Post on 13-Oct-2019
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Urinary system disorders Chapter 29
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The Nephron Anatomy
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1.25 L per minute blood flow 25% of Cardiac Output
Kidney compensates if one is lost - 2 weeks
Physiology
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1. Filtration 2. Reabsorption
w Diffusion w Osmosis w Active Transport
3. Secretion w Diffusion w Osmosis w Active Transport
4. Excretion
Urine Formation
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w Driven by pressure through glomerular membrane
Glomerular Filtration
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Glomerular Filtration
w Through 3 Selectively Permeable Layers w Capillary endothelium w Basement membrane w Epithelium of Bowman’s capsule
w podocytes
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w Basement Membrane w Selective Filter
w Slightly porous w Repels proteins
(negative charge) w Allows only water,
ions, and small molecules
Glomerular Filtration
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Renin
Angiotensinogen
Angiotensin I
ACE
Angiotensin II Aldosterone Release Vasoconstriction
Efferent Arterioles
Systemic Arteries
Renin-Angiotensin-Aldosterone System
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Renin-Angiotensin-Aldosterone System
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Renal Cystic Disease
w Fluid filled sacs or Dilated nephrons w Four types
w Simple kidney cysts w Acquired cystic disease w Medullary sponge kidney w Polycystic kidney disease
w Result of tubular obstruction w Enlarging cysts w Compresses vessels and renal tissue
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Polycystic Kidney Disease
w Autosomal dominant disorder characterized by multiple bilateral grapelike cysts that enlarge and replace functioning kidney tissue w Grossly enlarged kidneys w Slowly progressive w Destruction of renal tissue
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Polycystic Kidney Disease
w Complications w Pain from enlarging cysts w Hematuria from bleeding into a cyst w Pyelonephritis from ascending UTI w Hypertension due to compression of intrarenal blood
vessels and activation of R-A-A System w End stage renal failure after age 40
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Polycystic Kidney Disease
w Diagnosis and Treatment w Ultrasonography w Abdominal CT scanning
w Supportive treatment w Control hypertension w Prevention of ascending UTIs w Dialysis and Transplant
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Obstruction
w Urine accumulates behind blockage w Infection w Damage due to backpressure
w Classification w Site of obstruction w Degree of obstruction w Duration of obstruction
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Obstruction
w Site of Obstruction w Renal Pelvis w Ureter w Bladder and Urethra
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Obstruction
w Common Causes of Obstruction w Stones (Renal Calculi) w Pregnancy w Ureteral Stricture w Prostatic Hyperplasia
or Cancer
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Obstruction
w Mechanisms of Damage w Stasis of urine
w infection w stone formation
w Back pressure w interferes with blood flow w destroys renal tissue w kidney atrophies
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Obstruction
w Back Pressure (location is important) w Urethral Obstruction
w Accommodated in the bladder w Mild discomfort, Frequency
w Bladder or Ureter Obstruction w More severe w Pressure can irreversibly stretch the ureters
and renal pelvis w (hydroureter & hydronephrosis)
w May alter tubular transport and compromises blood flow to the kidney
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Hydronephrosis
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Obstructive Disorders
w Clinical Features w Vary depending on site, cause and rapidity of
onset w Pain w UTIs w Indications of Renal Dysfunction w Hypertension
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Kidney Stones
w Most Common Cause of Obstruction w Nephrolithiasis – stone within the kidney w Urolithiasis – stone anywhere in the urinary system
w Calcium Stones are Most Common w Theories of Stone Formation? w Calcium: idiopathic, hypercalciuria, alkaline urine w Struvite: from urease-producing bacteria, acidic urine
w Contributing Factors w immobilization w bone disease w vitamin D intoxication w decreased fluid intake
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Staghorn Kidney Stones
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Renal Colic
w Pain that accompanies urinary obstruction caused by kidney stones
w Symptoms: acute, intermittent, excruciating, upper quadrant/flank pain that may radiate to other areas; nausea/vomiting; cool, clammy skin
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Lower Urinary Tract Obstruction
w Neurogenic bladder often due to injury of urinary system or neurologic dysfunction w Dyssynergia : dyscoordination of the detrusor muscles
of the bladder and the external urethral sphincter muscles w Detrusor hyperreflexia: AKA overactive bladder.
