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Block 1 lectures > Pharmacology - Melega > Flashcards

Pharmacology - Melega Flashcards

1
Q

Melega lectures

medical model of disease

A

diseases are related to underlying derangement of normal function

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2
Q

Melega lectures

Quantal dose-response curves (d-r)

A
  • plots the fraction of population that responds to a given dose: response is recorded as either ‘present’ or ‘not present’ (it either occurs or does not occur). Log dose (x) vs %maximal response (or individuals responding)
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3
Q

Melega lectures

ED50

A

amount of drug that produces a therapeutic response in 50% of the people taking it

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4
Q

Melega lectures

TD50

A

amount of drug that produces a toxic response in 50% of the people taking it

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5
Q

Melega lectures

LD50

A

amount of drug that produces a lethal response in 50% of the people taking it

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6
Q

Melega lectures

TI

A

Therapeutic Index: TD50/ED50

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7
Q

Melega lectures

Pharmacodynamics

A

what the drug does to the body

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8
Q

Melega lectures

pharmacokinetics

A

what the body does to the drug ADME

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9
Q

Melega lectures

efficacy (drug)

A

refers to magnitude of response on d-r curve

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10
Q

Melega lectures

potency (drug)

A

Refers to effective concentration that produces 50% of its maximal response (EC50) when comparing two drugs with the same efficacy.

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11
Q

Melega lectures

full vs partial agonist

A

full: maximal efficacy, partial: partial efficacy

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12
Q

Melega lectures

spare receptors

A

even after brief introduction of irreversible antagonist, maximal efficacy still reached (bc cell had spare receptors that became activated)

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13
Q

Melega lectures

constitutive activity of receptors

A

receptor isomerization between active and inactive forms. receptors have some activity even in absence of agonist

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14
Q

Melega lectures

Kd

A

Kd is a measure of drug affinity (tendency to bind) for the receptor. Lower Kd = higher affinity since Kd=Koff/Kon

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15
Q

Melega lectures

4 main targets of drugs

A

(1) ligand gated ion channels (2) G coupled proteins (3) enzymes (4) transporters

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16
Q

Melega lectures

How does Exposure to Drug-Agonists Affect Receptor Function and Receptor Number

A

Short term: reduction in response tachyphylaxis. Long term response: decrease in receptor #. “receptor down regulation” less synthesis

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17
Q

Therapuetic window

A

the range of doses that produce a therapeutic response, without unacceptable side effects; - an index of drug safety. Seen on a plasma drug vs time graph

18
Q

Bioavailability

A

the fraction of administered drug that reaches the systemic circulation. AUCoral/AUCiv x100 = % bioavailability

19
Q

Factors affecting drug absorption

A

(1) route of administration (2) membrane diffusion (3) metabolism (first pass effect)

20
Q

enteral vs parental

A

via GI tract (oral and rectal); easy, but first pass effect reduces bioavailability. Not GI tract (IV, sub-cutaneous etc), for drugs not easily absorbed. good for drugs that are poorly absorbed in GI

21
Q

4 ways drugs cross membrane

A

(1) diffusion (gradient) (2) facilitated diffusion (3) active transport (4) pinocytosis

22
Q

First Pass Effect

A

The intestinal & hepatic degradation or alteration of a drug taken by mouth, after absorption, removing some of the active substance from the blood before it enters the general circulation.

23
Q

Ion trapping (drug distribution)

A

only neutral molecule can diffuse across the membrane. Once inside the weak base dissociates and is “trapped” inside. Thus ions can enter but not exit. How much diffuses depends on pH of solution and pka

24
Q

metabolism

Need for Drug metabolism

A

Drugs are usually lipophilic (important for absorption). This makes them hard to excrete. Metabolism makes them more hydrophilic

25
Q

metabolism

Main Categories of drug metabolism (2)

