin the body

Back 35

distribution

Front 36

removing drugs from teh body

Back 36

excretion

Front 37

in order to get drugs into, around, and out of teh body drugs must be able to __

Back 37

cross biological membranes

Front 38

what are two mechanisms of passive transfer?

Back 38

filtration, passive diffusion

Front 39

passive transfer of drug molecules by passage through membrane pores. this is the process for getting drugs out of circulation and into tissues in all areas EXCEPT the CNS; includes glomerular filtration of drugs into renal tubules for excretion

Back 39

filtration

Front 40

the most important proces for getting drugs across cell layers

Back 40

passive diffusion

Front 41

the passage of drugs by dissolving in and diffusing across the phospholipid bilayer

Back 41

passive diffusion

Front 42

what must happen to allow for passive diffusion to occur?

Back 42

the drug must be sufficiently "lipid soluble" due to te hydrophobic nature of teh interor of the phospholipid bilayer

Front 43

what happens to a drug in regards to passive diffusion if it is ionized or it contains water soluble functional groups?

Back 43

it will not diffuse easily

Front 44

in passive diffusion, net transfer is dependent on teh exisitence of a __ across the membrane

Back 44

concentration gradient

Front 45

drug transfer during passive diffusion will proceed until the __

Back 45

concentration is the same on both sides of the membrane (equillibrium)

Front 46

what maintains the concentration gradient in passive diffusion?

Back 46

tissue blood flow

Front 47

what are the three methods of carrier-mediated transfer?

Back 47

active transport, facilitated diffusion, uptake transporters

Front 48

kind of carrier mediated transfer where the drug is transfered across membranes by specific transporter proteins.

these are structurally selective and saturable; amenable to competitive inhibition.

Back 48

active transport

Front 49

active transport is energy dependent. it transports drugs __

Back 49

against concentration gradients

Front 50

in active transport, drug transfer proceeds until __ or __ is depleted

Back 50

drug stubstrate, ATP

Front 51

kind of carrier mediated transfer that is energy independent, it transports drugs WITH their concentration gradients. drug transfer proceeds until equilibrium is reached

Back 51

facilitated diffusion

Front 52

in carrier mediated transfer, __ move drugs in to cells, __ move drugs out of cells and tisseus

Back 52

uptake transporters, efflux transporters

Front 53

the percentage of administered drug that reaches the systemic circulation by any route

Back 53

bioavailability

Front 54

what are the bioabailability of drugs given IV?

Back 54

100%

Front 55

what 3 things does bioavailability depend on?

Back 55

1. chemical form of drug

2. amoutn of contact time with absorbing surface

3. presence fo drug metabolizing enzymes and efflux transporters that may eliminate the drug before it reaches the systemic circulation

Front 56

what are 3 effects of exercise on drug absorption?

Back 56

1. reduced splanchnic blood flow during or after exercise may reduce oral absorption

2. increased absorption for SC, transdermal, IM and inhalation due to increased blood flow

3. increased skin temp increases transdermal absortpoion of antianginal agent, nitroglycerin

Front 57

why is it important that tissue distrubtion of drugs throughout the body is not uniform?

Back 57

becuase drug concentration at the anatomical site of action determines the pharmacological effect

Front 58

what are three factors that determine drug distribution?

Back 58

1. blood flow and tissue mass/volume

2. capillary permeability

-periperal capillaries are porous (filtration into interstitial fluid is rapid)

-CNS and placental capillaries are non-porous; provides some limits to distribution to these tissues

3. lipid solubility of the drug vs lipid content of teh tissue (highly lipophilic drugs can accumulate in adipose tissue)

Front 59

defined as the volume (in liters per kg body weight) a drug appears to be containedin, relative to the concentration of drug in teh blood

Back 59

volume of distribution

Front 60

what is the equation of volume distribution

Back 60

Vd=amount of drug in teh body/concentration of drug in the blood

Front 61

what does volume distribution really tell you?

Back 61

is the drug mainly in tissues or in the blood

Front 62

what does a low Vd mean?

Back 62

the drug is confined to teh circulation and will be eliminated rapidly by teh kidnes

Front 63

what does a high Vd mean?

Back 63

drug will remain in teh body longer. kidneys will have difficulty eliminating the drug (unless it is metabolized)

Front 64

any drug in teh blood is present both __ and __

Back 64

free in solution, reversiblty "bound" to plasma protiens (mainly serum albumin)

Front 65

binding to plasma proteins are __

Back 65

saturable (when all binding sites are occupied, free drug concentration increases

Front 66

what is the basic purpose of drug metabolism?

Back 66

drugs that enter the body are usually too lipid soluble to be excreted rapidly enough to prevent toxicity. drug metabolizng enzymes turn these into more water soluble metabolites that can be excreted.

Front 67

enzymes that metabolize and transport drugs are concentrated at the __. this ___

Back 67

portals of entry; decreases the likelihood that chemicials will reach systemic circulation ina form which they might accumulate

Front 68

where are teh locations of enzymes that metabolize and transport drugs and which is teh most important, and initial

Back 68

liver (most important

small intestine (initial site of drug metabolism after oral dosing; conributes to 1st pass effect)

nasal epithelium and lung

skin

plasma

kidney

CNS

Front 69

what is the first pass effect?

Back 69

when metabolism of drugs by liver enzymes can be high enought ot remove most of teh drug from teh portal system passing through the liver

Front 70

what do phase 1 enzymes do?

Back 70

oxidizes drugs, product may be active, inactive, toxic, or nontoxic.

Front 71

what is the most important phase 1 enzyme?

Back 71

cytochrome p450

Front 72

what three CYP subfamilies account for teh metabolism of most drugs?

Back 72

3A, 2C, 2D

Front 73

what phase one enzyme is involved in the metabolism of >50% of all drugs?

Back 73

CYP3A4

Front 74

what do phase 2 enzymes do?

Back 74

convert drugs to inactive metabolites

Front 75

phase 2 enzyme that adds glucuronic acid to produces of phase 1; product is termed a glucuronide conjugate

Back 75

UDP glucuronyltransferase (UGT)

Front 76

phase 2 enzyme that adds sulfate; product is sulfate conjugate

Back 76

sulfotransferases (SULT)

Front 77

what are the 5 phase 2 enzymes?

