cns

Question 1

Barbiturates enhance {{c1::GABA}} (an inhibitory neurotransmitter) in the {{c2::sensory cortex, subcortical ganglia, and brain stem}}.

Question 2

Characteristic skin manifestation of barbiturate toxicity is {{c1::bullae formation at friction sites}} also known as {{c2::”barb burns”}}.

Question 3

The pupillary findings in barbiturate toxicity progress from {{c1::initially constricted and reactive}} to {{c2::hypoxic paralytic pupillary dilatation}}.

Question 4

Enhanced elimination of barbiturates is achieved through {{c1::forced alkaline diuresis}} and in severe cases {{c2::hemodialysis/charcoal hemoperfusion}}.

Question 5

Barbiturates are associated with {{c1::respiratory depression}}, {{c2::hypotension}}, and {{c3::coma}} in overdose.

Question 6

Benzodiazepines enhance the effect of GABA at the {{c1::GABAA receptor}}.

Question 7

The specific antidote for benzodiazepine overdose is {{c1::flumazenil}}, but it’s contraindicated in {{c2::chronic users}} because it may precipitate {{c3::seizures}}.

Question 8

Compared to barbiturates, benzodiazepines have a {{c1::higher therapeutic index}} and cause {{c2::less respiratory depression}}.

Question 9

Benzodiazepines rarely cause death when taken {{c1::alone}} but can be fatal when combined with {{c2::other CNS depressants}}.

Question 10

Clinical signs of mild benzodiazepine toxicity include {{c1::impaired cognition}}, {{c2::diplopia}}, {{c3::ataxia}}, and {{c4::slurred speech}}.

Question 11

{{c1::Barbiturates}} cause more neuronal depression while {{c2::benzodiazepines}} cause less.

Question 12

{{c1::Barbiturates}} have no specific antagonist while {{c2::benzodiazepines}} have flumazenil as antidote.

Question 13

{{c1::Barbiturates}} are potent enzyme inducers with more drug interactions, while {{c2::benzodiazepines}} are not enzyme inducers.

Question 14

{{c1::Barbiturates}} have higher dependence and tolerance potential compared to {{c2::benzodiazepines}}.

Question 15

CNS Stimulants: Amphetamines

Question 16

Amphetamines enhance the release of {{c1::catecholamines}} (causing central & peripheral effects) and {{c2::serotonin}} (causing hallucinogenic effects).

Question 17

Peripheral effects of amphetamines include {{c1::alpha stimulation}} (causing mydriasis, increased metabolic rate) and {{c2::beta stimulation}} (causing tachycardia and bronchodilation).

Question 18

In amphetamine toxicity, hypertension should be treated with {{c1::nitroprusside}}, while {{c2::beta blockers}} should be avoided due to {{c3::unopposed alpha effects}}.

Question 19

Despite amphetamine being a basic compound and excreted in acidic urine, acidification is {{c1::not recommended}} because it can {{c2::worsen nephrotoxicity from rhabdomyolysis}}.

Question 20

Severe amphetamine toxicity can lead to {{c1::agitation}}, {{c2::seizures}}, {{c3::hyperthermia}}, {{c4::rhabdomyolysis}}, and {{c5::cardiac complications}}.

Question 21

Chronic amphetamine abuse can cause {{c1::behavioral changes}}, {{c2::psychosis}}, and {{c3::withdrawal symptoms}} including anxiety, headache, lethargy, and depression.

Question 22

Designer drugs are {{c1::structural or functional analogs}} designed to mimic pharmacological effects while {{c2::avoiding classification as illegal substances}}.

Question 23

The three major categories of designer drugs are {{c1::synthetic cannabinoids}}, {{c2::synthetic stimulants}}, and {{c3::synthetic hallucinogens}}.

Question 24

Synthetic cannabinoids are also known as {{c1::K2 or Spice}} and cause effects similar to {{c2::cannabis}}.

Question 25

Crystal meth appears as {{c1::clear or blue-white crystals}} and causes {{c2::euphoria and CNS stimulation}}.

Question 26

DMT (Dimethyltryptamine) acts as a {{c1::non-selective agonist at serotonin receptors}} and produces {{c2::intense visual and auditory hallucinations}}.

Question 27

Signs of digitalis toxicity include arrhythmias and {{c1::hyperkalemia}} characterized by {{c2::peaked T-waves}}, {{c3::widened QRS}}, and {{c4::prolonged P-R interval}}.

Question 28

The specific antidote for digitalis toxicity is {{c1::digoxin-specific antibody fragments}} (Digibind).

Question 29

The classic anticholinergic toxidrome of atropine can be remembered as "{{c1::Hot as a hare}}, {{c2::blind as a bat}}, {{c3::dry as a bone}}, {{c4::red as a beet}}, {{c5::mad as a hatter}}."

Question 30

The physiological antidote for atropine poisoning is {{c1::physostigmine}}, which is a {{c2::cholinesterase inhibitor}}.

Question 31

Clinical Scenarios & Differential Diagnosis

Question 32

A patient presenting with bullae formation is most likely suffering from {{c1::barbiturate}} toxicity.

Question 33

A patient with small reactive pupils and respiratory depression is more consistent with {{c1::opioid}} toxicity rather than barbiturate toxicity.

Question 34

A patient with profound agitation, hyperthermia, and rhabdomyolysis is likely experiencing {{c1::amphetamine/stimulant}} toxicity.

Question 35

Differential diagnosis of amphetamine toxicity includes {{c1::cocaine toxicity}}, {{c2::sedative/hypnotic withdrawal}}, {{c3::autonomic hyperactivity}}, and {{c4::MAOI/food-drug interactions}}.

Question 36

The distinguishing feature between sympathomimetic toxidrome and anticholinergic toxidrome is {{c1::diaphoresis (wet skin) in sympathomimetic}} versus {{c2::dry skin in anticholinergic}}.

Question 37

The first priority in treating barbiturate overdose is {{c1::airway management and ventilation support}}.

Question 38

For benzodiazepine overdose, the mainstay of treatment is {{c1::supportive care}} with cautious use of {{c2::flumazenil}} in appropriate cases.

Question 39

In amphetamine toxicity, treatment priorities include {{c1::controlling agitation/hyperthermia}} and {{c2::managing hypertension}} (with nitroprusside, not beta blockers).

Question 40

In digitalis poisoning, treatment includes {{c1::digoxin-specific antibody fragments}}, {{c2::careful electrolyte management}}, and {{c3::continuous ECG monitoring}}.