Exam 1-Pharm 8903

Front 1

What is definition of pharmacology?

Back 1

Study of PK, PD, PT; study of action and reactions of drug therapies

Front 2

What is pharmacokinetics?

Back 2

Study conc. of drug in plasma during absorption, disturbution, metabolism, elimination

Front 3

What is pharmacodynamics?

Back 3

Study of physiologic mechanisms where drug produces intended therapuetic effect

Front 4

What is pharmacotoxicology?

Back 4

Study of physiologic mechanisms where drug produces toxic/adverse effect

Front 5

What is pharmacogenetics? How does affect future drug treatments?

Back 5

Study of genetic variations that cause differences in drug response among patients. Doctors may have to screen and adjust for these variations because pts can higher sensitivity to standard doses from genetics that decrease activity of enzyme that eliminates drug

Front 6

Differences between gene "knockout, knockdown, & knockin"?

Back 6

-out: breed homozygous animals where gene for receptor is absent or nonfunctional
-down: breed heterozygous with only limited suppression of function
-in: overexpress certain proteins of interest have been bred

Front 7

What is difference between trade vs. brand name? What is the formulation of drug?

Back 7

trade is patented trademark of drug; generic is common drug name but non-capitalized; formulation is to check for allergies or issuesof drug make-up

Front 8

What are the three fundamental characteristics of drugs?

Back 8

drugs only modify pre-existing functions, have multiple sites of action (for side effects/therapuetic uses), & dose is difference between drug vs. poison

Front 9

What are the four FDA criteria for drug approval?

Back 9

1. placebo controls
2. double-bind protocols
3. subjects randomly selected and appropriate for study
4. establishment of drug safety (acute vs. chronic toxicity)

Front 10

What are four problems/controversies with new drug development?

Back 10

animal models, genetic variation, uncontrolled variables, time and cost of drug development

Front 11

What are the three main ethical issues related to drug tx & development?

Back 11

automony (choice), beneficence (benefit patient), & justice (equal access)

Front 12

What is the differences between phases I-IV of clinical trials?

Back 12

I- low dose studies on healthy volunteers; II- sm group with dose response studies to establish efficacy; III- lg, multi-center dose response studies to check for eff. and toxicity; IV- post approval monitoring of drug on the general population

Front 13

What will decrease a drug's availability to target tissue, also called barriers?

Back 13

Protein binding and tissue deposits.

Front 14

What is an absorption profile?

Back 14

Change of concentration of drug in blood plasma over time. Should have concentration and time.

Front 15

What three variables are present at peak drug concentration on the absorption profile?

Back 15

Absorption, distrubution, and elimination.

Front 16

What does MEC and MTC mean and why are they important?

Back 16

MEC-minimal effective concentration. Minumum dose needed to see therapeutic effect.
MTC- minimum toxic concentration. Concentration when toxicity is seen.

Front 17

What are the C max and T max? Where are these points located on the oral absorption profile?

Back 17

C max= actual max "C"onc. of drug that peaks after administration; located at the peak of the curve from L side of graph (conc.)
T max= "t"ime takes after administration to reach peak max conc. in blood plasma; located at peak of curve down to designated time on graph

Front 18

What is the onset time and duration of action?

Back 18

Onset time-measure of time drug takes after admin. to work at MEC
Duration of action- elapsed time remains above MEC or how long produce therapuetic effect

Front 19

Explain what is half-life (T 1/2) of a drug.

Back 19

Measure of elapsed time it takes on absorption profile for drug to go from one conc. to 1/2 its conc.
dependant on drug absorption and usually is between MEC and MTC.

Front 20

What is the AUC?

Back 20

Area under the curve- total amt of drug enters into bld after administration, reflects PK of drug (characteristics of absorp profile), time drug appears till disappears

Front 21

What is bioavailability and how is it measured?

Back 21

% of total drug dosage that enters blood for available use; measured by AUC (mg)/dosage (mg) X 100, the remaining amt is loss % of drug

Front 22

What are two reasons oral bioavail. of most drugs is less than 100%?

Back 22

incomplete extent of absorption and first-pass elimination

Front 23

How does route of administration influence bioavail. of a drug? What are alternative routes of administration to avoid first-pass metabolism?

