Basic Pharmacology Exam I

Front 1

What is the most pimportant limiting factor for drug absorption?

Back 1

Because of the large number of lipid barriers, lipid solubility

Front 2

What is one way to enhance excretion of a lipid-soluble drug?

Back 2

Adjust urine pH to make most of the drug in its ionized form.
Weak acid in alkaline urine
Weak base in acidic urine

Front 3

True/False. Quarternary amines are always in their ionized form.

Back 3

True

Front 4

True/False. Acidic drugs with pKa favoring absorption from the stomach may undergo appeciable absorption from the intestine.

Back 4

True- due to large surface area of the microvilli

Front 5

A drug is very active if given IV, but not when given orally. What is one reason for this?

Back 5

First Pass effect

Front 6

What is the rate of clearance by filtration of a drug?

Back 6

Fraction of unbound drug in plasma (Fu) X GFR

Front 7

What are some drugs principally cleared by filtration?

Back 7

Digoxin
Gentamicin
Procainamide
Ethambutol

Front 8

What are some drugs eliminated by biliary elimination?

Back 8

chloramphenicol
digitoxin
morphine
refampicin
tetracycline

Front 9

What are organs that are rapidly perfused?

Back 9

endocrine glands, brain, liver, kidney, GI tract and heart

Front 10

How to calculate overall clearance of a drug

Back 10

Vd X k

Front 11

How to calculate the volume of distribution (Vd)

Back 11

Dose / initial concentration

Vd = D/Co

Front 12

What does a large Vd indicate?

Back 12

Drug is sequestered into fatty tissues (low plasma levels)

Front 13

What do zero order kinetics indicate?

Back 13

Rate of change is constant, regardless of amount or concentration

Front 14

What do first order kinetics inidcate?

Back 14

the rate is a constant fraction or proportion of the existing total

Front 15

Define elimination rate constant (k, or beta)

Back 15

the proportion of the drug eliminated per unit time

Front 16

How can k (or beta) be determined from a graph?

Back 16

It is the slope of % remaining versus time in a semilog plot

Front 17

How are the half-life and elimination rate constant related?

Back 17

Inversely.

t1/2 = 0.693 X k

Front 18

How to find the initial concentration of the drug given IV from a distribution curve (serum concentration vs dose) generated from a 2 compartment model?

Back 18

Extrapolate the elimination portion of the curve to the y-axis

Front 19

For a drug given other than IV, how do you determine the total amount of drug in the body?

Back 19

Serum concentration versus time, it is the area under the curve.

Front 20

What are 2 useful relationships using AUC?

Back 20

AUC = D/ Clearance

AUC = Co/ k (or beta)

Front 21

What is bioavailability (F)?

Back 21

Compares amount of drug that reaches blood by any non-IV route with IV
F = AUC(non-IV)/AUCiv

Front 22

How to calculate the steady state concentration (Css) ?

Back 22

Css = doing rate/clearance

Front 23

True/False. The amount of drug that accumulatesby the time steady state is reached depends only on the rate of administration.

Back 23

True, since the clearance of a drug generally remains constant.

Front 24

How to increase the steady state concentration of a drug?

Back 24

Increase infusion rate

Front 25

Define fluctuation

Back 25

the distance between the highest drug level and lowest for discontinuous administration

Front 26

How do you determine the loading dose for a drug?

Back 26

D* = Target Concentration (Css) X Vd

Front 27

Drugs that are weak bases are generally higher or lower concentrations in milk?

Back 27

higher- milk is relatively acidic to plasma

Front 28

Where are the majority drug metabolizing enzymes found at the cellular level?

Back 28

smooth ER

Front 29

What genetic defect results in ivermectin toxicity in certain dogs?

