Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
306 Cards in this Set
- Front
- Back
What are small molecule drugs? |
drugs with defined chemical structure, usually stable, <1000 D
|
|
What are biologics?
|
drugs are >2000D, structure not always well defined, tertiary structure will affect biologic activity, NOT stable ( sensitive to heat, light, etc)
|
|
Which type of drugs can legally have generic forms?
|
Small molecules drugs, biologics after ObamaCare
|
|
What is meant by biologics are not stable?
|
They are sensitive to heat, light, shaking, etc
|
|
Why are drugs expensive?
|
research, preclinical testings, clinical trials, evaluation, approval all are resouce consuming (time [many years] and money)
|
|
Who approves drugs before they can legally be sold in US?
|
FDA
|
|
Define drug.
|
Article intended for use in the diagnosis, cure, mitigation, treatment, or prevention of disease in man or other animals
|
|
Defined drugs are recognized where?
|
USP/NF (US Pharmacopeia & National Formulay - book of pharmacological standards) or HPUS (Homeopathic Pharmacopeia of US)
|
|
What is INAD?
|
Investigational New Animal Drug Application - drug sponsor (manufacturer) completes extensive testing to show effectiveness and safety
|
|
What is NADA?
|
New Animal Drug Application - supporting data from sponsor
|
|
*What is the FDA approval process?*
|
1. preclinical studies 2. clinical trials 3. FDA approval 4. Phase IV post market monitoring 5. Adverse events should be reported to FDA
|
|
*What are preclinical trials?*
|
animal testing to support initiation of clinical trials
|
|
*What are the phases of clinical trials?*
|
Phase 1 - safety and pharmacokinetics (on healthy patients) Phase 2 - efficacy Phase 3 - statistically significant safety and efficacy for patients with disease/contition to be treated (larger pop) Phase IV - post market monitoring
|
|
What does FDA approval mean?
|
The formulated drug is approved for particular indications and doses; the health benefit must outweigh the risk
|
|
T/F DVMs can prescribe drugs approved in EU and UK.
|
T
|
|
T/F Generics must be the same formulation and dose size as the approved drug
|
T
|
|
What does patent protection mean?
|
the window of time a company can recoup research expenses before generic versions can be sold
|
|
*What is brand/trade name?*
|
name chosen by the manufacturer (Heartgard)
|
|
*T/F There may only be one brand name despite differences in formulation
|
False, there can be multiple brand names based on formulation and company
|
|
*What is INN?*
|
International Nonproprietary Name (Ivermectin)
|
|
Which name is used by Plumb's?
|
INN
|
|
T/F INNs are the same in all countries
|
False, INNs are not the same in all countries (acetometaphin in US, paracetamol in UK; USAN [US adopted name] vs. BAN [British Approved Name])
|
|
*What is the chemical name?*
|
scientific name of active ingredient (22,23-dihydroavermectin B1a)
|
|
*What is the company code?*
|
name assigned by company during drug discovery phase (MK-933)
|
|
What is pharmacodynamics?
|
the effect of the drug on the body
|
|
What is pharmacokinetics?
|
the body's effect on the drug (ie metabolism)
|
|
T/F Drug effect is dependent on drug concentration
|
true!
|
|
What is a typical biological target?
|
a protein (enzyme, receptor)
|
|
Define reversible binder
|
Drug that interacts with protein through hydrogen bonding and Van der Waals interactions
|
|
Define irreversible binder
|
drug forms covalent bonds with protein aka "suicide inhibitor'
|
|
Which amino acid is most likely to bind with a drug?
|
cysteine
|
|
Are small molecule drugs selective?
|
Yes, but not perfectly, usually they also affect other biological targets, but to a lesser extent
|
|
What type of receptor uses secondary messengers?
|
G protein coupled receptors
|
|
What type of receptor allows drug interactions inside the cell?
|
Ligand gated channel receptors (nicotinic receptors)
|
|
What are secondary messengers?
|
Intracellular signaling molecules that trigger physiological changes such as proliferation, differentiation, survival
|
|
Define full agonist
|
drug that can combine with receptors to elicit a maximal response
|
|
define partial agonist
|
drug that is capable only of eliciting a submaximal response despite increased dose
|
|
define antagonist
|
drug that inhibits the function of the target. Also, if administered previously or simultaneously with agonist, will diminish the anticipated respnse to agonist
|
|
define competitive antagonist
|
inhibitory effect depends on relative concentrations of agonist and antagonist
|
|
define non-competative antagonist
|
the intensity of antagonism remains unchanged in presence of increasing agonist concentration
|
|
define potency
|
the response is relative to drug concentration
|
|
T/F A less potent drug will have a decreased maximal effect compared to a more potent drug
|
False, maximum effect will be equal for less potent and more potent drugs, however, less potent drug will require a large dose
|
|
Define IC50
|
Inhibitory concentration at 50% inhibition - concentration of a drug that produces 50% of the maximal response - used to quantify drug activity
|
|
T/F EC50 = IC50
|
True, inhibitory typically used for inhibitory drugs but essentially mean the same thing
|
|
define MIC
|
minimal inhibitory concentration
|
|
Explain the Clark's Occupation Theory of Drug-Receptor interactions
|
the extent to which a tissue responds depends on the proportion of its receptor population occupied by the drug
|
|
Define Emax
|
Maximal effect - where receptors are fully activated
|
|
T/F Using the occupation theory, competitive and non-competitive antagonists may be distinguished on a dose-reponse curve by examine EC50 and Emax.
