Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase I > Anesthesia Drugs > Flashcards

Anesthesia Drugs Flashcards

1
Q

Atropine

A
  • Class: Anticholinergic
  • MOA: Competitivley anatagonize Ach at postganglionic muscarininc cholinergic receptor in PNS
  • Onset 1-5 min, duration 30
  • Rapid hydrolysis to inactive metabolites, some renal excretion
  • Increased HR, contractility; bronchodilation; mydriasis
  • Crosses BBB
  • Used as premed before reversing NM blockade (neostig, edrophonium)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Glycopyrrolate

A
  • Class: Anticholingeric
  • MOA: Competitively antagonize Ach at postgang muscarinic cholinergic receptor in PNS
  • Onset several minutes, duration ~1h
  • 4 times potency of atropine
  • Poorly lipid soluble, does not cross BBB; excreted unchanged in urine
  • No mydriasis, increase HR/contractility, bronchodilation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Epinephrine

A
  • Class: Natural catecholamine
  • MOA: Non-selective agonist of a1, a2, b1, & b2 adrenergic receptors
  • Low dose = beta - inc CO, myocardial O2 consumption,; decrease diastolic BP, dec PVR
  • High dose = a1 - marked increase SVR
  • Dec threshold for ventricular arrhythmias, esp with halothane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Norepinephrine

A
  • Class: Natural catecholamine
  • MOA: a1, a2, b1 agonist
  • Alpha effects predominate at clinically used doses (B1 at very low dose)
  • Coronary vasodilation
  • Similar arrhythmogenic effects to epi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Dopamine

A
  • Class: Natural catecholamine
  • MOA: D1, D2, a1, a2, b1, b2 - dose-dependent; release of endogenous norepi
  • Low dose (1-2ug/kg/min): D1/2 - vasodilation renal/mesenteric vasculature, increase UOP
  • Intermediate (<10): Beta effects inc contractility, HR, CO
  • High (>10) - alpha effects - inc SVR, splenic contraction
  • Discontinue in stepwise manner
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Dobutamine

A
  • Class: Synthetic catecholamine
  • MOA: Primarily B1, a1 and B2 at high doses (no a2)
  • Primarily used to inc CO in poor myocardial function
  • Possibly cause seizures in conscious cats
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Isoproterenol

A
  • Class: Synthetic Catecholamine
  • MOA: Potent B1, B2 agonist, no alph
  • Positive inotrope/chronotrope
  • Potent bronchodilator - increase anatomic deadspace and V/Q mismatch
  • Increase renal & splanchnic bloodflow via selective vasodilation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Phenylephrine

A
  • A1 adrenergic receptor agonist
  • Increase SVR and BP, may decrease CO via inc afterload
  • No CNS effects, dec renal & hepatic bloodflow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Clenbuterol/albuterol/terbutaline

A
  • Primarily used for management of bronchospasm
  • Cause tachycardia at high dose (B1), dec BP at lower dose (B2)
  • Drive K+ intracellular via stimulation of Na/K ATPase
  • B adrenergic agonist
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Ephedrine

A
  • Direct & indirect sympathomimetic - a1/2, b1/2
  • Inhibit monoamine oxidase on norepi - tachyphylaxis due to depletion in indirect effect
  • Used to manage anesthetic hypotension - longer duration of action = bolus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Prazosin

A
  • Quinazoline derivative, highly selective A1 antagonist
  • blocks A1 adrenergic receptors create functional UO via contraction of bladder neck/urethra
  • Vasodilation and dec SVR/BP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Phenoxybenzamine

A
  • Long-acting, non-selective alpha andrenergic blocker, a1 > a2
  • Irreversible receptor blockade, inhibits neuronal & extraneuronal uptake of catecholamines
  • Usually used for pre-operative management of pheochromocytoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Beta-blockers

A
  • Competitive antagonists of B1 & B2 receptors; some have sympathomimetic effect/partial agonist
  • Negative inotropic effect - decrease myocardial O2 demand, inhibit RAAS via blockade of JGA
  • Bronchospasma at high doses
  • Atenolol - B1 selective, used for cats with HCM
  • Esmolol - very B1 selective, lipophilic (rapid onset) - BB of choice for GA
  • Propanolol - non-selective, control HR/BP in hyperthyroid cats, presurgical mgmt pheo
  • Sotalol - non-selective; class III anti-arrhythmic, K+ channel blocking effects; decrease VPC in boxer/ARVC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Acepromazine

