URINARY TRACT DISORDERS[FLUID and ELECTROLYTES related DISORDERS]

Acute GLOMERULONEPHRITIS NEPHROTIC SYNDROME Acute and Chronic RENAL FAILURE

BPH (Benign Prostatic Hyperplasia) ** BURNS

Anatomy ReviewOrgan/s involved:Kidney – basic unit NEPHRONS

Lies on posterior abdominal wall with each kidney on either side of the vertebral column and behind the peritoneum [retroperitoneal area]

RENAL [nephron] flowRenal corpuscle (Bowman’s capsule and Glomerulus) ->

proximal/distal tubule -> Loop of Henle -> descending limb -> renal sinus -> ascending limb -> renal cortex (convoluted tubule and renal corpuscle) -> collecting duct -> papillary duct -> calyx -> renal pelvis -> Ureter ->

Urinary BladderUrine is formed via: filtration -> reabsorption -> secretionSecretes “Erythropoietin”

Hormone/s Involved:1. Anti Diuretic Hormone ADH

–hypothalamus -> POSTERIOR pituitary gland -> KIDNEYS

-released during: INCREASED and DECREASED osmolality of the blood

-Baroreceptors [Blood pressure] Dec. BP = Inc. ADH ; Inc. BP = Dec. ADH

-Regulates water reabsorbed by the distal tubules and collecting ducts by altering permeability allowing water to be reabsorbed from the filtrate.

2. Renin –Angiotensin –Aldosterone (RAAS)

DECREASED BP -> Renin (Juxtaglomerular apparatus in kidney) -> Angiotensinogen (Liver) -> Angiotensin I -> ACE (Lungs and Kidney) -> Angiotensin II -> Aldosterone (Adrenal Cortex) -> INCREASED Na and H2O reabsorption = INCREASED BP

3. Atrial Natriuretic Hormone (ANH)ANH (Cardiac muscle R. Atrium) -> Kidneys ->

DECREASE Na reabsorption -> INC. Na Excretion and INC. water loss = DECREASED BP

**NEPHROTOXINS [from MS nursing by Black 8th Ed] Antibiotics Aminoglycosides Tetracyclines Amphotericin B Cephalosporins Sulfonamides (co-trimoxazole) Bacitracin Polymyxin Heavy metals: Lead, mercury, Bismuth, Arsenic, Copper,

Cadmium,Gold, Lithium

Poisons Mushrooms, insecticides, Herbicides, Snake venom (bites) Anesthetics and Contrast Dyes [all] Analgesics Salicylates Acetaminophen Phenacetin NSAIDS Other Drugs: Probenecid, Phenytoin, Heroin, Dextran, Mannitol,

Interleukin 2, Cisplatin, Amphetamines, Aristocholic Acid (Chinese herb)

ACUTE GLOMERULONEPHRITIS-an inflammation of the glomerulus caused by numerous factors including: immunologic abnormalities, ischemia, free radicals, drugs, toxins, vascular disorders, and systemic diseases like DM and SLE. [Huether, McCance]-GLOMERULONEPHRITITS is the most common cause of END STAGE RENAL DISEASE [Huether, McCance]-ACUTE GLOMERULONEPHRITIS is often associated with a streptococcal infection (acute poststreptococcal glomerulonephritis). [Huether, McCance]-Begins abruptly usually 7-10 days after Streptococcal infection or usually occur between 10-21 days after infection; Glomerular injury is IMMUNE MEDIATED; The thickened glomerular membrane contributes to decreased GFR; Most individuals especially children recover without loss if renal function. [Huether, McCance]-encompasses a variety of diseases, most of which are caused by an IMMUNOLOGIC reaction that results in proliferative and inflammatory changes in glomerular structure; can either be acute or chronic and usually manifested by either a NEPHROTIC SYNDROME or nephritic syndrome. [Black, Hawks]

GLOMERULONEPHRITIS TYPES according to: Pathologic lesions [diffuse,focal,segmental,mesangial,membranous,proliferative,sclerotic,crescentic] Progression [ACUTE, Rapidly Progressive, Chronic] Clinical presentation [Nephrotic Syndrome, Nephritic syndrome and Acute and Chronic Renal Failure]

ASSESSMENTS/Sx Subjective/Objective1. Hematuria with Red blood cell casts Objective2. Proteinuria Objective3. Decreased GFR Objective4. Oliguria Objective5. Hypertension Objective6. Edema [eyes,feet,ankles] Objective7. Ascites and Pleural effusion [occasionally] Objective

DIAGNOSTICS-Percutaneous Renal Biopsy [to determine what type, and

the findings to assist in planning intervention and determining the PROGNOSIS (Complete recovery to End stage renal disease).]

