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146 Cards in this Set

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atropine

- 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

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





epinephrine (adrenaline)

- non-selective endogenous catecholamine




- increases inotropism and HR, causes vasodilation (beta2)/vasoconstriction (alpha1) and bronchodilation




- uses: anaphylaxis, asystole/CPR, CV support



norepinephrine (noradrenaline)

- endogenous catecholamine




- weak beta2 activity --> does not produce vasodilation/bronchodilation




- causes vasoconstriction and increased inotropism

dopamine

- non-selective endogenous catecholamine




- @ low doses: dopamine receptors enhances renal vasodilation


@ med doses: beta1 increases inotropism


@ high doses: alpha1 increases vasoconstriction

isoproterenol

- synthetic non-selective catecholamine




- most potent beta-agonist




- given to increase HR, but severe hypotension and arrhythmias limit use

dobutamine

- synthetic beta-1 selective catecholamine




- increases inotropism --> increased CO and muscular perfusion

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)

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

beta adrenergic antagonists

- "beta blockers" - i.e. Esmolol, atenolol




- used to suppress/reduce sympathetic tone, treat dysrhythmias, hypertension, and pheochromocytomas

beta adrenergic agonists

- i.e. albuterol




- mainly used as bronchodilators

vasopressin

- AKA anti-diuretic hormone




- causes vasoconstriction

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

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

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

Contraindications for parasympatholytics

- pre-existing tachyarrhythmias


- w/ alpha-2 agonists

tranquilizer

- aka - ataractic, neuroleptic




- increasing dosages do not produce increased sedation, but do cause increased adverse side effects

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

butyrophenones

- droperidol, azaperone

sedatives

- increased doses produce increased states of sedation, such that can resemble general anesthesia

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

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

midazolam (Versed)

- no propylene glycol


- once in blood, becomes more lipid soluble --> cross BBB


- produces retrograde amnesia

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

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

xylazine

- alpha-2 agonist


- dramatic species related dose differences

detomidine

- alpha-2 agonist


- more potent and longer lasting than xylazine


- used in horses

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

dexmedetomidine

- alpha-2 agonist


- active isomer from medetomidine


- uses: supplement to anesthesia, sedation in ICU, post-op analgesia

romifidine

- alpha-2 agonist


- good sedation and analgesia


- duration of action intermediate between xylazine and detomidine


- licensed for horses

alpha-2 antagonists

- reversal agents for alpha-2 agonists


- reverse both central and peripheral effects

atipamezole

- alpha-2 antagonist

yohimbine

- alpha-2 antagonist


- better at returning rumen motility in ruminants sedated w/ xylazine

metoclopramide

- prokinetic agent - decreases GI transit time, increases motility




- dopamine antagonist (inhibits inhibitor)




- side effects: crosses BBB, extrapyramidal effects - agitation, violence

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

sodium citrate

- anti-acid, non-particulate/clear




- buffers pH transiently, window of about 10 mins




- given 10 mins before induction

diphenhydramine (Benedryl)

histamine antagonist

dimenhydrinate (Dramamine)

histamine antagonist

ondansetron

- serotonin antagonist, antagonizes 5-HT3 receptors centrally (in CTZ) and peripherally

dexamethasone (Decadron)

- glucocorticoid

maropitant (Cerenia)

- neurokinin (NK1) receptor antagonist




- blocks action of substance P in CNS

opiates

- purified natural agents derived from opium

narcotic

- potent morphine-like analgesic drugs

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

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

morphine

- used in almost all species




- releases histamine, give slowly IV




- nauseating, emetic




- can be injected intraarticularly, applied topically to corneas, given epidurally

hydromorphone, oxymorphone

- synthetic




- most commonly used in cats, dogs




- nauseating, emetic




- hydromorphone can cause panting in dogs

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

fentanyl

- synthetic




- most common in cats, dogs. also small ruminants, camelids




- go-home analgesia as fentanyl patches

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

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

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

Simbadol

- extended release buprenorphine for cats




- one SQ dose for 24 hrs of analgesia , up to 3 total doses

naloxone, naltrexone

- opioid receptor antagonists




- displace MOR and KOR agonists, but don't activate the receptor




- reverse all opioid effects, including the analgesia

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)

side effects of NSAIDs

- GI: gastritis/enteritis, ulceration, perforation




- AKI




- hepatic toxicity

carprofen (Rimadyl)