A

(1) Phase 1 functionalization reactions: polar substrate is introduced via oxidation, reduction, hydrolysis. GOAL: make metabolites more H2O soluble.
(2) Phase II reactions: Conjugate reactions. GOAL: make metabolites even more H2O soluble.A substrate (parent drug or phase I metabolite) is coupled to an endogenous compound such as glucuronic acid, glycine, or sulfate

26
Q

metabolism

CYP P450 Enzymes

A

Most important enzyme system for Phase I. Catalyze oxidation of organic substances (monooxygenase rxn). p450 embedded in ER of cells. Highest concentration found in Liver (GI, skin, lung etc also). Metabolism and detoxification of compounds enterring the body p.o

27
Q

metabolism

Phase I: Alcohol metabolism

A

alcohol dehydrogenase: alcohol to aldehyde (oxidation). Then oxidized again to carboxylic A. Side effect of excessive alcohol: decreased NAD+ levels and increased NADH. Increase in NADH pathways and decrease in NAD+ pathways (extremely dangerous if taking acetaminophen like tylenol which will then overwhelm liver)

28
Q

metabolism

Phase I: monoamine oxidase

A

MAO: non p450 phase I oxidation. Amines–>aldehydes

29
Q

metabolism

Phase I: hydrolysis

A

Esterases are present in plasma and other tissues; they rapidly metabolize esters and amides to carboxylic acids. Ex:For short term anesthesia, succinylcholine is administered by infusion; its neuromuscular blocking effect is terminated rapidly by hydrolysis by plasma cholinesterase

30
Q

metabolism

prodrug

A

Drug is inactive before metabolism and is activated by metabolism. Designed to overcome delivery problems. 30% or all prescription drugs are prodrugs. Some metabolites of active drugs also are active (longer pharmacological action)

31
Q

metabolism

CYP p450: induction and inhibition

A

Induction: increase in p450 synthesis. protein synthesized so delayed effect–> higher metabolism and decreased drug effect. Inhibition: competition with other drugs for active site of p450. reduces metabolism and increases drug action

32
Q

metabolism

Factors affecting individual differences in drug metabolism

A

Age: less p450 in older people (lower the dose for elder;y). Genetic differences (EM and PM extensive and poor metabolizers). Environment (other drugs health etc)

33
Q

metabolism

alcohol metabolisma and polymorphism

A

Asians often have a atypical type two ALDH (aldehyde dehydrogenase- second enzyme in pathway) leading to build up in acetaldehyde (nausea, tachycardia, and flushing)

34
Q

B1W4Melega4-Pharmacokinetics

bioequivalence

A

two drugs are bioequivalent if bioavailabilities are similar after administration (same dose)

35
Q

B1W4Melega4-Pharmacokinetics

Volume of distribution: Vd

A

Vd(L/Kg) = D(mg/kg)/C(mg/L)

D=dose,C=plasma concentration. Def. Theoretical volume in which the total amount of drug would need to be uniformly distributed to produce the desired blood concentration of a drug. Therefore the dose required to give a certain plasma concentration can be determined if the VD for that drug is known.

36
Q

B1W4Melega4-Pharmacokinetics

Clearance

A

Cl= rate of elimination/plasma concentration. Clearance as a ratio is a constant. Most commonly measured as renal clearance but can also be liver clearance or total clearance when everything is summed

37
Q

B1W4Melega4-Pharmacokinetics

relation of 1/2life, clearance, and Vd

A

T1/2 = .693 Vd/Cl, since Cl = K x Vd and .693/K = T1/2

38
Q

B1W4Melega4-Pharmacokinetics

steady state concentration (Css)

A

input=output, no net change in concentration

39
Q

B1W4Melega4-Pharmacokinetics

loading dose

A

an initial higher dose given to push blood concentration into therapuetic range early on and after which a maintenance dose can be prescribed. loading dose = Vd x C(desired)

40
Q

B1W4Melega4-Pharmacokinetics

capacity limited elimination

A

saturation of enzyme or transporter

41
Q

B1W4Melega4-Pharmacokinetics

zero order kinetics

A

drug eliminated at a constant rate

Block 1 lectures (29 decks)

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