-Urinalysis shows: scant, dark, smoky, cola-colored, or red brown hue. Protein (+) produces persistent and excessive foam, urine pH is lower than normal, specific gravity is: midnormal to highnormal

-SERUM CREATININE and Urea Nitrogen is elevated, Creatinine Clearance is decreased, Hematocrit and Hemoglobin may indicate anemia if RENAL FAILURE is imminent.

GOALS/OUTCOMES/PLANNING Maintain Fluid and Electrolyte Balance Reduce inflammation Prevent Thrombosis

Minimize Protein Los

PATHOPHYSIOLOGY [Acute Glomerulonephritis] (MS nursing by BLACK, et al. and Pathophysiology by Huether, McCance)

Modifiable Risk Factors: Previous Streptococcal infection (impetigo and pharyngitis), post bacterial endocarditis, post varicella and Hep B and C infection

Non-Modifiable Risk factors: Systemic Lupus Erythematosus, [Cell mediated immune mechanisms, Antibody deposition, Complement activation, Hemodynamic alterations, Influx of WBC]

Glomerular Injury = Altered GFR, altered glomerular filtration membrane permeability

Streptococcal antigen antibody complexes are deposited in the GBM (Glomerular basement membrane). The antigen antibody complex activates complement and release of inflammatory mediators that damage the endothelial and epithelial lying on the GBMRedness, Heat, Swelling, Pain and Loss of Function (HIPER process)Increased Permeability of membrane

Fever Chills nausea and vomiting Generalized edema FACIAL and PERIORBITAL SWELLING Anorexia Increased BMR FatigueAltered physical mobility d/t edema

Prolonged inflammatory response in the body

Inflammation and increased cells in the GLOMERULUS d/t antigen antibody complexes produced by an infection elsewhere in the body trapped in the

GLOMERULUS **The sources of infection are either exogenous (strep) or endogenous (disease

such as SLE)**

Ascites, Pleural effusion, Heart Failure

Hematuria, Proteinuria, decreased GFR, Oliguria, HYPERTENSION

Prolonged and progressive glomerular and tubular damage

ASSESSMENT-Previous respiratory infections, skin infections, scarlet fever, or previous history of Glomerulonephritis, or SLE, scleroderma, amyloidosis, Hypertension-Examine urine closely for color, amount and abnormal substances-Check VS closely, MONITOR BP especially.NURSING DIAGNOSIS

-Imbalanced Nutrition: Less than body requirements r/t anorexia and increased metabolic demands

-Excess fluid volume r/t decreased urine output-Fatigue r/t increased metabolic demands-Risk for impaired skin integrity r/t edema

-Risk for infection r/t altered immune response secondary to treatment

GOALS/OUTCOMES/PLANNING-The client will maintain adequate nutritional intake as

evidenced by no weight loss, an absence of negative nitrogen balance and normal electrolytes

-The client will maintain balanced intake and output as evidenced by no manifestations of edema or fluid overload.

-The client will conserve energy through an adequate balance of rest and activity as evidenced by absence of complaints of fatigue.

-The client will maintain tissue integrity, tissue will remain intact.

