Urology Ppt

U R O L O G Y

THE RENAL SYSTEM

• STRUCTURES:– KIDNEYS

• RETROPERITONEAL• RENAL ARTERY & VEIN• NEPHRON

– URETER– URINARY BLADDER– URETHRA

Here is a normal adult kidney. The capsule has been removed and a pattern of fetal lobulations still persists, as it sometimes does. The hilum at the mid left contains some adipose tissue. At the lower right is a smooth-surfaced, small, clear fluid-filled simple renal cyst. Such cysts occur either singly or scattered around the renal parenchyma and are not uncommon in adults.

In cross section, this normal adult kidney demonstrates the lighter outer cortex and the darker medulla, with the renal pyramids into which the collecting ducts coalesce and drain into the calyces and central pelvis.

THE RENAL SYSTEM

• 4 MAIN FUNCTIONS OF THE KIDNEYS:

– EXCRETION OF WASTE PRODUCTS• FILTRATION• TUBULAR REABSORPTION• TUBULAR SECRETION

– REGULATION OF FLUID & ELECTROLYTES– BLOOD PRESSURE REGULATION– ERYTHROPOEITIN SECRETION

THE RENAL SYSTEM

PHYSIOLOGY:• RENIN-ANGIOTENSIN

• ERYTHROPOEITIN

• PROSTAGLANDIN

RELEASED BY CELLS NEAR THE GLOMERULUS WHEN GFR IS LOW OR WHEN SYMPA-NS IS STIMULATED

RELEASED IN RESPONSE TO HYPOXEMIA

•IS RELEASED BY RENAL MEDULLA; VASODILATOR; REGULATE RENAL BLOOD FLOW

THE RENAL SYSTEM

PHYSIOLOGY:• METABOLISM OF VIT D – FOR CALCIUM

METABOLISM

• DEGRADATION OF INSULIN• URGE TO VOID : 200-300 ml OF URINE

• BLADDER DISTENTION: 400 ml• PARASYMPA-NS : DESIRE TO VOID

• SYMPA-NS: MUSCLE RELAXATION & ELIMINATION

Double ureters are seen exiting from each kidney and extending to the bladder that has been opened. A small segment of aorta is seen between the normal, smooth-surfaced kidneys. A partial or complete duplication of one or both ureters occurs in about 1 in 150 persons. There is a potential for obstructive problems due to the abnormal flow of urine and the entrance of two ureters into the bladder in close proximity, but most of the time this is an incidental finding

RENAL DISORDERS

• RENAL FAILURE• GLOMERULONEPHRITIS• NEPHROTIC SYNDROME• NEPHROSCLEROSIS• HYDRONEPHROSIS• INFECTIONS • NEUROGENIC DISORDERS• BENIGN PROSTATIC HYPERTROPHY

CASE STUDY

• Draco, 54 y.o., with history of uncontrolled DM-II, came in because of difficulty of breathing & anuria.

• VS = 38 O; 113; 30; 170/120

• He has bipedal edema & pruritus

CASE STUDY

• What is your first nursing action?

• What other assessment would you do?

• What are your plans?

RENAL FAILURE (R. F.)

INABILITY OF THE KIDNEY TO FXN NORMALLY & EFFECTIVELY

• ACUTE RENAL FAILRE

• CHRONIC RENAL FAILURE

ACUTE RENAL FAILURE

SUDDEN DETERIORATION OF KIDNEY FUNCTION

3 PHASES:1. OLIGURIC

2. ANURIC

3. POLYURIC / RECOVERY + WASTING OF Na, K, & base HCO3

ACUTE RENAL FAILURECAUSES:• PRERENAL

– SHOCK – MISMATCHED BT

• RENAL – NEPHRITIS– NEPHROTOXIC INFECTION

• POST RENAL – RENAL CALCULI

CHRONIC RENAL FAILURE

CAUSES:• PRERENAL

– GOUT– DM– SUBACUTE

BACTERIAL ENDOCARDITIS

• RENAL– SLE– GLOMEROLU-

NEPHRITIS

• POSTRENAL– PROSTATIC

OBSTRUCTION

R. F. - SIGNS & SYMPTOMS

• UO ALTERATIONS• WEAK• INCREASINGLY

DROWSY• RESTLESSNES• INSOMIA• DRY SKIN & MUCOUS

MEMB• URINEFEROUS

BREATH

• NAUSEA/ VOMITING• CNS

– IRRITABILITY– ANXIETY– HALLUCINATION– MUSCLE TWITCHING– CONVULSIONS– COMA

• HPN• ANEMIA• EDEMATOUS• BRUISE EASILY

R. F. - MANAGEMENT

MODALTIES:

1. CONSERVATIVE TREATMENT

2. AGGRESSIVE TREATMENT

CONSERVATIVE TREATMENT

• DIET– P, K, & Na RESTRICTED– GIORDANA-GIOVANETTI : LOW P (MINIMAL

ESSENTIAL A.A.), 20g; controlled K, 1.5g

• TREATMENT OF INFECTION– ANTIBIOTICS

• TREATMENT OF ALTERATIONS OF BODY CHEMISTRY

ALTERATIONS IN BODY CHEMISTRY

I. SUBSTANCES FROM PROTEIN METABOLISM:– UREA– CREATININE– URIC ACID

MGT:• PROTEIN RESTRICTION• PREVETION OF INFECTION• ANABOLIC HORMONES – CAUSE TISSUE BUILD

UP & REVERSE BREAKDOWN

ALTERATIONS IN BODY CHEMISTRY

II. ELECTROLYTES:I. HYPERKALEMIAII. HYPOKALEMIAIII. HYPERNATREMIAIV. HYPONATREMIAV. HYPOCALCEMIA, HYPERPHOSPHATEMIA,

& BONE DSEVI. ACIDOSIS

HYPERKALEMIA

CAUSES IN RF:

• SECRETED out from the cell TOGETHER WITH H ions IN EXCHANGE FOR Na

• DECREASED EXCRETION FROM DECREASED G.F.R.

HYPERKALEMIA

S/SX:• FLACCID PARALYSIS

• SLOW RESPIRATION

• ANXIETY

HYPERKALEMIA

MANAGEMENT:

• K RESTRICTED DIET

• ION EXCHANGE RESIN: KAYEXALATE; SORBITOL IS GIVEN

• IF WITH CARDIAC ARRHYTHMIA : Ca GLUCONATE

• IV NaH2CO3

• GLUCOSE & INSULIN

HYPOKALEMIA

S/SX:

• MUSCLE WEAKNESS• PARALYSIS• LOSS OF REFLEXES• CARDIAC ARRHYTHMIA

(PVC, TACHYCARDIA)• DIGITALIS TOXICITY CAN

DEVELOP

ECG CHANGES:• DEPRESSED T WAVE• ELEVATED U WAVE

MANAGEMENT:• PARENTERAL POTASSIUM

HYPERNATREMIA

SSX:• FLUID RETENTION• WEIGHT GAIN• CHF• PULMONARY EDEMA• HPN

MANAGEMENT:• LIMIT Na INTAKE• DRUGS: DIGITALIS, DIURETICS, ANTIHPN

HYPONATREMIA

S/SX:• DHN• DRY MOUTH• LOSS OF SKIN TURGOR• MUSCLE CRAMPS, TWITCHING• COMA

MANAGEMENT:• INCREASE DIETARY SODIUM• Na H2CO3, Na Citrate

Ca, Ph, & BONE DSE

• HYPOCALCEMIA• HYPERPHOSPHATEMIA• BONE DEMININERALIZATION

MANAGEMENT:• LARGE DOSE OF VIT D

ACIDOSIS

S/SX:• LETHARGY• DISORIENTATION• INCREASED HR• KAUSMAUL’S RESP

MANAGEMENT:• NaHCO3, NaLACTATE

Large love

AGGRESSIVE TREATMENT

• HEMOFILTRATION

• PERITONEAL DIALYSIS

• HEMODIALYSIS

HEMOFILTRATION

• CONTINUOUS ARTERIOVENOUS HEMOFILTRATION (CAVH)

INDICATION:• FLUID OVERLOAD FROM OLIGURIA• RENAL FAILURE

A-V SHUNTULTRAFILTRATION

HEMOFILTRATION

ADVANTAGE:

