Chapter
1st
Pharmacology of Intravenous anesthetic agents
51. Choice of
Inhalational agent for shock patient?
A. Halothane
B. Desfluran
C. Sevoflurane
D. Enflurane
52. Inhalational
agent of choice for renal patients is?
A. Halothane
B. Desflurane
C. Sevoflurane
D. Methoxyflurane
53. Which of the
following does not cause tachycardia?
A. Halothane
B. Desflurane
C. Isoflurane
D. Ether
54. Most common
cause of death after chloroform anesthesia
A. Respiratory depression
B. ARDS
C. Ventricular fibrillation
D. Malignant hyperthermia
55. Which
inhalational agent has increased intracranial tension?
A. Halothane
B. Desflurane
C. Isoflurane
D. Sevoflurane
56. Percentage of
thiopentone used in induction is?
A. 0.5%
B. 1.5%
C. 2.5%
D. 4.5%
57. Sodium
thiopentone acts by?
A. Rapid metabolism
B. Rapid distribution
C. Rapid excretion
D. Rapid absorption
58. Untrue about
thiopentone?
A. Hypokalemia
B. High protein binding
C. Good analgesic
D. Anticonvulsant
59. All are true
about thiopentone except?
A. Fast recovery
B. Causes laryngospasm
C. Tendency to cause postoperative discomfort
D. Stage of delirium is absent
60. Which of the
following IV anesthetic can cross the placenta quickly?
A. Gallamine
B. Morphine
C. Thiopentone
D. Succinylcholine
61. Bradycardia
is not seen with?
A. Morphine
B. Pentazocine
C. Fentanyl
D. Alfentanil
62. Chest wall
rigidity (wooden chest syndrome) is seen with?
A. Morphine
B. Sufentanil
C. Fentanyl
D. Alfentanil
63. Agent of
choice for decreasing hallucinations after ketamine
A. Propofol
B. Midazolam
C. Diazepam
D. Thiopentone
64. Thiopentone
if injected in artery, the first symptom is?
A. Pain
B. Analgesia
C. Paralysis
D. Skin infection
65. Propofol vial
once opened should be used within?
A. 1 hour
B. 6 hours
C. 12 hours
D. 48 hours
66. Induction
agent contraindicated in asthma?
A. Thiopentone
B. Ketamine
C. Propanidid
D. Theophylline
67. Which of the
following agents is used to produce “street fit” person following surgery?
A. Thiopentone
B. Ketamine
C. Propofol
D. Etomidate
68. Which of the
following anesthetic agents decreases the cortisol level?
A. Thiopentone
B. Ketamine
C. Propofol
D. Etomidate
69. In
neurolept-analgesia droperidol and fentanyl are in ratio?
A. 2:1
B. 20:1
C. 50:1
D. 10:1
70. Reversal of
which benzodiazepine is most difficult with flumazenil?
A. Lorazepam
B. Midazolam
C. Nitrazepam
D. Diazepam
71. When
barbiturates constrict cerebral vasculature, the most consistent combination of
effects is:
A. ↑ cerebral blood flow, ↑ intracranial pressure
B. ↓ cerebral blood flow, ↓ cerebral blood volume, ↓ intracranial pressure
C. ↓ cerebral blood flow, ↑ cerebral blood volume, ↑ intracranial pressure
D. ↑ cerebral blood flow, ↓ cerebral blood volume, ↑ intracranial pressure
72. How do
induction doses of etomidate influence adrenal function?
A. They permanently destroy adrenal enzymes
B. They transiently inhibit enzymes involved in cortisol and aldosterone
synthesis
C. They increase cortisol synthesis
D. They have no effect on adrenal enzymes
73. The primary
site of action for barbiturates is best described as:
A. A site on the NMDA receptor
B. Binding to GABA_A receptor to potentiate GABA action
C. Blocking acetylcholine receptors
D. Stimulating adrenergic receptors
74. During
repeated doses of thiopental, the patient’s recovery depends mainly on which
factor?
A. Redistribution to fat and muscle
B. Hepatic metabolism and elimination
C. Renal filtration
D. Plasma protein binding
75. Why can’t
thiopental be mixed with acidic drugs in the same syringe?
