Reading...
Play button
Play button
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;
295 Cards in this Set
- Front
- Back
|
why is regulation important?
|
protection of our food supply, maintaining efficacy of important human drugs, maintain integrity of the veterinary profession
|
|
|
true or false: US food supply is safest and most available food supply in the world
|
TRUE
|
|
|
avoiding __________is critical to maintaining a safe food supply
|
residues from drugs/chemicals
|
|
|
what is the reason for many of the regulations governing antibiotics?
|
maintaining efficacy of important human drugs
|
|
|
there are concerns that antibiotic use in food animals leads to the development of:
|
resistant human pathogens
|
|
|
what is the primary goal of food animal drug regulations/
|
residue avoidance
|
|
|
why are residues a concern?
|
direct toxic/allergic affects, genotoxicity, mutagenicity, potential carcinogenicity, reproductive and developmental toxicity, adverse affects on normal human intestinal flora
|
|
|
what is the primary method of residue avoidance?
|
observance of appropriate withdrawal times following any drug use in food animals
|
|
|
define withdrawal time
|
time from last drug administration until the animal or animal products can be legally marketed
|
|
|
the withdrawal time is the time
|
required for 99% of the animals to deplete a drug or its metabolites given at label dosage to less than the established tolerance limit in the target tissues
|
|
|
define tolerance limit
|
the maximum level of the drug that has been determined to be safe for human consumption
|
|
|
_____ is determed by the TOL and the time it takes for the drug to deplete to a level less than the TOL
|
withdrawal times
|
|
|
what is useful for estimating withdrawal period?
|
the half life (T1/2)
|
|
|
after _____ T1/2s, 99.9% of the drug will be eliminated
|
10
|
|
|
ELDU
|
extra label drug use
|
|
|
what legislation permits ELDU?
|
AMDUCA- 1994
|
|
|
when can a drug be used extra label?
|
when there is a valid VCPR, the drug is approved for another purpose, it is used for therapeutic purposes, use does not result in violative residue
|
|
|
what does ELDU not apply to?
|
feed additives
|
|
|
is ELDU allowed for all drugs?
|
No
|
|
|
what is a therapeutic purpose?
|
the animal must be at risk of suffering or death if not treated-- cannot be for production purposes
|
|
|
how can a vet determine WDT for ELDU?
|
consult literature, develop based on available PK/PD data (research, other countries, etc)
|
|
|
simple rule of thumb for determining WDT for ELDU?
|
10x the elimination half life in the species and tissue of interest (t1/2 will vary depedning on dose, route of administration and target tissue)
|
|
|
possible scenarios where a drug might need to be used Extra label?
|
need for increased dose, animal has altered metabolism due to dz state, administration to a species not included on the label, etc.
|
|
|
FARAD
|
food animal residue avoidance and depletion program
|
|
|
what is FARAD
|
resource provided by the USDA to assist veterinarians with determining appropriate WDTs for ELDU
|
|
|
when should FARAD be contacting?
|
before using the drug
|
|
|
what if sufficient data is not available to estimate WDT, and the ELDU has already occurred?
|
the animal is no longer eligible to be a food animal
|
|
|
when is compounding legal in food animal practice?
|
all requirements of routine ELDU must be met. No FDA approvaed drug in its available form will appropriately treat the patient, compounded product must be made from an FDA approved commercially available drug.
|
|
|
true or false: you can compound a human a drug even if an animal approved drug is available
|
FALSE
|
|
|
who can perform compounding?
|
licensed vet, or licensed pharmacist on the order of a vet
|
|
|
can a pharmacist establish WDT for a compounded drug?
|
no, must be a veterinarian
|
|
|
can you generally compound a specific antidote from bulk substances?
|
yes
|
|
|
true or false: compounding should be very common in food animal practice
|
FALSE
|
|
|
what are feed additives?
