Transcript Urinary System Diseases

Urinary System Diseases
Pathophysiology
Review of Urinary Anatomy & Physiology
• Located:
– Under back muscles
– Behind peritoneum
• Thus: retroperitoneal
– Below level of lowest ribs
– Right lower than left
– Adrenal gland on top of
kidney
• Cortex
• Medulla
– Contains Pyramids &
Papilla
• Pelvis
– Calyx = division of pelvis
• Pleural = calyces
• Bladder
– Lined with transitional
epithelium
• Can stretch
– Lined with rugae
– Trigone
• On posterior wall
• Where ureters & urethra
open
• Rigid area with NO rugae
– Micturition (voiding,
urination)
• Internal urinary sphincter
– Involuntary
• External urinary sphincter
– Voluntary
• Stretch receptors in
bladder wall
• Nephron = functional unit
– Consists of:
• Renal Corpuscle
• Renal Tubules
• Renal Corpuscle contains:
– Bowman’s capsule
• Part of collecting
system
– Glomerulus
• Afferent arteriole
• Efferent arteriole
• Renal Tubules
1. Proximal convoluted tubule
2. Loop of Henle
3. Distal convoluted tubule
4. Collecting tubule
• Key point:
– The cortex contains
all the structures of
the nephron
– The medulla contains
only the collecting
ducts & the loop of
Henle
•
Functions of the kidney
1.
Removes nitrogenous wastes
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2.
1.
2.
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3.
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Juxtaglomerular
apparatus
RAA system
» Renin
» Angiotensin
» Aldosterone
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4.
Occurs in proximal
convoluted tubule
Also occurs in distal
convoluted tubule
It takes things back into
blood
Secretion
–
Via blood filtration &
formation of urine
Occurs in renal corpuscle
Reabsorption
–
Regulation of Blood
Pressure
–
Filtration
–
Fluid balance
Electrolyte balance
Acid-base balance
Excretory Organ
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4.
Urine formation
Maintains homeostasis
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3.
Urea
Uric acid
Creatinine
Ammonia
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Occurs in distal
convoluted tubule
Blood gives things up to
the urine
Concentration
–
Occurs in collecting
tubules
See next slide
Some Key Points of Renal Physiology
• Nitrogenous wastes primarily come from breakdown of proteins
• Aging & renal function
• By age 35, one begins to lose nephrons
• By age 80, one has approx. 30% reduction in nephron capacity
• GFR = glomerular filtration rate
– Normal = 125cc/min (7500cc/hour)
– 99% of filtered product is reabsorbed
» Normal urine output = 60cc/hour (1500cc/day)
• All along the duct system water is reabsorbed
– Includes the prox. conv. tubule, loop of Henle, distal conv. Tubule, & collecting tubule
– Sodium follows water
• Key elements involved in each process
– Reabsorption = H2O(Na), proteins (amino acids), & sugars (glucose)
– Secretion = ions(K+), drugs, ammonia
– Concentration = more reabsorption of H2O
•
2 key factors determine volume of urine produces
1. Glomerular filtration rate (GFR)
– Determined by the unique arrangment of blood
vessels
2. Hormonal secretion
– Determined by fluid & electrolyte balance
Volume of urine also controlled by glomerular filtration rate
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Unique arrangment of blood vessels
– Afferent arteriole -----to----capillary bed-----to----efferent arteriole -----to----capillary bed ----to---- veins
• First capillary bed = glomerular capillaries
• Second capillary bed = peritubular capillaries
Purpose of this = to control the pressure in the glomerular capillaries &
consequently the glomerular filtration pressure
3 factors control this:
• (1) autoregulation
• Local feedback from muscle tension in afferent arteriole
• Local feedback from DCT at JGA
• Mediated via endothelial
secretions of glomerular capillaries
• (2) sympathetic nervous system
• (3) renin
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•
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B = increase fluid volume; overhydration; high output heart failure
C = kidney pathology
D = hypertension; arteriolar spasm
– Hormones help control the volume of urine via fluid & electrolyte
balance
• The concentration factor essentially deals with urine volume
– Usually more the volume = more the dilution [a direct proportion]
1. Aldosterone
» From adrenal cortex
» Works on distal convoluted tubule
» Causes H2O & Na+ retention
2. Atrial natriuretic hormone(ANH)
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From atrial wall of heart
Works on distal convoluted tubule
Works in opposition to aldosterone
Causes H2O & Na+ loss
3. Antidiuretic hormone
» From posterior pituitary
» Works on collecting tubules
» Causes reabsorption of H2O (Na+ goes with it)
Diagnostic Tests - Urinalysis
1. Physical Characteristics &
Measurements
– appearance
– color
– odor
– volume
– specific gravity
2. Chemical Measurements
– pH
– protein; glucose
– ketones
– bilirubin; urobilinogen
– leukocytes; nitrite
– blood
