Alterations of Renal and Urinary Tract Function Flashcards
Most common urinary dysfunction
-Infection (stones, tumors, inflammation)
Urinary Tract Obstruction
- Blockage or urine flow -Can be anatomical or obstructive
- Severity is based on (location, completeness, involvement of one or both upper urinary, duration)
Upper Urinary Tract Obstruction
- Complications: Hydroureter, hydronephrosis, ureterohydronephrosis, tubulointerstitial fibrosis, leads to excess cellular destruction and death of nephrons
- Compensatory hypertrophy hyperfunction
Kidney stones
- Renal calculi or urolithiasis
- Masses of crystals, proteins, or mineral salts form in the urinary tract may obstruct the urinary tract
- Risk factors: Male, most develop before 50 years, inadequate fluid intake
- Can be located in the kidney, ureters or urinary bladder
Kidney Stone Treatment
- Parenteral and/or analgesics for acute pain
- Medical therapy that promotes stone passage
- High fluid intake
- Alteration in urine pH
- Removal of stones using percutaneous nephrolithotomy, ureteroscopy, or ultrasonic or laser lithotripsy to fragment stones for excretion
Lower Urinary Tract Obstruction
- Neurogenic bladder
- disorders of the lower urinary system are typically related to storage of the urine in the bladder or emptying of urine from the bladder
Neurogenic bladder dysfunctions
-Dyssynergia, detrusor hyperflexia, detrusor areflexia
Causes of lower urinary tract obstruction
- prostate enlargement
- Urethral stricture
- Severe pelvic organ prolapse
- Low bladder wall compliance
Clinical manifestation of lower urinary tract obstruction
- Frequent daytime voiding
- Nocturia
- Urgency
- Dysuria
- poor force of stream, intermittency of urinary stream
- Feelings of incomplete bladder emptying, despite micturation
Cytometric test
- uses a catheter and manometer to evaluate urine volume and pressure in relation to involuntary bladder contraction and urge to void
- Used in evals w/ lower urinary tract obstruction
Lower urinary tract obstruction: Prolapse
- Pessary: rubber or silicone device designed to compensate for vaginal wall prolapse
- Intravaginal hormone replacement therapy and regular follow-up
- Surgery
- Pessary-can be removed, cleansed, and/or replaced at home or during a clinic visit
Overactive bladder syndrome
- Chronic syndrome of detrusor overactivity
- Symptoms syndrome of urgency w/ or w/out incontinence, usually w/ frequency and nocturia
- Urodynamic eval to confirm dx
- Tx: lifestyle modification, behavioral therapy, neuromodulation, antimuscarinic agents, surgery
Renal tumors
- Renal adenomas: benign
- Renal transitional cell carcinoma: rare-arises from renal parenchyma and renal pelvis
- Renal cell carcinoma: most common (hematuria, dull and aching flank pain)
Bladder tumors
- Urothelial (transitional cell) carcinoma: most common
- Risk factors: smoking, exposure to meatbolites of anline dyes or other aromatic amines or chemicals, high arsenic in drinking water, heavy consumption of phenacetin
- Inner lining of the bladder
Bladder tumor Tx
- Transurethral resection or laser ablation, combined w/ intravesical chemo or immunotherapy
- Radical cystectomy w/ urinary diversion
- Adjuvant chemo
- Radiation therapy
UTI
- Inflammation of urinary epithelium after invasion and colonization by some pathogen in the urinary tract
- Retrograde movement of bacteria in urethra or bladder
- Can occur at any point along the urinary system (cysitis-bladder inflammation, pyelonephritis-inflammation of upper urinary tract)
UTI protective urinary mechanisms
- Washed out of the urethra during micturation
- Low pH and high osmolality of urea
- Presence of tamm-horsfall protein
- Secretions from the uroepithelium: bactericidal effect
- Ureterovesical junction: closes to prevent reflux of urine to the ureters and kidneys
- Women-mucus secreting glands
- Men: length of male urethra
- Lewis blood group
UTI pathogens
-Escheriicia coli, staphylococcus saprophyticus
Painful bladder syndrome or interstitial cystitis
- Nonbacterial infectious cystitis, noninfectious cystitis and interstitial cystitis (autoimmune, hypersensitivity)
- S/s: longer than 6 wks but w/ negative urine cultures and no other known cause, bladder fullness, frequency, small urine volume and pelvic pain laster longer than 9 mo
- TX: oral and intravesical therapies, sacral nerve stimulation, onabotulinumtonxia;surgery
- Usually in women w/ neg urine cultures
Pyelonephritis
- Acute infection of the ureter, renal pelvis, and/or renal parenchyma
- s/s: flank pain, fever, chills, costovertebral tenderness, purulent urine
- Eval: WBC casts
- Tx: abx
Chronic pyelonephritis
- Can see deposition of scar tissue, fibrosis, and atrophy of affected tubules; can see shrinking of the size of the kidney
- Recurrent infection of kidneys
- Dx: urine culture, UA, clinical signs
- TX: Abx
Glomerular disorders
- Disorders that directly affect the glomerulus
- Significant cause of chronic kidney disease and end-stage renal failure worldwide.