Back 23

(hepatic elimination)-the overall (oral) process of drug being absorbed/metabolized via gut wall and portal blood (liver, bile) before hits systemic circulation, which can decrease bioavail. of drug; alt routes: IV, subling, IM, transdermal, inhalation, SC

Front 24

What is the onset time for IV route of administration and why?

Back 24

No onset time because no delay in absorption in blood plasma due direct absorption; initial dilution/mixing in 1min-> distrubtion within 30min-> elimination begins after 30min

Front 25

What happens during the initial mixing concentrations following bolus IV administration?

Back 25

Bolus is not completely mixed with blood, with high initial conc. of drug and will come down as mix with blood/begin to dilute; can be toxic prior to mixing with blood with initial dose in first min. due to initial dose

Front 26

Why are IV bolus doses contraindicated in most drugs? Give two example of these drugs.

Back 26

the initial high dose side-effects they produce,
e.g. isoproterenolol can cause cardiac dysrrhythmias; thiopentol can induce respiratory depression/arrest.

Front 27

What drug is one of the exceptions to IV bolus contraindication principle and why?

Back 27

phenytoin- bolus doses for control of seizures; highly bound to plasma binding proteins so initial conc. are buffered by this binding

Front 28

What two things are mainly affected during the absorption profile of tetracycline when given with dairy vs. tetracycline alone? Why?

Back 28

C max and AUC would be reduced; related to absorption issues from calcium in dairy product that causes precipitate in gut that prevents absorption of drug

Front 29

What is bioequivalence? What are the two main criteria?

Back 29

guideline that requires that two preparations of the same drug (trade vs. generic) have identical AUC and C max values; usually suggests that drugs will have same biological effects

Front 30

What are the four mechanisms of drug absorption (permeation)?

Back 30

1. Diffuse passively thru aqueous channels in between cells (tight junctions)
2. Through lipid cell membranes
3. If drug has appropriate characteristics, may be moved by carriers into and out of cell
4. Bind to cell surface receptors inside cell by engulfing into IC space and expelling into EC space
via cell membrane

Front 31

What is plateau principle and how can it be affected by the frequency of administration?

Back 31

When drug given over equal periods of time to reach plateau conc. in a steady state (goal bet. MEC & MTC); rate of absorption becomes = to rate of metabolism and elimination (the balance of PK); Very important to follow the appropriate frequency for therapeutic effect and try to prevent potential of toxic dosage or blood levels will be all over place

Front 32

What is chronopharmacology?

Back 32

study of drug effects that are timed to body's biological rhythm

Front 33

Discuss the drugs cisplatin, "statins", and glucocorticoids on chronopharmacology.

Back 33

cisplatin-chemo drug given at pm R/T when UO is maximal to reduce renal tox.
"statins"-given in evening when rates of cholesterol synthesis in liver are highest
gluco- given in am when cortisol production naturally peaks making more alert and dec. some side effects

Front 34

How does drug formulations affect absorption in tablets, coated tabs, and capsules? What are examples?

Back 34

to regulate absorption by changing formulations;
tabs- asa, compressed powder that quickly breaks in stomach
coated tabs- triaminic, coated that passed stomach and dissolves slowly in intestine
caps- Darvon, gelatin covered to dissolve in either stomach or intestine

Front 35

What happens to absorption when coated tabs are chewed/crushed vs. swallowed?

Back 35

Get different absorption which goes above MTC when change the way drug taken (chewed- more quickly vs. swallow- slows absorption to intestines of EC tabs)

Front 36

What variables of an absorption profile (conc. vs time) would be most profoundly effected by a drug that is administered in oil vs. saline vehicle?

Back 36

Onset time because prolonged absorption and dissolves slowly with oil vs. rapidly absorped with NSS

Front 37

What are three drug vehicles?

Back 37

NSS, oil, epinephrine (localized vasoconstriction for slow absorption and prolonged local effects

Front 38

What is difference between drug-antibody conjugates and liposomes with examples?

Back 38

conjugates- e.g. smart drugs that chemically link to antibody to help to target specfic cancer cells
liposomes- artificial membrane vehicles that encapsulate drug (amp B to reduce renal tox)

Front 39

What is molecular weight vs. lipid solubility?

Back 39

mol wgt- larger size of molecule wgt more difficult/slower rate absorption (types of insulin)
lipid solubility- more soluble faster onset of action and rate of absorption (barbituates)

Front 40

What is difference between strong and weak acids?