|
true!
|
|
What effect will a competive antagonist have on the agonist dose-response curve?
|
EC50 increases, Emax is unchanged
|
|
What effect will a non-competitive antagonist have on an agonist dose-reponse curve?
|
Emax decreases, EC50 remains inchanged
|
|
Define efficacy
|
The ability of a drug to produce the desired effect
|
|
Expain Paton's Rate theory
|
drug effect is proportional to rate of drug-receptor combination rather than the proportion of receptors occupied by the drug; explains persistent drug effect on tissue (tachyphylaxis)
|
|
MOS
|
Margin of Safety - ratio of theraputic dose and first toxic dose
|
|
NOAEL
|
No observed adverse events level - plasma concentration for the dose that had no observed adverse events
|
|
MED
|
Minimum effective dose - dose that produces the desired effect in vivo
|
|
MIC
|
Minimum inhibitory concentration - minimum plasma concentration of drug needed to inhibit pathogen (abx)
|
|
MTD
|
maximum tolerated dose - largest dose tolerated of a drug that is less than toxic dose
|
|
toxic dose
|
first dose that shows an unacceptable toxicity that is monitorable and reversible - NOT lethal
|
|
LD50
|
lethal dose to 50% population - 50% of population is killed by this dose - used for cell culture = not as relevant
|
|
How is MOS calculated?
|
MTD/MED using plasma drug concentrations
|
|
What is theraputic index?
|
LD50/ED50 = lethal dose/effective dose
|
|
What is theraputic ratio?
|
LD25/ED75
|
|
Define tolerance
|
with successive administration of a drug, increasing doses are required to elicit the same effect
|
|
Is tolerance caused by pharmacokinetic effect or pharmacodynamic effect?
|
both
|
|
define tachyphylaxis
|
pharmacodynamic tolerance that develops rapidly
|
|
define additive effects of agonists
|
response of 2 drugs combined
|
|
define synergistic effects of agonists
|
response of 2 drugs combined is greater than expected
|
|
define potentiation
|
an increase in potency of one drug caused by another drug that does not have the same pharmacological effect (not an agonist)
|
|
What does ADME stand for? DADME & LADME?
|
Absorption, distribution, metabolism and excretion; dissolution/liberation ADME
|
|
Define absorption
|
movement of drug into the central compartment (bloodstream)
|
|
define distribution
|
movement of drug to the tissue where it is acting
|
|
define metabolism
|
chemical of modification of the drug by the body
|
|
define excretion
|
elimination of drug from the body
|
|
define bioavailability
|
the percentage of drug administered that reaches the systemic circulation
|
|
define first pass effect
|
phenomenon of drug metabolism in which the concentration of a drug is greatly reduced before it reaches the systemic circulation - fraction lost to liver and gut wall
|
|
oral bioavailability
|
percent of drug in plasma from PO dose compared to IV dose
|
|
how is bioavailability calculated?
|
AUC (route of admin)/AUC (IV) |
|
define tablet
|
crystal of drug pressed into a pill |
|
define gelatin capsules
|
suspension or solution of drug in capsule
|
|
define powder/granule
|
crystalline solid drug, usually not amporphous
|
|
define suspension
|
crystals of drug are in the liquid (cloudy or white)
|
|
define aqueous solution
|
drug is completely dissolved (clear liquid)
|
|
Which drug forms need to be dissolved?
|
tablets, gelatin cap, powder/granule, suspension
|
|
What is the only suspension/non-clear liquid that can be given IV?
|
propofol
|
|
define emulsion
|
tiny droplets of one liquid in another liquid - drug dissolved in liquid
|
|
What drug formulation is injectable?
|
aqueous solution
|
|
T/F Drug formulation effects drug exposure
|
True.
|
|
What drug administration methods avoid first pass metabolism?
|
IV, IM, SC, transdermal
|
|
T/F Absorption of oral drugs is less predictable in monogastric species than in ruminants.
