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Phase 1 > Anethestic Drugs > Flashcards

Anethestic Drugs Flashcards

1
Q

What effect does hypoalbuminemia have on anesthetic drugs

A

Decreases bound fraction of some drugs (increases free drug) which can result in changes in volume of distribution, plasma concentration, and drug effect (e.g. NSAIDs are tightly protein bound)

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2
Q

Which direction do opioids shift the CO2 response curve when given alone

A

When given alone, opioids shift the CO2 response curve to the right with little change in slope

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3
Q

What is the primary analgesic effect of tramadol

A

Metabolism of tramadol to M1 and M1 acts as a full mu opioid agonist

Analgesia via opioid and non-opioid (monoamine uptake inhibition) mechanisms

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4
Q

How is tramadol excreted

A

Excreted largely unchanged in the urine - no liver metabolism

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5
Q

Why is efficacy of tramadol weak in dogs

A

Dogs do not produce large amounts of M1 and studies show in humans that don’t form M1 from tramadol have little to no effect of the drug.

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6
Q

Fentanyl potency

A

100x more than morphine

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7
Q

Fentanyl pitfalls

A

More likely to cause apnea and bradycardia when given as a bonus compared to other opioids
Can cause wooden chest - chest wall rigidity

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8
Q

Remifentanil - what is it, metabolism, and benefit

A

Analogue of fentanyl
Metabolized by plasma esterases therefore it has a short half life.
Good if you want a patient to wake up quickly

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9
Q

Methadone potency

A

2x more than morphine

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10
Q

Why does methadone cause less excitation in cats

A

It is an NMDA antagonist

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11
Q

Buprenorphine potency

A

40x more potent than morphine

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12
Q

Buprenorphine advantages

A

Causes less ileus
Ceiling effect - not associated with increased analgesia but higher doses do cause longer duration

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13
Q

Advantages of Alfaxalone over propofol

A

Less decrease in cardiac output and apnea
Can be given IM

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14
Q

Alfaxalone MOA

A

Steroid anesthetic
Enhances GABA and glycine mediated CNS depression

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15
Q

Propofol MOA

A

Unrelated to steroid anesthetic
GABA agonist: Inhibits CNS

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16
Q

Disadvantages of propofol compared to Alfaxalone

A

Benzyl alcohol formulation shouldn’t be given repeatedly or in CRI to cats (can cause CNS toxicity - hyperesthesia and depression)
More likely to cause apnea
CV effects: Hypotension from vasodilation; decrease in SVR and CO

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17
Q

Propofol advantages

A

Appropriate for patients with liver failure - extrahepatic metabolism sites
Used to treat refractory status epilepticus and reduces ICP

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18
Q

Lipid solubility of morphine

A

Relatively low lipophilicity

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19
Q

Dopamine MOA

A

Stimulates endogenous norepinephrine from presynaptic storage sites at adrenergic receptors to cause sympathomimetic effect

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20
Q

Dopamine dosing and what receptors predominate

A

Low dose (1-2 mcg/kg/min) - dopamine and DA-2 receptors
Medium dose - B1 and B2 adrenergic receptors
High dose >10 mcg/kg/min - A1-adrenergic receptors

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21
Q

Effects of B1 and B2 adrenergic receptor stimulation by dopamine

A

Increases myocardial contractility, HR, CO, and coronary blood flow

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22
Q

Effects of A1-adrenergic receptor stimulation by dopamine

A

Increases SVR, pulmonary vascular resistance, venous return, and PCV (via splenic contraction)

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23
Q

MOA of vasopressin

A

Non-catecholamine vasopressin that acts on the peripheral vessels (V1a, V1b, and V) while decreasing cellular hyperpolarization and increasing intracellular calcium concentration

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24
Q

What is the MOA of doxapram and its effects on glottal gap

A

Analeptic (CNS stimulant) with central and peripheral effects. Increases activity of the respiratory nuclei of the medulla
When given to dogs with larpar: glottal gap area at inspiration was reduced and significantly greater during exhalation

