Urinary Disorders Part 2

Urolithiasis

Stones or calculi may form anywhere in the urinary tract

Nephrolithiasis: renal calculus

Urolithiasis - Predisposing factors

High concentration of salts in urine saturates urine causing salts to precipitate and form calculi

– Urinary tract infections reduce solubility of salts in urine; clusters of bacteria are sites where urinary salts may crystallize to form stone

– Urinary tract obstruction causes urine stagnation, promotes stasis and infection, further increasing stone formation– urinary salts crystallize

– Some become impacted in the ureter and need to be removed-

– Bladder stones

Etiology of Urolithiasis

Chronic dehydration

Urinary tract obstruction

Diet

Recurrent UTI

Genetic disorder

Idiopathic

Signs & Symptoms Of Urolithiasis

costovertebral angle pain (flank pain) or abdominal pain when stone   Involves kidney  

Distinctive pain = renal colic->pain when lodged in the ureter, pain radiates to the groin, hematuria 

Pain in pelvic region and during urination if stone in bladder

nausea, vomiting, diarrhea can also be seen with

calculi

Many can be passed and excreted in urine

Bladder stones

Urinary Calculi or Kidney Stones Risks

10% of the population

Urinary Calculi or Kidney Stones Symptoms:

costovertebral angle pain (flank pain) or abdominal pain when stone is high in tract

Distinctive pain = renal colic

   pain when lodged in the ureter, pain radiates to the groin, hematuria,

Urinary Calculi or Kidney Stones Diagnosis

Urinalysis, blood analysis

– Radiographs, IVP, or ultrasound

– Stone analysis

Treatment of Kidney Stones

Medication that partially dissolves the stone and then it may be passed in the urine, or medication that prevents uric acid formation and pain medication

Physical treatment is lithotripsy, the crushing of kidney stones

Cystoscopy: snares and removes stones  lodged in distal ureter

Surgery

Prevention Of Kidney stones

Increase fluid intake, suggested 8 ounces of water per hour during the day in order to keep the urine a light color

Diet: reduce sodium (salt) and protein (nitrogen)-- Red meat, organ meats, and shellfish—predispose to increase uric acid secretion by kidneys

Urinary obstruction

Blockage of urine outflow leads to progressive dilatation of urinary tract proximal to obstruction, eventually causes compression atrophy of kidneys

results in atrophy of the parenchyma caused by increased pressure exerted by the urine

Manifestations Fo Urinary Obstruction

Hydroureter: dilatation of ureter

Hydronephrosis: dilatation of pelvis and calyces

• Result of obstruction of outflow of urine distal to renal pelvis

• Leads to tissue damage in chronic cases

Etiology Urinary Obstruction

Bilateral: obstruction of bladder neck by enlarged prostate or urethral stricture

Unilateral: ureteral stricture, calculus, tumor

Complications Of Urinary Obstruction

structural damage , stone formation; infections from stagnation of urine

lead to increase in the degree of obstruction

Diagnosis and treatment Of urinary obstruction

pyelogram, CT san

relieve obstruction

Renal Failure

Inability to clear creatinine and urea; increases in BUN and serum creatinine

Retention of excessive byproducts of protein metabolism in the blood

Renal Failure: Etiology

Lack of blood flow – ischemia

Blockage

Hemorrhage

Various poison

Infections

neoplasia

Acute renal failure (acute kidney injury)

Renal function usually returns

–Develops suddenly; loss of kidney function

Chronic renal failure

From progressive, chronic kidney disease; > 50% from hypertension and diabetes

Others include congenital polycystic kidney disease, nephrosclerosis, autoimmune disease

Kidney is unable to excrete waste products or control blood volume

90 – 95% of nephrons affected

 Etiology: Of Chronic Renal Failure

Can be the result of long-standing kidney disease (e.g.chronic glomerulonephritis, polycystic kidney disease, autoimmune)

hypertension (damage to glomeruli) or diabeticnephropathy resulting from diabetes mellitus –most common 

Pathophysiology Of Chronic Renal Failure

Decline in population of nephrons

Tubular damage results from the damage to blood vessels

Kidneys are smaller than normal because they begin to atrophy and formation of scar tissue and leads to End stage kidney disease with less than 10% of kidney function remains

