Nephritis Flashcards
(39 cards)
0
Q
Glomerulonephritis:
A
Is an inflammation of the glomerular capillary membrane
1
Q
Nephritis:
A
- Inflammation of the Kidneys
2. Different classifications based on area of involvement or etiology
2
Q
Classifications of Nephritis:
A
- Acute postinfectious glomerulonephritis (APIGN)
- Acute proliferative glomerulonephritis
- Chronic glomerulonephritis
- Rapidly progressive glomerulonephritis
3
Q
Acute postinfectious glomerulonephritis (APIGN):
A
- May develop as a response to a gourp A beta-hemolytic streptococal infections of the skin or pharynx or as a result of infection by the Staphylococcus, Pneumococcus, or Coxsackie virus.
- Give antibiotics to ensure eradication of origianl infectious agent
4
Q
Acute proliferative glomerulonephritis
A
- Glomerular damage results from immune complex reaction that localizes on the glomerular capillary wall.
- Antibody-Antigen complexes become lodged in the glomeruli -> inflammation and obstruction
- Glomerular membranes are thickened and capillaries in the glomeruli are obstructed by damaged tissue cells, leading to decreased GFR.
- Vascular permeability increases-> protein, RBCs, red cell clasts are excreted.
- Sodium & water are retained-> expanded intravascular volume & interstitial compartments and resulting in characteristic edema.
5
Q
Chronic Glomerulonephritis:
Causes
A
- Typically end stage of other glomerular disorders: Lupus Nephritis, Diabetic nephropathy, rapidly progressive glomerulonephritis.
- In many cases however, no previous disease has been identified
6
Q
Chronic Glomerulonephritis:
Characteristics
A
- Slow, progressive decline of glomeruli and a gradual decline in renal function
- Kidneys decrease in size symmetrically
- Kidney surfaces become granular or roughened
- Eventually, entire nephrons are lost
- Symptoms are INSIDIOUS, disease is often not recognized until signs of renal failure develop.
7
Q
Lupus Nephritis:
Cause
A
- Consequence of Systemic Lupus Erythematosus (SLE)
- 40-85% of clients w/SLE develop nephritis
- Autoimmune disorder affects connective tissues of body
- Immune complexes form in glomerular capillary wall are usual trigger for glomerular injury.
8
Q
Lupus Nephritis:
Symptoms
A
- Ranges from microscopic hematuria to massive proteinuria
2. Progression may be slow and chronic or fulminant- sudden onset and rapid development of renal failure
9
Q
Goodpasture’s Syndrome:
Cause
A
- Rare autoimmune disorder of unknown etiology
- formation of antibodies to the glomerular basement membrane. These antibodies may also bind to alveolar basement membranes, damaging alveoli and causing pulmonary hemorrhage.
- Usually affect young men (18-35), may occur at any age, also affects women.
10
Q
Goodpasture’s Syndrome:
Patho
A
- Although the glomeruli may be nearly normal in appearance and function, extensive cell proliferation and crescent formation characteristic of RPGN are common.
11
Q
Goodpasture’s Syndrome:
Manifestations
A
- hematuria, proteinuria, endema
- Rapid progression to renal failure may occur
- Alveolar membrane damage can lead to mild or life threatening pulmonary hemorrhage.
- Cough, SOB, hemoptysis
12
Q
Tubulointerstitial Nephritis
A
Results form injury to the renal tubules and interstitium often secondary to glomerular damage and renovasuclar disease.
13
Q
Risk Factors for Nephritis:
A
- Diabetes Mellitus
- HTN
↪️ secondary to vascular damage to the fragile vessels in the nephron. - Bladder Infections- can travel to kidney or cause scarring-> urine retention-> damages nephron
- Over use of painkillers & drug abuse
- Prematurity
- Trauma
- Family history
- Sickle cell anemai, AIDS, CHF
14
Q
Clinical Manifestations of Nephritis:
A
- Many clients are asymptomatic
- onset may be abrupt- flank or midabdominal pain
- irritiability
- Malaise
- Fever
- Microscopic or gross hemtauria- present in all cases -> Tea colored urine
- Mild periorbital edema- occurs early
- Dependent edema of feet & ankles
- Ascities
- Pulmonary effusion-> dyspnea, cough, crackles
- Acute HTN-> encephalopathy-> headache, N/V/, seizures
- Oliguria may or maynot be present
15
Q
Acute Postinfection glomerulonephritis
Manifestations
A
- abrupt onset of hematuria, proteinura,
- Salt & water retention-> increases extracellualr fluid volume-> HTN, Edema
- evidence of Azotemia (10-14 days after initial infection)
- Urine is brown or cola colored
- Edema primarialy in face, around eyes. Dependent- hands, & upper extremiteis.
- Fatigue, N/V/H.
16
Q
Older Adult manifestation:
A
- May have fewer symptoms
- Nausea, malaise, arthralgias, proteinuria- common
- HTN, Edema - seen less often
- Pulmonary infiltrates- may occur early due to worsening of preexisting condition such as heart failure.
17
Q
Acute phase
A
- Bed rest is a key component of treatment plan during acute phase.
- Edema & midle to moderate HTN should be treated with sodium restriction and diuretic- Lasix.