A. It crystallizes in acid because its solution is very alkaline
B. It binds to acids forming active complexes
C. It neutralizes the acid making it stronger
D. It forms harmless bubbles
76. Which drug
classically produces “burst suppression” on EEG when given in large doses?
A. Benzodiazepines
B. Barbiturates
C. Ketamine
D. Etomidate
77. Muscle
relaxation is seen to a little extent with which intravenous agent?
A. Methohexitone
B. Propofol
C. Midazolam
D. Thiopentone
78. Naloxone does
not completely reverse the actions of which drug?
A. Morphine
B. Pentazocine
C. Buprenorphine
D. Thiopentone
79. One ketamine
metabolite that retains anesthetic activity is:
A. Norketamine
B. Propofol glucuronide
C. Fospropofol
D. Ketamine phosphate
80. A patient
with depleted catecholamine stores (e.g., prolonged sepsis) receives ketamine
for induction. What cardiovascular outcome is most likely?
A. Increase in SVR and BP
B. Myocardial depression and hypotension
C. Hypertensive crisis
D. No change in hemodynamics
81.
Dexmedetomidine metabolites are primarily excreted in:
A. Feces
B. Exhaled air
C. Urine
D. Sweat
82. All of the
following drugs increase the mean arterial blood pressure, except:
A. Dopamine
B. Norepinephrine
C. Epinephrine
D. Isoproterenol
83. Stimulation
of α₂ receptors causes:
A. Hypertension
B. Bradycardia
C. Salivation
D. Anxiety
84. Compared with
thiopental, etomidate causes:
A. Less nausea
B. Increased seizure threshold
C. Greater myoclonic activity
D. Greater histamine release
85. The best
initial treatment for anaphylaxis during general anesthesia is:
A. Methylprednisolone
B. Famotidine
C. Diphenhydramine
D. Epinephrine
86. True
statement regarding flumazenil is:
A. It binds irreversibly with benzodiazepine receptor
B. It causes hypertension and tachycardia
C. It has a shorter duration of action than midazolam
D. It reverses opioid-induced respiratory depression
87. Midazolam can
be administered through all of the following routes, except:
A. Oral
B. Sublingual
C. Transcutaneous
D. Transnasal
88. Which of the
following statements about local anesthetics is false?
A. They are weak bases
B. They contain either ester or amide linkage
C. It is their charged form that interacts with the receptor
D. They bind the receptor inside the cell
89. All of the
following can lead to hyperkalemic response to administration of
succinylcholine, except:
A. Burn injury
B. Spinal cord injury
C. Prolonged ICU stay
D. Cerebral palsy
90. Which of the
following choices is correct regarding the blood-gas partition coefficient?
A. Nitrous oxide 0.47
B. Desflurane 0.62
C. Isoflurane 2.4
D. Sevoflurane 0.85
91. Which of the
following classes of drugs is most likely to be responsible for an anaphylactic
reaction during general anesthesia?
A. Neuromuscular-blocking drugs
B. Opioids
C. Antibiotics
D. Radio contrast dyes
92. Which of the
following statements about propofol infusion syndrome is most likely false?
A. Mortality rate in an established case is very high
B. Rhabdomyolysis is one of the diagnostic criteria
C. Tachycardia is an early sign of this syndrome
D. Cardiac dysfunction is very common in this condition
93. A 68-year-old
man is undergoing exploratory laparotomy for intestinal obstruction. Cause of
obstruction is found to be an ileal carcinoid tumor. Suddenly, the patient
develops bronchospasm, and the peak airway pressure increases from 24 to 45 cm
of H₂O. Which of the following is the best treatment for the bronchospasm in
this situation?
A. Dexamethasone
B. Sevoflurane
C. Ketamine
D. Somatostatin
94. Which of the
following can precipitate an episode of myotonia in a patient with myotonic
dystrophy?
A. Lidocaine administration
B. Neostigmine administration
C. Nondepolarizing neuromuscular-blocker administration
D. Hypothermia
95. Which of the
following statements about dexmedetomidine is most likely true?
