Term
| What are some of the meds to control fleas and ticks? |
|
Definition
-Organophosphates/carbamates
-amitraz
-pyrethrins/permethrins
-fipronil
-imidacloprid
-methoprene, pyriproxifen
-lufenuron
-nitenpyram
-spinosad |
|
|
Term
| What is the job of the FDA in regards to insecticides? |
|
Definition
-FDA regualtes ectoparaciticides with active ingredients that are systemically distributed
-classified as drugs |
|
|
Term
| What is the job fo the EPA in regards to insecticides? |
|
Definition
-regulates ectoparasiticides with active ingredients that do not exert effects by systemic absorption
-also concerned with environmental impact of chemical in question |
|
|
Term
| What is the general MOA of organophosphates and carbamates? |
|
Definition
| -parasympathomimetics that act as chilinesterase inhibitors |
|
|
Term
| Where do organophosphates and arbamates work in the insect? What about in the mammal? |
|
Definition
-in the insect: works at the cholinergic synapses in the cNS
-in mammal: could potentially work at para, symp, and CNS junctions |
|
|
Term
| What do organophosphates cause at the synaptic fleft? |
|
Definition
-inhibit action of AChE, thus there is an accumulation of AChE at the synaptic cleft
-this causes a continued depolarization of the post-synaptic membrane |
|
|
Term
| What are the physiologic effects or organophosphates? |
|
Definition
| -leads to continuous activation of nicitinic, muscarinic, and CNS cholinergic synapses that may progress to paralysis |
|
|
Term
| Do organophosphate bind irreversibly or reveresibly to AChE? What about carbamates? |
|
Definition
| -organophosphates bind irreverisbly while carbamates bind reversibly |
|
|
Term
| Which animals are more susceptible to organophosphates and carbamates? |
|
Definition
| -youg, old, debilitated, and cats |
|
|
Term
| What are the clinical signs of organophosphate/carbamate toxicity? |
|
Definition
-muscarinic, nicotinic, and CNS signs
-OP-induced delayed neuropathy
-pancreatitis |
|
|
Term
| What are the muscarinic signs due to organophosphates/carbamates? |
|
Definition
-SLUDDE: Salivation, lacrimation, urination, defecation, dyspnea, emesis
-bradycardia
-miosis
-as well as: anxiety, ataxia, abdominal pain, vomiting, diarrhea, seizures, genralized muscle weakness |
|
|
Term
| What are the nicotninic signs due to organophosphate/carbamate toxicity? |
|
Definition
-skiletal msucle fasciculations
-generalized msucle tetany, stiffness (Saw-horse stance)
-generlized weakness of limb, neck, and resp mm
-weakness wiht paresis
-paralysis secondary to inadequate repolarizaiton |
|
|
Term
| What is OP-induced delayed neuropathy? What are its symptoms? |
|
Definition
-develops several weeks after acute toxicity or after long-term low level OP exposure
-symptoms: weakness, ataxia, CP deficits of pelvic limbs |
|
|
Term
| Rate the most susceptible species to leadst for organophosphate/carbamate toxicity. |
|
Definition
| -chickens > cats > rodents |
|
|
Term
| HOw do we diagnose OP/Carbamate toxicity? Explain the test. |
|
Definition
-Atropine response test
-If msucarinic signs are present, give pre-anesthetic dose of atrophine and signs should mostly resolve if it is OP/carbamate toxicity |
|
|
Term
| How do we treat OP/CArbamate toxicity? |
|
Definition
-2-PAM is the specific antivodte
-can also give atropine to fix muscarinic effects but doesn't fix it long-term
-bathe with dish soap for dermal exposure
-give methobarbamol for tremors
-give diphenhydramine for nicotinic signs |
|
|
Term
| How do we give 2-PAM to treat OP/Carbamate toxicity? |
|
Definition
