Pharmacology

Question 1

zero order elimination. What is it, and what are examples

Answer 1

PEA, phenytoin, ethanol, aspirin. zero order means that rate of elimination is constant regardless of Cp.

Question 2

first order elimination. What is it

Answer 2

rate of elimination is proportional to Cp

Question 3

Weak acid drugs: Examples, where are they trapped, how to treat overdose

Answer 3

phenobarbitol, methotrexate, apririn. they are trapped in basic environments. treat overdose with bicarbonate.

Question 4

Weak base drugs: Example, where they are trapped, how to treat an overdose

Answer 4

Amphetamines. they are trapped in acidic environments. Treat overdose with ammonium chloride

Question 5

What is phase 1 drug metabolism

Answer 5

redox, hydrolysis. via Cyp450 system. Yields slightly polar metabolites that are often still active. Geriatric patients lose phase 1 first!

Question 6

What is phase 2 drug metabolism

Answer 6

Geriatric patients still have this, still have GAS, glucoronidation, acetylation, and sulfation. usually yields very polar, inactive metabolites that are renally extracted.

Question 7

What is efficacy.

Answer 7

refers to the maximum effect that a drug can produce. Examples of high efficacy drugs include analgesics, antibiotics, antihistamines, decongestants. a partial agonist is less efficacious than a full agonist.

Question 8

potency

Answer 8

the amount of drug needed for a given effect. if there is increase potency, there is increased affinity for the receptor. examples of highly potent drugs include: chemodrugs, antihypertensives, lipid lowering drugs.

Question 9

competitive antagonist

Answer 9

decrease potency, no change in efficacy. can be overcome by increasing agonist. Flumezanil is a competitive antagonist on GABA receptors

Question 10

noncompetitive antagonist

Answer 10

decreases efficacy. Is not overcome by increasing agonist concentration. Ketamine is a noncompetitive antagonist on NMDA receptors.

Question 11

irreversable competitive antagonist

Answer 11

decreases efficacy. is not overcome by increasing agonist concentration. phenoxybenzamine is an irreversible competitive antagonist on alpha receptors

Question 12

flumazenil

Answer 12

competitive antagonist on GABA receptors

Question 13

Ketamine

Answer 13

noncompetitive antagonist on NMDA receptors

Question 14

phenoxybenzamine

Answer 14

irreversible competitive antagonist on alpha receptors

Question 15

partial agonist

Answer 15

acts at same site as full agonist but lower efficacy, independent of potency. buprenorphine is a partial agonist of mu opioid receptors when compared to morphine.

Question 16

bupronorphine

Answer 16

partial agonist of mu opioid receptors

Question 17

Therapeutic index. what does it represent, how to calculate it, and examples of drugs with low TI values.

Answer 17

TITE. Therapeutic index is TD50/ED50. Higher is better. Low TI drugs include digoxin, lithium, theophylline, and warfarin.

Question 18

parasympathetic uses which NTs?

Answer 18

ACh on muscarinic receptors.

Question 19

sympathetic uses which NTs?

Answer 19

ACh at the preganglionic neuron. For Sweat glands, ACh at postgang. Usually Norepi at postgang. Dopamine for renal vasculature and smooth muscle. ACh straight from spinal cord for the adrenal medulla (which then releases NE and E).

Question 20

Nicotinic ACh receptors are found where?

Answer 20

they are ligand gated Na/K channels. they are found in autonomic ganglia (Nn), and neuromuscular junction (Nm).

Question 21

Muscarinic ACh receptors are found where?

Answer 21

G protein coupled receptors that usually act through 2nd messengers. there are 5 subtypes M1-M5.

Question 22

Alpha 1 GPCRs. What G protein class and major functions

Answer 22

G protein class q
Major functions:
1. increase VSMC contraction
2. Pupil dilatory muscle contraction. Mydriasis
3. intestinal and bladder sphincter muscle contraction

Question 23

Alpha 2 GPCRs. What G protein class and major functions

Answer 23

G protein class i
Major functions:
1. decreases sympathetic outflow
2. deceases insulin release
3. decreases lipolysis
4. decreases platelet aggregation

Question 24

Beta 1 GPCRs. What G protein class and major functions

Answer 24

G protein class s
Major functions:
1. increase heart rate,
2. increase contractility
3. increase renin release
4. increase lipolysis

