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Pharmacology drugs 2
CNS-Anesthesia
| Question | Answer |
|---|---|
| what is the oldest antiepilectic drug? | potassium bromide |
| how does bromide ion work as an antiepilectic? | it blocks the Cl- ion channels and is more permable than Cl- |
| Diazepam, aka valium, works as what? | anticonvulsant, anti-anxiety, muscle relaxant, appitite stimulant |
| how does diazepam work? | affects GABA binding and channel kinetics |
| how do barbiturates work? | change channel kinetics to increase the effects of GABA |
| what is the drug of choice for status epilepticus? | diazepam |
| why is diazepam such a good drug? | highly lipid soluble and crosses BBB |
| what drug is used when barbiturates fail? | KBr |
| how does levetiracetam work? | presynaptically |
| how do phenytoin and carbamazepine work? | limits frequency of Na channel opening by enchancing channel inactivation |
| how does zonisamide work? | reduces Ca+2 currents and increases Na+ channel inactivation |
| Which drugs are excreted largely unchanged by kidneys and used in animal with liver problems? | Bromide & levetiracetam |
| which compounds are commonly used in motivation, attention, and arousal are controlled by specific brain areas | Norepi, epi, serotonin, dopamine |
| which drugs are used as neuroleptics? | Phenothiazines - block multiple receptor types Acepromazine, chlorpromazine, azaparone Buterophenones - more selective for dopamine receptors Droperidol, haloperidol |
| how do neuroleptic drugs work? | block catecholamine receptors |
| how do Alpha-2 adrenergic neuro drugs work? | provides feedback inhibition of release |
| what are the alpha-2 adrenergic neuro drugs? | Xylazine, detomidine, medetomidine |
| what are the reversal letters of alpha-2 adrenergic drugs? | Yohimbine, telazoline, atapamazol |
| why do you give an animal endrophium? | to test if the animal has myasthenia gravis |
| how does the endrophium test work? | its a cholinesterase inhibitor and increases the amount of ACh and ACh receptors on the post-synaptic neuromuscular membrane |
| what is the gold standard test for myasthenia gravis? | measure for serum ACh antibodies |
| what are the side effects of the endrophium test? | SLUDD and bronchoconstriction |
| what are the two most common cholinesterase inhibitors used to treat MG? | pyridostigmine (PO) and neostigmine (IM) |
| what are the side effects of muscarinic receptors with cholinesterase inhibitors? | SLUDD, bradycardia, bronchoconstriction, weakness |
| what re the side effects of nicotinic receptors with cholinesterase inhibitors? | paradoxical muscle weakness |
| what do you use for immunomodulaiton of MG? | corticosteroids |
| what are the side effects associated with immunomodulation? | iatrogenic cushings, wasting, muscle weakness, pu/pd, polyphagia, personality changes |
| what are the treatment options for organophosphate toxicity? | atropine, diphenhydramine, 2-pam |
| what type of compound is atropine? | systemic use muscarinic cholinergic blocker |
| what type of compound is diphenhydramine? | systemic use nicotinic cholinergic blocker |
| what type of compound is 2-pam | cholinesterase enzyme reactivator |
| what genus of ticks causes tick paralysis in the US? | dermacentor |
| what genus of ticks causes tick paraylsis in Australia | ixodes |
| what are the indications for using a Neuromuscular blockind drug? | thoracotomy; obese animals intraocular surgeries; improve surgical access Reducing muscle contracture; endoscopy/intubation; balanced anesthesia |
| what must you keep in mind as far as precautions go when using Neuromuscular blocking drugs? | no analgesic properties ventilatory assistance required |
| what is the most common depolarizing neuromuscular blocking drug? | succinylcholine |
| what are the most common non-depolarizing neuromuscular blockind drugs? | pancuronium, atracurium, vecuronium |
| list, from most sensitive to least sensitive, the body organs you commonly use neuromuscular blocking drugs for. | eyes, larynx, jaw, trunk/limbs, diaphragm |
| how do non-depolarizing NMB work? | compete with ACh at the receptor site and minimize ability of the muscle to contract. It is reversible with neostigmine |
| how do depolarizing NMB work? | cause contraction of the muscle to the point of fatigue. It is NOT reversible. |
| which nerves do you monitor for a neuromuscular blockade? | tibial, facial, ulnar |