Back 77

UGT, SULT, GST, NAT, MT

Front 78

phase 2 enzyme that acetylates drugs

Back 78

N-acetyltransferase (NAT)

Front 79

phase 2 enzyme that methylates drugs

Back 79

methyltransferase (MT)

Front 80

enzymes that act in concert with pahse 1 and 2 enzymes to trasnfer drugs and their metabolites across membranes

Back 80

pahse 3 (efflux transporter proteins)

Front 81

explain what ATP binding cassette (ABC) transporters are

Back 81

MDR! (P-glycoprotein)

pumps drugs from cells itno urine, bile, and intestinal lumen

pumps drugs out of the brain

pumps anti-cancer drugs out of cancer cells

Front 82

what happens if a drug is metabolized too rapidly or too slowly?

Back 82

rapidly: may never reach a therapeutic blood level

slowly: accumulates and causes an excessive clinical response/toxicity

Front 83

what three things effect drug metabolism?

Back 83

enzyme induction

enzyme inhibition

pharmacogenetics

Front 84

what is enzyme induction and how does it affect metabolizing?

Back 84

a reversible, adaptive response that INCREASES the rate of drug metabolism and or transport

Front 85

how can enzyme induction affect the body by increasing drug metabolism?

Back 85

reduces therapeutic blood levels necessitating an increase in dosage

may increase the production of toxic metabolits

Front 86

how does enzyme inhbition decrease the rate of drug metabolism?

Back 86

decreases the rate of drug metabolism and or transport

Front 87

how does enzyme inhibition occur?

Back 87

when two or more drugs compete for the same drug metabolizing enzyme

Front 88

__ is the major cause of drug interactions in patient taking multiple drugs

Back 88

enzyme inhibition

Front 89

grapefruit juice causes the enzyme CYP3A4 in GI epithelium to increase oral bioavailability of many drugs. this is an example of __

Back 89

enzyme inhibition

Front 90

tobacco smoke increasing CYP1A1, Charcoal broiled foods increasing CYP1A2, ethanol incresaaing CYP2E1, and st. johns wort increassing CYP3A$ and PgP are all examples of __

Back 90

enzyme induction

Front 91

the individual variability in drug responses

Back 91

pharacogenetics

Front 92

ethinic subpopulations with faster or slower raes of drug metabolism like CYP2D6 causing poor, extensive, and ultra-rapid metabolizers of certian drugs and NAT-2 causing fast and slow acetylators of certain drugs (TB drug isoniazid) are examoples of __

Back 92

pharmacogenetics

Front 93

genetic variation accounting for pharmacogenetics can occur from __, __, and __

Back 93

SNP (polymorphisms), duplications, or deletions

Front 94

how does overall excretion of drugs occur?

Back 94

can be removed by kidneys if sufficiently hydrophilic. lipophilic drugs are eliminated by metabolism but their hydrophilic metabolitse must be revomed by the body by teh kidneys

Front 95

what are the components of total urinary excretion?

Back 95

glomerular filtration+(passive diffusion-passive reabroption)+ (carrier mediated efflux-carrier mediated reuptake)

Front 96

how does biliary excretion occur?

Back 96

active transport of comparatively large mostly anionic molecules from liver or bile, which is secreted itno the duodenum.

the glucoronide metabolizes the drug in the bile back to the free drug and be reabsorbed (enterohepatic recirculation)

Front 97

how does enterohepatic recirculation occur?

Back 97

gluconruonide conjugates excreted into the bile can be metabolized to the free drug by GI bacterial B-glucuronidase; free drug can then be reabsorbed.

Front 98

what are thee other(minor) routes of excretion?

Back 98

pulomonary (volitile comounds ie ethanol/anesthetic gases)

sweat and saliva

breast milk

Front 99

any drug taken via the stomach-proximal colon goes to the __ vien

Back 99

portal. to the liver to be processed

Front 100

__ and __ and entereal rounts of admnistration which avoid the liver.

Back 100

sublingual, rectal

Front 101

what does intrathecal injection mean?

Back 101

injection into sub-arachnoid space

Front 102

what route of administration might be better for a drug that needs slow distribution?

Back 102

dermal

Front 103

blood with drugs from teh stomach/proximal colon go into the __ into the liver to be metabolize

Back 103

portal vein

Front 104

what does intrathecal mean?

Back 104

injecting a drug into the subarachnoid space

Front 105

how does the body maintain a concentration gradient from the blood to itssues?

Back 105

the blood washes drugs away maintaining the gradient

Front 106

carrier mediated transfer can become __ and has an __ for certain drugs

Back 106

saturated, affinity

Front 107

efflux transporters are important for __ functions

Back 107

barrier

Front 108

explain volume of distribution

Back 108

its a ration of teh amount of drug in teh tissues to the amount of drug in teh blood. the higher the Vd, the more in the tissues. the lower the Vd, the more in the blood

Front 109

most important phase 2 enzyme

Back 109

UGT

Front 110

drug metabolizing enzymes that conjugate drugs to make them inactive

Back 110

phase 2 enzymes

Front 111

allows metabolites to leave cells b/c they’re too hydrophillic to do so on their own.

Back 111

phase 3 enzymes

Front 112

most important phase 3 enzyme

Back 112

ABC (ATP binding cassette)

Front 113

drug inhibition occurs when __

Back 113

two drugs are competing for the same enzyme

Front 114

how do you find the therapeutic range?

Back 114

its the difference between the minimal effective does and the minimal toxic dose.

Front 115

why is it more effective to use an infusion than a bolus?

Back 115

an infusion accumulates to a constant level whereas a bolus is continually eliminated

Front 116

what is the clinical significance of drug levels in teh blood?

Back 116

although the blood is not the site of action for ost drugs, there is a direct correlation between therapeutic and toxic responses in tissues and teh amount of drugs in teh blood. thus, a minimum effective level in teh blood can be defined for most drugs

Front 117

a period of latency between drug adminisration and onset of teh desired effect; depends on teh rate of absorption

Back 117

time to onset

Front 118

the maximal level attained after drug administration; usually correlates with the intesnity of the pharmacological effect

Back 118

peak drug level (Cmax)

Front 119

the amount of time spent above teh minimal effective level

Back 119

duration of action

Front 120

what determines the duration of action?

