DEFINITIONS:
Pulmonary Tuberculosis is an infectious disease that attacks the lungs caused by Myobakterium Tuberculosis.
Etiology:
Type of rod-shaped bacteria, 1-4/um length and thickness from 0.3 to 0.6 / um. Most of the bacteria in the form of fats / lipids that bacteria resistant to acids and is more resistant to chemical, physical. Other properties of aerobic bacteria is an area that many oksigin love, more pleasure in this region of high oxygen content is epikal lung area, this area is the prediction of the disease Tuberculosis.
Pathophysiology:
The disease is controlled by an intermediary immune response effector cells (macrophages), whereas limphosit (T cells) are cells imonoresponsifnya. Immunity usually involves macrophages are activated in place of infection by lymphocytes and lymphokines, this response is called a hypersensitivity reaction (slow). Tubercle bacillus reaches the surface of the alveolar be inhaled as a unit (1-3 basil), clumps of bacilli larger canals tend to be restrained nose and bronchial large branches and do not cause disease. That is the bottom dialveolus upper lobe pulmonary tubercle bacillus makes inflammation. Polymorphonuclear leukocytes appear in tempay and mempagosit, but do not kill the bacilli. The following days leukocyte replaced by macrophages, alveolar consolidation and attacked experiencing symptoms of acute pneumonia. Cellular pneumonia can be cured by itself. This process can go on, and continue dipagosit basil or multiply in the cells. Basil also spread through the lymph nodes. Macrophage infiltration into the hold longer and some unity formed epithelioid cell tubercles surrounded by lymphocytes (takes 10-20 days). Necrotic lesions of the central section gives a relatively solid and like cheese (caseating necrosis). Areas that experienced necrosis and granulation tissue surrounded by epithelioid cells and fibroblasts will cause different responses. Granulation tissue fibroblasts would be forming scar tissue and finally form a capsule surrounded by tubercles
SIGNS & SYMPTOMS
Complaints can vary or even without a complaint, which most are:
1. Fever: subfebril, febrile (40-41derajat C) intermittent.
2. Cough: is due to irritation of the bronchi, cough is to remove / eject the production of inflammation, starting from a dry cough to cough purulenta (produces sputum)
3. Shortness of breath: when is advanced in which up to half a lung inflammatory infiltration.
4. Chest pain: This is rare, occurs when the infiltration of inflammatory pain up to the pleura causing pleuritis.
5. Malaise: found beripa anorexia, decreased appetite, weight decreased, Sakir headache, muscle pain, night sweats diwaktu
In atelectasis there is any clinical manifestations are cyanosis, shortness of breath, collapse. The patient does not move the chest during breathing and heart pushed to the other side of the sick. In Pictures Torax appear on the affected side silhouette and diaphragms stand up.
DIAGNOSTIC EXAMINATION:
Physical examination:
• At an early stage is difficult to know.
• Ronchi wet, rough and loud.
• hipersonor / tympanic cavity if there is enough and vote umforik auscultation.
• Atrophy and intercostal retractions on the state information and fibrosis.
• When the pleura is pleural effusion occurs (percussion dullness vote)
Radiological examination:
• At an early stage picture looks like patches of clouds with no clear boundaries.
• In the shadow in the form of a ring cavity.
• In the shadow of calcification appear dense patches of high density.
Bronchografi: a special inspection for damage bronchus or lung damage due to TB.
Laboratory:
• Blood: leukocytes rose, LED rose
• Sputum: BTA found on culture
• Tuberculin Test: Mantoux test (induration of more than 10-15 mm)
MANAGEMENT:
• Extension
• Prevention
• Provision of drugs:
1. OAT (anti-tuberculosis):
2. Bronchodilatator
3. Expektoran
4. OBH
5. Vitamin
• Physiotherapy and rehabilitation
• Consultation on a regular basis
NURSING ASSESSMENT
a. The pattern of activity and rest:
Fatigue, shortness of raised strenuous activity (shortness of breath), Difficulty sleeping, sweating at night
b. Pattern Nutrition:
Anorexia, nausea, bad stomach, decreased BB
c. Respiration:
Productive cough (on stage), shortness of breath, chest pain.
d. Family History:
Usually there are a couple of people who have the same difficulties (the same disease)
e. Environmental history:
Unhealthy environment (pollution, waste), a densely, home ventilation less, the number of members of the family a lot.
f. Psychosocial Aspects:
• Feeling isolated
• Unable to communicate freely, pulling away.
• Usually in poor families.
• Issues related to economic conditions, to heal it takes a long time and cost a stout.
• Concern about the future / job patients.
• Do not get excited, to lose hope.
g. Previous disease history:
• Have a long coughing illness, and did not recover well.
• Once treated, but not cured.
• Once treatment but not regular (drop out).
DIAGNOSIS TREATMENT THAT MAY ARISE:
1. Impaired gas exchange with respect to the presence of risk factors:
• Reduced effectiveness of the surface of the lung, atelectasis.
• Damage to the alveolar capillary membrane.
• discharge is thick
• Bronchial edema.
