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72 Cards in this Set

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Primary objectives of general anesthesia?
Blunting of consciousness
Suppression of autonomic reflexes
Muscle relaxation
Diethyl Ether
First useful anesthetic. Complete anesthetic.
Major disadvantages: slow induction, flammable, respiratory irritation.
Halogenated hydrocarbons--properties/disadvantages
Less soluble in blood than ether leading to faster rates of induction and recovery. Non flammable and less irritating.
Disadvantages: depress respiratio, decrease BP, dilate cerebral blood vessels, relax uterus, low incidence malignant hyperthermia.
Class: halogenated hydrocarbon inhalation anesthetic.
Poor skeletal muscle relaxant and poor analgesic. Combined w/ other drugs giving balanced anesthesia. Sensitizes myocardium to catecholamines-->arrhythmias.
Inhalation anesthetic
Halogenated hydrocarbon inhalation anesthetics.
Enflurane: may induce seizure patterns
Isoflurane: respiratory irritant effect
Sevoflurane: partial hepatic metabolism
Desflurane: fastest onset and recovery
Halogenated hydrocarbons
Nitrous oxide
Inhalation anesthetic
Rapid onset and recovery
Excellent analgesic
Inadequate potency--second gas effect during induction accelerating onset of anesthesia by other inhaled anesthetic.
Diffusion hypoxia during recovery--tx with 100% O2.
Barbiturates as IV anesthetics
Thiopental: Rapid onset of anesthesia d/t high lipid solubility. Short duration d/t redistribution.
Use: induction of anesthesia, short anesthesia.
Properties: Marked respiratory and CV depression, weak skeletal muscle relaxant, antianalgesic activity, highly alkaline.
IV anesthetic. No cumulative effects of redistribution and can be used for long anesthesia.
Fewer post-op complications (NV, drowsiness). Can reduce BP.
Opioids as IV anesthetics
Fentanyl, sufentanil, alfentanil.
Properties: good analgesia, euphoria, respiratory depression (reversed by nalxone), muscle rigidity, nausea, vomiting. Little CV depression.
Can be combined w/ droperidol to produce neuroleptanalgesia.
H20 soluble benzodiazepine w/ rapid onset and short duration. May induce respiratory deperssion reversible by flumazenil (BDZ antagonist).
Local Anesthetics
1. Mechanism
2. Effect on action potential
1. Reduce changes in Pna and Pk in activated nerve membrane. No effect on resting membrane.
2. Effect on action potential: reduction in amplitude, rate of rise, and conduction velocity; blockade of axonal conduction.
Sensory blocked b/f motor b/c less myelin and smaller.
Structural components of Local Anesthetics (3)
1. Lipophilic aromatic residue
2. Hydrophilic amino group. Only uncharged form crosses nerve cell membrane. Converted to charged form w/in axon. pKa must be between 7 and 9.
3. Intermediate chain--determines metabolism. May be ester or amide.
Local Anesthetics--Esters (4)
Broken down by butyrylcholinesterases in the blood.
1. Cocaine-used topically
2. Procaine-metabolized to PABA
3. Chloroprocaine-most rapid metabolism
4. Tetracaine-potent and toxic
Local Anesthetics-Amides (3)
Metabolized by aminidases in the liver.
1. Lidocaine
2. Mepivacaine
3. Bupivacaine
Toxic effects of Local Anesthetics
1. Myocardial depression d/t Na+ channel blockade
2. Vasodilation-->fall in BP
3. Anxiety or depression and convulsions
4. Hypersensitivity-especially w/ esters.
Administration of Epinephrine w/ Local Anesthesia
Reduces blood flow from anesthetized area leading to reduced bleeding, prolonged anesthesia b/c of slowed loss, and reduction of systemic concentration.
Epi is NOT used with cocaine b/c cocaine is also a vasoconstrictor. Also not used on end-appendages.
Treatment of local anesthetic toxicity
1. oxygen to reduce hypoxia
2. Vasopressors or IV fluids to increase BP
3. Diazepam to reduce convusions
Common mechanism of Sedative-Hypnotic and Antianxiety Drugs + SEs
Mechanism: Enhanced inhibitory effects of GABA in CNS.
1. Decreased REM sleep
2. Drowsiness, hangover
3. Tolerance d/t increased metabolism by MFOs
4. Repiratory depression d/t decreased sensitivity of medullary respiratory ctrs to CO2. Cause of death in OD. Tolerance does not develop to respiratory depression.
5. Abuse potential and physical dependence.
Antianxiety preparations-BDZ
Usually have long durations of action.
1. Chlordiazepoxide
2. Diazepam
3. Alprazolam
Hypnotic preparations--BDZ
Shorter durations of action than antianxiety drugs. Used for sleep.
