1. Monitor ABGs PO2 > 80 mm Hg; PCO2 35-45 mm Hg; HCO3 21-28 mEq/L; pH 7.35-7.45 2. Chronic bronchi- tis Airway destruction Chronic sputum with
... [Show More] cough production on a daily basis for a minimum of 3 months in 2 consecutive years Reduced responsiveness of respiratory center to hypox- emia stimuli Precipitating factor: higher incidence in smokers "Blue bloaters" - generalized cyanosis of lips, mucous membranes, face, and nail beds Right-sided heart failure (distended neck veins, crackles) Lowest FiO2 possible to prevent CO2 retention Monitor for fluid overload Maintain PO2 between 55 and 60 Administer bronchodilators and anti-inflammatory agents 3. Emphysema Alveoli destruction Increased air trapping (increased AP diameter) Increased work, increased O2 consumption Precipitating factor: cigarette smoking "Pink puffers" Barrel chest, pursed-lip breathing, wheezing Lowest FiO2 possible to prevent CO2 retention Administer bronchodilators and anti-inflammatory agents Teach prolonged expiratory phase to clear trapped air 4. Asthma Unlike COPD, asthma is an intermittent disease with re- versible airflow obstruction and wheezing 5. COPD Emphysema and chronic bronchitis Characterized by bronchospasm and dyspnea Compensation occurs over time in clients with chronic lung disease and ABGs are altered The amount of O2 in the blood decreased (hypoxemia) and the amount of CO2 in the blood increases (hypercap- nia) causing chronic respiratory acidosis, which results in metabolic alkalosis as compensation 6. Clients at risk for pneumonia 7. Adrenergics and sympathomimet- ics Altered LOC Depressed or absent gag and cough reflexes Susceptible to aspirating oropharyngeal secretions (alco- holics, anesthetized individuals) Brain injury Drug overdose Stroke victims Immunocompromised Epinephrine; Albuterol (Proventil); Terbutaline (Brethine); Salmeterol (Serevent); Metaproterenol (Alupent); Lev- abuterol (Xopenex) Bronchodilation Adverse reactions: anxiety, increased HR, N/V, urinary retention 8. Methylxanthine Aminophylline (IV); Theophylline (PO) Bronchodilation Adverse reactions: hyperactivity, tachycardia, sleepless- ness, cardiac dysrhythmias Monitor therapeutic range Crosses placenta 9. Corticosteroids Prednisone (PO); Solu-Medrol (IV); Budesonide (Pulmi- cort); Fluticasone (Flovent); Triamcinolone (Azmacort) Anti-inflammatory Encourage oral care after use 10. Anticholinergics Ipratropium (Atrovent); Tiotropium (Spiriva) Bronchodilator; control of rhinorrhea Adverse reactions: dry mouth, blurred visions, cough 11. O2 delivery O2 must be humidified if given at >4 L/min or delivered directly to the trachea 12. Tuberculosis Airborne precautions***** Symptoms: fever with night sweats, anorexia, weight loss, malaise, fatigue, cough, hemoptysis, dyspnea, pleuritic chest pain with inspiration, positive sputum culture, re- peated upper respiratory infection Client may return to work after 3 negative sputum cul- tures Place client in respiratory isolation while hospitalized (mask for anyone entering room; private room; client wears mask if leaving room) Isoniazid (INH): metabolism primarily by liver and excre- tion by kidneys; increased phenytoin (Dilantin) levels Rifampin (Rifadin): used in conjugation with at least one other antitubercular agent; suppression of effect of birth control fills; orange body secretions; increases metabo- lism of digoxin and oral hypoglycemics Ethambutol: vision check before starting therapy and monthly thereafter Pyrazinamide Rifapentine 13. Chest tubes Used to remove or drain blood or air from the intrapleural space, to expand the lung after surgery, or to restore subatmospheric pressure to the thoracic cavity Keep all tubing coiled loosely below chest level Observe for air bubbling in the water seal chamber and fluctuations (tidaling) Do not strip or milk chest tubes Chest tubes are not clamped routinely. If the drainage system breaks, place the distal end of the chest tubing connection in a sterile water container at a 2-cm level as an emergency water seal If the chest tube is accidentally removed from the client, the nurse should cover with a dry sterile dressing Fluctuations (tidaling) in the fluid will occur if there is no external suction. These fluctuating movements are a good indicator that the system is intact; they should move upward with each inspiration and downward with each expiration. If fluctuations cease, check for kinked tubing, accumulation of fluid in the tubing, occlusions, or change in the client's position, because expanding lung tissue may be occluding the tube opening. When external suction is applied, the fluctuations cease. 