| what are the two most commonly used stimulation tests when testing if an animal has a neuromuscular block? | train of four; double burst |
| describe the characteristics of succinylcholine? | rapid onset (30s) but short lived (5min in cats, 20 min in dogs)action depolarzing NMB precautions= incr intra-ocular/cranial pressure hyperkalemia muscle fasiculation and pain malignant hyperthermia |
| what are the characteristics of atracurium? | intermediate duration of action non-depolarizing NMB (~35 min) few cardiovascular effects high histamine release metabolised through hoffman elimination not altered by hepatic or renal disease |
| what are the characteristics of pancuronium? | it's a long acting non-depolarizing NMB (40min) causes NorEp to be released hepatic and renal disease will prolong effects of drug vagolytic effect |
| what are the characterisitics of vercuronium? | intermediate duration of action (25 min) non-depolarizing neuromuscular blocker little effect on Aminoglycosides prolonged effects with hepatic and renal disease |
| what are the characterisitics of mivacurium? | short acting non-depolarizing NMB causes histamine release |
| what is an opiate? | drug derived from opium |
| what is an opioid? | Term used to describe ALL drugs with morphine-like activity |
| what is a narcotic? | Derived from the Greek word for stupor. Narcotic has historically been used to describe opioids. |
| what drug reverses the effects of opioids? | naloxone |
| where are the receptors for opioid drugs located? | Cerebral cortex, thalamus, PAG, spinal cord dorsal horn Peripheral sensory neurons and non-neurologic tissue |
| what are the endogenous mu ligand receptors? | endomorphins |
| what are the endogenous kappa ligand receptors? | dynorphins |
| what are the endogenous delta ligand receptors? | enkephalins |
| which opioid receptor's effects are not reversed by naloxone or netrexone? | sigma |
| which opioid receptor is stimulated by non-opioid related drugs? | sigma |
| what is the purpose for using anesthesia? | Humane restraint Efficiency Control convulsions Prevent recognition of pain Euthanasia Induction of anesthesia/Sedation/Maintenance |
| modifications to which carbon molecule of barbiturates confers sedative and hypnotic properties? | C5 |
| what activity do barbiturates have? | anticovulsant, hypnotic, sedative Respiratory depressants (dose dependent) Cardiovascular effects: increased heart rate negative inotrope blood pressure/cardiac output changes variable |
| barbiturates inhibit the release of which biological substances? | GABA, NE, ACh, glutamate |
| most common oxybarbiturate? how long lasting is it? | pentobarbitol; short |
| most common thiobarbiturate? how long lasting is it? | thiopental; ultra-short |
| which barbiturate is used in euthanasia solutions? | pentobarbitol |
| which drug can evoke oxidative damage to feline RBC with repeated administration? | propofol |
| what cardiovascular and respiratory effects does propofol cause? | Cardiovascular Effects: Vasodilation (hypotension), negative inotrope. Enhances the dysrhythmogenic effects of epinephrine Respiratory Effects: depressant |
| Etomidate causes what side effects? | -Inhibition of steroidogenesis (11-beta hydroxylase -Myoclonus, pain on injection -Hemolysis (propylene glycol effect) |
| Guaifenesin is normally given in conjunction with what other drugs? | xylazine, ketamine, or thiopental |
| List what makes an ideal anesthetics | Stable w/o preservatives; Inexpensive; Nonflammable; Easily vaporized; Low blood solubility; Very potent; No CV depression; Nonirritating to airways; Compatible with vasoactive drugs; skeletal muscle relaxation; Resists degradation; Nontoxic |
| What are the most accepted theories to explain the mechanism of action of local anesthetics? | Meye-Overton Theory Protein Receptor Hypothesis Alterations in Neurotransmitter availability |
| Which organic inhalant anesthetic is not an ether? | halothane |
| what are characteristics of the organic inhalant anesthetics? | contain aliphatic hydrocarbon ethers (mostly) all are halogenated all agents require some mechanism for converting the liquid to a vapor (except NO) |
| why is thymol added to halothane? | to better stabilize it and increase shelf life |
| Halogenation with Cl- and Br- do what to an inhalant anesthetic? | increase potency |
| Fl- is added to an inhalant anesthetic why? | to increase stability usually |
