ACUTE BIOLOGIC CRISIS

ROWELL G. TRINIDAD, RN

OBJECTIVES

OBJECTIVES
On completion of this concept, the students will be able to: 1. Compare and contrast a termed neonate from a preterm neonate. 2. Use the nursing process as a framework for the care of a preterm neonate.

OBJECTIVES
3. Explain cardiac physiology in relation to cardiac anatomy and the conduction system of the heart. 4. Identify the clinical significance and related nursing implications of the various tests and procedure used for diagnostic assessment of patients with Myocardial Infarction and arrythmias.

OBJECTIVES
5. Describe diagnostic tests used for assessment of suspected neurologic disorders and related nursing implications. 6. Use the nursing process as a framework for care of the patient with endocrine disorders.

CONCEPT OUTLINE .

CONCEPT OUTLINE I Prematurity a. Physiologic handicaps of premature d. Review of the characteristics of a termed neonate b. Termed versus Premature neonate c. Sudden Infant Death Syndrome (SIDS) II Cardiac Disorders .

Review of the structure and function of the heart.Diagnostic examination . Cardiogenic Shock .CONCEPT OUTLINE a.Management c. Myocardial Infarction .Types . b.

CONCEPT OUTLINE d. Arrhythmia . Review of the different glands b.Management III Endocrine Disorders a. Addison s disease .Symptoms .Types .

Diabetes mellitus e. Hyperthyroidism -Acute hyperthyroidism -Chronic hyperthyroidism IV Neurologic Disorders . Liver cirrhosis f.CONCEPT OUTLINE c. Cushing s syndrome d.

Adult Respiratory Distress Syndrome .CONCEPT OUTLINE a. Increased Intracranial Pressure c. Myasthenia Gravis b. Spinal Cord Injury d.

PREMATURITY .

PREMATURITY Termed Neonate birth between the thirtythirty-eighth and forty-second week of fortygestation. . Preterm (Premature) birth at less than 36 week s gestation. regardless of weight.

2. Body is normally pink with slight cyanosis of hands and feet (acrocyanosis) 3.PREMATURITY Characteristics of a TERM infant: 1. Heart rate is rapid and regular (120 to 180 beats per minute) . Appropriate for gestational age (AGA) weight falls between 10th and 19th percentile for age.

Fine. Head and chest circumference nearly equal with chest slightly smaller than head.PREMATURITY 4. 5. Respirations are abdominal and irregular with a rate of 30 to 56 breaths per minute. downy hair growth over the entire body. . 6.

2 degrees Celsius or 36. Temperature maintained at 36. 8.6 degrees Celcius.PREMATURITY 7. .fats and proteins readily. environmental factors may affect temperature. Digest simple carbohydrates .

Enlargement of breasts in males (gynecomastia) and females is normal as a result of hormones transmitted to infant by mother 10.PREMATURITY 9. Initial weight loss of 5% to 10% of birth weight is normal and usually regained by tenth day of life. .

eyebrows are absent. blood vessels and bony structures are visible). lanugo present on face. .PREMATURITY Characteristics of a PRETERM infant: 1. Less subcutaneous fat (wrinkled skin. 2. ears are poorly supported by cartilage. the fontanels are small and bones are soft. Circumference of the head is large in comparison with the chest. breast buds size is small with underdeveloped nipples.

random movements are common with slightest stimulus. HARLEQUIN sign is present. Posture is one of complete relaxation with marked extension of the legs and abduction of the hips. . 4. Skin color changes when infant is moved.PREMATURITY 3.

heat loss caused by large skin surface area and lack of subcutaneous and brown fat. Heat regulation poorly developed because of immaturity of CNS.poorly developed respiratory center with diminished oxygen consumption causing asphyxia. . . .PREMATURITY 5.weak heart action. .

6. .PREMATURITY .insufficient heat production caused by inadequate metabolism. retraction at xiphoid process is evidence of air hunger. Respirations are not efficient because of muscle weakness of lungs and rib cage and limited surfactant production.

rapid & irregular respirations. 8. . intercostal or suprasternal retractions. Greater tendency toward capillary fragility. Atelectasis can occur. grunting on expiration. manifested by: cyanosis that decreases with crying. flaring of nostrils.PREMATURITY 7. red and white blood cell counts are low with resulting anemia during first few months of life.

Higher incidence of intracranial hemorrhage. abnormal respirations. small capacity of stomach. manifested by muscle twitching. cyanosis. . shrill cry. 10. and a short. slow emptying time of the stomach. convulsions. Weak sucking and swallowing reflexes. low gastric acidity.PREMATURITY 9.

Reduced glomerular filtration rate results in decreased ability to concentrate urine and conserve fluid. Respiratory rate and effort. Nursing Care of Preterm infants: 1. Oxygen concentrations by pulse oximeter . blood pressure. heart rate. 2.PREMATURITY 11. temperature.

nutritional status 6. Daily weight. Skin color and integrity 4. Parents ability to cope with preterm birth . Ability of infant to suck.PREMATURITY 3. fluid and electrolyte status 5.

Risk for aspiration 2. Inability to sustain spontaneous ventilation 4. Hypothermia 5. Impaired gas exchange 3. Altered nutrition: less than body requirements . Risk for infection 6.PREMATURITY Nursing Diagnosis: 1.

. Maintain airway. 2. Observe for changes in respiration.PREMATURITY Nursing Management: 1. position to promote ventilation. check respirator function if used. maintain temperature of environment. suction when necessary. color and vital signs.

Check efficacy of Isolette: maintain heat. administer oxygen if necessary. 4. monitor oxygen carefully to prevent retinopathy of the newborn. humidity and oxygen concentrations. Maintain aseptic technique to prevent infection .PREMATURITY 3.

6. Institute phototherapy should hyperbilirubinemia occur. Observe weight-gain patterns. 8. . Determine blood gases frequently to prevent acidosis. Adhere to the techniques of gavage feeding for safety of infant. weight7.PREMATURITY 5.

. Support parents by letting them verbalize and ask questions to relieve anxiety.PREMATURITY 9. 10. 11. Arrange follow-up before and after followdischarge by a visiting nurse. allow them to participate in care. Provide liberal visiting hours for parents.

Maintains body temperature within acceptable limits 3.PREMATURITY Nursing Evaluation/Outcomes: 1. Remains free from infection 4. Gains weight . Maintains respiratory functioning 2.

SUDDEN INFANT DISTRESS SYNDROME (SIDS) .

.SUDDEN INFANT DISTRESS SYNDROME The sudden death of any infant or young child. and in which a thorough postmortem examination fails to demonstrate an adequate cause of death. It is the cessation of breathing for more than 20 seconds or a shorter episode associated with bradycardia. cyanosis or pallor.

95% occur by 6 months Pulmonary edema and intrathoracic hemorrhages found on autopsy. incidence of 1.SUDDEN INFANT DISTRESS SYNDROME The number one cause of death in infants between 1 month and 1 year of age.4 in every 1000 live births. . Peak age of occurrence: healthy infants 2 to 4 months of age .

Apnea related to organic disorders: a. Gastroesophageal reflux c. Sepsis. Significant anemia d. 2.SUDDEN INFANT DISTRESS SYNDROME Etiology: 1. Seizure disorders b. severe infection . Unknown may result from many different pathologic processes.

Maternal cocaine abuse 3. High risk factors: a. Prematurity b. Impaired regulation of breathing g. History of SIDS in the family .SUDDEN INFANT DISTRESS SYNDROME e. Hypoglycemia f.

Infants sleeping on abdomen or on softer bedding. Low-birth weight: newborns with Lowlow APGAR score e. Males d. and sheepskin g. quilts. Infants with CNS disturbance f. Infants with respiratory disorders such as bronchopulmonary dysplasia . pillows.SUDDEN INFANT DISTRESS SYNDROME c. comforters.

substance abuse. Clinical Manifestations: 1. Sudden. Frothy. smoking during pregnancy. blood-tinged fluid fills mouth bloodand nose .SUDDEN INFANT DISTRESS SYNDROME h. unexplained death of an infant under 1 year of age 2. Maternal factors such as youth.

or neglect 2. . abuse. Support parents 3. Be nonjudgmental about parents attempts at resuscitation. Avoid implying wrongdoing.SUDDEN INFANT DISTRESS SYNDROME Therapeutic Interventions: 1.

Altered family processes 4. Parental support system Nursing Diagnosis: 1. Parental knowledge of SIDS 2.SUDDEN INFANT DISTRESS SYNDROME Nursing Assessment: 1. Family coping: potential for growth 2. Ineffective family coping: disabling 3. Dysfunctional grieving .

SUDDEN INFANT DISTRESS SYNDROME Nursing Intervention: 1. Reassure the parents that they could not have prevented the death or predicted its occurrence 3. Know signs of SIDS to distinguish it from child neglect or abuse. do or say nothing that instill guilt in the parents 2. Reinforce that an autopsy should be done on every child to confirm diagnosis .

Visit the parents at home to discuss the cause of death and help them with their guilt and grief. 5.SUDDEN INFANT DISTRESS SYNDROME 4. refer the parents to a national SIDS parent group .

Parents maintain supportive relationship with other children .SUDDEN INFANT DISTRESS SYNDROME Nursing Evaluation: 1. Family exhibits appropriate bereavement behavior 4. Family exhibits positive coping behavior 2. Family uses support services 3.

STRUCTURE & FUNCTION of the HEART .

STRUCTURE & FUNCTION of the HEART .

STRUCTURE & FUNCTION of the HEART Structure and function of the cardiovascular system: Heart is a hollow. muscular organ lies in the mediastinum and rests on the diaphragm. .

contains 20 to 30 ml. of serous fluid which protects the heart from trauma and friction. Pericardium a thin. outer parietal layer. Heart wall is a specialized muscle tissue consisting of three tissue layers: .STRUCTURE & FUNCTION of the HEART 1. membranous sac that encase the heart that has a visceral layer in contact with the heart and an layer. 2.

serous outer layer b. Heart Chambers a membranous muscular septum divides the heart into two distinct sides. Myocardium the thick. muscular middle layer c.STRUCTURE & FUNCTION of the HEART a. Endocardium the smooth inner layer that comes in contact with blood 3. . Epicardium the thin.