14. Ineffective breathing pattern 15. Daily urine out- put 16. Acute renal fail- ure (ARF)/ acute kidney injury (AKI) Inability of air sacs to fill and empty properly (emphysema, cystic fibrosis) Obstruction of the air passages (carcinoma, asthma, chronic bronchitis) Accumulation of fluid in the air sacs (pneumonia) Respiratory muscle fatigue (COPD, pneumonia) 1 mL per kg per hour Total daily UO: 1,500-2,000 mL Occurs when metabolites accumulate in the body and urinary output changes - may be reversible! Sodium and chloride are the primary extracellular ions; potassium and phosphate are the primary intracellular ions History of taking nephrotoxic drugs (salicylates, antibi- otics, NSAIDs, ACE inhibitors, ARBs) Oliguric phase: increased BUN/creatinine; hyperkalemia; hyponatremia; acidosis; fluid overload; high urine specific gravity Diuretic phase: decreased fluid volume; hypokalemia; fur- ther hyponatremia; low urine specific gravity Monitor I&Os - give only enough fluids in oliguric phase to replace the losses (usually 400-500 mL/24 hr) Body weight is a good indicator of fluid retention and renal status***** Provide low protein, moderate fat, high carbohydrate diet 17. Hyperkalemia Dizziness, weakness, cardiac irregularities, muscle cramps, diarrhea, and nausea Sodium polystyrene (Kayexalate) may be prescribed if potassium is too high 18. Hypokalemia Dry mouth, thirst, weakness, drowsiness, lethargy, mus- cle aches, and tachycardia 19. End stage renal disease (ESRD) Progressive, irreversible damage to the nephrons and glomeruli, resulting in uremia Accumulation of waste products from protein metabolism is the primary cause of uremia - protein must be restricted in ESRD clients****** However, if protein intake is inadequate, a negative nitro- gen balance occurs, causing muscle wasting Labs: azotemia; increased creatinine/BUN; decreased calcium (function of the kidney to reabsorb calcium); el- evated phosphorus and magnesium (decreased calcium = increased phosphorus); anemia Provide a low protein, low sodium, low potassium, low phosphate, high calorie diet Administer phosphate binders with food because client is unable to excrete phosphates No magnesium-based antacids Monitor for fluid overload Admister erythropoietin (Epogen) to treat anemia (due to decreased production of erythropoietin in ESRD); do not shake vial (shaking may inactivate the glycoprotein) Beware of digoxin toxicity (excreted by the kidneys) 20. Digoxin toxicity N/V, anorexia, visual disturbances, restlessness, headache, cardiac dysrhythmias, pulse < 60 bpm 0.8 - 2.0 ng/mL 21. Urinary tract in- fection 22. Urinary tract ob- struction (renal calculi) 23. Transurethral re- section of the prostate (TURP) Consume oral fluids up to 3 L/day Avoid urinary tract irritants such as alcohol, sodas, citrus juices, and spices Administer narcotic analgesics Apply moist heat to the painful area High oral fluid intake will help dislodge the stone Strain all urine and send stones to lab for analysis**** most important intervention Bladder spasms frequently occur after TURP Inform client that the presence of the oversized balloon on the catheter (30 to 45 mL inflated) will cause a continuous feeling of needing to void. The client should not try to void around the catheter because this can precipitate bladder spasms Administer antispasmodics Check the urinary drainage system for clots Use only sterile saline for bladder irrigation after TURP because the irrigation must be isotonic to prevent fluid and electrolyte imbalance Urine should progress to clear yellow by the fourth day 24. Cholesterol Total < 200 mg/dL LDL < 100 mg/dL HDL > 60 mg/dL Triglycerides < 150 mg/dL 25. Angina EKG will show ST-segment depression and T-wave inver- sion during an attack Sexual activity may be resume after exercise is tolerated, usually when able to climb two