| what are the inorganic inhalant anesthetics? | Nitrous Oxide |
| What is the difference between a gas and a vapor? | Gas- an agent that exists in its gaseous form at room temperature and sea level pressure Vapor- the gaseous state of a substance that, at room temperature and sea level pressure, is a liquid |
| define saturated vapor pressure. | maximum concentration of molecules in the vapor state that can exist for a given liquid at each temperature |
| Why is the saturated vapor pressure important to medicine? | Anesthetics with a high SVP will require a smaller proportion of the total gas flowing through the vaporizer to pass through the vaporizing chamber to produce a given concentration than will anesthetics with a low SVP |
| What determines whether or not the animal will go to sleep? | Partial pressure of the Gas in the brain (not the concentration of the gas in the brain) |
| Which inhalant anesthetic has a boiling point near room temperature? | desflurane |
| what is a partition coefficient and how is it clinically important when applied to inhalation anesthetics? | The ratio of the concentration of anesthetics in 2 phases such a blood and gas. (describes the affinity of an anesthetic for one solvent over another) indicates speed of anesthetic induction, recovery, and change of anesthetic depth |
| Increased solubility in the blood (larger blood/gas PC)--> ? | increased uptake of anesthetic into blood |
| increased cardiac output--> ? | increased uptake of anesthetic into blood |
| How does a decreased cardiac output affect how quickly and animal will go to sleep when being anesthetized with an inhalant anesthetic? | prolongs time of how quickly the animal will go to sleep |
| Define minimum alveolar concentration (MAC). | minimum alveolar concentration of an anesthetic that prevents gross purposeful movement in 50% of the subjects exposed to a noxious stimulus ~ED50 |
| what does the MAC represent? | MAC represents alveolar concentration not inspired or delivered. |
| what factors affect MAC? | pregnancy status, age |
| What are the differences in the cardiovascular effects of the ether anesthetics and halothane? | Halothane decreases CO to change BP; Ether anesthetics vasodilates to change BP |
| by what enzyme does inhalant anesthesia metabolism occur? | liver metabolism by cytochrome p450 |
| list, from most to least, the order of metabolism of halothane, methoxyflurane, sevoflurane, isofluran. | methoxyflurane> halothane> isflurane> sevoflurane |
| Compound A is associated with which inhalant anesthetic? | Sevoflurane |
| T/F: Compound A is directly nephrotoxic? | False: its metabolites are nephrotoxic |
| 1. How do local anesthetics work? | Inhibit propagation (conduction) of nerve impulses; block Na+ channels which cause rapid depolarization by allowing rapid inward movement of Na+ |
| 2. Briefly describe a differential blockade? | Larger concentration block all pain and muscle function temporarily lost Smaller concentration block local pain and muscle function remains intact |
| 3. In a basic environment are local anesthetics more ionized or non–ionized? Why? | ionized b/c anesthetic is a weak base. |
| 4. What causes the local block to wear off after local anesthetic is injected near a nerve? | Local block worn off by systemic circulation Intrinsic action on nerves Rremoval by systemic circulation Local anesthetics themselves have vascular effects Cause vasodilation at clinical doses (except cocaine) |
| 5. Why is epinephrine sometimes added to lidocaine? | to produce vasoconstriction to prolong the local anesthetic's effect |
| 6. What topically applied local anesthetic can cause hemoglobin damage, especially in cats? | benzocaine |
| 7. What are the generic names of the 3 most commonly used local anesthetics in veterinary medicine? Which is the longest acting and which is the shortest acting? | lidocaine (shortest) < bupivicaine < Mepivicaine (longest) |
| 8. Of the 3 drugs in question 7 which is most cardiotoxic? | bupivicaine |
| 9. Briefly describe the differences between local infiltration of local anesthetic and a peripheral nerve block. | local infiltration is where you are trying to anesthetize a region/local area, a peripheral nerve block is when you’re aiming for a specifically named nerve |
| 10. 2% lidocaine contains how many milligrams/milliliter? | 0.02mg/ml |
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