Pharmacology C7

MOA: Increases cholinergic neurotransmission by inhibiting cholinesterase.

Treats: All stages of Alzheimer's Disease.

Tox: Nausea, vomiting, and bradycardia.

Key: Taken once daily; produces small cognitive improvements but does not stop progression.

MOA: Increases the frequency of GABA_A chloride channel opening.

Treats: Acute anxiety, panic attacks, status epilepticus, and alcohol withdrawal.

Tox: Anterograde amnesia and physical dependence.

Key: Flumazenil is the specific reversal agent.

MOA: Cholinesterase inhibitor that increases acetylcholine levels in the brain.
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Toxicities: Cholinergic side effects (GI distress) occur in approximately 20% of patients.
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High Yield Info: Available as a daily skin patch approved for all stages of Alzheimer's.

MOA: NMDA receptor antagonist; limits glutamate-cell interactions.

Treats: Moderate to severe Alzheimer's Disease.

Tox: Dizziness, confusion, and hallucinations.

Key: Helps slow decline in thinking skills in later stages.

MOA: Monoclonal antibodies that target and remove beta-amyloid plaques.

Treats: Early-stage Alzheimer’s Disease.

Tox: Brain swelling or small brain bleeds.

Key: Can slow cognitive decline by ~30%.

MOA: Dopamine precursor; crosses the blood-brain barrier via L-amino acid transporter (LAT).

Treats: Parkinson's Disease (especially bradykinesia).

Tox: Dyskinesias (involuntary writhing) and "on-off" fluctuations.

Key: Does not improve cognitive decline or dysphagia; effectiveness fluctuates over time.

MOA: COMT inhibitor; prevents peripheral degradation of levodopa.

Treats: Parkinson's (adjunct to levodopa).

Tox: Enhances levodopa-related dyskinesias.

Key: Only acts in the periphery; used to increase levodopa's duration.

MOA: Non-ergot dopamine agonists; Pramipexole is D3 selective, while Ropinirole is D2 selective.
​Toxicities: Anorexia, nausea, postural hypotension, and dyskinesias.
​High Yield Info: Better tolerated than older ergot derivatives (like Bromocriptine) which caused heart valve disease.

MOA: Selective inhibitors of MAO-B (monoamine oxidase type B), the enzyme that metabolizes dopamine in the brain.
​Toxicities: Insomnia, mood changes, dyskinesias, GI distress, and hypotension.
​High Yield Info: Lacks the "cheese effect" (hypertension) of non-selective MAOIs used in depression.

MOA: Antimuscarinic (anticholinergic class); blocks excitatory cholinergic neurons in the striatum.

Treats: Parkinson's tremorigidity and antipsychotic-induced extrapyramidal symptoms.

Tox: Dry mouth, constipation, and urinary retention.

Key: Little effect on bradykinesia.

MOA: VMAT2 (vesicular monoamine transporter 2) inhibitor that reduces dopamine storage.
​Toxicities: Sedation and parkinsonism-like symptoms.
​High Yield Info: Used to treat chorea in Huntington’s Disease.

MOA: Facilitate GABA_A receptor activity by increasing the duration of chloride ion channel opening.
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Toxicities: Severe respiratory and cardiovascular depression; precipitates porphyria.

​High Yield Info: Induce P450 liver enzymes, causing many drug interactions. Steeper dose-response curve than BZDs (more lethal in overdose).

MOA: Selectively binds to BZ_1 receptors.

Treats: Insomnia.

Tox: Minimal daytime impairment or withdrawal.

Key: Lack anticonvulsant or muscle-relaxing properties.

MOA: Serotonin 5-HT_1A partial agonist.

Treats: Generalized Anxiety Disorder (GAD).

Tox: Tachycardia and GI distress.

Key: Slow onset (>1 week); no sedation, addiction potential, or alcohol interaction.

MOA: Activates melatonin receptors (MT_1, MT_2) in the suprachiasmatic nucleus.
​Toxicities: Minimal; lacks rebound insomnia or withdrawal symptoms.
​High Yield Info: No direct effect on GABA-ergic systems; used for sleep onset insomnia.

MOA: Blocks NE and 5-HT reuptake; also blocks muscarinic, H_1, and alpha_1 receptors.

Treats: Major depression and chronic neuropathic pain.

Tox: Atropine-like effects and dangerous cardiac arrhythmias in overdose.
Coma, Convulsions, and Cardiotoxicity

Key: Overdose management focuses on lidocaine for arrhythmias and bicarbonate for acidosis.

MOA: A TCA that is a more selective inhibitor of 5-HT reuptake compared to others in its class.

Toxicities: Similar to other TCAs (anticholinergic, sedation).


High Yield Info: Historically important for Obsessive-Compulsive Disorder (OCD), though SSRIs are now the first-line choice for safety.

MOA: Selective Serotonin Reuptake Inhibitor (SSRI).

Treats: Depression, anxiety disorders, and bulimia.

Tox: Sexual dysfunction and insomnia.

Key: Longest half-life; inhibits CYP2D6, which can interfere with Tamoxifen activation.

MOA: Selective inhibition of SERT.

Toxicities: GI distress, jitters, and sexual dysfunction. Citalopram overdose can cause QT prolongation.

High Yield Info: Often the best choice for elderly patients due to lower autonomic side effects compared to TCAs.

MOA: Weak reuptake inhibitor of NE and Dopamine (NDRI).

Treats: Major depression and nicotine withdrawal.

Tox: Seizures at high doses.

Key: Least likely to cause sexual dysfunction.