flights of stairs without exertion 26. Antianginals Nitrates: nitroglycerin (NTG), isosorbide dinitrate (Isor- dil), isosorbide mononitrate (Imdur); anginal prophylaxis, acute attack; adverse effects include headache, flushing, dizziness, weakness, hypotension, and nausea; protect medication from light Beta blockers: propranolol HCl (Inderal), Atenolol (Tenormin), nadolol (Corgard), metoprolol (Toprol); angi- nal prophylaxis; monitor apical heart rate; do not stop medication abruptly; clients with HF, bronchitis, asthma, COPD or renal insufficiency have adverse reactions Calcium channel blockers: Verapamil, Procardia, Cardizem; anginal prophylaxis; monitor serum potassium; do not stop abruptly; adverse effects include dizziness hypotension, headache, syncope, hypokalemia, HF, and dysrhythmias 27. Antilipemics Bile sequestrants: bind to lipids and eliminate in stool; alteration in absorption of other oral medications HMG-CoA reductase inhibitors ("statins"): block the pro- duction of cholesterol in the liver; may elevate liver en- zymes Fibric acid derivatives: obtain baseline labs (liver function, CBC, electrolytes) every 3-6 months Water-soluble vitamins: decrease lipoprotein and triglyc- eride synthesis and increase HDL; give with milk or food to avoid GI irritation; hepatotoxicity with extended release forms 28. Myocardial in- Differs from anginal pain in its sudden onset; pain is farction (MI) unrelieved by nitroglycerin Serum cardiac markers: creatine kinase (CK) rises 3-12 hours after MI; troponin rises 3-12 hours after MI; CK-MB (recognized indicator of MI by most clinicians) onset 4-8 hours after MI EKG changes occur as early as 2 hours post-MI IV morphine sulfate acts as a peripheral vasodilator and decreases venous return Administer thrombolytic/ fibrinolytic agents within 1 to 4 hours of MI, but not more than 12 hours of MI 29. Stroke The number one cause of a stroke in hypertensive clients is noncompliance with medication regimen. Studies have shown that the more clients know about their hyperten- sion medications, the more likely they are to take it. 30. Diuretics Thiazide: useful in severe HTN; observe for postural hy- potension; administer potassium supplements Loop: furosemide (Lasix); rapid action, causes volume depletion; adverse effects include hypokalemia, hyper- uricemia, glucose intolerance, hypercholesterolemia, and sexual dysfunction Potassium-sparing: spironolactone (Aldactone); volume depletion without significant potassium loss; adverse ef- fects include hyperkalemia and renal failure in those treat- ed with ACE inhibitors or NSAIDs 31. Antihyperten- Alpha-adrenergic blockers: Minipress, Cardura; used as sives peripheral dilator that acts directly on the blood vessels Combined alpha/beta blockers: carvedilol (Coreg); pro- duces decrease in BP without reflex tachycardia or brady- cardia; CI with HF, heart block, COPD, and asthma Beta blockers ("lol"): block the sympathetic nervous sys- tem, especially to the heart, produces a slower heart rate, lowers blood pressure, reduces O2 consumption 32. Peripheral vas- cular disease // Arterial during myocardial contraction; adverse reactions include bradycardia; check apical pulse daily, do not discontinue abruptly, monitor for shortness of breath and give cau- tiously with bronchospasm, CI with asthma Central-acting inhibitors: Catapres, Aldomet; decreases BP by stimulating central alpha receptors, resulting in decreased sympathetic outflow from the brain; monitor for rebound HTN if abruptly discontinued Vasodilators: hydralazine HCl (Apresoline); decreases BP by decreasing peripheral resistance; adverse effects in- clude headache, tachycardia, and fluid retention Angiotensin II receptor blockers ("sartans"): blocks the vasoconstrictor and aldosterone-producing effects of an- giotensin II in vascular smooth muscle Angiotensin-converting enzyme (ACE) inhibitors ("pril"): decreases BP by suppressing renin-angiotensin aldos- terone system and inhibiting conversion of angiotensin I into angiotensin II; useful with clients diagnosed with diabetes; observe for acute renal failure, routine renal function tests Calcium channel blockers (CCB): inhibit calcium ion in- flux during cardiac depolarization, decreases SA/AV node