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GUILLAIN BARRE SYNDROME

A disorder of the CNS characterized by bilateral symmetrical polyneuritis leading to ascending muscle paralysis.

A. Predisposing Factors
1. Autoimmune 2. Antecedent viral infections such as LRT infections

B. Signs and Symptoms


1. Clumsiness (initial sign) 2. Dysphagia 3. Ascending muscle weakness leading to paralysis. 4. Decreased of diminished deep tendon reflex 5. Alternate hypotension to hypertension ** ARRYTHMIA (most feared complication) 6. Autonomic symptoms that includes a. increase salivation b. increase sweating c. constipation

C. Diagnostic Procedures
1. CSF analysis reveals increase in IgG and protein.

D. Nursing Management
1. Maintain patent airway and adequate ventilation by: a. assist in mechanical ventilation b. monitor pulmonary function test 2. Monitor strictly the following a. vital signs b. intake and output c. neuro check d. ECG 3. Maintain side rails to prevent injury related to fall 4. Prevent complications of immobility by turning the client every 2 hours 5. Institute NGT feeding to prevent aspiration 6. Assist in passive ROM exercise

7. Administer medications as ordered a. Corticosteroids suppress immune response b. Anti Cholinergic Agents Atrophine Sulfate c. Anti Arrythmic Agents Lidocaine, Zylocaine Bretylium blocks release of norepinephrine to prevent increase of BP 8. Assist in plasma pharesis(filtering of blood to remove autoimmune anti-bodies) 9. Prevent complications a. Arrythmia b. Paralysis or respiratory muscles/Respiratory arrest * Sengstaken Blakemore Tube for liver cirrhosis to decompress bleeding esophageal varices (prepare scissor to cut tube in case of difficulty in breathing to release air in the balloon for hemodialysis prepare bulldog clips to prevent air embolism.

CONVULSIVE DISORDER/ CONVULSION


A disorder of CNS characterized by paroxysmal seizure with or without loss of consciousness, abnormal motor activity alternation in sensation and perception and changes in behavior. Seizure First convulsive attack Epilepsy Second or series of attacks Febrile seizure Normal in children age below 5 years

A. Predisposing Factors
1. Head injury due to birth trauma 2. Genetics 3. Presence of brain tumor

4. Toxicity from a. lead b carbon monoxide

5. Nutritional and Metabolic deficiencies


6. Physical and emotional stress 7. Sudden withdrawal to anti convulsant drug is predisposing factor for status epilepticus (drug of choice is Diazepam, Valium)

B. Signs and Symptoms


Dependent on stages of development or types of seizure I. Generalized Seizure 1. Grand mal Seizure (tonic-clonic seizure) a. Signs or aura with auditory, olfactory, visual, tactile, sensory experience b. Epileptic cry is characterized by fall and loss of consciousness for 3 5 minutes c. Tonic contractions - direct symmetrical extension of extremities d. Clonic contractions - contraction of extremities e. Post ictal sleep unresponsive sleep2. 2. Petit mal Seizure absence of seizure common among pediatric clients characterized by a. blank stare b. decrease blinking of eyes c. twitching of mouth d. loss of consciousness (5 10 seconds) II. Partial or Localized Seizure 1. Jacksonian Seizure (focal seizure) Characterized by tingling and jerky movement of index finger and thumb that spreads to the shoulder and other side of the body. 2. Psychomotor Seizure (focal motor seizure) a. automatism stereotype repetitive and non propulsive behavior b. clouding of consciousness not in contact with environment c. mild hallucinatory sensory experience

III. Status Epilepticus A continuous uninterrupted seizure activity, if left untreated can lead to hyperpyrexia and lead to coma and eventually death. Drug of choice : Diazepam, Valium and Glucose

C. Diagnostic Procedures
1. CT Scan reveals brain lesions 2. EEG reveals hyper activity of electrical brain waves

D. Nursing Management
1. Maintain patent airway and promote safety before seizure activity a. clear the site of blunt or sharp objects b. loosen clothing of client c. maintain side rails d. avoid use of restrains e. turn clients head to side to prevent aspiration f. place mouth piece of tongue guard to prevent biting or tongue 2. Avoid precipitating stimulus such as bright/glaring lights and noise 3. Administer medications as ordered a. Anti convulsants (Dilantin, Phenytoin) b. Diazepam, Valium c. Carbamazepine (Tegretol) Trigeminal neuralgia d. Phenobarbital, Luminal 4. Institute seizure and safety precaution post seizure attack a. administer O2 inhalation b. provide suction apparatus 5. Document and monitor the following a. onset and duration b. types of seizures c. duration of post ictal sleep may lead to status epilepticus d. assist in surgical procedure cortical resection