Lesions above C2, pontine micturation center, upper motor neuron disease, Guillain-Barre
w Detrusor areflexia: muscle fails to contract in response to the stretch of filling urine. MS, spinal lesion below S1, lower motor neuron disorder
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Urinary Tract Obstruction
w Compensatory hypertrophy: the functional side increases in size and “makes up for” the loss of function on the other side. Due to w Obligatory growth: due to growth hormone w Compensatory growth: hormones unknown
w Postobstructive diuresis:large increase in excretion of urine after obstruction is removed
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Urge incontinence: I feel like I need to go but the bladder is not as full as it feels, maybe nervous or inflammatory stimulus
Stress incontinence: weak muscles and fascia so coughing, laughing, jumping results in urine leaks
Overflow incontinence: bladder is just too full to hold that much urine, you waited too long to void
Functional incontinence: urinary system and nerves going to and from it work, but you are cognitively demented (Alzheimer’s)
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Urinary Tract Infections
w Etiology w Escherichia coli (E. coli) w Any microorganism that has contaminated or
colonized in the urethra, vaginal or perineal area can cause an UTI
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Urinary Tract Infections
• Acute Cystitis – Lower UTI of the
bladder – Symptoms:
increased frequency of urination, burning & pain on urination, lower abdominal discomfort
– Also associated with urethritis or vaginitis
• Acute Pyelonephritis – Upper UTI that affects
the tubules and interstitium of the kidneys
– Bacterial infection caused by catheterization and urinary instrumentation, vesicoureteral reflux, pregnancy, neurogenic bladder
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Urinary Tract Infections
w Host Defenses w Washout phenomenon w Protective mucin layer of the bladder and urethra
w Estrogen may play a role in women w Local immune response
w IgA as an antibacterial defense w Prostatic secretions in men w Genetic polymorphism increases E. coli ability to
attach in some women
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Urinary Tract Infections
• Women – Shorter urethra – Urethra proximity to
openings of vagina and rectum leads to easy contamination
– Hormonal and anatomical changes during puberty and sexual activity contribute to UTI
– Common during pregnancy
• Men – Longer urethra – Prostatic
secretions help protect from UTI until age 50 when prostatic hypertrophy leads to obstruction and UTI
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Urinary Tract Infection (UTI) w Nonbacterial infectious cystitis: viral, fungal, chlamydia
w Interstitial cystitis: cause??? unknown, though several theories have been put forward (these include autoimmune theory, nerve theory, mast cell theory, leaky lining theory, infection theory and a theory of production of a toxic substance in the urine. Other theories are neurologic, allergic, genetic and stress-psychological w Manifestations
w Most common in women 20 to 30 years old w Bladder fullness, frequency, small urine volume,
chronic pelvic pain w Treatment
w No single treatment effective, symptom relief
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Glomerulonephritis
w Bilateral inflammation of the glomeruli w Most common cause of chronic renal failure w Uncertain cause but immune mechanism is likely (Type
2 cell lysis Strep A ab, Type 3 SLE immune complex)
w Injury to Glomeruli (Glomerulopathies) w Allows Proteins to enter tubules with filtrate
w Proteinuria w Allows RBC’s to enter tubules with filtrate
w Hematuria
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Glomerular Disorders
w Increased glomerular capillary permeability and loss of negative ionic charge barrier result in passage of plasma proteins into the urine
w Resulting hypoalbuminemia encourages plasma fluid to move into the interstitial spaces w Edema
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w Glomerular capillaries and Bowman’s capsule are both made of epithelial cells sitting on a basement membrane
w They are so tightly attached to each other that they share one basement membrane
w The epithelial cells of Bowman’s capsule stand up from the basement membrane on foot processes, leaving pores between the feet for filtration Blood in
capillary
Urine
Basement membrane
Foot processes
Epithelial cell
Structure of the Glomerulus
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Circulating immune complexes lodge in glomerular membrane
Antibodies to glomerular basement membrane proteins
Immune Damage to the Glomerulus
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Acute Proliferative Glomerulonephritis
w The most common form of glomerulonephritis w Follows infections caused by strains of group A Strep w Inflammatory response due to an immune reaction
w Capillary membrane swells w Becomes permeable to plasma proteins and cells
w Also called post-streptococcal glomerulonephritis w Occurs 7 – 12 days post infection w Oliguria is first sign followed by proteinuria and
hematuria w Approximately 95% full recovery - spontaneously
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Glomerulonephritis
w Rapidly progressing glomerulonephritis w Antiglomerular basement membrane disease
(Goodpasture syndrome: glomerulonephritis and hemorrhaging of the lungs), autoimmune Type II hypersensitivity reaction
w Chronic glomerulonephritis, diabetes mellitus, SLE
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Rapidly Progressive Glomerulonephritis
w Unknown cause w Perhaps - immunologic mechanism
w Immune complex: Strep A w Anti-glomerular membrane: Goodpasture’s
w Rapidly progressive w Treatment
w Plasmapheresis w Immunosuppressive drugs
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IgA Nephropathy