conduction; avoid grapefruit juice with these drugs (in- creases serum levels, resulting in hypotension)*** Predisposing factors: arteriosclerosis, advanced age, Raynaud disease, Buerger disease, diabetes, acute oc- clusion Skin: smooth, shiny, loss of hair, thickened nails, dry, thin, cool Decreased or absent pulses Sharp pain that increases with walking and elevation Intermittent claudication relieved by rest Ulcers: very painful, small but deep, circular in shape, not edematous Treatment: elimination of smoking***, topical antibiotics, saline dressing, and bed rest Change positions frequently, wear non-restrictive cloth- 33. Peripheral vas- cular disease // Venous ing, avoid crossing legs or keeping legs in a dependent position, wear shoes Predisposing factors: history of DVT, valvular incompe- tence, varicose veins, thrombophlebitis, venous stasis ulcers Skin: warm, cyanotic when dependent Normal pulses Persistent, aching, full feeling, dull sensation Relieved when horizontal, nocturnal cramps Ulcers: weeping, uneven edges, superficial but large, marked edema, slightly painful Treatment: systemic antibiotics, compression dressing, limb elevation, fibrinolytic agents and anticoagulants for thrombosis Change positions frequently, wear non-restrictive cloth- ing, avoid crossing legs or keeping legs in a dependent position, wear shoes 34. Anticoagulants Heparin sodium: avoid IM injection (can be given SQ or IV), assess stools for occult blood, asses PTT to deter- mine efficacy; antagonist - protamine sulfate Warfarin sodium (Coumadin): given orally, assess PT to determine efficacy, avoid sudden change in intake of foods; antagonist - vitamin K Low-molecular weight heparins (Lovenox): prevention of thrombolytic formation Advise client to wear medical alert symbol, avoid aspirin/ NSAIDs, avoid safety razors, and elevate extremity 35. Abdominal aortic aneurysm Most common symptom is abdominal pain or low back pain, with the complaint that the client can feel his or her heart beating Abdominal radiograph to confirm Symptoms of rupture: hypovolemic or cardiogenic shock with sudden, severe abdominal pain Assess peripheral pulses frequently 36. Dysrhythmias Causes: drugs, acid-base and electrolyte imbalances, marked thermal changes, disease and trauma, and stress Determine serum electrolyte levels, especially K+ and Mg++ Atrial fibrillation: chaotic activity in the AV node, no true P wave visible, irregular ventricular rhythm; anticoagulant therapy to decrease risk for stroke, antidysrhythmic drugs, cardioversion Atrial flutter: saw-toothed waveform***, fluttering in chest, ventricular rhythm stays regular; cardioversion Ventricular tachycardia: synchronized cardioversion if pulse present (if no pulse, treat as ventricular fibrillation) Ventricular fibrillation: cardiac emergency! No cardiac output; defibrillate as quickly as possible Premature ventricular contractions (PVC): a contraction originating in an ectopic focus in the ventricles, wide and distorted in shape 37. Pacemaker Instruct client to report pulse rate lower than set rate, avoid leaning over an automobile with the engine running, stand 4 to 5 feet away from electromagnetic sources (operating microwave overs), avoid MRI testing 38. Digoxin (Lanox- in) Indications: HF Increases the contractility of cardiac muscle, slows heart rate and conduction (chronotropic effect) Therapeutic range: 0.5-2.0 mg Check apical pulse for one full minute before adminis- tering and hold if below 60 bpm and notify healthcare provider Hypokalemia increases the risk for toxicity Antidote - Digibind 39. Epinephrine (adrenaline) Indications: cardiac arrest 40. Left-sided HF Results in pulmonary congestion due to the inability of the left ventricle to pump blood to the periphery Symptoms: dyspnea, "wet" lung sounds, cough, fatigue, tachycardia bed, and low-dose heparin therapy Fractures of long bones predispose the client to anemia - monitor hematocrit levels 79. Joint replace- INFECTION is the main concern postoperatively ment Joint pathology: OA, RA, fracture Pain unrelieved by medication Poor ROM in the affected joint A suction drainage device usually accompanies the client to the postoperative floor - check drainage often Monitor functioning of