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25
Q

What class of drugs are atropine and glycopyrrolate

A

Anticholinergics, parasympatholytics, antimuscarinics

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26
Q

Anticholinergics and GI motility and other GI effects

A

Dose required to decrease GI motility via blockade of M3 receptors is higher than that required to treat bradycardia

Decreases lower esophageal sphincter function which may lead to increased risk of gastroesophageal reflux

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27
Q

Atropine MOA
Does it cross the BBB

A

Anticholinergic- competitive, reversible antagonist of muscarinic receptors (M1- M5) inhibiting ACh release
Yes and blood placenta barrier
Can cause sedation

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28
Q

Glycopyrrolate and GI motility

A

Decreased for up to 30 minutes in dogs

29
Q

Glycopyrrolate BBB and blood placenta barrier

A

Does not cross

30
Q

Dobutamine MOA

A

Synthetic catecholamine
Primarily B1 adrenergic
Higher doses - B2 and A1 adrenergic receptors
Augments CO states associated with reduced myocardial function

31
Q

Dobutamine effects

A

Limited effects on BP
Increases CO, HR, and SVR

32
Q

Dexdormitor and its receptors

A

Mainly alpha 2 agonist with some peripheral alpha 1 agonist

33
Q

What are the alpha 1 agonist effects of dexdormitor

A

Vasoconstriction, hypertension, arrhthmogenicity, and paradoxical excitation.
Reflex bradycardia due to hypertension which leads eventually to hypotension

34
Q

Side effects of dexdormitor

A

Hyperglycemia, diuresis, and respiratory depression

35
Q

What are the consequences of giving an Anticholinergics with dexdormitor

A

Greater hypertension which increases the myocardial work

36
Q

Gabapentin MOA

A

Structural analogue of GABA but does not interact with GABA, NMDA, or dopamine
Inhibits N-type voltage dependent neuronal calcium channels

37
Q

Gabapentin excretion

A

By the kidneys

38
Q

What was amantadines original use

A

Antiviral agent then for Parkinson’s, TBI and pain

39
Q

Amantadine MOA

A

Dopamine agonist and NMDA agonist

40
Q

Ketamine in terms of somatic pain and dosing

A

Subanesthetic doses of ketamine produce profound analgesia especially in situations of somatic pain

41
Q

Can ketamine be given via an epidural

A

Yes

42
Q

Ketamine side effects

A

Catatonic state Increases salivation, ICP and IOP
Eyes remain open and swallowing reflex is maintained
Produces mild sympathomimetic effect - increases myocardial work

43
Q

What are the two categories of NMBAs and name an example of each

A

Depolarizing - Succinylcholine
Non-depolarizing - Atracurium

44
Q

Atracurium duration of action

A

Dose dependent duration of action 5-30 minutes

45
Q

Succinylcholine MOA and possible disadvantage

A

Mimics effects of acetylcholine
Initial depolarization of all skeletal muscle - looks like fasciculations
Trigger for malignant hyperthermia

46
Q

Elimination of Atracurium

A

Degraded by Hofmann elimination - independent of liver and renal excretion

47
Q

What is the TOF - train of four

A

In relation to NMBA
When 70% of receptors are occupied by a NMBA the twitches will fade beginning with the 4th, then the 3rd, then the 2nd then the 1st

48
Q

NMBA reversals

A

Anticholinesterase
Edrophonium, neostigmine, and pyridostigmine

49
Q

NMBA reversals MOA and side effects

A

Inhibit enzyme anticholinesterase increasing the concentration of ACh molecules at the neuromuscular junction

Can cause cholinergic crisis - SLUDD signs - give Anticholinergic to treat

50
Q

Edrophonium MOA

A

Reversible inhibition of electrostatic attachment to the an ionic site and by H bonding at the esteratic site on acetylcholinesterase