STRUCTURE & FUNCTION of the HEART .

STRUCTURE & FUNCTION of the HEART a. Right Ventricle c. Right Atrium b. Left Atrium d. Two types of heart valves are atrioventricular and semilunar valves . Heart valves connect the chambers and outflow tracts of the heart. Left Ventricle 4.

located between the left atrium and ventricle. Mitral valve (bicuspid valve) with two leaflets. . 2. Atrioventricular (AV) valves separates the atria from the ventricles 1. Tricuspid valve contains three leaflets.STRUCTURE & FUNCTION of the HEART a. located between the right atrium and ventricle.

STRUCTURE & FUNCTION of the HEART

STRUCTURE & FUNCTION of the HEART b. Semilunar valves - each containing three cusp, located between each ventricle and its corresponding artery. 1. Pulmonic valve located between the right ventricle and pulmonary artery. 2. Aortic valve located between the left ventricle and aorta.

STRUCTURE & FUNCTION of the HEART

STRUCTURE & FUNCTION of the HEART c. Papillary muscle is a muscle bundles on the ventricular walls, Chordae tendinae fibrous bands extending from the papillary muscles to the valve cusps. - keep the valves closed during systole, this maintains unidirectional blood flow through the AV valves and prevents backflow of blood.

STRUCTURE & FUNCTION of the HEART 5. Cardiac Conduction System consist of specialized cardiac cells that initiate or propagate electrical impulses throughout the myocardium as a precursor to cardiac muscle contraction. a. Electrical Impulses 1. Sinoatrial (SA) node located at the junction of the right atrium and superior vena cava, functions as the pacemaker of the myocardium, initiating rhythmic electrical impulses at 60 to 100 impulses per minute.

STRUCTURE & FUNCTION of the HEART .

a. conducts impulses from AV node. Bundle of His bundle of specialized muscle fibers in the myocardial septum.STRUCTURE & FUNCTION of the HEART 2. Right bundle branch (RBB) conducts impulses down the right side of the septum . AV node located in the septal wall of right atrium .receives impulses from SA node and relays them to the ventricles. 3.

STRUCTURE & FUNCTION of the HEART .

Left bundle branch conducts impulses into right and left fascicles that fan out into the left ventricular muscle Purkinje fibers where RBB and LBB terminate which propagate electrical impulses into the endocardium and on to the myocardium. .STRUCTURE & FUNCTION of the HEART b.

STRUCTURE & FUNCTION of the HEART .

STRUCTURE & FUNCTION of the HEART b. . Q. S and T P wave represents atrial depolarization PR interval represents the time from the beginning of atrial depolarization to the beginning of ventricular depolarization. Electrical impulse activity electrical impulses traveling through the cardiac conduction system can be measured and recorded by ECG. 1. Phases of electrocardiogram (ECG) P. R.

P waves precede each QRS complex . .Heart rate: 60 to 100 beats/min. Normal sinus rhythm .STRUCTURE & FUNCTION of the HEART QRS complex represents ventricular depolarization T wave represents ventricular repolarization 2.

12 to 0.QRS complex is 0.04 to 0.STRUCTURE & FUNCTION of the HEART .supply the heart with blood from branches that originate in the right or left sinus of valsalva of the aortic valve cusps. .Rhythm is regular with no abnormal delay 6.Conduction is forward and cyclical through the conduction system . . Coronary arteries .20 sec.PR interval is 0. .1 sec.

. Right coronary artery supplies blood to the right heart wall. supplies most of the blood to the left heart wall.STRUCTURE & FUNCTION of the HEART a. Left main coronary artery which divides into the left anterior descending coronary artery and the circumflex artery. b.

Cardiac output (CO) is defined as the volume of blood ejected by each ventricle in a minute.STRUCTURE & FUNCTION of the HEART Functions of the Heart: 1. Cardiac output (CO) = Stroke volume (SV) X Heart rate (HR) .

2. Stroke volume is the amount of blood ejected by the left ventricle with each heart beat. Afterload resistance to left ventricular ejection. increases by increased systemic arterial pressure.STRUCTURE & FUNCTION of the HEART a. Preload the end-diastolic filling endvolume of the ventricle. . increases by increased returning volume to ventricle. Factors affecting Stroke volume: 1.

Cardiac cycle each complete heartbeat or cardiac cycle consists of two phases in response to electrical stimulation.STRUCTURE & FUNCTION of the HEART b. normal: 60 to 100 beats per minute. Heart rate is the number of hearbeats per minute. Diastole is the relaxation (filling) phase . Systole is the contraction phase b. a. 2.

is often normal in persons younger that age 30 but pathologic in older persons and occurs during the rapid ventricular filling stage of diastole. S3 known as ventricular gallop.STRUCTURE & FUNCTION of the HEART 3. S2 is associated with aortic and pulmonic valve closure c. S1 is associated with tricuspid and mitral valve closure b. . a. Heart sounds result from vibrations caused by valve closure and ventricular filling.

4. Sympathetic nervous system stimulation release of norepinephrine.STRUCTURE & FUNCTION of the HEART d. is linked to resistance to ventricular filling as in hypertrophy or injury of the ventricular wall. increased heart rate and a positive inotropic effect. S4 known as atrial gallop. results in arteriolar vasoconstriction. . Neurologic factors regulating heart function a.

results in decreased heart rate and slowed AV conduction. . Parasympathetic nervous system stimulation with release of acetylcholine. to decreased O2 and increased CO2 concentrations is to increase the heart rate. c.STRUCTURE & FUNCTION of the HEART b. Chemoreceptors located in the carotid and aortic bodies.

Baroreceptors located in the aortic arch. . vena cava. resulting in blood pressure changes.STRUCTURE & FUNCTION of the HEART d. pulmonary arteries and atria is to decrease or increase heart rate. carotid sinus.

NURSING PROCESS OVERVIEW for the CARDIOVASCULAR SYSTEM .

NURSING PROCESS Assessment 1. course.Elicit a description of present illness and chief complaint (onset. duration. location and precipitating & alleviating factors) Cardinal signs & symptoms of altered cardiovascular function: . Health history: history: .

. and down arms. neck. beltbelt-squeezing pain that may radiate to shoulders. Palpitations characterized by rapid irregular or pounding heartbeat. 3. 2. Intermittent claudication characterized by extremity pain with exercise.NURSING PROCESS 1. Pain over the lower sternal region & the upper abdomen characterized by heavy vicelike.

or sudden onset at night (ie. Orthopnea). Paroxysmal nocturnal dyspnea) 5. in the supine position (ie. Edema or weight (>3 lbs. Fatigue with or without activity. (ie. 6. Diaphoresis with associated clamminess and cyanosis 8. in 24hrs) . Dyspnea on exertion). Dyspnea characterized by difficult breathing or shortness of breath with activity (ie. Syncope with or without dizziness 7.NURSING PROCESS 4.

Explore the client s health history for risk factors associated with cardiovascular disease (atherosclerosis) a.) c.o. b. Race: mortality is greater for nonwhites than whites . Positive family history for cardiovascular disease. Gender (greater in men than women. decrease after menopause) d.NURSING PROCESS 2. Age (high risk >40 y.

Diabetes j. Sedentary lifestyle i. Obesity h. Physical Assessment . Stress k. Use of oral contraceptives 2. Hypertension f. Hyperlipidemia (HDL & LDL ratio) g.NURSING PROCESS e.

assess jugular venous pressure & observe for venous distention c.NURSING PROCESS a.inspect the lips and buccal mucosa for central cyanosis .observe general appearance for signs of distress. anxiety and altered LOC .inspect peripheral extremities for cyanosis & a capillary refill time of less 3 seconds . Palpation . Assess the vital signs b. Inspection .

brachial. dorsalis pedis & anterior tibial Grade 0 no pulse 1+ . radial.NURSING PROCESS .palpate the precordium to locate the point of maximal impulse (PMI) or the apical pulse .palpate all peripheral pulses including carotid.bounding . femoral.normal 3+ . popliteal.weak 2+ .normal 4+ .

& friction rub. mitral area & tricuspid area e.NURSING PROCESS d.Hemoptysis (acute pulmonary edema) .Cough (pulmonary congestion) . Perform respiratory assessment . pulmonary area.Crackles or Wheezing ( airway narrowing. covering four main areas: aortic area. atelectasis or left ventricular failure) . murmurs.Cheyne-Stokes respiration (severe left Cheyneventricular failure) . Auscultation systematically auscultate the heart for normal & abnormal heart sounds.

NURSING PROCESS f.Liver enlargement & ascites (decreased venous return secondary to right ventricular failure) . Perform abdominal assessment .Bruits above umbilicus (abdominal aortic obstruction or aneurysm) .Bladder distention (decreased cardiac output) .

b.2 mmol/L LDL: 80-190 mg./dl. mm.2 mmol/L 401.92 mmol/L 802.04(females) ./dl.04-2.68 mmol/L 300. Lipid profile examine cholesterol (HDL & LDL) and triglycerides cholesterol normal level: 150-200 mg. 40-85 mg. WBC detect signs of infection normal level: 5.07HDL: 30-65 mg.78(males).000/cu./dl. or 1503. Laboratory and Diagnostic studies: a.93.9-5.000 to 10. or 0.07-4./dl. or 1. or 2.78-1.NURSING PROCESS 3.

Troponin & Lactate CPKdehydrogenase d. Blood coagulation studies: Prothrombin time 9. Cardiac enzymes: Creatinine phosphokinase (CPK) males: 5050325.5Partial thromboplastin time 20-45 sec.5-12 seconds 9. females: 50-250 U/L 50isoenzymes: CPK-MB.NURSING PROCESS c. 20- .

NURSING PROCESS
e. Chest radiography determine heart size and silhouette & visualize the pulmonary system f. Electrocardiography evaluates the heart s electrical activity g. Holter monitoring (ambulatory ECG) allows for 2424-hour continuous measurement of the heart s electrical activity h. Exercise ECG (grade exercise test) evaluates electrical activity during physical stress, chemical induced ECG stress test is used if the client is unable to walk or bike for a long period of time.

