Lecture 4 (Drugs)

Question 1

Ethnopharmacology

Answer 1

The study of substances use by society

Question 2

ethopharmacology

Answer 2

the study of substances used by animals

Question 3

dose

Answer 3

a single treatment

Question 4

dosage

Answer 4

treatment regime

Question 5

routes of drug ingestion:

Answer 5

1.) Ingestion
2.) Inhalation
3.) Dermal contact
4.) Injection

Question 6

Dermal contact

Answer 6

patches that dissolve drug into skin. only for lipid soluble products

Question 7

subcutaneous

Answer 7

injections into fat under the skin

Question 8

intramuscular

Answer 8

injections into the muscle under the skin

Question 9

intravenous

Answer 9

injections directly into the bloodstream

Question 10

Intraperitoneal

Answer 10

Injections into the abdomen

Question 11

intracerebroventricular

Answer 11

injections into the cerbral ventricles (into the CSF)

Question 12

Intracerebral

Answer 12

Injections into a discrete location of the brain tissue that you are studying

Question 13

intrathecal

Answer 13

injections into the spine

Question 14

Blood brain barrier (why and how)

Answer 14

endothelial cells are much tighter together in CNS, drugs cannot diffuse past them
protects to neurons in brain from toxins (as they do not regenerate much)

Ways around:
* gases, small fat soluble drugs
* glymphatic system = astrocytes control blood flow in local regions move material form CSF to the brain
* specialized ultrasound

Question 15

Ways around the Blood Brain Barrier:

Answer 15

• gases, small fat soluble drugs
• glymphatic system = astrocytes control blood flow in local regions move material form CSF to the brain
• specialized ultrasound

Question 16

Ligand

Answer 16

Any substance that binds to a receptor

Question 17

Types of Drug Actions (three:)

Answer 17

1.) Agonist = stimulates the action of an endogenous substance
2.) Antagonist = counters the action of an endogenous substance
3.) Inverse Agonist = acts oppositely to an agonist (blocks)

Question 18

Some synaptic drug effects:

Answer 18

1.) alters axonal transport (such as blocking transport or signals)

2.) alterations in synthesis (such as more transmitter being produced)

3.) alterations in storage (reseperine = makes vesicles leaky, no transmitter when they rupture)

4.) re-uptake (such as prozac)

5.) Alterations in metabolic breakdown (such as inactivating enzymes that break down neurotransmitter)

Question 19

Some post-synaptic drug effects:

Answer 19

1.) Inhibitors (such as MAOA’s, reduce breakdown of monamines in the cleft, more reuptake in pre-synaptic membrane)

2.) Direct effect on receptors (activate the receptors themselves, or a receptor sub-type)

3.) Block receptors (antagonists)

4.) Alter second messenger function

5.) Alter gene transcription (steroids?)

Question 20

endogenous

Answer 20

made inside the the body

Question 21

exogenous

Answer 21

made outside the body

Question 22

“orphan receptor”

Answer 22

receptors inside the brain. We don’t yet know what endogenous substances interacts with it. But they must must exist…?

Question 23

Three subtypes of Opioids + how many endogenous classes of opioids are there?

Answer 23

• mu, delta, kappa
• there are three classes

Question 24

Antagonist to Opioids

Answer 24

Naloxone (reverse affects of overdose!)

Question 25

Drug-receptor equilibrium means that?

Answer 25

drugs are binding and dissociating from receptors all the time at an equal rate

Question 26

Receptor Affinity

Answer 26

A drug has varying infinity for different receptors (#1 favourite, #2 favourite ect.)
No drugs have only one receptor
Increase dosage (bind to more receptors)

Question 27

Saturation

Answer 27

Drug binds to all high affinity receptors. Receptors are completely filled up with the drug.

Question 28

Is saturation ever 100%?

Answer 28

No, drugs are always binding and dissociating

Question 29

is 100% saturation necessary for best effects?

Answer 29

No, 60% for example saturation (for example) may be enough for good effects to be observed

Question 30

Secondary binding

Answer 30

All higher affinity receptors are saturated. Drug bids to lower affinity sites and saturates them. Causes side effects.