Question 25

Parasympathetic M1. What G protein class and major functions

Answer 25

G protein class q. Major Functions: 1. CNS, enteric system

Question 26

Parasympathetic M2. What G protein class and major functions

Answer 26

G protein class i. Major functions: 1. decease heart rate 2. decrease atrial contractility

Question 27

Parasympathetic M3. What G protein class and major functions

Answer 27

G protein class q Major Functions: 1. Increase endocrine gland secretions (lacrimal, salivary, gastric) 2. increase gut peristalsis 3. increase bladder contraction 4. bronchoconstriction 5. increase pupillary sphincter muscle contraction (miosis) 6. ciliary muscle contraction (accomodation)

Question 28

Dopamine D1. What G protein class and major functions

Answer 28

``` G protein class s Major functions: 1. relaxes renal vascular smooth muscle ```

Question 29

Dopamine D2. What G protein class and major functions

Answer 29

G protein class i Major Functions: 1. Modulates NT release, especially in the brain

Question 30

Histamine H1 What G protein class and major functions

Answer 30

``` G protein class q. Major Functions: 1. increase nasal and bronchial mucus production 2. increase vascular permeability 3. contraction of bronchioles 4. pruritis 5. pain ```

Question 31

Histamine H2. What G protein class and major functions

Answer 31

``` G protein class s. Major functions: 1. increase gastric secretions ```

Question 32

Vasopressin V1. What G protein class and major functions

Answer 32

``` G protein class q. Major functions: 1. increase vascular smooth muscle contraction ```

Question 33

Vasopressin V2. What G protein class and major functions

Answer 33

``` G protein class s. Major functions 1. increase H2O permeability and reabsorption in the collecting tubules of the kidney ```

Question 34

What do Gq receptors do?

Answer 34

activate phospholipase C -> cleave PIP2 to IP3 and DAG. to activate Protein Kinase C and increase intracellular calcium

Question 35

What do Gs receptors do?

Answer 35

stimulate adenylyl cyclase to make cAMP and protein kinase A to increase Ca intracellularly in the heart, and block myosin light chain kinase in smooth muscle.

Question 36

What do Gi receptors do?

Answer 36

inhibit adenylyl cyclase to stop making cAMP and protein kinase A to decrease Ca intracellularly in the heart, and allow myosin light chain kinase in smooth muscle.

Question 37

action of hemicholinium in the ANS

Answer 37

blocks choline transport into axon terminals. (that choline is then used to acetylcholine). this drug is typically not used clinically

Question 38

action of vesamicol in the ANS

Answer 38

blocks acetylcholine entering into vesicles in the axon terminal. this drug is typically not used clinically.

Question 39

action of boutlinum in the ANS

Answer 39

blocks release of acetylcholine filled vesicle release from axon terminals

Question 40

action of metyrosine in the ANS

Answer 40

blocks tyrosine's conversion to DOPA on the way to forming dopamine and NE. not typically used in clinic

Question 41

action of reserpine in the ANS

Answer 41

blocks transport of dopamine into the vesicles in the axon terminals.

Question 42

action of amphetamines in the ANS

Answer 42

increases release of NT laden vesicles (dopamine or NE) into synapse, and deceases reuptake

Question 43

action of bretylium in the ANS

Answer 43

decreases release of NT laden vesicles (dopamine or NE) into synapse

Question 44

action of cocaine, TCAs,

Answer 44

decreases reuptake of NTs like dopamine and NE

Question 45

action of guanethidine in the ANS

Answer 45

blocks release of NT laden vesicles (dopamine and NE). not usually used in clinic

Question 46

action of angiotensin II in the ANS

Answer 46

increase release of NE from nerve endings

Question 47

action of Alpha 2 receptors in the ANS

Answer 47

blocks release of NE from nerve endings.

Question 48

bethanechol. action and clinical application

Answer 48

Used for postop ileus, neurogenic ileus, and urinary retention. actives bowel and bladder smooth muscle. it is resistant to AChE

Question 49

carbachol. action and clinical application.

Answer 49

used for glaucoma, pupillary constriction, relief of intraocular pressure. is a carbon copy of acetylcholine

Question 50

pilocarpine. action and clinical application

Answer 50

potent stimulator of seat, tears, saliva. used for both open angle and closed angle glaucoma. 1. causes contraction of cilliary muscle (open angle glaucoma). 2. contracts pupillary sphincter (closed angle glaucoma) it is resistant to AChE, you drool, cry and sweat on your PILOw