|
false ruminant absorption of oral drugs is less predictable
|
|
T/F Rumens have first pass metabolism
|
true.
|
|
T/F Rumens can inactivate some drugs
|
true.
|
|
Why is balance between aqueous and lipid solubility needed?
|
Because drugs need to be soluble in aqueous environments (blood, cytoplasm) and be able to permeate lipid membrane
|
|
What are the variables in Fick's Law of Diffusion?
|
rate of diffusion = D*P*deltaC / h where D is diffusion coefficient of drug, h is membrane thickness, deltaC is concentration gradient of drug across the membrane, P is the partition coefficient for the drug or lipophilicity
|
|
Define lipophilicity
|
drug solubility in octanol (a lipid mimic) / solubility in water
|
|
What are the factors affecting solubility?
|
inherent drug solubility, lipophilicity, degree of ionization (pKa)
|
|
T/F Acidic drugs are trapped in basic environments, Basic drugs are trapped in acidic environments
|
true.
|
|
What factors determine inherent drug solubility?
|
molecular weight, aromaticity, shape
|
|
Where are acidic drugs ionized? Soluble? permeable?
|
acidic drugs are ionized in the small intestine, soluble in the small intestine and more permeable in the stomach
|
|
Where are basic drugs ionized? soluble? permeable?
|
basic drugs are ionized in the stomach, soluble in the stomach, more permeable in the small intestine
|
|
What are some factors that contribute to food effect?
|
fed state changes gastric pH, bile acids released in stomach when fed can increase drug solubility, fatty foods can help solubilized lipophilic drugs and increase bile secretion, gastric motilityincreases when fed, food interactions
|
|
T/F Drugs with high solubility and high permeabilty are most likely to show a food effect
|
false! drugs with LOW solubility and LOW permeability are most likely to show a food effect
|
|
Order routes of administration from fastest to slowest absorption rate
|
IV > SC > IM >PO
|
|
Which route of drug administration is safest for a low MOS (TI) drug?
|
IV
|
|
Will food increase or decrease drug exposure for a lipophilic drug?
|
increase
|
|
What organ is responsible for first pass metabolism?
|
liver
|
|
How can neutral species pass through membranes?
|
via passive transport
|
|
What are the barriers to distribution?
|
Endothelial barriers and barrier-restricted compartments
|
|
What are the factors affecting drug distribution?
|
Lipid solubility of the drug, tissue perfusion, tissue capacity, binding to plasma proteins
|
|
What are the organs with high tissue perfusion?
|
brain, kidney, liver, heart
|
|
What are the organs with medium tissue perfusion?
|
muscle, skin
|
|
What are the organs with low tissue perfusion?
|
fat, skeleton
|
|
Why is transport important for drugs that target cell-surface receptors?
|
Oral drugs need to transport through the GI and drugs need to move from bloodstream to target tissue
|
|
Define Vd
|
Volume of distribution indicates the diffusion of drug into the body tissues at a certain time
|
|
How is Vd calculated?
|
total amnt of drug in the body (mg/kg) / plasma drug concentration = dose/ Cp
|
|
What does a large Vd result from? What does it indicate?
|
A low drug concentration in plasma relative to dose and indicates that the drug is distributed to the tissues
|
|
Organ toxicities are observed for drugs with large or small Vd?
|
large
|
|
_______ drugs often have large Vd values
|
Lipophilic
|
|
What plasma proteins are involved in drug binding?
|
Albumin (binds acidic and neutral drugs), alpha-1-acid glycoprotein, lipoproteins
|
|
What effect does drug binding to plasma proteins have?
|
Plasm protein binding affects tissue distribution and pharmacologic activity; protein bound drug is not absorbed from the plasma or metabolized; protein bound drug acts as a time release
|
|
What factors affect protein binding?
|
Age, pregnancy, species --> end effect is different exposure for patient
|
|
What parameters does protein binding affect?
|
Vd, Cmax, T1/2, CL, AUC
|
|
What's fu?
|
Fraction unbound = unbound drug concentration / total drug concentration
|
|
What's a higher fu value indicate?
|
More free drug in plama (not bound to protein)
|
|
What type of substances diffuse across brain capillaries? Which types are restricted?
|
Highly lipid soluble substances diffuse across brain capillaries. Water soluble or ionized molecules are restricted from diffusion across brain capillaries.
|
|
What results in breakdown of the BBB?
|
inflammation
|
|
What type of drugs do not easily pass through the placenta?
|
highly polar agents
|
|
What does the MDR1 gene code for?
|
P-glycoprotein, a drug transport pump that plays an impotant role in limiting drug absorption and distribution (especially to brain) and enhancing excretion of drugs
|
|
What is the effect of an MDR1 mutation?