• DOES NOT REQUIRE DIALYSIS MACHINE OR DIALYSIS PERSONNEL

DISADVANTAGE:• 36-48 HRS

DIALYSIS

INDICATION:• GFR FALLS BELOW 3ml/min

PURPOSE:• REMOVING WASTE PRODUCTS FROM THE BODY

TYPES:• PERITONEAL DIALYSIS• HEMODIALYSIS

PERITONEAL DIALYSIS

CONTRAINDICATION:

• EXTENSIVE ABDOMINAL ADHESION

• PERITONITIS

• GANGRENOUS OR PERFORATED BOWEL

PERITONEAL DIALYSIS

COMPOSITION OF SOLUTION:

• DEXTROSE: 1.5% & 4.5%

• PHYSIOLOGIC CONC OF ELECTROLYTES

• SLIGHTLY HYPERTONIC

PERITONEAL DIALYSIS

36-48 HRS P.D. = 6-8 HRS HEMO

3 PERIODS:• INSTILLATION

• EQUILIBRIUM: OSMOSIS, DIFFUSION & FILTATION

• DRAINAGE

PERITONEAL DIALYSIS

NURSING RESPONSIBILITIES:

• CYCLING THE FLUID

• OBSERVE FOR COLOR OF THE OUTFLOW

• ACCURATE RECORDING ON THE FLOW SHEET

• FREQUENT MONITORING OF VS, WEIGHT & GEN CONDITION

PERITONEAL DIALYSIS

NURSING RESPONSIBILITIES:

• PREVENT COMPLICATIONS OF IMMOBILITY

• CHECK TUBING PATENCY

• INFORM DOCTOR FOR FLLUID BALANCE EVERY SHIFT

• COLLECT SAMPLES OF DIALYSATE REMOVED

PERITONEAL DIALYSIS

NURSING RESPONSIBILITIES:

• TEST URINE FOR GLUCOSE EVERY 6 HRS

• OBSERVE FOR COMPLICATIONS:– PHYSIOLOGIC– TECHNICAL

PERITONEAL DIALYSIS

PHYSIOLOGIC COMPLICATIONS:

• PERITONITIS

• PROTEIN LOSS

• HYPERGLYCEMIA & HHONK

• PULMONARY EDEMA

PERITONEAL DIALYSIS

PHYSIOLOGIC COMPLICATIONS:

• PERFORATION OF INTESTINES

• HYPOTENSION

• HYPOSTATIC PNEUMONIA

• RESPIRATORY ACIDOSIS

• ABDOMINAL DISCOMFORT

PERITONEAL DIALYSIS

TECHNICAL COMPLICATIONS:

• INCOMPLETE/ SLOW DRAINAGE– TURN THE PATIENT SIDE TO SIDE– SEMIFOWLER’S + GENTLE PRSSURE ON THE

ABDOMEN

• LEAKAGE / BLEEDING– NORMAL DURING THE FIRST EXCHANGE

PERITONEAL DIALYSIS

NEWER TECHNIQUE:

CONTINUOUS AMBULATORY PERITONEAL DIALYSIS (CAPD)

• 30-40 MIN TO PERFORM• 4 x A DAY• 24/7

HEMODIALYSISINDICATION:

• ACUTE RENAL FAILURE• CHRONIC RENAL FAILURE

PURPOSE:

• LOWER THE LEVEL OF METABOLIC WASTE PRODUCTS:– UREA, CREATININE, URIC ACID

• CORRECT ABNORMAL ELECTROLYTE CONC

HEMODIALYSIS

• DIALYZER

• SHUNTS:

– CANNULA

– A-V SHUNT

HEMODIALYSIS

CARE OF THE SHUNT:

• DRY STERILE DRESSING

• ENSURE PATENCY

• BRUIT

• NOTIFY PHYSICIAN STAT WITH PRSENCE OF BLOOD CLOT

HEMODIALYSIS

CARE OF THE SHUNT:

• AVOID TRAUMA TO THE ARM WITH SHUNT

• ACCIDENTAL SEPARATION: DIRECT PRESSURE/ VASCULAR CLAMPS

• OBSERVE FOR SHUNT-RELATED INFECTION:– Fever, lethargy, elevated WBC

HEMODIALYSIS

COMPLICATIONS:

• TECHNICAL

• PROCEDURE COMPLICATONS

• MEDICAL

HEMODIALYSIS

TECHNICAL COMPLICATIONS:

• BLOOD LEAKS

• TUBING SEPARATION

• DIALYSATE CONC ERRORS– HEMOLYSIS, CEREBRAL DISTURBANCE

HEMODIALYSIS

PATIENT COMPLICATIONS DURING PROCEDURE:

• DIALYSIS DISEQUILIBRIUM SYNDROME

• HYPERTENTION

• HYPOTENSION

• NAUSEA & VOMITING

• HEADACHE

• ACUTE BLEEDING

HEMODIALYSISPATIENT COMPLICATIONS DURING

PROCEDURE:• FEVER

• MUSCLE CRAMPS

• CARDIAC ARRHYTHMIAS

• CHEST PAIN

• SHORTNESS OF BREATH

• RESTLESSNESS

• DEPRESSION & HOSTILITY

HEMODIALYSIS

MEDICAL COMPLICATIONS:

• HPN

• CHF & PULMONARY EDEMA

• ANEMIA

• HEPATITIS

• LOW SEXUAL POTENCY

RENAL TRANSPLANTATION

• AUTOGRAFT

• ISOGRAFT

• ALLOGRAFT/ HOMOGRAFT

• XENOGRAFT

RENAL TRANSPLANTATION

TREATMENT to prevent REJECTION:

• AZATHIOPRINE (IMMURAN)

• ADRENAL CORTICOSTEROIDS

• ANTILYMPHOCYTES GLOBULIN

• ACTINOMYCIN-C

• LOCAL IRRADIATION THERAPY

RENAL TRANSPLANTATION

S/SX OF TISSUE REJECTION:

• WEIGHT GAIN

• IRRITABILITY

• SWELLING OF THE OPERATIVE SIGHT

• DECREASED W.B.C.

MATRIX

GLOMERULONEPHRITIS

• ACUTE G.N.

• CHRONIC G.N.

ACUTE G.N.

• INFLAMMATORY REACTION TO GLOMERULI FROM AN IMMUNE MECHANISM

• FROM BETA HEMOLYTIC GROUP A STREP INFECTION: – THROAT– SKIN– SCARLET FEVER

ACUTE G.N. - PATHOPHYSIO

STREP THROAT

STREP TOXINS AS ANTIGENS

ANTIGEN-ANTIBODY COMPLEX IN THE CIRCULATION

Ag-Ab COMPLEX LODGE IN THEGLOMERULI

GLOMERULARINFLAMMATION

ACUTE G.N.

CLINICAL MANIFESTATIONS:

• PREVIOUS STREP INFECTION

• MALAISE, HEADACHE, FACIAL EDEMA, FLANK PAIN & TENDERNESS

• HPN

ACUTE G.N.

LABS:

• URINE : SCANTY & BLOODY, SG, RBC & WBC CASTS

• ASO

• BUN & CREATININE

• ANEMIA

ACUTE G.N.

MANAGEMENT:

• PROTECTION FROM INJURY

• TREAT COMPLICATIONS PROMPTLY

ACUTE G.N.

COMPLICATIONS:

• HPN

• ENCEPHALOPATHY

• C.H.F.

• PULMONARY EDEMA

ACUTE G.N.PROMPT TREATMENT OF

COMPLICATIONS

• PENICILLIN

• BED REST UNTIL LABS RETURN TO NORMAL

• DIET: P RESTRICTED ( RENAL INSUFFICIENCY) Na RESTRICTED (HPN, EDEMA & CHF) HIGH C TO REDUCE P CATABOLISM FLUIDS

CHRONIC G.N. – PATHOPHYSIO

ACUTE G.N.

REPEATED AG-AB REACTIONS

GLOMERULI BECOME SCARRED;RENAL ARTERIAL BRANCHES THICKENED

GLOMERULAR DAMAGE

KIDNEY: 1/5 OFORIGINAL SIZE

end stage of chronic glomerulonephritis. Notice their small size. They each measure about 2 x 3". These are severely contracted kidneys. Notice the cortices and the finely granular surfaces.

