Patho exam 3 urinary

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Urinary system components

• Kidneys

• Ureters

• Urinary bladder

• Urethra

Position/location of kidneys

• Positioned retroperitoneally lie on either side of the vertebral column, high on the posterior wall of the abdominal cavity

  • between the 12th thoracic and 3rd lumbar vertebrae

  • Surrounded by Renal fascia and renal fat

Blood supply

The glomerulus is a tuft of capillaries supplied by an afferent arteriole

• The capillaries of the glomerulus then recombine into an efferent arteriole, which in turn become the peritubular capillaries that supply the renal tubule

Urine formation includes

• Glomerular filtration

• Tubular reabsorption

• Tubular secretion

Glomerular filtration

• Substances move from blood to glomerular capsule

Tubular Reabsorption

• Substances move from renal tubules into blood of peritubular capillaries

• Glucose, water, urea, proteins

• Amino, lactic, citric, and uric acids

• Phosphate, sulfate, calcium, potassium, and sodium ions

Tubular secretion

• Substances move from blood of peritubular capillaries into renal tubules

• Drugs and ions

General diagnostic tests

• Urinalysis

• Reagents strips (dipsticks)

• Microscopic analysis

Urinalysis

Physical description of urine (i.e. color, clarity, smell), biochemical, and microscopic analysis

• Normal physical description

  • Odorless

  • Foul smell from infections

  • Sweet smell from diabetes mellitus

• Clear to slightly hazy,

  • Yellow to amber color

  • Color varies with concentration of solutes and water

Reagents strips (dipsticks)

• pH should be close to neutral

  • Vary from acid to basic

  • Diet can change pH

• Specific gravity should be between 1.001 (dilute) and 1.030 (concentrated Measurement of the dissolved materials in urine)

  • -distilled water=1.000

  • -indicator of concentrating ability of the kidneys

• All other tests should be negative

Microscopic analysis

• inspection for white blood cells, bacteria, red blood cells, or collections of cellular debris, crystals, and cast

  • Red blood cells and WBC’s up to 5/HPF can be normal

  • Increased RBC = hematuria

  • Increased WBC = pyuria

• Crystals can be associated with renal calculi

• Casts are substances secreted in the tubules and retain the shape of the tubule

  • Can be benign or associated with kidney disease

Normal excretion by kidneys

• Urea

• Uric acid

Urea

• By-product of amino acid catabolism by liver

  • From ammonia

• Plasma concentration reflects the amount or protein in diet

• Enters renal tubules through glomerular filtration

Uric acid

• Product of nucleic acid metabolism

• Enters renal tubules through glomerular filtration

• Increase levels in blood or decreased excretion in urine can lead to gout

Blood tests

• Blood urea nitrogen (BUN)

• Serum Creatinine

Blood urea nitrogen (BUN)

• Elevated BUN does not equal kidney dysfunction

• Can occur in dehydration

  • Results from increase concentration

• High protein diets

• Conditions with increase protein metabolism-trauma, surgery, burns, GI bleeding

Serum creatinine

Muscle breakdown product that is practically filtered at the glomerulus and is not reabsorbed by the tubules

Increase serum creatinine indicates decreased filtering of creatinine at the glomerulus

• Exceptions to rule

  • Persons with increased daily muscle breakdown may have abnormally high creatinine

• A frail person will have low amount of serum creatinine daily, elderly, for example

Azotemia

• Elevation of BUN and creatinine

• Related to decreased glomerular filtration rate

Imaging studies

• Ultrasound

• Intravenous pyelography

• Radiographs

• Computed tomography scans

• MRI

Renal biopsy

• A small sample of kidney tissue is removed with a needle.

• The test is sometimes used to evaluate a transplanted kidney.

• It is also used to evaluate an unexplained decrease in kidney function, persistent blood in the urine, or protein in the urine.

Etiology of kidney dysfunction is divided into 3 categories. What are those categories?

• Prerenal dysfunction

• Intrarenal dysfunction

• Post renal dysfunction

Prerenal dysfunction

• Caused by decreased blood flow and perfusion to kidneys

• Directly related to blood flow and renal perfusion

• Causes include decrease cardiac output or severe hypovolemia (decrease blood volume-hemorrhage e.g.), septic shock

• Large blood loss is a common cause of prerenal kidney injury caused by ischemia

Intrarenal dysfunction

• Develops secondary to actual injuries to the kidney itself

• Etiology: Direct damage to nephrons from trauma, toxins, infections or atherosclerosis causing decrease blood supply

• Most common cause is nephrotoxic drugs (aminoglycosides, NSAIDS), renal infections (post streptococcal glomerulonephritis), systemic illness

Post renal dysfunction

• Related to obstruction of urine outflow from the kidneys

• Etiology: obstructive uropathy - Examples: uroliths, prostatic enlargement

• Urine backs up within the ureter and kidneys resulting in a fluid filled kidney (hydronephrosis)

