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Drugs That Affect Parkinson Disease

This document discusses drugs used to treat Parkinson's disease and epilepsy. It covers how dopamine and acetylcholine levels are affected in Parkinson's and describes drugs that target the dopamine system like levodopa, MAO inhibitors, and dopamine agonists. It also discusses anti-parkinsonian drugs and their mechanisms and side effects. For epilepsy, it describes different seizure types and common anti-epileptic drugs like phenytoin, carbamazepine, and valproic acid. Nursing considerations are provided around monitoring drug levels, diet restrictions, and safety during seizures.

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174 views12 pages

Drugs That Affect Parkinson Disease

This document discusses drugs used to treat Parkinson's disease and epilepsy. It covers how dopamine and acetylcholine levels are affected in Parkinson's and describes drugs that target the dopamine system like levodopa, MAO inhibitors, and dopamine agonists. It also discusses anti-parkinsonian drugs and their mechanisms and side effects. For epilepsy, it describes different seizure types and common anti-epileptic drugs like phenytoin, carbamazepine, and valproic acid. Nursing considerations are provided around monitoring drug levels, diet restrictions, and safety during seizures.

Uploaded by

richardmd2
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as DOCX, PDF, TXT or read online on Scribd
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Pharmacology 2

December 9, 2010

Drugs that affect Parkinson Disease: 1817 (James Parkinson  Shaking Palsy)

- Acetylcholine (increased in secretion)


- Dopamine (decreased in secretion)

Extrapyramidal System:
1. Motor Control
2. Posture
3. Muscle Tone
4. Smooth muscle activity

Dopamine Release: Target receptor is D receptors (D1,D2, D3, D4)


1. Mesolimbic areas  Amygdala (EMOTIONS)  Schizophrenia (+ symptoms)
2. Mesocortical areas  Cerebral cortex  Schizophrenia (- symptoms)
3. Nigrostriatal areas (Substancia Nigra/Putamen)
4. Basal ganglia & Hypothalamus

Dopamine Hyperstimulation can be caused by:


a. Genetic or family history lineage
b. Tumor or abnormal mutations
c. Drug induced (L-Dopa overdose/Dopamine Agonist)
d. Tyramine Rich Foods precursor dopamine synthesis
KINDLY CHECK the TYRAMINE entry in Presynaptic cleft pls  BULAG KA!

Effects or Commonality:
1. Psychosis/Schizophrenia (Positive/Negative symptoms)
2. May also stimulate other adrenergic receptors (A1,A2, B1, B2)

Dopamine Hypostimulation can be caused by:


a. Drug induced (Anti-psychotic agents)
b. Neurotoxin (MPTP 1-methyl 4-phenyl 1,2,3,6 -tetrahydropyridine)
c. Aging
d. Wear and tear (free radical damage)
e. Head trauma
f. Infections that may damage dopaminergic sites
g. Genetic/ inborn errors (rare)
f. Metallic poisoning (Pb, Mercury, Fe+++)
d. Carbon Monoxide Poisoning
e. Hypoxia/Stroke survivor

Effects or Commonality if Dopamine is Reduced:


1. Parkinson like disease
- Bradykinesia
- Rigidity
- Tremor
- Postural
Effects or Commonality if Dopamine is Increased:
1. Dyskinesia
- Chorea
- Dystonia

ANTI-PARKINSON ANGENTS:

1. Anticholinergics (Benztropine, Bipiriden, Procyclidine, Trihexylperidine)


2. Anti-Histamine (Diphenhydramine)
3. Dopamine Receptor Agonist (Bromocriptine, Levodopa, Levodopa-carbodopa,
Pergolide)
4. Indirect Acting Receptor Agonist
MAO – B Inhibitor  (Selegiline)

1. MAO A  Norepinephrine & Serotonin Metabolism


2. MAO B  Dopamine Metabolism

NB: AVOID Tyramine rich food  Cheese, Milk


May cause  RISK HYPERTENSIVE CRISIS

Tyramine  DOPA  NOR  NOREPINEPHRINE SURGE  Apha 1

COMT Inhibitor (Entacapone)


Miscellaneous (Antiviral  used for influenza virus: Prevents attachment) 
Amantadine (Re-uptake)

DOPAMINE: Lipophobic or Hydrophillic in nature  Fails to pass in blood brain barrier


(cell membrane)

LEVODOPA: (Can pass through the CNS but can be converted to DOPA in the
Periphery via DD )