| -use lowest effective dose possible for 3 treatments and discontinue if no response |
|
|
Term
| What drugs should we avoid using iwht OP/Carbamate toxicity cases? |
|
Definition
| -Phenothiazine derivatives |
|
|
Term
| What are the two MOAs of Amitraz? |
|
Definition
-inhibits Monoamine oxidase
-Acts as an octopamine agonist |
|
|
Term
| Atropine inhibits monoaime oxidase. What does monoamine oxidase do? |
|
Definition
| -degrades the NT NE and serotonin, thus its inhibition results in an accumulation of these amines |
|
|
Term
| Atropine acts as an octopamine agonist. What does this do? |
|
Definition
| -increases nervous activity in ticks and mites and decreases feeding and reproductive behavior, ultimately resulting in death |
|
|
Term
| What species cannot receive amitraz? |
|
Definition
|
|
Term
| What is amitraz mainly used for? Where does toxicity originate in each of these cases? |
|
Definition
-generalized demodecosis: toxicity is from dipping
-tick repellence: toxicity is from collar ingesiton |
|
|
Term
| What are the clinical signs of amitraz toxicity? |
|
Definition
-sedaiton
-depression
-disorientation
-ataxia
-bradycardia
-hypotension
-hypothemia |
|
|
Term
| HOw do we treat Amitraz toxicity? |
|
Definition
-Detoxify: bathe, remove ingested collar
-Reverse effects with Yohimbine
-Supportive care |
|
|
Term
| What is the natural source of PYrethrins and Pyrethroids? |
|
Definition
|
|
Term
| What is the MOA of Pyrethrins and type I pyrehtroids? |
|
Definition
-keep Na chh open within neuronal memranes causing repetitive firing of nn
-insect effect is on peripheral and CNS |
|
|
Term
| What is the MOA of type II pyrehtroids? |
|
Definition
-hold Na ch open even longer htan type I
-psosible interfere with the binding of GABA and Glu Rc sites in the brain |
|
|
Term
| What is the major drawback to efficacy of pyrethroids? |
|
Definition
| -rapidly metabolized so some insects recover |
|
|
Term
| What are some synergists that are used to increase toxicity of pyrethroids? |
|
Definition
-piperonyl butoxide
-MGK264 |
|
|
Term
| What is the purpose of synergists used with pyrethroids? |
|
Definition
| -inibit mixed function oxidases thus extending the life of pyrethrins and pyrethroids in insets and mammals |
|
|
Term
| How are pyrethrins and pyrehtorids absormed? ARe they lipophilic or lipophobic? Why does this matter? |
|
Definition
-absorbed dermally, orally, and via inhalation]
-highly lipophilic thus they like to distribute to the fat, CNS, and PNS |
|
|
Term
| How are pyrethrins and pyrethroids eliminated? |
|
Definition
|
|
Term
| What is the deal with cats and pyrethrins and pyrethroids? |
|
Definition
| -cats re sensitive because they cannot effectively clear chemicals by hepatic glucuronidaiton |
|
|
Term
| What are the clinical signs of pyrethrin and pyrehtroid toxicity in the cat? |
|
Definition
-hyperesthesia
-generalized tremors
-msucle fasciculations
-hyperthermia
seizures |
|
|
Term
| HOw are cats usually poisoned by pyrethrins and pyrethroids? |
|
Definition
-usually by licensed dog roducts being applied to cats
-also by casual contact with dogs that are wearing them |
|
|
Term
| How do we treat pyrethrins/pyrethroid toxicity? |
|
Definition
-Methocarbamol/BArbituates, Propofol< Diaepam
-IVF
-Lipid emulsion if necessary
-Bathe if topically exposed
-NO ATROPINE |
|
|
Term
| Why is atropine contraindicated in the case of pyrethin/pyrethroid toxicity cases? |
|
Definition
| -it can produce CNS overstimulation |
|
|
Term
| What is fipronil used for? |
|
Definition
| -used for fleas and ticks in dogs and cats |
|
|
Term