A
  • Phenothiazine tranquilizer
  • Sedation primarily via blockade of D2 receptors
  • Also blocks a1, muscarinic, and H1 receptors
  • Decreases SV, CO, and BP by 20-30%, decreases PVC
  • Little pulmonary effects, MAC reducer, decreases platelet aggregation
  • Does NOT lower seizure threshold
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Diazepam

A
  • Benzodiazepine - enhance GABAa receptor affinity for GABA (primary inhibitory NT in CNS); hyperpolarize post-syn cell membrane via Cl-
  • Light-sensitive & binds to plastic
  • Rapid absorption via nasal or rectal route
  • Unreliable sedative but good central muscle relaxant and anti-convulsant
  • No CV or resp depression
  • Metabolized to active compounds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Midazolam

A
  • Benzodiazepine - enhance GABAa receptor affinity for GABA (primary inhibitory NT in CNS); hyperpolarize post-syn cell membrane via Cl-
  • Rapid IM absorption
  • Unreliable sedative but good central muscle relaxant and anti-convulsant
  • Minimal CV depressant effects, 10-20% HR/CO reduction
  • Inactive metabolite - better for hepatic dz
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Alpha-2 agonists

A
  • Sedative and supraspinal analgesic effects via decreased norepi release and binding in cerebral cortex & brainstem; also centrally mediated bradycardia/hypotension
  • Receptors in spinal cord and vascular endothelium - spinal analgesia, vasoconstriction, peripheral bradycardia
  • Variably some A1 agonist effect - excitation, increased motor activity
  • Normal to slightly decreased cerebral bloodflow/ICP
  • Blood gas parameters normally maintained, can decrease respiratory drive
  • Bradycardia via peripheral (reflex due to inc SVR) and central (dec sympathetic outflow) mechanisms. CO decreased and selectively decrease tissue blood flow
  • Reversal: yohimbine (xylazine), atipamezole
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Xylazine

A
  • Alpha2-agonist
  • 160:1 a2/a1 specificity
  • Persistent bradycardia due to central effects outweighing peripheral: hypertension progresses to hypotension (20-30%)
  • CO decreases up to 50%
  • Contraindicated for C-section - increased neonate mortality
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Dexmedetomidine

A
  • Alpha2-agonist, dextrorotatory isomer of medetomidine
  • 1620:1 a2/a1
  • Similar CV effects as xylazine/other A2
  • Neuroprotective effects, minimal effect on ICP, blunting of response to intubation, etc, - good for intracranial surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Opioids - MOA/Pk/Pd

A
  • G-protein coupled receptors - dec cAMP, inhibit Ca2+ channels presynaptic (decrease release of excitatory NT), increase K+ outflow postsynaptic (hyperpolarization/inc activation threshold)
  • Three receptors - u (b-endorphin), k (leucine- & methionine- enkephalin), d (dynorphin A)
  • Lipophilic so high Vd, cross BBB (variable efflux by P-gylcoprotein)
  • Receptors in brain, spinal cord, CTZ, GI, synovium, leukocytes, etc.
  • Easily cross placenta - naloxone for fetuses if given during c-section
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Opioids - systemic effect

A

-Analgesia is main effect: spinal and supraspinal (inhibit GABA interneurons in PAG), more effective on C-fibers than A-delta fibers; peripherally have anti-hyperalgesic effects
-Generally dose-dependent sedation (synergistic with other sedatives) , can see excitation (rapid IV administration)
-Dose-dependent resp depression - mediated by
supraspinal mu receptors; usually minor in vet species (inc PaCO2)
-Central anti-tussive effects (u and K at cough center in medulla oblongata)
-Clinical doses have minor CV effects - mild bradycardia (central enhanced parasympathetic activity), usually CO/BP maintained
-Emetic/anti-emetic depending on drug/route/rate: CTZ - delta emetic, u/k anti-emetic. IV generally anti, SQ/IM pro; morphine emetic low/1st dose (not with inc ICP)
-Inhibit release of motility-modifying neurotransmitters (5HT-2, NO, VIP, Ach) - ileus
-Urinary retention due to spinal cord inhibition of micturition with epidural (longer with morphine)
-Thermoregulation: act on preoptic anterior hypothalamus - alter setpoint and compensatory mechanisms: hyperthermia in cats, hypo due to panting in dogs
-Dose dependent MAC reduction; full-u more than others