1. Precursor for DOPAMINE production


2. Periphery converted into Dopamine that can stimulate Adrenergic Receptors:
(Dopamine Decarboxylase)  LEVODOPA DOPAMINE
a. Alpha 2  Vasodilation (Hypotension)
b. Beta 1: Tachycardia  arrhythmias
c. Beta 2: Bronchodilates
d. Beta 1: Iris  Mydriasis  Blurring of Vision , IOP (Glaucoma)
e. CTZ (CNS)  Nausea & Vomiting
ACTION:
a. Decreases Rigidity, Tremors

SIDE EFFECTS:
a. Dopaminergic Actions in Adrenergic Receptors in Periphery
Hint: Dopamine targets alpha 2  VASODILATION not Constriction
NOREPI/EPI target  Alpha1  VASOCONSTRICTION
b. On/OFF phenomenon ( Short Half Life  1-2 hours) Fluctuations in the level of
concentration of the Dopamine

INTERACTIONS:
a. High Protein Diet (Neutral Amino Acid/Leu/Isoleucine)  Impede GI Absorption
- Take NPO for 45 minutes before eating
b. Vitamin B6 (Pyridoxine), Foods rich in Vitamin B6 Degrades Levodopa
c. MAO- A Inhibitor (Phenelzine)  Hypertensive Crisis  Catechoamine
Production
d. Antipsychotic Agents  Contraindicated because decreases Dopamine Release

Drug Holliday  10 Days  method used to start treatment

CARBIDOPA: Dopamine Decarboxylase Inhibitor


1. It doesn’t pass in the CNS Barrier
2. Inhibits the conversion of Levodopa to Dopamine in GI & Periphery
3. Decreases the side-effects in the periphery due to lack of Dopamine Conversion

Changes in the URINE Color & Saliva  Brown (cathecoamine production melanin)
- HARMLESS
Deprenyl (Selegiline) : MAO B-I (Metabolize Dopamine) Inhibitor
MAO A-I (Metabolize Nor/Serotonin)  NO effect

Amantadine: Anti-viral (Influenza)


Bromocriptine: Hallucinogenic, Confusion, Nausea, Hypotension

Anti-Cholinergics:

a. Benztropine (Congentin)
b. Bipiriden (Akineton)
NURSING CONSIDERATIONS:

1. Bromocriptine  Suppress the milk “let down” process  Mothers who do not want
to breastfeed
2. Amantadine  Anti-viral agent

3. NURSES FOCUS ON:


a. Enhance, Promote and Check Activity of Daily Living
b. Motor Activity & Movement (Walking, Gait, Hand Movements)
c. Communication
d. DIET (constipation), Avoid tyramine Rich food if MAO-I B is used, Vit B6
e. Psychological: Hallucinations, Confusion because D1 receptor activation in the
Mesolimbic or Mesocortical Areas
g. Vital Signs: BP (Hypotension)  Orthostatic Hypotension  Risk Injury
h. Check history of Drug Allergy
i. Glaucoma Patients: Mydriasis
j. Nausea and Vomiting Evaluation

Drugs that reduces Intracranial Pressure:


a. Mannitol (is sugar that is doesn’t absorbed  retention on the blood vessels 
Osmotic Effect  Diuresis  loosing water that reduces  cerebral edema.
b. Reduce intraocular pressure by allowing removal of tears/aqueous humor
c. Osmotic Loose Bowel  Laxative

Monitor: FOR TREATMENT ICP


1. Hydration: serum Hct (increase)
2. LOC  Improvement
3. Urine output
4. Serum electrolytes: Sodium Loss
5. Vital Sign: BP  Hypotension (Blood volume loss  WATER loss)

Drugs that can cause Muscle to Relax:

- Used to relax muscles during uncontrolled muscular spasm (PAIN, Respiration


Effects)
a. Loss to Function
b. Pain, Parethesias (Tingling Sensation)

- Cases: Cerebral Palsy, Multiple Sclerosis, Trigeminal Neuralgiam, Stiff Neck


Muscle Relaxant Effects:
- DIZZINESS, LIGHTHEADEDNESS, DROWSINESS, FATIGUE
- Caution with highly stimulated activities (Driving, Control of Machines)

Types:

1. Centrally Acting Muscle Relaxants  ACTION IS IN THE BRAIN


a. Baclofen: Lioresal (GABA mimetic)

2. Direct Acting Muscle Relaxants  ACTION IS IN THE MUSCLE


a. Dantrolene: Dantrium (Inhibits Calcium Release in the muscle sarcoplasmic
reticulum)

Other Uses: For Malignant Hyperthermia

Drugs that affects the Seizure Activity:

