Introduction

Question 1

Define “Pharmacokinetics”

Answer 1

The branch of pharmacology dedicated to determining the fate of substances administered to an organism “what the body does to the drug”

Question 2

What does ADME stand for?

Answer 2

Adsorption (A), Distribution (D), Metabolism (M), Excretion (E)

Question 3

What factors determine the speed of adsorption?

Answer 3

1. Lipid solubility: Higher = Faster
2. Degree of ionisation of the drug: More ionisation = Slower
3. pH of drug and cellular fluids: If match = Faster
4. Size of the drug molecule: Bigger = Slower
5. Vehicle of drug preparation: Slow-release = Slower
6. Drug concentration either side of cellular membrane: Bigger difference = Faster

Question 4

Define “Half-life”

Answer 4

The time required for a drug’s concentration to reach half the peak plasma concentration

Question 5

Define “Pharmacodynamics”

Answer 5

The branch of pharmacology dedicated to the effects of drugs on an organism and their mechanism of action “what the drug does to the body”

Question 6

What are the nervous system branches for the brain?

Answer 6

Forebrain: telencephalon (hippocampus, amygdala) and diencephalon (thalamus, hypothalamus)

Midbrain: mesencephalon (tectum, tegmentum)

Hindbrain: metencephalon (pons, cerebellum) and myencephalon (medulla)

Question 7

What are the types of glia?

Answer 7

Astrocytes: structural support to neurones, involved in neurotransmission and repair after injury

Oligodendrocytes: myelination to neurones in CNS

Microglia: brains immune system

Ependymal cells: produce and circulate CSF

Question 8

Compare axons and dendrites

Answer 8

Axons: take info away from cell body, usually 1 axon per cell, can be myelinated

Dendrites: bring info to cell body, rough surface, many dendrites per cell, no myelination

Question 9

How does synaptic transmission work?

Answer 9

1. Action potential arrives at synapse. Triggers opening of voltage-gated Ca2+ channels.
2. Calcium enters the pre-synaptic terminal.
3. Calcium binds to neurotransmitters in vesicles, these fuse to cell membrane and release contents into synaptic cleft.
4. Neurotransmitters diffuse across synapse.
5. Neurotransmitters bind to receptors on post-synaptic cell.
6. Receptors are activated causing a change in conduction.
7. New action potential is created.

Question 10

How does an action potential work?

Answer 10

1. Cell is resting at -70
2. Voltage gated Na+ channels open, causing an influx of Na in the cell (depolarization).
3. Voltage gated K+ channels open and K+ will leave the cell.
4. When the membrane potential reaches +40, the Na+ ion channels will become refractory, no more enters the cell.
5. K+ continue to leave the cell, returns the membrane towards its resting potential (repolarisation).
6. K+ channels will then close, and Na+ will reset as membrane has gone past resting potental to -75 (hyperpolarization).
7. Extra K+ ions diffuse away and membrane returns to -70.
8. This propagates an action potential in an adjacent axon.

Question 11

What are the types of agonists?

Answer 11

Full agonist: mimics effect of neurotransmitter

Partial agonist: excerpts some degree of effect of a neurotransmitter

Inverse agonist: binds to same agonist site but produces a reaction that is opposite

Question 12

What are the types of antagonist?

Answer 12

Antagonist: prevents effect of neurotransmitter

Competitive antagonist: compete for same site on receptor as neurotransmitter

Non-competitive antagonist: act at another site of receptor to prevent effect of neurotransmitter

Question 13

What is the difference between excitation and inhibition?

Answer 13

Excitation: produce membrane depolarisation to increase the likelihood of firing action potentials

Inhibition: produce membrane hyperpolarisation to decrease the likelihood of firing action potentials

Question 14

What are the types of presynaptic drug actions?

Answer 14

Synthesis, storage and inhibition of release