Here's an end stage kidney of chronic glomerulonephritis. Notice again it is extremely contracted and finely granular. This is the kidney of a 38 year old man who presented with an insidious onset of the three signs of uremia, that is loss of appetite, lethargy, and the laboratory finding of an increased BUN. He had no antecedent history of acute glomerulonephritis.

CHRONIC G.N.

CLINICAL MANIFESTATION:

• ASYMPTOMATIC

• 1ST INDICATION OF DSE: EPISTAXIS, STROKE, CONVULSION

• FEET SLI. SWOLLEN @ NIGHT

• WEIGHT LOSS, HEADACHE, NOCTURIA

CHRONIC G.N.

CLINICAL MANIFESTATION:

• PHYSICAL EXAM:– YELLOW GRAY SKIN PIGMENTATION– PERIORBITAL & PERIPHERAL EDEMA– HPN– ANEMIA – PALE PALP CONJ

CHRONIC G.N.

MANAGEMENT:

• DIET ESP PROTEIN, Na & FLUIDS IS READJUSTED ACCORDING TO THE METABOLIC NEEDS OF THE PATIENT

• BED REST

• DIALYSIS EARLY IN THE COURSE TO MINIMIZE RISK OF RENAL FAILURE

NEPHROTIC SYNDROME

CAUSES:

• CHRONIC G. N.

• DIABETES MILLETUS

• AMYLOIDOSIS

• RENAL THROMBOSIS

NEPHROTIC SYNDROME

S/SX:

• PROTEINURIA

• HYPOALBUMINEMIA

• EDEMA

• HYPERLIPEDEMIA

NEPHROTIC SYNDROME

S/SX:

• SLOW ONSET OF FLUID RETENTION

• HEMATURIA

• URINARY STASIS

NEPHROTIC SYNDROME

MANAGEMENT:

• BED REST

• HIGH P DIET

• DIURETICS- EDEMA

• STEROIDS - PROTEINURIA

NEPHROSCLEROSIS

• HPN• RENAL ARTERIOSCLEROSIS

CLIN MANIFESTATION:

URINE: LOW S.G. SM PROTEIN OCC HYALINE & GRANULAR CAST

HYDRONEPHROSIS

OBSTRUCTION OF

URINARY FLOWDISTENTION OF PELVIS & CALYCES

THINNING OF RENAL PARENCHYMA

GRADUAL DESTRUCTIONOF THE KIDNEY

COMPENSATORYHYPERTROPHY OF THE

CONTRALATERAL KIDNEYIMPAIRMENT OFRENAL FUNCTION

HYDRONEPHROSIS

CLIN MANIFESTATIONS:

• Asymptomatic

• Flank & back pain

• Hematuria

HYDRONEPHROSIS

MANAGEMENT

• Urinary diversion: Nephrostomy

• Antimicrobials

INFECTIONS OF THE URINARY TRACT

PREDISPOSING FACTORS:

• FEMALE : PROXIMITY OF THE URETHRA TO THE VAGINAL-RECTAL ORIFICES

• INFANTS AFFECTED MORE OFTEN THAN OLDER CHILDREN

• ELDERLY

INFECTIONS OF THE URINARY TRACT

CAUSE:

• ORGANISMS FROM THE BOWEL– E. coli– Pseudominas – Enterococci

INFECTIONS OF THE URINARY TRACT

• Ascending infection & Vesico - Ureteral

reflux

• Sexual activity

• Instrumentation

- KIDNEY-

URETER

BLADDER

URETERO-VESICAL

JUNCTIONVESICO-

URETERALREFLUX

U.T.I. S/SX

CYSTITIS:

– FREQUENCY– URGENCY– DYSURIA– BLADDER SPASM– WALLS MAY BLEED WITH SEVERE

INFLAMMATION

This is an opened urinary bladder. The mucosa shows many petechial hemorrhages and is swollen and congested. This is hemorrhagic

cystitis. It is frequently seen with lower urinary tract infections and is particularly common in the

presence of an indwelling urinary catheter.