Back 120

the rate of elimination (metabolism+excretion)

Front 121

when drug levels fall below the __, the drug response ceases

Back 121

minimal effective limit

Front 122

what is the execption to the rule of drug effects ceasing after the drug level falls below the MEL?

Back 122

if drug action persists after drug levels fall below MEL when the response is due to irreversible binding of the drug to its target (eg aspirin effects on platelets). once the drugs effect a tissue, that tissues stays that way permenantly.

Front 123

indicate how cautious clinicians should be in using and instructing pts to use a drug. incorporates a margin of saftey.

Back 123

therapeutic range

Front 124

at therapeutic doses, most elimination processes (renal, hepatic metabolism) are __; ie the rate of elimination is proportional to the amount of drug present

Back 124

1st order

Front 125

what does it mean if an elimination process is 1st order?

Back 125

the more the drug there is, the faster the eliminatino

Front 126

explain how you can get information on first order kinetics of drugs elmination from a blood concentration curve?

Back 126

you take the log of the y axis to get a linear curve.

Front 127

what does teh beta from teh log curve for 1st order kinetics elimination tell you?

Back 127

how fast the drug is eliminated

Front 128

how can you use the the log curve for the drug concentration graph to find half life?

Back 128

you find how much drug is present at time 0 and see how long it takes for half the drug to be eliminated.

Front 129

half life is always the same b/c its a __ reaction

Back 129

1st order

Front 130

it takes __ half lives for a drug to efficently leave teh body

Back 130

4-5

Front 131

what is the equation fro volume of distribution?

Back 131

Vd=dose/concentration at time 0

Front 132

what do you do if volume of distribution is expressed in liters/kg body weight?

Back 132

you multiply by body weight (ie 70 kg)

Front 133

the volume of fluid from which a drug is completely removed in a given period of time (mL/min or L/hr) as it flows through teh body or through an individual organ

Back 133

clearance (CL)

Front 134

what can clearance be conceptualized as?

Back 134

the rate of drug elimination (liver metabolism + renal excretion) relative to drug concentration in teh blood

Front 135

what is the equation for clearnace?

Back 135

metabolism + excretion/drug concentration

Front 136

drugs with long half lives and large volumes of distribution have __ clearance and are __ soluble

Back 136

long, lipid

Front 137

what are 2 factors that affect volume of distrubtion?

Back 137

aging: reduced muscle mass->decreases Vd->decreases half life

obesity: increased adipose ->increased half life

Front 138

what are 3 factors taht affect clearance?

Back 138

CYP induction: increases CL->decreases half life->need dose elevation

CYP inhibition: decreases CL->increases half life-> dose reduction

hepatic/renal failure ->decreases CL -> increases half life -> dose reduction

Front 139

how is the clearance of creatinine used to adjust doses of drugs eliminated by the kidneys in pts with renal insufficiency?

Back 139

if creatinine drops, it means kidney function isn't as high

Front 140

explain the principle of multiple dosing regimins

Back 140

the 2nd does is taken before teh first does is eliminated. each next dose is taken at the same interval. accumulation of the drug up to a steady state level occurs when DRUG INTAKE = DRUG ELIMINATION. drug levels will then always be in the therapeutic range

Front 141

what factors affect steady state of multiple dose drug regimins?

Back 141

if CL of teh drug is 1st order and teh dose interval =half life, then it will take 4-5 half lives to reach steady state

Front 142

if a drug has a very long half life and its a multiple dose regimin, you may need a __

Back 142

loading dose

Front 143

drugs acting on enzymes usually try to __ them

Back 143

inhibit

Front 144

drugs that activate receptors (stimulates the receptors)

Back 144

agonists

Front 145

drugs that block receptors and prevent their activation preventing endogenous ligands binding to it

Back 145

antagonists

Front 146

determines how much drug it takes to bind to the receptor

Back 146

affininty

Front 147

what does a high or low affinity mean?

Back 147

high affinity means you don't need much drug, low affinity means you need a lot of drugs

Front 148

what are the four superfamilies of receptors?

Back 148

ligand-gated ion channels-opened by ligand, lets ions in. ie nicotininc ACh

G protein coupled receptors-largest class on surface of cells. bind to ligand, activate signalling cascade to activate protein synthesis

kinase linked receptors

nuclear receptors-receptor not on cell surface, in nucleus ie steroid receptors

Front 149

explain the drug response relationship

Back 149

drug receptor binding is reversible

the number of recetpors in finite

at some drug dose, all teh binding sites will be occupied and the response is "maximal"

Front 150

what does Kd on teh linear dose response curves represent?

Back 150

teh dose of agonist that occupies 50% of teh recetpors

Front 151

a measure of the affinity of the drug for teh receptor

Back 151

Kd (the lower the Kd, the higher the affinity)

Front 152

the dose that produces an "effective response" that is 50% of maximal

Back 152

ED50 (on log dose response curves)

Front 153

if antagonists bind to teh receptor, but do not activate it, their efects are produced by __

Back 153

preventing the agonists form binding

Front 154

the amount of drug required to generate a given fractional response aka how little/how much do you need to give for a response?

Back 154

potency

Front 155

how well the drug activates the receptor when its bound

Back 155

efficiacy

Front 156

produces 100% response when all teh receptors are bound

Back 156

full agonsit

Front 157

produces <100% response when all receptors are bound

Back 157

partial agonist

Front 158

the curve closest to the Y axis is the most __

Back 158

potent

Front 159

the curve that is higest is teh most __

Back 159

efficacious

Front 160

the __ the Kd, the more potent

Back 160

lower

Front 161

drugs that bind reversibly to the receptor and thus compete with agonists for binding

Back 161

competitive antagonists

Front 162

what is the effect of competative agonists?

Back 162

decrease teh potency of teh agonist

Front 163

in teh presence of a competitive antagonist, the agonist does response curve shifts to the __

Back 163

right

Front 164

the effect of a competitive antagonist can be reversed by __ the concentration of the agonist

Back 164

raising

Front 165

bind irreversibly to the receptor; no other agonists can "compete" for teh receptor

Back 165

non-competitive antagonists

Front 166

what is the effect of non competitive antagonists?

