Pharmacology: Drug Action & Handling

Front 1

Dose Effect Curve

Back 1

Drug Dose (x-axis) -vs- Intensity of Effect (y-axis)

Front 2

Log Dose Effect Curve

Back 2

% Effective Dose (x-axis) -vs- % Maximum Response (y-axis).
As the dose is increased, first the effect is zero, then a small effect, then a rapid increase (this is the therapeutic range), and finally a plateau (this is the maximum response).

Front 3

Define *potency*

Back 3

the amount of drug needed to produce an effect

Front 4

Potency of Agent (with log dose effect curves)

Back 4

the farther from zero the log dose appears on the x-axis, the less potent it is.

Front 5

Define *efficacy*

Back 5

the maximum effect of a drug, regardless of dose, e.g., no matter how much aspirin you give, it can only relieve mild to moderate pain. It will never be as efficacious as morphine, which relieves severe pain.

Front 6

True or False: The efficacy of a drug and its potency are directly related.

Back 6

False. They are not related at all.

Front 7

What is a drug's LD50?

Back 7

Median Lethal Dose, i.e., the dose when 50% of the subjects die. Only determined in animals.

Front 8

How many different neurotransmitters are there? Name a few.

Back 8

at least 50 including acetylcholine, norepinephrine/epinephrine, dopamine, serotonin, gamma-aminobutyric acid (GABA), and histamine.

Front 9

Name 2 *local chemical agents* that activate nerve impulse transmission, i.e., not hormones or neurotransmitters.

Back 9

Prostaglandin (uterine contraction) and histamine (allergic response)

Front 10

What are hormones?

Back 10

secreted by the endocrine system to produce effects throughout the body, e.g., insulin, thyroid hormone, and adrenocorticosteroids. Usually slower than neurotransmitters.

Front 11

Drugs can only _______ or ________ the body's natural response. They cannot make the cell perform a new function.

Back 11

enhance, block (You cannot make a neuron produce bile, you can only *block* or *enhance* its ability to send an impulse.

Front 12

define therapeutic effect

Back 12

a drug's intended action

Front 13

True or False? Different drugs sometimes compete for the same receptor sites.

Back 13

True. Whichever has the stronger affinity for the receptor will bind to more receptors than the other. The drug with the stronger affinity is more POTENT.

Front 14

Define *agonist*

Back 14

a drug that
1. has affinity for a receptor,
2. combines with the receptor, and
3. produces an effect.

Front 15

Define *antagonist*. Name the 3 variations.

Back 15

A drug that counteracts the action of the agonist.
1. Competitive Antagonist
2. Noncompetitive Antagonist
3. Physiologic Antagonist

Front 16

Define *competitive antagonist*

Back 16

a drug that:
1. has affinity for a receptor,
2. combines w/ the receptor, and
3. produces no effect.
This causes a shift to the right in the Dose-Response curve, i.e.. The agonist + antagonist are competing for the receptor and the affinity and concentration of each determines the outcome. If the concentration + affinity of the agonist is higher, its effect will overcome the antagonist.

Front 17

Define *noncompetitive antagonist*

Back 17

Bind to a different receptor site than the agonist. This reduces the maximum response of the agonist.

Front 18

What is a granule?

Back 18

A package of neurotransmitter made from precursors that waits at the membrane for a signal to dump its contents into the synapse.

Front 19

3 ways to remove a neurotransmitter from the synapse after transmission:

Back 19

1. broken down by enzymes,
2. migrate to the receptor and produce a response, or
3. reuptake (taken back into the presynaptic nerve ending)

Front 20

mydriasis

Back 20

dilated pupils (myDriasis = Dilated)

Front 21

myosis

Back 21

constricted pupils (myOsis = cOnstricted) Produced by cholinergic drugs

Front 22

cycloplegia

Back 22

loss of focus of vision. Produced by cholinergic drugs

Front 23

Direct-acting cholinergic effects on cardiovascular system

Back 23

1. heart rate slows (negative chronotropic effect) and has a weak muscle response (ionotropic).
2. Smooth muscle (in blood vessels) relaxes and vasodilates.

Front 24

Indirect-acting cholinergic effects on cardiovascular system

Back 24

increase in heart rate and cardiac output

Front 25

Cholingergic GI effects

Back 25

increase in smooth muscle activity, motility and secretions

Front 26

Cholinergic effects on the Eye

Back 26

miosis (contraction), cycloplegia (loss of focus), decreased intraocular pressure. Useful for trx of Glaucoma.

Front 27

Adverse Cholinergic effects

Back 27

large doses = SLUD (salivation, lacrimation, urination, defecation)
larger doses = neuromuscular paralysis

Front 28

How are cholinergic overdoses treated?

Back 28

pralidoxime and atropine (usually caused by insecticides, which are nerve gases, or organophosphates)

Front 29

Contraindications to Cholinergic agents

Back 29

Bronchial asthma - can cause bronchospasm
hyperthyroidism- increase risk in atrial fibrilation
GI or urinary tract obstruction--GI stimulation
severe cardiac disease--CVS activity decreases
myasthenia gravis treated with neostigmine (it occupies the receptors choinergics need)
peptic ulcer--gastric stimulation

Front 30

Direct acting uses of cholinergic drugs

Back 30

Glaucoma, myasthenia gravis (sometimes) and Xerostomia--pilocarpine (Salagen). Side Effects: perspiration, nausea, rhinitis, chills, flushing.

Front 31

Indirect acting uses of cholinergic drugs

Back 31

physostigmine (Antilirium) treats toxicity from anticholinergic agents (atropine) and agents w/ anticholinergic action like phenothiazines, tricyclic antidepressants & antihistamines.
Cholinesterase inhibitors like insecticides & nerve gas are irreversible.

Front 32

Anticholinergic effects on CNS

Back 32

stimulation (scopolamine) or depression (atropine), depending on dose. Tertiary agents penetrate brain, quaternary less likely to.

Front 33

Anticholinergic effects Exocrine Glands

Back 33

reduces flow and volume. used in dentistry to decrease salivation and create a dry field

Front 34

Anticholinergic effects on Smooth Muscle

Back 34

Relax smooth muscle in respiratory & GI systems. Trx for asthma and spasmodic GI.

Front 35

Anticholinergic effects on Eye

Back 35

mydriasis & cycloplegia. for eye exams

Front 36

Anticholinergic effects on Cardiovascular system

Back 36

large doses = tachycdardia; small doses = bradycardia

Front 37

Anticholinergic Adverse reactions

Back 37

xerostomia, blurred vision, photophobia, tachycardia, fever, urinary & gastrointestinal statis, flush from lack of sweating.

Front 38

Anticholinergic Contraindications

Back 38

Glaucoma: rise in pressure
Prostate hypertrophy
Intestinal/Urinary retention
Cardiovascular disease

Front 39

Anticholinergic uses

Back 39

preop med
Trx of GI disorders
eye exams
decreases Parkinson-like movements
motion sickness

Front 40

Alpha adrenergic receptors

Back 40

smooth muscle excitation = vaso-constriction

Front 41

Beta 1 adrenergic receptors

Back 41

increases heart rate & strength (1 heart)

Front 42

Beta 2 adrenergic receptors

Back 42

vasodilation of skeletal muscles = bronchodilation (2 lungs)