A.22

Question 1

Intravenous anesthetics. Perioperative medication

Answer 1

Propofol,
Etomidate,
Ketamine,
Dexmedetomidine,
-Barbiturates: No analgesia: Thiopental
-Benzodiazepines: Midazolam
-Opiods: Fentanyl,
-Parasympatholytic: Atropine,
-Perioperative medication: Metoclopramide, Antacid drugs, Antihistamines, analgestics

Question 2

Propofol

Answer 2

MOA: Glycine gated Cl- channels agonist, GABAA agonist→ Cl- influx;
Effect: causes decreased level of conciousness and amnesia;
IND: induction & maintenance of anesthesia, Outpatient anesthesia, Antiemetic effect (treat postoperative vomiting and nausea), a component of TIVA, sedation in mechanically ventilated patients in ICU;
Kinetics: short context-sensitive half-time, high protein binding, short acting (5-10min), rapid onset (30sec) and recovry, hepatic metabolism by conjugation;
SEs: hypotension (potent vasodilator effect), metabolic acidosis (→propofol infusion syndrome- after long application in higher doses it can cause disturbances in lipid metabolism), Pain at injection site, cardiac + respiratory depressant, Overdose can cause death; Extra: Fospropofol- water soluble used in ICU

Question 3

Etomidate

Answer 3

MOA: GABAA agonist→ Cl- influx;
IND: Only for induction of anesthesia in patients with limited cardiac or respiratory reserve (e.g. hypovolemic patients);
SEs: Pain at injection site, nausea + vomiting, supress normal stress-induced adrenal cortisol for hours (↓cortisol);
Kinetics: short acting, rapid onset, preserves cardiovascular + respiratory stability

Question 4

Dexmedetomidine

Answer 4

MOA: α2 agonist (at presynaptic neuron, inhibit release of NE);
IND: short term sedation of intubated and ventilated patients in ICU, HTN;
Kinetics: analgestic, sedative/anxiolytic and stress relieving effects, improves perioperative hemodynamic stability;
SEs: bradycardia, hypotension (possible reflex HTN as well due to weak α1 activation in periphery); ContraIND: hypotensive patients

Question 5

Thiopental

Answer 5

MOA: GABAA agonist→ Cl- influx;
IND: induction of anesthesia, Anesthesia for short surgical procedures;
Kinetics: ultra-short acting, rapid onset (<1min), hepatic metabolism (enzyme inducer), slow recovery due to accumulation in tissues→ long T1/2 (may produce “hangover”);
SEs: hypotension, negative inotropic, peripheral vasodilation, inhibition of baroreflex, Apnea, coughing, ↑HR, cardiac + respiratory depressant, cerebral vasoconstriction (→ ↓cerebral blood flow, volume, ICP)

Question 6

Midazolam

Answer 6

MOA: GABAA agonist→ Cl- influx;
IND: not real anesthetic (→effect is not narcosis, but deep sleep), preoperative sedation, induction of anesthesia, outpatient anesthesia (e.g. colonoscopy); Kinetics: short acting, slow onset;
SEs: cardiovascular +respiratory depression, antidote- Flumazenil;
Dosage: 0.1-0.2mg/kg i.v

Question 7

Fentanyl

Answer 7

MOA: synthetic strong μ-OR agonist, analgestic agent; IND: induction and maintenance of anesthesia, management of pain (e.g. cancer patients);
Kinetics: acts as long as it is infused;
SEs: strong CNS depressant, respiratory depression (reversed with naloxone)

Question 8

Atropine

Answer 8

MOA: strong and effective non-selective M-ACh-R antagonist;
IND: reduces salivation and bronchial secretions before surgery, decreases vagal tone due to administration of inhaled narcotics;
SEs: general anti-M SEs (dry eyes, blurred vision, hallucination, delirium, urinary retention, constipation, decreased secretions);
Dosage: 0.3-1.0mg

Question 9

Metoclopramide

Answer 9

MOA: DA D2-R antagonist;
IND: anti-emetic effect (high doses required) prevents emesis after anesthesia and chemotherapy-induced emesis, Prokinetic agent (low doses required) → GERD, gastroparesis;
Effect: central effect (→inhibition of D2 receptor in area postrema results in anti-emetic action + anti-nausea), peripheral effect (→↓DA→ ↑ACh release +effect →prokinetic effect mediated by ACh);
SEs: drug induced parkinsonism, extrapyramidal symptoms, hyperprolactinemia, QT prolongation

Question 10

Antacids

Answer 10

weak bases that neutralize gastric acid by reacting with protons in the lumen of the gut (antacid + water→increasing pH)

Question 11

Mg(OH)2

Answer 11

Chemistry: Mg(OH)2 + 2HCl → MgCl2 + 2H2O;
Kinetics: slow onset, poorly absorbed from bowel;
SEs: diarrhea (unabsorbed Mg salt), hypermagnesemia (bardycardia, hypotension)

Question 12

Al(OH)3

Answer 12

Chemistry: Al(OH)3 + 3HCl → AlCl3 + H2O + CO2; Kinetics: slow onset, poorly absorbed from bowel; Effect: protects mucosa→ AlCl3 is a gel-like substance; SEs: constipation, increased Al absorption→ encephalopathy

Question 13

Antihistamines

Answer 13

GI protective agents: H2R blockers, proton pump inhibitors

Question 14

Analgestics

Answer 14

pioids (fentanyl, morphine, hydromorphone) + NSAIDs

Question 15

Outpatient anesthesia

Answer 15

Also known as ambulatory anesthesia, outpatient anesthesia is administered for minor procedures where an overnight stay is not anticipated.

Question 16

Balanced anesthesia

Answer 16

Combination of different drugs to achieve the goals of surgical anesthesia and decrease the SEs of individual agents. Preoperative- sedation=analgesia, Intraoperative- neuromuscular blocking agents (e.g. I.V propofol / etomidate / thiopental + isoflurane / sevoflurane / desflurane)

Question 17

TIVA

Answer 17

Total intravenous anesthesia. Hypnosis→ analgesia→ muscle relaxation

Question 18

Dissociative anesthesia

Answer 18

patient remains conscious but has marked analgesia, amnesia and catatonia (lack of movement and communication)

Question 19

Context-sensitive half-time

Answer 19

Is the time that required for blood or plasma concentrations of anesthetic agents to decrease by 50% after discontinuation of intravenous anesthetics infusion.
Protein binding: as a general rule, drugs that have low protein binding can penetrate tissue better, while drugs that have high protein binding can stay longer in circulation