1. Flurazepam-active t1/2 may lead to daytime drowsiness
2. Temazepam-t1/2 is 10 hours
3. Triazolam-short t1/2 may lead to early morning awakening.
BDZ Effects/Side Effects
Effects: Calming behavior, reduction of anxiety, sleep induction, anticonvulsant activity, muscle reaction.
SE: Drowsiness, dependence, enhanced depression when combined w/ other CNS depressant drugs.
BDZ vs. Bartiburates
-Advantages of BDZ
BDZ increase frequency of Cl- channel opening while barbiturates increase duration of Cl- channel opening.
Advantages of BDZ: Less potential for abuse, higher TI (lower suicide potential), less reduction in REM sleep, milder withdrawal, less induction of MFOs. Flumazenil will reverse BDZ effects.
Hypnotic w/ little effect on sleep stages. Not a BDZ, but binds to a BDZ-receptor subgroup. Antagonized by flumazenil. Short t1/2.
Chloral hydrate
Hypnotic prodrug. Metabolized by alcohol dehydrogenase to active moiety. Gross taste. Low TI
Antianxiety drug.
Partial agonist at 5HT1A receptors. No abuse potential.
Antihistaine used for anxiety. No abuse potential.
Marked sedative adn anticholinergic effects.
Bartiburates-Three classes/examples
1. Ultrashort-acting: thiopental. High lipid solubility. Used for IV anesthesia
2. Short- and intermediate-acting: pentobarbital. Lower lipid solubilities and longer durations of action. Appropriate for sleeping pills.
3. Long-acting: phenobarbital. Lowest lipid solubility and longest duration of action.
Absolute contraindication for bartiburate use
Acute intermittent porphyria
Clinical uses of sedative-hypnotics and antianxiety drugs
anxiety or neuroses
Muscle relaxation
Replacement tx during withdrawal
IV anesthesia
Sedation before surgical procedures
-Mechanism (2)
Mechanism: Adenosine receptors are blocked; at high concentrations, phosphodiesterases are inhibited leading to increased cAMP.
Effects: CNS stimulation (greater w/ caffeine)
Myocardial stimulation
Constriction of cerebral blood vessels
1. Structure
2. Mechanism
3. Effects
1. Are phenylethylamines; the d-isomer is more potent.
2. Indirect sympathomimetics-act by release of endogenous catecholamines.
3. Effects: improvement of mood, increased motor activity, reduction of appetite, reduced fatigue.
Convulsants (3)
Picrotoxin-GABA receptor antagonist
Strychnine-glycine receptor antagonist
Tetanus toxin-blocks inhibitory (glyceine) interneurons.
Only clinical use is for repiratory stimulation, but rarely indicated.
Antipsychotic drugs:
1. Mechanism
2. SE
Mechanism: Block D2 dopamine receptors in the limbic system.
1. Blockade of D2 in the extrapyramidal system (BG) induces iatrogenic parkinsonism. Tx w/ anticholinergics (i.e. benztropine)
2. Blockade of D2 in the pituitary enhances prolactin release leading to galactorrhea.
3. Blockade of histamine receptors leads to sedation
4. Blockade of M-cholinoreceptors leads to anticholinergic sx
5. Blockade of alpha-adrenoreceptors leads to hypotension
D2 in EPS
D2 in pituitary
Histamine block
M-cholinoceptor block
Alpha-receptor block
Typical antipsychotics
Examples and potency
Phenothiazines include chlorpromazine and thioridazine (low potency) and fluphenazine (high potency).
Thiothixene and haloperidol are also high potency antipsychotics.
Atypical antipsychotics
3 examples w/ mechanism
1 important SE
1. Risperidone: 5HT2 recpetor activity and less extrapyramidal symptoms
2. Clozapine: 5HT2 receptor blocker with fewest extrapyramidal sx. CAN CAUSE AGRANULOCYTOSIS.
3. Olanzapine: similar to clozapine, but no agranulocytosis
SE of high potency antipsychotics
SE of low potency antipsychotics
High potency: Most extrapyramidal sx
Low potency: fewer EPS, more anticholinergic effects, more hypotension, more sedation.
One major complication from typical antipsychotics
Tardive dysinesia: orofacial sx predominate. Withdrawal must be undertaken, but sx may not reverse.
1. Clinical indication
2. SE
3. Antidote
1. Used in bipolar d/o for tx of acute manic or depressive phase. 7-10 day delay until onset of effects.
2. SE: tremor, NEPHROGENIC DI.
3. No specific antidote--thiazide diuretics will lead to lithium retention and enhance toxicity. High sodium diet may increase excretion.
Tricyclic antidepressants
1. Prototype/similar to...
2. Mechanism
3. SE
1. Imipramine is the prototype; effects similar to phenothiazines.
2. TCAs reduce amine reuptake, thereby increasing concentration of NE and 5-HT in CNS synapses. Onset is delayed (2-3 weeks); improvement only in depressed persons.
