CNS PART II Flashcards
Substance abuse -Nicotine
releases norepinephrine and epinephrine;tachycardia, even hypertension, and peripheral vasoconstriction from alpha 1 receptor activation.
-arousal, increased alertness, increased memory functions, increased cognitive functions, mood enhancement, improved attention and reaction time, and reduced aggressiveness.
- stimulates the secretion of hydrochloric acid
-Nicotine is a hepatic enzyme induce
-potentiates the action of sympathomimetic agonists.
- better to use the selective Beta-1 blockers rather than the non-selective (Beta-1 and 2 receptor blockers) to avoid the additional peripheral vasoconstriction
- antagonizes the action of the alpha-1 and selective beta-1 sympathetic blocker drugs
-enhances procoagulant effects of the exogenous estrogen drugs increases the inappropriat blood clotting noted with these drugs. Women who smoke and take estrogens have a higher risk of blood clots, including ischemic strokes.
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nicotine quitting meds OTC
-Nicorette-no more 24 pieces gum/day-no loner than 6 months-high relapse rate
-Nicotine lozenges-15 min after eating/drinking
Max20/day. DC after 12 weeks
-transdermal systems - MAX 12-20 weeks very high relapse start patch before quitting
nicotine quitting meds -prescription
-Nicotine nasal spray- two sprays, one in each nostril.
Max 40/day. daily as needed to reduce cravings for 8 - 12 weeks then taper over the next 4 - 6 weeks (use should not exceed 6 months).
-Nicotine inhaler- Four (4) mg. nicotine is delivered from a 10 mg. cartridge.
5 to 16 inhalations daily.as needed 8 - 12 weeks then taper 4 - 6 weeks.
- Bupropion (Wellbutrin) Increases noradrenaline and dopamine levels in the CNS . Dose reduced in the elderly and pts taking meds lowering seizure threshold.
May cause seizures, angioedema and psychosis.
- Varenicline (Chantix)-partial agonist of the nicotinic receptor. Binding to the receptor may limit the reinforcement effect of nicotine on brain reward pathways in cigarette smokers -Second line therapy for patients who fail nicotine patch and bupropion.
May cause nausea, insomnia, abnormal dreams and taste perversion.
Safe in patients with cardiovascular disease.
Ethanol
-activates GABA receptors in the brain
-affects the release of several neurotransmitters (norepinephrine, dopamine, serotonin, endorphin)
-Causes cutaneous vasodilatation;
-Has direct cardiotoxic effects on the heart resulting in impaired myocardial contraction.
- Inhibits the release of antidiuretic hormone
-Increase in HDL levels
-Relaxes uterine smooth muscle
-Blocks hepatic gluconeogenesis
-inhibit the hepatic metabolism both of ethanol and any other drug metabolized by these enzymes.
- up-regulation of hepatic drug-metabolizing enzymes
-potentiates the pharmacologic effects of sedative-hypnotics.
-potentiate the hypoglycemic effects of insulin and the other oral hypoglycemic drugs.
- potentiate the gastric irritative effects of other gastric irritant drugs (i.e., aspirin and the other non-selective NSAIDs).
Ethanol withdrawal benzos- -6 hrs after the “last drink” or may take as long as 6 days.
Benzodiazepines (long-acting drugs like diazepam and chlordiazepoxide
-potentiate GABA receptors and replace the CNS depressant effect of ethanol.
- Larger than normal doses needed RT increased hepatic metabolism by chronic ethanol consumption and effect as a hepatic enzyme inducer.
- If the patient has cirrhosis, short-acting benzo may be needed (metabolized more slowly and act like long acting drug)
naltrexone (ReVia - formerly Trexan)
-opiate antagonist- blocks the effects of endorphins which are released by ethanol and are possibly responsible for the pleasurable effects of ethanol.