2. Potential infection and the spread of infection in relation to:
• Immune system decline, decreased function of cilia, secretions were settled.
• Tissue damage due to infection spreading.
• Durability / low resistance to infection
• Malnutrition
• Contaminated by the environment.
• Lack of knowledge about infectious germs.
3. Impaired nutritional needs with respect to fatigue, frequent cough, sputum production presence, dyspnoe, anorexia, decreased financial / cost.
4. Cleaning Ineffective airway secretion in relation to a thick, sticky and bloody, tired and cough less effort, Oedema trachea / larink.
5. Lack of knowledge (hygiene needs), on the condition, treatment, prevention, due to no one explained that a wrong interpretation, limited knowledge / cognition, inaccurate, incomplete imformasi obtained.
Treatment:
1. Name drugs: INH
Dose: 1 x 400 mg
Pharmacokinetics:
• absorbed: from the digestive tract, reduce speed and rate of food absorption
• Peak: 1-2 hours
• Distribution: The whole body tissues and fluids, including the CNS, cross the placenta
• Metabolism: Not activated by acetylation in the liver
• Elimination: half time 1-4 hours, 75-96% diekresikan in the urine within 24 hours, excreted in breast milk
Side effects: usually associated with dose
• CNS: parestesias, perifeal neuropaty, headache, weakness, tinnitus, dizziness, vertigo, ataxia, somnolence, insomnia, amnesia, euphoria, toxis psychoses, behavioral changes, depression, memory impairment, hyperpireksia, hallucinations, convulsions, muscle spasms, excessive dreams, menstruation
• Eyes: blurred vision, impaired vision, optic neuritis, atrophy
• GI: Nausea, vomiting, epigastric distress, dry mouth, constipation
• Hematologic: agranulocytosis, hemolytic or aplastic anemia, thrombocytopenia, eosinophilia, methemoglobinemia
• Hepatotoxicity: chills, skin blisters (mosbiliform, macular papular, purpura, urticaria) limpadenitis, vasculitis
• Metabolic Endocrine: Decreased absorption of vitamin B12 deficiency, pridoksin (vitamin B6), pellagra, gynecomastia, hyperglikemia, glycosuria, hyperkalemia, hipophosphathemia, hypocalcemia, acetonia, metabolic acidosis, proteinemia
• Other: dyspnea, urinary retention, fever yangdisebabkan drugs, rheumatoid arthritis, lupus erythromatosus syndrome, irritation at the injection site of the former.
• Implications care:
Management:
• Oral medications INH better given before meals 1-2 hours before the food is absorbed, if GI irritation occurs, the drug should be administered with food
• Isoniazid is stored in the form of a solution in crystalline form and stored in a low temperature. If this occurs the drug stored in a warm or in room temperature.
• Local temporary pain after IM injection, massage the injection area by rotating the injection site
• Medicines should be kept sealed, temperature 15-30 C unless otherwise provided in
Assessment / drug effects:
• Test the weakness right, before giving therapy to detect possible resistant bacteria
• Effects therapetik usually becomes apparent within 2-3 weeks of the first administration therapy. More than 90% of patients who received therapy had a sputum decreased after 6 months
• Examination of the eye
• Monitor blood pressure during administration of drugs
• Patients should be carefully examined by interview and in monthly intervals for early detection of the signs and symptoms of hepatotoxicity
• Continuous Therapy INH after onset of hepatic dysfunction increases the risk of severe liver damage
• Isoniazid hepatitis (sometimes fatal) usually develops over 3-6 months, but may occur at any time during the provision of therapy, it is more frequency in patients with age 35 years or older or especially drinking alcohol every day
• Check body weight 2 times a week, under standard conditions
• Patients should be absorbed DM to loss of control of diabetes between the real and glycosuria benedik test positive; false immediately reported
• peripheral neuritis cause more toxic affect is often preceded by parestesikaki and hands. Patients were free of vulnerabilities include (included) or the patient's premises alcoholic liver disease, malnutrition, diabetic, inaktivator slow, pregnant women and power.
Health education to families and patients
• Memeperingatkan patient to foods containing tyramine (cheese, fish) is the cause of palpitations, blood pressure peningktan.
• instructions to report to the medical patient when there are signs and symptoms of the development of hepatotoxic
• Warn patients against histamine-containing foods (tuna fish) could be the cause of the palpitations increase drug response (headache, hypotension, palpitations, sweating, diarrhea)
• Generally INH therapy given 6 months - 2 years for the treatment of active TB, when used for preventive therapy, INH given 12 months.
2. Drug name: Ethambutol hydrochloride
Dosage: Adults 15 mg / kg (orally), for the re-start treatment with 25 mg kg / BW / day or 60 days, then reduced to 15 mg / kg / hr
Children :: 6-12 years: 10-15 mg / kg / day
Pharmacokinetics:
• Absorption: 70% - 80% is absorbed in the gastrointestinal tract
• Peak 2-4 hours
• Distribution: diodistribusi to all body tissues, the highest concentration in erythrocytes, kidneys, lungs, saliva, via the placenta, is distributed into breast milk.