A. It has more α₂ selectivity than clonidine
B. It can increase opioid-induced rigidity
C. Context-sensitive half time increases markedly after prolonged infusion of
dexmedetomidine
D. It has no effect on systemic vascular resistance
96.A 75-year-old
woman is scheduled for mitral valve repair. High-dose fentanyl is used to
induce anesthesia. In order to counteract the bradycardia caused by fentanyl,
pancuronium is administered. Pancuronium blocks the bradycardia caused by
fentanyl by acting on which of the following?
A. β-Adrenergic
receptors
B. Cardiac muscarinic receptors
C. Carotid baroreceptors
D. Central vagal nuclei
97. A 50-year-old
woman had cholecystectomy done under general anesthesia. Rocuronium was used as
muscle relaxant, and a combination of anticholinergic and anticholinesterase
was used for reversal of muscle-relaxant action. The patient is now
bradycardic. The combination of reversal agents most likely to cause the
bradycardia is:
A. Atropine and
edrophonium
B. Glycopyrrolate and edrophonium
C. Atropine and neostigmine
D. Glycopyrrolate and neostigmine
98.The shorter
duration of action of remifentanil compared with fentanyl is primarily due to
its:
A. Rapid
redistribution
B. Renal elimination
C. Metabolism by esterases
D. Hepatic extraction ratio
99.Which of the
following medications will prolong the neuromuscular blockade produced by
vecuronium?
A. Carbamazepine
B. Clindamycin
C. Quinidine
D. Verapamil
100.A 45-year-old
farmer is brought into the emergency room. He is agitated and confused. On
examination, he has dry skin with fever and rapid heart rate. Anticholinergic
poisoning is suspected. Which of the following medications is most appropriate
to treat his condition?
A.
Neostigmine
B. Pyridostigmine
C. Edrophonium
D. Physostigmine
Answers and Explanations
51. B Desflurane
Explanation: among the inhalational agent now available desflurane if given in
concertation >1MAC stimulates sympathetic system but at low concentration
i.e < 1MAC it produces vasodilation similar to isoflurane. Halothane and
enflurane decreases cardiac output very significantly. Sevoflurane also
decreases cardiac output in dose dependent manner.
52.B Desflurane
Explanation: as desflurane does not
release the fluorides so its inhalational agent of choice for renal patients.
53.A Halothane
Explanation: Isoflurane and desflurane by causing hypotension can causes reflex
tachycardia. Ether stimulates sympathetic system to cause tachycardia.
Halothane by vagomimetic action can cause bradycardia.
54.C Ventricular fibrillation
Explanation: chloroform can cause cardiac arrest and death dye ventricular
fibrillation.
55.A Halothane
Explanation: Among inhalational agents maximum increases in ICT is with
enflurane followed by halothane and minimum with isoflurane.
56.C 2.5%
Explanation: preferred percentage of thiopentone is 2.5%. local complications
of thiopentone are more if it used in higher concentration. , so 2.5%
concentration is desirable.
57.B rapid distribution
Explanation: the elimination half life
of thiopentone is 10.4 hours but consciousness is regained after 10 to 15
minutes due to redistribution which means drug from the highly vascular areas
like brain is redistributed to less vascular areas like fat and muscle.
58.C Good analgesic
Explanation: thiopentone is ant analgesic mean it does not causes analgesia. At
induction it causes mild hypokalemia. It is 85% bound to plasma albumin and it
is strong anticonvulsant too.
59.D stage of delirium is absent
Explanation: at inadequate depth
thiopentone predisposes for laryngospasm. Thiopentone may cause postoperative
discomfort. Restlessness, vertigo and even euphoria i.e stage of delirium
(although the incidence is very rare).
60.C Thiopentone
Explanation: thiopentone because of its high lipid solubility crosses the
placenta quickest and the fetal concentration is rapidly increased to attain
equilibrium with maternal concentration in 5 minutes
61.B Pentazocine
Explanation: All opioids causes bradycardia except pentazocine and pethidine.
62.C Fentanyl
Explanation: Although Rapid administration of
larger doses of opioids (particularly fentanyl, sufentanil, remifentanil, and
alfentanil) can induce chest wall rigidity severe enough to make ventilation
with bag and mask nearly impossible. But most commonly the wooden chest
syndrome ahs been seen with the Fentanyl.
