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Acetylcholine Formation Acetyl CoA + Choline -Choline Acetyltransferase-> Acetylcholine Important site of production: nucleus basalis of Meynert Acetylcholine is broken down by acetylcholinesterase into Acetate and Choline
Dopamine Formation Tyrosine -tyrosine hydrolase-> Dopa -dopa decarboxylase-> Dopamine -dopamine beta hydroxylase-> Norepeniphrine -phenylethanolamine N-methltransferase-> Epinephrine Dopaminergic neurons are in: substantia nigra pars compacta and ventral tegmental area
Gamma Aminobutyric Acid GABA Major inhibitory NT
Glutamate Major excitatory NT
Glycine inhibitory NT. Controls/modulates glutamate activity in brain and spinal cord.
Histamine In CNS responsible for sleep modulation and satiety. (Antipsychotics and tricyclic antidepressants can cause H1 receptor blockade leading to sedation and increased appetite and s/e) Histamine Neurons located: ventral posterior hypothalamus
Seratonin 5-Hydroxytryptamine Monoamine. Regulates mood, body temperature, sexuality and sleep. Seratonin released by raphe nucleus
Seratonin (5-Hydroxytryptamine) Formation Tryptophan -trytophan hydroxylase-> 5-Hydroxytrytophan -aromatic L amino acid decarboxylase-> 5-Hydroxytryptamine (Seratonin) Degredation: 5-Hydroxytryptamine -MOA-> 5-Hydroxindole acetaldehyde -Aldehyde dehydrogenase-> 5-Hydroxyindole acetic acid
Norepinephrine Formation Tyrosine -tyrosine hydrolase-> Dopa -dopa decarboxylase-> Dopamine -dopamine beta hydroxylase-> Norepeniphrine -phenylethanolamine N-methltransferase-> Epinephrine primary site of synthesis = locus ceruleus (in the upper pons)
Succinylcholine (short acting) MOA -Depolarizing neuromuscular junction agent -ACh receptor agonist -Phase I: binds aggressively, depolarizes at end plate. Resistant to AChE so remains bound. continued binding keeps Na+ channels closed, prevents repolarization
Succinylcholine MOA (2) Phase II- over time continued binding --> conformational change at NMJ --> to non depolarizing NMJ block that can't be reversed. Active in 30s, lasts 10min (duration limited by diffusion) Pseudocholinesterase metabolizes it before drug reaches site
Succinylcholine Use Temporary muscle paralysis in surgery, intubation only depolarizing agent approved for clinical use in US
Succinylcholine S/E -Cardio low dose: negative chronotropic and ionotropic affects -Cardio high dose: positive chronotropic and ionotropic effets; raises catecholamine levels -Fasciculations -Myalgia
Succinylcholine S/E (2) -Hyperkalemia (concern with burns/trauma, spinal cord injury, cardiac disease and/or metabolic abnormalities) -Malignant Hyperthermia
Non Depolarizing Agents Mivacarium - short acting Vecuronium- intermediate acting Rocuronium- intermediate acting Atracurium- intermediate acting Pancuronium- long acting Doxacurium- long acting
Non Depolarizing Agents MOA competitive antagonists at ACh receptor--> paralysis
Non Depolarizing Agents Metabolism Renal and heptaic Except Mivacarium- metabolized by pseudocholinesterase -safe in pts with hepatic or renal dysfunction Reversal of these drugs depends on metabolism or giving AChE inhibitor
Non Depolarizing Agents Use Similar to depolarizing agents: Intubation, prevention of fasciculations, decrease amount of inhalation agents needed, maintenence of paralysis
Non Depolarizing Agents S/E -Respiratory fxl from diaphragmatic paralysis -Tachycardia (pancuronium) -Histamine release (mivacurium)
Cholinesterase Inhibitors Neostigmine Pyridostigmine Edrophonium Physostigmine
Cholinesterase Inhibitors MOA Inactivate AChE by electrostatic or covalent binding --> increase in ACh for binding at receptors
Cholinesterase Inhibitors Use Reversal of nondepolarizing agents C/I for use with depolarizing agents because they will prolong block also used to diagnose (Edrophonium) and Rx (neostigmine) Myasthenia Gravis
Cholinesterase Inhibitors S/E Bradycardia Bronchospasm Excitation (physostigmine) Intestinal Spasm Increased bladder tone Pupillary constriction
Anticholinergic Drugs Atropine Scopolamine Benztropine Glycopyrrolate
Anticholinergic Drugs MOA Competativley block ACh receptors
Anticholinergic Drugs Use -In anesthesiology, but also have other uses -Glycopyrrolate is charged molecule and cannot cross the BBB to cause CNS effects -Scopolamine given for CNS effects (antiemetic)
