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urinary tract obstruction
can occur at any site along the urinary tract
obstruction impedes flow
causes:
kidney stone
compression from a tumour
inflammation
congenital
obstructive uropathy
anatomical changes in the urinary system caused by obstruction
hydronephrosis
progressive dilation of the renal collecting ducts and tubules
glomerular filtration continues, so pressure builds up, first in the renal pelvis and then in tubules
hydroureter
caused by obstruction within ureter
stasis of urine
increases possibility of infection and stone formation
kidney stones
most common cause of upper urinary tract infection
kidneys, ureters, and urinary bladder
also known as urinary calculi
age, fluid intake, diet
crystals, proteins or other substances
most common stones are composed of calcium oxalate or phosphate
small stones have 50% chance of spontaneous passage, where larger stones have almost no chance of spontaneous passage
renal colic
clinical manifestation of kidney stone
excruciating pain in the flank and abdomen caused by a 1-5 mm stone moving into the ureter and stretching it
neurogenic bladder
cause of lower urinary tract obstruction
bladder dysfunction caused by neurologic disorders (CNS or peripheral nerve damage)
physical obstruction
cause of lower urinary tract obstruction
scarring of the urethra( infection, surgery), enlarged prostate
glomerulonephritis
inflammation of glomerulus
causes: hypertension, immunologic responses, infection, diabetes mellitus
2nd leading cause of kidney failure
nephritic syndrome
manifestation of glomerular disease
sudden excretion of blood cells, protein, diminished GFR, oliguria
caused by: inflammation that blocks the glomerular capillary lumen and damages the capillary wall (typically associated with post infectious glomerulonephritis)
nephrotic syndrome
manifestation of glomerular disease
nephrosis
massive proteinuria and lipidura
edema (hallmark manifestation)
group of manifestations resulting from loss of protein that includes thrombotic complications, increased risk of infection, etc
caused by:
increase in glomerular permeability due to blood vessel damage from eg. diabetes mellitus, SLE
BUN
blood urea nitrogen
concentration of urea in blood
shows degree of :
glomerular filtration, urine concentrating capacity
acute kidney injury (AKI)
sudden (less than two days) decline in kidney function
decrease in glomerular filtration
accumulation of nitrogenous waste products in the blood (BUN and plasma creatinine)
potentially reversible, if can correct the cause before the permanent kidney damage has occurred
ranges from minimal changes in renal function to complete renal failure requiring renal replacement therapy:
spectrum is described by RIFLE criteria
RIFLE
based on glomerular filtration rate and urine output
Risk
Injury
Failure
Loss
End stage disease
pre-renal acute kidney injury
cause of AKI (acute kidney injury)
decrease in GFR is caused by renal hypo perfusion
if pressure continues to be low, lack of oxygen delivery can cause cell injury and necrosis\
high BUN:creatinine ratio
due to low filtration and slow flow in tubules, which allows more reabsorption of urea
post renal acute kidney injury
cause of AKI
urinary tract obstructive disorder
occurs with urinary tract obstruction that affects both kidneys
causes an increase in pressure upstream, resulting in decreased GFR
normal BUN:creatinine ratio
kidney words fine initially; problem is after the kidney makes urine
intrarenal acute kidney injury
usually results from tubular necrosis as a result of occurrences including:
ischemia associated with pre renal failure
sepsis
nephrotoxic effects of drugs
lower BUN:creatinine ratio
due to poor reabsorption of urea in the tubules
treatment of AKI
maintain life until renal function has been recovered
correct fluid and electrolyte balance
treat infections
maintain nutrition
continuous renal replacement therapy or hemodialysis may be required
chronic kidney disease
defined by kidney damage or a GFR <60 ml/min for 3 months of longer (normal >=90ml/min)
5 stages
risk factors:
hypertension, diabetes mellitus, chronic glomerulonephritis, obstructive uropathies
intact nephron hypothesis
unaffected nephrons are capable of hypertrophy and hyper function
puts stress on healthy nephrons, which hastens their failure
compensation
what is done to maintain the pH in response to disturbances
partially compensated
one of the systems is attempting to rectify the disturbance, but has not yet been successful, resulting in values for that system that are outside normal ranges
fully compensated
pH levels are within normal limits, but values for both systems are outside of normal limits (in opposite directions)
corrected state
all values are within normal limits
hypernatremia
retention or therapeutic infusion of sodium
retention cam be caused by over secretion of aldosterone or ACTH
IV infusion - sodium bicarbonate to treat acidosis
increased loss of fluids
sweating, watery diarrhea, excessive urination
decreased water intake
hyponatremia
decreased concentration of sodium ions in the blood
water moves into the cells (osmosis), causing cells to swell
hyperkalemia
excess potassium ions in the blood
caused by:
renal disease
under secretion of aldosterone
increased intake
a shift from intracellular to extracellular: changed cell permeability caused by trauma, hypoxia, acidosis
insulin deficits
hypokalemia
derceased concentration of potassium ions in the blood
due to
excessive loss of potassium
inadequate intake
increased entry into cells
hypocalcemia
due to decreased PTH, kidney disease, alkalosis
leads to increased excitability of both muscles and nerves
Trosseau’s sign and Chvostek’s sign
Magnesium
cofactor in many intracellular enzymatic reactions
nerve conduction
smooth muscle contraction and relaxation
hypermagnesemia
decreased excitability of both muscles and nerves
hypoactive reflexes
muscle weakness
brachycardia, respiratory distress
nausea, vomiting
hypomagnesemia
increased excitability of both muscles and nerves
increased reflexes
muscle cramps and convulsions
tachycardia
behavioural changes, irritability
azotemia
increased levels of serum urea and other nitrogenous compounds
uremic syndrome
the systemic signs and symptoms associated with the accumulation of nitrogenous wastes and toxins in the plasma brought about through kidney failure.
anasarca
general accumulation of fluid in body cavities and tissues
cardiovascular system
effect on body system
major cause od death in CKD (chronic kidney disease)
excess sodium leads to hypertension
excess LDL leads to increased atherosclerosis
pulmonary system
effect on body system
complications associated with fluid overload
acidosis results in kussmal respirations
hematologic system
effect on body system
anemia (erythropoietin is produced by the kidneys), impaired platelet function (possibly due to uremia)
immune system
effect on body system
overall suppression by high levels of urea and metabolic eastes
neurologic system
effect on body system
numerous effects of uremic toxins, including both peripheral and central nervous system
restless leg syndrome, muscle atrophy, headache, impaired concentration 0 with later stages, seizures, coma
gastrointestinal system
effects on body system
anorexia, vomiting, possibly due to breakdown of urea by intestinal bacteria
endocrine and reproductive systems
effects on body system
decrease in levels of sex steroids bring symptoms, such as impotence and amenorrhea
insulin resistance and alterations in thyroid hormone metabolism can occur