w Primary glomerulonephritis w IgA containing immune complexes w Unknown cause
w Possible defect in IgA molecule w Slowly progressive
w No known treatment
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Nephritic Syndrome
w Glomerular disorders in which inflammatory process damages the glomerular membrane
w Mild protein loss w Red and white blood cells escape into the urine
w Hematuria with red and white cell casts w Hemodynamic changes can decrease permeability of
glomerular membrane and decreases the GFR w Low proteinuria
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Nephritic Syndrome
w Complications w Renal Failure
w Pulmonary edema w Heart failure w Hypertension
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Nephrotic Syndrome
w Collection of clinical findings associated with glomerular disease characterized by marked proteinuria, hypoalbuminemia, hyperlipidemia and edema
w Increased glomerular permeability causes massive loss of plasma proteins w proteinuria
w Edema is common w Hypoalbuminemia allows plasma to leak into tissues w Reduced intravascular volume lowers GFR triggering
Angiotensin II and Aldosterone which increase sodium and water retention
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w Other proteins lost in urine: Immunoglobulins and complement à immune suppression Clotting and anti-clotting proteins à thrombosis Proteins that carry other blood components à imbalances in blood components; altered drug dosages
Nephrotic Syndrome
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Glomerular Damage
↑ Permeability to Protein
Proteinuria > 3.5 g/24hr
Hypoproteinemia (Albumin < 3 g/100ml)
Compensatory Protein Synthesis including
Lipoproteins ↓ Plasma Osmotic Pressure
Hyperlipidemia Plasma leaks into tissues ↓ Plasma Volume
↓ GFR
↑ Aldosterone ñNa / Water Retention EDEMA
Nephrotic Syndrome
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Nephrotic Syndrome
w Complications w Malnutrition w Infection w Coagulation disorders w Thromboembolic vascular occlusion w Accelerated atherosclerosis w Acute renal failure
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Nephrotic Syndrome
w Treatment w Correct underlying cause w Diuretics
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Nephrotic Syndrome w Membranous glomerulonephritis:one of the more
common forms of nephrotic syndrome. Caused by immune complexes binding to the glomerular basement membrane
w Focal glomerulosclerosis: common in kids, scarring of some of the glomeruli, there are several genetic causes
w Minimal change disease (lipoid nephrosis): in kids, cause is idiopathic, diffuse loss of (podocyte) foot processes., vacuolation, and growth of microvilli on the visceral epithelial cells.
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w Damage to tubules and surrounding tissues
w Generally due to: w Pyelonephritis w Toxic substances such as medications or ischemic
injury
w Urinalysis is neither nephrotic nor nephritic in Character w Mild Proteinuria ( < 1 gm/day )
Tubulointerstitial Disorders
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w Inability of kidney to maintain homeostasis and eliminate nitrogenous wastes
w Decline in GFR leading to azotemia w ↑ Creatinine w ↑ Urea
w Generally a decline in urine output w Oliguria = < 500 mL/day w Anuria = < 100 mL/day
w Non-oliguric failure is possible
Renal Failure
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Acute Renal Failure
w Sudden interruption of renal function w Classified as prerenal, postrenal & intrarenal w Often reversible if treated early w Three phases
w Oliguric phase w Diuretic phase w Recovery phase
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Acute Renal Failure
w Oliguric phase w Lasts for a few days to several weeks w Urine output drops to below 400 ml/day w Patient may become fluid overloaded w Cellular injury and necrosis of kidney
w Diuretic phase w Lasts days to weeks w Kidneys become unable to conserve sodium & water w Urine output increases
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Acute Renal Failure
w Recovery Phase w Lasts 3 to 12 months w Renal function gradually returns to normal
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Acute Renal Failure
w Prerenal failure: most common w Caused by diminished blood blow to the kidney w Kidney becomes ischemic
w Damages kidney tubules
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Acute Renal Failure
w Intrinsic failure (intrarenal failure) w Damage to the filtering structures of the kidney w May be nephrotoxic, inflammatory or ischemic
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Acute Renal Failure
w Postrenal failure w Bilateral obstruction to urine outflow
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Acute Renal Failure
Causes of Acute Renal Failure Prerenal Hypovolemia Decreased vascular filling
Heart failure Vasoconstrictive drugs
Postrenal Bilateral ureteral obstruction
Bladder outlet obstruction
Intrinsic (ATN) Prolonged ischemia Nephrotoxins
Acute renal disease
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Acute Renal Failure
w Complications w Infection w Heart failure w Hypertensive crisis w Electrolyte imbalance
w Diagnostic test findings w Elevated BUN, creatinine and potassium w Abnormal urinalysis
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Acute Renal Failure
w Treatment w Reverse the cause w Electrolyte and I.V. therapy
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Acute Tubular Necrosis
w Intrarenal acute renal failure w Injury to the nephron’s tubular segment w Resulting from ischemia or nephrotoxic injury
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Acute Tubular Necrosis
w Causes w Ischemic injury
w Hypotension w Trauma, hemorrhage, dehydration w Shock
w Nephrotoxic injury w Toxic chemical ingestion or inhalation w Hypersensitivity reaction to antibiotics etc.