COMPREHENSIVE NEURO EXAM GLASGOW COMA SCALE -objective measurement of LOC sometimes called as the quick neuro check Components 1. Motor response 2. Verbal response 3. Eye opening Survey of mental status and speech a. LOC b. Test of memory Levels of orientation Cranial nerve assessment Sensory nerve assessment Motor nerve assessment Deep tendon reflex Autonimics Cerebellar test a. Rombergs test 2 nurses, positive for ataxia b. Finger to nose test positive result mean dimetria (inability of body to stop movement at desired point) c. Alternate supination and pronation positive result mean dimetria Conscious 15 14 Lethargy 13 11 Stupor 10 8 Coma 7 Deep Coma 3

MAIN FOODSTUFF Anabolism/ Catabolism 1. Carbohydrates 2. Protein 3. Fats, Glucose, Amino Acids, Fatty Acids, Glycogen, Nitrogen, Free Fatty AcidsCholesterol- Ketones HYPERGLYCEMIA - increase osmotic diuresis Glycosuria, Polyuria and Cellular starvation- weight loss. Cellular dehydration. Stimulates the appetite/satiety center Stimulates the thirst center (Hypothalamus) (Hypothalamus) Polyphagia/Polydypsia* Liver has glycogen that undergo glycogenesis/
glycogenolysis GLUCONEOGENESIS

Formation of glucose from non-CHO sources Increase protein formation Negative Nitrogen balance Tissue wasting (Cachexia) INCREASE FAT CATABOLISM Free fatty acids Cholesterol Ketones Atherosclerosis, Diabetic KetoAcidosis

Hypertension, Acetone Breath, Kussmauls Respiration odor, MI, CVA, Death Diabetic Coma

DIABETIC KETOACIDOSIS
- Acute complication of type 1 DM due to severe hyperglycemia leading to severe CNS depression

A. Predisposing Factors
1. Hyperglycemia 2. Stress number one precipitating factor 3. Infection

B. Signs and Symptoms


1. Polyuria 2. Polydypsia 3. Polyphagia 4. Glucosuria 5. Weight loss 6. Anorexia, nausea and vomiting 7. Blurring of vision 8. Acetone breath odor 9. Kussmauls Respiration(rapid shallow breathing) 10 CNS depression leading to coma

C. Diagnostic Procedures
1. FBS is increased 2. BUN (normal value: 10 20) 3. Creatinine (normal value: .8 1) 4. Hct (normal value: female 36 42, male 42 48) due to severe dehydration

D. Nursing Management
1. Assist in mechanical ventilation 2. Administer 0.9 NaCl followed by .45 NaCl (hypotonic solutions) to counteract dehydration and shock 3. Monitor strictly vital signs, intake and output and blood sugar levels 4. Administer medications as ordered a. Insulin therapy (regular acting insulin/rapid acting insulin peak action of 2 4 hours) b. Sodium Bicarbonate to counteract acidosis c. Antibiotics to prevent infection

HYPER OSMOLAR NON KETOTIC COMA


- Hyperosmolar: increase osmolarity (severe dehydration)- Non ketotic: absence of lypolysis (no ketones)

A. Signs and Symptoms


1. Headache and dizziness 2. Restlessness 3. Seizure activity 4. Decrease LOC diabetic coma

B. Nursing Management
1. Assist in mechanical ventilation 2. Administer 0.9 NaCl followed by .45 NaCl (hypotonic solutions) to counteract dehydration and shock 3. Monitor strictly vital signs, intake and output and blood sugar levels 4. Administer medications as ordered a. Insulin therapy (regular acting insulin peak action of 2 4 hours)- for DKA use rapid acting insulin b. Antibiotics to prevent infection INSULIN THERAPY A. Sources of Insulin 1. Animal sources - Rarely used because it can cause severe allergic reaction- Derived from beef and pork 2. Human Sources - Frequently used type because it has less antigenicity property thus less allergic reaction 3. Artificially Compound Insulin B. Types of Insulin 1. Rapid Acting Insulin (clear) - Regular acting insulin (IV only)- Peak action is 2 4 hours 2. Intermediate Acting Insulin (cloudy) - Non Protamine Hagedorn Insulin (NPH)- Peak action is 8 16 hours 3. Long Acting Insulin (cloudy) - Ultra Lente- Peak action is 16 24 hours

