TUBERCULOSIS Mycobacterium Tubercle Bacilli

Transmitted thru LYMP KIDNEY,BONES,CEREBRAL CORTEX, ALVEO SYSTEM LYMP SYSTEM LI INFLAMMATORY REACTION Phagocytesneutrophils,macrophag es,TB specific lymphocytes(lyse the bacilli & normal cell)

Accumulation of exudates Granulomas (fibrous tissue in alveoli mass) Bronchopneumo nia Necrosis (CHESSY GHON TUBERCLE Scar Bacteria is dormant RELEASE CHESSY MATERIAL IN BRONCHI Possible activation Reason: Compromise person

LUNG BECOMES MORE INFLAMED S/S:

 LOW GRADE FEVER  COUGH (NON PRODUCTIVE MUCOPURULENT)  NIGHT SWEAT  FATIGUE  WEIGHT LOSS  HEMOPTYSIS DIAGNOSTIC TEST  X-RAY  PRESENCE AND EXTENT OF THE DISEASE  ACID FAST BACILLI  SPUTUM CULTURE  TUBERCULIN SKIN TEST- (MANTOUX TEST)-to determine whether the pt. has been infected with the TB bacillus. PPD-purified protein derivative -intradermal (4 inches below the elbow), 26-27 G needle, intermediate strength PPD

lesion on xray (minimal) IV.(-) new sputum/ lesion on xray(extensive II. Hyperuricemia E.↑10 significant in people who have normal or mildly impaired immunity  < 5 years old. (+) BCG. .ORANGE DISCOLORATION ANEMIA. Family History • 3. Sedentary lifestyle • 8. ≥ ID mm is (+)  > 5 years old. Peripheral neuropathy  CONVULSION. ALBUMINEMIA.Optic neuritis (do not give in ↓ 6 years old) S.THROMBOCYTOPENIA. Smoking • 6. Hypertension • 4.Males and post-menopausal females • 2. Neprotoxic. ≥ 5 mm is (+) Category Intensive Continuation I – (+) sputum . (-) BCG.(-) new sputum.0-4 mm not significant . Hyperlipedimia Most important MODIFIABLE factors: • Smoking • Hypertension • Diabetes • Cholesterol abnormalities Pathophysiology .-result read within 48-72hours -induration . DM • 5.Hepatotoxic. PHYCOSIS P.tinnitus or hearing impairment  OLIGURIA.Tx failure -relapse III. Age above 45/55 and Sex.Chronic (still (+) sputum after supervised and retreatment 2 RIPE 4 RI 2 RIPES/ 1 RIPE 2 RIPE 5 RIE 4 RI DOTS SIDE EFFECTS DANGER SIGNS R.5 and above significant in person who considered to be at risk.OLIGURIA I. Ototoxic.↑ LIVER ENZYME. RENAL IMPAIRMENT CAD results from the focal narrowing of the large and medium-sized coronary arteries due to deposition of atheromatous plaque in the vessel wall RISK FACTOR • 1. Obesity • 7. ALBUMINEMIA.

to reduce BP and HR • . Diaphoresis • 3. Dizziness and syncope • LABORATORY FINDINGS • 1.Fatty streak formation in the vascular intima  T-cells and monocytes ingest lipids in the area of deposition atheroma narrowing of the arterial lumen  reduced coronary blood flow  myocardial ischemia • There is decreased perfusion of myocardial tissue and inadequate myocardial oxygen supply • If 50% of the left coronary arterial lumen is reduced or 75% of the other coronary artery. results from coronary artery VASOSPASMS. Unstable angina • Occurs unpredictably during exertion and emotion. Chest pain. Eating heavy meals.to dilate the coronary arteries • Aspirin. relieved by rest and drugs and the severity does not change 2. Nausea and vomiting • 4. Cold clammy skin • 5. Administer prescribed medications • Nitrates. Emotions like excitement and anxiety and Extremes of temperature • Relieved by REST and Nitroglycerin • 2. may occur at rest ASSESSMENT FINDINGS 1. STABLE ANGINA • The typical angina that occurs during exertion. Ischemic changes may show ST depression and T wave inversion • 2. Sense of apprehension and doom • 6.ANGINA • The most characteristic symptom • PAIN is described as mild to severe retrosternal pain.to prevent thrombus formation • Beta-blockers. severity increases with time and pain may not be relieved by rest and drug 3. this becomes significant • Potential for Thrombosis and embolism Angina Pectoris • Chest pain resulting from coronary atherosclerosis or myocardial ischemia ANGINA 1. tightness or burning sensation • Radiates to the jaw and left arm • Precipitated by Exercise. squeezing. Variant angina • Prinzmetal angina. Cardiac catheterization • Provides the MOST DEFINITIVE source of diagnosis by showing the presence of the atherosclerotic lesions NURSING MANAGEMENT 1. ECG may show normal tracing if patient is pain-free.