NURSING PROCESS
i. Vectorcardiography provides a graphic representation of the direction and magnitude of the heart s electrical function. j. Echocardiography yields information about cardiac structures (especially valvular) & function k. Radionuclide testing evaluates ventricular function & myocardial blood flow & detects areas of myocardial damage. Types: Positron emission tomography (PET), MultipleMultiple-gated acquisition (MUGA) & Thallium scanning

NURSING PROCESS
l. Cardiac catheterization enables measurement of chamber pressures & oxygen saturation m. Arteriography visualizes coronary arteries with injections of radiopaque contrast media n. Ventriculography visualizes ventricles with injection of radiopaque contrast media o. Central venous pressure (CVP) reflects filling pressure of the right ventricle & help assess cardiac function & intravascular volume status

NURSING PROCESS
p. Pulmonary artery wedge pressure (PAWP) & Pulmonary artery pressure (PAP) measure left heart pressures q. Arterial line allows continuous monitoring of peripheral arterial pressures Nursing Diagnosis: 1. Decreased cardiac output 2. Impaired gas exchange

NURSING PROCESS
3. 4. 5. 6. 7. 8. 9. Activity intolerance Pain Risk for Infection Sleep pattern disturbance Anxiety Knowledge Altered family processes

Improved family functioning .Reduction of anxiety .NURSING PROCESS Planning & Outcome Identification Major goals: .Adherence to a self-care program with selfunderstanding of disease process & management .Prevention of pain & infection .Increased gas exchange & activity tolerance .Improved sleep pattern .Enhancement of cardiopulmonary status .

Monitor ABG & pulse oximetry . heart sounds. BP.Monitor ECG & telemetry . peripheral pulses. skin color & temperature./hr.Monitor I&O & maintain 30 ml. peripheral edema.NURSING PROCESS D. RR & lungs . HR & rhythm. Implementation 1. use urometer to ensure accurate output . output.assess LOC. Assess cardiopulmonary status .

NURSING PROCESS
2. Enhance cardiac output establish a patent intravenous line to administer fluids. 3. Promote gas exchange - encourage to maintain high fowler s position while resting in bed, keep client on bed or chair rest. - collaborate with respiratory therapist & administer O2 to maintain O2 saturation level of 95% to 100% if no other disease process is present - instruct to cough, breath deeply & turn frequently

NURSING PROCESS
4. Increase activity tolerance - balance period of rest & exercises - assist as needed with activities of daily living and self care 5. Promote comfort - assess client s description of chest discomfort, including location, radiation, duration & what precipitated pain

NURSING PROCESS
6. Prevent infection - Monitor skin integrity of lower extremities & incisions from cardiac surgery - Assess insertion sites from invasive procedures for signs of redness, warmth, edema & pain - Monitor V/S especially for fever - Assess breath sounds for changes associated with pneumonia in clients after surgery and those requiring bed rest

NURSING PROCESS
7. Promote adequate sleep - attempt to cluster nursing interventions to provide the client with several hours of uninterrupted sleep 8. Minimize anxiety - offer client opportunities to ventillate feelings, answer client s question truthfully & caring relationship with client & client s family

NURSING PROCESS
9. Provide client & family teaching - Teach family members or significant others about pathophysiology of the underlying disease process - Teach client the importance of low-fat, lowlowlowcholesterol, low sodium diet, smoking cessation & adequate amount of exercise - Teach energy conservation measures - Discuss medications, including possible adverse effects & interactions.

discuss danger S/S requiring prompt medical attention including chest pain. sudden onset of fever.NURSING PROCESS . in less than 24 hours .discuss with client the necessity of advance directives & durable Power of Attorney for health care . irregular heartbeats & weight gain of more than 2 lbs. increased shortness of breath.

Outcome evaluation 1.assist with adaptation to role changes caused disease related limitations & activity restrictions E. hemodynamic parameters and urinary output . vital signs. Enhance family functioning . The client demonstrate stable cardiac rhythm.NURSING PROCESS 10.

6. The client limits activities to a level that permits the heart to rest. 5. 3. The client demonstrate stabilization of the inflammatory process. 4. The client is free of systemic & local infection. The client verbalizes factors and events that precipitate pain. .NURSING PROCESS 2. The client responds to cardio pulmonary resuscitation.

The client sleeps at least 6 hours each night uninterrupted. 9. . and treatment of the disease process and the signs or symptoms that should be reported to the health care provider. Family members or significant others verbalize an understanding of cardiopulmonary resuscitation (CPR) & the pathophysiology of underlying disease.NURSING PROCESS 7. preventive measures. The client can verbalize a understanding. 8.

CARDIOVASCULAR DISORDERS .

or complete arterial occlusion by embolism or thrombus 2. . Decreased coronary blood flow due to hemorrhage or shock. causing a profound imbalance between myocardial oxygen supply & demand. coronary artery spasm. Coronary artery narrowing due to atherosclerosis.MYOCARDIAL INFARCTION Myocardial infarction (MI) is destruction of myocardial tissue in regions of the heart abruptly deprived of adequate blood supply because of reduced coronary blood flow Etiology 1.

Pathophysiology of Myocardial Infarction .

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thrombus. embolism. coronary artery spasm) Inadequate coronary blood flow Myocardial ischemia Depresses cardiac function Triggers autonomic nervous system response Exacerbate imbalance between myocardial supply & demand Persistent ischemia results tissue necrosis & scar tissue formation Permanent loss of myocardial contractility in the affected area Decreased myocardial contractility Inadequate CO Cardiogenic shock death .Etiology (atheroslcerosis. hemorrhage.

Decreased blood pressure i. Tachycardia or Bradycardia h. Chest pain b. Palpitations or Syncope f. Altered S3 heart sound. Restlessness & anxiety or feeling of impending doom g. Nausea & Vomiting d.MYOCARDIAL INFARCTION Clinical Manifestations a. Diaphoresis & cool. pale skin c. clammy. Dyspnea with or without crackles e. which indicates left ventricular failure .

ECG T-wave to be larger & inverted. Serum enzymes .elevated CPK & CPKCPKMB. LDH & Troponin levels c.MYOCARDIAL INFARCTION Laboratory & Diagnostic study findings a. ST depressed in endocardial myocardial ischemia. b. WBC count is elevated . ST elevation in epicardial myocardial ischemia.

MYOCARDIAL INFARCTION Nursing Management 1. thrombolytics & anticoagulants in acute situation or stool softeners during rehabilitation . Morphine. nitrates. nitroglycerin & aspirin (MONA) .Immediate treatment of MI. oxygen. Administer drug therapy .Administer morphine. antilipidemics.

Reassure the client & explain procedures as the situation warrants .Monitor hemodynamic parameters as necessary through the multilumen pulmonary artery catheter 3. Provide ongoing assessment .MYOCARDIAL INFARCTION 2. Minimize anxiety .Monitor cardiac enzymes .

advance to a low-sodium.PTCA (Percutaneous Transluminal Coronary Angioplasty) . lowlowlowlow-cholesterol. low-fat.institute a liquid diet. Prepare client for treatment . Minimize metabolic demands .MYOCARDIAL INFARCTION 4. solid diet as tolerated 5.CABG (Coronary Artery Bypass Graft) . .

Provide referrals .MYOCARDIAL INFARCTION 6.Coronary club .American Heart Association .encourage family members & significant others to take CPR course 7. Provide client & family teaching .Mended Hearts Cardiac Rehabilitation .

BODY S REACTION TO SHOCK Impaired organ function Vasoconstriction of peripheral veins and arteries Hyperventilation Tachycardia * Fluid shifts .

Etiology: 1. Cardiomyopathy 4.CARDIOGENIC SHOCK Cardiogenic shock is the insufficient tissue perfusion due to the heart s inability to pump enough blood. Congestive heart failure 3. Myocardial infarction 2. Pulmonary edema 5. Cardiac tamponade .

RR .CVP & PCWP decrease periphery perfusion .oliguria .PACO2 cardiovascular .Cough & Crackles .lethargy .Hypotension .restlessness .confusion .Low PAO2 .Rapid weak pulse .altered LOC respiratory system .cool & pale skin Reduced renal perfusion .Pathophysiology of CARDIOGENIC SHOCK Inability of the heart to pump adequate blood Inadequate tissue perfusion on the body s organs Result in systemic symptoms cerebral perfusion .

Prepare the patient for insertion of an intraaortic balloon pump. pulse oximetry & ABG s. Administer medications to improve CO (inotropic drugs. preload & afterload reducers. diuretics & sedatives) 2. Monitor oxygenation status including respiratory rate. 4. lung sounds. Monitor PCWP to determine left ventricular function 3. .CARDIOGENIC SHOCK Nursing Management: 1.

measure urine output hourly 8. Institute ventilator support. Maintain strict intake & output measurements.CARDIOGENIC SHOCK 5. Monitor vital signs closely 7. 6. Promote rest & provide comfort measures .

ARRHYTHMIAS .

altered impulse conduction. or both.ARRHYTHMIAS Arrhythmia or dysrhythmia refers to any sinus rhythm deviating from normal. Etiology: Arrhythmias results from altered impulse formation. .

Pathophysiology of Arrhythmia Etiology (altered impulse formation. altered impulse conduction) Injured myocardial cells/replaced scar tissue Decreased ability to respond to SA node impulses Other cells assume the pacemaker properties Initiates the heart beat Interrupts SA node impulses Arrhythmia occurs .

NORMAL SINUS RHYTHM .

Conduction is normal 6. SINUS TACHYCARDIA Sinus tachycardia is a heart rate greater than 100 beats per minute.I. PR interval is normal 4. Rhythm is regular . P waves precede each QRS complex 3. originating in the sinus node. Characteristics: 1. Rate is 100 to 180 bpm 2. QRS complex is normal 5.

SINUS TACHYCARDIA Etiology: 1. Anxiety 3. Hypovolemia 8. Shock . Heart failure 7. Drugs 5. Anemia 6. Fever 4. Exercise 2.

Administer prescribed treatment is directed at the primary cause. .SINUS TACHYCARDIA Clinical Manifestations: 1. Angina with cardiovascular disease Nursing Management: 1. Hypotension 3. Occasional palpitations 2.

Beta blockers (Atenolol. Nadolol. Propanolol) this is to reduce the heart rate quickly .carotid sinus pressure . Metoprolol.SINUS TACHYCARDIA .