U.T.I. S/SX

PYELONEPHRITIS

• PRIMARY LOWER UTI• FLANK PAIN• MUSCLE SPASM• CHILLS• FEVER• DYSURIA

This is another section of a kidney with acute suppurative pyelonephritis. Notice the

parenchyma is congested and swollen. There is a calculus in the calyx.

U.T.I.

TREATMENT:

• ANTIBIOTICS

• INCREASE FLUIDS – 3-4L /DAY

• EARLY TREATMENT TO PREVENT COMPLICATIONS

U.T.I.

COMPLICATIONS:

•SEPTICEMIA

•RENAL FAILURE

NEUROGENIC DISORDERS

• PARASYMPATHETIC NERVOUS SYSTEM – SACRAL CORD 2,3,4

• PERCEPTION TO URINATE:300-500 ML OF URINE

• MAXIMUM BLADDER CAPACITY:1L OF URINE

NEUROGENIC DISORDERS

TYPES:

• LESION ABOVE THE SACRAL MICTURITION CENTER (SMC)– SPASTIC, NEUROPATHIC BLADDER

• LESION BELOW THE SMC– FLACCID, NEUROPATHIC BLADDER

SPASTIC BLADDER• REDUCED CAPACITY• INVOLUNTARY DETRURSOR CONTRACTIONS• HYPERTROPHY OF THE BLADDER• SPASTICITY OF PELVIC MUSCLES• AUTONOMIC DYSREFLEXIA

S/SX:

• INVOLUNTARY URINATION• VOIDING CAN BE TRIGGERED BY

STIMULATION OF GENETALIA OR ABDOMEN, WITH SPASM OF EXTREMITIES

FLACCID (ATONIC) BLADDER

TYPES:• SENSORY• MOTOR

• LARGE CAPACITY• LACK OF VOLUNTARY DETRURSOR MUSCLES• MILD WALL HYPERTROPHY (TRABECULATIONS)• DECREASED TONE OF EXTERNAL SPHINCTER

FLACCID (ATONIC) BLADDER

• LOSS OF SENSORY / MOTOR SUPPLY TO THE BLADDER

• SHOCK PHASE OF SCI

• BLADDER : – FLACCID & DISTENDED– RETENTION WITH OVERFLOW INCONTENENCE– SMOOTH MUSCLE STILL ACTIVE + WEAK STRIATED

SPHINCTER MUSCLES = TRABECULATIONS

• GENITAL PROBLEMS : LOSS OF ERECTION

NEUROGENIC BLADDER

DIAGNOSIS:

• HISTORY

• NEUROLOGICAL EXAM & STUDIES (EMG)

• RADIOLOGIC EXAM (VOIDING CYSTOURETHROGRAM)

• UROLOGIC STUDIES (UTZ)

NEUROGENIC BLADDER

INTERVENTIONS:

• INTERMITTENT CATHETER DRAINAGE

• CREDE’S METHOD

• ALCOHOL, TEA & COFFEE AS DIURETICS

• ELECTRONIC STIMULATION OF THE BLADDER

UROLITHIASIS

CAUSE:

• URINARY STASIS• UREA- SPLITTING ORGANISMS

– E. coli– Proteus – Staph, Strep

UROLITHIASIS

Types of Stones:

• ACID STONES– URIC ACID– CYSTINE

• ALKALINE STONES– PHOSPHATE– CALCIUM OXALATE

Alkaline Stone formationAlkaline Stone formation

UREA-SPLITTINGORGANISMS IN

THE URINEURINE BECOMESALKALINE

CALCIUM PHOSPHATEBECOMES INSOLUBE

UROLITHIASIS

There was a large renal calculus (stone) that obstructed the calyces of the lower pole of this kidney, leading to a focal hydronephrosis (dilation of the collecting system). The stasis from the obstruction and dilation led to infection.

The infection with inflammation is characterized by the pale yellowish-tan areas next to the dilated calyces with hyperemic mucosal surfaces. The upper pole is normal and shows good corticomedullary demarcations.

Sometimes a very large calculus nearly fills the calyceal system, with extensions into calyces that give the appearance of a stag's (deer) horns. Hence, the name "staghorn calculus". Seen here is a horn-like stone extending into a

dilated calyx, with nearly unrecognizable overlying renal cortex from severe hydronephrosis and pyelonephritis. Nephrectomy may be performed because the kidney is non-functional and serves only as a source for infection.