|
substances added to feed to improve performance; prevent, control or treat dz; improve nutrient utilization; parasite control
|
|
|
medicated feed
|
any manufactured or mixed feed containing drug ingredients intended to promote growth or feed efficiency or to cure, mitigate, prevent or treat diseases in animals other than humans
|
|
|
category 1 drug
|
any drug that does not require a withdrawal period when used at the lowest continuous use level in all approved species
|
|
|
category 2 drug
|
any drug that requires a withdrawal period when used at the lowest continuous-use level in all approved species
|
|
|
type A medicated feed
|
a concentrated form of a medicted feed additive, consists of the drug and a carrier agent; used to make other medicated feeds
|
|
|
type B medicated feed
|
medicated feed containing an animal drug and a substantial amount of other nutrients, can be used to make other medicated feeds
|
|
|
type C medicated feed
|
medicated feed intended to be a complete feed, can be fed as the sole ration, top dressed, or free choice (not free choice blocks or minerals)
|
|
|
is extra label use of feed additives allowed?
|
no
|
|
|
why would antimicrobials be used sub-therapeutically?
|
to improve growth rate and feed efficiency, to prevent or reduce the incidence of a particular disease
|
|
|
what are the concerns with sub-therapeutic antimicrobials?
|
may lead to antibiotic resistance in human pathogens
|
|
|
VFD
|
veterinary feed directive- mediated feed that must be prescribed
|
|
|
MUMS act
|
minor use/minor species, passed in 2004
|
|
|
What does MUMS do?
|
provide incentives for companies to develop new drugs for minor uses in major species or for use in minor species.
|
|
|
what are major species?
|
dogs, cats, horses, pigs, cattle, turkeys
|
|
|
MUMS relevance to feed additives
|
ELDU of medicated feeds in minor species is of low regulatory priority, but still not legal
|
|
|
true or false: FDA has the ability to choose to make use of certain drugs a low priority issue
|
TRUE
|
|
|
what does the FDA's ability to make drugs a low priority do?
|
reduces the risk of prosecution of other legal action
|
|
|
what is phenylbutazone prohibited in
|
dairy cattle- any cow over 20 months of age regardless of whether she is lactating or not
|
|
|
what is compounding?
|
mixing together approved drugs; changing the form of an approved rug, creating a product from bulk chemicals
|
|
|
are compounded drugs regulated?
|
no
|
|
|
what are some concerns with compounded drugs?
|
accurate concentration, accurate formulations, bioavailability, shelf life, sterility, pyrogens
|
|
|
is there a use for compounded drugs in veterinary medicine?
|
YES
|
|
|
the _____ of compounded drugs may be illegal and you are putting yourself at risk- you assume liability, and are unnecessariliy endangering your patients
|
misuse
|
|
|
in order to legally compound a drug:
|
there must be a VCPR, the health of the animal must be threatened or suffering or death may result from failure to treat; there must be no FDA approved commercially available drug that will appropriately treat the patient; the product must be made from an FDA approved commercially available animal or human drug; must be compounded by vet or pharmacist
|
|
|
efficacy of compounded vs commercial drugs
|
differ in bioavailability, efficacy, concentration, absorption, etc
|
|
|
rate of contamination in compounded drugs
|
can be as high as 80% of products are contaminated
|
|
|
choosing a compounded pharmacy
|
1) are they ethical? 2) is there a licensed pharmacist on site? 3) where are the bulk chemicals coming from? 4) what quality testing is being done on end products? 5) how are sterile drugs formulated? 6) is there appropriate product labeling?
|
|
|
what should you do to protect yourself when using compounded products?
|
keep records, doing rechecks, get signed client release
|
|
|
mechanisms by which ectoparasites affect animal health
|
physical damage and irritation to skin (loss of condition/loss of production), allergic reactions, disease transmission
|
|
|
types of antiparasitic agents
|
macrocyclic lactones, filpronil, organochlorines, pyrethroids, metaflumizone, oganophosphates, carbamates, imdacloprid, nitenpyram, insect development/growth regulators, acaricidal dips
|
|
|
major mechanisms of action of antiparasitic drugs?
|
ligand gated chloride channels, voltage gated sodium channels, nicotinic receptor agonists/antagonists, acetylcholinesterase inhibitors
|
|
|
ligands for invertebrate ligand gated Cl channels
|
glutamate and GABA
|
|
|
ligand gated Cl channels: response to ligand
|
hyperpolarization, inhibitory effect on nerves and muscle.
|
|
|
how does the parasiticidal work at the ligand gated Cl channels?
|
may act as an agonist or antagonist, generally results in parasite paralysis
|
|
|
what three agents work at ligand gated chloride channels?
|
macrocyclic lactones, fipronil, lindane
|
|
|
why arent these agents toxic to the host?