the extremity (circulation, sensa- tion, movement) Provide proper alignment of the affected extremity Get client out of bed as soon as possible Do not flex the hip more than 90 degrees (hip replace- ment)*** Instruct the client not to lift the leg upward from a lying position or to elevate the knee when sitting after a hip replacement 80. Amputation Causes: PVD (clients with diabetes), trauma, congenital deformities, malignant tumors, infection Position client to relieve edema and spasms at residual limb (stump) site: elevate stump for the first 24 hours postoperatively Do not elevate the stump after 48 hours postoperatively Keep stump in extended position and turn client to prone position three times a day to prevent hip flexion contrac- ture Provide passive ROM until client is able to perform active ROM 81. Glaucoma Chronic open-angle glaucoma, also known as primary open-angle glaucoma, is a condition characterized by increased intraocular pressure (IOP), involving a gradual, painless loss of vision IOP > 22 mm Hg Can lead to BLINDNESS if left untreated Aqueous fluid is inadequately drained from the eye Generally ASYMPTOMATIC in early stages Late signs include loss of peripheral vision, seeing halos around lights, decreased visiual acuity not correctable with glasses, headache or eye pain that may cause N/V Tonometer measures IOP Gonioscope obtains direct visualization of the lens Glaucoma is a SIDE EFFECT of many medications (an- tihistamines, anticholinergics) Administer eye drops as prescribed to cause pupil con- striction allowing aqueous humor to flow out PILOCARPINE is commonly used*** Caution the client that vision may be blurred for 1 to 2 hours after administration of pilocarpine and that adap- tation to dark environments may be difficult due to pupil constriction*** Vision already lost cannot be restored Eye drops are needed for the rest of life Avoid activities that may increase IOP 82. Cataracts Condition characterized by opacity of the lens Aging accounts for 95% of cases Leading cause of blindness in the world Surgical removal is done when vision impairment inter- feres with daily activities; intraocular lens implants may be used Operation is performed under local anesthesia on an outpatient basis Symptoms include blurred vision, decreased color per- ception, photophobia, diplopia, deduced visual acuity (progressing to blindness), clouded pupil, progressing to milky-white appearance Postoperative teaching should include teaching that glasses or shaded lens should be worn during waking hours and an eye shield should be worn during sleep; avoid any activity that increases IOP; avoid lying on oper- ative side; keep water from getting into eye while shower- ing 83. Eye trauma Explain that an eye patch may be applied to rest the eye; reading and watching TV may be restricted for 3 to 5 days Report a sudden increase in eye pain 84. Detached retina Hole or tear in, or separation of the sensory retina from, the pigmented epithelium Resealing done by surgery Administer medication to inhibit accommodation and con- striction - cycloplegics (mydriatics and homatropine) are given to dilate pupil before surgery 85. Hearing loss Conductive hearing loss: sound does not travel well to the sound organs of the inner ear; if volume is raised, hearing is normal; usually results from cerumen (wax) impaction or middle ear disorders such as otitis media Sensorineural hearing loss: sound passes properly through the outer and middle ear but is distorted by a defect in the inner ear or damage to cranial nerve VIII, or both; common causes include infections, ototoxic drugs, trauma, neuromas, noise, and aging; it involves perceptu- al loss, usually progressive and BILATERAL; it is detected by tuning fork When communicating with client, speak in a LOW-PITCHED voice, slowly and distinctly 86. Glasgow coma scale (GCS) Maximum total is 15; minimum is 3 A score of 7 or less indicates coma*** Eye opening (spontaneous, to verbal command, to pain, no response) = 4 Motor response (to verbal command, to painful stimuli [localizes pain, flexes/withdraws, flexor posturing {decor- ticate}, extensor posturing {decerebrate}, no response]) = 6 87. Altered state of consciousness Verbal response (oriented and