• Metabolism: metabolized in the liver
• Elimination: half time 3-4 hours, 50% diekresikan in urine for 24 hours, 20-22% excreted in feces
Side effects:
• CNS: headache, dizziness / dizziness, confusion, hallucinations, paresthesia, peripheral neuritis, joint pain, weakness in the lower extremities
• Eyes: eye toxicity: retrabulbar optic neuritis, anterior optic neuritis likely to decrease in visual acuity, visual field narrowing broad, blindness red-green, scotoma in the central and peripheral, eye pain, fotophobia, retinal hemorrhage and edema.
• Digestive Tract: anorexia, nausea, vomiting, abdominal pain
• hypersensitivity: pruritis, dermatitis, anafilaktis
• Hyperuresemia, fever, malaise, leukopenia (rare), sputum containing blood, while disturbances in liver function (possible hepatotoxicity), nephrotoxicity, acute gout arthritis, ECG abnormalities, transpiration
Nursing Implications
• Ethambutol may be given after meals if gastrointestinal irritation occurs. Absorption is not so affected by the food in the stomach.
• Protect from light ethambutol, inertia and heat. Put the packaging hermetically sealed at a temperature of 15-30 C unless given direct.
Assessment and drug effects
• Culture and susceptibility tests should be determined prior to the commencement of the action / and repeat the treatment periodically as a whole.
• okuli toxicity generally appear within 1-7 months after the start of tyerapi. Symptoms usually do not appear for several weeks to several months after the drug was discontinued
• Test opthalmoskopik includes extensive visual field tests, tests for visual acuity using paper currency, and color discrimination tests for classification should be determined first to start therapy and in monthly intervals during therapy. Eyes should be tested separately as well as jointly
• Monitor the ratio of input and output in patients with renal impairment. Report any oliguria or significant changes in the ratio or the laboratory reports of kidney function. Accumulation of systemic toxicity can result from medications ekresi slow
• Renal and hepatic function tests, blood counts and determinants of serum uric acid should be determined at regular intervals in the treatment thoroughly.
Education of patients and families
• In general, therapy can be continued for 1-2 therapy longer, though irregular shorter treatment can be used with either
• If the patient is pregnant during treatment suggest to report to the doctor immediately. Drugs should be separate.
• Advise patient to report accurately to the doctor about the incident dissimulation of view, changes in color perception, sags wide field of view, some other visual symptoms. Patients should be periodically asked about his
• If detected early, visual defects are generally not seen more than a few weeks to several months. In some instances (rare), recovery may be slow. For a year or more or defect may be irreversible.
3. Name drugs: rifampicin
Dose: 1 x 450 mg
Pharmacokinetics:
• Absorption: Readily absorbed in the gastrointestinal tract
• Peak: 2-4 hours
• Distribution: distributed everywhere include CSF, via the placenta, is distributed into breast milk
• Metabolism: metabolized in the liver to metabolize the active and inactive enterohepatic cycle.
• Elimination: The half-life of 3 hours. Up to 30% diekresikan in the urine of 60% - 65% in feces
Side effects:
• CNS: fatigue, drowsiness, headache, ataxia, confusion, dizziness, inability to concentrate, general numbness, pain in the extremities, muscle weakness, impaired vision, conjunctivitis, low-frequency hearing loss, temporarily.
• GI: heart burn, epigastric distress, nausea, vomiting, anorexia, flaturens, cramps, diarrhea, pseudomembranous colitis.
• Hematologic: Thrombocytopenia, leukopeni while, anemia, covers (included) hemolytic anemia
• Hypersensitivitas: hot, pruritis, urticaria, skin eruptions, pain in the mouth and tongue, eosinophilia, hemolysis
• Renal: hemoglobinuria, hematuria, Acute Renal Failure
• Other: hemoptysis, light-chain proteinuria, syndrome "flulike", menstrual disorders, hepatorenal syndrome (intermittent therapy). Temporary increases in liver function tests (bilirubin, BSP, alkaline phosphatase, ALT, AST), pancreatitis
• Overdose: GI symptoms, increased lethargi, enlargement and hardening of the liver, jaundice, sweat, saliva, tears, feces
Nursing Implications
• Capsules can be opened and filled with drunk / diteguk with water or mixed with food
• Oral Suspension can be prepared from capsules for use in pediatric patients
• Beriakn 1 hour before or 2 hours after meals. The peak of serum levels slowed and possibly slightly lower when given with food
• Preservation should be kept in capsules are packaged in bottles, can become unstable in humid conditions
Assessment and drug effects
• Serologic tests and vulnerability should be determined during the primary and in a state / time positive cultures
• Suggested hepatic function tests periodically. Patients with liver disease should be monitored in a closed (closely)
• If the patient also gets anti-coagulants, prothrombin time should be determined on a daily or frequently to create and maintain the anticoagulant activity
Education to patients and families
• Inform patient that drug may give color to red-orange urine, feces, sputum, sweat and tears. Especially those that use contact lenses or colored glass more permanent
• Patients with oral contraceptives, should consider alternative methods of contraception. The same stuff used Rimfapisin and decrease the effectiveness of oral contraceptives for contraception and menstrual disorders (spotting, bleeding)
• Note the patient to keep the drug out of the reach of children
4. Drug name: Pyrazinamide
Dosage: 2 x 500 mg
Pharmacokinetics:
• Absorption: Direct absorption from the gastrointestinal tract
• Peak: 2 hours
• Distribution: Past the blood-brain barrier
• Metabolism: in metabolism in the liver
• Elimination: Part time 9-10 hours, diekresikan slowly in urine
Side effects:
• Astralgia, active gout, difficulty in urinating, headache, photosensitivity, urticaria, skin rash (rare), hemolytic anemia, splenomegaly, limphadenopathy, hemoptysis, peptic ulcer, serum uric asid, hepatotoxic, renal function tests were abnormal, decreased plasma prothrombin.
