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146 Cards in this Set
- Front
- Back
atropine
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- parasympatholytic, antimuscarinic - faster acting, much cheaper than glycopyrrolate - blocks postjunctional muscarinic receptors - prevent bradycardia (increasing ABP, CO), also reduces secretions, slows GI motility, causes bronchodilation |
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glycopyrrolate |
- parasympatholytic, antimuscarinic - similar effects to atropine; larger molecule, does not cross BBB reducing central effects - blocks postjunctional muscarinic receptors - prevents bradycradia (increasing ABP, CO), also reduces secretions, slows GI motility, causes bronchodilation |
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epinephrine (adrenaline) |
- non-selective endogenous catecholamine - increases inotropism and HR, causes vasodilation (beta2)/vasoconstriction (alpha1) and bronchodilation - uses: anaphylaxis, asystole/CPR, CV support |
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norepinephrine (noradrenaline) |
- endogenous catecholamine - weak beta2 activity --> does not produce vasodilation/bronchodilation - causes vasoconstriction and increased inotropism |
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dopamine |
- non-selective endogenous catecholamine - @ low doses: dopamine receptors enhances renal vasodilation @ med doses: beta1 increases inotropism @ high doses: alpha1 increases vasoconstriction |
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isoproterenol |
- synthetic non-selective catecholamine - most potent beta-agonist - given to increase HR, but severe hypotension and arrhythmias limit use |
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dobutamine |
- synthetic beta-1 selective catecholamine - increases inotropism --> increased CO and muscular perfusion |
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phenylephrine |
- synthetic selective alpha-1 agonist - causes profound vasoconstriction and increase in ABP, reflex bradycardia usu. occurs (despite increased ABP, CO usu. decreases d/t elevated SVR) |
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ephedrine |
- synthetic indirect alpha- and beta- agonist - stimulates releases of NE/Epi from adrenal gland, and has direct effects - longer acting than other natural catecholamines - causes increased HR, inotropism, ABP and CO |
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beta adrenergic antagonists |
- "beta blockers" - i.e. Esmolol, atenolol - used to suppress/reduce sympathetic tone, treat dysrhythmias, hypertension, and pheochromocytomas |
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beta adrenergic agonists |
- i.e. albuterol - mainly used as bronchodilators |
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vasopressin |
- AKA anti-diuretic hormone - causes vasoconstriction |
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Why do we premed? |
- calm the pt (sedation/anxiolysis) - provide analgesia - decrease the dose of other drugs needed to provide analgesia - smooth recovery from anesthesia - increase muscle relaxation - antagonize adverse side effects of other drugs - control airway secretion or bronchospasm - control nausea/vomiting - modify sympathetic responses - prophylaxis against allergic reactions |
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Pros and Cons of Parasympatholytics |
Pros: reduce secretions, prevent bradycardia, reduce gastrointestinal motility Cons: decreased GI motility, increased myocardial work and arrhythmias, no support for net benefit |
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When to use parasympatholytics as premedicants: |
- ophthalmic sx - sx for cervical spinal cord decompression - endoscopy - giving large doses of mu opioid - when using cholinesterase inhibitors |
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Contraindications for parasympatholytics |
- pre-existing tachyarrhythmias - w/ alpha-2 agonists |
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tranquilizer |
- aka - ataractic, neuroleptic - increasing dosages do not produce increased sedation, but do cause increased adverse side effects |
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acepromazine |
- phenothiazine (tranquilizer) - slow onset, long duration - antiemetic, antihistaminic, decreases circulating catecholamines, poss. induces seizures (??) - side effects: hypotension, hypothermia, decreased PCV, resp suppression, penile prolapse - contraindications: hypovolemia, hepatic dz, coagulopathies, young, old, breeding stallions |
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butyrophenones |
- droperidol, azaperone |
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sedatives |
- increased doses produce increased states of sedation, such that can resemble general anesthesia |
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benzodiazepines |
- may see paradoxical excitement, but still produces substantial reduction in subsequent anesthetic needs - relatively reliable sedation in young, old, sick - non-specific muscle relation - reversible w/ flumazenil |
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diazepam (Valium) |
- benzodiazepine - poorly water soluble, unreliable uptake from IM/SQ injection sites - suspended in propylene glycol, which can accumulate when given w/ CRI, and produces hemolysis, pain, thrombosis if bolused - minimal cardiopulmonary effects |
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midazolam (Versed) |
- no propylene glycol - once in blood, becomes more lipid soluble --> cross BBB - produces retrograde amnesia |
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zolazepam |
- combined w/ tiletamine in Telazol - cats: zolazepam lasts longer - prolonged but unexcited recovery - dogs: zolazepam metabolized quicker - see tiletamine effects (dissociation, rigidity, etc.) - useful when low volume of injection is needed - high therapeutic index |
