Alterations of Renal & Urinary Tract (BOLDED ONLY) Flashcards
upper urinary tract obstruction - compensatory hypertrophy and hyperfunction
loss of function of one kidney with obstructive disease leads an increase in size and increased function of the unaffected kidney
relief of upper urinary tract obstruction is usually followed by _______ and may cause fluid and electrolyte imbalance
obstructive diuresis
typically mild, but can cause dehydration and f/e imbalance
also called renal calculi or urolithiasis, and what are they made of?
kidney stones
-masses of crystals, proteins, or mineral salts form in the urinary tract and may obstruct the urinary tract
kidney stone risk factors
-male, less than 50, inadequate fluid intake, geographic location (temperature, humidity, rain fall, fluid, and dietary pattern
most common mineral salts kidney stones and what increases risk?
calcium oxalate and calcium phosphate (70-80%)
- alkaline urine increases risk
- can prevent with potassium citrate, pyrophosphate, and magnesium
kidney stone formation - precipitation of a salt from a liquid to a solid state - what influences this? what is most important?
temperature and pH or urine influence the risk of precipitation and calculus formation, but pH IS MORE IMPORTANT
s/s of kidney stones - renal colic that is mod to severe pain originating in the flank and radiating to the groin indicates?
indicates obstruction of RENAL PELVIS OR PROXIMAL URETER
renal colic that radiates to the lateral flank or lower abd = obstruction in _______
the midureter
lower urinary tract obstruction - overactive bladder syndrome (OAB)
syndrome of? characterized by?
- syndrome of detrusor overactivity
- characterized by urgency with involuntary detrusor contractions during bladder filling that are either spontaneous or provoked
- coordination b/w contracting bladder and external sphincter maintained
- detrusor too weak to empty bladder and results in urinary retention with overflow or stress incontinence
- symptom syndrome of urgency, with or without urge incontinence and associated with frequency and nocturia
renal tumors - renal adenomas…what kind of tumors? located where? can become what?
renal adenomas are typically benign tumors located near cortex of kidney, and can become malignant
renal transitional cell carcinoma is what?
rare
renal cell carcinoma (RCC) - m or w more? risk factors? what type of cancer? which has better and worse prognosis?
most common
men>women in 5th and 6th decade of life
risk factors: cigarette smoking, obesity, HTN
RCC are adenocarcinomas that arise from tubular epithelium in the renal cortex
Clear cell - better prognosis most common
Papillary - worst prognosis
classic clinical manifestations of renal tumors
early stages are often?
HEMATURIA, dull and aching flank pain, palpable flank mass in thinner individuals
early stages often silent
bladder tumors (urological tumors) - this was not bolded
urothelial carcinoma is also called? risk factors?
urothelial (transitional cell) carcinoma is the most common type of bladder tumor
risk factors: smoking, exposure to metabolites of aniline dyes or other aromatic amines or chemicals, high arsenic in drinking water, heavy consumption of phenacetin
clinical manifestations of bladder tumors (think urothelial/transitional cell carcinoma)
GROSS PAINLESS MICROSCOPIC HEMATURIA
hematuria episodes tend to recur, and are accompanied by lower urinary tract symptoms including daytime voiding frequency, nocturia, urgency, and urge urinary incontinence
more common in M over 60 and smokers
UTI - cystitis - what is it?
inflammation of the bladder
*most of the time cystitis is caused by a UTI
interstitial cystitis - caused by?
also called bladder pain syndrome
nonbacterial infectious cystitis
thought to be the result of autoimmune reaction responsible for inflammatory response that includes mast cell activation, altered epithelial permeability, and increased sensory nerve sensitivity
interstitial cystitis manifestations
- age 20-30 females
- bladder fullness, frequency, small urine volume, urgency, chronic pelvic pain
- urine cultures negative
- most common in immunocompromised
pyelonephritis - what is it?
infection of one or both upper urinary tracts (ureter, renal pelvis, and interstitium)
acute pyelonephritis - most common cause? what does it cause? primarily affects?
