NEPHROTOXI NS

Assessment

have specific, destructive effects on renal cells Carefully monitor renal function with use of tests to identify nephrotoxic reactions can cause acute tubular necrosis (most common), defects in tubular transport system, interstitial nephritis, vasculitis & neprohrotic syndrome nephrotoxic substances and renal injuries caused o Medications all types of renal injuries Antibiotics longer exposure + pre-existing renal disease High risk cephalosporins, sulfonamides, aminoglycosides, amphotericin B Others tetracylcines, bacitracin, polymyxin, colistin Analgesics salicylates, acetaminophen, phenacetin, NSAIDs acute tubular necrosis or chronic renal failure Anesthetics reduces vasoconstrictive ability of kidneys making it more vulnerable to effect of shock; methoxyflurane direct nephrotoxic effect,

Diagnosis

associated with fatal acute renal failure; halothane adverse effect on renal function Diuretics when used aggressively can cause hypovolemia Contrast dyes radioiodinated agents (CT) associated with acute tubular necrosis; risk factors are age over 60 yrs, pre-existing renal insufficiency (diabetic nehropathy), dehydration, low cardiac output with pre-existing renal dse, proteinuria, hypoalbulinemia, multiple myeloma; multiple contrast studies within 24 hr period Other drugs probenecid, phenytoin, LMW dectran, rifampin, phenindione o Heavy metals lead, mercury, arsenic, copper, lithium, gold o Posions- mushrooms, insecticides, herbicides, snake bites o Organic solvents glycols, gasoline, kerosene, turpentine, tetrachloroethylene
Plan/Implementation

1. Discontinue use or reduce dose of nephrotoxic medications 2. Maintain high fluid intake dilute

urine & prevent crystallization 3. Keep patient well-hydrated through out the test or Use of non-dye studies, if possible ; compare baseline and post study renal function tests; monitor urine output for several hours after test
Evaluation Outcome management??

Pyelonephritis

Inflammation of the renal pelvis and parenchyma caused by bacterial infection ( active or remnants of a previous infection)

Assessment Diagnosis

acute occurs after bacterial contamination of urethra or introduction of an instrument or device (catheter, cytoscope) chronic occurs after chronic obstruction with ureteral reflux or chronic disorders Bacteria may trigger inflammatory response, increase WBCs----->edema and swelling of involved tissue (papillae to cortex); if treated --->fibrosis and scar tissue formation

Plan/Implementation Evaluation

GLOMERULONEPHRI TIS
Assessment

Nephrotic syndrome: clinical manifestations caused by protein wasting secondary to diffuse glomerular damage; predisposed by allergic reactions, reactions to specific drugs, renal vein thrombosis, sickle cell disease and heart failure Nephritic syndrome clinical manifestations that includes hematuria plus one of the ffg: oliguria (less than 400 mL/24 hrs), HPN, elevated BUN or decreased GFR Caused by immunologic reaction that results in proliferative and inflammatory changes in glomerular structure; can be acute or chronic usually manifested by either a nephrotic or nephritic syndrome o Function filter blood o Results from Ag-Ab complexes trapped in the glomerulus --->inflammatory damage and impeded glomerular function,

Diagnosis

reducing glomerular membranes capacity for selective permeability o Source of Ag exogenous (after Strep infections) or endogenous formed in the kidney/ antibodies affixed to the glomerular basement membrane (Goodpastures syndrome) o Primary pathologic processes are proliferation and inflammation Nephrotic syndrome- set of clinical manifestations caused by protein wasting secondary to diffuse glomerular damage; predisposed by allergic reactions, reactions to specific drugs, renal vein thrombosis, sickle cell disease and heart failure Nephritic syndrome set of clinical manifestations that includes hematuria plus one of the ffg: oliguria (less than 400 mL/24 hrs), HPN, elevated BUN or decreased GFR -Common including immunoglobulin A (IgA) nephropathy

Plan/Implementation

Interventions: Reduce inflammation o Plasmapheresis to remove specific circulating Abs and mediators of the inflammatory response, in conjunction with corticosteroids & immunosuppressive agents (azathioprine and cyclophosphamide) o Antibiotic therapy for Strep organisms Maintain fluid and electrolyte balance o Treat volume overload and HPN diuretics, antiHPN, restrict dietary sodium and water o Appropriate monitoring VS, I&O, weight; measurement of legs, abdomen Adequate nutritional intake high caloric, low protein diet, offer hard candies, ice chips to quench thirst Adequate rest physical and emotional Prevent skin breakdown (edema) good hygiene, massage, position changes; other prophylactic measures (mattress) Boost clients immune defenses; prevent RT and UT infections

Evaluation

Pathophysiologic Mechanisms of Glomerulonephritis: Antibody deposition Cell-mediated immune mechanisms GLOMERULONEPHRITIS Influx of circulating leukocytes On-Off Switch Persistent Inflammation (chronic glomerulonephritis) Exit of anti-inflammatory molecules & leukocytes (acute glomerulonephritis) Hemodynamic alterations Complement activation