Back 166

decrease the efficacy of teh agonist

Front 167

in teh presence of a non-competitive antagonist, the agonist dose-response curve shifts __

Back 167

down

Front 168

the effect of the non-competitive antagonist __ be reversed

Back 168

cannot

Front 169

how do quantal dose response curves differ from "graded dose response curves?

Back 169

in that it measures discrete outcomes

Front 170

drug curve used to assess efficacy and safety of drugs in teh clinical trials

Back 170

quantal dose response curves

Front 171

how are quantal dose response curves recorded?

Back 171

for each dose, teh number of patients in a population who respond to the drug is recorded

Front 172

what is the equation for the therapeutic index?

Back 172

TD50/ED50

Front 173

waht is the equation for the margin of safety?

Back 173

TD01/ED99

Front 174

drug effect known from pharmacology and are dose-related; seldom fatal and are common

Back 174

augmented pharmacological effects

Front 175

drug effect that is unpredictable with high morbidity/mortality; uncommon

Back 175

bizarre effects (idiosyncratic)

Front 176

drug effects that only occur with prolonged treatment

Back 176

chronic effects

Front 177

drug effects that occur months to years after treatment; can occur in children of treated parents

Back 177

delayed effects

Front 178

drug effects that occur when drug is stopped suddenly (withdrawl)

Back 178

end of treatment effects

Front 179

the official FDA aproved name of a drug. every drug has 1 of these

Back 179

generic name

Front 180

the name each manufacturer gives its product; a drug can have many of these. first letter is capitalized

Back 180

trade name

Front 181

superfamily of receptor that uses the flow of ions that causes hyper/de polarization to cause cellular effects. takes milliseconds. examples are nicotinic and ACh receptors

Back 181

ligand gated ion channels

Front 182

superfamily of drug receptor that uses second messengers that causes phosphorylation and cellular effects. takes seconds. examples are muscarinic ACh

Back 182

g protein coupled receptors

Front 183

superfamily of drug receptors that cause protein phosphorylation, gene transcription, protein sysnthesis, and cellular effects. takes hours. examples cytokine receptors

Back 183

kinase linked receptors

Front 184

superfamily of drug receptor that occurs in teh nucleus, cuases gene transcription, protein synthesis, and cellular effects. takes hours. examples estrogen receptor

Back 184

nuclear receptors

Front 185

sympathetic nerves exit from the __ and __

Back 185

thoracic and lumbar spine

Front 186

parasympathetic nerves exit from the __ and __

Back 186

cranium and sacrum

Front 187

compare/contrast somatic and ANS nerves

Back 187

somatic: ganglia in CNS, 1 effert fiber, used for skeletal muscle, NT: ACh, denervation cuases muscle atrophy

ANS: gnglia outside CNS, 2 efferent nerve fivers (pre/post ganglionic (non-myelinated), smooth muscle/heart/exocrine glands, function: homeostasis, NT: NE and ACh, denervation reveals intrinic activity

Front 188

contrast sympathetic and parasympathetic pre/postganglioiic fibers

Back 188

SNS: short pre, long post

PNS: long pre, short post

Front 189

what is the importance of the multiple postganglionic fibers innervated by 1 SNS preganglionc?

Back 189

you can mobilize everything at once for fight/flight.

Front 190

what doesn't have dual innervation?

Back 190

blood vessels, sweat glands, and adrenal glands (only SNS)

Front 191

what physiological function is mediated by a cooporation of the SNS and PNS nervous system?

Back 191

sex

Front 192

describe the anatomical arrangement of the PNS

Back 192

long preganglionic, releases ACh, stimulates nicotinic subtype receptor.

short post ganglionic, releases ACh to affect muscarinic recepotr

Front 193

describe the anatomical arrangement of the 3 SNS nerves

Back 193

short preganglionic, releases ACh, affects nicotinic recepotr; long postganglionic, releases NE to affect alpha or beta recepotrs

short preganglionic, releases ACh, affects nicotinic recepotr. long post ganglionic, releases ACh, affects muscarninc recepotrs on SWEAT GLANDS

short preganglionic, releases ACh, affects adreneal medulla. releases epinephrine. binds to alpha and beta receptpors

Front 194

the PNS affect on teh SA node, AV node, atria, and ventricles of the heart use a __ receptor and cause __ response

Back 194

M2, decreased HR, decreased conduction velocity, decreased contractility

Front 195

the PNS affect on the VSM and endothelium of teh blood vessels use a __ receptor and cause __ response

Back 195

M3, constriction (NO release-dilation)

Front 196

teh PNS affect on the broncial muscle and glands of teh respiatory tract use a __ receptor and cause __ response

Back 196

M3, bronchiole constriction/secretion

Front 197

the PNS affect on the moltility and tone, sphincters, and proton pumps of the GI tract use a __ receptor and cause __ response

Back 197

M3, increase motility/tone, relax sphincters, secreted protons

Front 198

the PNS affect on the genitoruniiary tract uses a use a __ receptor and cause __ responses in bladder detrusor, trigone and shpincter, and penis respectively

Back 198

M3, contraction, relaxation, erection

Front 199

the PNS affect on teh sphincter muclse of the iris, and ciliary muscle of the lens use a __ receptor and cause __ response

Back 199

M3, contraction (miosis), contraction (near focus)

Front 200

the PNS affect on the salivary glands uses a __ receptor and causes a __ response

Back 200

M3, salaivation

Front 201

the SNS affect on sweat glands uses a __ receptor and cuases a __ response

Back 201

M, perspiration

Front 202

the SNS affect on the adrenal medulla uses a __ receptor and causes a __ response

Back 202

nictoinc, epinephrine release

Front 203

the SNS and PNS affect on autonomic ganglia use a __ receptor and cuase _

Back 203

nicotinic, stimulation

Front 204

the somatic affect on skeletal muscle uses a __ receptor and cuases __

Back 204

nicotinic, contractoin

Front 205

what is the SNS effect on the SA node, AV node, and atria/venticles of the heart and what receptor is used?

Back 205

inc HR, inc conduction velocity, inc contractility; beta 1

Front 206

what is the SNS affect on the BV of the skeletal muscle and skin/mucosa? what receptors are used?