Question 31

why does secondary binding causes side effects?

Answer 31

Because the lesser affinity receptors may not be as directly related to the target process so they affect more bodily systems

Question 32

Irreversible binding

Answer 32

Drug binds to receptor, and cannot detach. Not forever. The receptor waxes and wanes, breaks down fairly fast. (receptor metabolism!)

Question 33

What does the dose response curve look like?

Answer 33

A flattened out S

Question 34

LD50

Answer 34

Lethal dose for 50% of treatment subjects

Question 35

ED50

Answer 35

effective dose for 50% of treatment subjects

Question 36

therapeutic index

Answer 36

LD50 / ED50 = index

Question 37

LD50 / ED50 = ?

Answer 37

The therapeutic index (want a big difference between lD and ED)

Question 38

Alternative to the LD50?

Answer 38

TD50 (toxic dose for 50% of patients)

Question 39

Effect of secondary saturation on the dose response curve?

Answer 39

dose réponse curve becomes non-monatomic (deviates from the s-shape) due to side-effects

Question 40

Three types of tolerance?

Answer 40

1.) Metabolic tolerance = physiological changes that reduce the amount of drug that gets to to its target (body starts breaking down drug before it gets to the brain)

2.) Functional Tolerance = target tissue with successive exposure to drug may become less reactive (up or down regulation)

3.) Contigent Tolerance = drug effect must be experience for tolerance to occur (drug effect, need to have the drug before an experience? LOL help….)

Question 41

Physiological changes that reduce the amount of drug that gets to to its target (body starts breaking down drug before it gets to the brain)

Answer 41

Metabolic tolerance

Question 42

Target tissue with successive exposure to drug may become less reactive (up or down regulation)

Answer 42

Functional Tolerance

Question 43

drug effect must be experience for tolerance to occur (drug effect, need to have the drug before an experience? LOL help….)

Answer 43

contigent tolerance

Question 44

tolerance for one drug may generalized to similar drugs

Answer 44

cross-tolerance

Question 45

Types of neurotoxins!

Answer 45

1.) Ion channel blockers (irreversible binding, agonist that binds permanently to a receptor)

2.)Ion channel openers (causes channels to stay open)

3.) Excito-toxins = amino acids variants cause cell to become hyper excitable (causes cell death)

4.) Metabolic = shut down metabolism or impair cell functioning
*mimic inappropriately an endogenous substance

Question 46

Tetrodotoxin (TTX)

Answer 46

Animal toxin (pufferfish)
blocks voltage gated Na channels = no action potentials (OH NO, SO SAD) :(

Question 47

Bungarotoxin (Banded krait)

Answer 47

Animal toxin
snake venom
blocks nicotinic Acetochcoline AHc channels irreversibly (paralysis)

Question 48

Charybdotoxin

Answer 48

animal toxin
scorpion venom
irreversibly blocks potassium channels

Question 49

stimulants

Answer 49

activate excitatory post-synaptic potentials
or block (IPSP)

Question 50

depressants

Answer 50

reduce EPSP, or causes IPSP

Question 51

examples of depressants:

Answer 51

opiates
alcohol
benzodiazepines (anxiety drugs)

Question 52

MTPT (designer drug)

Answer 52

leads to Parkinson’s disease (kills dopamine receptors)

Question 53

route of drug administration (5 stages):

Answer 53

1.) route of administration
* dermal contact
*inhalation
*injection
*ingestion

2.) Absorption (if applicable)
*gases
* dermal contact (lipid soluble)

3.) Binding
* drugs bind to receptors
*depot binding (binds to fat stores and deactivate, reactivate at some point)

4.) Inactivation
* enzymes breakdown drug via synapses
* mostly occurs in the liver

5.) Elimination
*urine

Question 54

Set

Answer 54

Everything that someone brings with them (individually) to a drug experience

Question 55

setting (drugs)

Answer 55

the physical setting/location of drug use
*known settings (body prepares, down regulation of receptors prior to even taking the drug)