Anticholinergic Drugs Use (2) Atropine: -given for cardiovascular effects -first line Rx for organophosphate poisening -Reversing vagal stimulated bradycardia -Decreasing resp tract secretions -Bronchial smooth muscle relaxation -Reversal of antipsychotic extrapyramidal s/e
Anticholinergic Drugs S/E -CNS stimulation -Cutaneous blood vessel dilation -Urinary retention -Cycloplegia (paralysis of ciliary muscle of the eye, leading inability to accommodate) -Decreased secretions
Barbituates Phenobarbital Pentobarbital Thiopental Secobarbital
Barbituates MOA -Increase DURATION of Cl- ion channel opening -> enhanced GABAergic transmission -Can also block excitatory glutamate receptors -Also induce CYP-450 in liver-> increased metabolization of its target drugs
Barbituates Metabolism -Phenobarbitol 75% inactivated by liver, 25% excreted unchanged in urine
Barbituates Use -During anesthesia (short acting ones like Thiopental or Methohexital) -Anticonvulesents in tonic-clonic seizures, status epilepticus, and eclampsia (Phenobarbital) -Anxiolytics in mild anxiety and as sedatives -Insomnia (but lose REM sleep so no)
Barbituates S/E -Dependance (high risk) -Synergistic effects with alcohol and benzos (cross tolerance) -Resp, cardio, CNS depression -> coma/death -Induce CYP 450 -C/I in acute intermitten porphyria (activate ALA synthase, enzyme that catalyzes rate lim step in heme
Barbituates Overdose Rx ABCs and hemodyalysis in extreme cases. Alkalinaztion of urine aids in elimination of phenobarbital
Barbituates Withdrawal -Can mimic ETOH w/d -Dangerous- Rx in hospital -Gradual admin of Phenobarbital SXS: -anxiety -Irritability -Elevated HR and RR -Muscle pain -Nausea -Tremors -Hallucinations -Confusion -Seizures -Death possible if untreated
Benzodiazepines Diazepam Lorazepam Triazolam Temazepam Oxazepam Midazolam Chlordiazepoxide Alprazolam short acting = TOM thumb (triazolam, oxazepam, midazolam)
Benzodiazepines MOA -Bind GABA receptor -> increased FREQUENCY of Cl- channel opening. -Cl hyperpolarizes cell, reduces excitability. -Effects terminated via redisdribution and excretion (hepatic metabolism into active metabolites) Cross placenta
Bezondiazepines Use -Anxiolytics (inhibit neuronal circuits in limbic system) -Muscle relaxant for muscle spasm -Amnesic agents for endoscopic procedures -anticonvulsant
Benzodiazepines S/E -Synergystic effect with ETOH and barbs (cross tolerance) -Resp depression and coma -Drowsiness and confusion -Tolerance -Dependence -decrease latency to sleep onset and increase stage 2 of non REM sleep. Both REM and slow wave decreased
Benzodiazepines S/E Rx Reverse benzo with Flumazenil (comp antagonist at GABA receptor)
Benzodiazepines Withdrawal Long term use -> tolerance and dependence W/D similar to barbituate withdrawal, rarely as severe. SXS: -confusion -Anxiety -Agitation -Restlessness -Insomnia -Tension
Opioids Morphine Hydromorphone Oxymorphone Methadone Meperidine Fentanyl Sufentanil Alfentanil Remifentanil Codeine Hydrocodone Oxycodone Buprenorphine Heroin Dextromethorphan
Opioids MOA -Analgesics, act on CNS (agonists at mu receptor with differing strengths)- modifies pain pathways modulate synaptic transmission: Inhibit release of ACh, NE, 5-HT, glutamate, substance P.
Opioids Types -Either endogenous (formulated from proopiomelanocortin POMC- also precursor for ACTH, MSH and LPH) -these are endorphins, met- and leuenkephalins and dynorphins -or exogenous (structurally similar but altered to get dif properties)
Opioids Use -local analgesia (regional nerve blocks, epidural nerve blocks, spinal nerve blocks) -systemic pain relief (pt controlled analgesia) -chronic pain management (transdermal patches) -Antitussives (dextromethorphan) -Abused by IV drug users
Opioids S/E Tolerance Dependence Overdose potential Toxicity: respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Toxicity Rx with naloxone or naltrexone
Buspirone MOA -Partial agonist to seratonin (5HT-1A) receptors in the CNS -Does not affect GABAergic receptors so doesn't interact with ethanol and is not sedative -No risk of dependance or associated euphoria
Buspirone Use Rx GAD
Buspirone S/E May stimulate locus ceruleus -> increased NE release (causing increased anxiety) -May not work in pts with a history of benzodiazepine use or sever anxiety.