3. SE: sedation, anticholinergic effects, antiadrenergic effects (similar to phenothiazines)
Tx of TCA overdose
1. Supportive
2. Lidocaine to reduce arrhythmias
3. Physostigmine to reduce anticholinergic effects.
1. Class
2. Unique use (1)
1. TCA
2. Used to treat obsessive-compulsive behaviors.
1. Examples
2. Mechanism
3. SE
1. fluoxetine, sertraline, paroxetine
2. Inhibit serotonin reuptake but not NE reuptake.
3. Can cause sexual dysfunction and CNS stimulation leading to insomnia. No anticholinergic or antiadrenergic effects.
1. Examples
2. Mechanism
3. SE
4. Hypertensive crisis
1. Tranylcypromine, phenelzine
2. Competitive, irreversible inhibitors of MAOa and MAOb, thereby increasing concentrations of NE and other aines in granules, increasing amine release.
3. SE include hepatotoxicity, CNS stimulation, and postural hypotension.
4. Hypertensive crisis precipitated when MAOIs are combined w/ foods containing tyramine (cheese, beans, beer, wine) or OTC sympathomimetics.
Drugs for Parkinson's Disease
List (7 classes)
1. L-dopa
2. Carbidopa
3. DA agonists--bromocriptine adn pergolide (non-selective); pramipexole and ropinirole (D2 selective)
4. Anticholinergics--trihexyphenidyl, benztropine
5. Amantadine
6. Antihistamines
7. Selegiline

Efficacies: L-dopa > bromocriptine > amantadine > anticholinergics
L-Dopa (parkinsons disease)
1. Mechanism
2. Effects
3. SE (include on-off)
4. Peripheral metabolism
1. L-Dopa is metabolized by dopa decarboxylase to DA, thereby increasing DA concentration, which is an inhibitory neurotransmitter in the basal ganglia.
2. Especially useful for reducing rigidity and akinesia.
3. SE include: NV, and anorexia d/t stimulation of CTZ; postural hypotension; arrhythmias, choreiform mvt; psychological disturbances; On-Off effects indicate a wearing off phenomena at the end of dosing.
4. l-dopa is rapidly metabolized in peripheral tissues (only 1% reaches CNS). Pyridoxine (B6) increases peripheral metabolism; carbidopa decreases peripheral metabolism.
Peripheral dopa decarboxylase inhibitor which slows peripheral metabolism of L-dopa. L-dopa dosage can be reduced by 80% w/ carbidopa.
DA receptor agonists
1. Major usage
2. Examples (non-selective; selective)
1. Used with L-dopa and carbidopa to reduce on-off effects. Effects and side effects similar to L-dopa
2. Non-selective (bromocriptine, pergolide); D2 selective (pramipexole, ropinirole)
Anticholinergics in Parkinson's Dz
1. Examples
2. Use
3. SE
1. Trihexphenidyl, benztropine
2. Reduce cholinergic tone in the basal ganglia. Used w/ antipsychotics to reduce EPS from antipsychotics
3. SE d/t central and peripheral cholinoceptor blockade.
Amantadine in Parkinson's
Amantadine is an antiviral drug that reduces sx of Parkinson's disease temporarily (6 mo)
1. Mechanism
2. Use in Parkinson's
1. MAOb inhibitor
2. Slows metaboilsm of DA and enhances the effectiveness of L-dopa.
Anticonvulsants-Mechanism (general)
1. Three specific mechanisms
Anticonvulsants act by erducing excitability of focal and non-focal neurons.
1. Enhancing GABA inhibition leading to increased Pcl and hyperpolarization of neuronal membranes.
2. Prolong sodium permeability inactivation thereby enhancing effective refractory period of nerve cells.
3. Block T-type calcium channels
1. Mechanism
2. Seizure types
3. SE
4. Contraindications
1. Phenobarbital potentiates GABA transmission by increasing duration of Cl channel opening.
2. Tonic clonic/partial seizures in kids; antiepileptic of choice in pregnant women.
3. SE-PHenobarbital induces hepatic P450 system--drug interactions.
4. Contraindicated w/ acute intermittent porphyria or variegate porphyria b/c barbiturates can induce porphyrin synthesis.
