REPUBLIC OF THE PHILIPPINES UNIVERSITY OF NORTHERN PHILIPPINES Tamag Vigan City

COLLEGE OF HEALTH SCIENCES

PARKINSON'S DISEASE

A Case Study on

In Partial Fulfillment of the Requirements in RLE (NCM 105)

PRESENTED TO: Maria

Conception Malangen,RN. Clinical Instruction

PREPARED BY: Regina

Supnad BSN (L) III Garnet

JUNE 7, 2011

I. INTRODUCTION

Oscar Edpalina, 69 y/o, a resident of Parian, San Fernando City La union was admitted last May 6, 2011 @10:10 AM in Ilocos Training and Regional Medical Center. Diagnosed with Parkinson's Dse by Dr. Fernandez. Parkinson's Disease is an idiopathic syndrome characterized by disability from tremor and rigidity. Various other forms of parkinsonism cause similar clinical manifestations but have known causes. They include: Post encephalitic parkinsonism, which occurred after the large epidemic of encephalitis in 1919 Drug-induced Parkinsonism, occurring after long-term use of phenothiazines Toxin-induced parkinsonism, sometimes resulting from carbon monoxide,mercury or manganese exposure Exposure to agricultural herbicides and pesticides Trauma injury to the mid brain CLINICAL MANIFESTATIONS PD most often develops in people in their 60's,although it can strike much younger people as well. It occurs worldwide. About 1% of people over age 50 have PD. The disease has six cardinal features: (1)tremor at rest;(2)rigidity;(3)bradykinesia (slow movement);(4)flexed posture of the neck, trunk and limbs;(5)loss of postural reflexes;and (6) freezing movement. OUTCOME MANAGEMENT The manifestations of PD can be relieved by various medications,particularly levodopa and anticholinergic drugs. The purpose of levodopa is to provide dopamine to the basal ganglia. The purpose of anticholinergic drugs is to block release of acetylcholine, thereby creating a better balance between acetylcholine and dopamine. The most common levodopa drug is carbidopa-levodopa (Sinemet) -MANAGE THE PARKINSONIAN CRISIS Occasionally,clients with PD experience a parkinsonian crisis as a result of emotional trauma or sudden or inadvertent withdrawalal of antiparkinsoniamedication. Severecerbation of tremor,rigidity,and bradykinesia,accompanied by acute anxiety,sweating,tachycardia,and hyperpnea occur. Intervention parkinsonian crisis includes respiratory and cardiac support. The person should be placed in a quiet room with subdued lighting. Barbiturates may be prescribed,as well as antiparkinsonian drugs. -MANAGE THE ON/OFF RESPONSE An on/off response (rapid flactuation of clinical manifestations)may occur in clients with PD;the client may be mobile and active (on) one moment and akinetic and rigid (off)the next. This transition may happen quickly,within 1 to 2 minutes. Initially,the off periods tend to occur 3 to 4 hours after a dose of antiparkinsonian medication. -NURSING MANAGEMENT OF THE MEDICAL CLIENT Nursing care of the PD client includes health assessment,medication instruction an monitoring

OBJECTIVES GENERAL OBJECTIVE > This study enables the student to develop the right knowledge,skills and attitude towards quality care of patient who has Parkinson's Dse. SPECIFIC OBJECTIVES >To know more about Parkinson's Dse. >To recognize clinical manifestations and its onset >To know about the common diagnostic procedures >To administer proper medical care, diet and activities >To institute prevention strategies >To know its management and treatment >To assess risk factors and causes of the disease,for plan of care.