51
Q

Neostigmine and pyridostigmine MOA

A

Inhibit acetylcholinesterase by forming carbamyl-ester complex at the esteratic site of acetylcholinesterase

52
Q

List opioids from least to most potent

A

Meperidine -> Morphine -> Methadone -> Hydromorphone -> oxymorphone -> buprenorphine -> fentanyl

53
Q

Meperidine disadvantage

A

Causes severe histamine rerelease
When given with MAOI can cause serotonin syndrome

54
Q

NSAIDs MOA

A

Arachidonic acid is the predominant fatty acid in animal cell membranes and biotransforms into eicosanoids. Prostanoids are eicosanoids metabolized by prostaglandins (PGD2, PGF2a, and PGE2), PGI, and TXA2. Arachidonic acid is acted upon by COX or LOX enzymes to form eicosanoids.
NSAIDS inhibit COX enzymes and alter the formation of prostanoids

55
Q

COX - 1 (prostaglandin synthase-1): type of enzyme? Responsible for?

A

Constitutive enzyme
Responsible for normal physiologic function

56
Q

COX -2 (prostaglandin synthase-2): type of enzyme? Responsible for?

A

Inducible enzyme
Usually unregulated (induced) by inflammation
May be unregulated during renal stress as a protective mechanism
GI stress - protective and healing.

57
Q

Robenacoxib with or without food

A

Give fasted - cats absorption was 49% vs 10% when given with food. In dogs 84% absorption without food and 62% with food.

58
Q

NSAIDs effects on the spinal cord

A

NSAIDs inhibit prostaglandin in both the peripheral and nervous systems (spine and brain)

59
Q

NSAID GI toxicity

A

Direct irritation of the drug on the GI mucosa and prostaglandin inhibition
Inhibition of prostaglandins results in decreased cytoprotection, diminished blood flow, decreased synthesis of protective mucus, and inhibition of mucosal cell turnover and repair.

60
Q

What type of drug is carprofen

A

Selective COX-2 inhibitor

61
Q

Carprofen and phenobarbital

A

Animals on phenobarbital are more susceptible to hepatotoxicity

62
Q

NSAIDs mechanism of renal injury

A

Prostaglandins modulate tone of blood vessels and regulate salt and water balance in the kidneys
COX 1 and COX 2 maintain renal blood blow and ion transport within the nephron
AKI from inhibition of renal prostaglandin synthesis
AKI is characterized by decreased renal perfusion, sodium, and fluid retention, decreased tubular function, and azotemia

63
Q

Meloxicam in cats

A

Labeled for chronic use in cats outside of US
Give with food and when cats are euvolemic at a low dose 0.01-0.03 mg/kg/day

64
Q

How do NSAIDs aid in treating OA

A

Canine chondrocyte cell cultures revealed that carprofen increases rate of PGAG synthesis which can be chondroprotective
Dual inhibitors (COX and lipoxygenase) may slow progression of OA

65
Q

NSAIDs and liver injury

A

Idiosyncratic - carprofen and others
Intrinsic - aspirin and acetaminophen
Undergo extensive hepatic metabolism and the liver is exposed to high concentrations of the parent drug and its metabolites
Usually reversible with supportive care

66
Q

Misoprostal type of drug and what its used for

A

Synthetic PGE analog that prevents and helps heal GI ulceration

67
Q

Name four effects of PGE on the kidney

A

Maintains renal blood flow and ion transport within the nephron
Increases salt excretion and increases water excretion
Maintains water hemostasis and tubular function
Regulates the release of renin

68
Q

Name 5 effects of PGE on the stomach

A

Maintains gastric mucosal layer
Quality of gastric mucous
Mucosal blood flow
Production of gastric acid
Bicarb secretion

69
Q

Acetaminophen in cats and MOA of injury

A

Cats have a phase II/ acetaminophen metabolizing enzyme deficiency
acetaminophen is shunted to phase 1 enzymes which produce toxic oxygen radicals leading to methemoglobinemia and potentially hepatic necrosis

Phase 1 (71 decks)

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