|
defective ability to limit drug absorption and distribution and delayed excretion
|
|
What is P-gp?
|
an efflux transporter that pumps xenobiotics out of cell or compartment
|
|
Where are P-gp efflux transporters found? And where do they xenobiotics get pumped?
|
intestinal epithelium pumped to intestinal lumen, capillary endothelial cells of BBB pumped to capillary, liver cells to bile ducts, proximal tubule of kidney pumped to urine collecting ducts
|
|
For P-gp substrates, what effect will inhibition of P-gp have on drug exposure?
|
increased exposure
|
|
For P-gp substrates, what effect will induction of P-gp have on drug exposure?
|
decreased exposure
|
|
What are some examples of P-gp substrate drugs?
|
Ivermectin, digoxin, fexofenadine, vincristine
|
|
What are the routes of elimination for drugs?
|
Renal excretion, biliary and fecal excretion, and other (sweat, saliva, tears, milk)
|
|
What are the three forms of renal excretion?
|
glomerular filtration, active tubular secretion, passive tubular secretion
|
|
T/F Protein bound drug will be excreted through the glomerulus
|
False! protein bound drug is not excreted in glomerular filtration
|
|
Passive excretion is dependent on ________ and ______
|
urine flow and pH
|
|
Explain biliary excretion.
|
Liver cells transfer drug from plasma to bile
|
|
What types of drugs are excreted by mammary glands?
|
organic bases and antibacterial agents
|
|
Salivary excretion may be significant in ________
|
ruminants
|
|
The lung is the major organ of excretion for ______________
|
volatile substances
|
|
Excretion of highly lipid-soluble drugs that are not extensively metabolized is via ______ _______ ______
|
passive intestinal excretion
|
|
Define clearance
|
irreversible elimination of drug from systemic circulation
|
|
How is clearance expressed?
|
as a rate
|
|
What does a larger clearance indicate?
|
faster drug elimination
|
|
What is Kel or lz?
|
the elimination rate constant = -CLt/Vd
|
|
Define AUC |
drug/plasma exposure
|
|
How do you calculate total body clearance CLt?
|
dose/AUC
|
|
How do you calculate DR?
|
Maintenance dose rate (DR) = CL*Css
|
|
What does CL depend on?
|
rate of hepatic blood flow
|
|
Define instrinsic clearance?
|
intrinsic ability of the liver to eliminate drug (enzymatic rate)
|
|
Define half-life
|
time it takes half of the drug concentration to clear
|
|
What does half life depend on?
|
drug distribution (Vd) and elimination (CL)
|
|
Larger Vd will _____ T1/2
|
increase
|
|
Larger CL, will _____ T1/2
|
decreased exposure
|
|
What is extraction ratio?
|
Concentration in artery - Conc in vein / conc in artery
|
|
What are the phases of metabolism?
|
Biotransformation and conjugation
|
|
What occurs in Phase 1 of metabolism and where?
|
biotransformation - oxidation, reduction, hydrolysis, hydration - in liver
|
|
What occurs in Phase 2 of metabolism?
|
conjugation - glucuronidation, glucose conjugation, acetylation, methylation, sulfate/amino acid/glutathione conjugation
|
|
What is the objective of metabolism and how is it acheived?
|
Objective is to increase the rate of excretion or elimination of various compounds from the body and is typically achieved by increasing water solubility
|
|
T/F Metabolites are always less active than parent drug
|
false, generally less active but sometimes more active (codeine --> morphine)
|
|
T/F Metabolites are sometimes equally potent to parent drugs
|
true (aspitin --> salicylic acid)
|
|
T/F All drugs are metabolized
|
False, some are not metabolized at all
|
|
T/F Some metabolites are more toxic than the parent drug
|
True, generally metabolites are less toxic but some are more toxic (acetaminophen)
|
|
What is the importance of Cytochrome P450?
|
Main enzyme involved in phase 1 (biotransformation) reactions
|
|
Define CYP substrate
|
drug metabolized by CYP
|
|
Define CYP inhibitor
|
drug binds CYP and interferes with CYP activity; slowly metabolized
|
|
Define CYP inducer
|
drug that increases body's production of CYP
|
|
T/F CYP inducers also often increase P-gp production
|
true!
|
|
Generally, do carnivores or herbivores have lower clearance of drugs.
|
Carnivores most likely due to CYPs
|
|
The following species have deficiencies in synthetic metabolism. Name the deficiency for dogs, cats, pigs.
