• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/55

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

55 Cards in this Set

  • Front
  • Back
Which is most potent

Which is most potent

A

A

What is potency

how much it will take to achieve max response

Which is high affinity which is low

Which is high affinity which is low

What does simple occupancy theory of drug action state

More R --> More intense response

Law of mass action

Affinity is directly related to potency

What does it mean if somehting has Kd of 10^-6 M

that when [D] = 10^-6 M, 50% of R is occupied

Units of k1 and K-1

k1 = /s


k-1 = /M s

For D + R --> DR




Kd =

[D][R]


[DR]

3 Factors governing Drug Specificity

Molecules are not spherical


Steric Hinderance


Electrostatic interactions

T/F Dobutamine has only B1 agonist activity

F; partial alpha antag for + isomer

What is the spare R theory and where did it come from

observation that ED50 < Kd; so you can get 50% response without using 50% of R
Which Line has high efficacy? which has lowest

Which Line has high efficacy? which has lowest

A = High
D = Low

A = High


D = Low

What color is what type of Agonist

What color is what type of Agonist

Difference between inverse agonist and antag

Antag will bring 0% change from basal R levels, IA will decrease

Allosterism

When active site becomes available or disappears when reg. molecule binds allosteric site

T/F Allosteric modulations are competitive

F

T/F Antagonists have intrinsic activity with high affinity for R

F; no intrinsic activity

T/F Competitive inhibitors bind reversibly

T

Which is competitive antag? What are the net results?

Which is competitive antag? What are the net results?


What effects agonist potency

Competitive antag; NOT active site or allosteric site noncompetitive antags

What effects agonist efficacy

Active site or allosteric site noncompetitive antags; NOT Competitive antag;

TI is measure of drug ____

Safety

TI is measured by what 2 methods

LD50/ED50


and


TD50/ED50

CSF is another method of drug safety. what is formula

LD1/ED99

What are the 4 major R families

Ion channels


G-protein coupled


Receptor-linked enzymes


Nuclear R

Where are G protein coupled R found

Sensory


Secretory


Smooth and Cardiac Muscle


Metabolosm

What do kinases do

Phosphorylate

name 2 R linked enzymes

Tyrosine Kinases


phosphatases

Stimulation of Tyrosine K leads to

Jak/Stat

Advantages and Disadvantages of Enteral route

A: Simple, cost effective, safe, no infection, no pain




D: Harsh GI, 1st pass metab, slow

Advantages and Disadvantages of Parenteral (IV)

A: Rapid, high bioavailability, bypasses 1st pass




D: irreversible, infection, pain, fear, skill required

Advantages and Disadvantages of Mucous membrane (inhalers)

A: Rapid, no 1st pass, no GI, simple, can give direct to tissue




B: Few drugs available

Advantages and Disadvantages of Transdermal

A: simple, excellent for long term use, bypass 1st pass and GI




D; Needs lipophilic drug

What is absorption

Movement of drug from site of administration into blood

What does Rate and amount tell us about absorption

Rate: how fast




Amount: how intense

3 Main ways to cross cell membranes

Passive diffusion of lipid soluble


Passive diffusion of water soluble through water pore


Mediated transport

5 factors that affect drug absorption

Rate of dissolution


Surface Area


Blood Flow


Lipid Solubility


pH Partitioning

Henderson Hasselbalch

log (protonated/nonprotonated) = pka -pH




ph=pka whren prot = nonprot

Weak acids go to what body compartments

alkaline areas like urine (opposite true for weak bases, the go to acidic places like gut)

What is Tissue Distribution

Movement of drug into body compartments from blood

Factors influencing tissue distribution

Tissue blood flow


Plasma protein binding


BBB


Vd

What capillaries are porous

Typical; specialized are not

What is Vd =

Dose/[plasma]

Renal clearance =

Excretion rate/[plasma]

Excretion rate =

[urine] x urine vol/time

What most significantly limits the time course of action of drug

Clearance (Vol/time)

T/F Rate of elimation changes as amount changes for 1st order? 0 order?

T for 1st; F for 0

Slop of [plasma] x time =

-k; trace back to extrapolate [plasma] at time 0

what is t 1/2

(.693 x Vd)/k

What 2 factors determine 1/2 life

Clearance and Vd

What time is required to reach steady state with chronic dosing

1/2 life

Loading dose =

V * target [plasma]

Initial [x] =




Stead state [x] =




Elimination 1/2 life =

1. Loading dose/Vd


2. Fraction absorbed x maintainance dose/ (Dosing interval x clearance)


3. .693

T/F 1st ordeer kinetics will saturate and taper off in Therapeutic range

T; 0 will not