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alpha-2 agonists |
- reliable, dose-dependent sedation - provides analgesia - alpha-2 receptors pre- and post- synaptic in neuronal tissue, platelets, endothelium, beta-cells - sedative and anxiolytic effects from supra spinal activity - analgesia from dorsal horn activity - side effects: vasoconstriction, decreased thermoregulation, emesis, decreased GI motility, hyperglycemia, PU |
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xylazine |
- alpha-2 agonist - dramatic species related dose differences |
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detomidine |
- alpha-2 agonist - more potent and longer lasting than xylazine - used in horses |
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medetomidine |
- alpha-2 agonist - mix of isomers - only one of which is resp. for sedation/analgesia - no longer used for domestic spp; still used for capture/wildlife - lasts long time |
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dexmedetomidine |
- alpha-2 agonist - active isomer from medetomidine - uses: supplement to anesthesia, sedation in ICU, post-op analgesia |
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romifidine |
- alpha-2 agonist - good sedation and analgesia - duration of action intermediate between xylazine and detomidine - licensed for horses |
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alpha-2 antagonists |
- reversal agents for alpha-2 agonists - reverse both central and peripheral effects |
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atipamezole |
- alpha-2 antagonist |
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yohimbine |
- alpha-2 antagonist - better at returning rumen motility in ruminants sedated w/ xylazine |
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metoclopramide |
- prokinetic agent - decreases GI transit time, increases motility - dopamine antagonist (inhibits inhibitor) - side effects: crosses BBB, extrapyramidal effects - agitation, violence |
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famotidine |
- competitive histamine H2-receptor antagonist - raises gastric pH and reduces volume of secretions - give 45-60 mins IV before induction, or PO evening before - side effects: IV bolus can cause cardiac arrhythmias |
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sodium citrate |
- anti-acid, non-particulate/clear - buffers pH transiently, window of about 10 mins - given 10 mins before induction |
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diphenhydramine (Benedryl) |
histamine antagonist |
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dimenhydrinate (Dramamine) |
histamine antagonist |
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ondansetron |
- serotonin antagonist, antagonizes 5-HT3 receptors centrally (in CTZ) and peripherally |
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dexamethasone (Decadron) |
- glucocorticoid |
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maropitant (Cerenia) |
- neurokinin (NK1) receptor antagonist - blocks action of substance P in CNS |
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opiates |
- purified natural agents derived from opium |
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narcotic |
- potent morphine-like analgesic drugs |
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opioid |
- all exogenous substances that bind to opioid receptors and produce at least some agonist activity, can be synthetic or natural - (presynaptically) inhibit NT release and reduce NT production, (postsynaptically) hyperpolarize cells - upregulate antinociceptive neurons descending from the brain - inhibit NT release in peripheral neurons |
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Side Effects of Opioids |
- CNS depression/stimulation - thermoregulation - cough suppression - change in pupillary diameter - sound sensitivity - ventilatory depression - dose-dependent bradycardia - nausea/vomiting/ileus - urine retention |
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morphine |
- used in almost all species - releases histamine, give slowly IV - nauseating, emetic - can be injected intraarticularly, applied topically to corneas, given epidurally |
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hydromorphone, oxymorphone |
- synthetic - most commonly used in cats, dogs - nauseating, emetic - hydromorphone can cause panting in dogs |
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methadone |
- synthetic - most commonly used in cats, dogs - less emetic (may still be nauseating) - prolonged analgesia after SQ administration - mod. well absorbed across m.m. in cats |
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fentanyl |
- synthetic - most common in cats, dogs. also small ruminants, camelids - go-home analgesia as fentanyl patches |
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tramadol |
- synthetic - weak MOR agonist, serotonin and norepinephrine reuptake inhibitor, facilitates serotonin release - most commonly used PO in dogs - do not use concurrently w/ MAOIs or other serotoninergic drugs |
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butorphanol |
- competitive MOR antagonist, KOR agonist - limited analgesic efficacy - good for mild pain - "ceiling effect" w/ side effects - good sedative and antitussive - CRI for colic in horses |
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buprenorphine |
- semisynthetic, partial agonist - binds tightly and dissociates slowly from MOR - difficult to antagonize, longer duration of action - given oral-transmucosally in cats, IV is ideal |
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Simbadol |
- extended release buprenorphine for cats - one SQ dose for 24 hrs of analgesia , up to 3 total doses |
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naloxone, naltrexone |
