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Pharmacology FINAL (2nd sem) > A: 23, 24 > Flashcards

A: 23, 24 Flashcards

1
Q

Inhaled anasthestics

A

DIS flower is so calming

Administered as gases , where partial pressure/tension in the inhaled air/in blood/ in tissues is a measure of their conc,

  • Halogenated HC:
    • Desflurane
    • Isoflurane
    • Sevoflurane
    • halothane
    • enflurane
  • nitrous oxide (N2O)
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2
Q

inhaled anesthetic mechanism of action

A
  • Facilitate GABA-mediated inhibition
  • Block brain NMDA
  • inhinit AchR (nicotinic) at medium/high conc.
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3
Q

Desflurane
Isoflurane

SE

A
  • Pulmonary irritant, may cause bronchospasm (BOTH)
  • Isoflurane:
    • peripheral vasodialtion
    • sensitizes myocardium to catecholamines > Arrhythmias
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4
Q

Sevoflurane SE

A
  • Nephrotoxic ( with prolonger anesthesia)
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5
Q

Pharmacologic effects on inhaled anesthetics

A
  • NO2
    • Uterine contraction > spontanoues abortion
    • drug of abuse “laughing gas”
    • diffusional hypoxia
  • Desflurane:
    • Pulmonary irritant (bronchospasm)
    • Peripheral vasodialation (decrease BP)
  • Isoflurane
    • Peripheral vasodialation (decrease BP
    • sensitizes myocardium to arrhythmogenic effect of catecholamines
    • pulmonary irritant (bronchospasm)
  • Sevoflurane
    • Nephrotoxicity (with prolonged anesthesia)
    • Peripheral vasodialation (decrease BP
  • Enflurane
    • myocardial depressant
    • Nephrotoxicity (with prolonged anesthesia)
    • increased cerebral blood flow : high level of enflurane cause muscle twitch & spike-&-wave activity.
  • myocardial depression (decrease CO): Enflurane , halothane (NO2 least likely)
  • ALL decrease respiratory function
  • Halothanne , isoflurane (less) : sensitize myocardium to arrythmogenic effect of catecholamines.
  • lung irritation (desflurane, isoflurane)
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6
Q

Which has high Blood:gas partition coefficient?

A

Halothane
Sevoflurane

Sevo Stay in blood

Higher blood solubility > equilibrates with blood slower

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7
Q

Which has low Blood: gas partition coefficient?

A

Desflurane
N2O

Deso Dissolves in gas

equilibrates more rapidly with blood; drug passes into brain faster producing anesthesia

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8
Q

Most inhaled anesthetics inhibit —– at moderate-high conc.c

A

nictotinic AchR isoforms

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9
Q

Inspired gas partial pressure effect on inhaled anesthetics

  • A high partial pressure of gas in the lungs results in —–
A

Rapid achievement of anesthesitic levels in blood

Done by administering higher gas conc. than required for maintencance of anesthesia.

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10
Q

The greater the ventilation rate the ……..

A

more rapid is the rise in alveolar and blood partial pressure of agent & onset of anesthesia

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11
Q

Potency of inhaled anesthetics is roughly proportional to their ——-

A

lipid solubility

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12
Q

pulmonary blood flow effect on inhaled anesthetics

A
  • high pulmonary blood flow :
    • gas partial pressures rises at slower rates; speed of onset of anesthesia in REDUCED.
  • low pulmonary blood flow
    • faster onset of anesthesia

In circulatory shock, this effect may accelerate rate of onset of anesthesia with agent of high blood solubility.

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13
Q

Elimination of inhaled anesthtic

A
  • redistribution of drug from brain > blood> alveolar air> elimination by lung
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14
Q

CNS neurons in diff regions of the brain have different sensitivities to general anesthetics

what is inhibited first neurons involved in pain pathway VS neurons in midbrain reticular formation

A

neurons involved in pain pathway is inhibited first

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15
Q

rate of recovery from Low blood: partition coefficient VS high solubility drugs

A
  • rate of recovery from Low blood: partition coefficien : FASTER
    eg. desflurane, nO2 have low blood solubility ; shorter recovery time than older agents
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16
Q

Potency of inhaled anesthetic is best measured by ——

A
  • MAC (minimum alveolar anesthetic conc.)= alveolar conc. required to eliminate response to standarized painful stimulus in 50% of patients
  • each anesthetic has defined MAC, but value may vary among patients depending on
    • age
    • CV status
    • use of adjuvant drugs
  • NOTE: MAC for infants and elderly are lower than those for young adults
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17
Q

inhaled anesthetic pharmacokinetics

A
  • Rate of onset and recovery vary by blood:gas partition coeffient
    • drugs with low blood: gas coeff equilibrates more rapidly> faster anesthesic effect
  • Recovery mainly due to redistribution from brain>blood> alveolar air> other tissues
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18
Q