II.PATIENT'S PROFILE

NAME:Oscar Edpalina AGE: 69y/o SEX: male CIVIL STATUS: Married ADDRESS: Parian, Sn. Fernando La Union DATE OF BIRTH: Nov. 18, 1941 RELIGION: Roman Catholic CITIZENSHIP: Filipino HOSPITAL WARD: Close Watch (Medical) DATE OF ADMISSION: May 6,2011 @10:10 AM ADMITTING PHYSICIAN: Dr. Fernandez ADMITTING DIAGNOSIS: Parkinson's Dse. III.HISTORY OF ILLNESS PAST HISTORY Oscar Edpalina,69 and a resident of Parian, San Fernando City La Union sought medical consultations before (2008) with nephrologist regarding Parkinson's Dse. Medications taken (not stated ) with incomplete immunizations. He is an ex-smoker consuming about pack/day for 40 years (20 pack/year),occasional alcoholic drinker consuming 1 bottle per occasion.He worked for more than 30 years in a celophane factory located at Naguilian La Union. FAMILY HISTORY Positive family history of hypertension. No family history of asthma,diabetes,tuberculosis, heart or kidney dse.,cancer,anemia,epilepsy or mental illness. PRESENT HISTORY Oscar Edpalina,69,a resident of Parian, San Fernando City La Union was admitted last May 6,2011 @10:10AM @ Ilocos Training and Regional Medical Center .2 wks. PTA, patient has been experiencing on and off difficulty of breathing,body weakness and easy fatigability. It was relieved by rest, thus no consultation was done. The condition persisted until 1 day PTA, patient experiences sudden onset of DOB that is much severe in quality. It is associated with nonproductive cough. There are no associated fever and chest pain. Persistence of DOB prompted consultation. It was diagnosed as Parkinson's Dse. His admitting physician is Dr. Fernandez. IV. PHYSICAL ASSESSMENT

BODY PARTS

TECHNIQUE USED
Inspection

FINDINGS

SIGNIFICANCE

Hair

With white Normal; changes hair;oily;properly due to aging distributed (-) head injury Appears weak watery and bulging no secretions Dry Normal denotes pain uncomfortable denotes pain Normal

are

Head Face Eyes Nose Lips Neck Heart

Inspection Inspection Inspection Inspection Inspection Inspection Auscultation

and

may be a sign of dehydration; or side effect of diazepam

No anatomical abnormalities Normal Initial PR: 98 Normal

Chest Abdomen Upper extremities

Inspection; Palpation Inspection; Palpation Inspection

Initial RR: 20 Normal not enlarged Normal Presence of dry wound with minimal secretions Infection (blood + pus) no anatomical abnormalities Normal

Lower Extremities

Inspection

5-13-2011 06 PM BP T P R 130/ 90 39.9 0C 98 20 I0 PM 130/ BP 80 38.9 T 0C 93 P 19 R

5-14-2011 06 PM 10PM

90/ Patient 60 Died by 41.3 8:35 pm 0C 113 24

V. ANATOMY AND PHYSIOLOGY

Many different areas within the brain are involved in a complex chain of decisions required for even the smallest muscular movement. Take walking for example. The brain must first gather all the information it needs about your body position. Are you sitting, lying down, or already standing up? Where are your feet? Do you have your balance? Then, the brain must add in what it knows about where you will be going. Will you be crossing an open field of grass or a busy street (This information is sent by your eyes to the brain)? Is the ground is easy to walk on or could you lose your balance because it is bumpy or slippery (brain enlists the information sensed by your feet for this)?

The entire nervous system is made up of individual units called nerve cells. Nerve cells serve as a "communication network" within your body. To communicate with each other, nerve cells use a variety of chemical messengers called neurotransmitters. Neurotransmitters carry messages between nerve cells by crossing the space between cells, called the synapse Neurotransmitters also allow the nervous system to communicate with the body's muscles and translate thought into motion. One especially important messenger is dopamine, which is manufactured in the substantia nigra. Dopamine is crucial to human movement and is the neurotransmitter that helps transmit messages to the striatum that both initiate and control your movement and balance. These dopamine messages make sure that muscles work smoothly, under precise control, and without unwanted movement. When a dopamine message is needed, a nerve cell that produces dopamine gathers packets within itself filled with dopamine particles. These packets carrying the dopamine move to the end of the nerve cell, open a "window," and release the dopamine particles into the synapse. The dopamine particles flow across the synapse and fit into special pockets on the outside of the neighboring, or receiving, nerve cell (figure 3). The receiving cell is now stimulated to send on the message, so it gathers its own packets of dopamine and passes along the message to the next nerve cell in the same way. After the receiving cell has been stimulated to pass along the message, the pockets then release the dopamine back into the synapse. To fine-tune coordination of movement, these "used" dopamine particles, along with any excess dopamine that did not originally fit into a