|
differences between vert/invert receptors, blood brain barrier and associated p-glycoprotein pumps
|
|
|
GABA is ligand for
|
ionotropic and metabotropic receptors
|
|
|
macrocyclic lactones MOA:
|
stimulation of ligand gated chloride channels
|
|
|
ivermectin is well distributed to most tissues except
|
the CNS
|
|
|
factors that affect drug dispostion
|
lipid solubility of the drug, tissue perfusion, tissue capacity, binding to plasma proteins
|
|
|
p glycoprotein pumps are at the ____ surface of the BBB
|
apical
|
|
|
selemectin distribution
|
into sebaceous glands
|
|
|
fipronil indication
|
a phenylpyrazole insecticide that inhibits GABA regulated chloride channels, causing excitation of the insect nervous system
|
|
|
organochlorine products
|
DDT, lindane
|
|
|
organochlorine MOA
|
lindane acts on the ligand gated choride channel
|
|
|
can lindane cross the BBB?
|
yes, highly lipophilic
|
|
|
voltage gated sodium channel
|
generates the action potential for nerve transmission. Parasiticidal MOA: prolongs the opening of channels, first causes repetitive discharge followed by parasite paralysis
|
|
|
what agents act at voltage gated sodium channels?
|
pyrethroids, mutaflumizone
|
|
|
why arent pyrethroids and metafluminzone toxic to the host?
|
rapid biotransformation to inactive forms by vertebrates, but can be toxic at higher doses
|
|
|
late generation pyrethroids MOA
|
exerts rapid adulticide action by modulating voltage gated NA channels
|
|
|
why are cats more sensitive to pyrethroids than dogs?
|
deficiency in glucuronidation
|
|
|
metaflumizone MOA
|
blocks the voltage gated Na channel
|
|
|
acetylcholinesterase
|
involved in neurotransmission, degrades Ach ending its effect
|
|
|
acetylcholinesterase inhibitor MOA
|
inhibits Ach-esterase, prolongs effect of Ach and nerve stimulation
|
|
|
why arent acetylcholinesterase inhibitors toxic to the host?
|
P=S must be convereted to P=O for full action, and this conversion happens less in vertebrates. Verts also have faster elimination
|
|
|
topical and oral formulations of organophosphates use what MOA?
|
irreversible inhibition of acetylcholinesterase
|
|
|
toxicity of topical and oral formulations of organophosphates
|
muscarinic effects (SLUDD) due to acute intoxication, nicotinic effects ( fasciculations, bradycardia, respiratory muscle paralysis) CNS depression and seizures, organophosphate ester induced delayed neuropathy
|
|
|
treatment of organopshosphate toxicity
|
treat cholinergic signs with high dose atropine, treat nicitonic signs with pralidoxime,
|
|
|
carbamate MOA
|
reversible inhibition of acetylcholinesterase
|
|
|
carbamate toxicity
|
acute intoxication manifests as a combo of nicotinic and muscarinic effects (SLUDD), seizures/respiratory failure
|
|
|
ligands for nicotinic acetylcholine receptors
|
Ach, nicotine
|
|
|
response to ligand
|
neurotransmission
|
|
|
parasiticidal MOA
|
inhibitory or partial agonsist of insect receptors, hyperstimulation of nerves
|
|
|
what are the neonicotinoid agents that act at nicotinic acetylcholine receptors?
|
imadocloprid, nitenpyram, spinosad
|
|
|
why arent neonicotinoids toxic to host?
|
they have greater affinity for insect nicotinic receptors than for vertebrate
|
|
|
imidacloprid
|
a neonicotinoid insecticide. MOA is irreversible binding to nicotinic receptors prevents acetylcholine binding
|
|
|
nitepyram (capstar)
|
flea control. MOA is to bind and inhibit nicotinic receptors, interfereing with nerve transmission and leading to rapid flea death. Oral administration
|
|
|
spinosad (comfortis)
|
flea control. MOA is to bind and inhibit nicotinic receptors, interfereing with nerve transmission and leading to rapid flea death. Oral administration
|
|
|
spinosad toxicity
|
GI upset, interaction with high dose ivermectine, lower seizure threshold
|
|
|
ligands for nicotinic acetylcholine receptors
|
Ach, nicotine
|
|
|
lufenuron
|
insect development inhibitor for feal control . MOA is disruption of the synthesis and deposition of chitin, resulting in ovicidal and larvicidal activity. No direct adulticidal activity
|
|
|
lufenuron disposition
|
high lipophilicity, accumulation in fat tissues and then slowly released into blood
|
|
|
methoprene
|
an insect development inhibitor, mimics insect growth hormone, acting on eggs and larvae to prevent development
|
|
|
amitraz
|
formamidine acaricide, MOA is unique agonist of insect nervous system, but exerts alpha 2 agonist activity in the host.