Back 40

strong- HCL, H+ ion donor released ions to solution to make more acidic, lower pH
weak- asa, can release or pick up H+ (reversible)

Front 41

What is difference between HA vs. A- for acid-base characteristics?

Back 41

HA= unionized, lipid soluble of drug
A- = ionized, lipid insoluble

Front 42

What is pKa?

Back 42

equilibrium constant defined as pH (H+ concentration) at which the HA (unionized)concentration is equal to the A- (ionized) concentration; pH to keep it neutral/balanced; low pH=high H+

Front 43

How will weak acid respond in different environments (acidic, basic, pKa)?

Back 43

pKa=balanced, equal
Acidic- forces into unionized state, more readily soluble-more H+ ions
Alkaline- forces into ionized state, less soluble-less H+ ions
Because moves from higher to lesser conc.

Front 44

Describe method of how can find out how weak acid responds in different environments.

Back 44

1. look at pKa and pH; acid & acid= non-ionized; base & base= non-ionized
2. anything else is ionized
3. must decide if pH is more acidic or basic compared to your pKa

Front 45

At what point in absorption profile does drug metabolism and elimination dominate blood level of drug?

Back 45

Can be measured at half life (T 1/2), which is rate of how drug disappears

Front 46

What will happen to the absorption of a weak acid across walls of stomach when also given will proton pump inhibitor to treat ulcer?

Back 46

The absorption of weak acid will be decreased related to the proton pump inhibitor making the stomach acid more basic.

Front 47

What happens with lipid solubility and onset times of various (3) barbiturates?

Back 47

thiopental: highly lipid soluble; onset seconds to minutes (induce quick anesthesia)

pentabarbital: moderately lipid soluble; onset minutes to hours (can induce sedation and hypnosis)
phenobarbital: low lipid solubility; onset hours to days (anti-sz med)

Front 48

What is the difference between B vs. BH+ in acid-base characteristics?

Back 48

B is the unionized, lipid soluble form of the drug

BH+ is the ionized, lipid insoluble form of the drug

Base neutralizes acids by being H+ acceptor

Front 49

Lidocaine is a weak base; how would this characteristic affect drug absorption and fetal exposure to this drug during gestation?

Back 49

Lidocaine would accumulate in the fetus and potentially become toxic

(see flashcard on seperate sheet for drawing)

Front 50

What are (4) biological variables that influence the rates and extent of drug absorption?

Back 50

1. GI contents
2. Presence of intestinal flora
3. GI functions
4. Availability of transport proteins

Front 51

What would happen to the absorption of L-DOPA if it were administered orally prior to the ingestion of a meal that contained proteins?

Back 51

Would decrease absorption because proteins from food would take up or compete for the a. a. transport proteins.

Front 52

What GI functions (3) can affect absorption?

Back 52

vomiting and diarrhea can alter drug absorption;
stress can reduce blood flow to the G-I tract and reduce drug absorption

Front 53

How long does it take to reach steady state or plateau after a drug is administered?

Back 53

4-5 half lives. Thats why we give scheduled doses. Frequency of drug admin is very important to main steady state.

Front 54

Give an example of why intestinal flora affects drug absorption.

Back 54

due to bacterial metabolism, the bioavailability of digoxin is 60-80% while the combination of digoxin and some antibiotics increases the bioavailability of digoxin to near 100%; this effect results in an increase the incidence of digoxin side-effects;

Front 55

Give an example of why GI contents affect drug absorption.

Back 55

dietary fibers bind to digoxin and reduce its absorption; some antibiotics when ingested with dairy products form calcium precipitates that reduces drug absorption;

Front 56

How long does it take to reach steady state or plateau after a drug is administered?

Back 56

4-5 half lives. Thats why we give scheduled doses. Frequency of drug admin is very important to main steady state.

Front 57

What are four things that can affect distribution?

Back 57

plasma binding proteins, blood flow, tissue deposits, barriers

Front 58

Discuss the importance of the barriers in relation to distribution (BBB, blood testes, placental).

Back 58

BBB-no space for drugs to pass thru capillary so they must diffuse thru the membrane; increase permeability occurs with inflamm/infections and young/elderly

everywhere else (testes and placental) have a nonbrain capillary with space between endothelial cells.

Front 59

If you had to give a pregnant woman an anti-coagulant, would you give heparin or coumadin and why?