SINUS TACHYCARDIA .

Rate is less than 60 beats per minute 2. QRS complex is normal 5. PR interval is normal 4.II. SINUS BRADYCARDIA Sinus bradycardia is a heart rate less than 60 beats per minute originating in the sinus node. P waves precede each QRS complex 3. This arrhythmia may be normal in athletes Characteristics: 1. Rhythm is regular . Conduction is normal 6.

SINUS BRADYCARDIA Etiology: 1. Vagal stimulation 3. Hypothermia 6. Drugs 2. Sinus node involvement in MI . Anorexia 5. Hypoendocrine states 4.

Administer Atropine SO4 (anticholinergic) .SINUS BRADYCARDIA Clinical Manifestations: 1. 2. Lightheadedness 3. Maintain adequate CO through treating the underlying cause. Fatigue 2. Syncope Nursing Management: 1.

SINUS BRADYCARDIA .

12 seconds) 4. Characteristics: 1. QRS complex is normal 5. PR interval is shortened (0. PAROXYSMAL ATRIAL TACHYCARDIA and SUPRAVENTRICULAR TACHYCARDIA Paroxysmal atrial tachycardia (PAT) & Supraventricular tachycardia (SVT) is an abrupt onset & rapid heartbeat (palpitations) originating in the atria. Rhythm is regular . Rate is 150 to 250 bpm 2. P waves are ectopic & maybe found preceding T waves 3. Conduction is normal 6.III.

PAT & SVT Etiology: 1. Dyspnea 4. Alcohol. Extreme anger & fear 2. smoking & caffeine Clinical Manifestations: 1. Lightheadedness 3. Palpitations 2. Anginal pain . Drugs 3.

Propranolol & bretylium) . Lidocaine.Adenosine is drug of choice for SVT 3.PAT & SVT Nursing Management: 1.Antiarrhythmics (Quinidine. Flecainide. Assist with cardioversion .Assist with carotid sinus pressure or vagal maneuver 2.Cardiac glycosides (digoxin) . Administer prescribed medication .

PAT & SVT .

SUPRAVENTRICULAR TACHYCARDIA .

ATRIAL FIBRILLATION Atrial Fibrillation is a disorganized & uncoordinated twitching of atrial musculature caused by overly rapid production of atrial impulses. QRS is normal 5. Characteristics: 1. P wave is not discernible. Conduction is normal 6. Rhythm is irregular & usually rapid unless controlled . with an irregular baseline 3.IV. Rate: Atrial is 350 to 600 bpm & Ventricular 120 to 200 bpm 2. PR interval is not measurable 4.

Congenital heart disease 5. Atherosclerosis 2. Congestive heart failure 4.ATRIAL FIBRILLATION Etiology: 1. COPD 6. Rheumatic mitral valve stenosis 3. Hypothyroidism & thyrotoxicosis .

Assist with cardioversion 3. Signs of cerebrovascular insufficiency Nursing Management: 1. Dyspnea 3. Palpitations 2. Pulmonary edema 4. Administer prescribed medication (cardiac glycosides & Ca channel blocker) 2.ATRIAL FIBRILLATION Clinical Manifestation: 1. Implement anticoagulant therapy .

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ATRIOVENTRICULAR BLOCKS AV block . Third degree . First degree 2. Second degree 3.is a conduction defect within the AV junction that impairs conduction of atrial impulses to ventricular pathways. Types: 1.V.

Rate 1st degree 60 to 100 bpm or the inherent ventricular rate. atrial rate is 2 to 4 times faster than the ventricular rate 3rd degree rate is slowed. usually 40 to 60 beats per minute or the inherent ventricular rate . 2nd degree rate is slowed.ATRIOVENTRICULAR BLOCK Characteristics: 1.

P wave is normal & present in each type of block 3. PR intervals cannot be measured .ATRIOVENTRICULAR BLOCK 2. PR intervals: 1st degree PR intervals are prolonged at 0.20 second 2nd degree PR intervals may be progressively lengthening 3rd degree no relationship between P waves & QRS complexes exist.

conduction through the ventricles is abnormal 6. Conduction 1st degree is delayed in the AV junction 2nd degree impulses are not regularly conducted through the AV junction 3rd degree .all sinus impulses are blocked. QRS complex 1st & 2nd degree normal 3rd degree QRS is widened 5. Rhythm is regular in each type of block .ATRIOVENTRICULAR BLOCK 4.

vagotonic agents. BetaBetaadrenergic blockers .ATRIOVENTRICULAR BLOCK Etiology: 1. symphatholytic agents. Congenital 2. Hypokalemia 4. Certain drugs: digitalis. Atherosclerotic heart disease 3.

pacemaker . weakness & irregular pulse 3rd degree hypotension. angina & heart failure Nursing Management: 1st degree no treatment.ATRIOVENTRICULAR BLOCK Clinical Manifestations: 1st degree asymptomatic 2nd degree vertigo. discontinue causative drug if indicated 2nd degree administer Atropine SO4 3rd degree Atropine SO4.

st 1 degree AV Block .

nd 2 degree AV Block .

rd 3 degree AV Block .

Rate 60 to 100 bpm 2. premature beat has no P wave 3.VI. PREMATURE VENTRICULAR CONTRACTIONS PVC is caused by increased automaticity of ventricular muscle cells. premature beat has no PR interval . PR interval underlying rhythm is normal. Characteristics: 1. P wave underlying rhythm is normal.

PREMATURE VENTRICULAR CONTRACTION 4. Rhythm is usually irregular when premature beat occurs. QRS complex premature beat is bizarre and is multifocal resulting to different configurations 5. it may be in a regular pattern . Conduction is retrograde through conduction system 6.

Myocardial damage 2. Increased catecholamines 6. Digitalis toxicity 4.PREMATURE VENTRICULAR CONTRACTION Etiology: 1. Electrolyte imbalance 5. Exercise . Hypoxia 3.

Asses the cause 2.PREMATURE VENTRICULAR CONTRACTION Clinical Manifestations: 1. Lightheadedness Nursing Management: 1. Weakness 3. Palpitations 2. Assess fro life threatening PVC s of more than six per minute .

Administer lidocaine immediately (drug of choice) 6. Assess PVC s that occur in a vulnerable phase of conduction cycle (R & T wave) 5. quadrigeminy 4. Administer procainamide & quinidine for long term therapy . Administer an antiarrhythmic as ordered 7.PREMATURE VENTRICULAR CONTRACTION 3. trigeminy.Assess PVC that are bigeminy.

PREMATURE VENTRICULAR CONTRACTION .

P wave is blurred in the QRS but the QRS complex has no association with the P wave 3. VENTRICULAR TACHYCARDIA VT is three or more consecutive PVCs. Rate 100 to 250 bpm 2. PR interval is not present . It is considered a medical emergency because CO cannot be maintained because of decreased diastolic filling.VII. Characteristics: 1.

VENTRICULAR TACHYCARDIA 4. Rhythm is usually regular Etiology: 1. Conduction is abnormal through ventricular tissue 6. 5. Irritability of ventricular muscle . T wave is in the opposite direction. QRS complex is wide & bizarre.

VENTRICULAR TACHYCARDIA Clinical Manifestation: 1. Lightheadedness 2. Weakness 3. Unconsciousness Nursing Management: 1. procainamide or bretylium) . Administer antiarrhythmic drugs as prescribed (lidocaine. Dyspnea 4.

If the client is conscious or if lidocaine is unsuccessful assist with cardioversion. If rhythm deteriorates to ventricular or if the client is pulseless assist with defibrillation & use Advance Cardiac Life Support (ACLS) guide for resuscitation. . 3.VENTRICULAR TACHYCARDIA 2.

sternum & apex) & apply 20 to 30 lbs of pressure to ensure good skin contact 4. Always have saline pads between the paddles & the client s skin 3. Make sure that the correct is applied before defibrilating or cardioverting the client.VENTRICULAR TACHYCARDIA Important points for assisting with defibrillation or Cardioversion: 1. Always shout all clear & make sure that no one is touching the bed or client before discharging paddles. . 2.g. Make sure that paddles are correctly placed ( e.

. the client will be sedated.VENTRICULAR TACHYCARDIA 5. Cardioversion is an elective procedure. the client is alert & requires informed consent.

QRS complex is seen as undulation with no specific pattern . PR interval is not seen 4.VIII. with ineffective motions 2. Rate is rapid & uncoordinated. VENTRICULAR FIBRILLATION VF is rapid. ineffective quivering of ventricles that may be rapidly fatal. Characteristics: 1. P wave is not seen 3.

Sudden death . Possible seizures 6. Loss of consciousness 2. Electrolyte imbalance (hypokalemia & hypercalcemia) 3. Cessation of respirations 5. Loss of blood pressure 4. Hypothermia Clinical Manifestation: 1. Myocardial infraction (most common) 2. Pulselessness 3.VENTRICULAR FIBRILLATION Etiology: 1. Digitalis or quinidine toxicity 4.

Assist with defibrillation & CPR 2.VENTRICULAR FIBRILLATION Nursing Management: 1. Administer prescribed antiarrhythmic medications .

P wave may be visible but does not conduct through the AV node & ventricles 3. ventricular asystole is fatal. Rhythm is not present . palpable pulse & respiration. QRS complex is not present 4. heartbeat. without immediate intervention. Characteristics: 1. Conduction is possible through the atria only 5.IX. Rate is not present 2. VENTRICULAR ASYSTOLE Ventricular asystole is described as a lack of QRS complexes.

No respirations 3. Loss of consciousness 2. Causes of ventricular asystole may include any of the reasons for the previously described arrhythmias if medical treatment was not successful Clinical Manifestations: 1.VENTRICULAR ASYSTOLE Etiology: 1. Sudden death . Pulselessness 4.

Administer drugs such as Atropine SO4 & Epinephrine . Assist with CPR 2.VENTRICULAR ASYSTOLE Nursing Management: 1.

.

ENDOCRINE DISORDERS .