|
|
|
amitraz is well tolerated by most species except
|
gcats
|
|
|
lime sulfur dips are primarily used for
|
dermatophytosis, sarcoptic mange, demodecosis
|
|
|
what should be done prior to the initiation of prophylactic therapy
|
animals should be tested for the presence of microfilaria to avoid adverse hypersensitivy reactions
|
|
|
what should be done in infected animals prior to initiatd prophylactic therapy?
|
removal of adult heartworms and microfilariae
|
|
|
what should you do if you miss 1 dose of HW preventative?
|
continue the next month as planned
|
|
|
what should you do if you miss 2 or more doses of HW preventative?
|
retest
|
|
|
heartworm adulticide
|
melarsomine dihydrochloride (immiticide)
|
|
|
drug class that treats microfilariae
|
macrocyclic lactones
|
|
|
three drugs that can be used for prophylaxis
|
ivermectin, selamectin, milbemycin oxime
|
|
|
melarsomine dihydrochloride mechanism of action
|
an orgenic arsenical, exact MOA is unknown. Kills L5 - ault parasites (those greater than 4 months of age)
|
|
|
melarsomine dihydrochloride indication and dose
|
approved for the treatment of dirofilaria immitis in dogs. 2.5mg/kg IM 2x, 24 hours apart
|
|
|
how is melarsomine absorbed after IM injection?
|
very rapidly
|
|
|
what is the bioavailability of melarsomine after im injection?
|
high
|
|
|
what results in higher plasma concentrations of melarsomine for a longer duration?
|
slower clearance and less RBC binding
|
|
|
what type of therapeutic index does melarsomine have?
|
narrow
|
|
|
melarsomine toxicity
|
related to pulmonary thromboembolism and arsenical toxicity
|
|
|
how can melarsomine toxicity be reversed?
|
using the chelating antidote- dimercaprol
|
|
|
how does melarsomine compare to thiacetarsemide?
|
melarsomine has 2x the therapeutic index, 5% mortality in mildly/moderately affected dogs (compared to 30% with thiacetarsemide). 18% mortality in severely affected dogs (vs 50%)
|
|
|
Thiacetarsemide (caparsolate) was a strong
|
vesicant
|
|
|
what Is a vesicant?
|
a substance or medication that causes necrosis of any tissue it touches outside of the blood stream
|
|
|
MOA of macrolides
|
bind to ligand gated Cl channels, causing hyperpolarization and paralysis
|
|
|
what is ivermectin indicated for
|
prophylaxis against dirofilaria immitis in dogs. .006mg/kg PO monthly
|
|
|
what does ivermectin combined with pyrantel pamoate treat?
|
GI nematodes
|
|
|
what will ivermectin treat in cats?
|
prevent dirofilaria immitis, control immature and adult hookworms
|
|
|
ivermectin dose in cats?
|
24ug/kg PO monthly
|
|
|
ivermectin disposition
|
bioavailability high (95%), well distributed to most tissues except the CNS. Primarily eliminated unchanged in the feces
|
|
|
what is the T1/2 of ivermectin?
|
48 hours
|
|
|
what breeds can heartgard be used in?
|
all
|
|
|
what breeds may have adverse reactions to higher doses of ivermectin? What are these reactions?
|
Collie-type breds. Mydriasis, ataxia, tremors, paresis, recumbency, stupor, coma
|
|
|
mydriasis
|
pupillary diliation
|
|
|
is ivermectin teratogenic?
|
no
|
|
|
how old must a dog be to receive ivermectin?
|
6 weeks
|
|
|
milbemycin indication and dose
|
prophylaxis against dirofilaria immitis in dogs.control of a. caninum, t. canis, t. leonina, and t. vulpis. .5mg/kg PO at montly intervals
|
|
|
what can milbemycin be combined with to increase spectrum to include external parasites such as fleas
|
lufenuron
|
|
|
toxicity of milbemycin?