Chronic renal failure

Scarring

Resolution

SYSTEMIC LUPUS ERYTHEMATOS US

Chronic, inflammatory, autoimmune disorder characterized by a wide array of clinical manifestations in vascular and connective tissue Two types: systemic (most severe) and discoid (mild involving only the skin usually affecting face, neck and upper chest) Relatively rare; seen commonly in African American then Asians then whites; 10x more common women age 15-40 Acute forms- fever, musculoskeltal aches and pains, butterfly rash on face, pleural effusion, basilar pneumonia, generalized lymphoadenopathy, pericarditis, tachycardia, hepatosplenomegaly, nephritis, delirium, convulsions, psychosis and coma Chronic forms depend on organ involvement May include fever, malaise, weight loss, cutaneous discoid LE lesions, erythematosus of the exposed skin, generalized lymphadenopathy, severe hemolytic anemia, thrombocytopenic purpura, hypersplenism, pericarditis, pleural effusion, tachycardia, peripheral vascular syndromes (Raynauds phenomenon, gangrene), ulceratie mucuous membrane lesions, abdominal pains, nausea, vomitin, anorexia, bloody stools, hepatic dysfunction, focal glomerulitis progressing to glomerulonephritis, myalgia, arthralgia, neuritis, hemiplegia, convulsions and coma Cause- unknown Factors implicated: Genetic predisposition

Assessment

Diagnosis

Infection Environmental irritants Physical and emotional stress Exposure to UV B radiation Medications reversible forms Definite hydralazine, procainamide Possible chlorpromazine, ethosuximide, hydantoin, methyldopa, dPenicillamine, oral contraceptives, practolol and Quinidine Familial tendency- incidence of 25-50% for twins Pathophysiology Antinuclear antibodies (ANAs) against double (ds) DNA; formation of autoimmune complexes triggering the inflammatory response; Common deposition of Ag-ANAs in the kidney --- glomerulonephritis; also deposited in the brain and heart Defect in T suppressor cell --- infective protective process of preventing autoantibody formation Onset and Prognosis: May be rapid (acute fulminant course); insidious --- chronic with remissions and exacerbations More severe for young onset, live for 5 yrs (95% of cases) Potentially fatal, leading cause is renal failure Medical Management/Goals: 1. maintenance of skin integrity 2. promotion of healthy lifestyle and reduction of stress 3. maintenance of proper nutrition 4. promotion of comfort

Plan/Implementation

5. increase in clients independence 6. maintenance of emotional well-being checkup every 3 months with determination of CBC, creatinine and cholesterol levels, urinalysis, serum C3,C4 and anti-ds DNA based on organ system involved a. cardiac with pleural effusion, pericarditis IV pulse methylprednisolone followed by oral prednisone b. cutaneous antimalarial agents c. plasmapheresis efficacy not determined d. risk for coronary heart disease, HPN 1. lifestyle changes 2. reduce salt and fat/cholesterol intake e. avoid sun exposure triggers inflammatory response f. clients on immunosuppressants preventive/vaccines for pneumococal pneumonia and flu g. yearly assessment/checkups dental, ophtha to monitor for systemic infection, effects of medications h. avoid sulfa antibiotics tendency to cause allergy and flares i. Algorithm for management of clients with SLE Nursing Management: -depends on how client responds to condition and/or severity/specificity of manifestations Newly diagnosed knowledge deficits= advise Follow-up =review changes,

Evaluation

psychosocial assessment During exacerbations = physiologic support to prevent skin breakdown, maintain nutritional and metabolic status, minimize risk for opportunistic infections Grief reactions emotional support; refer for counseling Outcome management??

ALLERGIC REACTIONS 1. Hypersensitivity disorders allergic rhinitis, asthma, dermatitis

Assessment

Diagnosis

1. Clients history 2. manifestations experienced during and after allergen exposure 3. results of allergy tests a. skin testing b. RAST radioallergosorbent test to measure IgE levels to certain allergens in vitro; less sensitive than skin testing c. Pulmonary function tests for asthma d. Blood assays for IgE levels, presense of /elevated serum eosinophil levels IgE formation in response to an allergen Factors: Air pollution Sex, age Exposure to second hand smoke Hypersentivity rxn can be: 1. immediate humoral or antigen-antiboby; minutes after exposure 2. delayed cell mediated; prolonged response to the initial allergen Types: Type Cause Patholog ic Rxn Process
I Immediate IgE / anaphylac tic IgG IgM Compleme nt Ag-Ab complexes
Mast cell degranualti on --histamine and leukotriene release Complemen t fixation ---cell lysis Anaphylaxis Atopic dses Skin rxns

II Cytolytic/ cytotoxic III Immune complex

Deposition in vessels and tissue walls --inflmmation

ABO incompatibil ity Durginduced hemolytic anemias Arthrus rxn Serum sickness SLE Acute

GNephritis

IV Cellmediated/ delayed Sensitized T cells

Lymphokine release TB Contact dermatitis Transplant rejection

Plan/Implementation

Medical Management: 1. Identify allergen detailed hx 2. Avoid allergen - airborne 3. Control environment 4. Administer medications a. Antihistamines caution for drowsiness effect b. Decongestants limit use to 1 week c. Steroids caution for side effects d. Aerosols started before allergy season; regular use with dosing of 3-4x a day (expensive) e. Anticholinergics for common cold and asthma f. Bronchodilators beta-agonists to control bronchospasm in asthma g. Antleukotrienes to treat manifestations of asthma and anaphylaxis (leukotrienes contribute to airway edema, smoot muscle contraction, inflammation) 5. promote desensitization for type I Ig-E mediated/immunotherapy increase IgG antibody levels (interferes with IgE binding) and may increase suppressor T-cell function Nursing Management: 1. detailed hx all current clinical manifestations 2. assess for presence of animals, presence

of allergens in the clients environment, occupation 3. Provide appropriate health teaching

Evaluation

Relief from allergic manifestations