Chapter 30 - Alteration In Renal And Urinary Tract Function Flashcards
Most common urinary disorders are
-bladder infection
-stones, tumours, inflammation causing obstructed urinary tract
Disorders of kidney or systemic diseases affecting kidney can result in
-acute kidney injury
-chronic kidney injury
-kidney failure (life threatening)
Urinary tract obstruction
Interference with urinary flow along urinary tract
Impeded flow =
Increased risk of infection
Obstructive uropathy
Anatomical changes causing obstruction
Upper vs lower urinary tract
U: kidneys and ureters
L: bladder and urethra
Upper urinary tract infections
Obstruction of the UUT results in BACKING UP of urine
-dilation
Upper urinary tract infections: pressure is transmitted to
Glomerulus which causes reduced filtration
Hydroureter
Accumulation of urine in ureter
Hydronephrosis
Accumulation of urine in calyces and renal pelvis
What is an early response to obstruction
Dilation
Upper urinary tract infections: stasis
Cessation of urinary flow
-occurs above obstruction between obstruction and glomerulus
Within 7 days (of Upper urinary tract infections)
Tubulonintersitial fibrosis
-excessive collagen, hardening and scarring
Upper urinary tract infections: 14 days
Both distal and proximal nephron affected
Upper urinary tract infections: 28 days
Glomeruli damaged
Compensatory hypertrophy
Unobstructed kidney increases the size of glomeruli and tubules
-but not the total number of nephrons
Interstitial
Relating to spaces between cells, tissues or organs in the body
Kidney stones (CALCULI)
Masses of crystals, proteins etc
-located in kidneys ureters and bladder
Progression of stone formation (4)
- Supersaturation of salts in urine (many ions capable of forming salts)
- Precipitation of salts from liquid to solid state
- Aggregation of salts into stone
- Absence of stone inhibitors
Urine contributing factors: >7.0
Increased risk of calcium phosphate stone
Urine contributing factors: <5.0
Increased risk of urine acid stone
Size of stone determines
It’s ability to be passed out through urination
Moderate to severe pain in flank (sides and back of abdomen) radiating to groin indicates
Obstruction of renal pelvis
Lower abdomen pain =
Obstruction in mid ureter
Urgency to urinate or incontinence =
Obstruction in lower ureter
TX for kidney stones
-imaging studies to determine location
-medications
-high fluid intake to reduce
-surgery (laser lithotripsy)
Lithotrispy
To fragment stones
-ureteroscopy with laser
Lower urinary tract obstructions are related to
-urine storage in bladder
-emptying of urine
-neurogenic/anatomical (or both)
Common symptom associated with lower urinary tract obstruction
Incontinence
Neurogenic bladder
Bladder dysfunction caused by neurological disorders
Type of dysfunction is related to
Related nerve location
Above C2 is
Hyper-reflexia
Hyper-reflexia (above C2) is caused by
Stroke, TBI, MS, Alzheimer’s
Hyper-reflexia (above C2)
Urgency to urinate and urine leakage
-bladder empties automatically when full
Between C2-S1 is called
Hyper-reflexia with sphincter contraction
Hyper-reflexia with sphincter contraction (between C2-S1) is caused by
Spinal cord injury, Gillian barre syndrome, vertebral disc issues
Hyper-reflexia with sphincter contraction (between C2-S1)
Muscle contractions and external sphincter contraction at the same time
-causes functional obstruction of bladder
Below S1 is called
Atonic (without tone) bladder
Atonic (without tone) bladder (bellow S1) is caused by
Peripheral neuropathy, MS, spinal injury
Atonic (without tone) bladder (below S1)
Urine retention and distension
-full bladder is sensed, but destrusor does not contract and you have an unreactive bladder
Urethral constriction
Scarring that narrows urethra and restricts flow of urine from bladder
-mostly in men, rarely in women
TX urethral constriction
Urethrotomy
-surgical knife used to widen urethra
Prostate enlargement is caused by
Caused by acute inflammation, benign prostatic hyperplasia, cancer
TX for prostate enlargement
Medication (alpha blockers such as terazosin (hytrin) or tamsulosin (flomax))
Acute cystitis
Inflammation of bladder
-most common site of UTI
Acute cystitis: mild infection
Mucosa is hyperaemic (red)
Acute cystitis: hemorrhagic cystitis
More advanced, diffuse hemorrhage
Acute cystitis: suppurative cystitis
Pus forms on epithelial bladder surface
Acute cystitis as a prolonged infection
Can result in shedding of bladder mucosa
-causing ulcer formation and possible necrosis of bladder wall
When bacteria bind to bladder mucosa what is the natural response of the immune system
Shedding
What is the negative side effect of the immune system shedding
Bladder wall now is not protected from salts, toxins etc
Most common pathogens in Acute cystitis
E. coli, Staph. Saprophyticus and parasite schistosomiasis
How does bacterial contamination occur in Acute cystitis
Movement of gram negative e.coli from urethra eventually to kidney
What allows e.coli to bind to epithelium and resist flushing during micturtiion
Fimbriae
Result of Acute cystitis
Inflammation of bladder stimulates stretch receptors, intimating feeling of fullness with only small volumes in bladder
