Pharmacology of anesthetics Flashcards
What is the purpose of benzodiazepines in pre-anesthesia?
Reduce anxiety and induce amnesia.
Examples: Midazolam, diazepam
Why are antihistamines used pre-anesthesia?
Prevent allergic reactions (e.g., diphenhydramine).
May also reduce nausea or sedation.
Role of antiemetics in pre-anesthesia?
Prevent postoperative nausea/vomiting (PONV) and aspiration.
Examples: Ondansetron (corrected from “ondansetrone”), dexamethasone.
Why are opioids given pre-anesthesia?
Provide preoperative analgesia and reduce intraoperative anesthetic requirements.
Examples: Fentanyl, morphine.
Purpose of anticholinergics in pre-anesthesia?
Reduce salivary/bronchial secretions (e.g., glycopyrrolate).
Prevent bradycardia (e.g., atropine).
What are the four stages of general anesthesia?
Stage I: Analgesia (conscious but pain-free).
Stage II: Excitement/Delirium (involuntary movements, risk of vomiting).
Stage III: Surgical Anesthesia (unconscious, no reflexes).
Stage IV: Medullary Paralysis (respiratory/cardiovascular collapse).
🧠 Goal: Rapidly reach Stage III, avoid Stage IV!
What is MAC (Minimum Alveolar Concentration)?
The ED₅₀ of an inhaled anesthetic: the alveolar concentration needed to prevent movement in 50% of patients during surgical incision.
🖼️ Low MAC = High potency (e.g., sevoflurane). High MAC = Low potency (e.g., nitrous oxide).
Mechanism of general anesthetics?
Enhance GABAₐ and glycine receptors (inhibitory).
Block NMDA and nicotinic receptors (excitatory).
Example: Propofol → GABA potentiation. Ketamine → NMDA antagonism.
Balanced anesthesia components?
Pre-anesthetic meds: Benzodiazepines (midazolam), opioids (fentanyl), antiemetics (ondansetron).
Induction: IV agents (propofol).
Maintenance: Inhalational agents (isoflurane).
Muscle relaxants: Rocuronium.
Why does halothane risk hepatotoxicity?
Metabolized to trifluoroacetyl chloride, which binds liver proteins → immune-mediated necrosis.
⚠️ Avoid in repeated/recent exposures.
Ketamine vs. Propofol?
Ketamine: Dissociative anesthesia (NMDA blockade), preserves airway reflexes, ↑ BP.
Propofol: GABA potentiation, rapid onset/offset, ↓ BP.
🖼️ Use ketamine in shock; avoid propofol in hypotension.
Ratio of anesthetic solubility in blood vs. alveoli.
High λ (halothane): Slow induction (blood “stores” anesthetic).
Low λ (desflurane): Rapid induction/recovery.
Which inhalational agents risk malignant hyperthermia?
Volatile agents (e.g., halothane, isoflurane) + succinylcholine.
🧠 Treat with dantrolene (blocks RyR1 Ca²⁺ channels).
Local Anesthetics: Esters vs. Amides?
Esters: Procaine, cocaine. Metabolized by plasma esterases.
Amides: Lidocaine, bupivacaine. Metabolized by liver CYP450.
⚠️ Esters cause more allergies (PABA metabolites).
MOA of local anesthetics?
Block voltage-gated Na⁺ channels → prevent depolarization → inhibit nerve conduction.
🖼️ Small fibers (pain) blocked before large (motor).
Lidocaine vs. Bupivacaine?
Lidocaine: Medium duration, safer cardiotoxicity profile.
Bupivacaine: Long duration, higher cardiotoxicity risk (avoid in epidurals in pregnancy).
Spinal anesthesia contraindications?
Hypotension.
Bleeding disorders.
Sepsis at injection site.
↑ Intracranial pressure.
🧠 Use ropivacaine (less cardiotoxic) for safer regional blocks.
Trade Names:
Lidocaine
Bupivacaine
Propofol
Lidocaine → Xylocaine.
Bupivacaine → Marcaine.
Propofol → Diprivan.
Why avoid ester local anesthetics in sulfa allergies?
Esters metabolize to PABA (para-aminobenzoic acid), which cross-reacts with sulfonamides.
Adverse effects of local anesthetics?
CNS: Seizures, dizziness.
CV: Arrhythmias (bupivacaine), hypotension.
Allergy: Rare with amides.
💡 Use lipid emulsion for systemic toxicity rescue.