- opioid receptor antagonists - displace MOR and KOR agonists, but don't activate the receptor - reverse all opioid effects, including the analgesia |
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NSAIDs |
- inhibit eicosanoid production by inhibiting COX enzymes - COX-1: PGE2 (vasodilation, nociceptor sensitization, beneficial GI effects); TXA2 (vasoconstriction, platelet aggregation) - COX-2: renin release, alterations in renal blood flow, PGI2 (vasodilation, inhibits platelet aggregation, inflammation, GI effects) |
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side effects of NSAIDs |
- GI: gastritis/enteritis, ulceration, perforation - AKI - hepatic toxicity |
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carprofen (Rimadyl) |
- COX-2 preferential - one of most commonly used NSAIDs in dogs - w/ comprehensive safety record |
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Meloxicam |
- COX-2 preferential
- PO/injectable approved for dogs - low dose chronic use shown to be safe in cats; warning against multiple dosings at the label dose in cats |
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Coxibs (Deracoxib, Firocoxib) |
- COX-2 specific - deracoxib for dogs - firocoxib for dogs, horses |
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robenacoxib (Onsior) |
- SQ, PO - first dose 45 mins before sx, then post-op - impressive margin-of-safety studies for cat kidneys |
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flunixin meglumine |
- non-specific COX inhibitor - only NSAID approved by FDA for use in cattle - commonly used to treat colic pain |
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phenylbutazone |
- commonly used in horses, particularly for orthopedic pain - illegal in food animals (causes aplastic anemia in people) |
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propofol |
- opaque white IV induction agent - needs lipid vehicle (soybean oil) for emulsification (lecithin) --> supports microbial growth - decreases rate of dissociation of GABA from GABA-A receptors - no analgesic action - short duration of action due to rapid redistribution to other tissues and rapid metabolism |
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side effects of propofol |
- decreased cerebral metabolic rate, blood flow and intracranial pressure - decreased myocardial contractility, vasodilation --> hypotension w/ suppression of baroreceptor reflex - hypoventilation/apnea - decreased intraocular pressure - can be painful to inject - Heinz body anemia in cats w/ repeated administrations - no analgesia |
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dissociative anesthetics |
- dissociation between thalamocortical and limbic systems - causes catalepsy, hypertonus/myoclonus - good analgesia - non-competitive NMDA receptor antagonist, serotonin and norepinephrine reuptake inhibitor, opioid receptor agonist, voltage-gated Na+ and Ca++ channel blockade, antimuscarinic - highly lipid soluble, relatively short duration of action - excreted unchanged by the kidneys in cats |
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landmarks of brachial plexus block |
medial to the scapula; between the supraglenoid tubercle and the acromion |
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nerves in brachial plexus block |
(cranial to caudal) musculocutaneous n. - flexion radial n. - extension median/ulnar nn. - medial rotation |
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landmarks for femoral nerve block |
just cranial to palpating the femoral pulse. should feel "pop" when needle punctures fascia overlying nerve medial to the rectus femoris mm. and pectineus mm. |
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action of femoral n. |
stifle extension |
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landmarks for sciatic nerve block |
between greater trochanter and ischiatic tuberosity |
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action of sciatic n. |
stifle flexion |
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contraindications for epidurals |
- bleeding disorders - hypovolemia - infection at the injection site - sepsis/bacteremia |
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landmarks for epidural |
spinous process of L7, median sacral crest, lumbosacral space between L7 and S1 |
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nociception |
reception, conduction and processing of signals generated by stimulated nociceptors physiological process resulting in the perception of pain |
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noxious stimuli |
a stimulus that is actually/potentially damaging to tissue a stimulus of intensity/quality adequate to stimulate nociceptors |
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acute pain |
- usually a result of trauma, surgery, infection, etc. - events that begin abruptly and are relatively brief - has a biologic function - serves as a warning to incite protective behavioral change - relatively easy to treat w/ analgesics |
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chronic pain |
- continues beyond the course of acute pain - associated w/ chronic pathological processes - does not serve a biologic function - harder to treat w/ analgesics |
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nociceptive pain |
- pain caused by stimulation of nociceptors - i.e. surgery, trauma, osteoarthritis, etc. |
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neuropathic pain |
- pain caused by damage to the nervous system - does not respond to traditional analgesics - characterized by: spontaneous paresthesias and paroxysms, pain caused by normal movements, hyperalgesia, allodynia |
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nociceptors |
- non-encapsulated receptor organs - respond preferentially to noxious stimuli - parent neurons are nociceptive neurons w/ pseudounipolar structure |