63.B Midazolam
Explanation: Midazolam is often the drug of choice to manage ketamine-induced
hallucinations because it helps calm the brain and reduce anxiety or agitation
caused by ketamine’s dissociative effects. As a benzodiazepine, midazolam works
by enhancing the effect of GABA, a neurotransmitter that promotes relaxation
and sedation. This helps smooth out the emergence reactions like vivid dreams,
confusion, or hallucinations that can occur when ketamine wears off. It also
provides additional sedation without affecting ketamine’s pain relief or
anesthesia effects, making it a safe and effective combination.
64.A, Pain
Explanation: Thiopentone is highly alkaline and irritates
the arterial endothelium, causing intense vasospasm (sudden constriction of the
artery).This reduces blood flow to the tissues supplied by that artery, leading
to ischemia (lack of oxygen) and severe burning pain almost immediately.If not managed
quickly, it can progress to tissue necrosis, gangrene, or loss of limb function.
65.B, 6 hours
Explanation: Propofol does not contain any preservative and the egg lecithin is
a good culture media for bacterial growth and there have been death reports
following the use of contaminated propofol solution. So propofol vial once
opened should be discarded within 6 hours.
66.(A) Thiopentone
Explanation: (Thiopental sodium) is a barbiturate used as an induction agent
for anesthesia, However, it is contraindicated in asthma due to its potential to
cause bronchospasm.
Reason: Thiopentone can release histamine from mast cells.Histamine causes bronchoconstriction,
increased airway resistance, and wheezing — which can exacerbate asthma.Therefore,
thiopentone is not safe for asthmatic patients.
67.(C) Propofol
Explanation: After propofol patient
become ready home (street fit) which mean ready for discharge after 3 to 4
hours that’s why it is iv agent of choice for day care surgery.
68.(D) Etomidate
Explanation:
Etomidate is an intravenous induction agent
that is unique because it inhibits cortisol and aldosterone synthesis
in the adrenal cortex.
This happens due to inhibition of the enzyme 11-β-hydroxylase,
which is required for converting 11-deoxycortisol → cortisol in
the adrenal cortex (zona fasciculata)
69.(C) 50:1
Explanation: Droperidol and fentanyl are available in the brand name INNOVAR.
It contains droperidol 2.5mg + fentanyl 0.05mg i.e in a ratio of 50:1
70.(A) Lorazepam
Explanation: antagonism is most difficult with lorazepam due to its high
receptor binding potential
71.B. ↓ cerebral blood flow, ↓ cerebral blood volume, ↓ intracranial
pressure
Explanation (in simple words):
Barbiturates make the brain’s blood vessels narrower (vasoconstriction). This
reduces how much blood flows to the brain and how much blood is inside the
skull. As a result, the overall pressure inside the head (intracranial
pressure) also goes down.
72.B They transiently inhibit enzymes
involved in cortisol and aldosterone synthesis
explanation:
Etomidate affects the adrenal glands for a short time. It blocks an important
enzyme called 11β-hydroxylase, which is needed to make cortisol and aldosterone
— two key hormones that help the body handle stress and control blood pressure.
This blockage
isn’t permanent; it only lasts for a few hours after the drug is given. That’s
why a single induction dose of etomidate can temporarily reduce the body’s
stress hormone levels, but it doesn’t cause lasting damage to the adrenal
glands.
73.B Binding to GABA(A) receptor to potentiate GABA action
explanation:
Barbiturates mainly work in the brain by acting on GABA(A) receptors, which are responsible for calming
brain activity.
Here’s
how it works:
·
GABA is the main “inhibitory”
(calming) chemical messenger in the brain.
·
Barbiturates bind to the GABA(A) receptor and make GABA’s effect
stronger.
·
This allows
more chloride ions to enter nerve cells, making
them less likely to send signals.
74.B. Hepatic metabolism and elimination
Explanation: At first, thiopental’s effect wears off because it moves from the
brain into less perfused tissues (redistribution). But with repeated doses,
those tissues become saturated and can’t store more drug. Now, the only way the
drug level drops is through metabolism in the liver. So instead of “wearing
off” quickly, recovery slows because elimination—not redistribution—controls
the duration.