converses, disoriented and converses, uses inappropriate words, incomprehen- sible sound, no response) = 5 A client with an altered state of consciousness is fed via ENTERAL routes because the likelihood of aspiration is high with oral feedings The presence of 100 mL or more of residual in an adult indicates poor gastric emptying, and the feeding should be withheld Paralytic ileus is common in comatose clients; a gastric tube aids in gastric decompression Any client on bed rest or immobilized must have ROM ex- ercises every 4 hours and very frequent position changes - do not leave the client in any one position for longer than 2 hours; any position that decreases venous return, such as sitting with dependent extremities for long periods, is dangerous Position client for maximum ventilation: three quarters prone or semiprone position to prevent tongue from ob- structing airway, and slightly to one side with arms away from chest wall Tachycardia can indicate infection, thrombus formation, or dehydration Rising blood pressure or widening pulse pressure can indicate increase ICP If temperature elevates, take quick measures to decrease it because fever increases cerebral metabolism and can increase cerebral edema Restlessness may indicate a return to consciousness but can also indicate anoxia, distended bladder, covert bleed- ing, or increasing cerebral anoxia; do not oversedate, and report any symptoms of restlessness During all activities, tell the client what you are doing, regardless of the level of consciousness Rapid infusions of tube feedings may cause diarrhea; lack of fiber and inadequate fluids may cause constipation 88. Head injury Increased ICP is the main concern in TBI; it is related to edema, hemorrhage, impaired cerebral autoregulation, and hydrocephalus Symptoms of increased ICP include change in level of responsiveness, slowing of respirations, increase or de- crease in pulse, rising BP or widening PP, tempera- ture rise, headache, PROJECTILE VOMITING, pupillary changes, seizures, ataxia, abnormal posturing (decorti- cate or decerebrate), and CSF leakage through nose or ear Keep HOB elevated 30 to 45 degrees to aid venous return from the neck and to decrease cerebral volume Position client semiprone or lateral recumbent to prevent aspiration If temperature increase, take immediate measures to de- crease it (aspirin, acetaminophen, cooling blankets) When using intracranial monitoring, elevations of ICP over 20 mm Hg should be reported immediately Mannitol (Osmitrol) dehydrates the brain and reduces cerebral edema; use for SHORT-TERM therapy only; nev- er give to clients with cerebral hemorrhage; never give to clients with no urine output (ANURIA) - if output is < 30 mL/hr, accumulation can cause pulmonary edema and water intoxication Steroids (dexamethasone, methylprednisolone sodium succinate [Solu-Medrol]) are used to reduce brain edema Barbituates are used to reduce brain metabolism and systemic BP Avoid narcotics because they mask the level of con- sciousness*** Passive hyperventilation on ventilator leads to respirato- ry alkalosis, which causes cerebral vasoconstriction and decreased cerebral blood flow, therefore decreasing ICP 89. Spinal cord in- jury Injuries are described by location in the spinal cord Damage can range from contusion to complete transec- tion Permanent impairment cannot be determined until spinal cord edema has subsided, usually by 1 week Physical assessment should concentrate on respiratory status, especially in clients with injury at C3 to C5, be- cause the cervical plexus innervates the diaphragm Hypotension and bradycardia occur with any injury above T6 because sympathetic outflow is affected Maintain client in an extended position with cervical collar during any transfer High-dose corticosteriods are often given to help control edema during the first 8 to 24 hours Evaluate for spinal shock: a complete loss of all reflex, motor, sensory, and autonomic activity below the lesion; this is a medical emergency that occurs immediately after the injury! Symptoms include hypotension, bradycardia, complete paralysis, lack of sensation below lesion, blad- der and bowel distention Evaluate for autonomic dysreflexia: exaggerated auto- nomic responses