-The client will maintain a healthy immune status, free of infection, as evidenced by normal temperature and an absence of local or systemic manifestations of infection

INTERVENTIONS [hospitalized INITIALLY, outpatient afterwards usually]Independent Interventions RATIONALE-Monitor input and output -daily weighing = Determine progression of edema (assesses renal function)-Thirst relievers = candies, ice chips, lemon slices-bed rest = activity level is equal to amount of hematuria and proteinuria-encourage client to talk about fears and concerns and dealing with emotions

-provide appropriate diversionary activities to cope with prolonged physical immobility-health teaching on avoiding infection (UTI and respiratory)

-Accurate assessment = thorough and appropriate planning-Weight is the most accurate measurement of fluid status

-Relieve thirst without compromising fluid status-Bed rest allows recovery and minimizes possible further damage minimize usage of protein stores in the body (MUSCLE WASTING).

-Immobile clients need to promote physical activity even when on bed rest because if not muscles would become atrophied-Avoiding infection is important so as to promote early recovery of client

Dependent-Administer Corticosteroids and immunosuppressive agents (azathioprine, cyclophosphamide) as ordered by Physician

-Administering drugs that suppress the immune response would preserve the function of the kidneys and minimize use of protein

**ORALS TIP**: IMMUNOSUPPRESSED clients are more prone to infection, ASEPTIC Technique and INFECTION CONTROL is very important.

-PLASMAPHERESIS [CHECK for nursing responsibilities r/t this procedure]

-Administer Diuretics, anti-hypertensive agents as ordered

in muscle and tissue repair.

-This procedure removes specific circulating antibody or mediators of inflammation and the client’s plasma is cyclically removed and replaced with fresh frozen plasma through a continuous flow blood cell separator.

-Excessive fluids are removed via Diuretics and excessive RAAS stimulation causes hypertension, so these agents are carefully administered as ordered by the physician.

Collaborative-Regular follow up appointments, adherence to medications, dietary restrictions, Blood Pressure regulation.

-Dietary restriction of Sodium and water, high calories, and low protein to preserve kidney function.

-For assessment and further evaluation if client is improving and readjustment of medications and activities to promote client’s improved health status-Sodium and water attract each other; High Calories provide energy and Low Protein diet helps the kidneys not to strain too much thus preserving Kidney function and promoting tissue repair.

Nephrotic Syndrome-is the excretion of 3.5g or more of protein in the urine per day and is characteristic of glomerular injury; is more common in children than in adults; Lipoid nephrosis, membranous glomerulonephritis, and focal glomerulosclerosis are directly related to Nephrotic Syndrome, although these conditions can occur with other types of glomerular disease. [Huether, McCance]-SECONDARY forms occur in systemic diseases like: Diabetes Mellitus, amyloidosis, SLE, and Henoch-Schonlein purpura; also seen with certain drugs, infections, malignancies and vascular disorders. When present as a secondary complication it often signifies a serious prognosis. [Huether, McCance]-is a set of clinical manifestations caused by PROTEIN WASTING secondary to diffuse GLOMERULAR DAMAGE. Manifestations include: Proteinuria, hypoalbuminemia and edema. Abnormal permeability of the glomerular basement membrane (especially ALBUMIN) results in loss of protein in the urine, then hypo albuminemia alters ONCOTIC PRESSURE in the vascular tree and the fluid moves into the interstitial spaces, causing edema. This movement stimulates RAAS and the kidney retains sodium and water, thus adding to the extracellular fluid. [Black, Hawks]

- Hypoalbuminemia d/t urinary loss of albumin and decreased synthesis of replacement albumin of the liver because of decreased intake of dietary proteins due to anorexia and/or malnutrition [Huether, McCance]

ASSESSMENTS/Sx Subjective or Objective

1. Proteinuria 1. Objective 2. Hypoalbuminemia 2. Objective3. Hyperlipidemia 3. Objective4. Lipiduria 4. Objective5. Weight Gain 5. can be Both6. Edema 6. can be Both

DIAGNOSTICS-Renal Biopsy (confirmatory diagnosis)-24 hour urine test (Protein loss of >3.5g, Creatinine clearance [DECREASED], Urine Lipid [Increased]-CBC [LOW level ALBUMIN, DECREASED protein, HIGH lipid concentration, DECREASED hemoglobin and Hematocrit, INCREASED or DECREASED blood clotting proteins]

PATHOPHYSIOLOGY [Nephrotic Syndrome] (MS nursing by BLACK, et al. and Pathophysiology by Huether,