- COX-2 preferential




- one of most commonly used NSAIDs in dogs




- w/ comprehensive safety record

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

Coxibs (Deracoxib, Firocoxib)

- COX-2 specific




- deracoxib for dogs




- firocoxib for dogs, horses

robenacoxib (Onsior)

- SQ, PO




- first dose 45 mins before sx, then post-op




- impressive margin-of-safety studies for cat kidneys

flunixin meglumine

- non-specific COX inhibitor




- only NSAID approved by FDA for use in cattle




- commonly used to treat colic pain

phenylbutazone

- commonly used in horses, particularly for orthopedic pain




- illegal in food animals (causes aplastic anemia in people)

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

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

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

landmarks of brachial plexus block

medial to the scapula; between the supraglenoid tubercle and the acromion

nerves in brachial plexus block

(cranial to caudal)




musculocutaneous n. - flexion


radial n. - extension


median/ulnar nn. - medial rotation

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.

action of femoral n.

stifle extension

landmarks for sciatic nerve block

between greater trochanter and ischiatic tuberosity

action of sciatic n.

stifle flexion

contraindications for epidurals

- bleeding disorders


- hypovolemia


- infection at the injection site


- sepsis/bacteremia

landmarks for epidural

spinous process of L7, median sacral crest, lumbosacral space




between L7 and S1

nociception

reception, conduction and processing of signals generated by stimulated nociceptors




physiological process resulting in the perception of pain

noxious stimuli

a stimulus that is actually/potentially damaging to tissue




a stimulus of intensity/quality adequate to stimulate nociceptors

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

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

nociceptive pain

- pain caused by stimulation of nociceptors




- i.e. surgery, trauma, osteoarthritis, etc.

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

nociceptors

- non-encapsulated receptor organs




- respond preferentially to noxious stimuli




- parent neurons are nociceptive neurons w/ pseudounipolar structure



A-delta fibers

- "first pain"


- pricking, sharp, aching pains


- light myelination


- 2-5 microns


- faster conduction velocity

C fibers

- "second pain"


- burning pain


- unmyelinated


- thinner, <2 microns


- slower conduction velocity

Transduction

translation of physical energy into electrical activity by nociceptors via transducers

Transmission

propagation of an action potential along peripheral neurons and in/thru the CNS

Modulation

modification of nociception in the dorsal horn of the spinal cord

Perception

perception of pain by higher brain centers

hyperalgesia

inappropriately increased response to a noxious stimuli, which occurs by sensitization of nociceptors

characteristics of a sensitized neuron

- decreased threshold




- increased response




- spontaneous activity

How do inflammatory mediators cause peripheral sensitization?

inflammatory mediators bind to metabotropic receptors and activate intracellular signaling cascades

major nociceptive pathway in carnivores

spinocervicothalamic tract

major nociceptive pathway in the head

trigeminothalamic tract

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

reticular activating system

responsible for making sure an organism pays attention to noxious stimuli

limbic system

ensures an organism will link noxious stimuli w/ negative emotions

primary NT released by first-order nociceptive neurons in the spinal cord dorsal horn

glutamate

post-synaptic receptors that bind glutamate

AMPA, NMDA

termination sites of A-delta neurons

I, IV-V

termination sites of C neurons

I, II

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

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

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

mechanisms of opioids peripherally

opioid receptor agonist




inhibits NT release

opioid receptors

mu - important for analgesia, kappa, and delta

endogenous opioid peptides

endorphins, diorphins, enkephalins

side effects of opioids

- hypo- or hyperthermia


- nausea/emesis


- hypoventilation


- mild dose-dependent bradycardia


- ileus


- urine retention

COX selectivity

related to adverse effects in GI tissues




unrelated to efficacy in a given patient

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

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

neuroma

tangled web of nerve endings that forms when a nerve is transected

tonicity

holds organs in a state of intermediate activation




can be increased or decreased




controlled in central ANS centers (not well known)