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Morphine

A
  • Full-u agonist, kappa agonist at high doses
  • Baseline of opioid potency - 1
  • Less lipophilic - slower entry into and diffusion from CNS -> ideal for epidural administration
  • Histamine release after IV administration in dogs
  • 50% hepatic/50% extrahepatic metabolism (most opioids near 100%)
  • Can be given intra-articular
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Oxymorphone

A
  • Full-u, 10x potent as morphine
  • No histamine release, generally less GI side-effects
  • Expensive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Hydromorphone

A
  • Full-u, 8x morphine potentcy

- No histamine release, most associated with hyperthermia in cats (though documented in many)

25
Q

Fentanyl

A
  • Full-u, 100x morphine
  • Less GI side effects, antiemetic
  • Short duration (30m - 2h depending on dose)
  • Transdermal solution - effective within 4 hours, last 3-4d
  • Trandermal patch: 12h to SS in cat, last 3-4d; 24h in dogs, last 2-3d
26
Q

Methadone

A
  • U-agonist (2x morphine) with NMDA antagonist effects - better for chronic pain
  • Synergistic with some other mu (morphine)
  • Metabolism inhibited by chloramphenicol
27
Q

Meperidine

A
  • U (0.1x morphine), serotonergic effects (not with monoamine inhibitors)
  • More histamine release IV than morphine
  • Negative inotropic effects, anti-muscarinic effects
  • Basically sucks, no one uses in small animal
28
Q

Hydrocodone

A
  • U-opioid
  • Poor bioavailability in dog but variably metabolized to hydro
  • Antitussive
29
Q

Codeine

A
  • Classified as u-opioid

- 4% bioavailability in dogs (no morphine metabolite); codeine-6-glucuronide may have some effects along with norcodeine

30
Q

Fentanyl derivaties (su- remi- alf-)

A
  • Full-u

- Remifentanil: metabolized by plasma-esterases (6min T1/2)

31
Q

Etorphine/carfentanil

A

-Used for wildlife capture, will kill you if you poke yourself with needle

32
Q

Buprenorphine

A
  • Partial-u (will partially reverse full); 25-40x morphine
  • pH of cat mouth yields could OTM absorption
  • Simbadol - SID (x3) SQ for cats
  • SR bup - up to 72h, not approved
33
Q

Butorphanol

A
  • U-antagonist/partial agonist; kappa-agonist
  • Anti-tussive and sedative PO but not analgesic
  • Dose reduce with MDR1
34
Q

Nalbuphine/Pentazocine

A
  • U-antagonist/kappa-agonist

- Like butorphanol but not as good

35
Q

Tramadol

A
  • Centrally acting analgesic; codeine analogue with some activity at u-receptor
  • Not metabolized to M1 (active form in humans). Of dubious efficacy in dogs (LJ agrees with this, JT says it is good orally in dogs)
  • Activity as serotonin and norepi reuptake inhibitors (likely method of analgesia in dogs according to LJ)
  • Cats do make M1, may be effective
  • Metabolized in liver and kidney
36
Q

Opioid antagonists

A
  • Naloxone - primary antagonist, mostly mu but some kappa/delta; convulsions d/t GABA antagonism
  • High naloxone dose with antagonize central opioid effects - acute pain, sympathetic stimulation - titrate slowly to effect
  • Low-dose naloxone block TLR4 allodynia from morphine
  • Naltrexone - mu/kappa/delta; longer duration used for wildlife reversal
  • Methylnaltrexone - low lipid solubility - does not reverse CNS effects
37
Q

Dantrolene

A
  • Ryanodine receptor antagonist - peripherally acting muscle relaxant
  • Treatment for malignant hyperthermia & rhabdomyolysis
38
Q

Doxapram

A
  • Analeptic (central nervous system stimulant)
  • Respiratory stimulant via combination of central and peripheral effects
  • Dose-dependent with activation of peripheral aortic & carotid receptors
  • Increase RR and TV to increase minute ventilation but very short-lived - used to assess laryngeal function
  • Dose in one study: 1.1mg/kg for lar-par (no change in glottal size; different study increased
39
Q

Famotidine

A
  • H2 receptor antagonist (~5x more potent than ranitidne, 20-50 more than cimetidine)
  • Demonstrated to be superior in prevention of gastric ulcer to no treatment (saline) or ranitidine, but inferior to PPI
40
Q