|
safe in all breeds over 4 weeks. Safe in pregnant and nursing animals
|
|
|
selamectin indication and dose
|
dirofilaria immits, control of fleas/ar mites in dogs and cats. Sarcoptic mange and ticks in dogs. Hooks and rounds in cats. Dose: 6 mg/kg topcailly monthly
|
|
|
moxidectin
|
proheart- dirofilaria immitis in dogs. Advantage- dirofilaria, fleas, nemotodes
|
|
|
when is proheart counterindicated?
|
in sick, debilitated or underweight animals, animals with a history of weight loss, or animals that have been vaccinated in the past month.
|
|
|
why is proheart considered risky?
|
because it is in the muscle, there is no way to reverse it or remove it should a problem arise
|
|
|
interceptor is effective agaisnt
|
dirofilaria l4 larvae, trichuris, toxocara, toxascaris, ancyclostoma
|
|
|
what is heartgard effective against
|
dirofilaria l4 larvae
|
|
|
what is nemex effective against?
|
toxocara, toxascaris, ancylostoma, uncinaria
|
|
|
heartgard plus is effect agaisnt
|
dirofilaria l4 larvae, toxocara, toxascaris, ancylostoma, uncinaria
|
|
|
revolution is effective against
|
dirofilaria l4 larvae
|
|
|
what is the susceptibility gap?
|
the treatment gap when d. immitis are not considered to be susceptible to either treatment (macrocyclic lactone or melarsomine)
|
|
|
antinematodal agents
|
benzimidazolse, nicotine like paralytic agents, heterocyclic compounds, macrolides, lactrophilin rc
|
|
|
antitrematodal agents
|
clorsulon, albendazole
|
|
|
anticestodal agents
|
praziquantal, epsiprantal
|
|
|
benzimidazole examples
|
fenbendazole, albendazole, mebendazole
|
|
|
benzimidazole MOA
|
binding to nematode b-tubulin prevents its polymerization during microtubule assembly
|
|
|
benzimidazole indication
|
approved for tx of nematodes, cestodes and trematodes
|
|
|
are benzimidazoles absorbed from host GI tract
|
poorly except for albendazole
|
|
|
albendazole may be ___ and ____
|
teratogenic and fetotoxic
|
|
|
nicotine like paralytic agent examples
|
pyrantel, levamisole
|
|
|
nicotine like paralytic agent MOA
|
cholinergic agonist (nicotine like action)- causes neuromuscular junction depolarization. Acts on all sites served by ACh as a neurotransmitter (autonomic ganglia, carotid and aortic bodies, NMJ)
|
|
|
nicotine like paralytic agent indication
|
approved for the tx of nematodes
|
|
|
pyrantel tartrate salt
|
strongid
|
|
|
pyrantel pamoate salt
|
nemex
|
|
|
which salt is well absorbed from GI tract?
|
tartrate salt
|
|
|
levamisole disposition
|
well absorbed from GI tract, rapid metabolism/elimination
|
|
|
levamisole toxicity
|
well tolerated at therapeutic dosages
|
|
|
levamisole is also used as an _______
|
immunostimulant
|
|
|
heterocyclic compound example
|
piperazine
|
|
|
heterocyclic compound MOA
|
ACh antagonist- causes neuromuscular hyperpolarization
|
|
|
piperazine disposition
|
well absorbed from GI tract, rapid elimination- primarily renal
|
|
|
macrolides example
|
ivermectin
|
|
|
ivermectin MOA
|
agonist at ligand gated chloride channels
|
|
|
ivermectin indication
|
use against nematodes, including GIT nematodes and migratory stages, and external parasites of a wide range of species
|
|
|
ivermectin therapeutic index
|
wide
|
|
|
what can result from ivermectin injections
|
pain, discomfort at injection site
|
|
|
can ivermectin be used in pregant and breeding animals?
|
yes
|
|
|
is ivermectio bioavailability higher in monogastrics or ruminants?
|
monogastrics
|
|
|
how is ivermectin eliminated?
|
metabolism and intestinal excretion
|
|
|
eprinomectin MOA is similar to other
|
avermectins
|
|
|
eprinomectin is approved for
|
GIT nematodes, lungworms, cattle grubs, lice, mange mites, and horn flies of beef/dairy cattle
|
|
|
what is the withdrawal time for eprinomectin?