C. Nursing Management for Insulin Injections 1. Administer at room temperature to prevent development of lipodystrophy
(atrophy, hypertrophy of subcutaneous tissues)

2. Place in refrigerator once opened 3. Avoid shaking insulin vial vigorously instead gently roll vial between palm
to prevent formation of bubbles

4. Use gauge 25 26 needle 5. Administer insulin either 45o 90o


depending on amount of clients tissue deposit

6. No need to aspirate upon injection 7. Rotate insulin injection sites to prevent development of lipodystrophy 8. Most accessible route is abdomen 9. When mixing 2 types of insulin aspirate first the clear insulin before 10. Monitor for signs of local complications such as a. Allergic reactions b. Lipodystrophyc.

cloudy to prevent contaminating theclear insulin and promote proper calibration.

Somogyi Phenomenon rebound effect of insulin characterized by hypoglycemia tohyperglycemia ORAL HYPOGLYCEMIC AGENTS - Stimulates the pancreas to secrete insulin

A. Classsification1. First Generation Sulfonylureas a. Chlorpropamide (Diabenase) b. Tolbutamide (Orinase) c. Tolamazide (Tolinase) 2. Second Generation Sulfonylureas a. Glipzide (Glucotrol) b. Diabeta (Micronase)

HISTOPLASMOSIS
Acute fungal infection caused by inhalation of contaminated dust or particles with histoplasma capsulatum derived from birds manure.

A. Signs and Symptoms


PTB or Pneumonia like 1. Productive cough 2. Dyspnea 3. Fever, chills, anorexia, general body malaise 4. Cyanosis 5. Hemoptysis 6. Chest and joint pains

B. Diagnostic Procedures
1. Histoplasmin Skin Test positive 2. ABG analysis PO2 decrease C. Nursing Management 1. Enforce CBR 2. Administer oxygen inhalation

3. Administer medications as ordered a. Antifungal- Amphotericin B- Fungizone (Nephrotoxicity, check for BUN and Creatinine, Hypokalemia) b. Steroids c. Mucolyticsd. Antipyretics 4. Force fluids to liquefy secretions 5. Nebulize and suction as needed 6. Prevent complications bronchiectasis 7. Prevent the spread of infection by spraying of breeding places

COPD (Chronic Obstructive Pulmonary/Lung Disease)Chronic Bronchitis


Inflammation of bronchus resulting to hypertrophy or hyperplasia of goblet mucous producing cells leading to narrowing of smaller airways

A. Predisposing Factors
1. Smoking 2. Air pollution

B. Signs and Symptoms


1. Productive cough (consistent to all COPD) 2. Dyspnea on exertion 3. Prolonged expiratory grunt 4. Anorexia and generalized body malaise 5. Scattered rales/ronchi 6. Cyanosis 7. Pulmonary hypertension a. Peripheral edema b. Cor Pulmonale(right ventricular hypertrophy)

C. Diagnostic Procedure
ABG analysis reveals PO2decrease (hypoxemia), PCO2increase, pH decrease

Bronchial Asthma
Reversible inflammatory lung condition due to hypersensitivity to allergens leading to narrowing of smaller airways.

A. Predisposing Factors (Depending on Types)


1. Extrinsic Asthma ( Atopic/ Allergic ) Causes a. Pollen b. Dust c. Fumes d. Smoke e. Gases f. Danders g. Fursh. Lints 2. Intrinsic Asthma (Non atopic/Non allergic) Causes a. Hereditary b. Drugs (aspirin, penicillin, beta blocker) c. Foods (seafoods, eggs, milk, chocolates, chicken d. Food additives (nitrates) e. Sudden change in temperature, air pressure and humidity f. Physical and emotional stress 3. Mixed Type 90 95%

B. Signs and Symptoms


1. Cough that is non productive 2. Dyspnea 3. Wheezing on expiration 4. Cyanosis 5. Mild Stress/apprehension 6. Tachycardia, palpitations 7. Diaphoresis