Back 29

MDR1- a plasma transport protein

Front 30

Phase I reaction

Back 30

introduce or expose a funcitonal group: typically oxidation, reduction or hydrolytic reactions

Front 31

Phase II reactions

Back 31

formation of covalent linkages between functional group and glucuronic acid, sulfate, glutathione, acetate or amino acids

Front 32

True/False. Drugs are most likely metabolized by a single enzyme.

Back 32

False. Due to wide overlap of substrate specificity it is unlikely

Front 33

Which Cytochrome P450 enzyme is responsible for over 50% of CYP mediated drug transformations in the liver?

Back 33

CYP3A4

Front 34

What are the most abundant type of Phase II enzymes?

Back 34

UDP-glucuronosyltransferases

Front 35

True/False. Acyl glucuronides tend to be unstable.

Back 35

True. May contribute to adverse side effects of NSAIDs

Front 36

Drugs may induce their own metabolism

Back 36

Pharmacokinetic tolerance

Front 37

How does enzyme induction occur?

Back 37

inducing agent binds to a receptor which is translocated to nucleus to promotor region of a gene

Front 38

Metabolism of structurally related may be induced

Back 38

Pharmacokinetic cross-tolerance

Front 39

Give an example of increased toxic side effects due to induction

Back 39

Alcohol increases metabolism of acetaminophen to a more toxic metabolite

Front 40

Name 3 clinical implications of induction

Back 40

pharmacokinetic tolerance and cross-tolerance

Increase of toxic side effecs

Affect metabolism of endogenous substances

Front 41

Define allometric scaling

Back 41

extrapolation from one species to another based on body size

Front 42

What are species defects in regard to drug metabolism?

Back 42

metabolic pathways that are common to most species but be essentially absent in another

Front 43

Name a species defect in drug metabolism in cats and one in dogs

Back 43

cats: glucuronidation of phenols

dogs: N-acetylation or aromatic amines

Front 44

In general, enzyme activity is higher/lower in males than females

Back 44

Higher

Front 45

True/False. Type II enzymes are most likely to be effected in liver disease or old age.

Back 45

False. Phase I

Front 46

Define "counterfeit incorporation mechanism"

Back 46

a structural analog of a biological chemical incorporated into cellular components and alter function

Front 47

How to find EC or ED 50 from a graded dose response curve

Back 47

Is the same as the Kd if we assume number of occupied receptors is proportional to effect.

Front 48

Hyperreactive

Back 48

drug produces an effect at a very low dosage

Front 49

hypersensitive

Back 49

allergy

Front 50

supersensitive

Back 50

increased sensitivity following denervation or long-term treatment with a receptor antagonist

Front 51

Hyporeactive versus tolerant

Back 51

Tolerant connotes hyporeactivity acquired as a result of exposure to the drug

Front 52

Tachyphylaxis

Back 52

Fast development of tolerance to a drug

Front 53

What is it called when a maximal effect is achieved when a relatively small fraction of receptors is occupied?

Back 53

Spare receptors.

Front 54

What effect does a competitive inhibitor have on maximal effect and Kd?

Back 54

Maximal effect is unchanged, but Kd is increased

Front 55

What effect does a noncompetitive inhibitor have on maximal effect and Kd?

Back 55

Maximal effect is lowered, but Kd is unchanged

Front 56

True/False. If a competitor acts outside the active site, then it may be competitive/irreversible and noncompetitive/reversible.

Back 56

True. Any combination can occur if it is acting outside the active binding site.

Front 57

What is TI?

Back 57

TI = TD50/ED50

Front 58

What are 3 general mechanisms of toxicity?

Back 58

Extension of therapeutic action
Action on same receptor through different pathway
Toxic effect through a different receptor

Front 59

Which process asks how the drug gets into the patient?

Back 59

Pharmaceutical

Front 60

Which process asks whether the drug is getting to the site of action?

Back 60

Pharmacokinetics

Front 61

Which processes asks whether the drug is producing the required effect?

Back 61

Pharmacodynamics

Front 62

What are ways to slow down diffusion of drug from site of injection?

