Pharmacology Exam 1

Front 1

What's missing in this Rx:

DVM, Clinic, Address, Phone #

Patient, Client, Address

Drug, Dose, Qty, Directions

DEA#

DVM print/signature

Back 1

Date

Species

Refills

Front 2

Species differences are notable in _____.

Back 2

Pharmacokinetics

*not noticeable in pharmacodynamics (drug action does not change)

Front 3

What are the implications of using a drug that is extra label?

Back 3

VCPR
exam
no other drug suitable/ available
drug will tx the diagnosed dz
no residues in food animals/ est. withdrawal times...
etc etc.

Front 4

What schedules of drugs require prescriptions? Which is nonrefillable?

Back 4

CII, CIII, CIV, CV

CII is nonrefillable


*CI are illegal illicit drugs and therefore not included

Front 5

Which level of regulation is usually more strict with drug control? Federal or State?

Back 5

State

Front 6

Which drug schedules require DEA#s?

Back 6

ALL schedules require DEA numbers

except for schedule I, i guess since it is not a Rxable drug to begin with... (illicit drugs-- see your corner drug deaeler for details)

Front 7

LD50/ED50

Back 7

Therapeutic Index

Front 8

Parallel curves are required to determine what "safety study" of drugs?

Back 8

Therapeutic Index

Front 9

Certain Safety Factor (aka Margin of Safety) =

Back 9

TD01/ED99

*curves may differ

Front 10

T/F: all drugs have a margin of safety.

Back 10

False

*in order for a drug to have a margin of safety, MS> 1

Front 11

How would you determine low-dose toxic effects on a dose-response curve? (ie: LD01 or ED99)

Back 11

Use PROBITS to straighten the ends

*a probit is a standard deviation from the ED50 or LD50

Front 12

acid drugs are ___ when pH<pKa

Back 12

unionized

Front 13

acid drugs are ____ when pH >pKA

Back 13

ionized

Front 14

weak bases are ____ when pH > pKa

Back 14

unionized

Front 15

weak bases are ____ when pH <pKa

Back 15

ionized

Front 16

The relationship of ____ to the environment determines the status of the drug as a weak acid or base.

Back 16

pKa

*environment assume is giving you pH

Front 17

Types of Conjugations....

works on -OH, -COOH, -NH2, -SH

Back 17

Glucuronic acid

Front 18

Types of Conjugations...

works on AROMATIC -OH, AROMATIC -NH2, and AROMATIC -COOH

Back 18

Sulfate Conjugation

Front 19

Types of Conjugations

works on HALOGENS, -NO2,

Back 19

Mercapturic Acid

Front 20

Types of Conjugations...

works on aromatic NH2, aliphatic NH2, SO2, NH3

Back 20

Acetylation

Front 21

What tissues can biotransformation occur in?

Back 21

LIVER
skin
kidney
GI
adrenal
blood

Front 22

What is the purpose of biotransformation?

Back 22

Change polarity of the drug to allow translocation

Front 23

How are Phase 1 reactions different from Phase 2 reactions?

Back 23

Phase 1: may activate or deactivate

Phase 2: increase MW, deactivate only

Front 24

What reaction adds -OH, O or removes a methyl group?

Back 24

Oxidations

Front 25

Esters, Amides, Glucuronidde conjugates, glycosides are most likely to be ____.

Back 25

Hydrolyzed

Front 26

What is the order of importance for Phase II biotransformation reactions?

Back 26

Glucuronidation, Sulfation, Mercapturic acid formation

Front 27

What reaction predominates in the mitochondria?

Back 27

Oxidation

Front 28

What reactions occur in the Microsomes?

Back 28

Oxidation
Reduction (requires anaerobic environment)
Hydrolysis
glucuronidation

Front 29

What Phase II biotransformation reactions are Reversible?

Back 29

Methylation
Glucuronidation

Front 30

What are the Cell Compartments that biotransformation may take place in?