Back 206

contriction/dilation of skeletal muscle, constriction of skin/mucosal; alpha 1 and beta 2 for skeletal muscle, alpha 1 for skin/mucosa

Front 207

what is the SNS affect on brinciole muscle and what receptor is used?

Back 207

relaxation; beta 2

Front 208

what is the affect on teh bladder detrusor muscle by the sns and what is the receptor used?

Back 208

relaxation; beta 2

Front 209

what is the effect on the trigone and sphincter muscles by teh SNS and what recetpor is used?

Back 209

contraction, alpha 1

Front 210

what is the effects of SNS on the penis and what recetpor is used?

Back 210

ejactulation; alpha 1

Front 211

what is the effect of the sns on the radial muscle of the iris and what receptor is used?

Back 211

contraction (mydriasis); alpha 1

Front 212

what is the effect of the sns on the cilliary muscle (lens) and what recetpro is used?

Back 212

relaxation (far focus), beta 2

Front 213

what is the effect of the sns on the ciliary body and what recetpor is used?

Back 213

aqueous humor secretion; beta

Front 214

what is the effect of the sns on the uterus and what are the recetptors

Back 214

contraction/relaxation; alpha 1/beta 2

Front 215

what is the effect of the sns on the kidney and what recetpor is used?

Back 215

inc release of renin; beta 1

Front 216

explain the basics of synaptic neurotransmission

Back 216

nerve impulse arrives a terminal button; opens Ca channels, Ca couses NT vessicles to exocytose and release NT into synaptic cleft.

Front 217

onabotulinumtoxinA, muscarine, atropoine, noicotine, tubocurarine, mehtyldopa, and cocaine all affect teh __ fuction

Back 217

presynaptic termianl function

Front 218

what characteristic of ACh makes it very transportable in the body?

Back 218

a postive charge on teh N atom, making it hydrophilic

Front 219

what enzyme breaks down ACH into acetate and choline

Back 219

acetycholine esterase

Front 220

how does botulinum toxin work?

Back 220

botulinum is a protein which gets inot the nerve terminal. prevents fusion of storage vessicle with terminal membrane. prevents release of ACh from nerve. causes flacid paralysis.

Front 221

used for therapeutically treat muscle spasms/dystonias; facial wrinkles; hyperhidrosis, and urge incontinence by causing temporary cholinergic denervation

Back 221

onabotulinumtoxinA

Front 222

what are the side effects of botulinum?

Back 222

if drug spreads beyond site of injection, dyphagia, breating difficulties; muscle weakness (ptosis), allergic reaction (rash)

Front 223

teh duration of action for botulinum toxin is __. you may get an allergic reaction from it b/c its a __

Back 223

3-6 months, forgein protein

Front 224

what are two important points to educate PT pts on botlinum toxin use?

Back 224

may have allergic reaction b/c its a foreign protein, effects are temporary

Front 225

what are the effects of muscarine and atropine?

Back 225

muscarine (stimulates muscarinic recepotrs)

atropoine (blocks muscarinnc recepotrs, leaves sympathetic nerves unopposed)

Front 226

muscarine is a muscarinic __

Back 226

agonist

Front 227

atropine is a muscarininc __

Back 227

antagonist

Front 228

muscarinine __ activate nocotininc recepotrs

Back 228

DOESN'T

Front 229

substance found in amanita muscaria, a mushroom that produces all cholinergic responses, worst of all in GI tract

Back 229

muscarine

Front 230

found in deadly night shade, which roman women used to cause pupillary dilation

Back 230

atropine

Front 231

muscarine and atropoine are selective for the __ recepotr

Back 231

muscarinic

Front 232

compare teh two nicotininc recepotrs

Back 232

Nn (ganglia): nictoine stimulates this receptor. Mecamylamine is an antagonist of this recepotr subtype

Nm (neuromuscular): nictoine stimulates this recepotr (tubocurarine is a competitive antagonists)

Front 233

_ is an antagonist for Nn recepotrs

Back 233

mecamylamine

Front 234

__ is a competitive antagonists for Nm recepotrs

Back 234

tubocurarine

Front 235

__ is used as a neuromuscular blocking drug by copetitively antagonising the Nm recepotrs

Back 235

tubocurarine

Front 236

how does nicotine affect nictoinc recepotrs?

Back 236

nicotine is selective for nicotinic receptors at teh NM junction and ganglia (Nm and Nn). it DOES NOT ACTIVATE TEH MUSCARININC RECEPTOR!!!. nictoine activates teh nicotinic receptors

Front 237

explain the synthesis of catecholamine NT

Back 237

all adrenergic NT come from tyrosine. then it gets converted to specific NT based on the tissues. tryosine->DOPA->dopinine (in BG)-.NE (SNS post-ganglionic neurons)->epinephrine (adrenal medulla)

Front 238

explain the differences between how NT action in a synapse is decrease in cholinergic and andrenergic transmission?

Back 238

cholinergic=enzyme

adrenergic=NET transporter

Front 239

explain andrenergic transmission

Back 239

NE is created in teh cell by converting tyrosine->DOPA->dopamine->NE. it is then packeaged into vessicles.

MAO (monoamine oxidase) is an enzyme in teh mitochondira that degrades dopamine/NE in teh cytosol)

once NE is released into the synapse, it is either removed by NET (pumps it back into teh presynaptic neruonr), it may stimulate alpha 2 recepotrs on teh Presyn cell which negatively feed back to decrease exocytosis. if NE gets to teh blood it will be removed by the ENT transporter

Front 240

tranporter in teh blood which can have an affect on IV given NE like drugs

Back 240

ENT

Front 241

tranposrter in teh presynaptic cell that pumps NE back inot it

Back 241

NET

Front 242

receptor on the presynaptic andrenergic cell that negatively feeds back to inhibit NE release

Back 242

alpha 2

Front 243

how does dyramine affect the presynaptic cell?

Back 243

tyramine is a dietary substance found in ceratin foods that gets into the nerve and dumps NT from teh cessicles into the cytosol. this reverses the concentration gradient for NET making the transporter dump NE into the synapse.

Front 244

drug found in aged cheeses, beer/wine, smoked meats, etc, that deplaces all the NE form nerve terminals at once, changing the concentation gradient for NET, reversing its flow.