Back 59

Heparins with MWs > 1000 do not pass placental membranes
While warfarin which has a MW of less than 500 passes placental membranes and is a fetal toxin;

Front 60

What does polarity and lipid solubility of drug have to do with distribution of drug to fetus?

Back 60

Insoluble are highly polar drugs- do not pass placenta membranes (e.g. succ.)

lipid soluble so more unionized so readily absorbed and becomes toxic in a fetus (e.g.- thiopental)

Front 61

Name the two forms of plasma binding proteins and the differences between them.

Back 61

Bound- “DP” large biologically inactive proteins; stays contained in plasma, unable to leave walls of capillaries

free- biologically active to circulate thru blood plasma and able to leave to go to target tissues

Front 62

A drug that circulates in the blood in its highly bound form to plasma binding proteins wld be expected to have shorter biological half life than drugs that circulate in their unbound form?

Back 62

Disappears more slowly in blood because it is bind (inactive) and harder to eliminate until converts into free form, longer half life so strongly disagree

Front 63

What happens when ASA (50% B) and warfarin (99% B)are given together in relation to being both bound drugs?

Back 63

ASA knocks warfarin off of its binding state making it more free form to be absorbed in blood, which increase toxic effects of increasing bleeding

Front 64

What can malnutrition, liver, or kidney diseases do to drug responses in variations of PBP's?

Back 64

reduce blood levels of PBP’s and increase drug toxicities because would increase the free form

Front 65

What is biological importance of plasma binding proteins?

Back 65

Initial concentration (displacement) will increase (free form) which can be toxic, but after period of time it will change its concentration and equal out with metabolism and elimination, Timing is Key!

Helps with interpretation of measured drug concentrations

Front 66

Name the (4) major tissue deposits and the role.

Back 66

(1) adipose tissue = 15-50% of body wt.
(2) muscle
(3) bone/teeth
(4) placenta/mammary tissue, etc.

By taking up the drug they reduce drug that is in plasma that is available to target tissues

Front 67

How does blood flow affect distribution of drug?

Back 67

more blood=more drug

very rich group (VRG: brain, liver, heart); muscle group (MG: skeletal muscle); very poor group (VPG: fat, skin, bone, ligament, hair, teeth)

Front 68

Biological importance of tissue deposits.

Back 68

Serves as drug reservoir, alter drug dosage, sites of drug interactions, sites of drug toxicity

Front 69

What is the difference between loading/induction/priming and maintenance doses?

Back 69

loading or induction doses of a drug are given to saturate tissue deposits with a drug and to maintain MEC

Maintenance- maintain MEC after saturation of tissue deposits

Front 70

Explain why the Vd for digoxin changes in the elderly and explain how this change might alter the toxic side-effects of this drug. Speculate on how anoxexia nervosa might alter the toxicity of digoxin in a patient.

Back 70

Elderly has less muscle mass and dehydration which is decrease Vd because digoxin is usually stored in tissue deposits it wld make higher concentrations of drug in plasma which could lead to higher toxicity of drug

Same for anorexic patients (dehydration) and less tissue deposits

Front 71

What is volume distribution and how is it measured?

Back 71

total amount of a drug that is in body (mg) is divided by the concentration of the drug in the blood plasma (mg/l) an apparent volume distribution can be calculated (l).

Front 72

What are the types of PBPs?

Back 72

1. albumen-most abundant
2. globulins; sex steroid binding globulins
3. alpha
4. lipoproteins

Front 73

What is the relationship betweed Vd. and PBPs?

Back 73

Highly bound has less Vd- higher conc. in bld plasma

Weakly bound has high Vd- most goes to tissues so when bld taken, bld conc of drug looks more diluted in lg vol.

Front 74

What are the phases of drug metabolism?

Back 74

phases = Phase I: CYP-catalyzed oxidation or hydrolysis

Phase II: conjugation reactions

Front 75

What are the differences between the (3) types of metabolic enyzmes?

Back 75

CYP- Takes a drug and convert to a metabolite

1. catalyzed oxidation- Bind to drug and interact with other enyzmes, combine with O2 to form oxidated form of drug

2. hydrolysis- Genetic situations when taking local anesthetic and pt doesn’t have enzymes to break drug down
Uses water to break hydrogen bonds

3. Conguation reactions- Take a drug and join to certain molecules to for conjugation product which then becomes biological inactive and increases water which increase rate of elim.