ENDOCRINE SYSTEM In conjunction with the nervous system. controls and integrates body function Endocrine system sends it messages in the form of hormones in the bloodstream .

external secretion Liver.any structure of animals.ENDOCRINE SYSTEM GlandsGlands. mammary gland. lacrimal gland . plants.releases secretion into ducts . or insects that produces chemicals 2 TYPES ExocrineExocrine.

parathyroid . pituitary.ENDOCRINE SYSTEM EndocrineEndocrine.discharge their secretions (Hormones) directly into the bloodstream Islet of langerhans Gonads( ovaries and testes ) Adrenal. thyroid.

ENDOCRINE SYSTEM .

Hormones are chemical substances secreted by endocrine glands directly into the blood stream to act on specific target cells. adaptation to stress & metabolism .ENDOCRINE SYSTEM Structure & Function of the endocrine system A. fluid & electrolyte balance. reproduction. Hormones regulate growth & development.

insulin. Steroids act intracellularly to modify protein synthesis (cortisol. Amine hormones or amino acids act on cell membranes (e. ACTH) 2.ENDOCRINE SYSTEM Types of hormones: 1. GH also called somatotropin. estrogen & testosterone) Hormone regulation hormone secretion is regulated through feedback mechanisms. vasopressin.g.g. norepinephrine) 3. Protein or peptide act on cell membranes by binding to receptors (e. . epinephrine.

anterior lobe: 1. Thyroid-stimulating hormone (TSH) stimulates thyroid hormone production 4. ACTH stimulates adrenal cortex to produce steroids (cortisol) 5. Prolactin affects mammary glands to stimulate milk production Thyroid3.ENDOCRINE SYSTEM I. GH affects growth of bones and muscles 2. Pituitary gland a. Follicle-stimulating hormone (FSH) Folliclestimulates ovaries to develop follicles & secrete estrogen or stimulates testes to develop seminiferous tubules & perform spermatogenesis .

Oxytocin stimulates uterine & mammary gland contractions 2. initiate ovulation & produce progesterone or stimulates testes to secrete testosterone. posterior lobe: 1. b. Antidiuretic hormone (ADH. vasopressin) acts on distal renal tubule to increase water reabsorption .ENDOCRINE SYSTEM 6. Luteinizing hormone (LH) stimulates ovaries to form a corpus luteum.

surround posterior thyroid tissue. difficult to locate & may be removed accidentally during thyroid or other neck surgery.ENDOCRINE SYSTEM II. it lowers blood calcium levels by inhibiting bone resorption. intestines & bones . Thyrocalcitonin secreted in response to high blood calcium levels. Parathyroid glands . Parathyroid hormone (PTH) raises blood calcium levels by increasing calcium resorption from kidneys. 1. 1. Thyroxine (T4) & Triiodothyronine (T3) regulate cellular metabolic activity 2. III. Thyroid gland a butterfly-shaped gland butterflylocated in the neck behind the trachea.

prepares the body for the fight-orfight-orflight response by converting glycogen. stored in the liver. Epinephrine accounts 90% of gland secretions. . to glucose & increasing cardiac output 2. 1. reacts to autonomic nervous system signals to release catecholamines.ENDOCRINE SYSTEM IV. adrenal medulla in the center of the gland. Norepinephrine exerts effects similar to epinephrine & produces extensive vasoconstriction. Adrenal glands a.

1. & decrease protein synthesis. secretion of adrenal androgens is controlled by ACTH. Glucocorticoids (cortisol) released in response to ACTH. 3. is stimulated by ACTH to produce corticosteroids. Adrenal sex hormones (androgens & estrogen) govern development of certain secondary sex characteristics. increase Na reabsorption & potassium loss primarily through the renal tubules 2. increase blood glucose by stimulating gluconeogenesis & lipolysis.ENDOCRINE SYSTEM b. . adrenal cortex outer portion of the glands. suppress the inflammatory response & promote sodium retention & potassium loss. Mineralocorticoids (aldosterone) released in response to angiotensin II & ACTH.

Alpha cells secrete glucagon. Pancreas a slender. elongated organ lying horizontally in the posterior abdomen behind the stomach. Functions: 1. which increases blood glucose through gluconeogenesis b. Beta cells secrete insulin c. beta & delta cells of the islets genesis a. Endocrine functions are controlled by the alpha.ENDOCRINE SYSTEM V. Delta cells secrete somatostatin (inhibitory hormone) & gastrin . Exocrine functions involve secretion of pancreatic digestive enzymes by specialized cells 2.

ENDOCRINE DISORDERS .

insuffficient ADH signscan cause dehydration whereas oversecretion cause excessive water retention PalpitationsPalpitations.eating more and loosing wt may indicate DM or hyperthyroidism while losspeople with hypothyroidism may gain wt Polydipsia and polyuria.increase body tempdue to hypothyroidism.increase nervousness.possible indication for hyperthyroidism FatigueFatigue.changes in mood.loss of menstrual cycle. changesdepression Changes in vital signs.abnormal thirst plus passage of large amount of urine may polyuriaindicate DM Changes in bowel status.may signify emotional stress WeaknessWeakness. while statusconstipation can indicate hypothyroidism Abnormalities involving the sex organs and libido.frequent loose stools are a sign of hyperthyroidism.mental confusion.increase heart rate can occur in hypothyroidism TremorsTremors.watch for polyphagia or anorexia changesWeight loss.indicates neurologic problems Appetite changes. impotence .MANIFESTATIONS THAT DEVELOP IN SOME ENDOCRINE DISORDERS Mental status changes. loss of libidolibido.

axillary and pubic hair loss may indicate a pituitary disorder.exopthalmus is an important characteristic of hyperthyroidism. A number endocrine disorders are inherited or at least associated with a familial trend . thin extremities and truncal obesity Growth abnormalities.acromegaly produces enlargement of hands and appearancefeet while cushing s syndrome is manifested by moon face. abnormalitiesexcessive(gigantism) or inappropriate(acromegaly) Skin and tissue changes. poor tissue healing and susceptibility to infection are associated with DM HairHair. problemcyst and fractures. hair feels soft and silky in hyperthyroidism while coarse.growth maybe delayed.people with hyperparathyroidism often develop bone pain. dry. one serious complication of DM is blindness Bone and joint problem. brittle in hypothyroidism EyesEyes. cushing syndrome produces a rapid breakdown of bone When assessing a person with endocrine disorder inquire into the family history. stunted(dwarfism).NURSING ASSESSMENT Untoward changes in appearance.hyperpigmentation occurs in chronic adrenocortical changesinsufficiency(addison s disease).excessive hair in women may indicate ovarian or adrenocortical disorders.

sometimes medullacalled symphatoadrenal system .the brain ( hypothalamus ) controls the release of two potent hormones epinephrine and norepinephrine ( symphatomimetics ) . adrenal medulla.ADDISONS DISEASE Adrenal gland ( suprarenal gland ) .small vital endocrine structures that cap the kidneys 2 LAYERS A.inner core.

ADDISONS DISEASE Epinephrine during stressful situation .increase cardiac output . pounding heart.converts glycogen to glucose for energy . deep rapid breathing and wide eyed alertness in times of emergency .produces cold sweat.

the SNS compensates for its loss .ADDISONS DISEASE Norepinephrine during stress reactions .extensive vascular constriction . should the medulla destroyed or removed.increase blood pressure * Overactivity of the adrenal medulla can be life threatening usually caused by cathecolamine producing tumor called pheochromocytoma which produces oversecretion of epinephrine and norepinephrine.

destruction or removal of this vital structure causes death within few days .ADDISONS DISEASE B. is essential for survival without therapeutic replacement of adrenocortical hormones.makes up the outer shell. adrenal cortex.produces adrenocortical hormones/ steroid hormones ( corticosteroids ) * Both are important for survival and well being but only the adrenal cortex is essential for life . cortexunlike the adrenal medulla.

mineralocorticoidsdesoxycorticosterone.helps maintain normal blood pressure and cardiac output . corticosterone .they regulate electrolyte balance by promoting sodium retention and potassium excretion . mineralocorticoids.ADDISONS DISEASE 3 CLASSIFICATIONS OF CORTICOSTEROIDS A.includes aldosterone.

cortisone and corticosterone . Glucocorticoids.increase levels of mineralocorticoids leads hypertension and hyperkalemia B.produces anti insulin effect .decrease levels of mineralocorticoids(addison s disease) person suffers hypotension. decrease cardiac output and hyperkalemia .ADDISONS DISEASE .regulate blood glucose levels Glucocorticoidsincludes cortisol.

lactate. pyruvates metabolismare converted in the liver to glucose(gluconeogenesis) which raises the blood glucose levels * excessive secretion can produce DM * fluid and electrolyte balance.acts to suppress immunityinflammation in response to stress but too much impedes healing and lowers resistance to infection .overabundance of balanceglucocorticoid secretion results in hypovolemia and hypertension owing to sodium water retention * inflammatory and immunity.ADDISONS DISEASE Effects of glucocorticoids on the body * glucose metabolism.amino acids.

while too much estrogen causes gynecomastia .release of glucocorticoids during stressorsstress the person can cope up but insufficient production of gucocorticoids(addison s disease) decrease the resistance to stress C.adrenal cortex secretes very hormonessmall amount of androgens and even smaller amounts of estrogen than the large amount release by the gonads.ADDISONS DISEASE * stressors.too much release of adrogens causes virilism. . Sex hormones.

pituitary destruction or removal 3. hemorrhage into the adrenal gland 3. neoplasm 5.pituitary axis from exogenous hypothalamicsteroid use 2.I. autoimmune process. ADDISON S DISEASE Adrenal hypofunction is a deficiency of adrenocortical hormones.circulating autoantibodies react specifically processagainst adrenal tissue 2. inadequate cortisol replacement. Etiology: Addison s disease 1. suppression of the hypothalamic. fungal infection & tuberculosis Secondary adrenal insufficiency 1. adrenalectomy 4. especially during time of stress .

abdominal pain or diarrhea 2. fatigue. nausea. dry skin. decreased body hair & possible increased pigmentation with excessive ACTH stimulation .ADDISON S DISEASE Clinical Manifestation: a. addison disease 1. anorexia. vomiting. weight loss 5. muscle weakness & arthralgias 3. decreased alertness & confusion 4.

hyperthermia Laboratory & diagnostic study: Suggestive findings 1. serum sodium level 3. pallor & extreme weakness 5. white blood cell count . hypotension 2. addisonian crisis (acute adrenal insufficiency)insufficiency)often unrecognized 1. serum potassium level 4.ADDISON S DISEASE b. rapid. serum blood glucose 2. weak pulse 3. rapid respiratory rate 4.