MOA: Antagonist at presynaptic alpha2 adrenoceptors (increasing amine release) and 5-HT2 receptors.

High Yield Info: Useful for depressed patients with insomnia or severe weight loss.

Toxicities: Marked sedation and significant weight gain

MOA: Postsynaptic 5-HT_2A receptor antagonist.

Toxicities: Highly sedating.

High Yield Info: Widely used as a sleeping aid in depressed patients with insomnia.

MOA: Irreversible inhibition of both MAO-A and MAO-B, increasing vesicular stores of NE, 5-HT, and Dopamine.

Toxicities: CNS stimulation (agitation/convulsions), and orthostatic hypotension in the absence of tyramine.

High Yield Info: "Cheese Reaction": Hypertensive crisis when combined with tyramine-rich foods (aged cheese, wine). Can cause life-threatening Serotonin Syndrome if combined with SSRIs.

MOA: Strong blockade of Dopamine D_2 receptors.

Treats: Schizophrenia, acute mania, and Tourette syndrome.

Tox: High risk of Extrapyramidal Symptoms (EPS) and hyperprolactinemia.

Key: EPS (like acute dystonia) is treated with parenteral benztropine.

MOA: D_2 receptor blockade.

Treats: Antiphsychotic; Schizophrenia

Toxicities: High antimuscarinic effects (dry mouth, constipation) and alpha_1 blockade (orthostatic hypotension). Retinal Pigmentation (browning of vision); this is its "classic" specific toxicity.

High Yield Info: Thioridazine is associated with retinal pigmentation (brown vision) and lethal cardiac arrhythmias in overdose.

MOA: High affinity for 5-HT_2 receptors with low D_2 affinity.

Treats: Treatment-resistant schizophrenia.

Tox: Agranulocytosis (1-2%) and weight gain.

Key: Requires regular blood monitoring; low risk of EPS.

MOA: Blockade of both 5-HT_2A and D_2 receptors.

Toxicities: Significant weight gain and hyperglycemia (diabetogenic action), especially with Olanzapine.

High Yield Info: Improve the negative symptoms of schizophrenia. Quetiapine/Olanzapine are often first-choice in pregnant patients with bipolar disorder to avoid lithium risks.

MOA: Antagonist at D_2 and 5-HT_2A; agonist at 5-HT_1A.

Treats: Schizophrenia and bipolar disorder.

Tox: Significant risk of QT prolongation.

Key: Little or no weight gain compared to other atypicals.

MOA: Partial agonist at D_2 and 5-HT_1A receptors; strong antagonist at 5-HT_2A.

Toxicities: Generally well-tolerated; least sedating of the newer agents.

High Yield Info: Low risk of weight gain, hyperglycemia, or hyperprolactinemia.

MOA: Used for the manic phase of bipolar disorder.

Toxicities: Tremor, sedation, ataxia, Nephrogenic Diabetes Insipidus (polyuria/thirst), and edema.

High Yield Info: Thiazide diuretics decrease lithium clearance, increasing the risk of toxicity. Low-salt diets also increase lithium levels.

MOA: Inhibits alcohol dehydrogenase (ADH).

Toxicities: Headache and nausea.

High Yield Info: Treats acute methanol or ethylene glycol intoxication to prevent toxic metabolite formation.

MOA: Pure opioid receptor antagonist.

Toxicities: Nausea and potential hepatotoxicity at high doses.

High Yield Info: Treats alcohol dependence long-acting and oral, used for maintenance/craving

MOA: Strong full $\mu$-opioid receptor agonist with a long half-life.

Toxicities: Respiratory depression and constipation.

High Yield Info: Used for opioid detoxification (withdrawal) and long-term maintenance programs.

MOA: Intravenous agent that facilitates GABA neurotransmission.

Toxicities: Significant respiratory and circulatory depression.

High Yield Info: Primarily used for induction of anesthesia and sedation in the ICU. has a unique antiemetic property, making it a favorite for "day surgery" where patients want to go home without nausea.

MOA: Blocks voltage-gated Na+ channels from the cytoplasmic end.

Toxicities: CNS excitation (seizures) and arrhythmias at high levels.

High Yield Info: Treats local anesthesia for minor surgery and is an antiarrhythmic agent.

MOA: Competitive antagonist at opioid receptors.

Toxicities: Precipitates immediate, severe withdrawal in dependent individuals.

High Yield Info: Treats acute opioid overdose short-acting and used for acute emergencies.

MOA: Depolarizing neuromuscular blocker; nicotinic receptor agonist.

Toxicities: Hyperkalemia and malignant hyperthermia.

High Yield Info: Used for rapid endotracheal intubation. Causes initial muscle fasciculations.

the only depolarizing agent used clinically. its blockade is potentiated (made worse) by cholinesterase inhibitors in Phase I.

MOA: Blocks Ca^2+ release from the sarcoplasmic reticulum (RyR1 blocker).

Toxicities: Significant muscle weakness.

High Yield Info: Treats malignant hyperthermia and chronic spasticity.

MOA: Inhibits T-type Ca^2+ channels in thalamic neurons.

Toxicities: GI distress, nausea, and sedation.

High Yield Info: Drug of first choice for generalized absence seizures.

MOA: Blocks Na+/ Ca2+ channels and inhibits GABA metabolism.

Toxicities: Fatal hepatotoxicity and neural tube defects (spina bifida).

High Yield Info: Treats tonic-clonic, absence, and myoclonic seizures, and acute mania.

it is the drug of choice for Trigeminal Neuralgia.