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Acute Tubular Necrosis
w Pathophysiologic Changes w Decreased urine output, hyperkalemia and elevated
renal function tests w Complications
w Heart failure w Pulmonary edema w Anorexia and vomiting
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Acute Tubular Necrosis
w Diagnostic test findings w Abnormal urinalysis w Abnormal blood tests of renal function
w Treatment w Reverse cause w Long term fluid management
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Chronic Renal Failure
w End result of gradual tissue destruction and loss of renal function w Occasionally due to acute destruction of kidney w Fatal without treatment
w Nephron damage is progressive and permanent w Relatively asymptomatic until 75% loss of nephrons
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Chronic Renal Failure
w Diminished renal reserve w Nephrons are working as hard as they can w GFR is 50 – 89% of normal
w Renal insufficiency w Nephrons can no longer regulate urine density w GFR is 20 – 50% of normal
w Renal failure w Nephrons can no longer keep blood composition normal w GFR is 5 – 20% of normal
w End-stage renal disease w GFR is Less than 5% of normal
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Chronic Renal Failure
w As GFR decreases azotemia and uremia develops w Azotemia = accumulated nitrogenous wastes in blood
w Early asymptomatic sign of renal failure w Elevated BUN
w Uremia = urea and other nitrogenous wastes increase in blood w Constellation of symptoms due to systemic
complications attributed chronic renal failure (increased BP, edema, nausea, vomiting, neurological problems due to toxic levels of nitrogenous wastes)
w These appear when azotemia becomes significant
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Chronic Renal Failure
w Renal filtering function decreases w Altered fluid and electrolyte balance
w Acidosis, hyperkalemia, salt wasting, hypertension w Wastes build up in blood
w Increased creatinine and BUN w Toxic to CNS, RBCs, platelets
w Kidney metabolic functions decrease w Decreased erythropoietin w Decreased Vitamin D activation
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Body System Manifestations Hematologic Anemia, bleeding tendencies, immunocompromised Cardiovascular Hypertension, CHF, pulmonary edema, arrhythmias Gastrointestinal (GI) Anorexia, nausea, vomiting, GI bleeding Musculoskeletal Muscle weakness, bone pain, spontaneous fractures Neurologic Headache, anorexia, lethargy, delirium, coma, seizures Body fluids Metabolic acidosis, hyperkalemia, hypocalcemia Genitourinary Impotence, amenorrhea, loss of libido
Chronic Renal Failure
These are not usually seen in Acute Renal Failure
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Chronic Renal Failure
w Causes w Endocrine disease (diabetes) w Chronic glomerular disease (glomerulonephritis) w Chronic infection w Congenital anomalies w Vascular disease (hypertension etc.) w Obstruction w SLE
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Chronic Renal Failure
w Treatment w Low protein, high calorie, fluid restricted diet w Medications w Dialysis w Kidney transplant
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Acute Renal Failure (ARF)
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Chronic Renal Failure
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Tumors
w Renal tumors w Renal adenomas w Renal cell carcinoma (RCC)
w Bladder tumors w Transitional cell carcinoma w Gross, painless hematuria w Most common in males older than 60 years w Chronic heavy smokers