ADDISON S DISEASE Definitive findings: 1. methylprednisolone) .glucocorticoids (hydrocortisone Na succinate. cortisone. Administer prescribed medications .mineralocorticoids (fludrocortisone) . ACTH stimulation test reveals a low to normal cortisol response Nursing Management: 1. prednisone. dexamethasone. serum cortisol levels are decreased 2.

Provide immediate treatment for an addisonian crisis.take precautions to avoid unnecessary activity & events that may be stressful .ensure hospitalized & acutely ill client on long term glucocorticoid therapy receive additional doses to compensate for stress .Corticosteroid replacement & vasopressors may be administered . Help prevent addisonian crisis . glucose & electrolytes administration .ADDISON S DISEASE 2. .client must avoid exertion 3.IVF.

hirsutism. Provide client & family teaching. cataracts & hypertension . discuss hormonal therapy (purpose. side (purpose. effects. mood swings. infection.ADDISON S DISEASE 4. a. weight gain. diabetes mellitus. osteoporosis. report to health care providers about the steroid replacement therapy d. if overreplacement of glucocorticoids is indicated. muscular weakness. symptoms of abnormalities report to medical doctor c. explain the purpose & side effects (cushingoid appearance. duration) b.

cortisol injected SQ causes sterile abscess.ADDISONS DISEASE PHARMACOLOGIC INTERVENTION .assess for signs of cushing syndrome due to long term cortisol therapy .administer oral cortisol with meals or antacids to lessen gastric irritation and possible development of peptic ulcer . abnormalities in pigmentation .fludrocortisone taken daily causes sodium retention -deoxycorticosterone correct electrolyte imbalance .administer parenteral cortisol deep into gluteal muscle not into deltoid .synthetic corticosteroids taken daily .cortisone or hydrocortisone on a daily basis correct metabolic imbalances . tissue atrophy.

hyperplasia of adrenal cortex caused by overproduction of ACTH .II.hyperfunction of the adrenal cortex causes excessive production of glucocorticoids. cortisol secreting adrenal tumor.30 % of tumorcases 2. CUSHING S SYNDROME Cushing syndrome ( glucocorticoid oversecretion ). mineralocorticoids and sex hormones Etiology 1.

truncal obesity. frequent infections. weight gain & altered fat distribution moon face & buffalo hump at C7. acne & thinning of scalp hair . potassium depletion leading to hypokalemia. poor wound healing and lowered resistance to stress owing to suppressed inflammatory response 4. muscle weakness and renal disorders 3.cardinal S/S limbs2. hyperglycemia result to DM 5. menstrual disturbances (amenorrhea) 7. slender limbs. arrythmias.CUSHING S SYNDROME Clinical Manifestation: 1. mental status changes & mood swings due to increase levels of glucocorticoids and ACTH 6. bruises. diminished libido 8. striae.

eosinophils & lymphocyte counts 4. plasma cortisol & 24-hour urine cortisol 24results ACTH5. ACTH (indicative of ACTH-mediated cushing syndrome) 6. serum glucose level 3. selected radiographic & axial CT studies may determine the site of ectopic ACTH production (e.g. bronchogenic oat cell carcinoma) .CUSHING S SYNDROME Laboratory & diagnostic study findings: 1. serum potassium level 2.

aminoglutethimide (cytadren). assess skin integrity regularly . mitotane (lysodren) 2.CUSHING S SYNDROME Nursing Management: 1. a. Administer prescribed medications. Take measures to protect the client from injury & infection a. adrenocortical steroid inhibitors ketoconazole (nizoral).

strong soaps) c.g. treatment & mental status . if indicated (bilateral adrenalectomy) 4. body image. promote good hygiene d. Encourage the client & family to ask questions & verbalize concerns about disease pathology.CUSHING S SYNDROME b. Prepare the client for surgery. tape. modify the environment to remove or minimize hazards 3. Avoid agents that can damage skin (e.

synthesize by alpha cells glucagon. glucagon.raises blood sugar level by promoting the conversion of glycogen( principal storage form of carbohydrate ) to glucose with in the liver . functioncarbohydrates and fats Endocrine function.a hyperglycemic agent .carried out by the islets of langerhans which contains functionalpha and beta cells 2 Hormones secreted by the islet : a.secrete enzyme that catalyze the digestion of proteins. insulin.lowers the blood sugar levels by promoting the passage of glucose into cell b. controls fat and protein metabolism insulin.synthesize by the beta cells.DIABETES MELLITUS Pancreas large fish shaped organ that lies behind the stomach both an exocrine and endocrine gland Exocrine function.powerful hypoglycemic agent .

Stimulate protein synthesis with in tissues . Regulates the rate at which carbohydrates are used by cells for energy . To cross the cell membrane glucose must be bound to insulin and hook up with the receptor sites on cell * Some people with DM have enough insulin but few receptor sites which reduces insulin to transport into the cell *Others have inadequate insulin. glucose remains outside the cell raising the blood glucose concentration above normal . Promotes the conversion of fatty acids into fat which can be stored as adipose tissue . Stimulate the active transport of glucose into muscle and adipose tissue cells.DIABETES MELLITUS Specific function of insulin . Inhibit conversion of fats to ketone bodies .

hydrogen and oxygen ) is one of the body s major fuel Carbohydrates. fats are metabolized in the liver to ketones which can be released into the circulation Increased amount of ketones in circulation due to decrease insulin can lead to ketoacidosis and coma . proteins and fats can all be catabolized by the body for energy but the body uses carbohydrates for energy Glycogen is converted to glucose in the liver for energy In cases body obtain energy protein or fats.NORMAL CARBOHYDRATE METABOLISM Carbohydrate glucose( composed of carbon.

heredity .overweight body needs more insulin to metabolize food and decrease insulin receptor sites Types: 1. Average life expectancy decrease about one third . accounts 5% to 10% of cases & typically occurs in person younger than 25 years of age.III. 3rd leading cause of death in the US because of complications . It s either the pancreas produces subnormal insulin or the person requires high amounts(obese) INCIDENCE . Even diabetes does not kill it produces permanent disabilities ETIOLOGY . Imbalance between insulin demand and supply . .age 40 yrs old . DIABETES MELLITUS Diabetes mellitus is a disorder of carbohydrate metabolism resulting from deficiency of or resistance to available insulin & is characterized by hyperglycemia. . Type 1 Insulin dependent diabetes mellitus (IDDM) insulin deficiency & risk of ketosis characterize it.

. insulin resistance & little risk of ketosis characterize it. Type II non-insulin dependent diabetes nonmellitus (NIDDM) accounts for 90% of cases & most commonly affects persons older than 40 years old. defects in insulin release & use. Gestational diabetes is a transitory glucose intolerance during pregnancy that resolves after delivery. accounts 2% to 5% of all pregnancies. high risk of developing overt diabetes later in life.DIABETES MELLITUS 2. 3.

Diabetes associated with other conditions is described as glucose intolerance caused by other diseases. autoimmune caused by virus c. Etiology: 1. genetic factors . drugs.DIABETES MELLITUS 4. Type I (IDDM) a. exact cause unknown b. or agents.

pancreatic diseases b. genetics 3. antiinsulin effects of progesterone. Gestational diabetes a. & human placenta lactogen. Type II (NIDDM) a.DIABETES MELLITUS 2. which increases the amount of insulin needed to maintain glycemic control. hormonal abnormalities estrogenc. drugs (glucocorticoids. estrogen-containing preparations) . cortisol. Diabetes associated with other conditions a. 4. obesity b.

DIABETES MELLITUS
Acute complications: 1. Diabetic ketoacidosis (DKA) an acute insulin deficiency resulting in metabolic acidosis from ketone bodies (acid end-products of fat endbreakdown), occurring in clients with type I diabetes Causes: a. failure to take prescribed insulin b. increased physical stress (infection & surgery) c. psychological stress 2. Hyperglycemic hyperosmolar nonketotic coma (HHNK) occurring in older client s with type II diabetes, is a severe hyperglycemia & hypertonic dehydration without significant ketoacidosis.

DIABETES MELLITUS
Common in type II DM because of enough insulin to prevent development of ketoacidosis Extremely elevated blood glucose levels can lead to polyuria, dehydration and coma Extremely elevated blood sugar with no ketosis causes profound hyperosmolar state that leads to serios volume depletion and shock TPN may precipitate HHNK if person receives solutions containing large amounts of glucose

DIABETES MELLITUS
Causes: a. Stress (infection, surgery & hyperalimentation) b. ingestion of certain drugs (thiazide diuretics, glucocorticoids, phenytoin & sympathomimetics) 3. Hypoglycemia is an excessive insulin to blood glucose ratio linked to excessive use of hypoglycemic drugs agents (e.g. insulin, oral agents), decreased food intake, increased physical activity, excessive alcohol consumption or renal failure , it occur in client s with type I or type II diabetes

Early manifestations
Headache Weakness Irritability Lack of muscular coordination Apprehension DiaphoresisDiaphoresis- due to epinephrine released when blood glucose drops abnormally low Drunk or bizarre psychotic fashion Brain damage develops when deprived of glucose after a drastic drop in blood sugar. Hypoglycemic shock is more dangerous than diabetic coma INTERVENTION . Depends on severity . Mild- glass of orange juice, sugar cubes, candies Mild. Severe- IV glucose ASAP, 20 to 50 ml of D 50% glucose Severe. Never force an unconscious or semi conscious person to drink liquids . ID card or bracelet tags

DIABETES MELLITUS
Chronic complications: 1. Microangiopathy is thickening of capillary basement membrane, most prominently in the eyes causing vascular degeneration in the retina leading to microaneurysm, retinal hemorrhage and blindness whereas in the kidneys it leads to intercapillary glumerulosclerosis and renal failure. 2. Macroangiopathy is atherosclerotic changes accelerated by lipid abnormalities exacerbated by elevated blood glucose level. . May lead to premature CAD . Results in reduced blood supply to the feet causing intermittent claudication, cold feet, infections, inadequate healing of foot lesions, ulceration and gangrene of extremities. 3. Neuropathy is abnormal nerve function, possibly caused by alteration in enzyme systems & affecting nerve sheaths or neural cell function. . Vascular insufficiency and high blood sugar levels both lead to metabolic disturbance in the neuron . Painless neuropathy is a dangerous condition people may be unaware of the injury particularly of the lower extremity 4. Increased susceptibility to infection results from an impaired ability of granulocytes to respond to infectious agents. . Infected areas heal slowly due to damaged vascular system due to insufficient oxygen, nutrients and antibodies to the injured site

weight loss 3. kussmaul respiration 4. visual disturbance 5. tachycardia 3. Diabetes Mellitus 1. vulva & urinary tract infections b. acetone breath & decreased LOC 5. abdominal pain . fatigue & weakness 4. recurrent skin.DIABETES MELLITUS Clinical Manifestations: a. nausea & vomiting. DKA 1. polydipsia & polyphagia 2. polyuria. dehydration 2.

decreased LOC 3. Cool. tremor. headache leading to loss of consciousness & seizure . hypotension d. moist skin or pallor 2. confusion 4. Hypoglycemia 1.DIABETES MELLITUS c. paresthesia. HHNK or HHNC 1. tachycardia 3. dehydration 2. tachycardia 4.