Implications care
• Medicines should not proceed if there is a reaction liver (jaundice, pruritis, sclera jaundice, yellow skin) or hyperursemia and acute gout
• Place in a closed place (temperature 15-13 C)
Drug effects
• Patients should be observed and instructed medical supervision
• Patients should be checked regularly, and the possible presence of toxic signs: enlargement of the liver, jaundice, damage the integrity of the vascular (echymosis, ptekie, abnormal bleeding)
• Hepatic reactions are more common in patients receiving high-dose
• liver function tests (AST, ALT, serum bilirubin) should be checked 2-4 weeks during therapy
Health education to patients in the family
• Report any difficulties in emptying
• Patients should desire for fluid intake 2000 ml / day if possible
• Patients with diabetes mellitus should be open to monitor and seek advice on the possibility of losing control of glycemia
5. Drug name: Aldactone
Dosage: 2 x 100 mg
Pharmacokinetics:
• Absorption: 73% digestive canals, onset: slowly.
• Peak: 2-3 days, max. the effect of 2 weeks.
• Duration: 2-3 days or more.
• Distribution: through placenta, distributed through breast milk.
• Metabolism: in the liver and kidneys.
• Elimination: The half-life: 1.3 to 2.4 hours kompound parent, 18-32 hours metabolized, 40-57% in ekskresikan in the urine, 35-40% in the bile.
Side effects:
• Lethargy, fatigue (rapid weight loss), headache, and ataxia.
• Endocrine: genekomastik, inability to maintain an erection, the effects of endogenous (menstrual irregularity, hersutisme, vote in), changes in the thyroid, reduced glukosetoleransi.
• GI: abdominal cramps, nausea, vomiting, anorexia, diarrhea.
• Skin: maculopapular, erythematosus rash, urticaria.
• Other: fluid and electrolyte imbalance (hyperkalemia, hyponatremia), increased BUN, acidosis, agranulasitosis, SLE, hypertension (post sympatectomi), hiperurecemia, Gout.
Implications care:
Management:
• Give with food to enhance absorption of food.
• Puree with a fluid tablet before administration chosen by the patient.
• Medication is stored in covered, in light-resistant packaging, in the form of suspension I hold within months under refrigeration.
Assessment and muscle effects:
• Check blood pressure before treatment is given.
• Serum electrolytes should be monitored, particularly during the beginning of therapy and be prepared if there are signs of an electrolyte imbalance.
• Monitor intake and output every day and check the edema, report deficiencies diuretic response or progression Odem.
• Report when there are effects mental changes, lethargy, stupor in patients with liver disease.
• adverse reactions, occurring generally reversible with medication discontinued. Ginekomastik associated with the dose and duration of therapy. This is all done even if the drug has been discontinued.
Education of patients and families:
• Inform the patient and family deuretik maximum drug effects may not occur until the third day of therapy. And deuretik continuously for 2-3 days after the drug is stopped.
• Intruksikan patient to report signs of hyponatremia, which is more common in patients with severe serosis.
• Generally, patients should avoid intake of foods high belebihan potassium and salt.
REFERENCES
Alsagaff Hood, Abdul Mukty, (1995). Basic - Basic Sciences Pulmonary Disease. Airlangga University Press. Surabaya.
Muhammad Amin, Hood Alsagaff. (1989). Introduction Lung Disease. Airlangga University Press. Surabaya.
Blac, MJ Jacob. (1993). l.uckman & Sorensen's Medical surgical Nursing A Phsycopsicologyc Approach. W.B. Saunders Company. Philapidelpia.
Barbara engram. (1999). Medical Surgical Nursing Care Plans. Vol. 1. Publisher EGC. Jakarta.
Marylin E Doengoes. (2000). Nursing care plans guidelines for Perencnaan / documentation of Patient Care. EGC.Jakarta.
Soeparman, Sarwono Waspadji. (1990). Medicine Volume II. Hall Publisher FKUI. Jakarta.
Sylvia Anderson Price, Lorraine McCarty Wilson. (1995). Pathophysiology Clinical Concepts Process - Process disease. EGC. Jakarta.
Faisal Yunus. (1992). Pulmonology Clinic. Section of Pulmonology FKUI. Jakarta.