CAD 2. Refer patient to proper agencies MYOCARDIAL INFARCTION Death of myocardial tissue in regions of the heart with abrupt interruption of coronary blood supply .• • • • • • • • • • • • • • • • • Calcium-channel blockers. take another tablet and wait for 5 minutes Another tablet can be taken (third tablet) If unrelieved after THREE tablets seek medical attention 3.hemorrhage.percutaneous transluminal coronary angioplasty • To compress the plaque against the vessel wall. Assist in possible treatment modalities PTCA. Hypercholesterolemia 2. ETIOLOGY and Risk factors 1. Coronary vasospasm 3. Obesity 5.coronary artery bypass graft • To improve the blood flow to the myocardial tissue 6. Coronary artery occlusion by embolus and thrombus 4. Assist client to identify risk factors that can be modified 8. increasing the arterial lumen CABG. Conditions that decrease perfusion. Hypertension 4. Teach the patient management of anginal attacks Advise patient to stop all activities Put one nitroglycerin tablet under the tongue Wait for 5 minutes If not relieved.to dilate coronary artery and reduce vasospasm 2. shock Risk factors 1. Promote myocardial perfusion Instruct patient to maintain bed rest Administer O2 @ 3 lpm Advise to avoid valsalva maneuvers Provide laxatives or high fiber diet to lessen constipation Encourage to avoid increased physical activities 5. Obtain a 12-lead ECG 4. Provide information to family members to minimize anxiety and promote family cooperation 7. Smoking 3. Stress 6. Sedentary lifestyle PATHOPHYSIOLOGY Interrupted coronary blood flow myocardial ischemia anaerobic myocardial metabolism for several hours myocardial death  depressed cardiac function  triggers autonomic nervous system response  further imbalance of myocardial O2 demand and supply • • • • • • • • • • • .

elevated CK-MB. thallium scans. ECG. Provide adequate rest periods 5.may show elevated WBC count • 4. cold clammy skin 5. crushing substernal discomfort Radiates to the neck. low cholesterol and low fat diet 6. hypotension 9. arm. Administer medications • Morphine to relieve pain • nitrates. jaw and back Occurs without cause. Semi-fowler’s 2.• • • • • • • • • • • • ASSESSMENT findings 1. Dyspnea 3. Provide client teaching • Medical Management • 1. S3 and dysrhythmias Laboratory findings • 1. Minimize anxiety • Reassure client and provide information as needed 7. Minimize metabolic demands • Provide soft diet • Provide a low-sodium. T wave inversion. Test after the acute stage. Assist in treatment modalities such as PTCA and CABG 8. CHEST PAIN Chest pain is described as severe. Myocardial enzymes. restlessness. persistent. sense of doom 7.the ST segment is ELEVATED.Exercise tolerance test. Monitor for complications of MI. ACE . primarily early morning NOT relieved by rest or nitroglycerin Lasts 30 minutes or longer 2. CBC. Minimize patient anxiety • Provide information as to procedures and drug therapy 4. N/V 6. tachycardia or bradycardia 8. thrombolytics.especially dysrhythmias. cardiac catheterization 1. Provide Oxygen at 2 lpm. aspirin and anticoagulants • Stool softener and hypolipidemics 3. since ventricular tachycardia can happen in the first few hours after MI 9. presence of Q wave • 2. Diaphoresis 4. ANALGESIC • The choice is MORPHINE • It reduces pain and anxiety • Relaxes bronchioles to enhance oxygenation • 2. LDH and Troponin levels • 3.

on the chair for 30 minutes TID • 5.• Prevents formation of angiotensin II • Limits the area of infarction • 3. Progress with dangling of the feet at side of bed • 4. Proceed with sitting out of bed. Alteplase • Dissolve clots in the coronary artery allowing blood to flow NURSING INTERVENTIONS AFTER ACUTE EPISODE • 1. Provide passive ROM exercises • 3. Thrombolytics • Streptokinase. Maintain bed rest for the first 3 days • 2. Proceed with ambulation in the room toilet hallway TID Cardiac rehabilitation • To extend and improve quality of life • Physical conditioning • Patients who are able to walk 3-4 mph are usually ready to resume sexual activities .

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