pocket on the receiving cell, are broken down by a chemical in the synapse called MAO-B (figure 4). This is an important step in the precise control of muscle movement. Too much or too little dopamine can disrupt the normal balance between the dopamine system and another neurotransmitter system, and interfere with smooth, continuous movement. Acetylcholine is another neurotransmitter system that works in conjunction with the dopamine system to produce smooth movement. Some of the nerve cells in the brain are specialized to use either dopamine or acetylcholine to send different messages, depending on what it is you want to do. What Happens in Parkinson's Disease In Parkinson's disease, for reasons that are not fully understood, nerve cells in the part of the brain that produces dopamine, the substantia nigra, begin to decrease in number. This causes
a decrease in the amount of the available dopamine. Also, the chemical in the synapse that breaks down the dopamine (MAO-B) continues to deplete what little dopamine is left. The overall effect is a large loss of dopamine in the brain. This throws off the normal dopamine/acetylcholine balance, since the level of acetylcholine remains normal.and there is not enough dopamine to keep balance with the acetylcholine. The basal ganglia are thus prevented from modifying the nerve pathways that control muscle contraction. As a result, the muscles are overly tense, causing tremor, joint rigidity, and slow movement. Most drug treatments increase the level of dopamine in the brain or oppose the action of acetylcholine.

VI. DIAGNOSTIC PROCEDURES Complete Blood Count RESULTS Hemoglobin Hematocrit Platelet WBC 81 24 243 19.4 NORMAL VALUE 120-180 g/L 38-54 10^12/L 150-450 10^g/L 4.5-11 10^g/L SIGNIFICANCE Due to blood loss Due to blood loss and dietary deficiency Normal Infection is present

Department of Radiology Interpretation The liver is unenlarged. Parenchymal echotexture is regular and medium in level. The intra and extra hepatic ducts are not dilated. The portal Venous radicles and inferior vena cava are not dilated. No hepatorenal fluid noted. Gallbladder is normal in size. Its wall is not thickened. No intraluminal echoes noted Pancreas is normal in size The right kidney measures about 8.13 x 3.13 cm The left kidney measures about 8.12 x 3.5 cm Urinary bladder not filled Free fluid collection is detected at the right costophrenic sulcus Impression Diffuse renoparenchymal change Note of right sided pleural effusion Sonographically unremarkable liver, gallbladder, spleen and pancreas TEST Total Protein ABG ANALYSIS RESULT 49.138 g/L NORMAL VALUE 62.000-80.000 SIGNIFICANCE Due to dietary insufficiency

RESULT PH PCO2 7.4 21mmHg

NORMAL VALUE 7.35-7.45 35-45 mmHg

SIGNIFICANCE Normal Respiratory alkalosis alternatively hypocapnia hyper- or over ventilation Patient receives more of

PO2

117 mmHg

80-100 mm Hg

the normal O2 consumption BF ccf HCO3 TCO2 SO2 (-) 12 mm Hg 13 mmol/L 14mmol/L 99.00% 96-100% Normal 22-26 mmol/L Metabolic acidosis

PROTHROMBIN TIME RESULT time INR % activity control 14.7 1.25 58.9 11.9 NORMAL VALUE 12.00-16.00 sec. SIGNIFICANCE normal

ACTIVATED PARTIAL THROMBOPLASTIN TIME RESULT time control 43.9 34 NORMAL VALUE 26.00-38.00 sec. SIGNIFICANCE Due to deficiencies in Vitamin K

TEST Potassium Glu (hexo) Cholesterol Triglyceride HDL Cholesterol LDL Cholesterol Uric acid

RESULT 3.7 mmol/L 3.786 mmol/L 2.532 mmol/L 0.576 mmol/l 0.834 mmol/L 1.58 mmol/L 521.903 u mmol/L

NORMAL VALUE 3.50-5.30 mmol/L 3.900-5.830 mmol/L 2.600-4.130 mmol/L 1.700-5.600 mmol/L 0.750-0.850 mmol/L 2.60-4.94 mmol/L 155.000-428.000 u mmol/L

SIGNIFICANCE Normal Due to dietary insufficiency Due to dietary insufficiency Due to dietary insufficiency Normal Normal Due to low zinc intake

VII.

PATHOPHYSIOLOGY

A.) Algorithm
Herbicides and pesticides Drug induced (Phenothiazines) Toxin induced (CO, mercury, Manganese

Degeneration of dopamine- producing cells in the substantia nigra

Degeneration of dopaminergic neurons in the basal ganglia

Loss of postural reflexes

Freezing movement

Tremor at rest

rigidity

bradykinesia

B.) Explanation PD is the most common form of parkinsonism. PD involves degeneration of dopamineproducing cells in the substantia nigra, which leads to degeneration of dopaminergic neurons in the basal ganlia. Once cell loss in the substantia nigra reaches 80%, manifestations appear. The cause of nigral cell degeneration is not known. The net result of the loss of the dopaminergic neurons is an imbalance of dopamine in relation to Ach in the basal ganglia, which leads to the clinical characteristics of PD.