UROLITHIASIS

S/SX:

• CVA PAIN – COLICKY & EXCRUCIATING – RADIATES TO THE LABIA OR SCROTUM

• ASHEN FACE• DIAPHORESIS• FREQUENCY• HEMATURIA• FEVER - INFECTION

UROLITHIASIS

MEDICAL TREATMENT:

• ACID STONES - ALKALINE ASH DIET: • FRUITS • VEGETABLES • MILK

• ALKALINE STONES - ACID ASH DIET : • MEAT • FISH • EGGS • CEREALS

UROLITHIASIS

MEDICAL TREATMENT:

• RESTRICT CALCIUM

• ALUMINUM HYDROXIDE – PHOSPHATE STONES

• PERCUTANEOUS STONE REMOVAL

– NEPHROSTOMY. NEPHROLITHOTOMY (LASER, UTZ, ELECTROHYDRAULIC)

– STONE DISSOLUTION - CHEMOLYSIS

UROLITHIASIS

SURGICAL PROCEDURES:

• PYELOLITHOTOMY – RENAL PELVIS

• NEPHROLITHOTOMY

• NEPHRECTOMY

• URETEROLITHOTOMY

• CYSTOLITHOTOMY

UROLITHIASIS

STONE DESTRUCTION:

LITHOTRIPSY

– ULTRASONIC

– ELECTROHYDRAULIC

RENAL TUMORS

• INSIDUOUS & SLOW

• HEMATURIA- EROSION OF PELVIS

• BLADDER TUMOR – RARE

• DIAGNOSIS – CYSTOSCOPY WITH BIOPSY

• TX : SURGERY, IRRADIATION, CHEMOTHERAPY

In the upper pole of this kidney is a well circumscribed tumor which has a

yellowish-brown color and shows central necrosis. This is a renal cell carcinoma.

obstructive disease . In the center of the photograph is the sigmoid colon and rectum of a patient with adenocarcinoma of the rectum. This has invaded the bladder and has occluded the orifices of the ureter on both sides. The right ureter shows extreme hydroureter.

BENIGN PROSTATIC HYPERTROPHY

S/SX:

• INCOMPLETE EMPTYING

• FREQUENCY• INTERMITTENCY• URGENCY

• WEAK STREAM• STRAINING• NOCTURIA• CYSTITIS• HYDRONEPHROSIS• URINARY CALCULI

BENIGN PROSTATIC HYPERTROPHY

DIAGNOSIS:

• DRE : SMOOTH, FIRM & ELASTIC ENLARGEMENT

• IMAGING : IVP OR RENAL UTZ

• PSA - OPTIONAL

BENIGN PROSTATIC HYPERTROPHY

MANAGEMENT:

• MILD SYMPTOMS : – WATCHFUL WAITING + MEDICATIONS

• SURGERY :– PROSTATECTOMY

BENIGN PROSTATIC HYPERTROPHY

MEDICATIONS:

• ALPHA – BLOCKERS – (eg PRAZOSIN)

• 5 ALPHA REDUCTASE INHIBITOR– (eg FINASTERIDE)

T.U.R.P.

TRANSURETHRAL RESECTION OF THE PROSTATE

• MOST COMMON APPROACH

• RESECTOSCOPE PASSED THRU URETHRA

• EXCESSIVE PROSTATIC TISSUE IS CAUTERIZED

• LARGE FOLEY CATH – FOR HEMOSTASIS & URINARY DRAINAGE

T.U.R.P.

PRE OP NURSING CARE:

• EXPLAIN ABOUT CATHETER & OCC DECOMPRESSION DRAINAGE

• INSTRUCT: NO STRAINING WITH VOIDING SENSATIONS

• INSTRUCT: TCDB

T.U.R.P.

POST OP NURSING CARE:

• PREVENT COMPLICATIONS

• URINARY DRAINAGE

• HEALING HEALTH HABITS

• HELPING CLIENT ADJUST TO CHANGES IN SELF-CONCEPT

T.U.R.P.