Front 76

What is difference between inducing and inhibiting enyzmes? Give examples.

Back 76

Inhibiting agents are CYP inhibitiors (cimitidine,quinidine,verapamil,
grapefruit juice)

Inducing agents induce CYP (phenobarbital,phenytoin,rifampin,tobacco,troglitazone,St. John’s wort,Ethanol)

Front 77

What is the importance of drug metabolism?

Back 77

drug biotransformation: alterations in the chemical structure of drugs that leads to:
1 drug inactivation: most drugs

2 drug (pro-drug) activation: e.g. loratridine (Claritin) and naproxen

3 drug bioconversion; e.g. some anabolic steroids can be converted to estrogens

4 production of toxic drug metabolites (e.g. tylenol)

Front 78

Explain relationship of acetaminophen and to depletion of glutathione in liver. How does OD tylenol result in liver failure-draw picture.

Back 78

Basically nothing for glutathione to bind with anymore after tylenol –accum of covalent bonds
Chemical metabolite accumulates and cause bonds in liver proteins thus destroying leading to liver failure

Front 79

Draw absorption profiles for theophylline and show how the Cmax and the T1/2 would differ between a non-smoker and smoker.

Back 79

theophylline would be higher c max and longer duration of action to non-smoker vs. smoker with increased cyps causing faster elimination

Front 80

What does sulbactam inhibit in relation to drug manipulation of metabolism?

Back 80

Inhibits the area of resistance or enzyme (beta-lactamases) that bacteria begin to do to resist pcn form working thus pcn is able have therapeutic effect

Front 81

What are some things that can affect metabolism?

Back 81

Ethnic diversity, gender, individual genetic variability, induction and inhibition of metabolic enzymes, diseases/injuries, occupation, food/prep (char-broiled)

Front 82

What is a heptan and what does it have to do with individual genetic variability of metabolism for PCN?

Back 82

some drug metabolites are converted to heptans that
creates a foreign protein complex that induces allergic responses
The difference in CYPs inherited thus when pcn given body makes heptan which body thinks is foreign and causes allergic response

Front 83

What is drug resistance?

Back 83

Cancer will begin to destroy metabolic enyzmes causing to be metabolized out of body faster thus decreasing therapuetic response

Front 84

Rate of renal elimination is determined how?

Back 84

= GFR + secretion - reabsorption

Front 85

Discuss the importance of renal clearance.

Back 85

Volume of bld cleared of drug by kidney per unit of time- effects kidney function

Front 86

One strategy for reducing side effects produced by OD of amphetamines would be to increase its rate of excretion. Amphetamine is a weak base and thus its excetion could be increased by:

Back 86

Making urine more acidic

Front 87

Draw absorption profile of pcn and indomethacin with/without probenecid

Back 87

Secretion if from blood into nephron thus if inhibit secretion it will increase duration of action and half-life of pcn

Front 88

What happens to the rate of elimination in ionized/insoluble weak acids/bases?

Back 88

Ionized base/acid is increased in excretion in kidneys because insoluble form

Front 89

What effects does renal diseases have on drug excretion?

Back 89

alterations (reductions) in renal blood flow (RBF) or
glomerular filtration rates (GFR) increases drug toxicities by increasing the Cmax and T1/2 of drugs

Front 90

Who would be more sensitive to liver toxicity from tylenol (ped or adult) and why?

Back 90

Ped because of cyps and liver not fully developed yet to help conjugate the tylenol

Front 91

What functions does conjugation enzymes have in the control of drug activity and elimination?

Back 91

Rate of excretion increases and conjugates are inactive

Front 92

The half life of a drug given to a neonate would likely be extended when compared to the half life in a healthy young adult.

Back 92

Liver and kidney not fully matured to excrete so strongly agree

Front 93

Is it safe to assume that all the genetic diversity in drug metabolism is the result in differences in CYP enzymes? What about succinylcholine; genetic variation?

Back 93

CYP's are NOT only genetic variations; another example is succ. (lead to MH)

Front 94

What is the measurement difference between absorption and dose-response curves?

Back 94

Conc vs. time= absorption curve
Dose of drug vs. intensity of response that a drug produce = DR curve

Front 95

What is the definitions of ED 50 and ED 100?