Back 244

tyramine

Front 245

why do we not get advers affects from tyramine normally?

Back 245

its normally degraded byMAO in teh GI tract. systemic absorption can occur with pts taking MAOIS for depression

Front 246

what is an adverse effect for people taking MOAI's which allow tyrosine to have affect?

Back 246

hypetensive crisis

Front 247

hwo does methydopa work?

Back 247

it insertes itself into the biochemical pathway for NE/E production. it creates methyl'ed dopaine, NE< and E. these do not stimulates postsynaptic receptors but DOES HAVE AN AFFINITY FOR THE A2 RECEPTOR. this increases the negative feedback to decrease NE release.

you get decreased alpa 1 recepotrs in BV and B recepotrs in the heart. this decreases blood pressure.

Front 248

what was methy-dopa used for, what are its adverse effects, and what is it used for now?

Back 248

used as an antihypertensive, gave you parkinsons like symptoms b/c it got into dopminergic nerves in teh brain. its now used to treat high bp in pregnant women b/c its safe for the fetus

Front 249

methydopa is __ which is converted to methyl-NE in adrenergic nerves

Back 249

prodrug

Front 250

what is teh mechanism of action of methyldopa?

Back 250

agonist at alpha 2 adrenergic recepotrs, reducing sympathetic outflow from CNS

Front 251

what is methyldopa used for?

Back 251

antihypertensive

Front 252

waht are the side effects for methydopa?

Back 252

parkinsons like symptoms, sedation, dry mouth

Front 253

what do you need to keep in mind as a PT iwth pts who are on methydopa? (2)

Back 253

check BP, stay away from interventions that would increase vasodilation

Front 254

how does cocaine affect the nerves?

Back 254

it blocks the NET tranposrter. causing excess stimulation of post-synatpic recepors.

also has periphery affects: causes heart problems b/c of inceased B1 stimulation (increases HR)

blocks NA channels on axons, giving it local anesthtic affect

Front 255

what is the mechanism of actin for cocaine?

Back 255

blocks NET leaving NT in synapse.

blocks Na channels in sensory nerves

Front 256

what are the therepueitc uses for cocaine?

Back 256

local anesthetic for ENT

Front 257

all adrenergic receptor subtypes are __

Back 257

coupled to G proteins

Front 258

alpha 1 receptpors are on __ and cuase __

Back 258

smooth muscle, contraction

Front 259

alpha 2 receptors are on __ and cause __

Back 259

nerves, inhibitory effects (negative feedback)

Front 260

beta 1 receptors are in teh __ and __ and cause __/__ effects

Back 260

heart, kidney, excitatory/contraction

Front 261

beta 2 receptors are in the __ , __, and __ and cause __

Back 261

lung, skeletal muscle vasculature, uterus, relaxation

Front 262

alpha 1's are on teh __ synaptic cel; alpha 2's are on teh __synaptic

Back 262

post, pre

Front 263

beta 1's cause and increase in __ and __

Back 263

HR, contractility

Front 264

beta 2 recepotrs cause __

Back 264

relaxation

Front 265

metabolzer of catecholamines that degrades NE/E, tyramine, histamine.

clears catecholamines in teh nere terminals

inhibitors elevate transmitter leves in neruons

Back 265

monoamine oxidase (MAO)

Front 266

metabolizer of catecolamines, cleasrs circualting catecholaines in teh liver/kidney.

inhibitors are used for parkinsons disease

Back 266

catecholo O methytransferase (COMT)

Front 267

what are teh pharmacokinetics of the drug acetylcholine?

Back 267

IV administration: poor lipid solubility (bad bioavailability; short duration of action (<10) due to lots of cholinesterase in tissues; non selective (acts on both nicotinic and muscarininc recepotrs

Front 268

acetylcholine is __, meaning it acts on both nicotinic and muscarinic recepotrs

Back 268

non-selective

Front 269

what are the 2 cardiovascular effects of aceytlcholine?

Back 269

vasodilation (sitmulates muscarinic recetpors an vascular endothelium

stimulation of these receptors releases NO

NO diffuses inot vascular smooth muscels and cuases relaxation

Front 270

what are 2 cardiac effects of acytelcholine?

Back 270

negative rate (chronotropic) effects

negative contractility (inotropic) effects

Front 271

what are teh smooth muscel effects of acetylcholine?

Back 271

increases tone, amplitude of contraction, peristalitic activity, and secretory activity of GI.

contracts bronchiolar, uterine, urinary smooth muscles

Front 272

what are the glandular effects of aceytlcholine?

Back 272

salivary, lacrimal, diestive, and tracaeobronchial secreation

sweat gland stimulation (sympathetic)

Front 273

what are teh occular effects of acytelcholine?

Back 273

contraction of sphincter mucle of iris, produces miosis (pupil constirction)

contraction of ciliary muscle (focuses eyes for near vision)

Front 274

what is the clinical use for acytelcholine?

Back 274

opthalmic

Front 275

how do synthetic choline esters and alkoloids differ from acytelcholine?

Back 275

there are more selective and have a more prolonged action

Front 276

synthetic choline esters and alkaloids act via __ of __ receptors

Back 276

direct stimulation; muscarinic

Front 277

what are the main differeces between synthetic choline esters and alkoloids?

Back 277

esters do not penetrate the blood brain barrier. alkaloids do.

Front 278

what is bethanechol?

Back 278

a choline ester that is resistant to hydrolysis by AChE; has a longer action than ACh

Front 279

with oral dosing of bethanechol, there is a selectvity for __ and __ muscarinic receptors

Back 279

GI, bladder

Front 280

what is the effect of bethanechol when administered orally?

Back 280

increased smooth muscle contraction of urinary bladder (detrusser muscle) whcih helps people pee. reduces need for catheters

Front 281

the therapeutic use for bethanechol are __

Back 281

postoperative and postpartum urinary retetion

Front 282

what is cevimeline?

Back 282

an alkaloid that is a selective muscarnic agonist. used to stimulate muscarinic receptors in salivitory glands.

Front 283

what is cevimeline used to treat?

Back 283

xerstomia from sjogrens syndrome and head/neck radiation

Front 284

name a synthetic choline ester and allkoloid

Back 284

bethanechol, cevimeline

Front 285

what are teh main adverse effects from muscarinic agonists?