Valproix Acid MOA Binds Na+ channels favoring inactivated state - Role in decreasing Ca++ influx across cell membrane through T-type Ca++ channels, reducing Ca++ current in thalamic neurons.
Valproic Acid USE 1st line for Generalized and Partial Tonic Clonic - 2nd line for Generalized Absence (after ethosuxamide) - bipolar disorder, intermittent expolisve disorder and prophylaxis for migraines.
Valproic Acid S/E GI distress - increased appetite and weight gain - tremor - sedation - alopecia - hepatotoxicity - decreased platelets - polycystic ovarian syndrome - folate antagonist-> neural tube defects - C/I in pregnancy
Phenobarbitol MOA A barbituate, GABA agonist, increases CNS inhibition and raises seizure threshold.
Phenobarbitol Use Role as anticonvulsant is for status epilepticus 1st line in pregnant women and children
Phenobarbitol S/E Sedation - Tolerance - Dependence - Induction of CYP450 system
Carbamazepine MOA Reduces recovery rate of voltage gated Na+ channels-> blocks rapid successive firing of APs associated with partial seizures and generalized tonic-clonic seizures
Carbamazepine Use 1st line for trigeminal neuralgia - 1st line for Generalized Tonic Clonic - Rx partial seizures - Also for bipolar
Carbemazepine S/E Diplopia - nystagmus - Aplastic Anemia - Agranulocytosis - gingival hyperplasia - hirsutism - SIADH - Stevens Jhonson's syndrome - Hyponatremia - Induces CYP450 enzymes -> increased metab of many drugs including self and OCP
Phenytoin MOA Slows rate of recovery of voltage gated Na+ channels (like carbemazepine)
Phenytoin Use Used to Rx all seizures except absence - 1st line for Generalized Tonic Clonic - 1st line for status epilepticus prophylaxis
Phenytoin S/E Toxicity at high levels: Nystagmus - Diplopia - Ataxia - Sedation - Gingival hyperplasia - Megaloblastic anemia - SLE-like syndrome - Induction of CYP450 - Fetal hydantoin syndrome
Lamotrigine MOA Prolongs inactivation of Na+ channels - Reduces glutamate release
Lamotrigine Use Partial - Generalized Tonic Clonic - focal epilepsy - Lennox-Gastaut syndrome - bipolar disorder
Lamotrigine S/E -Dizziness -Nausea -H/A -Skin Rash (hypersensitivity reaction) -Stevens-Johnson syndrome (avoided by increasing slowly)
Pregabalin MOA binds to alpha2-delta subunit of high voltage activated Ca channels. Increases density of GABA transporter protein and increases rate of functional GABA transport. -Reduces presynaptic release of glutamate, NE, and substance P.-Antinociceptive/Antiseizure
Pregabalin Use Rx neuropathic pain associated with diabetic nephropathy and postherpetic neuralgia. -Adjunctive Rx of partial seizures and fibromyalgia.
Pregabalin S/E Dizziness - Somnolence - Weight gain
Gabapentic MOA binds to alpha2-delta subunit of high voltage activated Ca++ channels -> modulate their function. - Also presynaptically reduces glutamate release.
Gabapentin Use Rx partial seizures, pain (neuropathic), peripheral neuropathy, bipolar, anxiety, used for sedation because it is highly lipid soluble.
Gabapentin S/E Sedation - Weight gain - ataxia
Topiramate MOA/Use/SE Epilepsy Drug - Blocks Na+ channels, increases GABAa action SE- Sedation, mental dulling, kidney stones, weight loss
Tiagabine Use/MOA 1st line for absence seizures - Blocks thalamic T-type Ca++ channels
Vigabatrin MOA/Use Irreversibly inhibits GABA transaminase -> increased GABA - Used for simple and complex seizures
Levetiracetam MOA/Use Unknown MOA, may modulate GABA and glutamate release - simple, complex and tonic clonic seizure Rx
Ethosuxamide MOA Reduced Ca current in thalamic neurons (thalamus responsible for 3Hz spike and wave rhythms seen in absence seizures. By reducing T type currents ->stop rhythmic discharge associated with absence seizure
Ethosuxamide Use 1st line for absence seizures
Ethosuxamide S/E GI distress - Lethargy - H/A - Urticaria - Stevens-Johnson syndrome
Memantine MOA Noncompetative block of NMDA receptors preventing glutamate to stimulate (normally depolarization causes magnesium to block receptors which is relieve and Ca+ enters cell to ->damage). This leads to less intracellular Ca++, sparing neurons
Memantine Use Rx moderate to severe Alzheimer's disease. Role in vascular dementia.