McCance)Modifiable Risk Factors: membranous glomerulonephritis, DM, Amyloidosis, Hepa B, syphilis, carcinoma, leukemia, pre-eclampsia,; renal vein thrombosis, and heart failure

Non-Modifiable Risk Factors: sickle cell disease, SLE, allergy to drugs such as: Penicillamine, anti convulsants, Probenecid, captopril, gold salts, heroin, and NSAIDS, UNKNOWN, Age, Gender, Heredity

Abnormally increased permeability of the Glomerular basement membrane alters the filtering capacity of the Glomerulus

Proteinuria >3.5 g/day

Edema

Protein Loss

Decreased BP

RAAS activation

INCREASED Sodium and water retention

Albumin Immunoglobulin

Increased EDEMA formation;

puffiness in the eyes at morning and pitting

edema

HYPOALBUMINEMIA

Fluid loss in intravascular space

Liver lipoprotein synthesis =

HYPERLIPIDEMIA

Increased Susceptibility to infections

Fibrinogen

Decreased Blood coagulation ability

Complications

Calcium Loss by urine = HYPOCALCEMIAARF(Acute Renal Failure) d/t hypovolemiaVitamin D deficiency d/t lost thyroxin proteinMalnutrition r/t anorexiaRenal vein thrombosisAtherosclerosis d/t increased cholesterol in bloodFluid overload Pleural effusion, Ascites and CHF

LIPIDURIA – fat droplets in urine

ASSESSMENT-Previous respiratory infections, skin infections, scarlet fever, or previous history of Glomerulonephritis, or SLE, scleroderma, amyloidosis, Hypertension-Examine urine closely for color, amount and abnormal substances-Check VS closely, MONITOR BP especially.

NURSING DIAGNOSIS-Imbalanced Nutrition: Less than body requirements r/t anorexia and increased metabolic demands-Excess fluid volume r/t decreased urine output-Fatigue r/t increased metabolic demands-Risk for impaired skin integrity r/t edema-Risk for infection r/t altered immune response secondary to treatment

GOALS/OUTCOMES/PLANNING-The client will maintain adequate nutritional intake as evidenced by no weight loss, an absence of negative nitrogen balance and normal

electrolytes-The client will maintain balanced intake and output as evidenced by no manifestations of edema or fluid overload.-The client will conserve energy through an adequate balance of rest and activity as evidenced by absence of complaints of fatigue.-The client will maintain tissue integrity, tissue will remain intact.-The client will maintain a healthy immune status, free of infection, as evidenced by normal temperature and an absence of local or

systemic manifestations of infection.

INTERVENTIONS [hospitalized INITIALLY, outpatient afterwards usually]Independent Interventions RATIONALE-Monitor input and output -daily weighing = Determine progression of edema (assesses renal function)-Thirst relievers = candies, ice chips, lemon slices-bed rest = activity level is equal to amount of hematuria and proteinuria-encourage client to talk about fears and concerns and dealing with emotions

-provide appropriate diversionary activities to cope with prolonged physical immobility-health teaching on avoiding infection (UTI and respiratory)

-Accurate assessment = thorough and appropriate planning-Weight is the most accurate measurement of fluid status

-Relieve thirst without compromising fluid status-Bed rest allows recovery and minimizes possible further damage minimize usage of protein stores in the body (MUSCLE WASTING).

-Immobile clients need to promote physical activity even when on bed rest because if not muscles would become atrophied-Avoiding infection is important so as to promote early recovery of client

Dependent-Administer Corticosteroids and immunosuppressive agents (azathioprine, cyclophosphamide) as ordered by Physician **ORALS TIP**: IMMUNOSUPPRESSED clients are more prone to infection, ASEPTIC Technique and INFECTION CONTROL is very important.

-PLASMAPHERESIS [CHECK for nursing responsibilities r/t this procedure]

-Diuretics, anti-hypertensive agents [ACE inhibitors] + diuretics : reduces proteinuria

-Anticoagulants: reduce blood clot risk

-Albumin infusion + Furosemide (Lasix) -Prednisone (Orasone) Glucocorticoid, -Cyclophosphamide (Cytoxan) –Antineoplastic

-Administering drugs that suppress the immune response would preserve the function of the kidneys and minimize use of protein in muscle and tissue repair.