Back 62

Oil
Epinephrine
Physical form, such as size of crystals

Front 63

What are the criteria for using drugs in combination?

Back 63

Frequency of administration must be the same
Fixed doses are optimally effective

Front 64

How is bioavailability represented graphically?

Back 64

Plot of plasma concentration over time, bioavailability is the AUC

Front 65

Why administer drugs IV during shock?

Back 65

Absorption from a particular site is dependent on the blood flow. Severely lowered blood flow to GI and peripheral tissues is a hallmark of shock.

Front 66

Which drugs are absorbed more readily with Celiac's disease?

Back 66

propranolol
tribrissen
cephalexin

Front 67

Name 3 therapeutic advantages to using a pro-drug

Back 67

Improved absorption
prevent adverse side effect
improved distribution

Front 68

What would be considered a phase III reaction?

Back 68

excretion from the body by any route

Front 69

For changes in protein binding to be of therapeutic importance, what 2 criteria must be met?

Back 69

Bound drug must constitute >90% of total in plasma
Distribution of drug to the tissues must be small

Front 70

What drugs are known to displace other protein-bound drugs?

Back 70

sulfonamides
salicylates
phenylbutazone

Front 71

Benefits of metabolism of an active drug to active metabolite?

Back 71

faster onset
shorter duration
less toxic

Front 72

Drugs whose distribution is affected by renal failure

Back 72

insulin
digoxin

Front 73

Drugs whose distribution is affected by cardiac failure

Back 73

antiarrhymics

Front 74

Drugs whose distribution is affected by hyperthyroidism

Back 74

cardiac glycosides

Front 75

What are the 3 types of drug-receptor interactions and pharmacological effect?

Back 75

DR interaction reversible, pharmacological effect reversible

DR Interaction not reversible, effect prolonged

DR interaction reversible, effect prolonged

Front 76

What are the main causes of therapeutic problems?

Back 76

failure to respond to treatment
adverse reactions
drug-drug interactions

Front 77

Some problems with the pharmacokinetic process?

Back 77

malabsorption
altered protein binding
increase of apparent Vd
increase in clearance

Front 78

Drug resistance would be considered a complication in which process of therapeutic process?

Back 78

pharmacodynamic

Front 79

Hyperthyroidism increases the clearance of which drugs?

Back 79

carbimazole
propranolol
practolol
hydrocortisone

Front 80

What are the 2 types of adverse drug reactions?

Back 80

Type A (dose related or augmented)
Type B (bizarre)

Front 81

If a drug accumulates in plasma faster due to kidney disease, what can be done to keep levels below toxic?

Back 81

Reduce maintenance dose
OR
Extend dosing interval

Front 82

How to redetermine dose because of renal failure?

Back 82

Patient dose = (patient Creatinine/Normal Creatinine) X normal dose

Front 83

How might a diuretic result in hepatic encephalopathy?

Back 83

Hypokalemia
H+/K+ exchange resulting in alkalosis
Increased NH3 absorption and retention in kidney
hepatic coma

Front 84

Distinguishing features of allergic drug reactions?

Back 84

no relation to pharmacological effects
delay between exposure and subsequent reaction
no dose-response curve

Front 85

What are some drugs known t cause allergic reactions?

Back 85

sulfonamides
penicillins
barbiturates
phenothiazenes and tetracyclines

Front 86

What are symptoms associated with drug induced allergic reactions?

Back 86

fever
connective tissue disease (looks like lupus)
Blood disorders
repsiratory disorders
rashes

Front 87

What features make a drug more likely to be precipitant in a drug-drug reaction?

Back 87

highly protein bound and likely to displace other drugs
alter metabolism
affect renal clearance

Front 88

What features make a drug more likely to be an object drug?

Back 88

steep dose-response curve
low therapeutic index

Front 89

What are pharmaceutical interactions?

Back 89

physiochemical interactions of either a drug with an IV infusion solution or 2 drugs in the same solution.