|
none
|
|
|
moxidectin is more _________ than ivermectin
|
lipophylic
|
|
|
moxidectin is approved to treat
|
cattle: GIT nematodes, lungworms, cattle grbs, lice, mange mites, and horn flies. Horses: variety of nematodes and encysted cyathosomes. Dogs: HW prophylaxis. Also nematodes in sheep, cats.
|
|
|
emodepside indication
|
intestinal nematocide in cats
|
|
|
emodepside MOA
|
lactrophilin Rc
|
|
|
how is emodepside administrated?
|
topically
|
|
|
clorsulon indication
|
effective against mature (>14wk) and immature (>8 week) F. hepatica
|
|
|
clorsulon MOA
|
inhibits enzymes involved in the glycolytic pathway, depriving flukes of metabolic energy
|
|
|
closulon disposition
|
lipid soluble, well absorbed after oral dosing
|
|
|
what is clorsulon not labeled for use in?
|
dairy cattle
|
|
|
albendazole indication
|
nematodes, cestodes, protozoa, adult f. hepatica
|
|
|
albendazole toxicity
|
teratogenic in early pregnant animals
|
|
|
praziquantal and epsiprantal indications
|
cestodes of dogs, cats, horses
|
|
|
praziquantal and epsiprantal MOA
|
increased membrane permeability to calcium, results in spastic paralysis and vacuolization of worms
|
|
|
which worms on adults tapeworm stages only?
|
epsiprantel
|
|
|
praziquaantal disposition
|
good absorption after oral administration, extensive distribution including CNS
|
|
|
is epsiprantel absorbed?
|
no, retained in GIT
|
|
|
fenbendazole is effective against
|
monieza and taenia; not dipylidium
|
|
|
when is pyrantel effective against equine anoplocephala perfoliata
|
when given at 2x the nematode dose
|
|
|
does drug exposure create resistance?
|
no, instead it selects for survival of resistant organisms
|
|
|
the genetic diversity of an oganism is correlated with ____
|
resistance
|
|
|
mechanisms of resistance
|
alterations in the target molectle (b-tubulin for benzimdazoles; glutamate gated Cl channels for avermectins). Multiple drug resistant P-glycoprotein pumps in the apical membranes of worm digestive and excretory systems export drugs from cells
|
|
|
general factors promoting development of resistance
|
overuse of antiparasitics, failure to ID primary target species, use of inadequate dosage or rapid elimination resulting in suboptimal drug concentrations at siteoo of action
|
|
|
cost and time taken to develop new antiparasitic agents precludes reliance on:
|
approval of new mechanistic groups of agents
|
|
|
guidelines to prevent resistance
|
appropriate drug use, appropriate dosages, use of combination drugs, timing of treatment to maximize parasite killing, alternation of antihelmintics, rotation of pastures and age of animals on pasure, good pasture management
|
|
|
role of refugia and preventing resistance
|
refugia needs to be maintained- antihelmintic use during conditions of low refugia may increase resistance
|
|
|
what can be used to treat babesial infections in horses and dogs
|
imidocarb
|
|
|
imidocarb MOA
|
DNA effect on parasite
|
|
|
imidocarb toxicity
|
severely nephrotoxic when overdosed, anticholinesterase effects may also be seen
|
|
|
what is a labeled tx for giardia?
|
none in the US
|
|
|
what can be used extralabel to tx giardia?
|
fenbendazole (approved in europe), metronidazole,
|
|
|
which is more effective against giardia?
|
fenbendazole
|
|
|
EPM therapy (combination drug) and why
|
pyrimethamine + sulfadiazine;; sequential block of folic acid metabolism. TX for >120 days
|
|
|
pyrimethamine + sulfadiazine toxicity
|
anemia, leukpenia, diarrhea. Teratogenic
|
|
|
what other drugs can be used to treat EPM?
|
ponazuril, diclazuril
|
|
|
the first drug approved for use In EPM therapy
|
ponazuril
|
|
|
ponazuril toxicity
|
mild, loose feces
|
|
|
ponazuril and diclazuril are
|
benzeneacetonitriles
|
|
|
prophylactic coccidia tx
|
inhibit penetration/development of coccidia. Most effective means to reduce losses, morbidity due to coccidiosis.