-This procedure removes specific circulating antibody or mediators of inflammation and the client’s plasma is cyclically removed and replaced with fresh frozen plasma through a continuous flow blood cell separator.

-Excessive fluids are removed via Diuretics and excessive RAAS stimulation causes hypertension, so these agents are carefully administered as ordered by the physician.

-Clients loose Blood proteins and has an altered Blood pH so administration of anticoagulants promote reduced risk of clot formation.-it is administered to prevent heart failure and pulmonary edema-It decreases permeability of glomerulus to protein -It is given if responding poorly to Glucocorticoids to promote

Collaborative-Regular follow up appointments, adherence to medications, dietary restrictions, Blood Pressure regulation.-Dietary restriction of Sodium and water, high calories, and low protein to preserve kidney function.

-For assessment and further evaluation if client is improving and readjustment of medications and activities to promote client’s improved health status-Sodium and water attract each other; High Calories provide energy and Low Protein diet helps the kidneys not to strain too much thus preserving Kidney function and promoting tissue repair.

Acute Renal Failure-is the abrupt loss of kidney function; over a period of hours to a few days the GFR decreases while BUN and serum Creatinine increases. [Black, Hawks]-usually associated with Oliguria (Output of less than 30ml/hr or less than 400ml/day) [Huether, McCance]-Pre-renal causes of ARF are those that interfere with renal perfusion. Intrarenal causes of ARF involve parenchymal changes by disease or nephrotoxic substances. Postrenal causes of ARF arise from an obstruction in the urinary tract, anywhere from the tubules to the urethral meatus. [Black, Hawks].-Most clients with ARF recover within 4-10weeks and renal function improves up to 12months after onset of ARF. The client is also susceptible to renal injury at this time. [Black, Hawks]-BUN interferes with platelet aggregation = bleeding tendencyASSESSMENTS/Sx Subjective/Objective

1. Oliguria/anuria or Non-oliguria 1. Objective2. Fluid and electrolyte imbalance 2. objective3. Acidosis 3. objective4. Anemia 4. objective5. Platelet dysfunction 5. objective6. GI complications

(anorexia,n/v,constipation/ diarrhea)6. Objective

7. Uremic encephalopathy (apathy, defective recent memory, episodic obtundation, dysarthria, tremors, convulsions and coma)

7. objective

8. Impaired wound healing 8. Objective

Classifications of ACUTE Renal Failure according to cause [Huether, McCance]

Possible Causes

PRE-RENAL Hypovolemia, Hemorrhagic blood loss, loss of plasma volume, water and electrolyte loss, hypotension or hypoperfusion, septic shock, cardiac failure or shock, massive pulmonary embolism, stenosis or clamping of renal artery

INTRA-RENAL Acute Tubular necrosis, glomerulopathies, acute interstitial necrosis, vascular damage, malignant hypertension, vasculitis, coagulation defects, renal artery/vein occlusion, bilateral acute pyelonephrities

POST-RENAL Obstructive uropathies, Ureteral destruction, bladder neck obstruction, neurogenic bladder

Diagnostics Diagram for ARF MS nursing by BLACK, et al.

Sudden loss of ability of the kidneys to excrete wastes, concentrates urine, and conserves electrolytes. Evaluate for possible causes, especially if potentially reversible

Acute tubular necrosis (intra-renal) Infection

(pre-renal)

Decreased blood flow (pre-renal)

Trauma, complicated

surgery, septic shock,

hemorrhage, burns,

dehydration or poor intake

Disorders of the blood or autoimmune

disorders (intra-renal)

LABORATORY EVALUATION: CBC,

coagulation studies, peripheral blood smear

Stricture of ureters, GU

tumor, kidney or ureteral

stones, nephrocalcinosis, or enlarged

prostate

Urinary tract obstruction (post-renal)

Overexposure to metals, solvents,

radiographic contrast materials, certain

antibiotics (intra-renal)

Biopsy of the Kidney may be indicated to confirm cause

Diagnostic Tests:Urinalysis abnormal, can show casts; serum Creatinine will increase in the short term; Creatinine clearance likely to decrease; BUN shows sudden increase

Radiological study depends on suspected cause: can be plain abdominal films, ultrasound, CT, MRI

PATHOPHYSIOLOGY ACUTE RENAL FAILURE MS nursing by BLACK, et al.