to stimuli Suction with caution to prevent vagus nerve stimulation, which can cause cardiac arrest A common cause of death after spinal cord injury is UTI - bacteria grow best in alkaline media, so keep urine dilute and acidic 90. Brain tumor Without treatment, benign as well as malignant tumors lead to death Symptoms include headache that is more severe on awakening, vomiting not associated with nausea, pa- pilledema with visual changes, behavioral and personality changes, seizures, aphasia, hemiplegia, ataxia, cranial nerve dysfunction, and abnormal CT scan/ MRI Institute nursing interventions that are similar to those for increased ICP Elevate the HOB 30 to 45 degrees; maintain neutral head position Craniotomy preoperative medications: corticosteroids, osmotic diuretics (to reduce secretions), phenytoin, pro- phylactic antibiotics 91. Multiple sclero- sis (MS) 92. Myasthenia gravis (MG) Demyelinating disease resulting in the destruction of CNS myelin and consequent disruption in the transmission of nerve impulses Onset is insidious, with 50% of client still ambulatory 25 years after diagnosis Symptoms involving motor function usually begin in the upper extremities with weakness progressing to spastic paralysis; bowel and bladder dysfunction occurs in 90% of cases Progression is not "orderly" Symptoms include optic neuritis (loss of vision or blind spots), visual or swallowing difficulties, gait disturbances, intention tremors, unusual fatigue, weakness, numbness (particularly on one side of face), impaired B&B control, speech disturbances Teach client that for muscle spasticity, stretch-hold-relax exercises are helpful, as are riding a stationary bike and swimming; take precautions against falls As incontinence worsens, client may need to learn clean self-catheterization, condom catheter Administer steroid therapy and chemotherapeutic drugs in acute exacerbations to shorten length of attack: ACTH, cortisone, cyclophosphamide (Cytoxan), and other im- munosuppresive drugs Biologic response modifiers such as interferon-beta prod- ucts are successful with MS relapses Disorder affecting the neuromuscular transmission of im- pulses in the voluntary muscles of the body Autoimmune disease characterized by the presence of acetylcholine receptor antibodies, which interfere with neuronal transmission Symptoms include diplopia, ptosis, masklike affect (sleepy appearance due to facial muscle involvement), weakness of laryngeal and pharyngeal muscles (dyspha- gia, choking, food aspiration, difficulty speaking), muscle weakness improved by rest, respiratory failure, B&B in- continence Bed rest often relieves symptoms 93. Parkinson dis- ease Myasthenic crisis: associated with undermedication; in- crease in symptoms (more difficulty swallowing, diplopia, ptosis, dyspnea); positive Tensilon test Cholinergic crisis: associated with anticholinesterase overdosage; symptoms include diaphoresis, diarrhea, fasciculations, cramps, marked worsening of symptoms; negative Tensilon test In clients with MG, be alert for changes in RESPIRATORY STATUS Administer cholinergic drugs (pyridostigmine bromide [Mestinon]) to inhibit the action of cholinesterase at the cholinergic nerve endings; cholinergic crisis with over- dose Atropine is antidote for drug-induced bradycardia*** Chronic, progressive, debilitating neurologic disease of the basal ganglia, affecting motor ability and character- ized by tremor at rest, increased muscle tone (rigidity), slowness in the initiation and execution of movement (bradykinesia), and postural instability (difficulties with gait and balance) The pathophysiology involves an imbalance between acetylcholine and dopamine, so symptoms can be con- trolled by administering a dopamine precursor (levodopa) Symptoms include rigidity of extremities, MASKLIKE FA- CIAL EXPRESSIONS with associated difficulty in chew- ing, swallowing, and speaking, DROOLING, stooped posture and slow, shuffling gait, tremors at rest, "PILL-ROLLING" movement, emotional lability Focus on SAFETY*** Schedule activities later in the day to allow client to per- form self-care activities without feeling rushed Encourage activities and exercise Serve a soft diet, which is easy to swallow Administer antiparkinsonian