Pulmonary Tuberculosis is an infectious disease that attacks the lungs caused by Myobakterium Tuberculosis.
Etiology:
Type of rod-shaped bacteria, 1-4/um length and thickness from 0.3 to 0.6 / um. Most of the bacteria in the form of fats / lipids that bacteria resistant to acids and is more resistant to chemical, physical. Other properties of aerobic bacteria is an area that many oksigin love, more pleasure in this region of high oxygen content is epikal lung area, this area is the prediction of the disease Tuberculosis.
Pathophysiology:
The disease is controlled by an intermediary immune response effector cells (macrophages), whereas limphosit (T cells) are cells imonoresponsifnya. Immunity usually involves macrophages are activated in place of infection by lymphocytes and lymphokines, this response is called a hypersensitivity reaction (slow). Tubercle bacillus reaches the surface of the alveolar be inhaled as a unit (1-3 basil), clumps of bacilli larger canals tend to be restrained nose and bronchial large branches and do not cause disease. That is the bottom dialveolus upper lobe pulmonary tubercle bacillus makes inflammation. Polymorphonuclear leukocytes appear in tempay and mempagosit, but do not kill the bacilli. The following days leukocyte replaced by macrophages, alveolar consolidation and attacked experiencing symptoms of acute pneumonia. Cellular pneumonia can be cured by itself. This process can go on, and continue dipagosit basil or multiply in the cells. Basil also spread through the lymph nodes. Macrophage infiltration into the hold longer and some unity formed epithelioid cell tubercles surrounded by lymphocytes (takes 10-20 days). Necrotic lesions of the central section gives a relatively solid and like cheese (caseating necrosis). Areas that experienced necrosis and granulation tissue surrounded by epithelioid cells and fibroblasts will cause different responses. Granulation tissue fibroblasts would be forming scar tissue and finally form a capsule surrounded by tubercles
SIGNS & SYMPTOMS
Complaints can vary or even without a complaint, which most are:
1. Fever: subfebril, febrile (40-41derajat C) intermittent.
2. Cough: is due to irritation of the bronchi, cough is to remove / eject the production of inflammation, starting from a dry cough to cough purulenta (produces sputum)
3. Shortness of breath: when is advanced in which up to half a lung inflammatory infiltration.
4. Chest pain: This is rare, occurs when the infiltration of inflammatory pain up to the pleura causing pleuritis.
5. Malaise: found beripa anorexia, decreased appetite, weight decreased, Sakir headache, muscle pain, night sweats diwaktu
In atelectasis there is any clinical manifestations are cyanosis, shortness of breath, collapse. The patient does not move the chest during breathing and heart pushed to the other side of the sick. In Pictures Torax appear on the affected side silhouette and diaphragms stand up.
DIAGNOSTIC EXAMINATION:
Physical examination:
• At an early stage is difficult to know.
• Ronchi wet, rough and loud.
• hipersonor / tympanic cavity if there is enough and vote umforik auscultation.
• Atrophy and intercostal retractions on the state information and fibrosis.
• When the pleura is pleural effusion occurs (percussion dullness vote)
Radiological examination:
• At an early stage picture looks like patches of clouds with no clear boundaries.
• In the shadow in the form of a ring cavity.
• In the shadow of calcification appear dense patches of high density.
Bronchografi: a special inspection for damage bronchus or lung damage due to TB.
Laboratory:
• Blood: leukocytes rose, LED rose
• Sputum: BTA found on culture
• Tuberculin Test: Mantoux test (induration of more than 10-15 mm)
MANAGEMENT:
• Extension
• Prevention
• Provision of drugs:
1. OAT (anti-tuberculosis):
2. Bronchodilatator
3. Expektoran
4. OBH
5. Vitamin
• Physiotherapy and rehabilitation
• Consultation on a regular basis
NURSING ASSESSMENT
a. The pattern of activity and rest:
Fatigue, shortness of raised strenuous activity (shortness of breath), Difficulty sleeping, sweating at night
b. Pattern Nutrition:
Anorexia, nausea, bad stomach, decreased BB
c. Respiration:
Productive cough (on stage), shortness of breath, chest pain.
d. Family History:
Usually there are a couple of people who have the same difficulties (the same disease)
e. Environmental history:
Unhealthy environment (pollution, waste), a densely, home ventilation less, the number of members of the family a lot.
f. Psychosocial Aspects:
• Feeling isolated
• Unable to communicate freely, pulling away.
• Usually in poor families.
• Issues related to economic conditions, to heal it takes a long time and cost a stout.
• Concern about the future / job patients.
• Do not get excited, to lose hope.
g. Previous disease history:
• Have a long coughing illness, and did not recover well.
• Once treated, but not cured.
• Once treatment but not regular (drop out).
DIAGNOSIS TREATMENT THAT MAY ARISE:
1. Impaired gas exchange with respect to the presence of risk factors:
• Reduced effectiveness of the surface of the lung, atelectasis.
• Damage to the alveolar capillary membrane.
• discharge is thick
• Bronchial edema.
