Test #29 (PRR Week 2N Block 12: Neuro Pharm) Flashcards
Explain blood gas/partition coefficient of gas anesthetic & what it means in terms of drug properties
Onset of action of a gas anesthetic depend on its solubility in blood (blood/gas partition coefficient). Drugs with high blood/gas partition coefficients are more soluble in the blood, demonstrate slower equilibration with brain, & have longer onset times
Classify first generation antipsychotics based on characteristic side effect profiles
Low potency: non-neurologic side effects (e.g., sedation, anticholinergic side effects, orthostatic hypotension); High-potency: extrapyramidal sx (Think: “Potency = ExtraPyramidal)
Explain/Dx: 55 yo man with chest pain while watching tv, PMH of htn, asthma, diabetes, smokes 2 packs cigs daily, tx in ED for chest pain & becomes short of breath, bp now 135/85 mmHg and heart rate 65/min, PE reveals prolonged expirations and wheezes in bilateral lung fields
Beta-adrenergic blockade reduces blood pressure and cardiac work, which is beneficial in acute tx of myocardial iscemia. However, when noncardioselective agents used, adverse effects like bronchoconstriction (dose-dependent) may be seen
(1) Dx: 55 yo farmer confused disoriented, otherwise healthy, not use any meds, bp 110/70 mmHg, HR 50/min, pupils symmetric, 2 mm, and reactive to light, tearing considerably, scattered wheezes bilaterally on lung auscultation, patient’s skin flusedhed and sweating profusely (2) Explain
(1) Organophosphate poisoning (2) Exposure to certain insecticides => organophosphate poisoning. Profound and prolonged cholinesterase inhibition because organophosphates bind irreversibly to cholinesterase, causing state of cholinergic excess: excessive salivation, lacrimation, diaphoresis, urinary incontinence, diarrhea, emesis, miosis, and bradycardia
(1) Mechanism of Benzodiazepines (2) Other drugs sharing this mechanism
(1) Allosteric binding to GABA receptor (2) Benzodiazepines, Barbiturates, and alcohol all bind to different components of GAGAa receptor & facilitate inhibitory action of GAGA. Note: GABAa & GAGAc = ion channels while GABAb receptor = G-protein linked
(1) Mechanism of Timolol (2) Explain its use in glaucoma
(1) Beta-blocker (2) Glaucoma due to increased intraocular pressure, due to decreased outflow or increased production of aqueous humor. Timolol and other beta-blockers decrease aq. hum. prod. by ciliary epithelium
(1) List 1st and 2nd generation H1 blockers. (2) Which given to patient with hx of falls, and why?
(1) 1st generation: Diphenhydramine, dimenhydrinate, chlorpheniramine; 2nd generation: Loratadine, Fexofenadine, Desloratidine, Cetirizine (2) 2nd generation, because have minimal sedative (and antimuscarinic) effects
(1) Tx: patient complains of weakness in right arm and leg 5 days after resolve of subarachnoid hemorrhage
Calcium channel blockers (espeically Nimodipine) can be used to assist in prevention of cerebral vascular spasm following SAH. This is an alternative use of calcium channel blockers.
(1) Contraindicated drug in this patient: 65 yo male undergoing rehabilitation after stroke, given diazepam in order to decrease muscle spasticity involved extremities (2) Explain
(1) 1st generation H1-histamine receptor antagonists, including diphenydramine and chlorpheniramine, (2) can cause significant sedation, especially when used with other meds that cause CNS depression (e.g., benzodiazepines)
(1) Compare side effect profile of SSRIs to TCAs (2) Relatively common side effect of SSRIs
(1) Better side effect profile (2) Sexual dysfunction relatively common side effect of SSRIs & limits use in many patients
Indication of clinical movement after edrophonium administration in myasthenia gravis patients
Clinical movement after edrophonium admin. indicates that pt. is undertreated (myasthenic crisis)
Barbiturates effect on warfarin therapy
Barbiturates induce hepatic microsomal enzymes, increase warfarin metabolism and reducing its anticoagulation activity
(1) Dx: 15 yo male, 3 mo. hx periodic, sudden-onset, arrhythmic jerking movements, muscle contractions usually happen early in AM, soon after wakening, aggravated by sleep deprivation, movements neither suppressible nor preceded by an urge to make a movement, never lost consciousness, no other PMH, family hx reveals seizure disorder in uncle (2) Tx of choice & its mechanism
(1) Myoclonic seizure (2) Sodium valproate (valproic acid) is drug of choice for myoclonic seizures. This drug suppresses abnormal electric activity in cortex by affecting GABA and NMDA receptors, as well as Na+ and K+ channels
Meds causing seizures
Bupropion (antidepressant), Clozapine (antipsychotic at high doses), Isoniazid (anti-tuberculosis drug, if given without pyridoxine), Ciprofloxacin (antibiotic), & imipenem (antibiotic)
(1) Dx: 8 yo Asian immigrant, brief loss of consciousness, fell on floor & ‘started shaking and jerking’, also seen ‘staring in space’ that occurs several times a day for last year, boy seems sleepy although oriented in time and place, several hours later, alert & wants to go home (2) Tx of choice
(1) Absence & associated tonic-clonic seizures (2) Sodium valproate
Mechanisms of following: (1) Anticholinergic poisoning (2) Botulism (3) Organophosphate toxicity
(1) Inhibit postsynaptic action of acetylcholine (2) Blocks presynaptic exocytosis of acetylcholine vesicles (3) Prevent degradation of acetylcholine within synaptic cleft
(1) Mechanism of most opioid narcotics (2) Purpose & mechanism of Pentazocine (3) Warning about Pentazocine use
(1) Majority of opioid narcotics selective mu receptor agonists that work by binding to mu receptors and mimicking effects of endogenous opioid receptors (2) Opioid narcotic specifically designed to produce analgesic effects with little to nose abuse potential. Pharmacologically, works through partial agonist activity and weak antagonist activity at mu receptors. (3) Because of its weak antagonistic effects, can cause withdrawal sx in patients who are dependent or tolerant to morphine or other opioids
Entacapone: (1) Type of drug (2) Mechanism (3) Other drug in this type/class
(1) Catechol-O-methyl transferase (COMT) inhibitor (2) Increase levodopa availability in brain (3) Tolcapone
(1) Type of drug amitriptyline is (2) Most common cause of death in patients with this kind of drug overdose (3) Explain (4) Intervention
(1) TCA (2) Refractory hypotension & cardiac arrhythmias (3) Inhibition of fast sodium channels in cardiac myocytes (and His-Purkinje system) is thought to be major underlying cellular event. (4) Fluid resuscitation with normal saline and hypertonic sodium bicarbonate administration are crucial in these patients
(1) Halothane toxicity (2) Mechanism (3) Clinical/Lab finding
(1) Massive hepatic necrosis is rare but severe complication of halothane exposure (2) Occurs due to direct liver injury by halothane metabolites & formation of autoantibodies against liver proteins (3) Light microscopy shows massive centrilobular hepatic necrosis.
(1) type of drug amitriptyline is (2) Comparison of its and similar drugs’ anticholinergic properties to other drugs (3) Patient population to take caution with using this drug & why
(1) TCAs such as imipramine, doxepin, amitriptylin, and clomipramine have (2) stronger anticholinergic properties than heterocyclics or SSRIs & (3) should be used with caution in pts with benign prostatic hyperplasia (BPH), as they may cause urinary retention
Mechanism of resistance against cephalosporins
Change in structure of penicillin binding proteins