C. Diagnostic Procedure
1. Pulmonary Function Test- Incentive spirometer reveals decrease vital lung capacity 2. ABG analysis PO2 decrease- Before ABG test for positive Allens Test, apply direct pressure to ulnar and radial artery to determine presence of collateral circulation

D. Nursing Management
1. Enforce CBR 2. Oxygen inhalation, with low inflow of 2 3 L/min 3. Administer medications as ordered a. Bronchodilators given via inhalation or metered dose inhaler or MDI for 5 minutes. b. Steroids decrease inflammation

c. Mucomysts (acetylceisteine) d. Mucolytics/expectorants e. Anti histamine 4. Force fluids 5. Semi fowlers position 6. Nebulize and suction when needed 7. Provide client health teachings and discharge planning concerning a. Avoidance of precipitating factor b. Prevent complications- Emphysema- Status Asthmaticus (give drug of choice)- Epinephrine- Steroids- Bronchodilators c. Regular adherence to medications to prevent development of status asthmaticus d. Importance of follow up care

BRONCHIECTASIS
Abnormal permanent dilation of bronchus leading to destruction of muscular and elastic tissues of alveoli

A. Predisposing Factors
1. Recurrent lower respiratory tract infections 2. Chest trauma 3. Congenital defects 4. Related to presence of tumor

B. Signs and Symptoms


1. Productive cough 2. Dyspnea 3. Cyanosis 4. Anorexia and generalized body malaise 5. Hemoptysis (only COPD with sign)

C. Diagnostic Procedure
1. ABG PO2 decrease 2. Bronchoscopy direct visualization of bronchus using fiberscope Nursing Management PRE Bronchoscopy 1. Secure inform consent and explain procedure to client 2. Maintain NPO 6 8 hours prior to procedure 3. Monitor vital signs and breath sound POST Bronchoscopy 1. Feeding initiated upon return of gag reflex 2. Avoid talking, coughing and smoking, may cause irritation 3. Monitor for signs of gross 4. Monitor for signs of laryngeal spasm prepare tracheostomy set

D. Treatment
1. Surgery (pneumonectomy , 1 lung is removed and position on affected side) 2. Segmental Wedge Lobectomy (promote re expansion of lungs)- Unaffected lobectomy facilitate drainage

EMPHYSEMA
Irreversible terminal stage of COPD characterized by a. Inelasticity of alveoli b. Air trapping c. Maldistribution of gases d. Over distention of thoracic cavity (barrel chest)

A. Predisposing Factors
1. Smoking 2. Air pollution 3. Allergy 4. High risk: elderly 5. Hereditary it involves deficiency of ALPHA-1 ANTI TRYPSIN (needed to form Elastase, for recoil of alveoli)

B. Signs and Symptoms


1. Productive cough 2. Dyspnea at rest 3. Prolong expiratory grunt 4. Anorexia and generalized body malaise 5. Resonance to hyperresonance 6. Decrease tactile fremitus 7. Decrease or diminished breath sounds 8. Rales or ronchi 9. Bronchial wheezing 10. Barrel chest 11. Flaring of alai nares 12. Purse lip breathing to eliminates excess CO2 (compensatory mechanism)

C. Diagnostic Procedure
1. Pulmonary Function Test reveals decrease vital lung capacity 2. ABG analysis reveals a. Panlobular/ centrilobular - Decrease PO2 (hypoxemia leading to chronic bronchitis, Blue Bloaters)- Decrease ph- Increase PCO2- Respiratory acidosis b. Panacinar/ centriacinar - Increase PO2 (hyperaxemia, Pink Puffers) Decrease PCO2 - Increase ph- Respiratory alkalosis

D. Nursing Management
1. Enforce CBR 2. Administer oxygen inhalation via low inflow 3. Administer medications as ordered a. Bronchodilators b. Steroids c. Antibiotics d. Mucolytics /expectorants 4. High fowlers position 5. Force fluids 6. Institute pulmonary toilet 7. Nebulize and suction when needed 8. Institute PEEP (positive end expiratory pressure) in mechanical ventilation promotes maximum alveolar lung expansion 9. Provide comfortable and humid environment 10. Provide high carbohydrates, protein, calories, vitamins and minerals 11. Health teachings and discharge planning concerning a. Avoid smoking b. Prevent complications- Atelectasis- Cor Pulmonale- CO2 narcosis may lead to coma- Pneumothorax c. Strict compliance to medication d. Importance of follow up care

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