2. Potential infection and the spread of infection in relation to:
• Immune system decline, decreased function of cilia, secretions were settled.
• Tissue damage due to infection spreading.
• Durability / low resistance to infection
• Malnutrition
• Contaminated by the environment.
• Lack of knowledge about infectious germs.
3. Impaired nutritional needs with respect to fatigue, frequent cough, sputum production presence, dyspnoe, anorexia, decreased financial / cost.
4. Cleaning Ineffective airway secretion in relation to a thick, sticky and bloody, tired and cough less effort, Oedema trachea / larink.
5. Lack of knowledge (hygiene needs), on the condition, treatment, prevention, due to no one explained that a wrong interpretation, limited knowledge / cognition, inaccurate, incomplete imformasi obtained.
Treatment:
1. Name drugs: INH
Dose: 1 x 400 mg
Pharmacokinetics:
• absorbed: from the digestive tract, reduce speed and rate of food absorption
• Peak: 1-2 hours
• Distribution: The whole body tissues and fluids, including the CNS, cross the placenta
• Metabolism: Not activated by acetylation in the liver
• Elimination: half time 1-4 hours, 75-96% diekresikan in the urine within 24 hours, excreted in breast milk
Side effects: usually associated with dose
• CNS: parestesias, perifeal neuropaty, headache, weakness, tinnitus, dizziness, vertigo, ataxia, somnolence, insomnia, amnesia, euphoria, toxis psychoses, behavioral changes, depression, memory impairment, hyperpireksia, hallucinations, convulsions, muscle spasms, excessive dreams, menstruation
• Eyes: blurred vision, impaired vision, optic neuritis, atrophy
• GI: Nausea, vomiting, epigastric distress, dry mouth, constipation
• Hematologic: agranulocytosis, hemolytic or aplastic anemia, thrombocytopenia, eosinophilia, methemoglobinemia
• Hepatotoxicity: chills, skin blisters (mosbiliform, macular papular, purpura, urticaria) limpadenitis, vasculitis
• Metabolic Endocrine: Decreased absorption of vitamin B12 deficiency, pridoksin (vitamin B6), pellagra, gynecomastia, hyperglikemia, glycosuria, hyperkalemia, hipophosphathemia, hypocalcemia, acetonia, metabolic acidosis, proteinemia
• Other: dyspnea, urinary retention, fever yangdisebabkan drugs, rheumatoid arthritis, lupus erythromatosus syndrome, irritation at the injection site of the former.
• Implications care:
Management:
• Oral medications INH better given before meals 1-2 hours before the food is absorbed, if GI irritation occurs, the drug should be administered with food
• Isoniazid is stored in the form of a solution in crystalline form and stored in a low temperature. If this occurs the drug stored in a warm or in room temperature.
• Local temporary pain after IM injection, massage the injection area by rotating the injection site
• Medicines should be kept sealed, temperature 15-30 C unless otherwise provided in
Assessment / drug effects:
• Test the weakness right, before giving therapy to detect possible resistant bacteria
• Effects therapetik usually becomes apparent within 2-3 weeks of the first administration therapy. More than 90% of patients who received therapy had a sputum decreased after 6 months
• Examination of the eye
• Monitor blood pressure during administration of drugs
• Patients should be carefully examined by interview and in monthly intervals for early detection of the signs and symptoms of hepatotoxicity
• Continuous Therapy INH after onset of hepatic dysfunction increases the risk of severe liver damage
• Isoniazid hepatitis (sometimes fatal) usually develops over 3-6 months, but may occur at any time during the provision of therapy, it is more frequency in patients with age 35 years or older or especially drinking alcohol every day
• Check body weight 2 times a week, under standard conditions
• Patients should be absorbed DM to loss of control of diabetes between the real and glycosuria benedik test positive; false immediately reported
• peripheral neuritis cause more toxic affect is often preceded by parestesikaki and hands. Patients were free of vulnerabilities include (included) or the patient's premises alcoholic liver disease, malnutrition, diabetic, inaktivator slow, pregnant women and power.
Health education to families and patients
• Memeperingatkan patient to foods containing tyramine (cheese, fish) is the cause of palpitations, blood pressure peningktan.
• instructions to report to the medical patient when there are signs and symptoms of the development of hepatotoxic
• Warn patients against histamine-containing foods (tuna fish) could be the cause of the palpitations increase drug response (headache, hypotension, palpitations, sweating, diarrhea)
• Generally INH therapy given 6 months - 2 years for the treatment of active TB, when used for preventive therapy, INH given 12 months.
2. Drug name: Ethambutol hydrochloride
Dosage: Adults 15 mg / kg (orally), for the re-start treatment with 25 mg kg / BW / day or 60 days, then reduced to 15 mg / kg / hr
Children :: 6-12 years: 10-15 mg / kg / day
Pharmacokinetics:
• Absorption: 70% - 80% is absorbed in the gastrointestinal tract
• Peak 2-4 hours
• Distribution: diodistribusi to all body tissues, the highest concentration in erythrocytes, kidneys, lungs, saliva, via the placenta, is distributed into breast milk.