|
|
|
metaphylaxis
|
treat entire susceptible group
|
|
|
treatment of clinical coccidiosis
|
treat by killing gamonts.
|
|
|
why is tx of clinical coccidiosis of limited value?
|
the coccidial life cycle is nearly complete, the mucosa is already damaged
|
|
|
when is treatment of clinical coccidiosis warranted?
|
during an acute outbreak to prevent further formation of occysts
|
|
|
what can be used for coccidia prophylaxis?
|
decoquinate, low dose amprolium, ionophores, sulfa drugs, benze acetonitriles (diclazuril)
|
|
|
what is used to treat coccidiosis
|
high dose amprolium, benze acetonotriles, sulfa drugs
|
|
|
are sulfa drugs very effective agaisnt gamonts?
|
no, but may prevent secondary bacterial ifnections
|
|
|
sulfonamide examples
|
sulfadimethoxine, sulfaquinoxaline
|
|
|
quinolone example
|
decoquinate
|
|
|
decoquinate MOA
|
interfere with cytochrome mediated electron transport in the mitochondria
|
|
|
decoquinate is a _____ agent. It actas only be inhibiting penetration of _____
|
prophylactic; sporozoites
|
|
|
amprolium
|
a structural analog of thamine that inhibits thaimine metabolism in coccidia. Prophylactic at lower doses, may inhibit sexual cycle at higher doses.
|
|
|
amprolium side effect
|
high dose may cause thiamine deficiency
|
|
|
ionophore examples
|
monensin, salinomycin, lasalocid,
|
|
|
how do ionophores work?
|
form complexes with cations, altering the permeability of biological membranes. Used prophylactically
|
|
|
can monensin be given to horses?
|
NO
|
|
|
halofuginone
|
anticoccidial in poultry, in cattle- cryptosporidium control in calves
|
|
|
immunostimulant that is also an antiparasitic
|
levamisole
|
|
|
in most species, sympathetic neurons innervating this particular effector release ACH to activate cholinergic rc on the effector cells. What is the end organ innervated by these sympatethic cholinergic neurons?
|
sweat gland
|
|
|
activation of a rc in the SNS is typically stimulatory except for those in the
|
GI tract
|
|
|
isorproterenol is used to treat bronchospasm due to its ability to
|
activate beta adr rc
|
|
|
pilocarpine is a direct muscarinic agonist. If instilled into the eye
|
contraction of the ocular sphincter m and ciliary muscle will occur
|
|
|
at low dosages, dopamine will
a) activate b1 rc in cardiac m b) incrase NE release in symp fibers innervating the heart c) increase renal blood flow through activation of D rc d) activate a1 rc in peripheral vessels e) all except d |
e) all except d
|
|
|
epi causes an increase in BP following system administration. Coexposure to an a blocker causes
|
hypotension because of a net incraesed activation of b2 rc by epi
|
|
|
ephedrine (mixed adr agonist) could be used:
|
dilate bronchioles, treat urinary incont, treat nasal congestion
|
|
|
drug to incrase bladder detrusor m motility
|
neostigmine
|
|
|
cat presents with excessive secretions, fasciculations, miosis, labored breathing with secretions. Atropine is administered and all signs except fasciculations improve. Most likely explanation?
|
c) cat was exposed to ACHE inhibiting insecticide
|
|
|
metaclopramide acts as a parasympathometic (prokinetic agent) it elieces this response by
|
directly activating serotonin rc in gi smooth m
|
|
|
atropine in horses
|
NO, causes colic
|
|
|
aminopentamide has a relative selectivity for muscarinic rc in the
|
GI smooth m
|
|
|
dysautonomia (SNS or PNS)
|
PNS
|
|
|
pelvic n is a
|
Parasym nerve that releases ACH
|
|
|
clenbuterol is a selective b2 rc agonist. Use when _______ is needed
|
decreased bronchial smooth m contractions
|
|
|
what drug would be expected to increase NE release by blocking adrenergic autoreceptors on SNS nerve terminals?