Risk factors for ARF: PRE-renal = vasoconstriction, hypotension, hypovolemia, hemorrhage, decreased cardiac output; INTRA-renal = Tubular obstruction theory, Back leak theory, alterations in renal blood flow theory; POST- renal = Urinary tract obstruction, neurogenic bladder

Decrease Glomerular filtration rate

Renal hypoperfusion [pre] Acute Tubular Necrosis [intra] Anuria with flank pain or polyuria [post]

ACUTE PRE-RENAL

ACUTE INTRA-RENAL

Tubular Lumen Edema

ACUTE POST- RENAL

Nephron injury

Acute Tubular Necrosis

S/Sx:

Fluid and electrolyte imbalances due to OSMOTIC changes in the BloodAcidosis r/t Decreased Kidney Function which impairs ACID-BASE BalanceIncreased susceptibility to secondary infections d/t decrease excretion of waste productsAnemia r/t Decreased Erythropoietin secretionPlatelet dysfunction r/t loss of Blood ProteinsGI complications r/t vagal nerve stimulationIncreased incidence of pericarditis r/t poor excretion of infectious materialUremic encephalopathy d/t Urea retentionImpaired wound healing d/t loss of Blood Proteins

ASSESSMENT-Monitor those people with risk factors for ARF.-Assess fluid and electrolyte balance-Assess for hypovolemia, because it’s the common cause-Assess for complications such as: Pleural effusion, pericarditis, acidosis, and uremia.

NURSING DIAGNOSIS-Deficient fluid volume r/t loss from a variety of causes-Excess fluid volume r/t inability of the kidneys to produce urine secondary to ARF-Imbalanced nutrition less than body requirements r/t anorexia and altered metabolic state secondary to ARF.-Risk for impaired skin integrity r/t poor cellular nutrition and edema.-Risk for infection r/t lowered resistance

-Anxiety r/t unknown outcome of disease process

GOALS/OUTCOMES/PLANNING-The client will maintain fluid balance, as evidenced by a balanced intake and output.-The client will maintain adequate nutritional status, with sufficient nutrients to meet metabolic needs.-The client will maintain skin integrity, as evidenced by intact skin and mucous membranes.-The client will maintain immune status, resisting infection as evidenced by normal vital signs, normal WBC count and no outward manifestations of infection.-The client will manage anxiety as evidenced by calmness and an ability to focus.

INTERVENTIONS Independent Interventions RATIONALE-Monitor input and output and compare 24 hour to 48 hour trends-Check VS (especially postural BP and apical pulse), skin turgor, mucous membranes every 4 hours depending on severity of the illness.-daily weighing = Determine progression of edema (assesses renal function)-Assess urine specific gravity, abnormal heart sounds, breath sounds and mental status.-careful monitoring of fluid intake as ordered

-Thirst relievers = candies, ice chips, lemon slices-provide appropriate diversionary activities to cope with prolonged physical immobility such as ROM exercises.-Provide pleasant environment during mealtime.-Provide meticulous skin care, frequent turning and special mattresses.

-Maintain aseptic technique at all times and at all procedures.

-Accurate assessment = thorough and appropriate planning-Blood Pressure,skin turgor and fluid status changes occur so frequent assessment findings can show improvement or decline in Kidney function

-Weight is the most accurate measurement of fluid status-To assess heart related complications due to Fluid overload

-CAREFUL and ACCURATE recording of Fluid intake is important to determine overall status of patient-Relieve thirst without compromising fluid status-Immobile clients need to promote physical activity even when on bed rest because if not muscles would become atrophied

-Pleasant preparation of meals stimulates the appetite-Skin is easily broken down due to fluid overload, skin breakdown would predispose client to infection other complications-Avoiding infection is important so as to promote early recovery of client

-give frequent, careful explanations and provide emotional and psychological support.