At the 2-hour sample 2- . or postprandial blood glucose level above 200 mg/dL.DIABETES MELLITUS Laboratory & diagnostic study findings: a. Glycosylated hemoglobin (A1C) reveals an elevated blood glucose level over the previous 2 to 4 months 3. FBS level above 140 mg/dL. Diabetes mellitus 1. Glucose tolerance test reveals blood glucose over 200 mg/dL. Measured on more than one occasion 2.

arterial blood gas (ABG) values indicate acidosis c. urine specimen reveals an absence of ketosis 4. ABG studies reveals possible mild lactic acidosis 5. serum electrolytes reveals hypernatremia & hypokalemia . renal function test detects azotemia 6. serum blood glucose is higher than 700 mg/dl 2. HHNK or HHNC 1.DIABETES MELLITUS b. DKA 1. serum K levels are elevated 2. serum blood osmolarity is higher than 330 mOsm/kg 3.

monitor & administer electrolytes as prescribed. biguanides 2. serum blood glucose level is less than 70 mg/dL. major electrolyte concern is potassium DIABETES MELLITUS .d. Administer prescribed medications a. Nursing Management: 1.90% NSS) at high rate followed by hypotonic NSS (0. administer IVF NSS (0. Hypoglycemia 1. thiazolidinediones. Intervene as indicated for a client exhibiting signs & symptoms of DKA a. Type II (NIDDM) sulfonylureas.45% NSS) b. Type I (IDDM) insulin insulin b.

assess vital signs. lungs. monitor blood glucose values hourly e. intake & output & monitor ketones f. assess for precipitating factors 3. provide treatment similar to that of DKA b. intervene as indicated to manage HHNK a.DIABETES MELLITUS c. continuous rate d. monitor for CHF & cardiac arrhythmias . infuse regular insulin intravenously at a slow. because clients are usually older.

intravenous glucose (50% dextrose) .6 to 10 Life-savers Life. fruit juice or regular soda .2 to 4 tablets of commercially prepared glucose . administer glucose.glucagon (IM or SQ administration) . monitor blood glucose levels b.4 to 6 oz.2 to 3 tsp. sugar or honey .DIABETES MELLITUS 4. provide care for a client experiencing hypoglycemia a. sources include .

American diabetes Association. Provide teaching to client & family 6. protect the client injury 5. National Diabetes Information Clearinghouse. Provide referrals .DIABETES MELLITUS c. American Association of Diabetes Educators & Medic-Alert MedicFoundation . administer a source of long-acting longcarbohydrate to prevent subsequent episodes d. advise the client to carry simple sugar at all times. e.

sulfonylureas.banned in 1977 due to increase risk of Biguanideslactic acidosis .ORAL HYPOGLYCEMIC AGENTS Insulin is given parenterally because it is destroyed by the GI enzymes 2 classifications a. it also increases the number of insulin receptor sites ex. Tolbutamide(Orinase) Chlorpropramide(Diabenase) Glipizide(Glucotrol) b. Biguanides.lowers the blood sugar by stimulating sulfonylureaspancreatic beta cells to release insulin.

Laennec cirrhosis(micronodular) . LIVER CIRRHOSIS Liver cirrhosis is a chronic. Biliary cirrhosis . Common in individual who chronically abuse alcohol . massive loss of liver cells with irregular pattern of regenerating cells 3. Disorganization of liver architecture by widespread fibrosis and nodule formation and scarring of the liver Hepatocytes(major liver cells) die and replaced by scar tissue Liver regenerate in abnormal pattern forming tiny balls known as nodules Peak incidence occurs between ages 40 & 60 years The incidence of cirrhosis is twice as high among men as women. Postnecrotic cirrhosis(macronodular) . degenerative liver disease marked by diffuse destruction & fibrotic regeneration of hepatic cells. Most common worldwide.IV. Types: 1. Also in non drinkers and ddue to hepatotoxins substance intake 2. Bile flow is decreased with concurrent cell damage to hepatocytes around bile ducts .

Reverse blood flow and enlargement of esophageal veins . decrease liver function b.metabolites and toxins from the digestive organs to the liver for processing and detoxification Portal hypertension. It carries nutrients.a disease process that alter the flow of blood through the hypertensionliver or it s major vessels Increase pressure in the portal vein causes the ff : .receives blood from intestine and spleen veinnormal blood flow to and from liver depend on the proper functioning portal vein .develop in severe cirrhosis hypertensionPortal vein. Incomplete clearing of metabolic waste . portal hypertension. Ascites .LIVER CIRRHOSIS 2 major clinical problems a.

constipation or diarrhea 4. Alcoholism & chronic nutritional deficiencies (Laennec cirrhosis) 2. chronic dyspepsia & splenomegaly 3.Etiology: 1. enlarged. Ascites. dilated abdominal blood vessel 8.plasma leaks directly from the liver Ascitescapsule and congested portal vein into the peritoneal cavity LIVER CIRRHOSIS . gradual weight loss & ascites 7. firm liver 2. Hepatitis (Posthepatic cirrhosis) Clinical Manifestation: 1. S/S of portal hypertension (late) 9. Bile duct disorders (Biliary cirrhosis) 3.

serum protein levels reveal hypoalbuminemia 5.LIVER CIRRHOSIS Laboratory & diagnostic study findings: 1. Liver biopsy detects destruction & fibrosis of liver tissue 2. liver scan reveals abnormal thickening & masses 3. AST & LDH levels are elevated 4. liver function test results for ALT. PT is elevated .

limit visitors & orient the client to date. turn the client every 2 hours b. minimize metabolic derangements that can cause further deterioration of mental status d.LIVER CIRRHOSIS Nursing Management: 1. Promote adequate nutrition. time & place f. Protect client from injury a. assist with ambulation & raise side rails . restrict dietary CHON e. soft soap c. use mild. a. ensure a nutritious. diet supplemented with vitamins as prescribed 2.

Provide referrals a. portal hypertension. Develop a nursing care plan to address the complications of liver (e. bleeding esophageal varices) 4.LIVER CIRRHOSIS 3. American Liver Foundation & Alcoholics Anonymous .g. Provide health education 5. jaundice. hepatic encephalopathy.

excessive formation of bile pigments in the blood(hyperbilirubinemia) and in the skin Portal hypertension Bleeding esophageal varices.portal HPN rise to varicesabdominal wall veins and esophagogastric veins dilate and distend Hepatic encephalopathy.COMPLICATION OF LIVER CIRRHOSIS JaundiceJaundice.elevation of ammonia encephalopathylevels in the blood and CSF due to inability of the liver cells to convert ammonia to urea and damage liver cells and necrosis occurs .

Carbohydrate. just below the cricoid cartilage glandShaped like a letter H ThyroxineThyroxine. Regulate body metabolism .HYPERTHYROIDISM Thyroid gland. Resistance to infection . fat and protein metabolism . Ensures that oxygen consumption and heat production keep pace with the body s needs and activities * Too much thyroxine causes dangerous speeding of metabolism and high rate of oxygen consumption. In contrary too little results in sluggish metabolism. Regulate growth and development both physical and mental .located at the neck. a slowing physical and mental function in adults and retardation of growth and development in child .one of the 3 major hormones produced Major role .

salicylates) .much more potent than thyroxine Thyrocalcitonin(TCT) capable of lowering both plasma calcium and phosphate . Exposure to prolong heat Triiodothyronine(T3)Triiodothyronine(T3). ingestion of sufficient protein and iodine b. release of anterior pituitary hormone called TSH Factors that depress thyroxine secretion . Ingestion of certain drugs(sulfonamides. Excessive intake of goitrogens known to inhibit thyroxine production .HYPERTHYROIDISM Thyroxine production depends on a.

antibodies react against dysfunctionthyroglobulin(storage form of thyroxine)that lead to enlargement of the thyroid gland and secretion of excess thyroid hormone 2. Etiology: 1. Autoimmune dysfunction. disease is greatest between the ages 30 to 40 & is higher among women than men. which may be acute. subacute or chronic (e.V. Hashimoto disease) . HYPERTHYROIDISM Hyperthyroidism is a metabolic imbalance resulting from excessive thyroid hormone production. toxic nodular goiter b. Genetic factors and other factors like a. exposure to iodine c.g. Thyroiditis. Grave s disease is the most common form. TSH-secreting pituitary tumor (rare) TSHd.

nervousness. menstrual irregularities & decreased libido .HYPERTHYROIDISM Clinical Manifestation: a. insomnia & interrupted sleep 6. easy fatigability & exercise intolerance 3. frequent stools & diarrhea 7. irritability. weakness. Hyperthyroidism 1. weight changes (loss or gain) & increased appetite 5. hyperactivity. heat intolerance and profuse diaphoresis 4. emotional lability & decreased attention span 2.

elevated systolic blood pressure. cyclic moods. exopthalmos. hyperkinesia & hyperreflexia 10.HYPERTHYROIDISM 8. bruits over thyroid gland 14. goiter 13. retracted eyelids & staring gaze 11. excessive hyperactivity leads to extreme fatigue and depression . widened pulse pressure & S3 sound 15.mild euphoria to extreme hyperactivity or delirium moods17. hair appears thin and soft 12. tremor. warm. heart failure & AF (elderly clients) 16. sweaty. flushed skin with a velvety-smooth texture & velvetyspider telangiectasias owing to an accelerated circulation to tissues 9.