If several inhaled anesthetic agents used simultaneously their MAC values are —–

A

Additive

eg. 0.5 MAC NO2 +
0. 5 MAC desflurane = 1MAC inhaled anesthetic

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19
Q

Toxicities of inhaled anesthetics

A
  • Extensions of effects on
    • brain:
      • decreased brain metabolic activity
      • increase cerebral blood flow; increased ICP
        • high conc. enflurane cause spike-and-wave activity and mucle twitching
    • heart/vessels
      • decrease arterial BP (less likely with no2)
      • isoflurance, desflurane, sevoflurane > peripheral vasodialation
    • lungs:
      • RR increase
      • dose-dep decrease in TV, Minute ventilation> increased arterial CO2 tension
      • most are bronchodilators
  • Drug interactions:
    • additive CNS depression with opoids & sedative-hypnotics
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20
Q

prolonged exposure to no2 causes

A

megaloblastic anemia (due to decreased methionine synthase activity)

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21
Q

SE when using inhaled anesthetic together with Neuromuscular blockers (esp succinyl choline_

A

malignant hyperthermia (sign: masseter hypertonia)

due to mutations in gene loci of RYR1 and

skeletal muscle L-type Ca channel

uncontrolled release of Ca by SR of skeletal m leads to

  • muscle spasm
  • hyperthermia
  • autonomic lability

Dantrolene indicated + supportive

22
Q

What anesthetics Facilitate GABA-mediated inhibition

A
  • Inhaled anesthetics
  • Barbiturates: thiopental
  • Benzodiazepine: midazolam
  • etomidate
  • propofol

y-aminobutyric acid

23
Q

Stages of anesthesia

A
  • stage 1: analgesia
    • Patient has decreased awareness of pain
    • Amnesia (sometimes)
    • conciousness impaired, BUT not lost
  • stage 2 : Disinhibition
    • ​patient is in delerious and excited
    • amnesia occurs
    • reflexes are enhanced
    • irregular respiration
    • retching and incontinence (lack of voluntary control over urination or defecation) may occur
  • stage 3: surgical anesthesia
    • ​Unconcious
    • no pain reflexes
    • respiration is regular
    • BP maintained
  • stage 4: Medullary depression
    • Patient develops severe respiratory & CV depression
    • requires mechanical and pharmacologic support to prevent death
24
Q

general anesthetic VS conventional sedative-hypnotics

A
  • general anesthetics are CNS depressants with actions that can be induced and terminated more rapidly
25
Q

general anesthesia definition

A
  • state of
    • unconciousness
    • analgesia
    • amnesia
    • skeletal muscle relaxation
    • loss of reflexes
26
Q

IV anasthestics

A

PEKMully? TFuu.פחמימות לוריד ישר

Propofol- GABA-A inhibition
Etomidate- GABA-A inhibition
Ketamine- NMDA inhib. (central glu R)
Midazolam(benzo)- GABA-A inhibition
Thiopental (barbiturate)- GABA-A
Fentanyl- opioid u-r agonist

Dexmedetomidine - ( centrally-acting alpha-2 agonist)

27
Q

ketamine mechanism

A
  • Antagonist of action of excitatory glutamic acid on the NMDA-r
28
Q

Special SE of Ketamine

A
  • Cardiovascular stimulant
  • Intracranial hypertension
  • disorientation, excitation, hallucination, delerium, vivid nightmare
29
Q

D2-R antagonist sedative

A

Metoclopramide - antiemetic ( perioperative)

מתוק לו כשאין דופמין
כי דופמין מוריד פרולקטין וחלב זה מתוק אז כשאין דופמין יש חלב מתוק

30
Q

Preoperative sedation

A

Midazolam

31
Q

Perioperative agents

A
  • anxiolytics: benzo (midazolam, lorazepam)
  • Analgesics :
    • ​opioid ( fentanyl, morphine, hydromorphone)
    • NSAIDS (ketorolac, diclofenac, meloxicam)
  • Anti-emetic
    • Metoclopramide (D2-r blocker) oral, parenteral
    • droperidol
  • GI protective agents
    • H2 blockers : Cimetidine, famotidine, ranitidine, nizatidine
    • PPI
    • sucralfate
  • Anti-muscurinics
    • Atropine: (non-selective) -oral, parenteral : anti spasmodic , anti diarrhea, reversal of AV block, managing bradyarrythmias (IV)
  • Antibiotic prophylaxis
    • Ampicillin
    • cefazolin
    • cefuroxime
  • Acid-supressing agents (ANTACID) - weak bases neutralise stomach acid
    • NaHCO3
    • Mg(OH)2
    • AL(OH)3
32
Q

Barbiturates drugs and mechanism of action

A
  • Intravenous anesthetic
  • Facilitates GABA-mediated inhibition at GABA-A receptor
  • Thiopental
  • thiamylal
  • methohexital
33
Q