-Client’s family need to be aware and be supported by the nurse emotionally and be explained regarding the improvement or deterioration of the client

Dependent-Medications to alleviate discomfort of nausea and stomatitis, Enteral or parenteral nutrition may be used.-use of procedures such as Kidney Dialysis or CRRT (Continuous renal replacement therapies ). -Use of Furosemide and Mannitol while monitoring Kidney function.-Electrolyte replacement of Potassium while carefully monitoring its serum blood levels-Use of Sodium bicarbonate, sodium lactate or sodium acetate to treat Acidosis.-Initial treatment with NSAIDS or steroids, recombinant erythropoietin for anemia, Phenytoin for seizures, correct vitamin K deficiencies for those with bleeding tendencies.

-To relieve loss of appetite of client

-Done to reduce body weight and to balance Intake and output

-This somehow maintains fluid balance by pushing out excess fluids in the body-Potassium is easily lost in the Urine, replacement is necessary and so is monitoring to prevent arrhythmias-Acid Base balance is compromised due to poor renal function so these are used to compensate for the buffering system-Correcting other existing problems to prevent complications of the disease.

Collaborative-Collaboration with dietitian to make foods more palatable and avoiding foods rich in Magnesium such as: dark green vegetables, unrefined grains, seeds, nuts, legumes, and antacids and osmotic laxatives containing Magnesium.-Promote high calorie low protein diet, may also be Low sodium, magnesium, phosphate and potassium;

-Use of Electrocardiographic monitors to assess for effects of hypo or hyperkalemia,

-promoting a good diet will enhance recovery and tissue repair

- Proteins are lost yet also retained, careful giving of proteins to compensate for tissue repair is important. Also these proteins must be COMPLETE PROTEINS to reduce nitrogenous wastes.-ECG monitoring is important because Potassium imbalances are common among Renal Failure patients.

BURNS PATHOPHYSIOLOGY [Burns] (MS nursing by BLACK, et al)

Modifiable Risk Factors: Exposure to temperature extremes, exposure to potentially dangerous objects, sites or areas.

contact with strong acids, alkalis, or organic compounds as well as the duration of contact, determine the severity of a chemical injury

contact with flame, hot liquids, semiliquids (steam), semisolids (tar), or hot objects.

- Exposure to asphyxiants, smoke poisoning and Direct thermal injury to Lungs

caused by heat that is generated by Electrical energy as it passes through the body

Exposure to a radioactive source and prolonged exposure to UV rays

THERMAL BURNS

Non-Modifiable Risk Factors: Job, Profession, environmental conditions

ELECTRICAL BURNSCHEMICAL BURNS

RADIOACTIVE BURNS

Exposure to asphyxiants (Carbon Monoxide) and smoke

INHALATION INJURY

HEAT from external source is conducted to skin Exposure to asphyxiants,

smoke poisoning and Direct thermal injury to Lungs

Destroys tissue depending on LENGTH of EXPOSURE to heat and TEMP.

104-111.2 0F or 40-440C CAUSES:-cellular enzyme and cellular systems fail-SODIUM-POTASSIUM pump FAILS

CELLULAR EDEMA

at 440C causes CELL NECROSIS OCCURS

FREE RADICALS produced and FURTHER produce cellular damage

Heat generated by electricity travels throught the body causing INTERNAL TISSUE DAMAGE

-amount of RADIOACTIVE energy and distance from

source is important.

The voltage, type of current moisture content at site, composition of skin and duration of contact are considered in the damage.

AC(ALTERNATING CURRENT)

-produces more heat related injury d/t rapid flow of electricity-ventricular fibrillation-Tetanic muscle contractions-long bone/vertebral compression fractures-can cause acute renal failure

- Hemoglobin, Myoglobin RELEASED from muscles into bloodstream after DEEP BURN injuries involve muscle damage -> it passes to the urine -> if larger than the tubules it could cause obstruction causing RENAL DAMAGE.-Could also cause Cataract formation in HIGH voltage injury on head or neck

-Systemic toxic effects result from CUTANEOUS absorption of offending agent. -ORGAN FAILURE and DEATH from PROLONGED contact

-causes cell death and damage if prolonged.