|
dogs - acetylation; cats - glucuronidation; pigs - sulfation
|
|
Define Tao
|
dose interval
|
|
Define Cpss
|
plasma concentration at steady state
|
|
Target concentration (Css) is equal to
|
IV dose rate / CL
|
|
PO dose rate =
|
IV dose rate/ F (F=bioavailibilty)
|
|
How is Cpss calculated? May not need to know
|
(1.44 * T1/2 * F * dose)/(Vd * tao)
|
|
Loading dose =
|
Cpmax * Vd
|
|
How do you calculate dose? May not need to know
|
Cpmax * Vd * (1-e-kTao) or Cpmin * Vd * (ektao -1)
|
|
How do you calculate time to reach steady state?
|
5 * T1/2
|
|
Why should drugs with low theraputic indices be monitored? How are they monitored?
|
To decrease their frequency of toxicity and to increase their efficacy; monitoring is done by measuring plasma concentrations and adjusting dose to optimize therapy
|
|
When should samples for drugs with low theraputic indices be collected?
|
After absorption and distribution are complete
|
|
How does half-life affect how many monitoring samples should be collected?
|
Drugs with a long half-life or that are given by constant infusion, one blood sample is sufficient; for drugs with short half-life, 2 blood samples should be drawn (1 prior to next dose "trough" and one immediately after dose but after distribution "peak")
|
|
If a dose is doubled, how is withdrawl time affected?
|
Doubling dose increases withdrawl time by 1 half-life
|
|
What equation is used for dose adjustment after drug monitoring?
|
New dose = (Desired Cp/Observed Cp) * old dose
|
|
Give 2 reasons why cats should not be given Chloramphenicol
|
Cats are not capable of glucoronidation necessary to metabolize chloramphenicol therefore ~25% is excreted unchanged and its also toxic to humans leading to fatal aplastic anemia and reversible bone marrow suppression
|
|
T/F At steady state, each dose replaces the amount of drug eliminated during the previous dosage interval
|
true.
|
|
Why is steady state not reached immediately if the same dose is given and elimination capacity of animal remains stable>
|
with each successive dose, drug in plasma accumulates until the point where amount eliminated equals drug added to system
|
|
What is allometric scaling?
|
method used to determine dosing for different species
|
|
What is drug compounding?
|
manipulation of a drug beyond what is stipulated on the drug label (flavoring, mixing 2 drugs, diluting)
|
|
Who regulates compounding?
|
FDA and state govts
|
|
What should you look for when selecting a compounding pharmacy?
|
Compliant with US Pharmacopeial Convention standards, pharmacist is trained in veterinary compounding, registered with state board, vertification by Vet-VIPPS
|
|
T/F The federal regulation regarding compounding states that a FDA approved drug may be compounded when needed to adequately medicate a non-food animal diagnosed with a medical condition
|
true. not to save $
|
|
T/F Compounding can be ahead of time.
|
False. Compounding need to be done on an individual patient basis
|
|
T/F Formulation affects bioavailabilty and absorption
|
true!
|
|
Changing the formulation of a drug is especially risky for drugs with...
|
low TI, low solubility, low permeability
|
|
Zeros ____ not ____
|
Zeros LEAD not FOLLOW
|
|
The theraputic window is between?
|
MEC (minimum effective dose) and MTC (maximum tolerated dose)
|
|
Why would a cat with low body temp appear more sedated with a normal dose of sedative? What can be done in anticipation?
|
Enzymes are temp dependent so at lower temp, reaction rates are slower and less drug is metabolized; warming patient before sedative administration
|
|
T/F Large amounts of most drugs reach bile by diffusion
|
False, only small amounts of most drugs reach bile by diffusion
|
|
What types and sizes of drugs have reported active biliary secretion?
|
organis anions, cations and polar, uncharged molecules
|
|
What are the pharmological effects of enterohepatic circulation?
|
creates a reservoir of recirculating drug (~20% of drug in body) and prolongs the duration of action of such drugs
|
|
What is the effect of Cyp inhibitors on first pass metabolism?
|
Cyp inhibitors (ex: grapefruit juice) decrease metabolism of certain drugs increasing serum levels thus decreased first pass metabolism effect
|
|
What does the Food, Drug and Cosmetic Act of 1938 do?
|
Created FDA and does not allow marketing of drugs unless proven safe
|
|
What does the Durham-Humphrey Amendment of 1951 state?
|
Creates 2 classes of drugs OTC drugs with adequate direction for use and medically supervised Rxs
|
|
What amendment requires drugs marketed in Us to be safe and effective?
|
Kefauver-Harris Amendment of 1962
|
|
Which amendment allows generics?
|
Waxman-Hatch Amendment of 1987
|
|
Which amendment involves use in animals?
|
1968 Amendment - do not produce residues in food manufactured from treated animals
|
|
What is the backbone for veterinary use of pharmeceuticals?
|
American Medicinal Drug Use Clarification Act of 1994 (AMDUCA)
|
|
What does the Animal Drug Availability Act of 1996 do?