Omeprazole

A
  • Proton-pump inhibitor - prevents acid secretion by parietal cells (gastrin, H2, M3)
  • Acts on proton-pump on luminal side of cell
  • Theoretical concern about changing gastric fauna/bacterial overgrowth
41
Q

Maropitant

A
  • Neurokinin (NK1) receptor antagonist - reduces binding of Substance P in brainstem nuclei, centrally acting anti-emetic
  • Extensive hepatic metabolism by CYP3A
  • Possible analgesic properties related to NK1 receptors on sensory afferents in CNS and PNS
  • MAC reduction of 16-30%
42
Q

Methocarbamol

A
  • Centrally acting muscle relaxant - inhibits spinal & supraspinal polysynaptic reflexes via action on interneurons; no direct effect on skeletal muscle
  • Use for tetanus, pyrethrin/permethrin toxicity, acute muscle strain
43
Q

Metoclopromide

A
  • Multiple sites of action: serotonin antagonism in CNS, D2 antagonism in CNS and GI
  • Anti-emetic (weak), increases GE sphincter tone and promotes duodenal peristalsis
  • Reduction in risk of GE reflux in orthopedic surgeries
44
Q

Ondansetron/dolasetron

A
  • Serotonin (5HT-3) receptor antagonist
  • Often used as an antiemetic prior to chemo: effective at preventing vomiting from cisplatin (acts on gastric mucosa stimulating 5HT3)
45
Q

Procainamide

A
  • Class 1a antiarrhythmic, effective at treating SVT and VT
  • Na+ channel blockade to slow rise of phase 0 of cardiac action potential, raise threshold, prolong refractory period
  • Often 2nd line for VT refractory to lidocaine, similar efficacy as sole agent
46
Q

Sodium Nitroprusside

A
  • Potent arterial and venous dilation through liberation of NO
  • Risk of inadvertent hypotension, tachycardia.
  • If overdose or hepatic/renal insufficiency, potential for cyanide or thiocyanate toxicity
47
Q

Vasopressin (ADH)

A
  • Vasoconstrictor - acts on V1a receptor on smooth muscle (also V1b pituitary and V2 renal collecting duct)
  • Alternative to epineprhine, works in acidic environment & in CIRCI
  • No b1 effects so less risk of myocardial ischemia
48
Q

Desmopressin (DDAVP)

A
  • Synthetic analogue of vasopressin with reduced vascular effects
  • Used to manage central DI, peri-operative management of Von Willebrands
49
Q

Amantadine

A
  • Dopamine agonist & NMDA antagonist
  • Used in Parksinson’s and possible role in TBI (in people, being studied in rats)
  • Some evidence for use in chronic arthritic pain in dogs/cats
50
Q

Amitriptyline/Notriptyline

A
  • Tricyclic antidepressant used for behavioral disorders/FLUTD, possible use for neuropathic pain
  • SSRI but also Na+ channel blockade, NMDA antagonism, antihistamine activity
  • Caution in animals with renal insufficiency
51
Q

Gabapentin/pregabalin

A
  • Structural analogues of GABA but no action at GABA receptors (or NMDA, Dopamine)
  • Suggested inhibition of N-type voltage-dependent neuronal calcium channels
  • Historically used as anticonvulsant, currently used for neuropathic pain
52
Q

Tapentadol

A
  • Higher mu receptor affinity (50x) than tramadol but lower than M1 metabolite
  • Similar potency as tramadol for norepi reuptake inhibition, less (5x) for serotonin reuptake inhibition
  • Low oral bioavailability in dogs, extensive hepatic metabolism (glucuronidation) to inactive metabolite
53
Q

Succinycholine

A
  • Depolarizing NMBA
  • Structurally is two Ach molecules combined
  • Rapidly degraded in plasma by pseduocholinesterase - can give large doses and get rapid onset without prolonged duration
  • Not broken down in cleft by acetylcholinesterase - channel remains open, no repolarization of postjunctional membrane
  • Pseudocholinesterase synthesized in liver - decreased by liver disease, chronic anemia, pregnancy, reglan, burns, etc
54
Q

Atracurium (and other non-depolarizing NMBA)

A
  • Non-depolarizing NMBA
  • Dose-dependent onset of ~5min and duration of 30 min in dog
  • Competitively binds to alpha subunit blocking Ach binding and depolarization
  • About 1/2 undergoes Hoffman elimination - not prolonged in hepatic/renal disease; pH and temperature dependent
  • Potential for histamine release (not seen with cisatracurium isomer)
  • Also affect muscarinic receptors on cardiac muscle (arrythmias, inc or dec HR) and parasymp NS in ganglia, less CV effects with newer NMBA
  • Large, hydrophilic - do not cross placenta, may gain entry into CSF
  • Reversal with anticholinesterase drugs - edrophonium, neostigmine, pyridostigmine; edrophonium shorter duration and less muscarinic cholinergic effects (do not need to premed with anticholinergic)
55
Q