Etiology (Prerenal) Of Acute Renal Failure

impaired blood flow to  kidneys (most common cause)

is reversible with prompt treatment

Hypovolemic, cardiogenic, septic shock will result in decrease perfusion

Leads to acute tubular necrosis (ATN)

Shock=failure of cardiovascular system to provide blood to tissue with widespread impairment of aerobic cellular metabolism

Etiology (Intrinsic) Of Acute Renal Failure

nephrotoxic drugs (NSAIDS, aminoglycosides)  or poisons (ethylene glycol)

•Leads to ATN

• trauma

•Infections (pyelonephritis)

Post renal

Secondary to obstruction

Acute tubular injury

most common cause of acute disease

Acute renal failure with tubular injury/necrosis

Encountered in the absence of glomerular disease by:

•Impaired renal blood flow causes tubular necrosis

• Decreased or interrupted blood flow

• Example: Hypovolemic Shock  and Marked drop in blood pressure impairs blood flow to kidneys necrosis of tubules

•Toxic drugs and chemicals or endogenous agents (hemoglobin)

• Many drugs are excreted by kidneys direct toxic injury

Pathophysiology of Acute tubular necrosis

Blood supply to tubules is via the efferent artery

• Alterations of blood flow cause decrease in GFR resulting in reduced glomerular blood flow and reduced oxygen delivery to the tubulesà Leads to tubular necrosis

Phase 1 of acute kidney disease

Initial: last hours to days and is time from insult to clinical signs

– asymptomatic

Phase 2 of acute kidney disease

Oliguria: associated with decrease GFR, retention of fluid, urea, creatinine, electrolytes

• Hypertension from hypervolemia

• Electrolyte disturbances—sodium and potassium

• Azotemia (increased BUN and Creatinine)

• Acidosis

Phase 3 of acute kidney disease

Diuretic phase: kidneys are beginning to recover—cells regenerate, but tubules are not able to concentrate urine

• Increased urine output

• Electrolyte disturbances (low potassium-hypokalemia)

• Dehydration

• hypotension

Phase 4 of acute kidney disease

Recovery: time needed for final repair of renal damage; nephrons are compensating by becoming super nephrons- they hypertrophy and demonstrate hyperfiltration

• Urine becomes concentrated

• BUN and Creatinine return to normal

• Tubular function gradually recovers with treatment

• May take months

• Depends on phase of disease and underlying cause

Kidney Failure

Electrolyte abnormalities (Na+, K+, Ca++)

Vitamin D is not able to be activated results in decrease absorption of calcium ->hypocalcemia

Hyperkalemia

cardiac dysrhythmias and muscle weakness

Clinical outcome Of Kideney failure

Hypoalbuminemia

Metabolic acidosis from retention of acids that would normally be excreted

–Decrease H+ elimination

–Decreased bicarbonate reabsorption

Hypoalbuminemia

Glomerular damage

Proteinuria is a classic sign

Fluid imbalance

In early end stage disease excessive water loss dominates because the loss of reabsorptive capacity by the tubules exceeds the reduction of filtration

– Sodium is not reabsorbed, and water does not get reabsorbed into the blood

Later, as the glomerular function is further reducedleads to uremia

Uremia

urine in blood stream

Uremic Breath

ammonia smell from accumulation of waste (urea)

Uremia-clinical syndrome

End result of kidney failure-when renal excretion drops to about 10% of normal

Waste products (urea and creatinine) accumulate to a poisonous level in the blood

urea

is converted to ammonia, which acts as an irritant in the gastrointestinal tract to produce nausea, vomiting, and diarrhea.

•The nervous system is affected; vision becomes dim, mental ability is decreased, and convulsions or coma may ensue.

•Low protein diets are recommended because remaining healthy nephrons have difficulty removing nitrogenous wasted from blood

Treatment of wtv

Fluid and electrolyte management

•Hemodialysis and peritoneal dialysis

•Renal transplant

Hemodialysis

Substitutes for the functions of the kidneys by removing waste products from patient’s blood

Waste products in patient’s blood diffuse across a semipermeable membrane into a solution (dialysate) into the other side of the membrane