Back 285

you get the full range of muscarinic effects. most comon are sweating, hypotension, and upset stomach.

Front 286

name 2 antidotes for muscarinic agonist poisoning

Back 286

atropine, epinephrine

Front 287

name 3 muscarninc agonists

Back 287

bethanacol, cevimeline, aceytlcholine

Front 288

what are 4 muscarinic antagonists?

Back 288

atropine, ipratropium bromide, scopolamine, tolterodine

Front 289

what is the mechanism of action of atropoine?

Back 289

competitively blocks muscarinic receptors, produces the opposite effect of muscarinic stimulation

Front 290

atropine is a lipophilic drug that can cross teh __

Back 290

blood brain barrier

Front 291

atropine has no effect on the __ becuase theres no receptors there

Back 291

blood vessels

Front 292

what are the central nervous system effects of atropine?

Back 292

mild intoxication at low doses

toxic doses produce hallucinations and psychosis

Front 293

what are teh occular effects of atropine?

Back 293

mydriasis (blocks sphincter muscle)

cycloplegia (blocks ciliary muscle)

Front 294

what are the cardiovascular effects of atropine?

Back 294

tachycardia (blocks vagal nerve)

NO EFFECT ON CIRCULATION B/C IT HAS NO PNS INNERVATION

Front 295

what are the genitourinary effects of atropione?

Back 295

suppresses detrusor muscle contraction, contracts trigone and sphincter (urinary retention, need to go but can't)

antispasmodic for pts with overactive bladder

Front 296

what are the respiratory effects of atropine?

Back 296

decreases bronchial secretions

relaxes bronchial smooth muscle (asthma)

Front 297

what are teh GI effects of atropine?

Back 297

inhibits salivation

reduces tone and motility of GI (constipation)

reduced GI acid secretion

Front 298

what are 3 therapeutic uses for atropine?

Back 298

bradycardia during surgery

mydriasis for opthalmic procedure

poison antidote for amanita mushrooms and organophosphate insectides

Front 299

dry mouth, blurred vision, photophobia, tachycardia, GI distress, hot and dry skin are adverse effects of __

Back 299

atropine

Front 300

when is atropine contraindicated?

Back 300

urinary retention (males with BPG)

Front 301

what is a drug interaction you must be mindful with atropine?

Back 301

additive anticholinergic effects with antihistamines, antipsychotic, and antidepressant

Front 302

what is a main PT concern for atropine?

Back 302

pts will be at cardiac risk and have altered thermoregulation

Front 303

a drug similar to atropine but used as a sedative at low doses

Back 303

scopolamine

Front 304

what is scopolamine used for?

Back 304

suppresses emesis and motion sickness (atropine does not)

Front 305

used as a preventative treatment for motion sickness and nausea/vomitting associated with recovery from anethesia

Back 305

scopolamine

Front 306

quaternary amine that is always charged so it does not diffuse across cell membranes. approved as a bronchodilator in treatment of COPD and asthma. limited absorption when inhaled, so atropine like side effets are minimal

Back 306

ipratropium bromide

Front 307

a muscarinic antagonist administered by inhalationto treat asthma. allows teh SNS to take over and dilate the bronchiols

Back 307

ipratropium bromide

Front 308

muscarinic antagonist used to treat frequenc or uncontrolled urination (urge incontinence). effects are modest, atropine like effects

Back 308

tolterodine

Front 309

name 5 anticholinesterase agents

Back 309

nestigmine, physostigmine, doneqezil, malathoid, pralidoxime

Front 310

what is the mechanism of action of the acytelcholine esterase inhibitors?

Back 310

competitive inhibition of AChE. enhances effects of ACh.

Front 311

in therapeutic doses, AChE inhibitor effects are limited to __ receptors and __ receptors

Back 311

M, N (at NMJ)

Front 312

AChE inhibitor that is used to treat myesthenia gravis.

Back 312

neostigmine

Front 313

explain the neuromuscular effects of neostigmine at low and high doses

Back 313

low: increased force of contraction

high doses: reduced force of contraction b/c receptors are sensitized

Front 314

neostigmine is used to treat __ and __

Back 314

myesthenia gravis, glaucoma

Front 315

neostigmine has adverse effects by causing __ like respiratory depression. these can be treated with __

Back 315

excessive muscarinic stimulation. atropine

Front 316

AChE inhibitor that has an action similar to neostigmine; but crosses the blood brain barrier. used to treat poisoning by atropine and other drugs that cause muscarinic blockade. reverses muscarnic blockade in CNS

Back 316

physostigmine

Front 317

AChE inhibitor used to counteract the cognitive decline from alzheimers disease.

Back 317

donepezil

Front 318

is a more selective AChE inhibitor that targets AChE in the brain, rather than in the periphery

Back 318

donepezil

Front 319

what is an important drug interaction to know for donepezil?

Back 319

anticholinergics can cause an ultimate decline in cognitive function

Front 320

an irreversible AChE inhibitor that is an insecticide. its a highly lipid souble compound absorbed from all routes including the skin. is a common source of accidental and agricultural poisoning. therapeutically used to treat head lice

Back 320

malathion

Front 321

profuse sweating, salivation, miosis, bronchorrea/bronchospasm, bradycardia involuntary urination and defecation (muscarinic)

muscle weakness, fasciculation, paralysis (nicotinic)

confusion, ataxia, convulsions, coma, respiratory depression (CNS) are all sings of a __ caused by exposure of irreversible AChE inhibitors

Back 321

cholinergic chrisis

Front 322

what are 2 treatments for a cholinergic chrisis

Back 322

atropine, pralidoxime

Front 323

used to treat cholinergic crisis, give in large repeated doses; antagonizes muscarinic effects

Back 323

atropine

Front 324

used to treat a choliergic crisis. reactivates AChE at the NMJ. must be administed before aging occurs

Back 324

pralidoxime

Front 325

name 4 andrenergic agonists

Back 325

epinephrine, phenyephrine, terbutaline, methylphenidate

Front 326

what are 4 adrenergic antagonists?

Back 326

prazosin, tamsulosin, propranolol, metoprolol

Front 327

what are 4 mechanisms of action of sympathomimetics?