Seizure: Brief, 1st Time


a. Metabolic  hyponatrmia, metabolic acidosis
b. Hyperthermia  Febrile Convulsion
c. Drug Induced  Antibiotics * 3rd generation cephalosporin, Cocaine
d. Hypoxia
e. Infection
f. Toxic Substances: Alcohol withdrawal, Vitamin B6 Deficiency

Epilepsy: Chronic, and repeats overtime, unpredictable


a. Organic or structural damage/abnormality

Convulsion: Muscular Contractions

Types:
1. Primary Epilepsy (CNS cause origin)
2. Secondary Epilepsy (Tumor, Head Injury, Edema, Alcohol Withdrawal, Fever)

Location: Affected part of the brain is local (1 part)


Partial Seizures (FOCAL)  NO LOSS OF CONSCIOUSNESS
a. Simple
b. Complex

DOC: Phenytoin , Carbamazepine


Generalized  LOSS OF CONSCIOUSNESS, HALLUCINATION
(Both hemisphere are damaged/affected)

a. Tonic-Clonic (Grandmal) : DOC: Phenytoin , Carbamazepine


b. Absence (Petitmal) : DOC: VALPORIC ACID
c. Myoclonic: DOC: VALPORIC ACID, CLONAZEPAM
d. Febrile Seizures: DOC: Phenobarbital
e. Status Epilepticus: DOC Phenytoin, Diazepam

Effects of Seizure/Epilepsy
1. Injury Risk  fracture, head trauma
2. Airway Obstruction  Aspiration
3. Airway Ventilation  Breathing (Stop rise/fall of the chest wall)
4. LOC  Amnesia, confusion, hallucinations
5. Brain Damage

Steps:
1. Establish Safety
2. Airway
3. Avoid restraints
4. Re-orient the patient

ANTI-EPILEPTIC AGENTS:

1. Carbamazepine
2. Clonazepam
3. Diazepam
4. Phenytoin
5. Valporic Acid

Phenytoin: Dilantin
Therapeutic Index of Safety:10-20mcg/ml (Narrow/risk for toxic effects)
MONITOR BLOOD SERUM LEVELS REGULARLY

1. ACTION: Decreases the flux of Na ions to reduce electrical synaptic (-90MV) activity
2. Can cause Drowsiness  (Nystagmus & Ataxia)
3. Do not use with Abscence Seizure (Valporic Acid)
4. ORAL: Chronic Users & IV: Status Epilepticus (Diazepam)
5. Gingival Hyperplasia
6. Megaloblastic Anemia (Vitamin B12 interaction)
7. Inhibits Insulin release  Hyperglycemia
8. Teratogenic Agent  FETAL HYDRANTOIN SYNDROME (Cleft palate, Cleft lip,
CHD)

9. Drug Interactions: Chloramphenicol, Dicumarol, Cimetidine, INH


10. Increases Liver Metabolizing Action  cP450  Increases Metabolism Medication
11. Hirsutism and Dilantin Facies
12. Osteoporosis  loss of calcium deposits

Risk for Skin Allergy  STEVEN JOHNSONS (Carrier HLA B Allele Ch. 12)

Carbamazepine:
1. DOC for Trigeminal Neuralgia
2. Can cause respiratory depression and Coma, Blurring of Vision  higher dosage
3. Gastric Irritant: Nausea and Vomiting (Give w/meals)
4. Aplastic Anemia, Agranulocytosis, Thrombocytopenia  BONE DEPRESSION
5. Hepatotoxic Agent
6. Skin: Exfoliative, Stevens-Johnson

Check Serum levels:


a. RBC, Platelets, WBC
b. Liver Function Test, Renal Function

Valporic Acid:
1. GABA mimetic
2. DOC : Myoclonic Seizure, Absence
3. Hepatotoxic and Pancreatoxic
4. Transient Hairloss
5. Weight Gain

AVOID MILK & CARBONATED DRINKS  Affect the pH of the Valporic acid

Nursing Considerations:
1. Keep Medical and Symptoms Diary  Caregiver
2. Skin rashes develop Stop agent  inform the doctor
3. Wearing an alert bracelet/ necklase with medications and type of epilepsy
4. Give meals before taking agent for CARBAMAZEPINE
5. Do not mix with Milk and Carbonated Drinks (Valporic Acid)
6. Seizure withdrawal occur if drug is stopped abruptly (rebound seizure)
7. Skin becomes Photosensitive
8. Avoid Smoking, Caffeinated agents  Increase seizure activity
9. Blood serum levels are screened regularly for toxic effects
10. Identify what type of Seizure that the patient has

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