75.A. It crystallizes in acid because its solution is very alkaline
Explanation: Thiopental sodium has a pH around 10, which keeps it soluble.
Mixing it with acidic substances drops the pH, causing the barbiturate to
revert to its insoluble acid form. The result is precipitation in the syringe
or line—potentially clogging it or injecting crystals into a vein.
76.B. Barbiturates
Explanation:
Barbiturates such as thiopentone are well-known for producing a burst
suppression pattern on EEG when administered in large doses. This pattern
shows alternating periods of high-voltage electrical bursts followed by periods
of electrical silence. It indicates profound cerebral depression, often used in
cases like refractory status epilepticus or to provide cerebral protection
during neurosurgery.
The mechanism involves barbiturates
enhancing GABA-mediated chloride influx, leading to strong neuronal inhibition.
Other agents like benzodiazepines and etomidate can cause EEG slowing but do
not typically produce true burst suppression. Hence, barbiturates are the
classical agents associated with this pattern.
77.C
Midaozlam
Explanation: among iv agents only
benzodiazepines produces muscle relaxation to some extent due to central action
78.C. Buprenorphine
Explanation:
Buprenorphine is a partial opioid agonist with very high affinity for
the µ-opioid receptor. This means it binds tightly and does not easily get
displaced by antagonists like naloxone. As a result, naloxone cannot fully
reverse its effects, including respiratory depression.
Drugs like morphine and pentazocine,
on the other hand, are more easily reversed by naloxone because they have lower
receptor affinity. Buprenorphine’s strong receptor binding is beneficial for
maintenance therapy in opioid dependence but problematic in overdose situations
since naloxone is less effective.
79.Norketamine (A)
Explanation:
Ketamine is metabolized in the liver mainly by cytochrome P450 enzymes to norketamine,
an active metabolite that still has anesthetic and analgesic properties, though
about one-third as potent as ketamine itself. Norketamine contributes to the
prolonged effects of ketamine, especially when given by continuous infusion.
Other options like propofol glucuronide, fospropofol, or ketamine phosphate
either do not exist as active metabolites or are unrelated drugs. Thus,
norketamine is clinically significant as an active metabolite with residual
anesthetic and analgesic activity.
80.B. Myocardial depression and
hypotension
Explanation:
Ketamine usually increases blood pressure and heart rate by stimulating the
sympathetic nervous system and releasing catecholamines. However, in patients
with depleted catecholamine stores (like those with sepsis, shock, or chronic
illness), this indirect mechanism fails. In such cases, ketamine’s direct
myocardial depressant effect becomes evident, leading to hypotension and
decreased cardiac output.
Therefore, while ketamine is generally
considered cardiostimulatory, in catecholamine-depleted states it can
paradoxically cause cardiac depression and hypotension. This is important
to remember in critically ill or septic patients.
81.C. Urine
Explanation:
Dexmedetomidine is a sedative drug mainly used in anesthesia and
intensive care. After the body breaks it down in the liver (through metabolism), the resulting waste
products — called metabolites — are removed
mainly through the kidneys in the urine.
Only a small amount leaves through feces.
So, most of the drug’s byproducts exit your body when you pee, not through stool, breath, or sweat.
82.D. isoproterenol
Explanation:
explanation: Effect of
sympathomimetic drugs on the mean arterial blood pressure is mediated through
their effect on the adrenergic receptors they stimulate. Ultimate effect is
generated through complex interaction of different factors based on baseline
sympathetic tone, patient’s volume status, and condition of the heart. Although
isoproterenol increases contractility through its action on β2 receptors, it
also stimulates β1 receptors in big vascular beds like muscle, causing
vasodilatation and decreasing the systemic vascular resistance. So despite
increasing contractility of the heart and increasing the cardiac output, the
mean arterial blood pressure can decrease with administration of this drug.
Other medications increase the mean arterial blood pressure by their effect on
α1 and β1 receptors.
83.B. Bradycardia
Explanation:
Stimulation
of α2 receptors causes inhibition of release of norepinephrine, thus decreasing
the activity of the sympathetic nervous system. Hypotension and bradycardia are
side effects that sometimes limit the use of medications like clonidine and
dexmedetomidine. In the past, these drugs were used mainly as
antihypertensives, but applications based on their sedative, anxiolytic, and
analgesic properties are becoming increasingly common. Dry mouth may also
result from the use of dexmedetomidine.