drugs: anticholinergics (at- ropine sulfate, Cogentin); dopamine replacements (lev- odopa, Sinemet) Adverse effects of anticholinergic drugs include increased HR, postural hypotension, dry mouth, constipation, uri- 94. Guilain-Barre syndrome nary retention, and blurred vision; CI in narrow-angle glaucoma, urinary retention Clinical syndrome of unknown origin involving peripheral and cranial nerves Usually preceded by a VIRAL respiratory or GI infection 1 to 4 weeks prior to the onset of neurologic deficits Constant monitoring of these clients is required to prevent the life-threatening problem of acute respiratory failure*** Full recovery usually occurs within several months to a year after onset of symptoms About 30% of those diagnosed with Guilain-Barre are left with a residual disability Symptoms include paresthesia (numbness and tingling), muscle weakness of legs progressing to the upper ex- tremities, trunk, and face, paralysis of the ocular, facial, and oropharyngeal muscles, causing marked difficulty in talking, chewing, and swallowing, increasing pulse rate and disturbances in rhythm, transient HTN, orthostatic hypotension, and weakness or paralysis of the intercostal and diaphragm muscles (may develop quickly) 95. Stroke Cerebral vascular accident (CVA)/ brain attack Sudden loss of brain function resulting from a disruption in the blood supply to a part of the brain; classified as thrombotic or hemorrhagic Atrial fibrillation and atrial flutter produce a high incidence of thrombus formation, following dysrhythmia caused by turbulence of blood flow through all valves and heart chambers*** Presenting symptoms relate to the specific area of the brain that has been damaged Generally, motor loss exhibited as hemiparesis or hemi- plegia, communication loss, perceptual disturbances, and impaired mental acuity Left hemisphere: aphasia, agraphia, unable to discrimi- nate words and letters, reading problems, deficits in right visual field, slow, cautious behavior, anxious when at- tempting new tasks, depression, quick anger and frustra- tion Right hemisphere: disoriented memory, cannot recognize faces, visual/spacial deficits, neglect of left visual field, loss of depth perception, impulsive, unaware of neuro- logical deficits, euphoric, denies illness, overestimates abilities, loses ability to hear tonal variations Rehabilitation is begun as soon as the client is stable The quicker movement is recovered, the better the prog- nosis is for full or improved recovery Assess functional abilities (mobility, ADLs, elimination, communication) Risk for falls, risk for aspiration*** Control HTN to prevent further stroke Reassure client that bladder control tends to be regained quickly Reassure client that regaining speech is a very slow process Teach that swallowing modifications may include a soft diet (pureed foods, thickened liquids) and head position- ing Steroids are administered after a stroke to decrease cere- bra edema and retard permanent disability H2 inhibitors are administered to prevent peptic ulcers 96. Apraxia Inability to perform purposeful movements in the absence of motor problems 97. Dysarthria Difficulty articulating 98. Dysphasia Impairment of speech and verbal comprehension; difficul- ty swallowing 99. Aphasia Loss of the ability to speak 100. Agraphia Loss of the ability to write 101. Alexia Loss of the ability to read 102. Anemia Diet lacking in IRON (red meats, organ meats, spinach), FOLATE (green vegetables, liver, citrus fruits), and/or VITAMIN B12 (glandular meats, yeast, green leafy veg- etables, milk, cheese) Family history of genetic disease such as sickle cell or congenital hemolytic anemia Medication history of anemia-producing drugs, such as salicylates, thiazides, and diuretics Hgb < 10 g/dL Hct < 36% RBCs < 4 x 10^12 Administer blood products Instruct in food selection and need for vitamin supplemen- tation Take iron on an empty stomach and with vitamin C to enhance absorption Give liquid iron through a straw to prevent staining of teeth Clients with pernicious anemia should receive vitamin B12 parenterally 103. Administration of iron Use Z-track method*** (to prevent staining the skin) Do not use deltoid muscle Do not massage injection site [Show Less]