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62 Cards in this Set

  • Front
  • Back
What are the clinical features of Parkinson's Disease? (4)
1. Tremor (at rest)
2. Rigidity
3. Bradykinesia = extreme slowness in movement
4. Mask-like expression
What can Parkinson's Disease be a complication of?
1. Influenza epidemic of 1918
2. certain medications
3. MPTP toxicity
4. other neurologic disorders
-Progressive Supranuclear Palsy
-Shy-Drager Syndrome
-Creutzfeld-Jacob Disease
What is the pathophysiology of Parkinson's Disease?
Loss of Nigrostriatal Dopamine neurons = pale Substantia Nigra

Loss of Dopaminergic innervation of the Basal Ganglia
What are the 2 families of Dopamine receptors?
D1-like = D1 & D5

D2-like = D2, D3, & D4
What is important for the greatest efficacy in therapeutic strategy for Parkinson's treatment?
balance between D1 & D2
What is the Primary Strategy in Parkinson's treatment? Secondary?
Primary = replace Dopamine

-Dopamine agonists
-block Dopamine catabolism
Since Dopamine does not cross the BBB, what is given to replace it?

"The Lazy Dog Naps Easily"
What are the pharmacological effects of L-DOPA?
Motor = reversal of rigidity, tremor, & bradykinesia

-improved mental function
-sense of well-being
What are the Early Side Effects of Levodopa (L-DOPA)?
GI = N/V = due to stimulation of the Chemoreceptor Trigger Zone (CTZ) (very common)

-Postural Hypotension (very common) = due to stimulation of D1 Dopamine receptors in Kidney & Vasculature
-HTN, esp. w/ Sympathomimetics

-decreased Prolactin secretion = due to stimulation of D2 receptors in Pituitary
What are the long-term Motor side effects of L-DOPA?
1. fluctuations in efficacy

2. "on-off" - symptoms reappear periodically

3. "wearing off" - effects don't last as long
What are the long-term Neurological side effects of L-DOPA?
Abnormal movements

**this is very common
What are the long-term Psychic effects of L-DOPA?
Hallucinations, Paranoia, Mania, Anxiety, Depression
-due to stimulation of dopamine receptors in targers of the Mesolimbic & Mesocortical pathways
-can lower dose or treat with newer Antipsychotics that do not tend to produce EPS
What are the long-term Neuroendocrine side effects of Levodopa?
Renewed Sexual interest & behavior

L-DOPA Pharmacokinetics:
1. Route of Administration
2. Absorption
3. Peak Levels
4. t1/2
5. Metabolism & excretion
1. Oral
2. dependent on GI transit time
3. 1/2 to 2 hrs after administration
4. 1-3 hours
5. >95% decarboxylated in periphery & excreted in urine
What is L-DOPA virtually always administered with? Why?

-Increases Levodopa to the brain
-can used decreased doses
-decrease side effects, esp. GI
Non-ergot D2/D3 Dopamine agonists
1. Pramipexole

2. Ropinerole

"Ropin some Prami's" with D2/D3
2 Ergot Dopamine Agonists

D1/D2 Dopamine agonist
What is the mechanism of action of the Dopamine agonists?
Agonist at D2 & other Dopamine receptors

Activity at D3 receptor may confer greater efficacy & may mediate neuroprotective effects
Which Dopamine agonists may be used as Monotherapy or with L-DOPA?
D2/D3 agonists = Pramipexole & Ropinerole

**others are used with L-DOPA in pts with "on-off" or whose symptoms are not controlled by L-DOPA
What are the side effects of the Dopamine Agonists?
Postural Hypotension
Selective MAO-B inhibitor that blocks that catabolism of Dopamine

"Select a Gel Line" that inhibits sweating "My Ass Off" (MAO-B)
What is the use of Selegeline?
Adjunct to L-DOPA
-increases efficacy
-decrease L-DOPA dose
-decreases "on-off" effect
2 COMT inhibitors that block catabolism of Dopamine


"Al CAPONE watched the COuntry Music Television Inhibitor"
What are the uses of COMT inhibitors?
Adjunct to L-DOPA
-increases efficacy
-decrease L-DOPA dose
-decreases "on-off" effect
What side effect can MAO inhibitors cause?
Hypertensive Crisis
-esp. MAO-A inhibitors
What drugs can decrease GI motility and result in decreased absorption of L-DOPA?
What drug can increase L-DOPA metabolism?
Pyridoxine = vitamin B6
What are 2 Anticholinergics used to treat Parkinson's Disease? Why are they used?

Block the actions of Striatal Interneurons = curb the excess Cholinergic activity
What are the side effects of Trihexyphenydyl & Benztropine?
1. Constipation
2. Urinary Hesitance, retention
3. Mental confusion
4. Hallucinations
What antiviral is used to treat Parkinson's disease? What is a proposed mechanism?