84.(D) Greater
myoclonic activity
Explanation:
Etomidate actually causes a decrease in the seizure threshold, and is thus
useful in cases of electroconvulsive therapy for severe depression. Spontaneous
movements characterized as myoclonus occur in more than 50% of patients
receiving etomidate and may be associated with seizure-like activity on the
EEG. Another side effect is an increased incidence of nausea and vomiting in
the postoperative period. It does not cause histamine release in contrast to
thiopental, which has been shown to release histamine in vitro
85.D. Epinephrine:
Explanation:
Although all of these medications may be useful in the event of
anaphylaxis. during a general anesthetic, epinephrine is considered to be the
drug of choice and is indicated as the first line of treatment. Dose depends on
the severity of the reaction and may be anywhere from 10 μg to 1 mg if cardiac
arrest develops. Its α1 action counteracts the severe vasodilatation, which is
the hallmark of this condition. Its β2 action helps treat bronchoconstriction
while β1 action helps support the cardiac output. H1- and H2-blockers are also
indicated in the treatment of anaphylaxis and help mitigate the effects of type
1 antigen antibody reaction on mast cells and other mediators, causing vascular
dilatation and increased capillary permeability, but their actions are neither
as rapid nor as profound as epinephrine. Steroids stabilize the cell membranes
of mast cells and eosinophils, thus decreasing the intensity of the immunologic
response, but their action takes 4 to 6 hours to develop, and there is little
evidence to support the use of steroids for the acute treatment of anaphylaxis
86.A. It binds irreversibly with benzodiazepine receptor
Explanation: Flumazenil is
useful as a specific reversal agent for benzodiazepine overdose. It has minimal
intrinsic activity on this receptor, but because of similarity in the chemical
structure, it acts as a competitive antagonist in the presence of agonist at
the receptor site. Duration of action is short (60–90 minutes), so repeated
doses or infusion is required if recurrence of sedation is desired. Reversal of
benzodiazepine action does not lead to cardiovascular side effects or evidence
of acute stress response. It does not have any effect on opioid receptor, so is
not useful to reverse respiratory depression caused by narcotic overdose.
87.C. Transcutaneous
Explanation:
Although most common route of
administration of midazolam in anesthesia is intravenous, this drug can be
given via many routes. Midazolam oral suspension is used routinely in pediatric
anesthesia. Intramuscular injection can be painful, but intranasal route
utilizing mucosal atomization device may be useful to treat seizure activity.
Bioavailability of sublingual midazolam is much better than orally administered
drug. Exposure of the acidic midazolam preparation to the physiologic pH of
blood causes a change in the ring structure that renders the drug more lipid
soluble, thus speeding its passage across the blood–brain barrier. There is no
preparation available for transcutaneous delivery of this drug in comparison to
fentanyl
88.C. It is
their charged form that interacts with the receptor
Explanation: Local anesthetics exert their
electrophysiologic effects by blocking sodium ion conductance. This effect is
primarily mediated by interaction with specific receptors that are within the
inner vestibule of the sodium ion channel
89.D. Cerebral palsy
Explanation: Any time
prolonged skeletal muscle inactivity or extensive muscle damage exists, patient
may be susceptible to hyperkalemia after the administration of succinylcholine
and is dependent on development of extrajunctional atypical receptors. In some
patients, potassium levels may exceed 10 mEq/L. This can lead to serious
cardiac arrhythmias and even cardiac arrest. The duration of susceptibility to
the hyperkalemic response to succinylcholine is unknown but probably decreases
after 3 to 6 months of denervation injury. Although cerebral palsy seems to be
a muscular problem, consensus is that it is safe to use succinylcholine for
these patients if airway management will be facilitated by its use
90.A.Nitrous oxide
0.47
Explanation:
The relative solubility of an anesthetic in air, blood, and tissues is
expressed as partition coefficients. Each efficient is the ratio of the
concentration of the anesthetic gas in each of the two phases at equilibrium.