Back 30

Cytosol (supernatant)
Mitochondria
Microsomes

Front 31

All Phase II reactions require ___ enzymes.

Back 31

transferase

Front 32

How do Phase II reactions increase Molecular weight?

Back 32

conjugation iwth a large moiety.

Front 33

What is the major problem with oral drugs that can be significantly reduced, if not entirely eliminated by other routes of administration?

Back 33

First pass effect

Front 34

T/F: Dehydrated patients absorb IM and SQ injections RAPIDLY due to their increased need for fluid.

Back 34

False: dehdyrated patients have decreased peripheral circulation and will not absorb IM/SQ injections

Front 35

What is the stipulation for drugs applied topically?

Back 35

They must be in suspension.

*drugs in unlike vehicles leave the vehicle to move to the skin whereas drugs in like vehicles will tend to stay in the vehicle

Front 36

What physiologic space is the greatest?

Back 36

intracellular

Front 37

T/F: intracellular and extracellular space exists only in the vascular compartment.

Back 37

False: it also exists in the tissue space.

Front 38

Movemtn of drugs occurs by
transcytosis, endothelial jx with inflammation, diffusion, protein carriers... what is the most common?

Back 38

diffusion

Front 39

______ limited distribution is controlled by the ability of the drug to permeate the tissues.

Back 39

Diffusion limited

Front 40

______ limited distribution is controlled by the circulation to the tissue.

Back 40

Blood flow limited

Front 41

Biotransformation converts a drug entity to a ____.

Back 41

metabolite

Front 42

T/F: Volume of distribution is always equal to a physiologic space.

Back 42

False:
It may not be equal.

Front 43

How long does it take to reach steady state?

Back 43

5 T1/2s

Front 44

T/F: Steady state depends on Dose as well as T1/2/

Back 44

False:
Steady state depends entirely on T1/2. Dose does not affect steady state unless you are using a loading dose (2x) but usually these are not used for their increased risk.

Changing the dose will require that 5 T1/2s pass before the NEW steady state is reached.

Front 45

What is being described when we say that doubling the dose doubles the effects?

Back 45

Dose independent behavior

* this is true for 99% of drugs

Front 46

What are the main differences between first order and zero order pharmokinetics?

Back 46

First order has a T1/2 and is plotted on a semi log graph (fractions of dose absorbed and eliminated)

Zero order has no T1/2 (drugs may accumulate indefinitely

Front 47

Volume of distribution vs concentration?

Back 47

Vz= strictly volume

Concentration = substance measured per unit volume.... generally in the blood

Front 48

You just gave a dog a high dose of a concentrated drug IV. You then measure the Vz and find that it is low. What does this mean?

Back 48

"The drug is stuck to the side of the tank"

* drug is distributed to places other than the vascular space (

Front 49

What does it mean if a drug is said to have a large Vz?

Back 49

the drug will distribute to many places in the body

Front 50

____ decreases with increasing Vz.

Back 50

effective clearance (aka time required for clearance increases)

this is because organs filtering the drug are required to work more to filter those large amounts.

Front 51

Why do we alter Neurotransmitter?

Back 51

To alter the effect of the synapse since there are no "receptors" as there are in the ANS.

Front 52

Antidopaminergenics

Back 52

tranquilizer
antiemetic

(acepromazine/ metaclopromide)

Front 53

Acepromazine is antiDA what is its pharmacologic class?

Back 53

indirect sympatholytic

Front 54

Acepromazine is antiDA, antiadrenergic, and anticholinergic. We only use it for the antiDA effect. Why do the other effects occur?

Back 54

Nonselectively affects other neurons.

*Ace works by decreasing dopamine which is the precursor for NEpi (the neurotransmitter for the Sympathetic Nervous system postganglion and also one of the Neurotransmitters in the CNS).

Front 55

Metaclopromide is AntiDA like acepromazine. But, metaclopromide falls in what pharmacologic class?