Back 95

ED 50- a measure of drug at ½ of max effect (effective dose)
ED 100- lowest dose of drug that produces max effect; if 200x or 300x dose will not effect max effect but will increase toxicities

Front 96

Explain the relationship of ED 50 vs. potency of drug?

Back 96

Lower ED 50, higher the potency

Front 97

What is intrinsic activity in relation to the target tissues?

Back 97

Compare height of ED 100 (measure biological effect); measure of the magnitude or intensity of a biological responserelative to the maximal attainable response that can be produced in a target tissue (alpha=1.0).

Front 98

Define the classifications of drugs based upon their intrinsic activity: agonist, partial agonist, antagonist

Back 98

agonists: drugs with high intrinsic activities (close to 1.0)
partial agonists: drugs with mid-range intrinsic activities (alpha = ~0.5)
antagonists: drugs with little or no intrinsic activity; often called “blockers” (eg. Beta-blocker)

Front 99

On a single figure, draw two dose-response curves; one for drug A and the second for drug B. Show how drug A would differ from drug B if drug A has a higher potency than drug B and drug B has a higher intrinsic activity than drug A.

Back 99

see notecard

Front 100

What is therapeutic index for drugs?

Back 100

measures drug safety; LD50/ED50; the higher the value (distance) for the therapeutic index the safer the drug
LD- lethal dose 50, usually done in animals for toxic effects
Potency, intrinsic activity, and safety is what dose-response curve discusses

Front 101

What is the difference between the types of drug target tissue interactions (2)?

Back 101

structurally non-specific interactions= mainly physical presence in a target tissue is all that's necessary; e.g. osmotic laxative or diuretics

structurally specific interactions= chemical
structure of the drug is essential for its biological activity because the drug generally forms reversible chemical bonds with some component in a target tissue; e.g. receptors and drug receptor can fits like a “lock and key”

Front 102

What happens to affinity and potency related to the lower the concentration of drug that binds to its receptor?

Back 102

Higher the affinity (lower dose it takes to occupy/saturate receptor) and higher its potency on a dose-response curve (low dose to produce its effect)
affinity and potency both have inverse relationship to drug concentration or dose

Front 103

A drug antagonist (low efficacy) can have a high affinity of a receptor?

Back 103

strongly agree but there is NO cause and effect relationship so can be any make-up

Front 104

Discuss agonist, partial agonist, and antagonist on efficacy.

Back 104

Bind the receptor but doesn’t activate drug-antagonist (wrong key)-little or no effect
Bind the receptor changes shape slightly-prt agonist (valet or maid key)-mod. effective
Bind the receptor lock and key-agonist (house or car key)-highly effective

Front 105

What is efficacy dependent on?

Back 105

the ability of a drug to induce a conformational change in the shape of receptor that leads to S.T. and the biological response.

Front 106

What is when receptor is in activated form, can produce sm observable effect in downstream mechanisms, even with absence of drug?

Back 106

Constitutive receptor activity

Front 107

Discuss allosteric binding in relation to benzos.

Back 107

drugs that bind to the same receptor molecule but do not prevent binding of agonist, may enhance or inhibit action of agonist; benzo’s- bind non-compet. to ion channels activated by neurotransmitter GABA, enhancing net activating effect of GABA on channel conductance

Front 108

What has a higher affinity for receptor inactive form, which reduces constitutive receptor activity and may produce a contrasting/opposite physiologic result?

Back 108

Inverse agonist

Front 109

What two different responses does epinephrine produce and why?

Back 109

coronary vasodilation and renal vasoconstriction
because of different types of receptors that cause these different actions

Front 110

What is an example of mechanism for allowing a target tissue to change its response to a drug?

Back 110

the “pre-term” uterus responds to ritodrine while the “term” uterus does not respond to ritodrine
Some receptors differ at different periods of times

Front 111

How does dopamine allow a drug produce an ordered sequence of responses?

Back 111

Dopamine changes responses that are ordered by the desired doses and subset receptors

Front 112

What are some examples of "up" regulation numbers of receptors?

Back 112

some breast cancers (HER), hyperthyroidism (tachy/cardiac tissue), propranalol (rebound HTN)

Front 113

What are some examples of "down" regulation numbers of receptors?

Back 113

NIDDM (hyperinsulinemia/resistance), albuterol (tolerance)