• Metabolism: metabolized in the liver
• Elimination: half time 3-4 hours, 50% diekresikan in urine for 24 hours, 20-22% excreted in feces
Side effects:
• CNS: headache, dizziness / dizziness, confusion, hallucinations, paresthesia, peripheral neuritis, joint pain, weakness in the lower extremities
• Eyes: eye toxicity: retrabulbar optic neuritis, anterior optic neuritis likely to decrease in visual acuity, visual field narrowing broad, blindness red-green, scotoma in the central and peripheral, eye pain, fotophobia, retinal hemorrhage and edema.
• Digestive Tract: anorexia, nausea, vomiting, abdominal pain
• hypersensitivity: pruritis, dermatitis, anafilaktis
• Hyperuresemia, fever, malaise, leukopenia (rare), sputum containing blood, while disturbances in liver function (possible hepatotoxicity), nephrotoxicity, acute gout arthritis, ECG abnormalities, transpiration
Nursing Implications
• Ethambutol may be given after meals if gastrointestinal irritation occurs. Absorption is not so affected by the food in the stomach.
• Protect from light ethambutol, inertia and heat. Put the packaging hermetically sealed at a temperature of 15-30 C unless given direct.
Assessment and drug effects
• Culture and susceptibility tests should be determined prior to the commencement of the action / and repeat the treatment periodically as a whole.
• okuli toxicity generally appear within 1-7 months after the start of tyerapi. Symptoms usually do not appear for several weeks to several months after the drug was discontinued
• Test opthalmoskopik includes extensive visual field tests, tests for visual acuity using paper currency, and color discrimination tests for classification should be determined first to start therapy and in monthly intervals during therapy. Eyes should be tested separately as well as jointly
• Monitor the ratio of input and output in patients with renal impairment. Report any oliguria or significant changes in the ratio or the laboratory reports of kidney function. Accumulation of systemic toxicity can result from medications ekresi slow
• Renal and hepatic function tests, blood counts and determinants of serum uric acid should be determined at regular intervals in the treatment thoroughly.
Education of patients and families
• In general, therapy can be continued for 1-2 therapy longer, though irregular shorter treatment can be used with either
• If the patient is pregnant during treatment suggest to report to the doctor immediately. Drugs should be separate.
• Advise patient to report accurately to the doctor about the incident dissimulation of view, changes in color perception, sags wide field of view, some other visual symptoms. Patients should be periodically asked about his
• If detected early, visual defects are generally not seen more than a few weeks to several months. In some instances (rare), recovery may be slow. For a year or more or defect may be irreversible.
3. Name drugs: rifampicin
Dose: 1 x 450 mg
Pharmacokinetics:
• Absorption: Readily absorbed in the gastrointestinal tract
• Peak: 2-4 hours
• Distribution: distributed everywhere include CSF, via the placenta, is distributed into breast milk
• Metabolism: metabolized in the liver to metabolize the active and inactive enterohepatic cycle.
• Elimination: The half-life of 3 hours. Up to 30% diekresikan in the urine of 60% - 65% in feces
Side effects:
• CNS: fatigue, drowsiness, headache, ataxia, confusion, dizziness, inability to concentrate, general numbness, pain in the extremities, muscle weakness, impaired vision, conjunctivitis, low-frequency hearing loss, temporarily.
• GI: heart burn, epigastric distress, nausea, vomiting, anorexia, flaturens, cramps, diarrhea, pseudomembranous colitis.
• Hematologic: Thrombocytopenia, leukopeni while, anemia, covers (included) hemolytic anemia
• Hypersensitivitas: hot, pruritis, urticaria, skin eruptions, pain in the mouth and tongue, eosinophilia, hemolysis
• Renal: hemoglobinuria, hematuria, Acute Renal Failure
• Other: hemoptysis, light-chain proteinuria, syndrome "flulike", menstrual disorders, hepatorenal syndrome (intermittent therapy). Temporary increases in liver function tests (bilirubin, BSP, alkaline phosphatase, ALT, AST), pancreatitis
• Overdose: GI symptoms, increased lethargi, enlargement and hardening of the liver, jaundice, sweat, saliva, tears, feces
Nursing Implications
• Capsules can be opened and filled with drunk / diteguk with water or mixed with food
• Oral Suspension can be prepared from capsules for use in pediatric patients
• Beriakn 1 hour before or 2 hours after meals. The peak of serum levels slowed and possibly slightly lower when given with food
• Preservation should be kept in capsules are packaged in bottles, can become unstable in humid conditions
Assessment and drug effects
• Serologic tests and vulnerability should be determined during the primary and in a state / time positive cultures
• Suggested hepatic function tests periodically. Patients with liver disease should be monitored in a closed (closely)
• If the patient also gets anti-coagulants, prothrombin time should be determined on a daily or frequently to create and maintain the anticoagulant activity
Education to patients and families
• Inform patient that drug may give color to red-orange urine, feces, sputum, sweat and tears. Especially those that use contact lenses or colored glass more permanent
• Patients with oral contraceptives, should consider alternative methods of contraception. The same stuff used Rimfapisin and decrease the effectiveness of oral contraceptives for contraception and menstrual disorders (spotting, bleeding)
• Note the patient to keep the drug out of the reach of children
4. Drug name: Pyrazinamide
Dosage: 2 x 500 mg
Pharmacokinetics:
• Absorption: Direct absorption from the gastrointestinal tract
• Peak: 2 hours
• Distribution: Past the blood-brain barrier
• Metabolism: in metabolism in the liver
• Elimination: Part time 9-10 hours, diekresikan slowly in urine
Side effects:
• Astralgia, active gout, difficulty in urinating, headache, photosensitivity, urticaria, skin rash (rare), hemolytic anemia, splenomegaly, limphadenopathy, hemoptysis, peptic ulcer, serum uric asid, hepatotoxic, renal function tests were abnormal, decreased plasma prothrombin.