|
Allows flexibility in product dosing - Veterinary Feed Directive allows vets to use drugs in animal feeds
|
|
What is the FDA Modernization Act of 1997?
|
any drug considered new has to be feild tested
|
|
What is the effect of the Medicare Modernization Act of 2003?
|
back-order of meds
|
|
What are Fast Track Products?
|
Investigational drug may be fast-tracked for use in terminal patient
|
|
What is a supplemental NDA (new drug app) used for?
|
changes to product
|
|
What is a conditional NDA (new drug app) used for?
|
minor use or use in minor species or conditional approval for rare disease or rare species
|
|
What makes a drug a controlled substance?
|
drug carries divergent or abuse potential
|
|
Who handles most controlled substance investigations?
|
State level, DEA focuses on high-level case investigations
|
|
What are the penalties of Federal Controlled Substance Act violations?
|
civil, criminal charges, loss of liscensure
|
|
Explain the closed system concept
|
responsibility falls on DVM prescribing and on pharmasist filling prescription
|
|
T/F Federal and state controlled substance schedules always match.
|
False, they do not have to, follow more stringent!!
|
|
What CS schedules are used for medical treatment?
|
C II - CV
|
|
What CS schedule drugs have no medical use? Example?
|
C I - heroin
|
|
Describe some recent schedule changes in CS
|
Tramadol used to not be CS and is now C IV and hydrocodone used to be C III is now C II
|
|
What does extra-label mean?
|
Use of drug in an animal in a manner not in accordance with the approved labeling
|
|
AMDUCA allows extra-label use if what requirements are met?
|
Vet-Client-Patient relationship is established, animal will suffer or die if not treated, animal's food animal status is considered (no other options, withdrawl time established)
|
|
When is extra-label use unsafe?
|
used by lay person, used in or on animal feed, resulting residue presents risk to public health
|
|
Define prescription
|
an order for medication which is dispensed for a ultimate user
|
|
What is required information on a prescription?
|
patient's full name, species, owner's name, address, practitioner's name, address, phone #, DEA registration #, drug name, strength, dosage form, quantity, directions for use, number of authorized refills, DAW/NS, withdrawl time for food animal
|
|
What is not required on a prescription but should be included for dose verification?
|
patient's weight
|
|
For a Class II drug, in what amount of time must the Rx be filled? How many refills can be authorized? Can they be called in or faxed in?
|
No federal time limit in which Rx must be filled but no refills are allowed and the Rx must be written
|
|
For Class III-V, does a Rx need to be written? How many refills are allowed?
|
Can be written, faxed, electronic, phoned-in and up to 5 refills must be authorized within 6 months after issue date
|
|
Rx records must be kept for how many years federally and in OR?
|
Federal 2 years, OR 3 years
|
|
Where do axons of the somatic nervous system originate and what do they release?
|
axons originate at the spinal cord and release ACh at neuromuscular junction
|
|
Where do preganglionic neurons of the sympathetic nervous system originate and where do post-ganglionic neurons synapse?
|
pre-ganglionic neurons originate from the thoracolumbar region of SC and synapse with post-ganglionic neurons close to the spinal cord
|
|
Where do preganglionic neurons of the parasympathetic nervous system originate and where do they synapse with post-ganglionic neurons?
|
Pre-ganglionic neurons originate from the cranialsacral region of SC and synpase with post-ganglionic neurons close to the effector tissue
|
|
Neurons that release catecholamines are referred to as? What catecholamines are released at most post-ganglionic sympathtic neurons? CNS? Adrenal medulla? GI? kidney?
|
Adrenergic! post-ganglionic sympathetic neurons release NE: CNS releases DA, NE; Adrenal medulla releases EPI; GI and kidney release DA
|
|
Neurons that release ACh are called? And where are they found?
|
Cholinergic foud in preganglionic symp and PS, post-gang PS, at neuromuscular junctions and in the CNS
|
|
In general ___ receptors are excitatory and ___ receptors are inhibitory.
|
alpha adrenergic receptors are excitatory; beta adrenergic receptors are inhibitory
|
|
Where are alpha adrenergic receptors not excitatory?
|
in the gut
|
|
Where are beta adrenergic receptors not inhibitory?
|
beta1 receptors are excitatory in the heart
|
|
Presynaptic receptors are ____ and are acted on by ______ to decrease _______.
|
alpha2 adrenergic receptors, released NE, further NE release
|
|
Dopamine receptors produce _______ of renal, mesenteric and coronary vessels
|
vasodilation
|
|
Where are muscarinic receptors found?
|
post-ganglionic PS in heart, glands, smooth muscle
|
|
Where are nicotinic receptors found?