1. Prodrug of what drug
2. Seizure types
1. Prodrug of phenobarbital
2. Used in tonic-clonic and partial
1. Mechanism
2. First line for one type of seizures
3. SE
4. Metabolism
1. Binds to voltage-sensitive Na channels, especially inactive channels.
2. First line for tonic-clonic; also used in status after benzos
3. Gingival hyperplasia, cardiac arrhythmias, and hirsuitism. Also teratogenic, causing fetal hydantoin syndrome.
4. Zero-order kinetics
1. Mechanism
2. Drug of choice in one seizure type
3. SE
4. Interactions
1. Binds to voltage-sensitive Na channels and prolongs ERP.
2. Drug of choice in partial seizures
3. SE: rash, rare blooc dyscrasias including aplastic anemia, agranulocytosis.
4. Induces P450 thereby decreasing drug levels of itself and other drugs.
Valproid Acid
1. Mechanism
2. Drug of choice in one seizure type
3. SE
1. Broad-spectrum; enhances GABA accumulation and inhibits repetitive neuronal firing.
2. Drug of choice in myoclonic seizures
3. Dose-related anorexia, nausea, vomiting; hepatotoxic
1. Mechanism
2. Drug of choice in one seizure type
1. Inhibits low threshold T-type calcium channels.
2. Drug of choice in absence seizures
1. Mechanism
2. Uses
1. Blocks neuronal and glial reuptake of GABA.
2. Adjuvant tx for partial seizures
1. Mechanism
2. Uses
1. Blocks action of glutamate at its receptors
2. Used in partial seizures as adjuvant or monotherapy.
Major features of antiepileptic drugs
1. Protein binding
2. Clearance
3. SE
1. Highly plasma protein bound
2. Cleared by hepatic metabolism; may inhibit or induce metabolism of other drugs.
3. SE include CNS depression, skin rashes, nystagmus
Treatment of Status Epilepticus
1. IV benzodiazepine (diazepam or lorazepam)
2. IF BDZ is ineffective, try IV phenytoin, IV phenobarb, or general anesthesia.
1. Mechanism
2. Therapeutic Effects
1. Acetylates adn irreversibly inhibits COX-1 and COX-2.
2. Major therapeutic effects include mild analgesia, antipyresis, and anti-inflammatory actions at high doses. All d/t reduced prostaglanding synthesis at various sites.
1. SE
2. Acute toxic effects
3. Mgt of overdose
1. May cause gastric ulcerations, which are increased by EtOH; inhibit platelet aggregation; hypersensitivity; reduced renal uric acid secretion at low doses w/ reduced uric acid reabsorption at high doses; Reye's syndrome in children
2. Tinnitus, increased respiration d/t direct medullary stimulation and uncoupling of oxidative phosphorylation. This leads to respiratory alkalosis and HCO3 excretion. Acidosis subsequently occurs d/t respiratory depression, acidic products of aspirin metabolism, and previous HCO3 loss.
3. Tx OD with emesis or lavage, fluids with HCO3.
1. Mechanism
2. Effects
3. Major adverse effects
4. Antidote
1. Inhibits COX, especially in CNS
2. Mild analgesic, antipyretic
3. Major AE is delayed hepatic necrosis d/t depletion of glutathione and buildup of a toxic phase 1 metabolite. More pronounced w/ EtOH
4. N-acetylcysteine--replenishes stores of glutathione
Ibuprofen and Naproxen
1. Mechanism
2. Effects
3. SE
1. Reversibly inhibit COX
2. Effects include mild analgesic, antipyretic, and anti-inflammatory
3. SE are milder than aspirin, but include GI bleed, increased bleeding time.
1. Indicaiton
1. Unusualy NSAID, can be given IM for acute pain.
1. Properties
2. Pharmacologic effects
3. Cause of death in OD
1. Lipid soluble; distributes to TBW; metabolized by glucuronide conjugation. Binding sites include mu, kappa, and delta subtypes.
2. Analgesia d/t inhibitor action on substance P release in spinal cord; respiratory depression (decreased medullary sensitivity to CO2); Physical dependence and tolerance; antitussive; emetic on initial doses; miosis (no tolerance develops); constipation
3. Respiratory depression
1. Mechanism
2. Clinical uses
1. Like morphien, binds to mu receptors, blocking nociceptive transmission. Weak agonist wrt morphine
2. Antitussive is unique use
1. Class
2. Clinical use
1. Opioid acting on mu-receptors
2. Antidiarrheal
1. Class/mechanism
2. Clinical use
1. Opioid agonist-antagonists; agonist at kappa-receptors and partial agnoist at mu-receptors.
2. Used as analgesia for moderate pain.
1. Class/mechanism
2. Clinical use
1. Opioid, primary a mu agonist.
2. Tx of opioid abstinence syndromes and heroin users.
1. Class/mechanism
2. Uses of Naloxone
2. Use of naltrexone
1. Opioid antagonists; pure antagonists at opioid mu-receptors.
2. Naloxone is fast acing and reverses respiratory depression from narcotic OD; incudes withdrawal in narcotic addict.
3. Naltrexone can be taken PO and has a longer duration of action. Used in mgt of narcotic addict to reduce euphoric effects of narcotics; also reduces craving for EtOH.