Implications care
• Medicines should not proceed if there is a reaction liver (jaundice, pruritis, sclera jaundice, yellow skin) or hyperursemia and acute gout
• Place in a closed place (temperature 15-13 C)
Drug effects
• Patients should be observed and instructed medical supervision
• Patients should be checked regularly, and the possible presence of toxic signs: enlargement of the liver, jaundice, damage the integrity of the vascular (echymosis, ptekie, abnormal bleeding)
• Hepatic reactions are more common in patients receiving high-dose
• liver function tests (AST, ALT, serum bilirubin) should be checked 2-4 weeks during therapy
Health education to patients in the family
• Report any difficulties in emptying
• Patients should desire for fluid intake 2000 ml / day if possible
• Patients with diabetes mellitus should be open to monitor and seek advice on the possibility of losing control of glycemia
5. Drug name: Aldactone
Dosage: 2 x 100 mg
Pharmacokinetics:
• Absorption: 73% digestive canals, onset: slowly.
• Peak: 2-3 days, max. the effect of 2 weeks.
• Duration: 2-3 days or more.
• Distribution: through placenta, distributed through breast milk.
• Metabolism: in the liver and kidneys.
• Elimination: The half-life: 1.3 to 2.4 hours kompound parent, 18-32 hours metabolized, 40-57% in ekskresikan in the urine, 35-40% in the bile.
Side effects:
• Lethargy, fatigue (rapid weight loss), headache, and ataxia.
• Endocrine: genekomastik, inability to maintain an erection, the effects of endogenous (menstrual irregularity, hersutisme, vote in), changes in the thyroid, reduced glukosetoleransi.
• GI: abdominal cramps, nausea, vomiting, anorexia, diarrhea.
• Skin: maculopapular, erythematosus rash, urticaria.
• Other: fluid and electrolyte imbalance (hyperkalemia, hyponatremia), increased BUN, acidosis, agranulasitosis, SLE, hypertension (post sympatectomi), hiperurecemia, Gout.
Implications care:
Management:
• Give with food to enhance absorption of food.
• Puree with a fluid tablet before administration chosen by the patient.
• Medication is stored in covered, in light-resistant packaging, in the form of suspension I hold within months under refrigeration.
Assessment and muscle effects:
• Check blood pressure before treatment is given.
• Serum electrolytes should be monitored, particularly during the beginning of therapy and be prepared if there are signs of an electrolyte imbalance.
• Monitor intake and output every day and check the edema, report deficiencies diuretic response or progression Odem.
• Report when there are effects mental changes, lethargy, stupor in patients with liver disease.
• adverse reactions, occurring generally reversible with medication discontinued. Ginekomastik associated with the dose and duration of therapy. This is all done even if the drug has been discontinued.
Education of patients and families:
• Inform the patient and family deuretik maximum drug effects may not occur until the third day of therapy. And deuretik continuously for 2-3 days after the drug is stopped.
• Intruksikan patient to report signs of hyponatremia, which is more common in patients with severe serosis.
• Generally, patients should avoid intake of foods high belebihan potassium and salt.
REFERENCES
Alsagaff Hood, Abdul Mukty, (1995). Basic - Basic Sciences Pulmonary Disease. Airlangga University Press. Surabaya.
Muhammad Amin, Hood Alsagaff. (1989). Introduction Lung Disease. Airlangga University Press. Surabaya.
Blac, MJ Jacob. (1993). l.uckman & Sorensen's Medical surgical Nursing A Phsycopsicologyc Approach. W.B. Saunders Company. Philapidelpia.
Barbara engram. (1999). Medical Surgical Nursing Care Plans. Vol. 1. Publisher EGC. Jakarta.
Marylin E Doengoes. (2000). Nursing care plans guidelines for Perencnaan / documentation of Patient Care. EGC.Jakarta.
Soeparman, Sarwono Waspadji. (1990). Medicine Volume II. Hall Publisher FKUI. Jakarta.
Sylvia Anderson Price, Lorraine McCarty Wilson. (1995). Pathophysiology Clinical Concepts Process - Process disease. EGC. Jakarta.
Faisal Yunus. (1992). Pulmonology Clinic. Section of Pulmonology FKUI. Jakarta.
May be useful.......................... .......................
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