Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
65 Cards in this Set
- Front
- Back
- 3rd side (hint)
|
Ondansetron
|
5-HT3 Receptor Antagonist
(Acts at GI tract and STN and CTZ zone) USE * Acute Chemotherapy N/V (not good for N/V >24 hours) * Post-op N/V * Post-radiation N/V NOT USED FOR MOTION SICKNESS!! INTERACTIONS * Potentiates L-Dopa: Inhibition of 5-HT increases DA. |
|
|
|
Prochlorperazine
|
Dopamine Receptor Antagonist--Phenothiazide
* Blocks D2 receptors in the Solitary Tract Nucleus, and CTZ zone. * Has no antipsychotic action...does not work at mesolimbic receptors. USE * Chemotherapy N/V CONTRAINDICATIONS * Parkinson's Disease INTERACTIONS * L-Dopa - decreases the effectiveness |
|
|
|
Droperidol
|
Dopamine Receptor Antagonist
* Blocks D2 receptors in the Solitary Tract Nucleus, and CTZ zone. * Butyrophenone class of typical anti-psychotics but has no antipsychotic actions (no blockade in the mesolimbic areas). USE * Postoperative N/V CONTRAINDICATIONS * Parkinson's Disease INTERACTIONS * L-Dopa - decreases the effectiveness |
|
|
|
Metoclopramide
|
Dopamine Receptor Antagonist
USE * Chemotherapy N/V * Postoperative N/V * Prokinetic (stimulates GI). CONTRAINDICATIONS * Parkinson's Disease INTERACTIONS * L-Dopa - decreases the effectiveness |
|
|
|
Aprepitant (Emend)
|
Anti-emetic
*Neurokinin Receptor Antagonist MOA: Blocks NK1 receptors in CTZ zone USE * Acute Chemotherapy N/V * Delayed Chemotherapy N/V Not used much b/c it is expensive. |
|
|
|
Scopolamine
|
Muscarinic Receptor Antagonist
* Acts at M1 receptors in Cerebellum, CTZ zone, and STN of brain. USE * Motion Sickness * N/V CANNOT GIVE ORALLY d/t anti-musc effects...don't want systemic effects. Must give as a transdermal patch behind ear...goes directly to CNS. SE * Sedation/ Confusion * Mydriasis * Dry mouth |
|
|
|
Diphenhydramine (Benedryl)
|
Histamine-1 Receptor Antagonist
Muscarinic Antagonist MOA * Crosses BBB. Blocks H1 receptors in the Cerebellum and STN to pvt nausea and motion sickness. * Blocks musc receptors in the nigrostriatal pathway to tx parkinson's disease (helps decr tremor...but NOT bradykinesia). USE * Motion Sickness * Chemotherapy Induced N/V * Insomnia * EPS Symptoms * Parkinson's Disease SE * Sedation via H1 Blockade |
|
|
|
Promethazine (Phenergan)
|
Anti-emetic/ Anti-histamine/ Phenothiazide
MOA: *Crosses BBB. Blocks H1 receptors in the Cerebellum and STN. (tx's nausea and motion sickness) * Muscarinic Antagonist * Dopamine Antagonist (some): Phenothiazide (with 2 carbon spacer in R2: ie no antipsychotic activity). (tx's nausea) USE * Motion Sickness * Post-op N/V SE * Sedation via H1 Blockade * PROMINENT Antimuscarinic Effects: AMS, dry mouth, constipation, blurred vision, urinary rtn, etc INTERACTIONS * L-Dopa - decr effectiveness |
|
|
|
Meclizine
|
Histamine-1 Receptor Antagonist
Muscarinic Antagonist * Crosses BBB. Blocks H1 receptors in the Cerebellum and STN. USE * Motion Sickness * Postop N/V SE * Causes less drowsiness than dimenhydrinate * Antimusc SE...dry mouth, mydriasis, etc. |
|
|
|
Phenytoin
|
Na Channel Blocker in the CNS.
* Causes blocked AP's in the brain and stops seizure SPREAD. EFFECTS * Decreased convulsive seizures * Some pain blockade USE --> Tonic Clonic Seizures --> Partial Convulsive Seizures --> Status Epilepticus (IV)..follows a benzo. ---> Trigeminal Neuralgia tx. (d/t compressed trigeminal nerve..very painful movement). (But DOC is carbamazepine) ---> Digoxin-Induced AV Block/ Ectopy (will reduce V-fib). --->NOT EFFECTIVE IN ABSENCE SEIZURES PHARMACOLOGY * Metabolized by Hepatic CYP450 Enzymes * Zero-order Elimination Kinetics...independent of plasma concentration. * Narrow Therapeutic Window (small TI). (Easy to have toxicity) * 79-95% Albumen-bound DOSE * EMPIRICAL DOSING: No halflife...must dose based on weight and an assumed halflife and titrate dose up or down to get dose with no seizures but no SE. * ALWAYS given with folate. SE * Burning on Injection, Cardiac dysrhythmias, and HOTN d/t propylene glycol added to solution. * Induces CYP450 Enzymes. Must increase dose of drugs metaboilzed by CYP450s. (Birth Control) * Tetatogenic...avoid in pregnancy. * CNS SE: from intoxication: ---> Nystagmus ---> Ataxia ---> Dysarthia (slurred speech) ---> Decreased Coordination ---> Mental confusion * Nausea/ Vomiting * Type IV Hypersensitivity Rxn ---> T-cell mediated rash. Can be mild or can develop into Steven Johnson's Syndrome. (Stop drug!!) * Hirsutism * Folic Acid Deficiency (90% of all pts) via blockage of intestinal conjugases, causing ---> Macrocytic Anemia (large RBC's) -50% ---> Megaloblastic Anemia (Large nucleus, immature) - < 1% * Osteomalacia ---> Decr Absorption of Vitamin D and Incr metabolism of Vit D (liver), leading to bone softening. Collagen is still there but no Ca to make the bone strong. This is called Rickets in Children. ---> Tx is to give a Vit D and Ca supplement. * Pregnancy category D ---> FA deficiency can cause neural tube defects ---> Fetal Hydantoin Syndrome (cleft palate, facial deformities, CV dysfunction) ---> Fetal Hemmorhagic Syndrome: d/t vit K deficiencies. Give the baby vit K at birth. INTERACTIONS --> Salicylates, Valproic Acid, and Sulfonamides DISPLACE IT FROM PLASMA PROTEINS. These drugs can cause Phenytoin Toxicity...excess drug cannot be cleared d/t zero order kinetics...can cause instant toxicity. You will not see it by drawing a plasma level b/c plasma levels measure both free and protein bound drug. --> All CYP450 Inhibitors (Cimetidine) will increase dose of Phenytoin and cause toxicity!! ---> Will decr the effectiveness of birth control. |
|
|
|
Phenobarbital
|
Barbituate: GABA-a Agonist
* Prolongs the duration of the Cl- Channel Opening..hyper-polarizing then neuron. USE: * Status Epilepticus (refractory to benzos and phenytoin) * Partial Seizures * Generalized Tonic Clonic Seizures DOSE: ALWAYS GIVE WITH FOLATE SE * Induces CYP450 enzymes...can decr effectiveness of drugs metabolized by them. (birth control). * CNS SE ---> Extreme sedation, ataxia, nystagmus, impaired cognition, hyperactivity in kids. (kids can be given a smaller dose to pvt hyperactivity). * Folic Acid Deficiency: Blocks intestinal conjugases. ---> This can cause macrocytic and megaloblastic anemia. * Pregnancy Cat D ---> Teratogenic ---> FA deficiency can cause neural tube defects ---> Hemorrhagic Disease in the Newborn (VitK def) CONTRAINDICATIONS * Black Box warning...contraindicated in ACUTE INTERMITTENT PORPHYRIA. ---> Buildup of porphorins causes pain and flareups. Phenobarbital makes this worse (induction of CYP450's) induces heme synthesis. |
|
|
|
Primidone
|
Barbituate: GABA-a Agonist
* THIS IS A PRODRUG THAT IS METABOLIZED INTO PHENOBARBITAL. (and PEMA-10%). * Prolongs the duration of the Cl- Channel Opening..hyper-polarizing then neuron. USE: * Partial Seizures * Generalized Tonic Clonic Seizures SE * Induces CYP450 enzymes...can decr effectiveness of drugs metabolized by them. (birth control). * CNS SE ---> Extreme sedation, ataxia, nystagmus, impaired cognition, hyperactivity in kids. (kids can be given a smaller dose to pvt hyperactivity). * Folic Acid Deficiency Blocks intestinal conjugases. ---> This can cause macrocytic and megaloblastic anemia. * Pregnancy Cat D ---> Teratogenic ---> FA Deficiency can cause neural tube defects ---> Hemorrhagic Disease in the Newborn (VitK def) CONTRAINDICATIONS * Black Box warning...contraindicated in ACUTE INTERMITTENT PORPHYRIA. ---> Buildup of porphorins causes pain and flareups. Phenobarbital makes this worse d/t induction of CYP450 enzymes, |
|
|
|
Carbamazepine
|
Anti-epileptic Med
MOA: Na Channel Blocker in the CNS (pvts seizure SPREAD). DOSE * Always give with folate USES: * Partial Seizures * Tonic Clonic Seizures * DOC for Trigeminal Neuralgia!!! ---> Blockage of Na channels in the brain also blocks pain tracts.) * Bipolar Disorder intolerant or refractory to Li. (lower efficacy than valproate). * Neurogenic DI (stimulates ADH release...could cause SIADH in a normal pt). Adjunct to vasopressin. (So if you had a bipolar pt on lithium who was developing nephrogenic DI...take them off the lithium and put them on carbamazepine). * Dyscontrol/ Impulsivity. * Never give carbamazepine ALONE in a mixed seizure disorder...will make the absence seizure WORSE. PHARMACODYNAMICS * Highly protein bound, (80%) BUT eliminated via 1st order kinetics...so if displaced... excess will be cleared by the kidneys. (Differs from Phenytoin). SE * Induces CYP450 Enzymes. This will decr the effectiveness of BC. * CNS SE: Dizziness, ataxia, vertigo, nystagmus, blurred vision. * Hemopoietic Complications ---> Thrombocytopenia ---> Agranulocytosis ---> Aplastic Anemia * Liver Toxicity: Causes cholestatic Jaundice * SIADH: Too much ADH..causes edema, HTN. * Pregnancy Cat D. --Teratogenic --->FA deficiency causes craniofacial and limb abnormalities and spina bifida ---> Causes hemorrhagic disease of the newborn (vit K def) CONTRAINDICATIONS * Absence Seizures (can make them worse)!!! |
|
|
|
Ethosuximide
|
Ca Channel Blocker in the CNS
USE * Absence Seizures - DOC!!! (stops the spread). Prevents the "spike and wave" on the EEG. SE * CNS: Drowsiness, Lethargy * GI: N/V * Drowsiness/ lethargy in a breast feeding baby. |
|
|
|
Clonazepam
|
Benzo - GABA-a Agonist
* Incr the freq of Cl channel opening. USE * Absence Seizures (stops spread) (good b/c can use for long term tx). * Anxiety Disorders SE * Drowsiness, ataxia, impared cognition, memory and behavioral changes, *Tolerance can develop. ...can have break-through absence seizures. |
|
|
|
Valproic Acid/
Divalproex Sodium |
Divalproex Sodium = Valproate and it's sodium salt.
