Basic ass shit

Question 1

Agonists do what

Answer 1

BBind and activate the receptor

Question 2

Antagonists do what?

Answer 2

BBind and do not activate the receptor

Question 3

How can affinity be measured

Answer 3

Dissociation constant, so when 50% of the receptors are occupied you do logkD. Lower the kD the higher the affinity

Question 4

Difference between concentration and dose

Answer 4

Concentration is the amount in given volume whilst dose is the amount administered

Question 5

Pharmokinetics is

Answer 5

body does to drugs

Question 6

Pharmodynamics is

Answer 6

Drugs does to the body

Question 7

Efficacy

Answer 7

The desired beneficial response to a drug, difference in maximal response

Question 8

What determines potency

Answer 8

Ec50 and pEC50

Question 9

Full anatgonism

Answer 9

Bind and elicit a maximal response but not all receptors are bound

Question 10

Partial antagonism

Answer 10

Bind and no not elicit a maximal response

Question 11

Receptor

Answer 11

Biological macromolecule or complex that binds another molecule and initiates or modulates signalling or effector activity within a cell

Question 12

Analgesic is what

Answer 12

A drug acting to relieve pain

Question 13

Where are alpha 1 and alpha 2 receptors found

Answer 13

Alpha 1 on blood vessels

Alpha 2 on nerve terminals

Question 14

Where are Beta1 and Beta2 fund?

Answer 14

Beta1 in heart

Beta2 in airways, some blood vessels

Question 15

Ionotropic receptor is what?

Answer 15

Agonist binds directly to and directly regulates the opening of an ion channel. Ligand gated ion channell

Question 16

Metabotropic

Answer 16

Agonist binding triggrs a series of intracellular events that produce second messengers to indirectly produce cellular responses

Question 17

Kinase linked receptors, how do they work and give an example?

Answer 17

Agonist binds to extracellular domain of a transmembrane protein, this activates enzymatic activity of the proteins cytoplasmic domain. Eg growth factor receptors, agonist binding causes receptor dimerisation activation of tyosine kinase (cytoplasmic domain) phosphorylates substrates that regulate cell growth

Question 18

Cytoplasmic nuclear receptors

Answer 18

Lipid soluble chemical signal enters the cell, this ligand binds to and activates intracellular receptor. Receptor may regulate gene transcription. Drug-receptor complex enters nucleus and binds to DNA to induce or repress genes. Slow onset, protein synthesis takes hours. Slow protein turnover.
Example is that glucocorticoid receptor activation inhibits synthesis of cyclo-oxygenase

Question 19

How does the glucocorticoid receptor work

Answer 19

The activation of this receptor inhibits synthesis of cyclo-oxygenase

Question 20

What are some examples of GPCR and how do they work?

Answer 20

Muscarinic ACh receptor and adrenoceptors .
GPCRs activate a particular G protein, G protein then anble to selectively interact with the effector protein such as ion channel or enzyme. Changes the activity of 2nd messenger that causes cellular modulation.

Question 21

Competitive surmountable antagonism, competitive reversible antagonism, describe the graph?

Answer 21

When the anagonism is present, it shifts the graph to the right. Reducing the potency, more agonist for same effect

Question 22

What is pA2

Answer 22

pA2 is the negative logaritihim of the concentration of antagonist required to cause a 2 fold rightward shift of the agonist concentration.
An indication of antagonist potency

Question 23

Where do cholinoceptors lie

Answer 23

Muscarinic - post ganglionic parasympathetic responses

Nicotinic - skeletal muscle responses and ganglionic transmission

Question 24

In sympathetic, what happens to the pupil and arteries and bronchi

Answer 24

Pupil dilation
Arteries constrict
Bronchi dilation