-must be not be drinking at time of the 1st dose, must be opioid-free minimum of 7 days and not receive opioid analgesics during therapy. Concurrent use of exogenous opioids may result in fatal overdose.
- A once-monthly injectable form (Vivitrol)
-Must avoid using in patients with active liver disease.
Beta blockers-for alcohol
Prevent tachycardia RT sudden withdrawal of the direct vasodilatory effects on peripheral arterioles.also prevent the HTN RT excessive ethanol consumption.
- Centrally-acting alpha-2 adrenergic agonists for alcohol withdrawal
- Prevent the hypertension frequently associated with excessive consumption of ethanol
- disulfiram (Antabuse) for alcohol withdrawal
Inhibits the enzyme acetaldehyde dehydrogenase resulting increase in the serum levels of acetaldehyde. Alcohol will also increase acetaldehyde=toxic effect blurred vision, dizziness, chest pain, confusion, palpitations, flushing of the face, nausea, vomiting, diaphoresis, weakness, and rarely, seizures, coma and death. Effects may last up to 14 days after the last dose.
Cocaine withdrawal meds
-Tricyclic antidepressants block the reuptake of dopamine and serotonin. By augmenting monoamine levels may relieve dysphoria and reduce cravings
- Bromocriptine -dopamine agonist
- Amantadine stimulates release of dopamine from dopaminergic neurons
- Anticonvulsants to control seizure activity
Cocaine
blocks the reuptake of norepinephrine, dopamine, and serotonin back into the nerve endings, increasing them and has a direct effect on dopaminergic neurons in the brain causing the release of dopamine from its storage sites
otentiate the pharmacologic effects of adrenergic agonist drugs.
- Cocaine can produce excessive peripheral vasoconstriction if administered together with the non-selective Beta blockers
Marijuana
- bronchodilatation with acute usage and -bronchoconstriction with chronic usage.
- decreased testosterone and decreased spermatogenesis and infertility in men;
-decreased FSH, LH, and prolactin hormone levels in women. - possibility of chromosomal damage from chronic use.
- Tolerance and dependence are rare; only occur with chronic use of very high doses
Tricyclic Antidepressants( ex-amitriptyline ,amoxapine , clomipraminel) for Depression
-long duration of action (weeks)
-Multiple uses; depression, insomnia, migraine, A, enuresis, etc.
-Takes weeks before action begins. Max effect may take 2 months
-anticholinergic adverse effects
- alpha-1 blocking effects commonly produce orthostatic hypotension, palpitations, tachycardia.
-cardiotoxic because they are proarrhythmic drugs
decrease the seizure threshold;
-Can cause extrapyramidal effects and changes in libido
-May cause bone marrow suppression and agranulocytosis
TetraCyclic Antidepressants
Low affinity for the muscarinic acetylcholine receptors; few or no anticholinergic side
- advantages similar to Tricyclic Antidepressants
-Disadvantages similar to the Tricyclic Antidepressants except few or no anticholinergic effects
Monoamine Oxidase Inhibitors (MAOIs)
isocarboxazid (Marplan)
Selegiline (EmSam)
phenelzine (Nardil)
tranylcypromine (Parnate)
-No anticholinergic effects
- Multiple uses; anxiety-depression, panic disorders, phobias
-Slow recovery from enzyme-blocking action, 2-3 weeks
- Potentiates the effects of sympathomimetic drugs;
- strict dietary limitations; tyramine-containing foods (wine, cheeses, beer, pickled products, sour cream, chocolate, yogurt, bananas, figs, raisins, liver, avocados, etc.), severe hypertension
Commonly produce adverse effects; dizziness, drowsiness, anorexia, orthostatic hypotension, hypertension, arrhythmias, constipation, sexual dysfunction
-Not first line drug
-Not for patients with suicidal depression; may increase the risk of suicide
- Not recommended in pregnancy, lactation, or seizure disorders
- Contraindicated concurrently with meperidine (Demerol); increased risk of cardiovascular instability