Back 55

Parasympathomimetic

* ace = sympatholytic

Front 56

Primary tone for blood pressure and bronchi...

Back 56

Sympathetic:
increases BP
increase bronchodilation

Front 57

Primary tone for Heart rate, GI, Urinary...

Back 57

Parasympathetic:
decrease heart rate (50:50 with SNS)
increase GI
increase Urinary

Front 58

would you use parasympathetic or sympathetic drugs to increase heart rate after heart surgery?

Back 58

parasympathomimetics: because they will have fewer adverse side effects on the the stability of the patient. .. unless i accidentally wrote PsM instead of PsL-- which would make more sense seeing as atropine increases HR.

*i really have no idea how this works, she just said it during the review... so you can probably just ignore it.

*remember that the heart is 50:50 SNS:PNS.

Front 59

Diazepam and Barbiturates act on what receptor?

Back 59

GABA direct agonists

Front 60

Ketamine works on what receptor?

Back 60

direct antagonist GLUTAMATE

Front 61

Morphine works on what receptor?

Back 61

direct agonist
mu, kappa (enkephalins)

Front 62

Butorphanol works on what receptor?

Back 62

direct agonist
kappa

Front 63

Acetylcholine
pilocarpin
neostigmine
atropine

have what kinds of receptors? so what nervous system are they involved with?

Back 63

Muscarinic

parasympathetic

Front 64

What is the big alpha2 agonist?

*decreases blood pressure= tranquilizer

Back 64

XYLAZINE

Front 65

What is the big beta blocker?

*results in decreased heart rate and bronchoconstriction

Back 65

PROPRANOLOL

Front 66

What do these drugs have in common?
theophylline
acepromazine
metaclopromide
neostigmine

Back 66

indirect action

Front 67

What do these drugs have in common?
epinephrine
norepinephrine
xylazine
isoproterenol
theophylline

Back 67

Sympathomimetic

Front 68

What do these drugs have in common?
propranalol
acepomazine
metaclopromide

Back 68

sympatholytic

Front 69

What do these drugs have in common?
acetylcholine
pilocarpine
neostigmine

Back 69

parasympathomimetic

Front 70

An antimuscarinic drug, atropine would be in what pharmacologic class?

ie: it is a direct ANTAGonist

Back 70

parasympatholytic

Front 71

T/F: morphine is more efficacious than butorphanol.

Back 71

true

Front 72

T/F: morphine is more potent than butorphanol.

Back 72

false
*morphine is more efficacious than butorphanol, but butorphanol is more potent.

Front 73

Clinical use of pilocarpine

Back 73

miosis
Rx: glaucoma

Front 74

clinical use of atropine

Back 74

increase heartrate
decrease secretions

Front 75

this drug is often used to Rx alzheimers

Back 75

neostigmine

* miotic.
*antidote for nondepolarizing NMJ blockers

Front 76

this drug is associated with catylepsy and dissociateive amnesia

Back 76

ketamine

Front 77

how do u distinguish diazepam from barbiturates?

Back 77

barbs can be used for euthanasia

Front 78

epinephrine is used to increase heartrate by exploiting its action onf what receptor.

Back 78

Beta > alpha

Front 79

xylazine is a tranquilizer that also decreases ____

Back 79

blood pressure

Front 80

isoproterenol can be used to increase ___ and also to ____

Back 80

increase heartrate

bronchodilate

Front 81

this beta blocker (antagonist) causes decreased heart rate and bronchoconstriction

Back 81

Propranolol

Front 82

isoproterenol acts on heart and lung. what receptors are involvoed?

Back 82

beta 1 and beta2

Front 83

administering acetylcholine will have what effect clinically?

Back 83

Primarily
parasympathomimetic =
increased gi motility
decreased heartrate
miosis

there will be other side effects because Ach is the NT at many sites pre and post ganglionic

Front 84

what drug has direct agonism antitussive effects?

Back 84

codein