Back 327

direct receptor stimulation (agonist)

promotion of NE release (tyramine)

inhibition of NE reuptake (cocaine)

inhibition of NE inactivation (MAOI's)

Front 328

what are teh differences between catecholamines and non-catecholamine sympathomimetics?

Back 328

catecholamines: not orally active, short duration of action, doesn't cross teh BBB

non-catecholamines: don't have catechol, orally effective, longer duration, produce CNS effects

Front 329

adrenergics have a strong __

Back 329

selectivity

Front 330

adrenergic selectiviey is __ related to dose. you can overcome a lack of affinity by having a lot of drug

Back 330

inversley

Front 331

what is a clinical affect of alpha 1 activation in the blood vessels, eye form adrenergics? (4,2)

Back 331

vasoconstriction: hemostasis, nasal decongestion, prolonged action of anesthetics, elevation of blood pressure

mydriasis without cycloplegia (doesn't cause blurred vision)

Front 332

what are the the A2 activation effects of andrenergic agonists in teh CNS and eye? (3)

Back 332

reduced sympathetic outflow

antihypertensive effect

reduced gluacoma

Front 333

what are the clinical applications of andrenergic agonists on teh Beta 1 receptors of teh heart? (2)

Back 333

cardiac stimulation, treatment of shock

Front 334

what are the clinical applications of Beta 2 activation by adrenergic agonists? (2)

Back 334

asthma and COPD treatment

delay preterm labor

Front 335

epinephrine activates __, __, __, and __ receptors

Back 335

alpha 1, alpha 2, beta 1, beta 2

Front 336

what are the cardiac effects of epinephrine?

Back 336

increased SA node automaticty (chronotropism)

increased contractility (inotropism)

Front 337

what are the vascular effects of epinephrine?

Back 337

reduced cutaneous blood flow (alpha 1)

decreased/increased skeletal muscle blood flow (alpha 1 or beta 2)

Front 338

when does epiephrine cause skeletal muscle vasculature to vasoconstrict or vasodilate?

Back 338

if its a low dose: you get a B2 dilation effect

if its a high dose, alpha 1 receptors constriction effect

Front 339

what are teh 2 respiratory effects of epinephrine?

Back 339

relaxation of bronchial smooth muscle (B2)

Front 340

epinephrine is used for a __, __, and __

Back 340

anaphylactic shock, topical hemostasis, cardiac arrest

Front 341

hypertensive crisis (alpha 1), dysrhthmias (B1), angina pectoris (B1), and hyperglycemia (B2) are all adverse effects of __

Back 341

epinephrine

Front 342

what are 3 drug interacitons to be aware of with epinephrine?

Back 342

MAOI's (additive effect), cocaine (block NE reuptake, additive effect), alpha/beta blockers (antagonised effects)

Front 343

phenylephrine is __ selective

Back 343

A1

Front 344

andrenergic agonist which acts on A1 receptors. cuases marked vasoconstirction, used as a nasal decongestant, pressor aganet, and mydriatic

Back 344

phenylephrine

Front 345

because it can cause reflex bradycardia, excitability, restlessness, hypertension, overdose, problems with geriatic pts, __ has FDA high alert status

Back 345

phenylephrine

Front 346

terbutaline is a __ selective drug

Back 346

B2

Front 347

what is teh cardiovascular effects of terbutaline?

Back 347

little effect due to B2 selectivity

Front 348

what are 2 therapeutic uses of terbutaline?

Back 348

reduces airway resistances

tocolytic (supresses premature labor by relaxing uterine smooth muscle

Front 349

indirectly promotes teh release of NE/DA and inhibits reuptake (amphetamine like CNS stimulant). used for ADHD in children and adults. also used as a narcoleptic.

Back 349

methylphenidate

Front 350

__ could have insomnia and appetitie supression as adverse effects

Back 350

methylphenidate

Front 351

what are the alpha 1 blockade effects from adrenergic antagonsits (4)

Back 351

hypertension, BPH, pheochromocytoma (catecholamine secreting tumor), reynauds disease

Front 352

what are 7 b1 blockade effects of adrenergic antagonists?

Back 352

hypertension, angina, CHF, hyperthyroidism, glaucoma, stage fright, migraine headache prevention

Front 353

prazosin is a __ selective drug

Back 353

a1

Front 354

an alpha 1 selective drug that blocks alpha 1 receptors, especially in teh vasculature. produces dilation of arteries and veins and relaxes smooth muscle of teh bladder neck and prostate capsule. used for hypertension

Back 354

prazosin

Front 355

the first dose effect (orthostatic hypotension), inhibitory ejaculation, nasal congestion are adverse effects of__

Back 355

prazosin

Front 356

tamsulosin is a __ selective drug

Back 356

alpha 1a

Front 357

a drug that selectively favors blockade of teh alpha 1A receptor in the prostate and bladder. has little effect on blood pressure and facilitates urination in males with BPH by reducing prostatic smooth muscle tone

Back 357

tamsulosin

Front 358

can cause abnromal (failed, decreased, retrograde) ejaculation

Back 358

tamsulosin

Front 359

what drug interactions are important for tamsulosin?

Back 359

vasdilator drugs for ED, can cause dangerous drop in BP and precipate MI

Front 360

the prototype beta blocker that nonselectively blocks beta receptors (B1 and B2). decreases HR and contractility, supresses impulse conduction through AV node, slowly developiong reduction in BP, supresses release of renin (blocks activation of renin-angiotension system), bronchoconstriction, and inhibits glycogenolysis in liver and skeletal muscle

Back 360

propanolol

Front 361

fatigue, lethargy, and coldness of extremities, exercise intolerance, sexual dysfunction, bradycardia/av block, and aggravation of asthma due to bronchoconstriction are all adverse effects of __

Back 361

propanolol

Front 362

what are 3 cases where propanolol is contraindicated/precautioned?

Back 362

diabetes (supresses tachycardia warning sign)

heart failure: exacerbates symptoms

contraindicated in asthmatics

Front 363

a b1 cardioselective drug that is used for hypertension, angina, CHF, and MI. less likely to cause bronchoconstriction and suppression of glycogenolysis

Back 363

metoprolol