May release Dopamine and/or have anticholinergic properties

**used as adjunt to L-DOPA
What are the side effects of Amantidine?
Similar to Dopamine agonists

May produce Livedo reticularis, Peripheral Edema, & Headache
What is the cause of Drug-induced Parkinsonism?
Blockade of Striatal Dopamine receptors
What drugs most commonly produces Drug-induced Parkinsonism? What is the treatment?
Antidopaminergic, antipsychotic drugs such as HALOPERIDOL

Tx = Trihexyphenidyl & Bentropine
What are the clinical features of Huntington's Disease?
1. Progressive Chorea = abnormal involuntary movements

2. Progressive Dementia
What is the pathology of Huntington's Disease?
Functional overactivity of Dopaminergic Nigrostriatal pathways due to loss of Striatal GABAergic neurons projecting to the Globus Pallidus
What is the treatment for Huntington's Disease?
What are the clinical features of Tourrette's Syndrome?

Involuntary movements or outbursts
What is the pathology of Tourette's Syndrome?
Unknown, but involves increased activity of Striatal neurons
What is the treatment of Tourrette's Syndrome?
What are Physiologic Postural Tremors? What receptors does it involve?
Normal phenomenon enhanced by anxiety, fatigue, thyrotoxicosis, or administration of Sympathomimetics

Beta-1 & Beta-2 receptors
What are Essential Tremors? What receptors are primarily involved?
Essential Tremor = neurological disorder characterized by shaking of hands (and sometimes other parts of the body including the head), evoked by intentional movements

Beta-1 receptors
What is the treatment for Tremors?
Physiologic & Essential = Propranolol (Beta-1 & 2 blocker)

Essential = Metoprolol (Beta-1 selective)
What is "Spasticity"?
Violent, painful, involuntary muscle contractions resulting from dysfunction or descending motor input
What can cause Spasticity?
Trauma, inflammation, or diseases such as Multiple Sclerosis & Cerebral Palsy
What is the site of action of Diazepam as an Antispastic drug? What is its mechanism?
Spinal & Supraspinal

Enhances GABAergic transmission at GABA-A receptors
What are the principal uses of Diazepam as an Antispastic drug?
All types of Spasticity associated with Spinal Cord lesions

Cerebral Palsy
Diazepam as an Antispastic:
1. Administration
2. Duration of action
1. Oral or IM

2. >24 hrs due to active metabolites
What is the site of action of Baclofen as an Antispastic drug? What is the mechanism?
Gamma motor neurons in the Spinal Cord

GABA-B agonist = inhibits release of excitatory transmitters & increases threshold for excitation thus decreasing mono- & polysynaptic spinal reflexes
What are the side effects of Baclofen?
1. Drowsiness
2. Insomnia
3. Weakness
4. Dizziness
5. Confusion

**side effects can be decreased with Intrathecal administration
What are the principal uses of Baclofen?
Spinal Cord injuries & Multiple Sclerosis
Baclofen pharmacokinetics:
1. Administration
2. Half-life
3. Excretion?
1. rapidly absorbed after oral administration
2. 3-4 hours
3. unchanged in urine
What is Dantrolene's site of action? What is its mechanism?

reduces muscle contraction by decreasing Ca++ release from Sarcoplasmic Reticulum
What are Dantrolene's side effects?
Generalized Muscle Weakness


*"Dan the Lean" man has muscle weakness & Liver problems
What are the principal uses of Dantrolene? What is another use?
Paralysis & Hemiparalysis
Cerebral Palsy
Multiple Sclerosis

Malignant Hyperthermia = hereditary condition in which certain anesthetics (e.g., halothane) cause high body temperatures and muscle rigidity
Dantrolene pharmacokinetics:
1. Administration
2. Plasma half-life
3. Metabolism & excretion
1. Orally
2. 9 hours
3. Hepatic metabolism & urine excretion

"Dan the Lean" man gets oral for 9 hours
What is Botox's site of action as an Antispastic drug? What is it's mechanism?

Acts on Cholinergic vesicles to inhibit ACh release
What are the principal uses of Botox?
Local muscle spasm & more generalized spastic disorders such as Cerebral Palsy
Botox pharmacokinetics:
1. Administration
2. Duration of action?
1. injected into muscle
2. weeks-months after a single injection
What 2 drugs are used for the treatment of acute muscle spasm cause by acute trauma or strain? What is their mechanism of action?
Cyclobenzaprine & Carisoprodol

Act as either a sedative &/or at the level of the brain stem or spinal cord

"Clarissa-Pro-Doll drives her Circle-Benz-aprine so much she gets sleepy (sedatives) & doesn't have muscle spasms"
What is Cyclobenzaprine structurally relted to? What is it not effective against?
Tricyclic Antidepressants

Spasms due to Cerebral Palsy or Spinal Cord injury
What is Carisoprodol metabolized into? What is the significance of this?
Meprobamate = sedative-hypnotic with abuse potential

"Clarissa the Pro Doll" has a daughter named "Me Probe a Mate" who is sedated all the time, with whom she is addicted to