  • Urine is toxic to cells

  • Urine stagnation predisposes to secondary infection

Glomerulonephritis Etiology

• infections, immune mediated disease, inherited

• can be acute or chronic

Glomerulonephritis

• Leading cause of chronic kidney disease

  • Inflammatory changes impair kidney’s ability to excrete waste and excess fluid

  • Injury to the glomerulus causes cellular changes that impair filtration of blood

• Decrease urine output (oliguria) from blocked glomeruli by inflammation

  • Leads to less blood filtered and therefore less urine formation

  • Decreases Glomerular filtration rate

    • Amount of blood filtered/time

• Less urine formation leads to less waste product being excreted (accumulate in blood)-increase BUN and Creatinine

• Protein (albumin) and red cells leak through damaged glomerular membrane

  • Leads to formation of casts

  • Leads to low albumin (protein)

• Low GFR leads to hypervolemia and increase in blood pressure

• Low albumin in blood (hypoalbuminemia) leads to diminished oncotic pressure

  • Causes edema

Nephrotic syndrome

• Refers to a group of abnormalities characterized by a severe loss of protein in the urine

  • Combination of clinical finding that occur when the glomerulus is damaged, which allows proteins to be lost in the urine

  • Proteinuria, hypoalbuminemia, massive generalized edema

Nephrotic syndrome etiology

• Glomerulonephritis-chronic and progressive

• Diabetes (causing glomerular changes)

  • Most common type

• Systemic lupus erythematosus, SLE-affect connective tissue; autoimmune disease

• Associated with NSAID use

Lower urinary tract infection UTI

• Bladder and urethra

• Cystitis: affects only the bladder

• Very common; maybe acute or chronic

• Most infections are caused by gram-negative bacteria

  • E. coli most common

• Organisms contaminate perianal and genital areas and ascend urethra

Conditions protective against Lower UTI’s

• Free urine flow

• Large urine volume

• Complete bladder emptying

• Acid urine: most bacteria grow poorly in an acidic environment

• Immunoglobulin A secreted by WBCs in urinary tract prevents adherence of bacteria to bladder wall

  • Some women are non-secretors of IgA

Predisposing factors to Lower UTI

• Any condition that impairs free drainage of urine

• Stagnation of urine favors bacterial growth

• Injury to mucosa by kidney stone disrupts protective epithelium allowing bacteria to invade deeper tissue

• Introduction of catheter or instruments into bladder may carry bacteria

Lower Urinary Tract Infection Etiology

• More common in women than men; shorter female urethra, and, in young sexually active women, sexual intercourse promotes transfer of bacteria from urethra to bladder

• Common in older men, because enlarged prostate interferes with complete bladder emptying—benign prostatic hyperplasia

  • common non-malignant enlargement of the prostate gland; common in men 50 years or older; Idiopathic

  • Prostate enlargement leads to urethral obstruction, which obstructs urine outflow

  • Predisposes to UTI, bladder calculi, hydronephrosis

Clinical Manifestations of lower urinary tract infection

• Burning pain on urination-

  • Dysuria= painful or difficulty urinating

• Desire to urinate frequently

• Urine contains many bacteria and leukocytes

• Elderly have high risk and may present with confusion

• Responds well to antibiotics

• May spread upward into renal pelvis and kidneys

  • Upper urinary tract infection

Lower urinary tract infections diagnostic tests

• Urinalysis: + leukocyte esterase and + blood and alkaline pH (typically)

• WBC/hpf >100/hpf

• RBC/hpf 2-5/hpf

• Casts None

• Other Many leukocytes

• Culture and sensitivity for definitive identification of organism and antibiotic

Pyelonephritis

• Suppurative inflammation of the kidney and renal pelvis, caused by Escherichia coli found in the colon; streptococci, and staphylococci are examples

• Can be acute or chronic

Pyelonephritis involvement of upper urinary tract

• Ascending infection from the bladder (ascending pyelonephritis)

  • Most common; higher incidence in young women

  • Older men with prostatitis

  • Obstructive uropathy  predisposes to infection

  • E. coli is most common

• Carried to the kidneys from the bloodstream (hematogenous pyelonephritis)

  • Less common

  • Staphylococcus aureus is most common

Pyelonephritis clinical manifestations

• Localized pain and tenderness over affected kidney

  • Back pain that spreads over the abdomen

• fever, chills

• Nausea and vomiting

• +/- gross hematuria

• Responds well to antibiotics

• Cystitis and pyelonephritis are frequently associated

  • Signs will include those of lower UTI

Chronic pyelonephritis signs/symptoms

• Some cases become chronic and lead to kidney failure

  • Kidneys will become shrunken and contain Increase scar tissue

  • Renal functions declines

Diagnostic tests for pyelonephritis

• urinalysis: hematuria, bacteria, wbc’s (pyuria) and wbc casts

• Culture and sensitivity for definitive diagnosis

• Imaging studies:

  • radiographs

  • ultrasound

Urinary calculi

Urolithiasis

• Stones or calculi may form anywhere in the urinary tract

• Nephrolithiasis: renal calculus

Urinary calculi 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-

  • Many can be passed and excreted in urine

• Bladder stones

  • Usually secondary to infection and urine stasis

Urinary calculi etiology

• Chronic dehydration

  • Low fluid intake → low volume of urine produced → high concentrations of tone forming solutes in urine

• Urinary tract obstruction

• Diet

  • High in animal protein—uric acid formation (Gout)

• Recurrent UTI

• Genetic disorder

  • Increase risk if family member with kidney stones

  • Idiopathic

Urinary calculi signs and symptoms

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 kidney stones

How to diagnose urinary calculi

• Urinalysis, blood analysis

• Radiographs, IVP, or ultrasound

• Stone analysis

Urinary calculi treatment

• 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

Urinary calculi prevention

• 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

Urinary obstruction manifestations

• 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

Hydroureter

• Dilation of ureter

Hydronephrosis

• Dilatation of pelvis and calyces

Urinary obstruction etiology

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

• Unilateral: ureteral stricture, calculus, tumor

Urinary obstruction complications

• Structural damage, stone formation; infections from stagnation of urine,

  • This can lead to increase in the degree of obstruction

Urinary obstruction diagnosis and treatment

• Pyelogram

• CT scan

• Relieve obstruction

Renal failure etiology

• Lack of blood flow – ischemia

• Blockage

• Hemorrhage

• Various poison

• Infections

• Neoplasia

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

  • Retention of excessive byproducts of protein metabolism in the blood

Acute renal failure (acute kidney injury)

• Renal function usually returns

• Develops suddenly, loss of kidney function

Acute renal failure etiology

• Prerenal

  • impaired blood flow to kidneys (most common cause)

  • Pre – renal and 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

• Intrinsic

  • 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 tubules Leads to tubular necrosis

First phase of acute kidney disease

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

  • asymptomatic

Second phase 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

Third phase 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

Fourth phase 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

Chronic renal failure

• From progressive, chronic kidney disease

• irreversible progressive disease, generally ending in death

• Kidney is unable to excrete waste products or control blood volume

• Kidneys can maintain normal function until about 75 % become nonfunctional

  • Few symptoms appear until >75% damage

• Disease develops over months to years

  • 90 – 95% of nephrons affected

Chronic renal failure etiology

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

• Hypertension (damage to glomeruli) or diabetic nephropathy resulting from diabetes mellitus –most common

Chronic renal failure pathophysiology

• Decline in population of nephrons

• Normal renal function can be maintained with only 20 – 30 % of nephrons.

  • Kidneys are resilient because huge number of nephrons

  • Can live with 1 kidney because have double the amount of nephrons needed to filter blood

• These surviving nephrons receive a larger volume of blood to process at a higher pressure

  • Compensate by hypertrophy and increasing their clearance capacity

  • Super nephrons

  • Eventually, glomerular injury from hyperfiltration

  • Glomeruli hypertrophy and will begin to harden (sclerosis) and GFR decreases

• Tubular damage results from the damage to blood vessels

  • Ultimately results in more nephrons being damaged

  • irreversible

• 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

Clinical presentation and diagnostic findings of chronic renal failure

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

  • Hyperkalemia: cardiac dysrhythmias and muscle weakness

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

    • Leads to neuromuscular irritability and seizures

    • PTH is secreted and results in demineralization of bone

      • Increase susceptibility of fractures (secondary hyperparathyroidism)

• Hypoalbuminemia

  • Glomerular damage

    • Proteinuria is a classic sign

• Metabolic acidosis from retention of acids that would normally be excreted

  • Decrease H+ elimination & Decreased bicarbonate reabsorption

• Fluid imbalance

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

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

    • The urine produced is dilute because of the tubules inability to concentrate urine

      • polyuria will present and polydipsia

• Later, as the glomerular function is further reduced leads to uremia

  • Leads to oliguria and eventually anuria

  • Eventually, fluid and salt retention -hypertension and edema (along with low albumin)

Uremia

• Urine in blood stream

• 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 a small molecule and can enter into RBCs and causes hemolysis → leads to anemia

  • Anemia also from failure of production of erythropoietin

• Loss of body weight from anorexia vomiting, and diarrhea induced by uremic toxins

• Uremic Breath = ammonia smell from accumulation of waste (urea)

• Uremic encephalopathy

• Typically, when uremia develops the diseased has progressed too far for treatment

Chronic renal failure treatment

• Fluid and electrolyte management

• Hemodialysis and peritoneal dialysis

  • 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

• Renal transplant