3. Microscopic
– cells (wbc, rbc, sperm)
– casts
– crystals
– bacteria
4. Detection of Bacteriuria
– nitrite test
• qualitative or screening test
– C&S
• Colony Count, if done,
make this a quantitative test
• NOTE: Step 4, qualitatively, is
done as part of step 2
• Appearance
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Clear = normal
Cloudy = ? Infection
If sediment = kidney disease
Dark = ?blood, ?bilirubin,
?concentrated
• Color
– Urochrome pigment = yellow
• comes from breakdown of
hemoglobin
– Concentration
• More Concentrated =
Deeper Yellow
– Change of Color From:
• Meds
– Vitamin = yellow
• Diseases
– Blood = red-brown
– Liver = Orange
• Foods
– Rhubarb = red-brown
• Odor
– Normal = ammonia-like smell
• from breakdown of urea
– Unpleasant = ? infection
• Quantity
– Average per 24 hours = 1500 cc
• 60 cc per hour
• GFR = 125 cc/min
– Thus, 7500 cc/ hour
• Urine Made Per Hour = 60 cc
• Urine GFR Per Hour = 7500 cc
– KEY: 1 % of filtered urine
remains urine; 99 % becomes
reabsorbed back into blood
– Oliguria = 100 - 400 cc per day
– Anuria = less than 100 cc per day
– Polyuria = diabetes, nerves, diuretics
• Specific Gravity
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Determines Concentration
Compares Test Liquid to H2O
Normal = 1010 - 1030
First AM Specimen = > 1020
In many kidney diseases, one
loses the ability to concentrate
urine
– 3 ways to do it:
1. Reagent Strip
2. Refractometer
3. Urinometer
• pH
– Determines Acidity or Alkalinity
– Normal = 6.0
– Range = 4.5 - 8.0
• Acidity example = diabetes
• Alkaline example = UTI
• Protein
– OK to have a Trace in the urine
– Benign Conditions:
• exercise
• exposure to cold
•  protein consumption
– Generally Means Kidney Disease
• Glucose
– Will only be in urine if exceed Renal
Threshold (160 - 180 mg/dl)
• Ketone (note Acetone is a Ketone)
– Ketones are products of Fat
Metabolism
– If cant breakdown Sugars for
energy, the body will begin using
Fat
– Seen in:
• Uncontrolled Diabetes
• Starvation
• Hi-Fat Diet
•
Bilirubin & Urobilinogen Formation
– When used-up RBC’s are broken
down by R-E System, a by-product
is Bilirubin
– Bilirubin removed from blood by
liver & excreted into intestine
– Bacteria in intestine convert
Bilirubin into Urobilinogen
– Some Urobilinogen reabsorbed into
blood
• Of this amount reabsorbed
some my be normally passed in
urine
• Bilirubin
– Normally None in Urine
– Found in urine if it can’t get from
the liver into G-I tract
• From Obstruction of Bile Ducts
– Found in urine if have:
• Liver Disease (hepatitis)
• Blood Disease (hemolysis)
• Urobilinogen
– generally follows whatever happens
to bilirubin
– may get none in urine if on
antibiotics (destruction of gut flora)
– usually get small amount in urine
• Blood
– None is normal
– But may see some if female is
menstruating
• Leukocytes
– from inflammation of kidney or
lower G-U tract
• Nitrites
– screening test for bacteriuria
– bacteria convert nitrate to nitrite
Other Diagnostic Tests
• Blood tests
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BUN / creatinine
CBC ------ anemia if decreased EPO production
Renin
Antistreptolysin titers
• Urine culture & sensitivity (C&S)
• Include colony count
• Imaging
• IVP
• Retrograde pyelography
• CAT/ MRI
• Surgical procedures
• Cystoscopy
• Biopsy
Urinary Tract Disorders
overall outline
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Incontinence & retention
UTI’s
Inflammatory disorders
Nephrotic syndrome
Urinary tract obstruction
• Stones
• Hydronephrosis
• Tumors
– Renal cell carcinoma
– Bladder cancer
• Congenital disorders
• Polycystic kidneys
• Wilm’s tumor (nephroblastoma)
• Renal failure
• Acute
• Chronic
• Dialysis
Incontinence, retention, & catheters
• Urinary Incontinence
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Loss of voluntary control of bladder
Frequently called “neurogenic bladder”
Many causes
Enuresis = involuntary control after age 4 or 5
Types:
– Stress
– Urge
– Overflow
• Urinary retention
– Called “residual urine”
– Causes :
– Anatomical defects
– Neurogenic defects
• Treated with “catheterization”
– Foley
– French
Urinary Tract Infections
Urethritis; Cystitis; Pyelonephritis
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Etiology
– Ascending infection ----- women > men
– Prostatic hypertrophy with urinary retention
– Incomplete emptying of bladder with urinary stasis
– Pregnancy associated with stasis
– Blood borne pathogens
Pathophysiology of UTI’s ----- see next slide
Dx
• Dysuria, urgency, & nocturia
• Systemically get fever & malaise
• CVA tenderness in pyelonephritis
Note glomerulonephritis is vastly different with regards etiology &
pathophysiology
•
Note etiologies
– Inflammation of
mucosa
– Trauma of mucosa
– Obstruction
– Vesicoureteral reflux
– Immobility
– Blood-borne
pathogens
• TB
• HIV
• Septicemia
Inflammatory disorders
(1) glomerulonephritis
(2) nephrotic syndrome
• Glomerulonephritis
– Acute
• Sx = proteinuria, edema, oliguria
• Etiol = 1-2 weeks post strept
infect.