HYPERTHYROIDISM b. hypertension 3. Thyroid scan reveals increased function in the thyroid gland (hot areas) . Increased serum T4 & T3 2. Thyroid storm 1. delirium 4. vomiting 5. hyperthermia 2. Radioactive iodine uptake test shows an increased uptake 3. Serum TSH assay reveals a nondetectable TSH level 4. tachyarrhythmias Laboratory & diagnostic study findings: 1.

SSKI: lugols solution) . Administer prescribed medications a. antithyroid drugs (levothyroxine: synthroid.HYPERTHYROIDISM Nursing management: 1. Surgery (subtotal or total thyroidectomy) .PTU.lessen palpitation and agenttremors 2. Assist the client & family members or significant others in exploring treatment options a.Adrenergic blocking agent.PTU.more potent than PTU . Radioactive iodine therapy c. Pharmocotherapy b.Methimazole.block thyroid hormone synthesis .Methimazole.

minimize client s energy expenditure by assisting ADL as necessary c. calm & quite environment b. Promote adequate nutrition a. provide increased calories & other nutritional support . Promote rest a. encourage client to alternate periods of activity with rest 4.HYPERTHYROIDISM 3. monitor nutritional status b.

HYPERTHYROIDISM 5. use cooling mattress & acetaminophen. artificial tears) ExopthalmosExopthalmos.protruding eyes and fixed stare due to accumulation of fluids in the fat pads and muscles that lies behind the eyeballs that push out the eyes that can lead to corneal ulceration and loss of vision 6. supply sufficient fluids to offset losses from diaphoresis c. provide eye protection with exopthalmos (patches. Prevent injury a. drops. avoid aspirin b. provide appropriate comfort measures for the febrile patient . Maintain normothermia a. intervene as needed to ensure safety b. assess the client s mental status & decision-making decisionability.

Provide postoperative care a. tetany. support the head & avoid tension on sutures b. hemorrhage. Provide referrals: Thyroid Foundation of America & National Graves disease Foundation .HYPERTHYROIDISM 7. laryngeal nerve injury & edema of the glottis) 9. encourage the client to comply with long-term longmedical follow-up therapy follow8. monitor for complications & intervene as needed (thyroid storm. Provide client & family teaching a. reassure the family that any abrupt changes in the client s behavior probably are disease related b.

NEUROLOGIC DISORDERS .

000 persons & is higher among women than men. initial symptoms occur between the ages of 20 & 40 years old Etiology: 1. The incidence is 1 case per 25. MYASTHENIA GRAVIS Myasthenia gravis is a progressive disorder affecting neuromuscular transmission of impulses in voluntary muscle.I. Autoimmune response .

Severe fatigue 2. Breathing difficulty because of weak respiratory muscle Laboratory & diagnostic study findings: 1. Impaired chewing & swallowing 5. Serum anti-ACHR antibodies are present anti- . Diplopia 4. Positive Tensilon test that confirm diagnosis 2. Drooping facial muscle & ptosis 3.MYASTHENIA GRAVIS Clinical Manifestation: 1.

If indicated assist the client undergoing medical procedure . neostigmine: prostigmine) 2. Administer prescribed medications a.MYASTHENIA GRAVIS Nursing Management: 1.thymectomy (decrease formation of anti-ACHR antiantibodies) .plasmapheresis (plasma exchange to reduce titer of circulating antibodies) . anticholinesterase (pyridostigmine: mestinon.

monitor pulmonary function test b.MYASTHENIA GRAVIS 3. provide small. frequent meals & keep suctioning equipment readily available 4. encourage effective coughing. Prevent problems associated with swallowing difficulty a. Encourage adjustment in lifestyle to prevent fatigue . Prevent problems associated with respiratory function a. Promote measures to maintain adequate c. chest physiotherapy & suctioning of secretions 5.

Maximize functional abilities a. administer medications 30 mins. set realistic daily schedule 6. Prevent problems associated with impaired vision resulting from ptosis of eyelid a. Before activities b. encourage client to tape eyes open for short intervals . prevent complications of immobility b.MYASTHENIA GRAVIS a. maximize effective communication 7. plan adequate rest period throughout day c. promote self-care selfc.

Determine the type of crisis by administering intravenous edrophonium (tensilon) .MYASTHENIA GRAVIS b. cholinergic with atropine . Treat myasthenic crisis with intravenous anticholinesterase. instill artificial tears & wear sunglasses when outside 8. Be prepared for emergency treatment of myasthenic or cholinergic crisis a. if crisis is myasthenic there is improvement & if cholinergic there is no improvement.

Brain tumor 5. Intracranial surgery . Head injury 2. The normal ICP depends on the position of the client & is 15 mmHg or less. INCREASED INTRACRANIAL PRESSURE ICP is the result of the amount of brain tissue. Inflammatory 4. intracranial blood volume & CSF within the skull at any time.II. Stroke 3. increased ICP is more than 15 mmHg Etiology: 1.

inequality) 3. Lethargy (earliest sign). dilated. Bradypnea & irregular breathing pattern 5. Bradycardia & Increase pulse pressure (called cushing reflex) 4. Headache 7. Blurred or double vision. slowed response. Hyperthermia (late sign of increasing ICP) 6. restlessness. Pupil changes (fixed. altered LOC.INCREASED INTRACRANIAL PRESSURE Clinical Manifestation: 1. slowing of speech 2. photophobia .

Osmotic diuretics. LOC. MRI scans. ischemic area) Nursing Management: 1. Monitor neurologic status (VS. radiographs. Oculomotor nerve. tumor. & sedatives 2. Administer prescribed medications a.g. analgesic. corticosteroids. ICP monitoring reveals an ICP greater than 15 mmHg 2. motor & sensory status) . & CT scans may identify the cause of the increased pressure (e.INCREASED INTRACRANIAL PRESSURE Laboratory & diagnostic study findings: 1.

position the client to prevent airway obstruction . Provide safety measures when administering sedatives & analgesics that may depress respiration & decrease LOC a. Maintain a patent airway a. elevate the head of the bed 30 degrees c.INCREASED INTRACRANIAL PRESSURE 3. suction PRN b. hyperoxygenate the client before suctioning 4. reduce or eliminate noxious stimuli b.

Manage hyperthermnia a. force fluids unless contraindicated 6. sterile technique for wound care b. Prevent infection a. use a hypothermia blanket.INCREASED INTRACRANIAL PRESSURE 5. administer antipyretics as prescribed d. insertion of ICP monitoring device & keeping it intact . provide only minimal bed coverings & clothing b. avoid rapid cooling c.

INCREASED INTRACRANIAL PRESSURE 7. provide familiar objects in the client s environment . give simple directions d. provide for adequate c. monitor intake & output b. Maintain fluid & electrolyte balance a. reduce external stimuli b. monitor for signs of dehydration 8. Help orient the client & reduce confusion a.

III. Gunshot wounds . contusions or compression of the vertebral column with damage to the spinal cord. Diving accidents 3. Sports injuries 5. Motor vehicle accidents 2. SPINAL CORD INJURIES Spinal cord injury is a fractures. Falls 4. Common sites of injury include the cervical spine & the junction of the thoracic & lumbar areas (T1 to L1) Etiology: 1.

Loss of sensation & altered motor functions Neurologic damage: 1. including independent respiratory function & bowel & bladder control . Paresthesia 3. Pain 2. Loss of consciousness 4.SPINAL CORD INJURIES Clinical Manifestations: 1. Below C4 loss of motor & sensory function from the neck down.

SPINAL CORD INJURIES 2. Below C8 loss of motor control & sensation to parts of the arms & hands. loss of bowel & bladder control 4. impaired intercostal muscle function. loss of bowel & bladder control . loss of bowel & bladder control. 3. Below C6 loss of motor & sensory function below the shoulders. loss of bowel & bladder control 5. Below T12 loss of motor control & sensation in the legs & pelvis. Below T6 loss of motor control & sensation below the mid-chest but with motor control & midsensation preserved in the arms & hands.

CT scanning can locate the area of cord damage & search for other injuries that often accompany spinal trauma . Below L4 loss of motor control & sensation in parts of the thighs & legs. Below L2 loss of motor control & sensation in the legs & pelvis.SPINAL CORD INJURIES 6. loss of bowel & bladder control 7. loss of bowel & bladder control Laboratory & diagnostic study findings: 1. Spinal radiography can locate the area of cord damage 2.

high dose corticosteroids (e.g. osmotic diuretics b. keep the neck aligned c. Administer prescribed medications a.g.g. Provide emergency treatment a. reduces disability if given within 8 hours after injury) .SPINAL CORD INJURIES Nursing Management: 1. muscle relaxants (e. immobilize the head & neck d. ABG s & pulse oximeter) 2. O2 therapy. maintain a patent airway (e. do not move the client b. Baclofen) c.

Prepare the client for surgery a. skeletal Tongs: GardnerGardner-Wells or Crutchfield tongs. applying skeletal traction (e.SPINAL CORD INJURIES 3. Prevent complication of immobility a. usually for repair of fractures or dislocations to stabilize the spinal column. halo tongs) 4. Assist with immobilization & reduction of dislocations & stabilization of the cervical vertebral column a.g. perform passive ROM exercises on paralyzed limbs to maintain joint mobility . 5.

teach the client transfer skills if appropriate c. work with other discipline in securing needed assistive devices b. Promote client and family coping a. Prepare client & family for ambulation & home maintenance management a. teach new coping strategies b.SPINAL CORD INJURIES 6. collaborate with the clients family to identify ways to adapt the home environment to the client s needs 7. evaluate the client s & family members coping strategies .

provide information on alternative means for achieving sexual satisfaction 9.SPINAL CORD INJURIES c. National Spinal Cord Injury Association . As appropriate. encourage the client & family members to verbalize concerns 8. Provide a referral a.