TX for Acute cystitis
Antibiotics
Painful bladder syndrome/interstitial cystitis: non bacterial
Viral or fungal
-most common in immunocompromised
Painful bladder syndrome/interstitial cystitis: non infectious cystitis
Associated with radiation, chemotherapy treatment for pelvic regions
Cause of Painful bladder syndrome/interstitial cystitis
Unknown
Symptoms of Painful bladder syndrome/interstitial cystitis
Bladder fullness, nocturia, chronic pelvic pain lasting longer than 9 months
TX for Painful bladder syndrome/interstitial cystitis
-sacral nerve stimulation
-surgery for refractory cases
Acute pyelonephritis
Sudden and severe kidney infection infecting one or both upper urinary ureters
Most common risk factors and gender common in Acute pyelonephritis
-urinary obstruction and reflux of urine from bladder
-women
What bacteria is primary in Acute pyelonephritis, and what does it do
-e.coli
-splits urea into ammonia = alkaline urine = increased risk of stone formation
Where does the infection mostly occur, and what does the infection cause (Acute pyelonephritis)
-renal pelvis and calyces
-causes influx of WBC into kidney medulla causing inflammation and Edelman
TX for Acute pyelonephritis
-AP responds well to 2-3 weeks of microorganism specific antibiotics
-bacteria will Dec until urine becomes sterile again
Chronic pyelonephritis
Persistent and recurrent infections leading to scarring of both kidneys
Chronic obstruction in Chronic pyelonephritis prevents
Elimination of bacteria
-there will be progressive inflammation causing tubule destruction and impaired urine concentration ability
Result of Chronic pyelonephritis
Chronic kidney disease
-can lead to kidney failure
TX for Chronic pyelonephritis
Related to specifics of underlying infections
Glomerulonephritis (what/cause)
Inflammation of glomerulus caused by primary glomeruli injury
Primary glomeruli injury can be caused by..
-immunological responses
-ischemia
-free radicals
-medications
-infections (strep)
What causes the major injuring in Glomerulonephritis, and what does it result in
Immune mechanisms
-damages glomeruli filter membrane
Glomerulonephritis: injury is caused by
Complement (from porins) and cytokines
-cause invasion of macrophage, neutrophils and T cells
Result of infiltration in Glomerulonephritis
Glomeruli filtration rate is reduced, causing hypoxic injury
Glomerulonephritis: loss of negative charge across glomeruli filter results in
Proteins (negatively charged) leaking into nephron
Chronic Glomerulonephritis leads to
Chronic kidney disease
-dialysis or kidney transplant may be required
Nephrotic syndrome
Occurs when filtration of proteins exceeds tubular reabsorption
Nephritic syndrome
Characterized by hematuria (RBC in urine) and RBC casts (cylindrical structures created by kidney containing red blood cells) excreted in urine
Nephrotic syndrome vs nephritic syndrome
Nephrotic: excretion of 3.5g or more of PROTEIN in urine per day, glomerular injury
Nephritic: bleeding in nephron, blood in urine
Acute kidney disease
Sudden decline in kidney function with a decrease in glomerular filtration and urine output
Results of Acute kidney disease
Accumulation of nitrogenous waste products in blood which is demonstrated by elevation in plasma creatinine and BUN levels
How can we tell there is in an inc of nitrogenous waste products in blood
Elevation in plasma creatinine and BUN levels
Acute kidney disease results from
Ischemic injury related to decreased renal blood flow, toxic injury from chemicals and sepsis induced injury
Acute kidney disease: injury initiates inflammatory response =
cell death = alterations in kidney function
Urea is composed of
Oxygen, carbon, nitrogen and hydrogen
BUN test measures
Nitrogen in blood
Nitrogen in blood = urea in blood
-inc urine in blood = kidney dysfunction
Acute kidney injury: oliguric phase
Less than 400ml/day urine output
-occurs 1 to u days of kidney injury
-casts, hyperkalemia (inc blood K+), hyponatremia (dec Na+), elevated BUN and creatinine
Acute kidney injury: diuretic phase
1-2 weeks or possibly longer
-urine output is normal to high (bc kidney has lost ability to concentrate urine)
-weight loss, hypovolemia/hypotension due to inc urine output, BUN and creatinine begin to normalize
Acute kidney injury: recovery phase
Begins with GFR normalization
-BUN and creatinine levels begin to normalize
Chronic kidney disease
Progressive loss of renal function
Chronic kidney disease is associated with
-diabetes mellitus (most significant risk factor)
-hypertension
-systemic lupus
-intrinsic kidney disease
Systemic lupus
Autoimmune disease where the immune system attacks its own tissues
Intrinsic kidney disease
Direct damage to kidneys and sudden loss in kidney function
Chronic kidney disease: sequences of events leading to scarring and fibrosis
-infiltration of damaged kidney with inflammatory cells
-loss of renal cells through apoptosis and necrosis
-production of fibroblasts
Mechanisms of accelerated progression of CKD
-systemic and intraglomerular hypertension
-glomerular hypertrophy
-inc Ca+ phosphate in kidney
Mechanisms in Chronic kidney disease lead to
Focal segmental glomerulosclerosis
-scar tissue in glomerulus