POST OP NURSING CARE:

• PREVENT COMPLICATIONS

• URINARY DRAINAGE

• HEALING HEALTH HABITS

• HELPING CLIENT ADJUST TO CHANGES IN SELF-CONCEPT

COMPLICATIONS- T.U.R.P.

HEMORRHAGE

• ARTERIAL BLEEDING : BRIGHT RED URINE WITH CLOTS

• MONITOR FOR SIGNS OF SHOCK

• VENOUS BLEEDING : NORMAL 48 HRS & 6-8D POST OP

COMPLICATIONS- T.U.R.P

THROMBOSIS & EMBOLISM

• TURNING

• EXERCISE LEG

• ENCOURAGE AMBULATION

COMPLICATIONS- T.U.R.PBLADDER SPASM

• PROPHYLACTIC ANTISPASMODIC

• AMBULATION

• DETERMINE PATENCY OF CATHETER

• IRRIGATE CATHETER AS ORDERED

• FREQUENCY OF SPASM SHOULD DECREASE WITHIN 48H

• AVOID RECTAL PRESSURE – STOOL SOFTENER, INCREASE BULK IN FOOD

T.U.R.P.

POST OP NURSING CARE:

• PREVENT COMPLICATIONS

• URINARY DRAINAGE

• HEALING HEALTH HABITS

• HELPING CLIENT ADJUST TO CHANGES IN SELF-CONCEPT

URINARY DRAINAGE

• F 18-16 3-WAY FOLEY CATHETER– HEMOSTASIS– OUTLET OF URINE

• FLUIDS – DILUTE URINE – MINIMIZE INFECTION

• MONITOR IRRIGATING SOLUTION– WATER INTOXICATION IS POSSIBLE

URINARY DRAINAGE• REFER IF NO VOIDING WITHIN 5-6H AFTER

CATHETER REMOVAL

• NORMAL: URGENCY, FREQUENCY & DYSURIA AFTER REMOVAL

• INCONTINENCE : – NOT NORMAL– CAUSED BY BLADDER SPASM

• FLUIDS: 12-14 GLASSES A DAY

• EXERCISE TO STRENGTHEN PERINEAL MUSCLES

T.U.R.P.

POST OP NURSING CARE:

• PREVENT COMPLICATIONS

• URINARY DRAINAGE

• HEALING HEALTH HABITS

• HELPING CLIENT ADJUST TO CHANGES IN SELF-CONCEPT

HEALTH HABITS

• ADEQUATE NUTRITION

• PERINEAL APPROACH – HOT SITZ BATH

T.U.R.P.

POST OP NURSING CARE:

• PREVENT COMPLICATIONS

• URINARY DRAINAGE• HEALING HEALTH HABITS

• HELPING CLIENT ADJUST TO CHANGES IN SELF-CONCEPT

ADJUSTING TO CHANGES IN SELF-CONCEPT

• POSSIBILITY OF PERMANENT/ TEMPORARY INTERFERENCE IN SEXUAL FXN

• STERILITY WITH SEVERING OF VAS DEFERENS

• CLOUDY URINE :T– EMPORARY RETROGRADE EJACULATION

FROM DAMAGE TO INTERNAL SPHINCTER

DISCHARGE INSTRUCTIONS

• MGH – IF ABLE TO EMPTY BLADDER SPONTANEOUSLY

• NO HEAVY LIFTING 6 WKS POST OP

• NO SEXUAL INTERCOURSE – 6 WKS POST OP

• HEMATURIA WITH VENOUS BLOOD IS NORMAL

• REPORT BRIGHT RED BLEEDING & DYSURIA

This is an opened urinary bladder and prostate below

The hyperplastic prostate gland has obliterated the lower part of the cystic cavity. There is hemorrhagic cystitis and prominent trabeculae in the hypertrophied bladder.

This is another enlarged prostate gland, but it does not show the sharply defined

capsule that you saw in hyperplasia of the prostate. This is adenocarcinoma of the

prostate gland which is invading the

pelvic tissue.

• A client who is in acute renal failure develops pulmonary edema. Nursing interventions for this person should include all of the following, except:

a. Oxygenb. Coughing & deep breathingc. Semi-fowler’s positiond. Replacing lost fluids