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A-delta fibers |
- "first pain" - pricking, sharp, aching pains - light myelination - 2-5 microns - faster conduction velocity |
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C fibers |
- "second pain" - burning pain - unmyelinated - thinner, <2 microns - slower conduction velocity |
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Transduction |
translation of physical energy into electrical activity by nociceptors via transducers |
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Transmission |
propagation of an action potential along peripheral neurons and in/thru the CNS |
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Modulation |
modification of nociception in the dorsal horn of the spinal cord |
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Perception |
perception of pain by higher brain centers |
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hyperalgesia |
inappropriately increased response to a noxious stimuli, which occurs by sensitization of nociceptors |
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characteristics of a sensitized neuron |
- decreased threshold - increased response - spontaneous activity |
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How do inflammatory mediators cause peripheral sensitization? |
inflammatory mediators bind to metabotropic receptors and activate intracellular signaling cascades |
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major nociceptive pathway in carnivores |
spinocervicothalamic tract |
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major nociceptive pathway in the head |
trigeminothalamic tract |
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How do nociceptive neurons travel from the viscera to CNS? |
glossopharyngeal/vagus nerve and a pair of spinal nerves OR two pairs of spinal nerves |
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reticular activating system |
responsible for making sure an organism pays attention to noxious stimuli |
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limbic system |
ensures an organism will link noxious stimuli w/ negative emotions |
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primary NT released by first-order nociceptive neurons in the spinal cord dorsal horn |
glutamate |
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post-synaptic receptors that bind glutamate |
AMPA, NMDA |
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termination sites of A-delta neurons |
I, IV-V |
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termination sites of C neurons |
I, II |
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spinal cord plasticity |
induced by an increase in intracellular Ca++ ions in second-order neurons in dorsal horn due to opening of ion channel in NMDA receptor. ion channel opens after glutamate/glycine binding and removal of Mg++ plug |
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inhibitory interneurons |
- stimulated by GABA/glycine, serotonin, norepinephrine
- inhibit first- and second-order nociceptive neurons - can be stimulated by A-beta fibers (innocuous touch) - the principle behind TENS and massage reducing pain - PAG and RVM project to dorsal horn of spinal cord where they release NT that stimulate inhibitory interneurons |
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mechanisms of opioids in CNS |
opioid receptor agonist increases K+ efflux and/or inactivates Ca++ channels --> inhibiting NT release AND inhibits adenylyl cyclase --> reduced NT production |
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mechanisms of opioids peripherally |
opioid receptor agonist inhibits NT release |
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opioid receptors |
mu - important for analgesia, kappa, and delta |
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endogenous opioid peptides |
endorphins, diorphins, enkephalins
|
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side effects of opioids |
- hypo- or hyperthermia - nausea/emesis - hypoventilation - mild dose-dependent bradycardia - ileus - urine retention |
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COX selectivity |
related to adverse effects in GI tissues unrelated to efficacy in a given patient |
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common causes of AKI w/ NSAID administration |
- overdose/toxicosis - w/ concurrent corticosteroids - hypovolemia - under poorly managed anesthesia (i.e. vasoconstriction, w/o fluids) - cardiac disease - pre-existing renal disease |
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contraindications of NSAIDs |
- hypovolemia - coagulopathy - pre-existing liver/kidney/GI disease - w/ concurrent NSAIDs or corticosteroids - w/ concurrent nephrotoxic drugs - mast cell tumors - neonatal/juvenille animals |
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neuroma |
tangled web of nerve endings that forms when a nerve is transected |
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tonicity |
holds organs in a state of intermediate activation can be increased or decreased controlled in central ANS centers (not well known) |
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origin of preganglionic sympathetic fibers |
thoracolumbar region (T1-L3) |
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origin of preganglionic parasympathetic fibers |
brainstem and sacral spinal cord |
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cholinergic receptors |
- muscarinic receptors (PNS effectors) - ganglia of both the PNS and SNS - nicotinic receptors at NMJ |
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effects of PNS |
- bradycardia, decreased inotropism - bronchoconstriction - increased airway secretions - salivation - GI hypermotility - increased gastric acid secretion |
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NT of PNS |
acetylcholine |
