Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

56 Cards in this Set

  • Front
  • Back
What are the signs of Parkinson disease (PD)
Bradykinesia; Muscular Rigidity; Tremors; Gait abnormalities; Postural istability
What neurotransmitter pathway is affected in PD
Dopaminergic pathway (inhibitory neurons) in the substanstia nigra and corpus striatum (neurotransmitter ratio shifts toward decreased DA and increased Ach)
What does increased levels of DA in the tuberoinfundibular tract lead to
Decreased prolactin levels
What does increased levels of DA in the CTZ lead to
Increased emesis
What does increased levels of DA in the mesolimbic-mesocortical tracts lead to
Increased psychomotor activity; Psychosis; Schizophrenia; Increased reinforcement
Which DA receptor subtype is implicated in PD
D2 receptor subtype (inhibitory receptor subtype that decreases cAMP levels in the corpus striatum)
Given the abnormal DA/Ach shift in the striatum, give two pharmacologic strategies in the treatment of PD
Medications that will increase DA levels; Medications that will decrease Ach levels
Do anti-Parkinson’s medications affect pathology, symptoms, or both
Name two antimuscarinic medications that are used in the treatment of PD
Benztropine; Trihexyphenidyl
Is benztropine more or less lipid soluble than atropine
More lipid soluble (therefore, greater CNS penetration)
Which characteristic of PD is not affected by anticholinergics
Is benztropine useful in the treatment of tardive dyskinesis
No (may actually exacerbate tardive dyskinesia)
What are the adverse effects of benztropine and trihexyphenidyl
Xerostomia; Blurred vision; Constipation; Urination retention; Sedation; Mydriasis
How does amantadine work in the treatment of PD
May inhibit reuptake of DA into presynaptic neurons; May increase DA release from presynaptic fibers
Amantadine is used to treat what condition other than PD
Influenza A
What is the name of the dermatologic adverse effect caused by amantadine
Livedo reticularis
What is livedo reticularis
A network-patterned discoloration of the skin caused by dilation of capillaries and venules
Which characteristic of PD is not affected by amantadine
Which selective MAOD inhibitor is commonly used as first-line treatment for PD
What is the mechanism of action of selegiline
Inhibition of DA metabolism in presynaptic neurons located in the CNS via inhibition of MAOB
What are the two active metabolites of selegiline
Amphetamine; Methamphetamine
What are the main adverse effects of selegiline
Cardiovascular stimulation (hypertension, tachycardia, palpitations; arrythmias; angina)
Name two ergot derivatives that act as DA agonists in the nigrostriatal system
Bromocriptine; Pergolide
Bromocriptine is used to treat what conditions other than PD
Prolactin-secreting adenomas; NMS; Acromegaly; Postpartum lactation
What are the adverse effects of bromocriptine
Headache; Dizziness; Nausea; Orthostatic hypotension; Dyskinesia; Hallucinations; Confusion; Psychosis
Name two nonergot DA agonists
Pramipexole; Ropinirole
What are the adverse effects of the nonergot DA agonists
Sedations; Syncope; Nausea; Vomiting; Hallucinations; Dyskinesia
What is the mechanism of action of tolcapone and entacapone
Inhibition of peripheral COMT thereby increasing CNS uptake of L-Dopa
What reaction does COMT catalyze
Conversion of L-Dopa to 3-O-methyldopa (partial DA agonist) in peripheral tissues
What are the adverse effects of COMT inhibitors
Orthostatic hypotension; Headache; Fatigue; Nausea; Diarrhea; Anorexia; Dyskinesia; Muscle cramps; Brown-orange urine discoloration; Hallucinations; Diaphoresis
Which of the COMT inhibitors is hepatotoxic
Are COMT inhibitors used as first-line therapy, adjunctive therapy, or both in the treatment of PD
Adjunctive therapy ( in combination with carbidopa/ levodopa)
Are the nonergot DA agonists used as first-line therapy, adjunctive therapy, or both in the treatment of PD
What is the precursor of DA
Levodopa (L-Dopa)
What enzyme converts L-Dopa to DA
Dopa-decarboxylase (DDC)
What is another name for DDC
Aromatic amino acid decarboxylase
Does DA cross the BBB
Does levodopa cross the BBB
Yes (converted to DA by dopaminergic neurons in the substantia nigra)
Is levodopa effective in treating PD when all of the dopaminergic neurons in the substanstia nigra have been destroyed
No (dopaminergic neurons in the substanstia nigra are required to convert levodopa to DA)
What is the mechanism of action of carbidopa
Inhibition of peripheral DDC thereby increasing the amount of levodopa that is available to cross the BBB into the CNS (this allows for lower doses of levodopa needed thereby decreasing levodopa adverse effects)
Does carbidopa cross the BBB
No (only inhibits peripheral DDC)
How does levodopa work in the treatment of PD
Decreases symptoms of PD, such as rigidity, bradykinesia, and tremors
What is the “on-off” phenomenon
Levodopa has such a short half-life (1 to 2 hours) that plasma concentrations may decline rapidly causing the patient to experience rigidity, bradykinesia, and tremors
Which amino acids compete with levodopa for GI absorption
Isoleucine: Leucine
What are the adverse effects of levodopa
Anorexia; Nausea; Vomiting; Tachycardia; Hypotension; Discoloration of saliva and urine; Mydriasis; Hallucinations; Dyskinesia; Increased intraocular pressure; Cardiac arrhythmias
Why should vitamin B6 (pyridoxine) not be used in combination with levodopa
Pyridoxine enhances peripheral metabolism of levodopa thereby rendering the medication ineffective
What is drug-induced parkinsonism
Parkinsonian symptoms can be caused by potent antipsychotic agents such as haloperidol because they block dopamine receptors
What is the treatment for drug-induced parkisonism
There are three treatment options:
Lower the drug levels
Change the drug to a less potent one
Use an anticholinergic agent
Define Huntington's disease
A genetic disorder due to a single defect on chromosome 4
What are the symptoms of Huntington's disease
Individuals who have this disease display dementia and/or chorea
What is the pathophysiology of Huntington's disease
This disease is thought to occur because of excessive dopaminergic activity and diminished GABA functions in the basal ganglia (caudate and putamen)
What is the treatment for Huntington's disease
Dopamine blockers such as haloperidol (Haldol) or tetrabenazine are used to treat this disorder
What is Tourette's syndrome
A disease characterized by abnormal tics and facial movements
What is the treatment for Tourette's syndrome
Clonidine (Catapres). Haloperidol has also been used
Define Wilson's disease
Wilson's disease is a genetic disorder of copper metabolism. Excess copper is deposited in the liver, brain, and other tissues
What is the treatment for Wilson's disease
A copper chelating agent known as penicillamine (Depen)