- Direct HEAT INJURY to upper airway CAUSES EDEMA, ERYTHEMA and ULCERATION in the UPPER airway.

-LOWER airway affectation causes LOCALIZED inflammation causingDECREASED Bronchial ciliary action, DECREASE alveolar surfactant, MUCOSAL EDEMA and after several HOURS tracheobronchial EPITHELIUM will slough off causing HEMORRHAGE

- Carbon Monoxide replaces O2 in RBC decreasing O2 supply. CAUSING HYPOXEMIA depriving tissues and ORGANS of O2 Supply.

PRESENCE of Tissue INJURY

LOCALIZED response if <25%TBSA

SYSTEMIC REPSONSE >25%TBSA

MINOR Burn Injury (LESS than 20% TBSA)

Release of Chemical Mediators

INCREASE Permeability of capillaries

FLUID shifting leading to edema and blister formation

Increased pressure on blood vessels and nerves

OBSTRUCTION of blood flow

ISCHEMIA and Necrosis

PAIN

BENIGN PROSTATIC HYPERPLASIA/HYPERTROPHY [BPH]-is the enlargement of the Prostate Gland. [Huether, McCance]-not primarily a RENAL disorder but a male reproductive tract disorder that affects the urinary tract of males-nonmalignant histologic growth of the glandular elements of the prostate [Black, Hawks]

ASSESSMENT-HISTORY taking (Ask about daytime voiding frequency, nocturia, urgency, urinary incontinence, force of urine stream, hesitancy, need to strain, perception of bladder emptying and prior episodes of acute urinary retention.- BUN, Creatinine clearance and serum creatinine, urine culture or serum prostate specific antigen [PSA]-Uroflowmetry [MS Nursing by Black, Hawks p.876]

NURSING DIAGNOSIS- Impaired Urinary Elimination; Urinary Incontinence; - Disturbed sleeping pattern; - Acute Pain [during urination]- Risk for Infection

GOALS/OUTCOMES/PLANNING- Relieve Urinary Retention- Promote Seep and Comfort at night- Prevent infection due to urinary stasis- Slow prostate growth through medications- Prepare for surgical management such as TURP [Transurethral Resection of the Prostate], etc

INTERVENTIONS- Provide teaching about BPH- Explain medications- Prepare for SURGERY if necessary [all below are mostly POST OP interventions]- Prevent catheter dislodgement- Prevent infection- Monitor for fluid retention- Assist in self-care [Perineal hygiene] If client cannot do for himself (Geriatric) - Teach pelvic muscle Rehabilitation- Prevent injury [post op]

PATHOPHYSIOLOGY: BPH [MS Nursing by Black, Hawks and Pathophysiology by Huether, McCance]

Risk factors for BPH: -Diet [Obesity (Increased abdominal girth), smoking, age, frequent use of alpha adrenergic agonists and OTC cold medications, diet pills INCREASES risk; -Lycopene in cooked tomatoes, green and yellow vegetables, traditional Japanese diet, INCREASED physical activity REDUCES risk

DHT [Dihydrotestosterone] and 5α Reductase imbalance

UNKNOWN or POORLY understood

CELLULAR apoptosis is compromised

Causing enlargement of the Prostate gland

OBSTRUCTION of bladder outlet

Compensation of the Detrussor Muscle in the bladder to push out the urine

[INCREASED force of contraction]

Causing S/Sx to appear after decompensation, while prostate still continues to grow in size obstructing further the urine flow at the Urethra

DECOMPENSATION will result to urine stasis and backflow causing COMPLICATIONS that damage and cause infection to

the parts of the URINARY tract [Urethra up to Kidneys]

Asymptomatic or minor difficulty in urination

S/Sx:-Palpable enlargement via DRE [Digital Rectal Examination], incomplete bladder emptying, daytime voiding frequency, urge urinary incontinence, Nocturia, sleep disturbancesComplications:-RENAL failure, hydronephrosis, hydroureter “fish hook” ureter, UTI and hematuria, Prostatitis