Barbiturates pharmacologic effects and pharmacokinetics (onset, duration, termination, elimination)

A
  • pharma effects:
    • Circulatory and respiratory depression
    • decrease intracranial pressure (ICP) - depress cerecral blood flow
  • High lipid solubility - which promotes rapid entry into the brain and results in surgical anesthesia in one circulation time (<1 min)
    • fast onset
    • short duration due to distribution
  • The anesthetic effects of thiopental are terminated by redistribution from the brain to other highly perfused tissues
  • but hepatic metabolism is required for elimination from the body
34
Q

Barbiturates

Toxicities and interactions

A
  • Extensions of CNS depressant actions
  • Additive CNS depression with many drugs
35
Q

Barbiturates drugs and indication

A

Thiopental

Metho-hexital

  • induction of anesthesia
  • for short surgical procedures.
36
Q

Propofol mechanism of action, pharmacokinetics

A
  • GABA-A inhibition
  • I.V anesthetic
  • Fast onset , Fast recovery due to inactivation
  • propofol produces anesthesia as rapidly as I.V barbiturate but recovery is more rapid!
  • Hepatic metabolism
37
Q

Propofol pharmacologic effect, toxities

A
  • Vasodialation and hypotension
  • negative inotropy : decreased contractility force
  • Anti-emetic effect
  • Hypotension (during induction)
  • CV depression
38
Q

propofol indication

A
  • General anesthesia
  • Outpatient anesthesia
  • Prolonged sedation in patients in Intensive care setting
  • Anti-emetic activity

I.V

39
Q

Etomidate mechanism of action and administraion, onset

A
  • Imidazole derivative
  • GABA-mediated inhibition at GABA-A receptors
  • I.V
  • Rapid onset and short duration of action due to distribution
40
Q

Etomidate pharmacologic effects and toxicities

A
  • This drug is not analgesic, its primary advantage is in anesthesia for patients with limited cardiac or respiratory reserve.
    • because it has Minimal effects on cardio-vascular and respiratory function
  • Pain on injection (may need opioid)
  • myoclonus
  • nausea and vomiting
  • Prolonged administration may cause adrenal suppression.
41
Q

Ketamine mechanism of action and administration, pharmacokinetics

A
  • Blocks excitation by glutamate at NMDA receptors
  • IV
  • Hepatic metanolism
  • moderate duration of action
42
Q

ketamine indication and toxicities

A
  • produces a state of “dissociative anesthesia” in which the patient
    • remains conscious but has marked
      • catatonia
      • analgesia
      • and amnesia
    • toxities:
      • Increased intracranial P ( due to Cardio-vascular stimulanting effect!)
      • emergence reactions (disorientation, excitation, and hallucinations) which occur during recovery from ketamine anesthesia, can be reduced by the preoperative use of benzodiazepines.
43
Q

Dexmedetomidine mechanism and administration

A
  • centrally acting α2-adrenergic agonist
  • when used intravenously has: analgesic and hypnotic actions
  • rapid clearance ; short elimination T1/2
44
Q

Dexmedetomidine indiation

A
  • mainly used for short-term sedation in an ICU setting.
  • When used in adjunct to general anesthesia, the drug decreases dosage requirements for both inhaled and intravenous anesthetics
  • achieves sedation with no respiratory depression

centrally acting alpha2 agonist has analgesic and hypnotic actions when used intravenously

45
Q

Midazolam mechanism and administration, metabolism

A
  • Benzodiazepine
  • Facilitates GABA-mediated inhibition at GABA-A receptors
  • I.V
  • Hepatic metabolism
  • post-operative respiratory depression reveresd by flumazenil
46
Q

Benzodiazepine action can be terminated by

A

effect terminated by flumazenil (accelerates recovery)

47
Q

flumazenil can terminate what drug action

does it work on ethanol or barbiturates?

A
  • Flumazenil (anatginost at benzo site on GABA-A r) can be used to reverse the CNS depressant effects of benzodiazepines,(midazolam)
  • but there is NO antidote for barbiturates or ethanol.
48
Q

midazolam indication and SE

A
  • Preoperative sedation
  • Induction anesthesia
  • outpatient anesthesia ( eg colonoscopy)
  • SE:
    • CV and respiratory depression
49
Q

BENZO compared with barbiturates

  • onset
  • duratuin
  • depressant
A

Benzos are

  • less depressants than barbiturates
  • slower onset
  • longer duration than barbiturates
50
Q

fentanyl mechanism . administration, metabolism

A
  • Opoid receptors (u) agonist
  • I.V
  • Hepatic metabolism
51
Q

fentanyl indication , SE

A
  • used with other CNS depressants (NO2, BENZO) in anasthesia resgimens
    • esp valuable in high-risk patients who might not survive ful general anesthesia
  • SE:
    • respiratory depression ( can be revesed postoperatively by naloxone)

Pharmacology FINAL (2nd sem) (37 decks)

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