MOA: * Increases the synthesis of GABA receptors. * Blocks Na channels DOSE: * Always give with folate!! * Get a liver fxn test before starting!! USE * ALL types of seizures: Tonic Clonic, Absence, Complex partial, etc * Bipolar Disorder (tx mania) * Migraine prophylaxis * Mood stabilizer - used in Li intolerant or Li hypersenstive pts * Rapid Cycling Bipolar Disorder * Mixed Mania (immediate control AND maintanance). SE *Hypersensitivity Rxn ---> Hepatitis ---> Pancreatitis (Get a liver fxn test before you initiate tx). * Alopecia * Fine hand tremor * Transient N/V (divalproex sodium is better - buffered version) * Pregnancy Cat D - Can cause FA deficiency and Spina Bifida. INTERACTIONS * Displaces phenytoin from plasma proteins...will cause phenytoin toxicity. |
|
|
|
Lamotrigine
|
1st Line Anti-Seizure Drug
MOA: * Blocks Na Channels in CNS (pvts seizure spread) * Suppresses the release of GLUTAMATE USE * Tonic Clonic Seizures * Absence Seizures * Complex Partial Seizures * Bipolar Disorder (mania) refractory to Li or intolerant of Li. ( Add-on agent). Maintenance but NOT acute control of mania. SE * Type 4 Hypersensitivity Rxn: Rash - Steven Johnson's Syndrome...D/C drug if you see a rash. !! |
|
|
|
Gabapentin
|
Narrow Spectrum Anti-seizure Drug Add-on
* GABA Analogue that crosses the BBB * 2nd Line tx for seizures...used when 1st line drugs fail MOA: --> Enhances GABA --> Reduces glutamate levels. USE * Partial seizure Adjunct * Secondary Tonic Clonic Seizure Adjunct (Not very effective as an antiseizure med when used alone) * Neuropathic Pain (most common use). |
|
|
|
Tiagabine
|
Narrow Spectrum Anti-seizure drug - Add-on
Second-line Tx: (add-on agent to standard AEDs) MOA * GABA uptake Inhibitor USE * Refractory partial and secondary generalized seizures. |
|
|
|
Felbamate
|
BROAD Spectrum Anti-seizure Add-on Drug.
MOA * Blocks NMDA receptors * Blocks Ca channels * Blocks Na Channels USE * Refractory, SEVERE Complex Partial Epilepsy * Refractory Lennox-Gastaut Syndrome ---> Childhood Epilepsy..difficult to tx SE * Aplastic Anemia * Hepatic Failure ..b/c of side effects...only used in people who seize constantly |
|
|
|
Topiramate (Topamax)
|
BROAD Spectrum Anti-seizure Add-on Drug.
MOA * Multiple! USE * Migraine prophylaxis (alone) * Epilepsy SE * Pupil Dilation (mydriasis) * Renal Stones CONTRAINDICATIONS * Angle Closure Glaucoma |
|
|
|
Fosphenytoin
|
Na Channel Blocker in the CNS.
* Causes blocked AP's in the brain and stops seizure SPREAD. * A PRODRUG FOR PHENYTOIN: water soluble, pH=8...MORE RAPID INFUSION AND LESS HOTN ON INJECTION!! USE --> Tonic Clonic Seizures --> Partial Convulsive Seizures --> Status Epilepticus (IV)..follows a benzo. ---> Trigeminal Neuralgia tx. (d/t compressed trigeminal nerve..very painful movement). (But DOC is carbamazepine) ---> Digoxin-Induced AV Block/ Ectopy (will reduce V-fib). --->NOT EFFECTIVE IN ABSENCE SEIZURES PHARMACOLOGY * Metabolized by Hepatic CYP450 Enzymes * Zero-order Elimination Kinetics...independent of plasma concentration. * Narrow Therapeutic Window (small TI). (Easy to have toxicity) * 79-95% Albumen-bound DOSE * EMPIRICAL DOSING: No halflife...must dose based on weight and an assumed halflife and titrate dose up or down to get dose with no seizures but no SE. * ALWAYS given with folate. SE * Induces CYP450 Enzymes. Must increase dose of drugs metaboilzed by CYP450s. (Birth Control) * Tetatogenic...avoid in pregnancy. * CNS SE: from intoxication: ---> Nystagmus ---> Ataxia ---> Dysarthia (slurred speech) ---> Decreased Coordination ---> Mental confusion * Nausea/ Vomiting * Type IV Hypersensitivity Rxn ---> T-cell mediated rash. Can be mild or can develop into Steven Johnson's Syndrome. (Stop drug!!) * Hirsutism * Folic Acid Deficiency (90% of all pts) causing ---> Macrocytic Anemia (large RBC's) -50% ---> Megaloblastic Anemia (Large nucleus, immature) - < 1% * Osteomalacia ---> Decr Absorption of Vitamin D and Incr metabolism of Vit D (liver), leading to bone softening. Collagen is still there but no Ca to make the bone strong. This is called Rickets in Children. ---> Tx is to give a Vit D and Ca supplement. * Pregnancy category D ---> FA deficiency can cause neural tube defects ---> Fetal Hydantoin Syndrome (cleft palate, facial deformities, CV dysfunction) ---> Fetal Hemmorhagic Syndrome: d/t vit K deficiencies. Give the baby vit K at birth. INTERACTIONS --> Salicylates, Valproic Acid, and Sulfonamides DISPLACE IT FROM PLASMA PROTEINS. These drugs can cause Phenytoin Toxicity...excess drug cannot be cleared d/t zero order kinetics...can cause instant toxicity. You will not see it by drawing a plasma level b/c plasma levels measure both free and protein bound drug. --> All CYP450 Inhibitors will increase dose of Phenytoin and cause toxicity!! ---> Will decr the effectiveness of birth control. |
|
|
|
Diazepam/ Lorazepam
|
Benzodiazepines
Diazepam: Highly lipid soluble: Enters and leave brain quickly (not good for status epilepticus b/c you want a drug that has a longer DOA. Lorazepam: Longer DOA..better for status epilepticus. |
|
|
|
Chloropromazine
|
ALIPATIC Phenothiazine Anti-Psychotic D2 Blocker
LOW POTENCY * Equal Efficacy as Piperadines and Piperazine!! EFFECTS: * NORMAL PERSON: Cause lack of initiative, Lack of Emotion, Disinterest, Drowsiness, Deminished motor fxn. * PSYCHOTIC PT: Cause DECREASED: agitation, aggressiveness, hallucinations, delusions, paranoia, and IMPROVED negative symptoms. USE: * Schizophrenia * Intractable hiccups SIDE EFFECTS: * Via D2 BLOCKADE outside of mesolimbic/cortical areas: (LITTLE EFFECT D/T LOW POTENCY!!!!!!!!!!) ----> Nigrostriatal Pathway: Causes EPS - Parkinsonism. ----> TARDIVE DYSKINESIA (mths to years!!): Repetitive, involuntary, stereotyped movements of the facial musculature, arms, and trunk (sticking out tongue, twitching, etc) d/t disuse sensitivity from chronic D2 blockade in nigrostriatal pathway. D2 receptors incr in # overtime. Occurs late in tx. Irreversible!! Equipredictable with high and low potency Phenothiazines. Depends on the duration of tx and the dose taken. So higher incidence in older pts. NOT EFFECTIVE TX! D/C antimusc, decr anti-psych or switch to Clozapine or other Atypical, BDZ, Propanolol, Lechithin/ Choline. ----> Tubero-infundibular Pathway: from Nucleus of hypothalamus to Ant Pit: Causes Hyperprolactinemia and Gynecomastia in men, galactorrhea and amenorrhea in women. (Equipotential of all Phenothiazides to cause.) * Via NON-D2 RECEPTORS: (INCREASED EFFECTS D/T LOW POTENCY...HIGHER DOSES!!) ----> H1 Blockade: Sedation ----> Lowered Seizure Threshold (for pts with epilepsy, CNS pathology or ETOH W/D). ----> Alpha-1 Blockade: Nasal Stuffiness, Orthostatic HOTN, Ejaculatory Disturbances (retrograde, sphincter can't close above.). ----> Muscarinic Blockade: Dry mouth, Blurred vision (mydriasis, lack of accomodation), constipation, urinary retention, decr sweating, male impotence (no erection). (BUT NOT AS MUCH AS THIORADAZINE). ---> Poiklyothermia: can't sweat and freeze in the cold..temperature dysregulation. ----> Obstructive (cholestatic) jaundice (b/n 2-4 wks of tx). This is a hypersensitivity rxn. ---> Photosensitivity: deposits in skin and absorbs UV radiation. Will kill neighboring cells. Avoid sun exposure. ---> Hyperpigmentation w/ chronic high dose tx. (unknown mech. depostis in skin??). PURPLE BLOTCHINESS ALL OVER BODY. CONTRAINDICATIONS * Pts with angle closure glaucoma * Pts with ischemic heart disease...antimusc effects would cause tachycardia. * Pts in the sun all day - can't sweat. INTERACTIONS * Antagonize L-DOPA and Bromocriptine * Additive Effect with CNS Depressants (opiods, ethanol, antihistamines, anesthesia, etc). |
|
|
|
Thioridazine
|
PIPERADINE Phenothiazine Anti-Psychotic D2 Blocker
MEDIUM POTENCY: Equal Efficacy as Alipatics and Piperazine!! ****** Also has antimuscarnic effects!!!! This makes it an exception of the piperadines...in that it is LESS likely that alipathic for causing EPS, and is has MORE anti-musc effects. **** EFFECTS: * NORMAL PERSON: Cause lack of initiative, Lack of Emotion, Disinterest, Drowsiness, Deminished motor fxn. * PSYCHOTIC PT: Cause DECREASED: agitation, aggressiveness, hallucinations, delusions, paranoia, and IMPROVED negative symptoms. USE * No anti-emetic effects * Schizophrenia * L- DOPA Induced Psychosis SIDE EFFECTS: * Via D2 BLOCKADE outside of mesolimbic/cortical areas: ----> NO EPS EFFECTS D/T ANTI-MUSC PROPERTIES. ----> TARDIVE DYSKINESIA (mths to years!!): Repetitive, involuntary, stereotyped movements of the facial musculature, arms, and trunk (sticking out tongue, twitching, etc) d/t disuse sensitivity from chronic D2 blockade in nigrostriatal pathway. D2 receptors incr in # overtime. Occurs late in tx. Irreversible!! Equipredictable with high and low potency drugs. Depends on the duration of tx and the dose taken. So higher incidence in older pts. NOT EFFECTIVE TX! D/C antimusc, decr anti-psych or switch to Clozapine or other Atypical, BDZ, Propanolol, Lechithin/ Choline. ----> Tubero-infundibular Pathway: from Nucleus of hypothalamus to Ant Pit: Causes Hyperprolactinemia and Gynecomastia in men, galactorrhea, false pos preg tests, and amenorrhea in women. (Equipotential of all phenothiazides to cause..) * Via NON-D2 RECEPTORS: (not as much as alipatics) ----> H1 Blockade: Sedation ----> Lowered Seizure Threshold (for pts with epilepsy, CNS pathology or ETOH W/D). ----> Alpha-1 Blockade: Nasal Stuffiness, Orthostatic HOTN, Ejaculatory Disturbances (retrograde, sphincter can't close above.). ----> Muscarinic Blockade: Dry mouth, Blurred vision (mydriasis, lack of accomodation), constipation, urinary retention, decr sweating, male impotence (no erection). (MORE THAN ALL THE OTHER PHENOTHIAZIDES). ---> Poiklyothermia: can't sweat and freeze in the cold..temperature dysregulation. ----> Obstructive (cholestatic) jaundice (b/n 2-4 wks of tx). This is a hypersensitivity rxn. (OCCURS MOST WITH ALIPATICS!!) ---> Photosensitivity: deposits in skin and absorbs UV radiation. Will kill neighboring cells. Avoid sun exposure. ---> Hyperpigmentation (purple blotchiness) w/ chronic high dose tx. (unknown mech. depostis in skin??). SIDE EFFECTS SPECIFIC TO THIORADAZINE: * Prolonged QT interval...d/t blocked K channels, leading to Torsades de Pointes. *PIGMENTARY RETINOPATHY - dose dependent effect ---> Pigment deposits spread from central retina to perphery causing blind spots (scotomas) and potential blindness. D/C ASAP!!! CONTRAINDICATIONS * Pts with angle closure glaucoma * Pts with ischemic heart disease...antimusc effects would cause tachycardia. * Pts in the sun all day - can't sweat. * Pts with dysrhythmias d/t prolonged QT interval * Don't use this drug unless nothing else has worked!! INTERACTIONS * Additive Effect with CNS Depressants (opiods, ethanol, antihistamines, anesthesia, etc). (ie..decrease MAC). |
|
|
|
Fluphenazine
|
PIPERAZINE Phenothiazine Anti-Psychotic D2 Blocker
HIGH POTENCY * Equal Efficacy as Piperadines and Alipatics!! EFFECTS: * NORMAL PERSON: Cause lack of initiative, Lack of Emotion, Disinterest, Drowsiness, Deminished motor fxn. * PSYCHOTIC PT: Cause DECREASED: agitation, aggressiveness, hallucinations, delusions, paranoia, and IMPROVED negative symptoms. SIDE EFFECTS: * Via D2 BLOCKADE outside of mesolimbic/cortical areas: (GREATEST EFFECT D/T HIGH POTENCY!!!!!!!!!!) ----> Nigrostriatal Pathway: Causes EPS - Parkinsonism. Occurs in 1st 3 mths of tx. Temporary but must be tx b/c very painful, uncomfortable ACUTE EPS: * Dystonia: (PAINFUL spasms of Neck, Eye (upward), jaw and tongue muscles). Tx w/ Benzotropine, Benedryl, Amantidine, or decr/change anti-psychotic. * Parkinsonism (2wks-2mths): tremor at rest, rigidity, akinesia/ bradykinesia, postural instability. Tx w/ Benztropine, Diphenhydramine, Amantadine, decr or change anti-psych. * Akathisia (1-3 mths): Extreme motor restlessness..ants in pants. Discern from agitation..they are tx'd oppositely! (MOST COMMON Acute EPS symptom.) Tx w/ Propanolol, Lorazepam, Benztropine, Benedryl, Decr or change anti-psych. * Neuroleptic Malignant Syndrome (hrs-mths): Med. Emergency: Hyperthermia, Muscle Rigidity, Autonomic Instability. Idiosyncratic Mechanism..antagonism of D2 receptors may contribute. Tx: Dantrolene IV, Bromocriptine (emergency), Diazepam, D/C Fluphenazine!! DO NOT CONFUSE W/ SEROTONON SYNDROME. CHRONIC EPS: * Tardive Dyskinesia (mths to years!!) * Repetitive, involuntary, stereotyped movements of the facial musculature, arms, and trunk (sticking out tongue, twitching, etc) d/t disuse sensitivity from D2 blockade. D2 receptors incr in # overtime. Occurs late in tx. Irreversible!! Equipredictable with high and low potency drugs. Depends on the duration of tx and the dose taken. So higher incidence in older pts. NOT EFFECTIVE TX! D/C antimusc, decr anti-psych or switch to Clozapine or other Atypical, BDZ, Propanolol, Lechithin/ Choline. ----> Tubero-infundibular Pathway: from Nucleus of hypothalamus to Ant Pit: Causes Hyperprolactinemia and Gynecomastia in men, galactorrhea and amenorrhea in women. (Equipotential of all Phenothiazides to cause.) * Via NON-D2 RECEPTORS: (LEAST EFFECTS D/T HIGH POTENCY...SMALLER DOSES!!) LESS THAN ALIPATICS AND PIPERADINES INTERACTIONS * Antagonize L-DOPA and Bromocriptine * Additive Effect with CNS Depressants (opiods, ethanol, antihistamines, anesthesia, etc). |
|
|
|
Haloperidol
|
Butyrophenone Typical Anti-psychotic
MOA: D2 Receptor Blockade USE * Initial tx of MANIA (until lithium kicks in) * Huntington's Disease (loss of cholinergic neurons in striatum) * Tourette's Disorder - Too much DA in the striatum. Tx the Tics but not the Coprolalia (swearing) * Acute OD of CNS stimulants causing psychosis (Cocaine, Amphetamine) * PCP/ Hallucinogen induced flashbacks * Intractable HIccoughs (Carbamazepine also works) * Epilepsy and Schizo combined (low potency pheno's lower seizure threshold). SE * Same as with a high-potency Phenothiazide...can cause EPS effects and Parkinsonism. * Via D2 BLOCKADE outside of mesolimbic/cortical areas: (GREATEST EFFECT D/T HIGH POTENCY!!!!!!!!!!) ----> Nigrostriatal Pathway: Causes EPS - Parkinsonism. Occurs in 1st 3 mths of tx. Temporary but must be tx b/c very painful, uncomfortable ACUTE EPS: * Dystonia: (spasms of Neck, Eye (upward), jaw and tongue muscles). Tx w/ Benzotropine, Benedryl, Amantidine, or decr/change anti-psychotic. * Parkinsonism (2wks-2mths): tremor at rest, rigidity, akinesia/ bradykinesia, postural instability. Tx w/ Benztropine, Diphenhydramine, Amantadine, decr or change anti-psych. * Akathisia (1-3 mths): Extreme motor restlessness..ants in pants. Discern from agitation..they are tx'd oppositely! (MOST COMMON Acute EPS symptom.) Tx w/ Propanolol, Lorazepam, Benztropine, Benedryl, Decr or change anti-psych. * Neuroleptic Malignant Syndrome (hrs-mths): Med. Emergency: Hyperthermia, Muscle Rigidity, Autonomic Instability. Idiosyncratic Mechanism..antagonism of D2 receptors may contribute. Tx: Dantrolene IV, Bromocriptine (emergency), Diazepam, D/C Fluphenazine!! DO NOT CONFUSE W/ SEROTONON SYNDROME. CHRONIC EPS: * Tardive Dyskinesia (mths to years!!) * Repetitive, involuntary, stereotyped movements of the facial musculature, arms, and trunk (sticking out tongue, twitching, etc) d/t disuse sensitivity from D2 blockade. D2 receptors incr in # overtime. Occurs late in tx. Irreversible!! Equipredictable with high and low potency drugs. Depends on the duration of tx and the dose taken. So higher incidence in older pts. NOT EFFECTIVE TX! D/C antimusc, decr anti-psych or switch to Clozapine or other Atypical, BDZ, Propanolol, Lechithin/ Choline. ----> Tubero-infundibular Pathway: from Nucleus of hypothalamus to Ant Pit: Causes Hyperprolactinemia and Gynecomastia in men, galactorrhea and amenorrhea in women. (Equipotential of all Phenothiazides to cause.) INTERACTIONS * L-Dopa - decr effectiveness CONTRAINDICATIONS * Parkinson's disease |
|
|
|
Droperidol
|
Butyrophenone Typical Antipsychotic
* Does not have the antipsychotic effects USE * Antiemetic * Neurolept Analgesia (Droperidol + Fentanyl) * Neurolept Anesthesia (Droperidol + Fentanyl + N2O) SE * Just like HIgh Potency Phenothiazides (Piperazines). * Via D2 BLOCKADE outside of mesolimbic/cortical areas: (GREATEST EFFECT D/T HIGH POTENCY!!!!!!!!!!) ----> Nigrostriatal Pathway: Causes EPS - Parkinsonism. Occurs in 1st 3 mths of tx. Temporary but must be tx b/c very painful, uncomfortable ACUTE EPS: * Dystonia: (spasms of Neck, Eye (upward), jaw and tongue muscles). Tx w/ Benzotropine, Benedryl, Amantidine, or decr/change anti-psychotic. * Parkinsonism (2wks-2mths): tremor at rest, rigidity, akinesia/ bradykinesia, postural instability. Tx w/ Benztropine, Diphenhydramine, Amantadine, decr or change anti-psych. * Akathisia (1-3 mths): Extreme motor restlessness..ants in pants. Discern from agitation..they are tx'd oppositely! (MOST COMMON Acute EPS symptom.) Tx w/ Propanolol, Lorazepam, Benztropine, Benedryl, Decr or change anti-psych. * Neuroleptic Malignant Syndrome (hrs-mths): Med. Emergency: Hyperthermia, Muscle Rigidity, Autonomic Instability. Idiosyncratic Mechanism..antagonism of D2 receptors may contribute. Tx: Dantrolene IV, Bromocriptine (emergency), Diazepam, D/C Fluphenazine!! DO NOT CONFUSE W/ SEROTONON SYNDROME. CHRONIC EPS: * Tardive Dyskinesia (mths to years!!) * Repetitive, involuntary, stereotyped movements of the facial musculature, arms, and trunk (sticking out tongue, twitching, etc) d/t disuse sensitivity from D2 blockade. D2 receptors incr in # overtime. Occurs late in tx. Irreversible!! Equipredictable with high and low potency drugs. Depends on the duration of tx and the dose taken. So higher incidence in older pts. NOT EFFECTIVE TX! D/C antimusc, decr anti-psych or switch to Clozapine or other Atypical, BDZ, Propanolol, Lechithin/ Choline. ----> Tubero-infundibular Pathway: from Nucleus of hypothalamus to Ant Pit: Causes Hyperprolactinemia and Gynecomastia in men, galactorrhea and amenorrhea in women. (Equipotential of all Phenothiazides to cause.) |
|
|
|
Clozapine
|
Atypical Antipsychotic
MOA * D2 Blockade in CNS * 5-HT2a Blockade in mesocortical, tubuloinfundibular, and nigro-striatal tracts. BENEFITS * Greater efficary for tx the negative symptoms * Lower incidence of acute EPS, or tardive dyskinesia. USE * Tx-resistant Schizophrenics * Tx- Intolerant Schizophrenics" ---> Those w/ Tardive Dyskinesia ---> Schizo caused by Parkinson's Drugs (L-DOPA) (you can't stop taking the L-Dopa and can't use a typical..except thioridazine) * Parkinson's combined with Schizo. SE * Same as Alipatic Phenothiazides. ----> Sedation!!, Lowered seizure threshold (black box warning!), Alpha1 Blockade and ortho. HOTN. ----> Anti-musc: Has more anti-musc effects than ALL THE ATYPICALS! ----> BUT does not cause EPS or hyperprolactinemia. * Agranulocytosis ---> Get a baseline WBC count before starting drug. ---> Get a weekly WBC count for 6 mths after starting. ---> Get a WBC count every OTHER week from then on. ---> If you show symptoms of agranulocytosis it is D/C'd and you can never use it again. * Sialorrhea * Weight Gain: avg 10 lbs in 10 wks |
|
|
|
Risperidone (Risperdal)
|
Atypical Antipsychotic
MOA * D2 Blockade in CNS * 5-HT2a Blockade in mesocortical, tubuloinfundibular, and nigro-striatal tracts. BENEFITS * Greater efficary for tx the negative symptoms * Lower incidence of acute EPS, or tardive dyskinesia. USE * Tx-resistant Schizophrenics * Tx- Intolerant Schizophrenics" ---> Those developing Tardive Dyskinesia ---> Schizo caused by Parkinson's Drugs (you can't stop taking the L-Dopa and can't use a typical (except thioridazine) * Parkinson's combined with Schizo. SE * Same as Piperazine Phenothiazides (high potency). . ----> BUT does not cause EPS very much and Tardive Dyskinesia rates are low. * Hyperprolactinemia * Weight Gain: avg 10 lbs in 10 wks |
|
|
|
Olanzepine (Zyprexa)
|
Atypical Antipsychotic
MOA * D2 Blockade in CNS * 5-HT2a Blockade in mesocortical, tubuloinfundibular, and nigro-striatal tracts. USE * Tx-resistant Schizophrenics * Tx- Intolerant Schizophrenics" ---> Those w/ Tardive Dyskinesia ---> Schizo caused by Parkinson's Drugs (you can't stop taking the L-Dopa and can't use a typical..) * Parkinson's combined with Schizo. SE * Same as Piperazine Phenothiazides (high potency). . ----> BUT does not cause EPS very much and Tardive Dyskinesia rates are low. * Hyperprolactinemia * Weight Gain: avg 10 lbs in 10 wks |
|
|
|
Quentiapine (Seroquel)
|
Atypical Antipsychotic
MOA * D2 Blockade in CNS * 5-HT2a Blockade in mesocortical, tubuloinfundibular, and nigro-striatal tracts. USE * Tx-resistant Schizophrenics * Tx- Intolerant Schizophrenics" ---> Those w/ Tardive Dyskinesia ---> Schizo caused by Parkinson's Drugs (you can't stop taking the L-Dopa and can't use a typical..) * Parkinson's combined with Schizo. SE * Same as Piperazine Phenothiazides (high potency). . ----> BUT does not cause EPS very much and Tardive Dyskinesia rates are low. * Hyperprolactinemia * Weight Gain: avg 10 lbs in 10 wks |
|
|
|
Ziprasidone (Geodon)
|
Atypical Antipsychotic
MOA * D2 Blockade in CNS * 5-HT2a Blockade in mesocortical, tubuloinfundibular, and nigro-striatal tracts. USE * Tx-resistant Schizophrenics * Tx- Intolerant Schizophrenics" ---> Those w/ Tardive Dyskinesia ---> Schizo caused by Parkinson's Drugs (you can't stop taking the L-Dopa and can't use a typical..) * Parkinson's combined with Schizo. SE * Same as Piperazine Phenothiazides (high potency). . ----> BUT does not cause EPS very much and Tardive Dyskinesia rates are low. * Hyperprolactinemia * Weight Gain: avg 10 lbs in 10 wks |
|
|
|
Arpiparazole (Abilify)
|
Dopamine System Stabilizer
* An adjunct anti-psych med to tx depression. MOA *Partial agonist at D2 receptors * Antagonist at 5HT2a receptors (not in mesolimbic pathway) Will be either an agonist or an antag depending on the amt of DA signalling in the pathway. --> In the mesolimbic pathway of a schizo pt, DA act is TOO HIGH, so abilify acts as a DA antag. --> In the mesocortical, nigrostriatal or tubuloinfundibular pathways of a schizo, if DA act gets TOO LOW, Abilify acts as an agonist and DA act is enhanced or preserved.....THIS PVTS SIDE EFFECTS. |
|
|
|
Fluphenazine Decanoate
Haldol Decanoate |
Decanoate – a fatty acid ester prep…inject it IM as a depot. It is slowly released over a month. Good for non-compliance. Never use it as an initial tx because you have no idea what the right dose or SE are…only use in pts that are well tolerant of the drug.
|
|
|
|
Imipramine (Tofranil)
|
Tri-Cyclic Antidepressant
MOA: Inhibits reuptake of NE and 5-HT ADMINISTRATION: Before Bed!!! USE: * Depression (major and d/t adjustment disorder) * Anorexia and Depression * Depression with Psychotic Features * Mixed Mania * TCA of choice for NOCTURNAL ENURESIS that is refractory to Desmopressin METABOLISM * This a tertiary amine that is metabolized by CYP450 phase 1 dealkylation into DESIPRAMINE, an active metabolite that has the same effects (inhibits NE and 5-HT reuptake). SE - same as low potency phenothiazines (more than SSRI's) * Sedation (H1 Blockade) * Antimuscarinic * Orthostatic HOTN * Cardiovascular: Inhibits fast Na and K Channels (prolongs QRS and QT interval) this will cause VENTRICULAR ARRYTHMIAS. * Weight Gain: d/t chg in appetite and NT at hypothalamus, which regulate body fat stores. * Lowered Seizure Threshold SE MORE COMMON IN SSRI'S than TCA's: * Agitation/ Insomnia * GI Distress * Sexual Dysfunction CONTRAINDICATIONS * Angle Closure Glaucoma d/t antimusc effects * Benign Prostatic Hyperplasia (can cause urinary retention) * Anticholinergics used already (could cause paralytic ileus)! * Anti-parkinson's anticholinergic use...will cause a paralytic ileus d/t so much blockade of PNS. * Dementia/ Cognitive Dysfunction (will make it worse!) * Pts with constipation * Be careful in the elderly d/t orthostatic HOTN * Pts with dysrhytmias and ischemic heart disease. * Use caution in Diabetes...will make them fatter. * Pts with bipolar disorder...can cause a provoked switch to mania * Pts with epilepsy...give an MAOI instead INTERACTIONS * MAOIs and TCAs/SSRIs can cause SEROTONIN SYNDROME (min-hrs) ---> Hyperthermia, Diaphoresis, Myoclonus, Hyperreflexia, Autonomic Instability, Coma, Death. NO TX!!! Symptoms only (ice packs, etc). * Inhibition of CYP450's (decr metab of some drugs) * Additive effect with other anti-muscarinics/ anti-cholinergics * Potentiate DA, Neo: Direct Acting Sympathomimetrics (by blocking PNS) * Block Indirect Acting Sympathomimetrics (Tyramine: uses a reuptake inhibitor to enter the neuron. TCA's block this reuptake port...Tyramine cannot work.) * Opposes the antihypertensive effects of alpha2 agonists (Clonidine, methyldopa)..cause more NE to build up in the cleft. OVERDOSE: #1 drug used for suicide d/t OD!!! * Prominent Antimusc SE: Agitation, Coma, Depressed Resp, Hyperthermia, HOTN, Mydriasis, Flushed Skin, Seizures, Ventricular Conduciton Block (prolonged QRS) and Ventricular dysrhythmias. * Tx: Gastric Lavage with activated charcoal. Tx the symptoms only...ie..don't give Physostigmine...will only make the dysrhythmias worse. |
|
|
|
Desipramine (Norpramine)
|
Tri-Cyclic Antidepressant
MOA: Inhibits reuptake of NE and 5-HT USE * Depression. Mixed Mania, Organic Mood Disorder, etc * Depression and Anorexia * ADHD as a backup to Ritalin * stop smoking ADMNISTRATION: At night before bed. SE - same as low potency phenothiazines (more than SSRI's) * Sedation (H1 Blockade) * Antimuscarinic * Orthostatic HOTN * Cardiovascular: Inhibits fast Na and K Channels (prolongs QRS and QT interval) this will cause VENTRICULAR ARRYTHMIAS. * Weight Gain: d/t chg in appetite and NT at hypothalamus, which regulate body fat stores. * Lowered Seizure Threshold SE MORE COMMON IN SSRI'S than TCA's: * Agitation/ Insomnia * GI Distress * Sexual Dysfunction CONTRAINDICATIONS * Angle Closure Glaucoma d/t antimusc effects * Benign Prostatic Hyperplasia (can cause urinary retention) * Anticholinergics used already (could cause paralytic ileus)! * Anti-parkinson's anticholinergic use...will cause a paralytic ileus d/t so much blockade of PNS. * Dementia/ Cognitive Dysfunction (will make it worse!) * Pts with constipation * Be careful in the elderly d/t orthostatic HOTN * Pts with dysrhytmias and ischemic heart disease. * Use caution in Diabetes...will make them fatter. * Pts with bipolar disorder...can cause a provoked switch to mania * Pts with epilepsy...give an MAOI instead INTERACTIONS * MAOIs and TCAs/SSRIs can cause SEROTONIN SYNDROME (min-hrs) ---> Hyperthermia, Diaphoresis, Myoclonus, Hyperreflexia, Autonomic Instability, Coma, Death. NO TX!!! Symptoms only (ice packs, etc). * Inhibition of CYP450's (decr metab of some drugs) * Additive effect with other anti-muscarinics/ anti-cholinergics * Potentiate DA, Neo: Direct Acting Sympathomimetrics (by blocking PNS) * Block Indirect Acting Sympathomimetrics (Tyramine: uses a reuptake inhibitor to enter the neuron. TCA's block this reuptake port...Tyramine cannot work.) * Opposes the antihypertensive effects of alpha2 agonists (Clonidine, methyldopa)..cause more NE to build up in the cleft. OVERDOSE: #1 drug used for suicide d/t OD!!! * Prominent Antimusc SE: Agitation, Coma, Depressed Resp, Hyperthermia, HOTN, Mydriasis, Flushed Skin, Seizures, Ventricular Conduciton Block (prolonged QRS) and Ventricular dysrhythmias. * Tx: Gastric Lavage with activated charcoal. Tx the symptoms only...ie..don't give Physostigmine...will only make the dysrhythmias worse. |
|
|
|
Amitriptyline (Elavil)
|
Tri-Cyclic Antidepressant
MOA: Inhibits reuptake of NE and 5-HT USE * Depression, Mixed Mania, Organic Mood Disorder, etc. * Anorexia with depression * Bulemia Nervosa * CHRONIC PAIN ADMINISTRATION: At night before bed. METABOLISM * This is a tertiary amine that is dealkylated(removes a methyl grp) by CYP450's into Nortriptyline (A prefix of "nor" or "des" means it's been dealkylated). Nortiptyline is an active metabolite and still has the same effects (inhibits NE and 5-HT reuptake). SE - same as low potency phenothiazines (more than SSRI's) * Sedation (H1 Blockade) * Antimuscarinic * Orthostatic HOTN * Cardiovascular: Inhibits fast Na and K Channels (prolongs QRS and QT interval) this will cause VENTRICULAR ARRYTHMIAS. * Weight Gain: d/t chg in appetite and NT at hypothalamus, which regulate body fat stores. * Lowered Seizure Threshold SE MORE COMMON IN SSRI'S than TCA's: * Agitation/ Insomnia * GI Distress * Sexual Dysfunction CONTRAINDICATIONS * Angle Closure Glaucoma d/t antimusc effects * Benign Prostatic Hyperplasia (can cause urinary retention) * Anticholinergics used already (could cause paralytic ileus)! * Anti-parkinson's anticholinergic use...will cause a paralytic ileus d/t so much blockade of PNS. * Dementia/ Cognitive Dysfunction (will make it worse!) * Pts with constipation * Be careful in the elderly d/t orthostatic HOTN * Pts with dysrhytmias and ischemic heart disease. * Use caution in Diabetes...will make them fatter. * Pts with bipolar disorder...can cause a provoked switch to mania * Pts with epilepsy...give an MAOI instead INTERACTIONS * MAOIs and TCAs/SSRIs can cause SEROTONIN SYNDROME (min-hrs) ---> Hyperthermia, Diaphoresis, Myoclonus, Hyperreflexia, Autonomic Instability, Coma, Death. NO TX!!! Symptoms only (ice packs, etc). * Inhibition of CYP450's (decr metab of some drugs) * Additive effect with other anti-muscarinics/ anti-cholinergics * Potentiate DA, Neo: Direct Acting Sympathomimetrics (by blocking PNS) * Block Indirect Acting Sympathomimetrics (Tyramine: uses a reuptake inhibitor to enter the neuron. TCA's block this reuptake port...Tyramine cannot work.) * Opposes the antihypertensive effects of alpha2 agonists (Clonidine, methyldopa)..cause more NE to build up in the cleft. OVERDOSE: #1 drug used for suicide d/t OD!!! * Prominent Antimusc SE: Agitation, Coma, Depressed Resp, Hyperthermia, HOTN, Mydriasis, Flushed Skin, Seizures, Ventricular Conduciton Block (prolonged QRS) and Ventricular dysrhythmias. * Tx: Gastric Lavage with activated charcoal. Tx the symptoms only...ie..don't give Physostigmine...will only make the dysrhythmias worse. |
|
|
|
Nortiptyline (Pamelor)
|
Tri-Cyclic Antidepressant
MOA: Inhibits reuptake of NE and 5-HT USE * Depression * Anorexia and Depression ADMINISTRATION: At night before bed. SE - same as low potency phenothiazines (more than SSRI's) * Sedation (H1 Blockade) * Antimuscarinic * Orthostatic HOTN * Cardiovascular: Inhibits fast Na and K Channels (prolongs QRS and QT interval) this will cause VENTRICULAR ARRYTHMIAS. * Weight Gain: d/t chg in appetite and NT at hypothalamus, which regulate body fat stores. * Lowered Seizure Threshold SE MORE COMMON IN SSRI'S than TCA's: * Agitation/ Insomnia * GI Distress * Sexual Dysfunction CONTRAINDICATIONS * Angle Closure Glaucoma d/t antimusc effects * Benign Prostatic Hyperplasia (can cause urinary retention) * Anticholinergics used already (could cause paralytic ileus)! * Anti-parkinson's anticholinergic use...will cause a paralytic ileus d/t so much blockade of PNS. * Dementia/ Cognitive Dysfunction (will make it worse!) * Pts with constipation * Be careful in the elderly d/t orthostatic HOTN * Pts with dysrhytmias and ischemic heart disease. * Use caution in Diabetes...will make them fatter. * Pts with bipolar disorder...can cause a provoked switch to mania * Pts with epilepsy...give an MAOI instead INTERACTIONS * MAOIs and TCAs/SSRIs can cause SEROTONIN SYNDROME (min-hrs) ---> Hyperthermia, Diaphoresis, Myoclonus, Hyperreflexia, Autonomic Instability, Coma, Death. NO TX!!! Symptoms only (ice packs, etc). * Inhibition of CYP450's (decr metab of some drugs) * Additive effect with other anti-muscarinics/ anti-cholinergics * Potentiate DA, Neo: Direct Acting Sympathomimetrics (by blocking PNS) * Block Indirect Acting Sympathomimetrics (Tyramine: uses a reuptake inhibitor to enter the neuron. TCA's block this reuptake port...Tyramine cannot work.) * Opposes the antihypertensive effects of alpha2 agonists (Clonidine, methyldopa)..cause more NE to build up in the cleft. OVERDOSE: #1 drug used for suicide d/t OD!!! * Prominent Antimusc SE: Agitation, Coma, Depressed Resp, Hyperthermia, HOTN, Mydriasis, Flushed Skin, Seizures, Ventricular Conduciton Block (prolonged QRS) and Ventricular dysrhythmias. * Tx: Gastric Lavage with activated charcoal. Tx the symptoms only...ie..don't give Physostigmine...will only make the dysrhythmias worse. |
|
|
|
Fluoxetine (Prozac/ Sarafem)
|
SSRI
Inhibits serotonin reuptake. USE * Atypical Depression (Oversleeping, overeating) * Premature Ejaculation * Depression, Mixed mania, organic mood disorder, etc. * BULIMIA NERVOSA (TCA's also) * Premenstrual Dysphoric Disorder * Exogenous Obesity ADMINISTRATION: In AM or early PM (causes stimulation) WITH FOOD d/t GI SE SE - same as phenothiazines (3 TCA's > 2nd TCA's > SSRIs) * Sedation (H1 Blockade) * Antimuscarinic: constipation, tachycardia, blurred vision, mydriasis, urinary rtn, etc. * Orthostatic HOTN * Cardiovascular * Weight Gain * Lowered Seizure Threshold SE MORE COMMON IN SSRI'S than TCA's: * Agitation/ Insomnia * GI Distress: Diarrhea/ N/V * Sexual Dysfunction * Lowered Seizure Threshold CONTRAINDICATIONS * Pts with insomnia * Pts with Bipolar Disorder...cna cause a provoked switch to mania. * Pts with epilepsy...give an MAOI instead INTERACTIONS * MAOIs and TCAs/SSRIs can cause SEROTONIN SYNDROME (min-hrs) ---> Hyperthermia, Diaphoresis, Myoclonus, Hyperreflexia, Autonomic Instability, Coma, Death. NO TX!!! Symptoms only (ice packs, etc). * Inhibition of CYP450's |
|
|
|
Sertraline (Zoloft)
|
SSRI
Inhibits serotonin reuptake. USE * Depression (oversleeping, overeating) * Premature Ejaculation * Mixed Mania * Organic Mood Disorder * Panic Disorder/Attacks And Agoraphobia (Paroxitine also) * Generalized and Social Anxiety Disorder (Paroxitine also) * PTSD (Paroxetine also) * Premenstrual Dysphoric Disorder (all SSRIs) ADMINISTRATION: In AM or early PM (causes stimulation) WITH FOOD d/t GI SE SE - same as phenothiazines (3 TCA's > 2nd TCA's > SSRIs) * Sedation (H1 Blockade) * Antimuscarinic: constipation, urinary rtn, blurred vision, mydriasis, tachycardia, can't sweat * Orthostatic HOTN * Cardiovascular * Weight Gain * Lowered Seizure Threshold (SSRI's = TCAs) SE MORE COMMON IN SSRI'S than TCA's: * Agitation/ Insomnia * GI Distress: diarrhea, N/V (take with food). * Sexual Dysfunction CONTRAINDICATIONS * Pts with insomnia * Pts with Bipolar Disorder...cna cause a provoked switch to mania. * Pts with epilepsy...give an MAOI instead INTERACTIONS * MAOIs and TCAs/SSRIs can cause SEROTONIN SYNDROME (min-hrs) ---> Hyperthermia, Diaphoresis, Myoclonus, Hyperreflexia, Autonomic Instability, Coma, Death. NO TX!!! Symptoms only (ice packs, etc). * Inhibition of CYP450's |
|
|
|
Paroxetine (Paxil)
|
SSRI
Inhibits serotonin reuptake. USE * Depression * Premature Ejaculation * Mixed Mania * Organic Mood Disorder * Panic Disorder/ Attacks and Agoraphobia (Sertraline also) * Generalized and Social Anxiety Disorder. (Sertraline also) * PTSD (Sertraline also) * Premenstrual Dysphoric Disorder (all SSRI's) ADMINISTRATION: In AM or early PM (causes stimulation) WITH FOOD d/t GI SE SE - same as phenothiazines (3 TCA's > 2nd TCA's > SSRIs) * Sedation (H1 Blockade) * Antimuscarinic: constipation, dry mouth, tachycardia, AMS, urinary retention, blurred vision, mydriasis * Orthostatic HOTN * Cardiovascular * Weight Gain SE MORE COMMON IN SSRI'S than TCA's: * Agitation/ Insomnia * GI Distress: Diarrhea, N/V (take with a meal) * Sexual Dysfunction * Lowered Seizure Threshold (SSRIs = TCAs) CONTRAINDICATIONS * Pts with insomnia * Pts with Bipolar Disorder...cna cause a provoked switch to mania. * Pts with epilepsy...give an MAOI instead INTERACTIONS * MAOIs and TCAs/SSRIs can cause SEROTONIN SYNDROME (min-hrs) ---> Hyperthermia, Diaphoresis, Myoclonus, Hyperreflexia, Autonomic Instability, Coma, Death. NO TX!!! Symptoms only (ice packs, etc). * Inhibition of CYP450's |
|
|
|
Buprobrion (Wellbutrin)
|
Anti-depressant
MOA: NE and DA reuptake inhibitor. USE * Depression (not very effective) * Smoking Cessation (Zyban) more DA so quitting is less unpleasant. Benefits: * NO SEDATION!! (no H1 Blockade). * No sexual dysfunction!! :) (does not change serotonin) SE * Insomnia or less restful sleep (prolonged REM) d/t incr NE and DA. May improve over time. *Psychosis d/t blocked DA reuptake in mesolimbic pathway * High Incidence of Seizures (dose dependent) (too much excitation) * |
|
|
|
Venlafaxine (Effexor)
|
Anti-depressant
MOA: *5-HT and NE reuptake inhibitor. (5-HT > NE) USE * Depression * Treatment of Generalized and Social Anxiety Disorder SE * Dose Dependent HTN (serotonin causes vasoconstriction). * Similiar to SSRI's: * Agitation/ Insomnia * GI Distress: Diarrhea, N/V (take with a meal) * Sexual Dysfunction * Lowered Seizure Threshold (SSRIs = TCAs) CONTRAINIDICATIONS * HTN |
|
|
|
Duloxetine (Cymbalta)
|
Anti-depressant
5-HT and NE reuptake inhibitor....similiar structure to a tricyclic but not a tricyclic. USE * Depression * Diabetic Neuropathy Pain * Post Herpetic Pain (shingles) SE * Similiar to TCA's - structure is similiar: * Sedation (H1 Blockade) * Antimuscarinic * Orthostatic HOTN * Cardiovascular: Inhibits fast Na and K Channels (prolongs QRS and QT interval) this will cause VENTRICULAR ARRYTHMIAS. * Weight Gain: d/t chg in appetite and NT at hypothalamus, which regulate body fat stores * Lowers Seizure Threshold |
|
|
|
Atomoxetine (Strattera)
|
Selective NE reuptake Inhibitor
NE reuptake inhibitor. USE * ADD/ ADHD SE * Similiar to TCA's * Hepatotoxicity |
|
|
|
Mirtazapine (Remeron)
|
Anti-Depressant
MOA: * 5-HT and NE INHIBITORY AUTORECEPTOR Blockers (5-HT2/3 and alpha2) * This incr the release of 5-HT and NE * Still takes 2-4 wks to work. SE * Weight Gain * Sedation |
|
|
|
Trazadone
|
Anti-depressant
ADMINISTRATION: At night SE * Sedation - H1 Blockade |
|
|
|
What are the FDA approved SSRI and TCA for OCD?
|
TCA - Clomipramine
SSRI - Fluvoxamine (this is not prozac) |
|
|
|
What drugs will boost the effect of anti-depressants?
|
Lithium
active thyroid hormone |
|
|
|
Phenelzine
|
MAOI - IRREVERSIBLE
MOA: * Binds to MAO-A and MAO-B irreversibly so that body must make new MAO. * Maximal Inhibition Achieved in a few days but antidepressant effect takes 2-3 weeks. * Anti-depressant effect is via MAO-A blockade ONLY. DOSE * > 80% Inhibition of platelet MAO is predictive of a clinically effective dose. * Give at night d/t sedation BENEFITS * Do NOT lower seizure threshold (unlike SSRI's and TCA's) USE * Major Depressive Disorder * Epilepsy and Depression * Refractory pts (d/t side effects) * Atypical Depression (better than TCA's) * Panic Attacks with Agoraphobia * OCD SE * CNS: SEDATION * Hepatotoxicity * Orthostatic HOTN INTERACTIONS * Tyramine (Aged Cheese, Red Wine, Smoked Meat)- Tyramine goes into the reuptake channels for NE, enters the vesicle, displaces NE, and causes NE release via backflow of the reuptake channel. In the GI tract, it is metabolized by MAO-A, so bioavaliability is zero. MAOI's allow tyramine to do it's dirty work - you end up NE dumping, VC, and a HTN crisis. * Direct and indirect acting sympathomimetic amines * TCA/ SSRI/ Meperidine (opiod agonist): Can cause serotonin syndrome!! * Increases MAC * L-Dopa: Increases DA by inhibiting MAO-B. Increases NE by inhibiting MAO-A. NE overload can lead to a HYPERTENSIVE CRISIS. Must d/c for 2 WEEKS BEFORE L-Dopa administration. CONTRAINDCATIONS * Bipolar Disorder - will provoke a switch to mania. OVERDOSE * Similiar to a TCA OD * Prominent Antimusc SE: Agitation, Coma, Depressed Resp, Hyperthermia, HOTN, Mydriasis, Flushed Skin, Seizures, Ventricular Conduction Block (prolonged QRS) and Ventricular dysrhythmias. * Tx: Gastric Lavage with activated charcoal. Tx the symptoms only...ie..don't give Physostigmine...will only make the dysrhythmias worse. * LONG DURATION d/t irreversible inhibitior of MOA's |
|
|
|
Tranylcypromine
|
MAOI - PSEUDOREVERSIBLE
MOA: * Binds to MAO-A and MAO-B irreversibly so that body must make new MAO. * Maximal Inhibition Achieved in a few days but antidepressant effect takes 2-3 weeks. * Anti-depressant effect is via MAO-A blockade ONLY. DOSE * > 80% Inhibition of platelet MAO is predictive of a clinically effective dose. * Give in the MORNING d/t arousal. BENEFITS * Do NOT lower seizure threshold (unlike SSRI's and TCA's) USE * Major Depressive Disorder * Epilepsy and Depression * Refractory pts (d/t side effects) * Atypical Depression (better than TCA's) * Panic Attacks with Agoraphobia * OCD SE * CNS: AROUSAL!! * Hepatotoxicity * Orthostatic HOTN INTERACTIONS * Tyramine (Aged Cheese, Red Wine, Smoked Meat)- Tyramine goes into the reuptake channels for NE, enters the vesicle, displaces NE, and causes NE release via backflow of the reuptake channel. In the GI tract, it is metabolized by MAO-A, so bioavaliability is zero. MAOI's allow tyramine to do it's dirty work - you end up NE dumping, VC, and a HTN crisis. * Direct and indirect acting sympathomimetic amines * TCA/ SSRI/ Meperidine (opiod agonist): Can cause serotonin syndrome!! * Increases MAC * L-Dopa: Increases DA by inhibiting MAO-B. Increases NE by inhibiting MAO-A. NE overload can lead to a HYPERTENSIVE CRISIS. Must D/C 2 WEEKS BEFORE L-Dopa Administration. CONTRAINDCATIONS * Bipolar Disorder - will provoke a switch to mania. OVERDOSE * Similiar to a TCA OD * Prominent Antimusc SE: Agitation, Coma, Depressed Resp, Hyperthermia, HOTN, Mydriasis, Flushed Skin, Seizures, Ventricular Conduciton Block (prolonged QRS) and Ventricular dysrhythmias. * Tx: Gastric Lavage with activated charcoal. Tx the symptoms only...ie..don't give Physostigmine...will only make the dysrhythmias worse. * LONG DURATION d/t irreversible inhibitior of MOA's |
|
|
|
Lithium
|
Mood Stabilizer
MOA: Inhibits G-protein receptors: * Inhibits IP3 signaling: Inhibits the enzymes that recycle IP3. * Inhibits Adenylate cyclase stim: Uncouples Gs from the receptor. (This causes the SE at TSH-R and ADH-R). * It also inhibits the release of NE and stimulates the reuptake of NE (the reverse action of TCA's)...this tx the mania. EFFECTS * Normal Person: No Effect * Manic Pts: Decr Mania * Bipolar pt: Mood stabilizer DOSE * Ther. Serum Conc = 0.9-1.4 mEq/L * BEFORE ADMIN: Get BASELINE TESTS: Serum Cr & Cr clearance, TSH (T3/T4), WBC w/ differential, Pregnancy Test * AFTER ADMIN: ---> Monitor serum conc Q 5 days until stabilized. ---> Once stabilized get a serum conc Q 3-6 mths. ---> Monitor baseline tests Q 6-12 mths. (Serum Cr, Cr clearance, TSH, T3/T4, WBC w/ differential, Preg test). ---> If you change the dose or see a toxicity..monitor serum conc until stabilized again. USE * Bipolar Disorder (after haldol for acute phase). * Major depressive disorder (to potentiate the anti-depressant). * Cyclothermia * Schizo-Affective * Impulsivity/ Explosive Behavior * SIADH...causes nephrogenic DI..adjunct to demeclocycline * Chemotherapy-Induced Neutropenia (Adjunct to filgrastim or sargramostim) * Prophylaxis of a Cluster Headache * Premenstrual Dysphoric Disorder PHARMACOKINETICS * Eliminated via kidneys. Renal Dysfunction alters clearance. * Lithium can substitute or Na in the body. -----> Incr Na intake: Incr Clearance: Leads to ineffectiveness -----> Decr Na intake: Decr Clearance: Leads to Toxicity * Therapeutic Index: 2-4 SE * GI: N/V, Diarrhea * Anorexia * Initiation Tremor (fine)..will resolve sponateously. * Polyuria/ Polydipsia (1st 24-48 hrs) - b/c you are excreting Na (body thinks Lithium is a salt). This is TRANSIENT. * Edema/ Weight Gain (Day 4-5) d/t incr aldosterone secretion s/t all the Na loss. Tx with Spironolactone. Will resolve in several days. * Hyperaldosteronism (Day-4-5) d/t incr aldosterone secretion s/t all the Na loss. Tx with Spironolactone. TOXICITY: * ACUTE: Can occur w/ diet changes d/t low TI: 2-4. Occurs when plasma conc > 1.4 mEq/L: --> Mild: Flu-like symptoms: Apathy, Lethargy, Nausea, Muscle Weakness, Irritability. Call MD ASAP!! --> Moderate: Course Tremor, Dysarthria, Unsteady Gait, Somnolence, muscle twitches. D/C Lithium!! --> Seizures, Coma, CV collapse, Death. D/C Li and give OSMOTIC DIURETICS AND HEMODIALYSIS. (other diuretics would deplete Na..bad). * CHRONIC: --> GOITROGENIC HYPOTHYROIDISM: Uncoupling the TSH-R from it's Gs protein. TSH can no longer stim thyroid hormone production...increase TSH causes hyperplasia and a goiter. Tx with Synthroid. --> NEPHROGENIC DI: Uncouples ADH receptor from it's Gs protein. Tx w/ Amiloride..blocks Na channels in the principal cells. --> LEUKOCYTOSIS: Increases neutrophils...good for leukopenia assoc with chemo..will incr their neutrophils. --> RENAL TUBULAR NECROSIS CONTRAINDICATIONS * Renal Insufficiency: Can incr Li toxicity d/t decr clearance. * Na Depletion: Sweating, low Na diet: Will leads to Li retention and toxicity. * Pregnancy - Category D!! Causes EBSTEINS ANOMALY: Tricuspid valve abnomalities. If you must use it in pregnancy: must incr the dose near term d/t increased Vd and renal clearance. Mom should NOT breast feed baby. Can also switch her to Carbamazepine. INTERACTIONS * NSAIDS - inhibit PGE2 and decr clearance - toxicity!! * Thiazide and Loop Diuretics: Na depleting...this increases Li reabsorption in the PT. --Toxicity!! * Methylxanthines (Caffeine/ Theophylline): These normally increase lithium clearance, when you stop them...you have toxicity! So caffeine withdrawal will cause Li toxicity. * Li Decreases MAC of volatiles. * TCA's d/t incr antimusc action and urinary retention this can cause lithium toxicity. * Phenothiazide Antipsychotics: will mask the signs of Li toxicity by pvting N/V (except for Thioridazine) |
|
|
|
Selegilline
|
Anti-Parkinson's Drug
MOA: Irreversible MAO-B Inhibitor. * Pvts conversion of MPTP to MPP+ * Decr Dopamine degradation in the brain (more DA avaliable). -->MPPP is a designer drug made from Meperidine. It is metabolized by MAO-B into MPP+. MPP+ is dangerous. It enter the neurons of the substantia nigra via the DA transporter and kills the neuron, causing Parkinson's Disease. So selegiline can have a neuroprotectant effect by inhibiting MAO-B. --> Paraquat is an herbicide with a similiar structure to MPTP...so it can also cause parkinson's. Selegilline also protects the brain from Paraquat. --> Due to these effects, Selegilline is given in the EARLY stages of Parkinson's to protect the brain from ALL possible environmental causes. Also, by inhibiting DA degradation, it increases levels of DA in the brain. DOSE: Take in the MORNING...causes insomnia EFFECTS * Reduces dose of L-Dopa (10-30%) * Extends duration of L-Dopa by pvting DA degredation * Reduces motor fluctuations w/ L-Dopa * Neuroprotective (monotherapy in early PD)...will NOT reduce the symptoms alone..just protects the brain. SE * Insomnia INTERACTIONS * Serotonin Reuptake Inhibitors: TCAs & SSRIs, Meperidine. Will cause SEROTONIN SYNDROME (myoclonus, rigidity, confusion, autonomic instability, coma, death). ...cause if you take too much selegiline...it can inhibit MAO-A too. (No tx for Serotonin Syndrome) |
|
|
|
Levo-Dopa
|
Prodrug for DA in the CNS
MOA * Crosses the BBB and is converted to DA in nigrostriatal neurons by AAAD and Vit B6. * Always given with Carbidopa as Sinemet. USE * Corner stone tx for parkinson's dz EFFECTS: incr DA SYNTHESIS in nigrostiatal pathway * Reduced: bradykinesia, rigidity, tremor * Elevated mood and sense of well-being. * Does NOT help with POSTURAL INSTABILITY OR SHUFFLING GAIT!!! (Why? Because you don't have enough DA receptors avaliable at that stage or the dz for the excess DA to act.). METABOLISM * PERIPHERY ---> AAAD and Vit B6 convert to DA (causing Orthostatic HOTN, Tachycardia, and N/V via D1 receptors in CTZ and BV). Tx w/ Carbidopa ---> Dopamine Beta Hydroylase converts L-Dopa to NE. This causes tachycardia and dysrhythmias. Tx w/ Carbidopa ---> COMT converts L-Dopa to 3-OMD. This competes with L-DOPA at organic transports to brain. So very little L-Dopa gets to brain (< 1%). Tx w/ Tolcapone. * CNS ---> AAAD and B6 convert to DA for effect. ---> COMT converts to 3-OMD (tx w/ tolcapone) ---> MAO-B degrades DA into metabolites (tx w/ selegilline) SIDE EFFECTS: * Decreased effectiveness overtime d/t neuron death * END-DOSE DETERIORATION: -->After 3 yrs of Parkinson's, the neurons start dying. That means you have less endogenous DA in the brain AND less neurons to release and receive DA synthesized from L-dopa...so when L-dopa plasma levels fall, parkinson's symptoms return quickly. (This does not happen in the 1st 3 years d/t more DA neurons in the substantia nigra to balance it out.). How to Tx:....... ---> Give Tolcapone to increase L-Dopa uptake and decr CNS DA degradation by COMT. Give bromocriptine. ---> Adjust medication combination: give smaller and more frequent doses of L-Dopa ---> Decrease dietary protein intake to incr DA uptake. * MOTOR FLUCTATIONS ---> Unexplained, unpredicatble On/Off motor fluctuations w/ steady L-Dopa levels. No TX. Vacation holiday from L-Dopa may be needed. Tolcapone, Bromocriptine, or Selegilline may help reduce these. * PERIPHERAL SE (explained above): Tachycardia, dysrythmias, N/V, Orthostatic HOTN (pvt with Carbidopa.) Decr CNS uptake (tx w/ tolcapone). * CNS SE: --> Schizo SE d/t incr DA in the mesolimbic/ mesocortical area: Confusion, Psychosis, Hallucinations --> Dyskinesia: Choreiform, ballistic, & dystonic (whole body writhing) movements d/t excessive dopaminergic stimulation in the striatum. Occurs w/ peak CNS levels. Happens more with LATER stages of Parkinson's b/c of more peaks and troughs. Sadly this state is often preferred for the pt over akinesia and rigidity. INTERACTIONS * PYRIDOXINE/ Vit B6 fluctuations - Cofactor for AAAD. Increases the activity of AAAD...this incr the conversion of L-Dopa to DA both in the PERIPHERY & CNS. For pts stabilized on L-Dopa, a decr in Vit B6 and Parkinson's will return. An incr in Vit B6 and could have CNS SE - Psychosis, Diskinesia. (NO EFFECT ON PERIPHERAL SE d/t Carbidopa..only acts peripherally to inhibit AAAD). So you tell your pt..DO NOT TAKE B6 AT ALL. This way they want have any changes. * PROTEIN: Dietary protein competes with L-Dopa for organic transporters into the brain. (reduce dietary protein to incr uptake) *D2 ANTAGONISTS (Typical Anti-psychotics (except Thioridazine), Metoclopramide, Droperidol, Haldol) - can decr it's effects. * ANTICHOLINERGICS - Reduce intestinal motility- Prolongs the transit time of L-Dopa in the GI tract. Bacterial agents metabolize L-Dopa into D-dopa, pvting it's absorption. * NONSPECIFIC MAO INHIBITORS (Phenylzine and Tranylcyclozine): Inhibition of MAO-B increases DA. Inhibition of MAO-A increases NE...which is synthesized from DA. You end up with NE overload and a HYPERTENSIVE CRISIS. (B/C of their long DOA, must wait at least 2 WEEKS after taking MAOI's for L-Dopa to be given.) CONTRAINDICATIONS * Be careful in the elderly...d/t orthostatic HOTN...as long as you give Carbadopa with L-Dopa you won't have to worry about it. * Psychotic Disorders: Will make them worse! ( more DA in mesolimbic) * Angle Closure Glaucoma - will make it worse! (Dilates the eye via D1 receptors) * Malignant Melanoma: black box warning. Can make them come out of remission and kill them. * Previous Hx of Cardiac Dysrhytmias (d/t potential peripheral SE). |
|
|
|
Carbidopa
|
Anti-Parkinson's Adjunct Drug
*ALWAYS given with L-Dopa (as Sinemet) to pvt peripheral SE. MOA: * AAAD inhibitor in the PERIPHERY ONLY. * Pvts the conversion of L-Dopa to DA & NE in the periphery. * This pvts the L-Dopa peripheral SE of ---> N/V (DA to D1 receptors) ---> Orthostatic HOTN (DA to D1-R) ---> Tachycardia (NE to B1) ---> Dyrhythmias (NE to B1) * It also allows more L-Dopa to get into the brain. EFFECTS * Increased potency/ decreased dose of L-Dopa. * Better control of L-Dopa Conc (evens out fluctuations) * Prolonged duration of L-Dopa * Decreased peripheral side effects. * Pvts Vit B6 stim of AAAD in the periphery...pvts degradation of L-dopa in the periphery d/t incr vit B6. (But NOT in the CNS) |
|
|
|
Tolcapone
|
Anti-Parkinson's Adjunct Drug
* Given with L-Dopa to increase CNS uptake. (Unlike Carbidopa, Tolcapone is not ALWAYS given with L-dopa..but can be added to boost tx.) * Crosses BBB. * ONLY GIVE WHEN PT IS REFRACTORY TO ENTACAPONE MOA * COMT Inhibitor---> REDUCES 3-OMD * COMT degrades L-Dopa in the periphery AND centrally to 3-OMD..which competes at organic CNS transporters..pvting L-Dopa uptake in the brain. * This drug works in the periphery AND in the CNS to inhibit COMT. In the brain the effect is to increase levels of DA. EFFECTS * Lower Dose of L-Dopa * Increased potency of L-Dopa * Prolonged duration of L-Dopa * Reduces end of dose deterioration -->After 3 yrs of Parkinson's, the neurons start dying. That means you have less endogenous DA in the brain AND less neurons to release and receive DA synthesized from L-dopa...so when L-dopa plasma levels fall, parkinson's symptoms return quickly. (This does not happen in the 1st 3 years d/t more DA neurons in the substantia nigra to balance it out.). * Reduces motor fluctuations --> Unexplained, unpredictable On/Off motor fluctuations w/ steady L-Dopa levels. No TX. Vacation holiday from L-Dopa may be needed. SE * Acute Hepatic Necrosis --> Pt needs a liver function test Q 2 wks!!!! |
|
|
|
Sinemet
|
Anti-parkinson's Drug
* L-Dopa + Carbidopa MOA of Carbidopa: * AAAD inhibitor in the PERIPHERY ONLY. * Pvts the conversion of L-Dopa to DA & NE in the periphery. * This pvts the L-Dopa peripheral SE of ---> N/V (DA to D1 receptors) ---> Orthostatic HOTN (DA to D1-R) ---> Tachycardia (NE to B1) ---> Dyrhythmias (NE to B1) * It also allows more L-Dopa to get into the brain. EFFECTS * Decr dose and incr potency of L-Dopa * Incr Duration of Action of L-Dopa |
|
|
|
Vitamin B6
|
Cofactor or AAAD (the enzyme that converts L-Dopa to DA.)
MOA * Increases the activity of AAAD...this incr the conversion of L-Dopa to DA both in the PERIPHERY & CNS. EFFECTS (for pts stabilized on L-Dopa) * If they DECREASE B6 intake: Parkinson's will return (decr DA). * If they INCREASE B6 intake: better tx..Parkinson's treated..but could have CNS SE. * NO EFFECT ON PERIPHERAL SE (d/t Carbidopa..only acts peripherally to inhibit AAAD). So you tell your pt..DO NOT TAKE B6 AT ALL. This way they want have any changes. |
|
|
|
Entacapone
|
Anti-Parkinson's Adjunct Drug
* Given with L-Dopa to increase CNS uptake. (Unlike Carbidopa, this is not ALWAYS given with L-dopa..but can be added to boost tx.) * Crosses BBB. * Preferred over Tolcapone d/t no hepatic necrosis MOA * COMT Inhibitor---> REDUCES 3-OMD * COMT degrades L-Dopa in the periphery AND centrally to 3-OMD..which competes at organic CNS transporters..pvting L-Dopa uptake in the brain. * This drug works in the periphery AND in the CNS to inhibit COMT. In the brain the effect is to increase levels of DA. EFFECTS * Lower Dose of L-Dopa * Increased potency of L-Dopa * Prolonged duration of L-Dopa * Reduces end of dose deterioration -->After 3 yrs of Parkinson's, the neurons start dying. That means you have less endogenous DA in the brain AND less neurons to release and receive DA synthesized from L-dopa...so when L-dopa plasma levels fall, parkinson's symptoms return quickly. (This does not happen in the 1st 3 years d/t more DA neurons in the substantia nigra to balance it out.). * Reduces motor fluctuations --> Unexplained, unpredictable On/Off motor fluctuations w/ steady L-Dopa levels. No TX. Vacation holiday from L-Dopa may be needed. |
|
|
|
Bromocriptine
|
Anti-Parkinson's Adjunct
MOA: D2 Agonist. DOSE: 1st Dose should be taken before sleep. EFFECTS * Reduces Motor Fluctuations * Improves Motor Function * Allows Lower-L-Dopa Doses * GIVE In Early PD: it minimizes wearing before Ldopa started * INCR In Late PD: Incr dose as DA neurons degenerate (L-Dopa will not work as much..) USE * Adjunct to L-Dopa in Parkinson's Dz * Neuroleptic Malignant Syndrome * Acromegaly * Hyperprolactinemia * Restless Leg Syndrome SE * Similiar to L-Dopa * GREATER Psychiatric Effects than L-Dopa * LESS Dyskinesia than L-Dopa * First Dose Syncope - Pt should take the first dose before they go to bed. |
|
|
|
Amantadine
|
Anti-parkinson's adjunct
MOA * Enhances the release of stored DA in the nigrostriatal pathway. EFFECTS * Decreased Tremor, Bradykinesia, Rigidity, and Dyskinesias USE * Early Parkinson's Disease: Monotherapy * Moderate Parkinson's Disesae: Adjunct to L-Dopa * Tx EPS symptoms of Anti-psychotics (except Akathisia) * Influenza tx (anti-viral agent). SE * CNS- Insomnia * LIVEDO RETICULARIS: A blue-reddish skin discoloration that is most often in the LEGS/ FEET. (not a big deal) |
|
|
|
Benztropine mesylate
|
Antimuscarinic Agent
MOA * Blocks Musc. Receptors in CNS USE * TX Parkinson's disease * Tx of EPS symptoms assoc with anti-psychotics EFFECTS * Decr Tremor and Rigidity * Does NOT improve Bradykinesia (you would need a dopamine agent for that) SE * Predictable Anitmuscarinic SE: Dry mouth, blurred vision, constipation, urinary retention, mydriasis, AMS, can't sweat. CONTRAINDICATIONS * Angle Closure Glaucoma * Benign Prostatic Hyperplasia * Constipation * Other drugs with anti-muscarinic action |
|
|
|
Diphenhydramine
|
Antimuscarinic Agent
MOA * H1 Antagonist and Musc Antagonist USE * TX Parkinson's disease * Tx of EPS symptoms assoc with anti-psychotics EFFECTS * Decr Tremor and Rigidity * Does NOT improve Bradykinesia (you would need a dopamine agent for that) SE * Predictable Anitmuscarinic SE: Dry mouth, blurred vision, constipation, urinary retention, mydriasis, AMS, can't sweat. CONTRAINDICATIONS * Angle Closure Glaucoma * Benign Prostatic Hyperplasia * Constipation * Other drugs with muscarinic action |
|
|
|
Dimenhydrinate (Dramamine®)
|
is a combination of diphenhydramine and 8-chlorotheophylline (stimulant)…this pvt sleepiness but allows tx of motion sickness
|
|
