A. BACKGROUND
Glomerulonephritis is a syndrome characterized by inflammation of the glomeruli followed by the establishment of several antigens that may be endogenous (such as circulating thyroglobulin) or exogenous (infectious agents or processes that accompany systemic disease) hospes (kidney) recognize the antigen as foreign and begins to form antibodies to attack it. This inflammatory response causing the spread of pathophysiological changes, including decreased glomerular filtration rate (LFG), increased permeability of the glomerular capillary wall to plasma proteins (mainly albumin) and HR, and abnormal sodium and water retention that suppress the production of renin and aldosterone (Glassok, 1988; In the book Sandra M. Nettina, 2001).
Pyelonephritis is an inflammation or infection of acute renal pelvis, tubules and interstitial tissue. The disease is caused by a bacterial infection enterit (most common is Escherichia coli) that have spread from the bladder into the ureters and kidneys due to reflux vesikouretral. Other causes urinary obstruction or pyelonephritis include infection, trauma, infection from blood, other kidney disease, pregnancy, or metabolic disorders (Sandra M. Nettina, 2001).
Common cause of glomerulonephritis is streptokokkus nemolitikus beta group A type 12 or 4 and 1, rarely by other causes. Signs and symptoms are hematuria, proteinuria, oliguria, edema, and hypertension (Sylvia A. Price and Lorraine M. Willson, 2005).
Cause
The most frequent cause of pyelonephritis was Escherichia coli. Signs and symptoms are sudden fever arises, chills, malaise, tender area kostovertebral, leukocytosis, and bacteriuria (Sylvia A. Price and M. Willson, 2005).
Based on the results of glomerulonephritis and pyelonephritis is more common in girls than boys. Because the urethra is shorter forms and adjacent to the anus. Epidemiological studies indicate the presence of significant bacteriuria at 1% to 4% of the girl students. 5% -10% of women of childbearing age, and about 10% of women whose age exceeds 60 years. In nearly 90% of cases, the patients were women. The comparison of this disease in women and men is 2: 1.
B. The purpose of writing
1. General Purpose
Increase knowledge and understanding of nursing care glomerulonephritis and pyelonephritis.
2. Specific Objectives
- To be able to carry out assessments on patients glomerulonephritis and pyelonephritis.
- To be able to establish nursing diagnoses in patients with glomerulonephritis and pyelonephritis.
- To be able to intervene in patients glomerulonephritis and pyelonephritis.
- To be able to carry out the implementation of the patient's glomerulonephritis and pyelonephritis.
- To be able to evaluate the patient's glomerulonephritis and pyelonephritis.
CHAPTER II DISCUSSION
I. BASIC CONCEPT OF DISEASE
A. Glomerulonephritis
1. Definition
Glomerulonephritis is inflammation and damage to blood purifier as well as capillary kidney (glomerulus) (Sandra M. Nettina, 2001).
Glomerulonephritis is a syndrome characterized by inflammation of the glomeruli followed by the formation of multiple antigens (Barbara engram, 1999).
Acute glomerulonephritis is a term often used broadly refers to a group of diseases in which inflammation occurs in the renal glomerulus (Brunner & Suddarth, 2001).
2. Etiology
a. Germs streptococcus.
b. Associated with other autoimmune diseases.
c. Drug reactions.
d. Bacteria.
e. Virus.
(Sandra M. Nettina, 2001).
3. Clinical Manifestations
a. Pharyngitis or tansiktis.
b. Fever.
c. Headache.
d. Malaise.
e. Pelvic pain.
f. Hypertension.
g. Anorexia.
h. Vomiting.
i. Acute Edema.
j. Oliguria, proteinuria, and brown urine.
(Sandra M. Nettina, 2001).
4. Pathophysiology
Prokferusi cellular (increased production of endothelial cells lining the glomerulus is). Leukocyte infiltration into the glomerular basement membrane produced or abdominal tissue and loss of surface filters. In glomerulonephritis enlarged kidneys, swelling and congestion. In fact the case, the stimulus of the reaction is an infection by the bacteria streptococcus A throat, which usually precede glomerulonephritis until 2-3 weeks interval. Streptococcal products act as antigens, stimulating circulating antibodies cause kidney injury (Sandra M. Nettina, 2001).
5. Diagnostic Examination
a. Urinalysis (UA).
b. Glomerular filtration rate (LFG).
c. Blood urea nitrogen (BUN) and serum creatinine.
d. Pielogram intravenous (PIV).
e. A renal biopsy.
f. Antistrepsomisin O titer (ASO).
(Sandra M. Nettina, 2001).
6. Management
a. Manifestations diet:
- Restrict fluid and sodium.
- Restrictions protein when BUN greatly increased.
b. Pharmacotherapy
- Immunosuppressive therapy such sitoksit agents and steroids to rapidly progressive glomerulonephritis.
- Diuretics, especially loop diuretics such as furosemide (Lasix), and bumex.
- Dialysis, for end-stage renal disease.
(Sandra M. Nettina, 2001).
7. Complication
a. Hypertension.
b. Dekopensasi heart.
c. ARF (Acute Renal Failure).
(Sandra M. Nettina, 2001).
B. Pyelonephritis
1. Definition
Pyelonephritis is a bacterial infection of the cup kidney tubules, and network interstinal of one or both kidneys (Brunner & Suddarth, 2002).
Pyelonephritis is an infection of the kidney that can arise ureterik hematogenous or retrograde flow (JCE Underwood, 2007).
2. Etiology
a. Bacteria (Escherichia coli, Klebsiella Pneumoniac, Streptococcus Fecalis).
b. Obstruction of the urinary track.
c. Reflux.
d. Pregnancy.
e. Diabetes.
f. Circumstances reduced immunity to fight infection.
(Barbara engram, 1988).
3. Clinical Manifestations
The most common symptoms may include sudden fever, and may be accompanied by chills, lower back pain, nausea and vomiting (Barbara engram, 1988).
4. Pathophysiology
Bacteria ascend to the kidney and renal pelvis and bladder through the urethra. Normal fecal flora such as E. Coli, Streptococcus Fecali, Pseudomonas aeruginosa, and Staphilococcus aureus is the most common bacteria that cause acute pyelonephritis, E. Coli causes about 85% of infections. In acute pyelonephritis, kidney inflammation causes enlargement of the ordinary. The cortex and medulla expands and multiple abscesses. Skin and renal pelvis also would berinvolusi. Resolution of inflammation produces fibrosis and scarring of chronic pyelonephritis appears after repeated periods of acute pyelonephritis. Kidney degeneratik changed and become small and atrophic. If the widespread destruction of nephrons, can progress to renal failure (Barbara engram, 1988).
5. Diagnostic Examination
a. Whole Blood.
b. Urinalysis.
c. Ultrasound and Radiology.
d. BUN.
e. Creatinine.
f. Serum Selectrolytes.
(Barbara engram, 1988).
6. Complication
a. Renal papillary necrosis.
b. Fionefrosis.
c. Perinefrit abscess.
(Barbara engram, 1988).
7. Management
a. Specific antimicrobial therapy organisms:
- Usually begins immediately to cover prevalent gram-negative pathogens, and then adjusted based on urine culture results.
- Treatments for 2 weeks or more.
b. Inpatient treatment with parenteral antimicrobial therapy if the patient is unable to tolerate oral intake and dehydration or acute illness.
c. Percutaneous drainage or antibiotic therapy is necessary to treat the old renal abscess or abscesses perinefrik.
(Barbara engram, 1988).
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