Memantine S/E Agitation - Urinary Incontinence - Insomnia - Diarrhea
Tacrine, Donepezil, Rivastigmine, Galantamine MOA Selective inhibitors of AChE in CNS. Increases ACh -> improved cognition. Because centrally acting, less peripheral s/e.
Tacrine, Donepezil, Rivastigmine, Galantamine Use Rx Alzheimer's ds cause they are centrally acting (cross BBB), unlike the AChE used for myasthenia gravis.
Tacrine, Donepezil, Rivastigmine, Galantamine S/E N/V - Diarrhea - Insomnia
Bromocriptine, Pergolide, Ropinirole, Pramipexole MOA DA receptor agonists. Pergolide at D1 and D2, Ropirinole and Pramipexole at D2 only, Bromocriptine D2 agonist and D1 ANTagonist. Bromocripine also antagonizes D1 receptors in hypothalamus.
Bromocriptine, Pergolide, Ropinirole, Pramipexole Use Rx Parkinsons Ds. Bromocriptine can be used to reduce rate of growth of pituitary adenomas and to Rx. acromegaly
Bromocriptine, Pergolide, Ropinirole, Pramipexole S/E H/A, N/V, Epigastric pain, hypotension/syncope intially leading to HTN over time
Levodopa (L-dopa) MOA metabolic precursor to dopamine, enters brain through L-amino acid transporter (dopamine can't cross BBB). In CNS decarboxylated to dopamine. Appears in urin as metabolites homovanillic acid (HVA) and dihydroxyphenylacetic acid (DOPAC).
Levodopa Use 1st line to Rx PD. Give with carbidopa to reduce peripheral conversion and s/e and increase CNS levels.
Levodopa S/E N/V - Tachycardia - Atrial Fibrillation - Dyskinesias - Depression - Agitation - Confusion C/I in psychosis and closed angle glaucoma.
Selegiline, Rasagiline MOA MAO-B (metabolizes dopamine, found in striatum) Inhibitor, selective irreversible
Selegiline, Rasagiline Use Rx PD - Selegiline available in skin patch that allows bypass of GI tract. Its low doses does not tyramine food interactions like other MOA inhibitors
Selegiline, Rasagiline S/E Serotonin Syndrome (can occur in comb with meperidine, TCAs or SSRIs)
Tolcapone, Entacopone MOA Catechol-O-Methyltransferase (COMT)Inhibitors - Tolcapone is peripheral and central - Entacopone is peripheral - prolong activity of L-Dopa by preventing its metabolism both centrally and peripherally. Entacopone preferred because less hepatotoxicity.
Tolcapone, Entacopone Use Used to increase levels of levodopa in the Rx of PD
Tolcapone, Entacopone S/E Dyskinesias - Nausea - Confusion
Stages of Anesthesia Stage 1: Analgesia (conscious and conversational) Stage 2: Disinhibition (Autonomic variations- changes in BP/HR/RR)Stage 3: Surgical Anasthesia (Unconscious and relaxed muscles) Stage 4: Medullary depression (Respiratory and vasomotor center depression)
Halothane, Isoflurane, Sevoflurane, Desflurane MOA, Use Inhaled anesthetics used in maintenence of anesthesia MOA poorly understood
Halothane, Isoflurane, Sevoflurane, Desflurane S/E Respiratory depression, Nausea, Emesis, Hypotension
Halothane, Isoflurane, Sevoflurane, Desflurane Toxicity Hepatotoxicity (halothane), Nephrotoxicity (methoxyflurane; no longer used in the US), Convulsions (enflurane), Malignant hyperthermia (all agents except nitrous oxide- Rx with Dantrolene- blocks Ca release from SR by binding ryanodine receptors).
Barbituates as IV anesthetic highly lipid soluble, enter brain rapidly, so useful for short procedures. Redistribution to other tx -> loss of effects. They are NOT analgesic and require supplementary analgesic. Can cause severe hypotn in pts who are hypvolemic or in shock
Benzodiazepines (Midazolam) as IV anesthetic 1st line for endoscopy, used with inhalational anesthetics and narcotics. Midazolam can cause severe postoperative respiratory depression and amnesia.
Ketamine (Arylcyclohexylamine) as IV anesthetic PCP analog that acts as dissociative anesthetic (high affinity for NMDA receptors). Causes sedation, amnesia, immobility, disorientation, and hallucinations
Opioids (Morphine, Fentanyl, Sufentanil) as IV anesthetic used with other CNS depressants during general anesthesia. Toxicity involves hypotn, respiratory depression and muscle regidity.
Propofol as IV anesthetic rapid induction anesthesia with short procedures, excitatory phase may occur with muscle twitching, spontaneous movements, hiccups. Can reduce ICP. Used in the resection of spinal tumors. can be used when assessing spinal cord function
Created by: stripedjeans



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