EDAIC I MCQs from the ESAIC sample paper with simplified explanations. Weekly free uploads by targetedaic. (4)

A. can cause postural hypotension B. reduces heart rate C. has an elimination half-life of 24 hours D. is a more potent alpha than a beta-adrenoceptor blocker E. may cause bronchoconstriction

A. TRUE B. TRUE C. FALSE D. FALSE E. TRUE

EXPLANATION: Due to the alpha1-receptor antagonistic activity of labetalol, blood pressure is lowered more in the standing than in the supine position, but this can lead to symptoms of postural hypotension.
Labetalol is both a selective, competitive, alpha 1-adrenergic antagonist as well as non-selective, competitive, beta-adrenergic (B1 and B2) blocker in a single agent. Activity ratio of alpha to beta-blockade has been estimated to be approximately 1:3 and 1:7 following oral and intravenous (IV) administration, respectively.

Labetalol is metabolized by the liver resulting in an inactive glucuronide conjugate. It has an onset of action within 2 to 5 minutes, reaches its peak effects at 5 to 15 minutes, has an elimination half-life of 5.5 hours, and a duration of action up to four hours.

Another important consideration for anesthesia providers in the perioperative period is that non-selective beta blockers that interact with beat receptors can result in bronchospasm in patients with a history of asthma or chronic obstructive pulmonary disease due to antagonism of beta receptors.

A. Hyperglycaemia B. Hypokalaemia C. Increased gastrointestinal motility D. Skeletal muscle tremor E. Increased contractility of the pregnant uterus

A. TRUE B. TRUE C. FALSE D. TRUE E. FALSE

EXPLANATION: Cardiac effects

1. Increase contractility (positive inotropy)
2. Increase relaxation rate (positive lusitropy)
3. Increase heart rate (positive chronotropy)
4. Increase conduction velocity (positive dromotropy)

Vascular effects

1. Smooth muscle relaxation (vasodilation)

Muscle effects:

1. Smooth muscle relaxation: bronchodilation, uterine relaxation, urinary bladder relaxation, vasodilation
2. Skeletal muscle
   1. uptake of potassium
   2. abbreviated active state and less conduction in slow conducting fibres
   3. enhanced muscle spindle firing

Metabolic effects:

1. Hepatic glycogenolysis and gluconeogenesis: ↑ blood glucose
2. Pancreatic release of glucagon: ↑ blood glucose
3. Renin release by kidneys

A. progressive metabolic acidosis B. abnormal electroencephalographic changes C. increased mixed venous oxygen tension D. constant response to low dose infusion of sodium nitroprusside E. a decrease in haemoglobin saturation

A. TRUE B. TRUE C. TRUE D. FALSE E. FALSE

EXPLANATION: Acute cyanide toxicity occurs when the cyanide ions bind to tissue cytochrome oxidase and interfere with normal oxygen utilization. This as a result leads to metabolic acidosis, cardiac arrhythmias, and increased venous oxygen content (as a result of the inability to utilize oxygen). Another early sign of cyanide toxicity is the acute resistance to the hypotensive effects of increasing doses of sodium nitroprusside (tachyphylaxis). (It should be noted that tachyphylaxis implies acute tolerance to the drug following multiple rapid injections, as opposed to tolerance, which is caused by more chronic exposure). Cyanide toxicity can usually be avoided if the cumulative dose of sodium nitroprusside is less than 0.5 mg/kg/h
Cyanide toxicity is often associated with the odour of almonds on the breath and can result in acidosis, tachycardia, mental status changes seizures (hence the EEG changes), and death.
Normal oxygen saturation on pulse oximetry is expected as there is adequate oxygen in the blood yet inability to use the oxygen that is present.

A. paralysis of the sphincter pupillae muscle B. paralysis of the ciliary muscle C. increase in intraocular pressure D. enophthalmos E. photophobia

A. TRUE B. TRUE C. TRUE D. FALSE E. TRUE.

EXPLANATION: On local application, ATROPINE causes relaxation/paralysis of the sphincter pupillae and ciliary muscles leading to mydriasis and cycloplegia (blocking of the accommodation reflex). This leads to photophobia.
It may cause increase in IOP especially in glaucomatous eyes and is not recommended.

A. halothane B. vecuronium C. thiopentone D. nitroglycerine E. ketamine

A. TRUE B. FALSE C. FALSE D. TRUE E. TRUE

EXPLANATION: Cerebral metabolism can be manipulated (reduced) and consequently CBF, cerebral blood volume and ICP is reduced. Hence, drugs that reduce the metabolic demand will reduce the cerebral blood volume by decreasing the CBF. Infusions of the barbiturate thiopentone are used in this manner to help control high ICP after head injury.
Anaesthetic drugs have a significant effect on cerebral blood vessels; volatile agents cause a reduction in the tension of cerebral vascular smooth muscle resulting in vasodilatation and an increase in CBF. Interestingly many of the newer drugs (isoflurane, sevoflurane) also reduce neuronal function and metabolic demands and as a result, this
can lead to uncoupling of flow-metabolism. This appears to be dependent on the concentration of volatile anaesthetic given. The vasodilatation can be countered by hyperventilation, without serious risk of cerebral ischaemia.
VASODIALATORS like NTG will increase the capacity of vascular tree and thus ↑ CBV.
Ketamine leads to increase in metabolic rate, cerebral blood flow and cerebral blood volume.
Vecuronium is a non-depolarizing muscle relaxant and decreases the metabolic demand of the skeletal muscles. Vecuronium neither induces histamine release nor does it change blood pressure. Pancuronium, vecuronium, rocuronium, and pipecuronium have little or minimal effect on CBF, ₂ , or ICP.