Lower the partition coefficient, higher the rate of equilibration. In other
words, for an anesthetic with a lower alveolar to blood partition coefficient,
the rate of rise of alveolar concentration, and thus alveolar partial pressure,
will be higher than an anesthetic with higher partition coefficient. Since it
is the alveolar partial pressure that determines the partial pressure in the
brain, more rapid rise of alveolar pressure is translated into faster
anesthetic induction. Another factor that plays a role in this regard is the
concentration effect. Nitrous oxide, being a less potent anesthetic with a MAC
of 104, is administered in much larger quantities to induce anesthesia than a
potent agent like sevoflurane. The massive inflow (higher concentration) of
nitrous oxide leads to higher rate of rise of alveolar concentration (FA) of
with a blood gas partition coefficient of 0.46 compared with desflurane with
partition coefficient of 0.42.
91.A. NMB DRUGS
Explanation: Anaphylactic reaction during
anesthesia is estimated to occur between 1 in 5,000 and 1 in 25,000 cases.
Neuromuscular-blocking drugs seem to be the most common agents causing this
reaction. Incidence is far too low to determine the relative frequency of
occurrence with individual neuromuscular blocker. Latex, antibiotics, and induction
agents are much less common etiologic agents in anesthesia. Opioids extremely
rarely cause anaphylactic reactions.
92.C. mortality rate in an
established case is very high
Explanation:
Propofol
infusion syndrome was first described in pediatric intensive care units, but
quite a few adult cases have been reported now. Earliest sign of syndrome is
metabolic acidosis because of impairment oxidative phosphorylation in the
mitochondria, anaerobic metabolism, and accumulation of lactic acid. Cardiac
dysfunction is also an early sign, which manifests early on as bradycardia, and
rightheart block is very common. Rhabdomyolysis is a hallmark of this
condition, and free myoglobin precipitates in the renal tubules, leading to
kidney failure. In an established case, the mortality rate is extremely high,
in excess of 80%. Higher cumulative dose of propofol over a relatively longer
period of time seems to be associated with higher incidence of this condition.
This has led to a drop in the popularity of this drug in the pediatric
intensive care setting.
93.D. Somatosatatin
Explanation:
Carcinoid
syndrome can be precipitated in the operating room when the carcinoid tumor is
manipulated by the surgeon. Cause is the release of massive amount of hormones
made by the carcinoid tumor into the systemic circulation. Signs and symptoms
during anesthesia may include flushing of head, neck, and upper thorax,
bronchospasm, and hypo or hypertension. Many carcinoid tumors contain
somatostatin receptors: a gastrointestinal regulatory peptide that reduces the
production and release of gastro pancreatic hormone. Somatostatin infusion can
avoid and treat the manifestation of this syndrome in the perioperative period.
A synthetic analogue: octreotide is used more often in contemporary practice. It
is recommended to be started 2 weeks prior to the scheduled surgery and
continued in the postoperative period. Ketamine is not indicated in this
condition, as it may increase the sympathetic nervous system discharge and
worsen the situation. Sevoflurane is helpful to treat bronchospasm acutely but
is not specific for this condition and may not be potent enough to treat
bronchospasm induced by these
hormones. Dexamethasone is not indicated for
the acute treatment of bronchospasm, as its onset of action measures in hours
and not in minutes.
94.D. Hypothermia
Myotonia is
characterized by continued involuntary contraction of a group of muscles. So
once triggered, muscles fail to relax. Myotonic dystrophy is the most common
form. Succinylcholine can cause severe hyperkalemia and is contraindicated in
this condition. Nondepolarizing muscle relaxants may not be able to reverse
this spasm. As neostigmine can also trigger myotonic episode, its use for
reversal of muscle relaxants is not indicated. For that reason, it is prudent
to avoid using longeracting nondepolarizing agents that may require reversal
agents. Hypothermia can trigger this condition, so precautions need to be taken
to avoid it during any anesthetic. Best treatment to relieve the spasm is to
inject local anesthetic into the muscle.
95.C. Context sensitive half time
increases…….
Explanation:
Dexmedetomidine
is an α2-agonist, which acts centrally to inhibit sympathetic nervous system
activity. Clonidine belongs to the same group of medicines. Dexmedetomidine
actually sometimes is used to treat spasm observed in cerebral palsy patients.