Barbituates (thiopental, pentobarbital, phenobarbital)

A
  • CNS depression via activation of GABAa, hyperpolarization of post-synaptic membrane
  • Lipophilic so rapid onset, quick redistribution from CNS to tissues; can have prolonged recovery was tissue equilibrate if multiple boluses/CRI given
  • CNS: CBF and ICP decreased, cerebral 02 consumption decreased by up to 55%; cerebral perfusion pressure maintained d/t ICP dec more than MAP
  • CV: dec SV and contractility, sensitizes to epi related arrhythmias; mild dec in MAP but inc HR
  • RESP: Dose-dependent dperession of resp centers, dec responsiveness to low O2/high CO2
  • Modest decrease renal and hepatic bloodflow
  • Crosses placenta, more effect on neonates than propofol
  • Avoid use in sighthounds - deficient in microsomal enzyme to metabolize
56
Q

Propofol

A
  • Exerts effects through GABAa receptors and inhibits NMDA receptor
  • Chemically distinct from all other anesthetics, rapid awakening
  • Rapidly moves into CNS, quickly redistributes. Extensive hepatic and extrahepatic metabolism so short half-life
  • CNS: reduces ICP and CMRO2, can have significant decrease in CPP in patients with elevated ICP
  • CV: Dec arterial BP, SVR, and CO. No compensatory inc HR
  • RESP: Dose-dependent ventilatory depression, postinudction apnea, dec responsiveness to O2 and CO2
  • No adverse effect on heaptic blood flow or GFR.
  • Crosses placenta but rapidly cleared from neonatal circulation
  • Oxidative injury to cat RBC with repeated administration
57
Q

Dissociatives (ketamine, tiletamine)

A
  • MOA: NMDA, opioid, monoaminergic, and muscarinic receptors, voltage gated Ca channels; NOT GABA
  • Rapid onset, short duration, also effective IM unlike other injectable anesthetics
  • Metabolized in liver, biotransformed to norketamine in cat - extrectd unchanged in urine
  • CNS: cataleptic state by dissociation of limbic and thalamocortical systems via NMDA antagonism; increase CBF and CRMO2, inc ICP; does not lower sz threshold, may be neuroprotective
  • CV: Negative inotrope, overcome by sympathetic stimulation; inc HR, systemic & pulm BP, CO, myocardial O2 (can see decrease if catecholamine stores exhausted - eg CIRCI)
  • Resp: No respiratory depressant effects; bronchodilator/decrease airway resistance
  • No hepatic, renal, GI effects
  • Little muscle relaxation, can have inc tone and spontaneous movement
  • Crosses placenta, most depression of neuro reflexes in neonates of injectable induction drugs
  • Good analgesic
58
Q

Etomidate

A
  • Imidazole derivative, acts at GABA receptor enhancing inhibitory effects
  • Rapid penetration to CNS, rapid, redistribution to inactive tissues. 75% albumin bound.
  • CNS: cerebral vasoconstriction, dec CBF and CRMO2. CPP unchanged due to maintenance of MAP, dec ICP. May precipitate sz in p with hx.
  • CV: No cardiovascular effects, ideal for p with severe cardiac dz
  • Resp/renal/GI/hepatic: No resp depression, no reduction in hepatic blood flow or GFR
  • Endocrine: adrenocortical supression via dose-dependent inhibition of convernsion of cholesterol to cortisol; contraindicated with Addison’s
  • Pain on IV injection; myoclonus, dystonia, tremors; intravascular hemolysis d/t hyperosmolality
59
Q

Alfaxalone

A
  • Neuroactive steroid; acts on GABA, modulate ion currents at low dose, agonist at high dose
  • CyP450 and conjugation-dependent metabolism
  • CNS: CBF, ICP, CRMO2 all decreased
  • CV: HR, CO, BO decrease in dose-dependent fashion
  • RESP: dose-dependent depression
  • (CV and RESP effects not as significnat at lower clinical doses)
  • Can be used as a CRI for TIVA; longer-recovery with minor adverse events

Phase I (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions