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Spring Pharm > Parkinson's Disease, Psychosis & Neurocognitive Disorders Pharm > Flashcards

Parkinson's Disease, Psychosis & Neurocognitive Disorders Pharm Flashcards

1
Q

Parkinson’s Disease

A

Degeneration of DA neurons in the extrapyramidal motor pathway; DA & ACh imbalance resulting in GABA stimulation
Symptoms –> rigidity, bradykinesia, tremors, masked facies (don’t show a lot of emotion), pill-rolling
Treatment –> anticholinergic drugs, DA replacement, DA agonists, MAO-B inhibitors, COMT inhibitors (most people are on a cocktail of meds depending on symptoms & severity)

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2
Q

Carbidopa-Levidopa

A

Dopamine replacement
MOA –> carbidopa prevents the breakdown of levodopa in the bloodstream & levodopa converts to DA
Common side effects –> anticholinergic (dry mouth, constipation), N/V (give with food), hypotension, dizziness, weakness, dark urine
Adverse reactions –> rebound parkinsonism, agranulocytosis, cardiac arrhythmias, NMS
MVIs are contraindicated, moderate alcohol can antagonize the drug effects, high protein diet may increase BUN and decrease effectiveness of drug in crossing the blood-brain barrier

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3
Q

Carbidopa-Levodopa Administration Considerations

A
  • MVIs are contraindicated (they may contain Vit B6 which decreases effects of levodopa)
  • moderate alcohol can antagonize the drug effects
  • high protein diet may increase BUN and decrease effectiveness of drug due to issues crossing the blood-brain barrier
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4
Q

Psychosis exists in these disorders

A
  • schizophrenia (positive symptoms-ie. hallucinations, delusions)
  • mania & depression (mood stabilizer)
  • drug/med intoxication
  • drug/med withdrawal
  • general medical conditions
  • delirium
  • traumatic brain injury
  • dementia
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5
Q

Antipsychotic black box warning

A
  • increased mortality in elderly patients with dementia-related psychosis treated with antipsychotic meds r/t cerebrovascular adverse events including stroke, heart failure
  • when used as a mood agent, black box warning for increased suicidal thoughts/ideation (usually upon starting & dose changes)
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6
Q

Antipsychotic therapy

A
  • Goal: complete remission/significant reduction of psychotic symptoms
  • maximum relief: achieved after several weeks or months
  • maintenance doses: 6-12 months, gradual taper to lowest dose
  • chronic persistent illness = long-term (but always question the need for continuation)
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7
Q

Conventional Antipsychotics (FGAs)

A
  • classified by potency in relationship to their ability to antagonize CNS D2 receptors
  • aren’t specifically selective to D2 receptor pathways that are associated with psychosis (i.e.. slam DA receptors when they can)
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8
Q

Atypical Antipsychotics (SGAs)

A
  • less D2 receptor blockade than traditional

- antagonize other D receptor subtypes & 5HT2 receptor subtype

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9
Q

1st generation antipsychotics classification by potency

A

Chlorpromazine –> low potency phenothiazine
Fluphenazine –> high potency phenothiazine
Haloperidol –> high potency non-phenothiazine; 1st line med for non-psychiatric hospitalized patients experiencing agitation and/or delirium

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10
Q

Conventional Antipsychotics MOA

A

MOA –> block D2 receptor sites in mesolimbic pathway (positive symptoms) & block other D2 receptors (causing EPSE, muscular and other side effects)

  • includes partial histamine antagonism, acetylcholine blockage & antagonism of alpha-adrenergic system
  • 2 groups: phenothiazines (block NE, causing sedative/hypotensive effects) vs nonphenothiazines (block DA)
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11
Q

Antipsychotic adverse effects

A

Occur with all antipsychotics, but more commonly seen with 1st gen

  • Extrapyramidal side effects
  • Neuroleptics toxicity
  • Neuroleptic malignant syndrome
  • Agranulocytosis
  • Hypotension (blocks alpha-1; tolerance develops in 2-3 months)
  • Sedation (blocks histamine; some block NE)
  • Seizures (lower the seizure threshold)
  • Arrhythmias associated with sudden death (i.e. QT prolongation)
  • Anticholinergic effects: dry mouth, nasal congestion, blurred vision, urinary hesitancy/retention, constipation
  • Dermatological: pruritic maculopapular rashes, jaundice
  • Metabolic: glucose dysregulation, weight gain & lipid dysregulation
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12
Q

Extrapyramidal side effects (EPS)

A
  • drug-induced movement disorders caused by DA receptor blocking agents
  • Acute dystonia
  • Parkinsonism
  • Akathisia
  • Tardive dyskinesia
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13
Q

Acute dystonia

A
  • severe muscle spasm that develops within 1st few days, often within hours or initiation or dose change
  • common muscles involved: tongue, neck, face (oculogyric crisis-involuntarily looking upward), back, laryngeal (airway obstruction)
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14
Q

Parkinsonism

A
  • develops within the 1st month & tends to resolve spontaneously if treated or med is stopped
  • common S/S: akinesia (lack or slowness of movement), muscle rigidity & posture changes, tremor, hyper salivation & drooling, mask-like facies
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15
Q

Akathisia

A
  • extremely uncomfortable profound sense of restlessness characterized by inability to sit or stand still
  • subjective reports of internal feelings of restlessness, anxiety & uneasiness
  • develops within first 2 months of use
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16
Q

Tardive dyskinesia

A
  • more serious side effect, but usually mild
  • common S/S: involuntary twisting movements, beginning with tongue/face & progressing to limbs/trunk
  • sometimes irreversible
  • onset: months to years
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17
Q

Treatment of EPS other than TD

A

Propanolol –> for akathisia
Benztropine & Trihexyphenidyl –> blocks central cholinergic receptors (DA deficiency results in excess cholinergic effects)
Diphenhydramine –> histamine blocker; treats EPS by suppressing central cholinergic activity & prolonging action of DA by inhibiting its re-uptake & storage

18
Q

Treatment for TD

A

-removal of causative drug via slow taper
-vesicular monoamine transporter 2 inhibitors
-switch to another agent with less potential for TD
-Clonazepam
-Vitamin E
(Convention may make it worse)

19
Q

Neuroleptic Toxicity

A

Overdose: hypotension, CNS depression, EPSEs (death by overdose is rare)
Atropine psychosis: psychotic delirium caused by excessive anticholinergic effects
-S/S: agitation, confusion, tachycardia, dry flushed skin

20
Q

Neuroleptic malignant syndrome

A

-caused by prolonged use
-fatality rate: 10-20%
Primary symptoms: (caused by D2 blockade)
-tongue: bag full of worms (tightly bound & wiggling around)
-severe rigidity & tremors
-sudden high fever
-severe sweating & drooling
-autonomic instability
-changing LOC with possible progression to seizures or death

21
Q

Agranulocytosis

A

severely decreased WBC

  • suspect if develops sore throat, fever, malaise during first two months of initiating medication
  • potentially fatal due to overwhelming infection
22
Q

Adverse effect differences by potency

A

Low potency –> more anticholinergic effects, sedation & hypotension common
High potency –> anticholinergic side effects less common, more ESPs

23
Q

Antipsychotic adverse effects by sex

A

Females –> gynecomastia, galactorrhea, menstrual irregularities, decreased libido & impaired ability to achieve orgasm
Males –> gynecomastia, decreased libido, erectile & ejaculatory dysfunction

24
Q

Benefits of Atypical antipsychotics

A
  • effective for both positive & negative symptoms of schizophrenia
  • cause fewer EPSEs
  • less risk for developing TD
25
Q

Negative Symptoms & Atypical antipsychotics

A
  • negative symptoms are the result of hypodopaminergic process in the frontal lobe
  • selective subtypes of 5HT inhibit DA & drugs that antagonize these subtypes will increase frontal lobe DA
26
Q

Adverse effects atypical antipsychotics

A
  • can have some side effects as first generation
  • decreased likelihood to cause EPS than FGAs but still possible
  • more likely to cause weight gain & metabolic syndrome
27
Q

Atypical antipsychotics & metabolic syndrome

A

-insulin resistance
-HTN
-high serum lipids
-obesity
-coagulation abnormalities
Product label warning for hyperglycemia & DM

28
Q

Aripiprazole

A

Dopamine-antagonist; Serotonin agonist

  • Dopamine system stabilizer –> regulates areas where you might need more DA & areas where you might need less DA (stimulates receptors at low levels, blocks at high levels)
  • has both DA and CNS stimulation blocking side effects & adverse reactions
29
Q

Clozapine

A
  • more effective at symptom management, but with increased risk
  • significant adverse reactions: seizures, agranulocytosis
  • requires blood draws for neutrophil counts –> weekly during first 6 months, every other week for second 6 months & every 4 weeks after one year & for duration of treatment
30
Q

Pharm management of schizophrenia

A

Medication selection & dosing –> individualized based on past hx, trials, family hx & genetic testing
Initial & maintenance treatment –> symptoms occur in 1-2 days & gradually improve over the first several months
Monitoring for EPSEs & other effects –>AIMS (abnormal involuntary movement scale)

31
Q

Preparations of antipsychotic meds

A

Traditional meds: oral, intravenous, intramuscular (including DEPOT)
Atypical meds: oral, quick dissolve, DEPOT forms (NO IV forms)

32
Q

Depot Preparations

A

long-acting, injectable formulations used for long-term maintenance therapy of schizophrenia and BPAD
-generally given monthly

33
Q

Benefits of depot preparations

A
  • increased adherence (need to come to clinic so you know they get the med)
  • maximize pharmacokinetic coverage & minimize antipsychotic withdrawal (achieve a steady state)
  • not influenced by first pass metabolism (decreased potential for drug-drug interactions)
  • no peaks & troughs of med (reduces side effects, which improves adherence)
34
Q

Interactions with antipsychotics

A

CNS depressants: antipsychotics increase CNS depression effects
Anticholinergics: increased anticholinergic responses
Antihypertensives: increased hypotension
Levodopa: counteracts effects
Smoking: increased metabolism of antipsychotics, decreased med-induces Parkinsonism

35
Q

Caution in combining antipsychotics with…

A

SSRIs: increased antipsychotic levels, EPSEs, possible serotonin syndrome
Lithium & 1st generation AP chlorpromazine: decreased antipsychotic effect
TCAs: increased serum levels of both drugs

36
Q

Minimizing adverse/enhancing therapeutic effects

A
  • lowest dose to maintain
  • treatment of side effects: especially anticholinergic & extrapyramidal
  • patient teaching: educate about side effects so they recognize them & come to you for help
  • therapeutic relationship
  • long-acting injectable meds
37
Q

Neurochemistry to Alzheimer’s Disease

A
  • decreased ACh due to a decrease in acetyltransferase (interferes with cholinergic innervation in the brain)
  • increased glutamate results in overstimulation of NMDA –> increased intracellular calcium –> neuron degradation & cell death
  • others: NE, 5HT, DA
38
Q

Rivastigmine

A

Acetylcholinesterase inhibitors

  • slow progression of DAT by preventing the breakdown of ACh
  • side effects: N/V, diarrhea, anorexia, dizziness, headache, cholinergic, bronchoconstriction
  • interactions: traditional antipsychotics, TCAs, antihistamines
39
Q

Memantine

A

NMDA receptor antagonists

  • used alone or in combo with cholinesterase inhibitors
  • MOA: inhibits glutamate, affects NMDA receptors which changes Ca2+ regulation
  • Adverse effects: dizziness, headache, confusion, constipation
40
Q

Potential Alzheimer’s pharm treatments

A

Nicotine patch –> may make things better or worse
NSAIDS –> may protect those with certain genes
Vitamin E –> may slow progression
Ginkgo Biloba??

Spring Pharm (8 decks)

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