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NTs of SNS |
epinephrine, norepinephrine, dopamine, isoproterenol |
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alpha-adrenergic receptors |
alpha-1: commonly found in vascular muscle - activation = vasoconstriction alpha-2: found pre- and post-synaptically - post-syn activation: vasoconstriction - pre-syn activation: mediate neg feedback for further norepinephrine release |
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beta-adrenergic receptors |
beta-1: predominates in myocardium, SA node, ventricular conduction system - activation: increased inotropism and chronotropism beta-2: located in smooth muscle of vessels and bronchi - activation: muscle relaxation |
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dopaminergic receptors |
localized in CNS, blood vessels - activation: vessel dilation |
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baroreceptor reflex |
stretch receptors sense changes in blood pressure, relay impulses to the medullary vasomotor center which mediates changes in heart rate and vascular tone |
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catecholamines |
- inactivated by MAO and COMT enzymes, cleared by lungs - effects usually short - generally not liposoluble, limited central effects |
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roles of GI drugs as premedicants |
- empty the stomach - neutralize the stomach contects w/ non-particulate agent - decreased gastric acid production |
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patients at high risk of GI reflux or aspiration |
- ER surgery - pregnancy - morbid obesity - diabetic gastroparesis |
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qualities of anesthesia |
- unconsciousness - analgesia - amnesia - immobility - AND stabilize the autonomic nervous system |
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drugs that are general anesthetics |
- vapors: iso-, sevo-, des- - nitrous oxide, xenon - barbiturates - propofol - dissociatives - steroids (i.e. alfaxalone) |
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amnesia |
- occurs at level of hippocampus, amygdala, and cortex - GABA involved in memory formation |
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arousal vs awareness |
arousal - responsiveness to stimuli awareness - mostly cortical function |
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immobility |
produced by inhibition of spinal reflex pathways |
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Meyer-Overton Rule |
correlation between anesthetic potency and lipid-solubility (doesn't always hold up) |
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how do anesthetics affect neurons? |
- neuronal excitability: anesthetics hyperpolarize cortical and spinal neurons - communication between neurons: synaptic transmission in excitatory and inhibitory pathways |
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major excitatory NT |
glutamate (act on NMDA, KA, and AMPA receptors) |
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major inhibitory NT |
GABA |
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affect of GA on voltage-gated ion channels |
some decreases subtypes of voltage-gated Na+ channel activity - a small decrease in Na+ channel activity creates a large decrease in synaptic function activate "leak K+ channels" HCN channels inhibited, reduction in amplitude |
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effects of locoregional anesthesia |
- less pain, decreased risk of chronic pain - earlier mobilization, improved rehabilitation - reduced duration of ileus |
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electrical nerve stimulation |
electrical impulses that reach a nerve are transmitted down the nerve fiber. if the fiber contains motor fibers, the current induces a muscle contraction at the effector muscle.
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epidural anesthesia |
blocking of nerve roots from the spinal cord with local anesthetic |
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layers to go through during epidural |
skin, SQ, muscle, interarcuate ligament, epidural space |
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drugs used for locoregional anesthesia |
local anesthetics, opioids, alpha-2 agonists |
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complications of epidurals |
- accidental improper drug administration - neural damage/neurotoxicity - infection - subarachnoid/spinal or subdural injection - intravascular injection |
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complications of epidurals (w/ drugs) |
- sympathetic blockade - Horner's syndrome - respiratory depression (rarely phrenic n. paralysis) - total spinal anesthesia |
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metabolic oxygen |
oxygen demand, per kg, per min minimum amount of oxygen you have to supply your patient |
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functional residual capacity |
volume of gas left in the lungs at the end of a passive expiration |
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closing volume |
volume of gas left in the lungs when small airways start to close |
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minimum alveolar concentration |
concentration of anesthetic vapor in the alveoli the produces immobility in 50% of patients exposed to a painful stimulus |
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factors that may contribute to a difficult airway |
- previous history of difficult airway - previous laryngeal surgery - problems at laryngeal inlet |
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management of difficult airway |
- aspiration prophylaxis (sodium citrate, famotidine)
- appropriate equipment (i.e. suction) - thorough pre-oxygenation - regional anesthesia, surgical airway - CANCEL PROCEDURE |