acute infection of the renal pelvis interstitium
e.coli most common cause
causes medullary infiltration of WBCs with renal inflammation, renal edema, and purulent urine
PRIMARILY AFFECTS TUBULES, GLOMERULI USUALLY SPARED
rarely causes renal failure
acute glomerulonephritis (the glomerulus is affected*) pathophysiology
clinical manifestations
formation of immune complexes (antigen/antibody) in the circulation with subsequent deposition in glomerulus
antibodies produced against the organism that cross-react with the glomerular endothelial cells
clinical manifestations: hematuria with RBC casts; smoky, brown-tinged (or cola colored) urine from RBCs, HTN d/t fluid retention…
nephrotic sediment vs nephritis sediment
nephrotic: contains massive amounts of PROTEIN AND LIPIDS and either a microscopic amount of blood or no blood
nephritic: BLOOD is present in the urine with RED CELL CASTS, WHITE CELL CASTS, AND VARYING DEGREES OF PROTEIN, which is not usually severe
nephrotic syndrome
clinical manifestations
- excretion of 3g or more of protein in the urine - causes foamy urine
- protein excretion as a result of glomerular injury
clinical manifestations: hypoalbuminemia (peripheral edema), prone to infection, vit D deficient, hyperlipidemia and lipiduria, hypothyroidism
nephritic syndrome caused by?
increased permeability of the glomerular filtration membrane
nephrotic syndrome caused by
altered glomerular permeability and loss of negative charge (loss of negative charge causes protein loss) - albumin is also negatively charged, and this usually prevents loss
RIFLE
classification of acute kidney injury
risk, injury, failure, loss, end-stage disease
- Risk GFR decrease > 25%, increased creatinine x1.5
- Injury GFR decreases >50%, creat x 2
- Failure GFR decreases >75%, creat x3
- Loss - persistent acute renal failure: complete loss of kidney function >4 weeks
- End-stage kidney disease - complete loss of kidney function >3months
acute kidney injury
sudden decline in kidney function with a decrease in glomerular filtration and accumulation of nitrogenous waste products in the blood
- increase in BUN and creatinine
- 3 categories: pre-renal, intra, and post
pre-renal acute kidney injury
renal hypo-perfusion: most common cause
reversible
elevation BUN and creatinine
GFR decline
intra-renal AKI
disorders involving the renal parenchymal or interstitial tissue
ACUTE TUBULAR NECROSIS (ATN) CAUSED BY ISCHEMIA IS THE MOST COMMON CAUSE
*occurs most often after surgery s/t hypovolemia and third spacing due to increase in inflammation, but ATN also associated with sepsis, obstetric complications, burns, trauma
*anesthesia can also mess with neural controls of the bladder resulting in retention
there is kidney damage
post-renal AKI
rare
disorders associated with acute urinary tract obstruction
Intra-renal AKI generally described as _____ or ______
POSTISCHEMIC - involves persistent hypotension, hypoperfusion, and hypoxemia producing ischemia, reduced ATP, and generate toxic oxygen-free radicals with loss of antioxidant production that causes cell swelling, injury, necrosis
or
NEPHROTOXIC produced by numerous abx; neomycin, gentamycin, and tobramycin are the major culprits
*drugs accumulate in renal cortex and can cause renal failure
post-renal
occurs with urinary tract obstructions that affect the kidneys bilaterally
*bilateral ureteral obstruction, bladder outlet obstruction -prostatic hypertrophy, tumors, or neurogenic bladder (extra renal), and urethral obstruction
clinical manifestations: pattern of several hours of anuria with flank pain followed by polyuria
*can occur after catheterization of ureter, which causes inflammation of the tubular lumen
the phases of AKI
initiation phase - prevention of injury possible, usually lasts 24-36 hours
oliguric phase - period of established renal injury and dysfunction after the initiating event has been resolved?
- may last from weeks to months
- urine output low, BUN + creat high, K+ high, Na+ and H20 overload, metabolic acidosis develops
recovery phase - renal injury repaired, GFR returns to normal, but the regenerating tubules cannot concentrate the filtrate, diuresis common, decline in serum BUN/creat
*polyuria can result in loss of sodium, water, K+
CKD causes four bolded things
immune system suppression d/t loss of proteins (Ig) - lack of response to vaccines, increase r/f infection
neurologic system - impaired concentration, memory loss, impaired judgement, seizures, coma - think toxin build-up uremia
endocrine and reproductive systems - decrease in sex steroids (loss of protein), decreased libido (loss of testosterone), insulin resistance, low thyroid hormone levels
integumentary system: anemia causes pallor (anemia from decreased EPO), bleeding - hematomas and ecchymosis (platelet dysfunction), retained urochromes = sallow skin color,
-hyperparathyroidism (probably d/t low calcium levels b/c PTH results in increased calcium) and uremic skin residues, known as uremic frost - causes irritation, and pruritus with scratching, excoriation, and increased r/f infection