|
pre-ganglionic symp and PS located in ganglia, neuromuscular junctions
|
|
What receptors are found in the heart?
|
B1
|
|
What receptors are found in the blood vessels?
|
alpha 1/2 - contriction and beta 1/2 - dilation
|
|
What receptors are found in the GI tract?
|
alpha and beta
|
|
What receptors are found in the lung?
|
B2
|
|
What receptors are found in the eye?
|
a1, b2
|
|
What receptors are found in the urinary bladder?
|
a1, b1
|
|
What is NANC?
|
Non-adrenergic, non-cholinergic = Nitric oxide
|
|
Where is constitutive NO found?
|
neurons and endothelial cells
|
|
What effects does NO produce?
|
vasodilation, bronchodilation, neurogenic control of penile erection, neuronal control of GI function
|
|
What are sympathomimetics? sympatholytics?
|
sympathomimetics=adrenergic agonists; sympatholytics=adrenergic antagonists
|
|
What are parasympathomimetics? parasympatholytics?
|
parasympathomimetics=direct and indirect cholinergic agonists, parasympatholytics=cholinergic antagonists
|
|
What are ganglionic agonists and antagonists?
|
non-specific
|
|
Of xylazine, medtomadine and dexmedetomadine, which has cyp inhibition? which does not? which has species dosing variations?
|
medetomadine has cyp inhibition; dexmedetomadine does not and xylazine has variations in dosing among different species
|
|
What is the main difference between potentcy and efficacy?
|
Potentcy can be changed by increasing dose while increasing dose will not affect a drug's relative efficacy
|
|
What is a direct-acting drug?
|
A drug that acts on the target receptor
|
|
What is an indirect-acting drug?
|
A drug that acts at the release site of the signal
|
|
What are mixed-acting drugs?
|
A drug that works at either release site or at receptor site
|
|
Examples of Sympathomimetic drugs
|
epinephrine, dopamine, dobutamine, isoproterenol, terbutaline, phenylpropalamine
|
|
Examples of Sympatholytic drugs
|
phenoxybenzamine, yohimbine, propanolol, atenolol
|
|
What effects do sympathomimetic agents produce?
|
peripheral excitatory and inhibatory actions, cardiac excitatory actions, glycogenolysis, fatty acid mobilization, ENS excitatory actions
|
|
What are the mechanisms of action of sympathomimetics?
|
direct stimulation of alpha & beta receptors; inhibit NE reuptake; increased release NE; inhibition of MAO (monoamine oxidase)
|
|
What is the consequence of inhibition of NE reuptake into the presynaptic terminal?
|
Increased NE levels in the synapse
|
|
What is the consequence of inhibition of MAO?
|
leads to accumulation of NE and EPI
|
|
How are isoproterenol and norepinephrine related?
|
Isoproterenol is a synthetic derivative of norepinephrine
|
|
How are sympathomimetics generally administered and why?
|
IV; because poorly absorbed PO due to rapid metabolism and SC, IM d/t vasoconstriction
|
|
Do sympathomimetics cross the BBB?
|
No
|
|
How are sympathomimetics eliminated?
|
Rapidly diffuse out of the synapse, uptake into presynaptic and effector cells, metabolized by MAO and COMT
|
|
Of NE, EPI, ISO, DA, which is mixed acting? What are all the others?
|
DA (dopamine) is mixed acting, and all others are direct-acting
|
|
What tissue are alpha receptors found and what is the response to activation?
|
Alpha receptors are found in the blood vessels and activation results in vasoconstriction
|
|
What tissue are the beta1 receptors found and what is the response to activation?
|
Beta1 receptors are found in the heart and activation results in positive inotropic and chronotropic effects
|
|
What tissue are the beta2 receptors found and what is the response to activation?
|
Beta2 receptors are found in the blood vessels and activation results in vasodilation
|
|
Which sympathomimetic decreases blood pressure?
|
Isoproterenol
|
|
Which sympathomimetic increases peripheral resistance?
|
Epinephrine
|
|
What are some adverse effects of sympathomimetics?
|
Anxiety, restlessness, excessive pressor responses, cardiac arrythmias, cerebral hemorrhage
|
|
What are the theraputic indications of Epinephrine?
|
bronchospasm, cardiac resuscitation, hypersensitivity, anaphylactic shock, vasoconstriction to prolong local anesthetics, localized hemorrhage
|
|
What are the theraputic indications of Isoproterenol?
|
cardiac stimulant in heart block, bronchospasm
|
|
What are the theraputic indications of dopamine?