|
yohimbine
|
|
|
xylazine reversal
|
atipamezole
|
|
|
muscarinic agent in the eye can
|
incraese aqueous humor flow through trabecular meshwork/canal of schlemm
|
|
|
a2 rc agonist has beneficial properties in that it can
|
decraese sympathetic outflow from CNS
|
|
|
three basic systems regulating urethral sphincter mm contraction (sympathetic, parasymp and somatic) Parasymp innervation leads to a net
|
relaxation of the urethral smooth m
|
|
|
treatment of reduced GI peristalsis
|
metoclopramide
|
|
|
drug to treat paralytic ileus
|
neostigmine
|
|
|
drug should be avoidedi n horses with colic
|
atropine
|
|
|
dopamine is useful to treat shock because
|
it cincreased blood flow thru renal and selected other vascular beds
|
|
|
drug for urinary incontince
|
ephedrine
|
|
|
atenolol is a b1 rc antagonist. Used for
|
treating tachyarrythmia
|
|
|
which drug has a mixed action at b1 rc?
|
dopamien
|
|
|
why is local admin of epi useful for restricting systemic absorption of a local anesthetic?
|
activates a1 rc in the local region --> vasoconstriction
|
|
|
pressor response following ISO admin when an alpha adrenergic rc blocker (phenoxybenzamine)
|
alpha blocker essentially has no effect on the pressor response to isproterenol
|
|
|
dobutamine prominent pharm effect is to
|
increase myocardial contractile force
|
|
|
where will NO relax smooth m?
|
urinary sphincter
|
|
|
1) If a dog was being treated with an alpha adrenergic receptor blocker such as prazosin to treat hypertension, and came into the clinic with an apparent hypersensitivity reaction, you might give epinephrine to treat the hypersensitivity. If you did, what would likely happen to blood pressure:
|
It would decrease because of activation of beta 2 receptors and concurrent block of vessel alpha receptors
|
|
|
primary difference between adr and cholin synapses?
|
one uses transmitter reuptake, other uses enzymatic degregation
|
|
|
drug used for short term tx of heart failure
|
dobutamine
|
|
|
an organophosphorus pesticide acts as an
|
indirect agonist
|
|
|
how does atropine increase heart rate?
|
blocks muscarinic m2 rc at the sinoatrial node
|
|
|
NT inovlved in signalling at all autonomic ganglia is
|
acetylcholine
|
|
|
selective agent to treat tachyarrythmia
|
atenolol
|
|
|
a beta 2 rc to test for anhidrosis in hroses. To observe sweating:
|
give ID injection and observed localized response
|
|
|
effect of hexamethonoim on urine outlfow?
|
decrased
|
|
|
atropine is muscarinic rc blocker. Used to treat:
|
incontinence, mydriasis, GI spasms, insecticide poisoning
|
|
|
why is metoclopramide effective as a prokinetic?
|
increases cholinergic signalling in the myenteric plexus
|
|
|
a dog with dysautonomia would show
|
thickened secretions, decreased urination, vasoconstriction, photophobia, anorexia, weight loss
|
|
|
dex-medetomidine reversal
|
atipamezole because it blocks a2 rc
|
|
|
treatment of babesiosis
|
imidocarb
|
|
|
monensin in horses
|
cardiotoxicity
|
|
|
TX of clinical coccidiosis
|
diclazuril
|
|
|
prophylactic against coccidia
|
monensin, diclazuril, decoquinate
|
|
|
pyrethroid toxicity tx
|
symptomatic
|
|
|
pyretheroid antiparasitic MOA
|
voltage gated sodium channels
|
|
|
class of drugs poorly absorbed from gI
|
benzimidazoles (except albendazole)
|
|
|
teratogenic antiparasitical
|
albendazole
|
|
|
A. perfoliate tx
|
praziquantal, 2x pyrantel
|
|
|
1) While on emergency duty, you are presented with an eleven year old neutered collie dog, “Blue”, with tremors, agitation, and diarrhea. You get a careful history from the owners and note that Blue received an amitraz dip from his regular veterinarian earlier that day. In addition, the owners have brought a bag of medications that Blue received earlier today: fluoxetine (a selective serotonin reuptake inhibitor), ivermectin (heartworm prophylaxis), and silymarin (a nutraceutical for treatment of liver disease). Given this information, the most likely explanation/treatment recommendation for Blue’s current signs is:
|
serotonin syndrome, needs serotonin antagonist
|
|
|
endoectocide drug
|
macrocyclic lactones
|
|
|
1. the oral administration of netobimin (a prodrug for albendazole) to cattle results in which of the following pharmacokinetic patterns:
|
a. A prolonged elimination phase for albendazole metabolites in the digestive tract as compared to plasma.
|