– Chronic
• Etiol = autoimmune disease
– e.g. lupus, diabetes, hepatitis C
• Can lead to irreversible kidney
damage
• Nephrotic Syndrome
– Glomerular disorder where one loses the capacity
to retain protein, especially albumin
– Sx
– severe edema (anasarca)
* can get skin breakdown since
impaired arterial flow
– proteinuria
– hypoalbuminemia
– oliguria
– Etiol:
» Toxic agents (lead, mercury)
» Toxic drugs (aminoglycosides)
» Diseases (diabetes, lupus
» Key = any significant problem with
glomerulus can lead
to nephrotic syndrome
Obstructive Disorders
• Renal Calculi
– Etiology: Calcium, Uric
acid, Urine crystals
– Symptoms: renal colic, N&V,
chills, fever
– Risk factors: prolong
dehydration, prolong
immobilization, infection
– Treatment:
surgery,lithotripsy
• Anomalies
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Strictures
Kinks
Ptosis
Pelvic kidney
• Tumors
– Note that primary
symptom = hematuria
– Renal Cell Ca = most
common, unilateral, adeno
Ca from tubular epithelium
• See picture
– Bladder Ca = usually from
transitional epithelium
• Neurogenic bladder
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•
These result in:
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Hydronephrosis
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Hydroureter
If these conditions
exist longer than 2
months get
destruction of
kidney
Major sites of urinary tract obstruction
Congenital Diseases
• Vesicoureteral reflux
• Due to ectopic insertion of ureter into bladder. If far away from
trigone, do not get adequate compression of ureter when voiding &
get reflux
• Incidence: 1/1000
• If one gets it each sibling(to be) has 50% incidence
• Girls> boys; 10:1 ratio
• Ectopic kidney
• May get kinking of ureter
• Usually in pelvis
• Asymptomatic
• Renal agenesis
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Usually unilateral & left kidney
2 types: (1) occurs randomly (2) genetic
Asymptomatic
Remaining kidney becomes large since compensatory hypertrophy
Congenital Diseases (cont)
• Polycystic kidney (2 types
– In adults
(see picture)
• Genetic etiol ----- autosomal dominant
• Clinically seen in adults
– Between age 30 – 40 one begins to get renal
failure
• Tx = transplant
– In children
• Genetic etiol --- autosomal recessive
• Manifest at birth; usually fatal or infant stillborn
• Rare
• Wilm’s tumor (nephroblastoma)
• Most common tumor of children; usually
unilateral
• Etiol = autosomal recessive (on chromosome 11)
• Manifests between age 2 – 5 years & presents as
abdominal mass
– May produce hypertension
• 5 year survival = 90%
Renal Failure
• Acute renal failure
– Abrupt decrease in renal function
• Nitrogenous wastes accumulate
– Usually reversible
– Sx:
• Oliguria
• Drowsiness
• Altered levels of consciousness
– Etiol:
• Glomerular disease
• Severe pyelonephritis
• Nephrotoxins that damages
tubular epithelium
• Ischemic causes
– shock
• ATN (acute tubular necrosis)
» e.g. burns(hgb
accumulates)
» e.g. trauma (myoglobin
accumulates)
• Chronic Renal Failure
– Get slow progressive loss
of neurons
– Usually irreversible
– Course = gradual
– Etiol:
• Vascular disease
– e.g.
hypertension
– Disease called
nephrosclerosis
• Glomerular disease
– e.g. diabetes
• Tubular disease
– e.g. toxins
Hypertension & the kidneys
Dialysis in renal failure
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•
2 types:
– Hemodialysis
– Peritoneal dialysis
Mechanism
– Simple diffusion for
wastes &
electrolytes
– Osmosis for water
balance