| What is fipronil commonly combined with? |
|
Definition
| -Methoprene for additional control of immature flea stages |
|
|
Term
| What is the MOA of fipronil? |
|
Definition
-binds GABA Rc in insect neurons and blocking hte lfow of Cl
-blockage results in stimulation of CNS and death of the arthropod |
|
|
Term
| How do we not kill animals with Fipronil? |
|
Definition
| -has a much, much, much higher binding affinity for insects than mammals |
|
|
Term
| Why does fipronil not kill mammals? |
|
Definition
-lipid soluble thus does not readily penetrate skin and has slow oral absorption
-it is metabolized by liver and excreted in urine and feces |
|
|
Term
| What are the clinical signs of fipronil hypersensitivity? |
|
Definition
-erythema
-pruritus
-irritation
-alopecia |
|
|
Term
| What is the treatment for fipronil hypersensitivity? |
|
Definition
-topic OD: bathe with dishwashing detergent (Dawn)
-oral OD: dilute iwth milk or water
-hypersensitivity: symptomatic care: usually a antihistamine or corticosteroid |
|
|
Term
| In which common product is imidocloprid found? |
|
Definition
|
|
Term
| What is the use of imidocloprid? WHat is it commonlycombined with? |
|
Definition
-kill adult fleas and larvae on dogs and cats
-combined with permetrhin in DOGS ONLY to kill ticks |
|
|
Term
| What is the MOA of imidocloprid? |
|
Definition
-mimics the aciton of ACh but is not degraded by AChE by binding to post-synaptic nicotinic ACh Rc
-causes persistent activation, prevents impulse transmission, and ACh build-up |
|
|
Term
| What does imidocloprid cause in the insect? |
|
Definition
| -causes hyperexcitation, convulsions, paralysis and death |
|
|
Term
| Why does imidocloprid have a low toxicity in mammals? |
|
Definition
| -due to a higher concentration of nicotinic acetylcholine receptors in insects and higher affinity for insect rc |
|
|
Term
| What are the general effects of imidocloprid in the mammal system? |
|
Definition
-not systemically absorbed: spreads over skin by translocation and goes to hair follicles and glands where it is shed in sebum
-if ingested, absorbed quickly from GIT but is eliminated via urine
-has poor penetration into BBB |
|
|
Term
| What are the clinical signs of imidocloprid toxicity even though it is rare? |
|
Definition
-Topical: dermal sensitivity
-Oral: vomiting, drooling, oral ulcers (cats) |
|
|
Term
| How do we treat the rare case of imidocloprid toxicity? |
|
Definition
-Topical OD: bathe with dishwasing detergent
-Oral OD: dilute wiht milk/water
-Hypersensitiviy: symptomatic care, antihistamine, corticosteroids |
|
|
Term
| What do methoprene and pyriproxifen do? |
|
Definition
-juvenile hormone analogue that binds to insect juvenile hormone receptor sites
-however the structual differences protect them from enzyme degredataion thus they arrest flea development by preventing insects from molting to the next stage |
|
|
Term
| How are methoprene and pyriprxifen absorbed in the mammal? What symptoms may they cause? How do we treat them? |
|
Definition
-absorbed orally and dermally, rapid excretion in urine nand feces
-can cause: letharyg, ataxia, young are more susceptible
-supportive treatment if any |
|
|
Term
| What is hte MOA of Lufenuron? |
|
Definition
| -Fhitin synthesis inhibitor that is ovicidal and larvicidal |
|
|
Term
| How is lufenuron absorbed in the mammal? |
|
Definition
| -40% of oral dose is absorbed in SI, enhanced with fatty meal b/c it concentrates in fat |
|
|
Term
| How do we administer lufenuron? Why? HOw would we treat the issues? |
|
Definition
-give oral
-b/c injection can cause local reaction