origin of preganglionic sympathetic fibers

thoracolumbar region (T1-L3)

origin of preganglionic parasympathetic fibers

brainstem and sacral spinal cord

cholinergic receptors

- muscarinic receptors (PNS effectors)




- ganglia of both the PNS and SNS




- nicotinic receptors at NMJ

effects of PNS

- bradycardia, decreased inotropism


- bronchoconstriction


- increased airway secretions


- salivation


- GI hypermotility


- increased gastric acid secretion

NT of PNS

acetylcholine

NTs of SNS

epinephrine, norepinephrine, dopamine, isoproterenol

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

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

dopaminergic receptors

localized in CNS, blood vessels


- activation: vessel dilation

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

catecholamines

- inactivated by MAO and COMT enzymes, cleared by lungs


- effects usually short


- generally not liposoluble, limited central effects

roles of GI drugs as premedicants

- empty the stomach


- neutralize the stomach contects w/ non-particulate agent


- decreased gastric acid production

patients at high risk of GI reflux or aspiration

- ER surgery


- pregnancy


- morbid obesity


- diabetic gastroparesis

qualities of anesthesia

- unconsciousness


- analgesia


- amnesia


- immobility




- AND stabilize the autonomic nervous system

drugs that are general anesthetics

- vapors: iso-, sevo-, des-


- nitrous oxide, xenon


- barbiturates


- propofol


- dissociatives


- steroids (i.e. alfaxalone)

amnesia

- occurs at level of hippocampus, amygdala, and cortex




- GABA involved in memory formation

arousal vs awareness

arousal - responsiveness to stimuli




awareness - mostly cortical function

immobility

produced by inhibition of spinal reflex pathways

Meyer-Overton Rule

correlation between anesthetic potency and lipid-solubility




(doesn't always hold up)

how do anesthetics affect neurons?

- neuronal excitability: anesthetics hyperpolarize cortical and spinal neurons




- communication between neurons: synaptic transmission in excitatory and inhibitory pathways

major excitatory NT

glutamate




(act on NMDA, KA, and AMPA receptors)

major inhibitory NT

GABA

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

effects of locoregional anesthesia

- less pain, decreased risk of chronic pain




- earlier mobilization, improved rehabilitation




- reduced duration of ileus

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.

epidural anesthesia

blocking of nerve roots from the spinal cord with local anesthetic

layers to go through during epidural

skin, SQ, muscle, interarcuate ligament, epidural space

drugs used for locoregional anesthesia

local anesthetics, opioids, alpha-2 agonists

complications of epidurals

- accidental improper drug administration


- neural damage/neurotoxicity


- infection


- subarachnoid/spinal or subdural injection


- intravascular injection

complications of epidurals (w/ drugs)

- sympathetic blockade


- Horner's syndrome


- respiratory depression (rarely phrenic n. paralysis)


- total spinal anesthesia

metabolic oxygen

oxygen demand, per kg, per min




minimum amount of oxygen you have to supply your patient

functional residual capacity

volume of gas left in the lungs at the end of a passive expiration

closing volume

volume of gas left in the lungs when small airways start to close

minimum alveolar concentration

concentration of anesthetic vapor in the alveoli the produces immobility in 50% of patients exposed to a painful stimulus

factors that may contribute to a difficult airway

- previous history of difficult airway




- previous laryngeal surgery




- problems at laryngeal inlet

management of difficult airway

- aspiration prophylaxis (sodium citrate, famotidine)



- appropriate equipment (i.e. suction)




- thorough pre-oxygenation




- regional anesthesia, surgical airway




- CANCEL PROCEDURE