|
hypotension/shock, acute heart failure
|
|
Tell me all about Dobutamine
|
direct alpha 1 agonist and antagonist, B1 agonist results in inotropic effects thus CO increased; for short-term tx of heart failure
|
|
Let's talk about selective Beta2 agonists
|
terbutaline, clenbuterol; direct B2 agonists; relax vasculature, uterine, bronchial smooth muscle; tx for bronchospasm and labor prevention (tocolysis)
|
|
Important things about Phenylpropanolamine
|
indirect agent that promotes release of endogenous NE that increases heart rate, contractility, blood pressure, peripheral resistance and smooth muscle contraction to tx incontinence and nasal decongestant
|
|
Tell me all about yohimbamine
|
competitive and selective antagonist of a2 receptors that stimulates CNS, increases HR, BP, insulin release; used for reversal of anesthesia/sedation induced by a2 agonists
|
|
Tell me about Phenoxybenzamine
|
irreversible inhibition of alpha receptors (a1>a2) that decreases peripheral resistance --> hypotension (reflex tachycardia); decreases urethral tone to tx urethral obstruction; dx pheochromocytoma and tx associated hypertension
|
|
Important things about propanolol
|
competitive and non-selective antagonist of B2 receptors that negatively affects HR, CO, conductance and automaticity; used to tx cardiac arrythmias, thyrotoxicosis and hypertension associated with pheochromocytoma
|
|
What type of effects do parasympathomimetic agents produce?
|
peripheral excitatory actions, cardiac inhibitory actions, rarely CNS excitatory actions
|
|
What receptors mediate peripheral excitatory actions of parasympathomimetics?
|
muscarinic receptors except nicotinic on skeletal muscles
|
|
What receptors mediate cardiac inhibitory actions produced by parasympathomimetics?
|
muscarininc receptors
|
|
Why are CNS excitatory actions rare with parasympathomimetics? Which type may produce CNS excitatory actions?
|
Rare d/t BBB, cholinesterase inhibitors may cause excitement followed by depression
|
|
What are the mechanisms of action of parasympathomimetics?
|
direct stimulation of muscarinic and nicotinic receptors; and indirect action involving inhibition of cholinesterases
|
|
What are the attachment sites for ACh on acetylcholinesterase?
|
esteratic site and anionic site
|
|
How do AChE inhibitors prevent metabolism of ACh?
|
AChE inhibitors prevent deacylation of ACh by binding to either or both the esteratic and/or anionic sites of AChE. May be reversible or irreversible.
|
|
What binds irreversibly to only the esteratic site?
|
organophosphates
|
|
What do the effects of cholinergic agents depend on?
|
Concentration used and whether ganglionic receptors are affected
|
|
Lets talk about atenolol
|
competitive and selective antagonist of B1 receptors that decrease HR, CO and BP for TX of cardiac arrythmias, hypertrophic cardiomyopathy, hypertension
|
|
What is Bethanechol?
|
choline ester related to ACh but more slowly metabolized produces muscarinic activity such as increased GI motility and secretion, urinary bladder contraction and sphincter relaxation used to stimulate bladder contractions
|
|
Tell me about Pilocarpine
|
natural alkaloid with direct muscarinic and nicotinic
|
|
Let's talk about Neostigmine
|
reversible, competitive inhibition of AChE via carbamylation producing increased GI motility & secretion, muscle fasciculations, miosis for reversal of tubocurarine-like neuromusclular blockade, paralytic ileus, atony of urinary bladder, myasthenia gravis
|
|
What about edrophonium and pyridostigmine?
|
reversible inhibition of AChE producing increased GI motility & secretion, muscle fascilutaions, miosis for reversal of turbocuranine-like neuromuscular block and dx (edrophonium) and tx (pyridostigmine) of myasthenia gravis
|
|
Of edrophonium and pyridostigmine, which is short-acting and which is relatively long-acting?
|
Edrophonium is short-acting and pyridostigmine is long-acting
|
|
Let's chat about atropine
|
plant alkaloid that competitively inhibits muscarinic receptors to produce mydriais, cylopeglia, tachycardia, decreased GI tone, decreased salivary, sweat & resp secretion, bronchodilation that is used for presnesthetic agent, bradycardia (sinus bradycardia, sinoatrial arrest, incomplete heart block), tx of anticholinesterase toxicity, myadriasis for eye exam
|
|
What else can be used to induce myadriasis for eye exam?
|
Tropicamide
|
|
What is propantheline?
|
antimuscarinic similar to atropine except it does not cross the BBB used for antipasmodic and antisecretory actions for diarrhea
|
|
Tell me about glycopyrrolate
|
antimuscarinic similar to atropine except it does not cross the BBB used as preanesthetic agent, tx for sinus bradycardia (SA arrest, incomplete AV block), and in conjunction with neostigmine for reversal of tubocurarine-like neuromuscular block
|
|
What is pralidoxime?
|
Selective antidote for organophosphate poisoning |