Its effect in opioid-induced rigidity is not well studied. Decay time of the
serum levels of dexmedetomidine after a short duration of infusion is very
fast, but if it used for longer time, for example, 10 hours, as it is sometimes
used in intensive care unit setting, the sedative action may take a long time
to dissipate. Dexmedetomidine decreases systemic vascular resistance, and that
is one of its mechanism by which it may cause a decrease in blood pressure.
96.D. Central vagal nuclie
Explanation:
Patients with
valvular heart disease are sometimes extremely sensitive to abrupt changes in
the heart rate. High-dose fentanyl has been shown to cause bradycardia through
its effect on the vagus nerve. To some extent, this may be desirable in a
patient with stenotic valvular lesion. In case of regurgitant lesions, this may
lead to critical decrease in cardiac output. In order to counteract this
bradycardia action of the fentanyl, some anesthesiologists like to use a muscle
relaxant that causes tachycardia. Pancuronium and an older nondepolarizing
muscle-relaxant gallamine were used for this purpose. Effect of pancuronium on
the heart rate is elicited at the level of sinoatrial node by blockade of the
muscarinic receptors. On the other hand, effect of fentanyl that caused
bradycardia was more through central nuclei of the vagus nerve. Carotid
baroreceptors and β adrenergic receptor are not involved in induction of
tachycardia noticed after administration of pancuronium.
97.C. Atropine and neostigmine
Explanation:
Administration
of anticholinesterase agents to reverse the action of nondepolarizing agent
allows the acetylcholine levels to build up not only in neuromuscular junction
of the skeletal muscle but also at the level of muscarinic receptors. That
leads to the problem of bradycardia if not effectively counterbalanced by
administration of an anticholinergic agent. Finding the best combination of
these agents is of great importance to an anesthesiologist. Older
anticholinesterase agent edrophonium causes the cholinesterase activity to
increase in cardiac muscarinic receptors, while neostigmine was found to have
additional direct action on these cardiac receptors. Despite that finding,
neostigmine-induced bradycardia is effectively prevented by administration of
anticholinergic agent compared with edrophonium, where this effect is not as
predictable. Another factor to consider is the onset of action of these drugs.
Atropine and edrophonium are very fast-acting, while neostigmine and
glycopyrrolate are slower in onset. As a result, if glycopyrrolate is injected
to counteract the cholinergic response induced by edrophonium, the chance of
development of bradycardia is greatest with this combination, as glycopyrrolate
will take much longer and may not reverse all of the cholinergic effect
produced by edrophonium.
98.C. metabolism
by esterases
Explanation: Remifentanil is metabolized by
nonspecific esterases found in blood and issues. This metabolism is so rapid
that action of remifentanil is terminated without the need for redistribution
or hepatic extraction. There is no accumulation of the drug in patients with
renal failure. Elimination half-life (6 minutes) is not prolonged even after a
prolonged infusion. Hypothermia during cardiac bypass does prolong its
elimination time up to 20%
99.D. Verapamil
Explanation: Many
physiologic factors and medications are associated with potentiation of action
of neuromuscular blockers. Calcium channel blockers like verapamil lead to
decreased sarcoplasmic concentration of calcium, which may potentiate the
muscle weakness as well as prolong the duration of action of
neuromuscular-blocking agents. Carbamazepine was originally used as
anticonvulsant but has been found to be useful in many other conditions. It is
not associated with prolonged action of neuromuscular-blocking agents. Many
antibiotics, notably aminoglycosides, prolong the actions of these drugs, but
clindamycin is safe to use and has not been shown to have any deleterious
effect when used concomitantly with drugs like vecuronium
100. D. Physostigmine
Explanation: Belladonna
alkaloids found in the nature sometimes lead to manifestations of
anticholinergic syndrome. Factors that need to be taken into consideration for treatment
of this condition include whether there is CNS involvement or not. In this
case, it seems that manifestations of CNS involvement are obvious. Neostigmine, pyridostigmine,
and edrophonium have quaternary ammonium ion in their chemical structure, making
them unable to cross the blood–brain barrier. Physostigmine being a tertiary
compound is able to cross this barrier and is able to antagonize the central
actions of these anticholinergic agents.
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