-treat local reaction with supportive care |
|
|
Term
| IN which product is nitenpyram found? |
|
Definition
|
|
Term
| What is the MOA of mitenpyram? |
|
Definition
| -blocks the ability ofr neural messages to transmit thorugh the CNS of the flea, causing instant death |
|
|
Term
| Why does nitenpyram not really do anything in the mammal? |
|
Definition
-little to no binding on vertebrate peripheral ACh receptors
-fat absorption
-little to no tissue absorption
-eliminated in urine unchanges |
|
|
Term
| From what bacterium is the active ingredient in Spinsad from? |
|
Definition
| -soil-dwelling Saccharopolyspora spinosa |
|
|
Term
| What is the MOA of spinosad? |
|
Definition
| -acitvation of nicoitnic ACh Rc |
|
|
Term
| What happens to insects treated with spinosad? |
|
Definition
-involuntary mm contractions
-tremors
-prolonged hyperexcitation results in prostration, paralysis, and death |
|
|
Term
| HOw is Spinosad absorbed in the mammal? How is it eliminated? |
|
Definition
-oral absorption
-eleminated in feces via bile |
|
|
Term
| What are the potential adverse effects of Spinosad in the mammal? |
|
Definition
-vomiting
-lethargy
-ataxia
-anorexia
-tremors
-lethargy |
|
|
Term
| What other medication should you be cautious of administering with spinosad? |
|
Definition
-ivermectin
-if occurs: emesis, activated charcoal, and supportive care |
|
|
Term
| What are the macrolide antiparasitic agents? |
|
Definition
| -avermectins and limbemycins |
|
|
Term
| What are macrolides licensed for? |
|
Definition
| -HW prevention in dogs and cats, some are licensed for the threatment of otodectes and hookworms |
|
|
Term
| What are some extra label uses for macrolides? |
|
Definition
| -scavies, lice, cheyletiella, demodecosis, GI nematodes, and microfilaria |
|
|
Term
| Do mcacrolides have a wide or narrow margin of safety? |
|
Definition
|
|
Term
| What is the mOA of macrolides? |
|
Definition
-bind Glutamate-gated Cl chh that are specific to invertebrates
-this causes an influx of Cl ions into |
|
|
Term
| What is the MOA of Macrolides? What does this cause in the insect? |
|
Definition
-bind Glutamate-gated chloride channels specific to invertebrates
-this causes an influx of chloride ions into parasite neurons leading to hyperpolarization, paralysis, and death |
|
|
Term
| What in the mammal anatomically prevents macrolide toxicity? Elaborate. |
|
Definition
-BBB
-P-glycoprotiein pumps specifically |
|
|
Term
| What animals have issues with macrolides? |
|
Definition
-animals lacking the ABCB1 gene
-Collies, Aussies mostly |
|
|
Term
| What are some drugs that increase the chance of Macrolide sensitivity? |
|
Definition
-Cyclosporine
-Ketoconazole
-Verapamil
-Tamoxifen |
|
|
Term
| What is the common cause of dog/cat macrolide toxicity? |
|
Definition
| -incorrect use of large animal products |
|
|
Term
| What are the clinical signs of macrolide toxicity? |
|
Definition
-mydriasis
-depression
-disorientation
-coma
-tremors
-ataxia
-stupor
-emesis
-hypersalivation
-hyperasthesia
-death |
|
|
Term
| How do we treat macrolide toxicity? |
|
Definition
-emesis if within 30-60 mins
-activated charcoal
-symptomatic and supportive care
-cautious use of diazepam, barbituates, propofol
-Physostigmine
-Flumazenil |
|
|
Term
| What can we do to shorten the duration of therapy for macrolide toxicity? What will this do? |
|
Definition
-IV lipid emulsion therapy
-acts as a sink to draw in lipophilic xenobiotics into plasma lipid phase to remove from target tissue and increase elimination |
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