18
Q
Severe HTN w/Cerebral dysfunction
A
- Medical emergency
2. give diazoxide or hydralazine IV
19
Q
Fluid requirements determined by careful monitoring of:
A
- Urinary Output
- Weigth
- Bloodpressure
- Serum electrolytes
- Dietary restriction of sodium and potassium may be necessary with severe azotemia, protein intake may need to be limited.
20
Q
Diagnostic Tests:
A
- Throat or Skin Cultures- defect infection by group A beta hemolytic streptococci
- Antistreptolysin O tieter- streptococcal exoenzymes
- ESR- elevated in APIGN or lupus nephritis
- KUB (Kidney, Ureter, Bladder)- abdominal x-ray- evaulates kidney size. Enlarged= acute nephritis, Small=late Chronic
- Kidney Scan
- Biopsy- most reliable diagnostic for glomerular disorders, helps determine type, prognosis, and appropriate treatment
- BUN- measures urea nitrogen (end product of protein metabolism)
- Serum Creatinine- creatinine in the blood, excreted by kidnesy= indicator or kidney function. level>4= serious impairment
- Urine Creatinine- levels decrease when renal function is impaired
- Creatinine Clearance- used to evaluate GFR. amount of blood cleared of creatinine in 1 minute, depends on pressure of blood
- Serum electrolytes-
- UA- RBCs. proteins- 24 hour specimen.
21
Q
Avoid Nephrotoxic antibiotics
A
- Aminoglycoside antibiotics, streptomycin, some cephalosporins.
22
Q
Agressive Immunosupressive Therapy used for:
A
- To treat the acute inflammatory process such as RPGN, Goodpasture’s, and exacerbations of SLE
- When begun early, significantly reduces risk of end-stage renal disease and renal failure.
- Prednisone- large dose of 1mg/Kg/day
23
Q
Ace inhibitors
A
- Reduce protein loss associated with nephrotic syndrome
- Reduce proteinuria and slow the progression of renal failure.
- Protective effect on the kidney in clients with diabetic nephropathy.
24
NSAIDs
1. Also reduce Proteinuira in some clients
| 2. Can increase Salt and water retention
25
Antihypertensives
1. Maintain blood pressure, which is important because systemic and renal hypertension is associated with a poorer prognosis in clients with glomerular disorders.
26
Bed Rest ordered during
Acute Phase!
27
If edema is significant or client is hypertensive...
1. Restrict sodium intake to 1-2g/day
28
If Azotemia is present...
1. Restrict proteins, thos included in the diet should be complete or high-value proteins. Compelte proteins supply amino acids required for growth and tissue maintenace.
29
Treatment for RPGN and Goodpastures's syndrome
1. Plasmapharesis- remove damaging antibodies from plasma
| 2. Used in conjunciton with immunosupressive therapy.
30
Nursing Diagnosis:
1. Excess Fluid Volume -#1
2. Risk for Infection
3. Risk for impaired Skin integrity
4. Risk for imbalanced nutrition: Less than body requirements
5. Fatigue
6. Ineffective Role Performance
31
Assessment:
| Health History
1. Complaints of facial or peripheral edema
2. weight gain
3. fatigue
4. N/V/F/H
5. abdominal or flank pain
6. Cough or SOB
7. Changes in amount, color, or character of urine
8. History of skin or pharyngeal streptococal infection
9. diabetes, SLE, or Kidney disease
10. Current medications
32
Assessment:
| Physical examination
1. General apperance
2. VS
3. Weight
4. Presence of periorbital, facial, or peripheral edema
5. Skin lesions
6. Infection
33
Goals of care
1. Client maintain or regains normal urine output
2. Client is able to meet nutritional needs
3. Client avoids infection
4. Client maintain skin integrity
5. Client maintains education or remain current with classmates
6. Client participates in diversional acitivities during period of bed rest.
34
Excess Fluid Volume:
1. Monitor VS, Fluid, Electrolytes, I&Os,
2. Watch for fluid shift from vascular to interstitial
3. Monitor degress of ascities- measure abdominal girth
4. Document specific gravity
5. Maintain fluid restriciton as ordered
6. Offer Ice Chips, requent mount care
7. Dietary consult on sodium and protein restricted diets.
35
Risk for Infections
1. Monitor for Fever, malaise, elevated WBC
2. Avoid or minimize invasive procedures
3. if Cath, use sterile intermittent or straight cath or maintain a closed drainage system for indwelling
4. Instruct pt. on good hand hygiene, limit visitors & screen for upper respiratory infections.
36
Risk for Impaired Skin Integrity:
1. Dependent areas or areas prone to pressure are vulnerable to skin breakdown.
2. Turn pt. frequently
3. pad bony prominences or susceptibe areas with sheepskin or protect skin with a transparent dressing.
4. Make sure bed is free of crumbs & wrinkles
37
Risk for Imbalanced Nurtirition: Less than body requirements
1. client follows a "no addes salt" and low-protein diet
2. To increase appetitie, encourage family to bring clients favorite foods fomr home, serve age appropriate quantities to children, and allow children to eat with other clients or with family members.
38
Fatigue:
1. Anemia, loss of plasma porteins, headache, anorexia, and nausea compund the fatigue
2. Schedule activites and procedures to provide adequate rest and energy conservation. Prevent unnecessary fatigue
3. Assist with ADLs as need
4. Reduce energey demands with frequent small meals and short periods of acitivity.
5. limit number of visitors and length.