- Secondary disorders (diabetes, SLE)
Acute Glomerulonephritis
- Patho: formation of immune complexes in the circulation
- Antibodies produced against the organism that cross-react w/ glomerular endothelial cells
- see in young children w/ strep
- SX: hematuria w/ RBC casts, proteinuria w/ albumin, smoky brown-tinged urine, edema, oliguria
Acute glomerulonephritis Tx
- Abx
- Corticosteroids
- Cytotoxic agents
- Anticoagulants
- dx by urinalysis, decreased GFR, elevated creatinine, plasma urea, and cystatin C levels
Chronic Glomerulonephritis
- Leading to chronic kidney failure
- some secondary causes: diabetes nephropathy, lupus nephritis
- S/s: proteinuria, hypercholestermia
- TX: Dialysis, and transplant
Diabetic nephropathy
- develops from metabolic, inflammatory, and microvascular complications related to chronic hyperglycemia
- Will see proteinuria w/ progression to chronic renal failure
Nephrotic syndrome
- Excretion of 3g or more of protein in urine
- Protein excretion as a result of glomerular injury
- s/s: hypoalbuinemia, peripheral edema, prone to infection, vitamin D deficiency,
- tx: normal protein, low fat diet, salt restrictions, diuretics, immunosuppression, and heparinoids, immunosuppressive drugs and ACE inhibitors used w/ steroid-resistant
Eval of nephrotic syndrome
-24 hr urine collection-see an increase in protein, decrease in serum albumin, concentrations of cholesterol, phospholipids, and triglycerides increase
Nephritic syndrome
- Hematuria, RBC casts, proteinuria
- caused by increased permeability of the glomerular filtration membrane
- Advanced stages-htn, uremia, oliguria
- Same tx of nephrotic syndrome
Classification of kidney dysfunction
- Acute or chronic, reversible or irreversible
- Renal insufficiency
- Renal failure
- End-stage renal failure (less than 10% of renal function remains)
Uremia
- Syndrome of renal failure
- Elevated blood urea and creatinine levels
- Fatigue, anorexia, nausea, vomiting, pruritus and neurologic changes
- Retention of toxic wastes, deficiency states, electrolyte disorders and proinflammatory state
Azotemia
- increased serum urea levels and frequently increased creatinine levels
- Renal insufficiency or renal failure, causing azotemia
- Both azotemia and uremia accumulate of nitrogenous waste products in the blood
Acute kidney injury
- sudden decline in kidney function w/ decrease in GFR and accumulation of nitrogenous waste products in the bloods
- Increased creatinine and BUN
AKI Classification
- RIFLE: Risk, injury, failure, loss, end-stage disease
- Risk: increased creatinine levelx1.5 or GFR decrease >25%, UOP <0.5mL/kg/hr x6hrs
- Injury: Increased creatinine levelx2 or GFR, decreased >50%, UOP <0.5mL/kg/hrx12HR
- Failure: increase creatinine levelx3 or GFR decrease >75%, UOP <0.3mL/kg/hrx24 hr or anuria
- Loss: persistent acute renal failure, complete loss of kidney function >4wks
- Endstage kidney disease: complete loss of kidney function >3mo
AKI type
- Prerenal: renal hypoperfusion: most common cause
- Intrarenal: disorders involving the renal parenchymal or interstitial tissue, acute tubular necrosis caused by ischemia most common cause
- Postrenal: rare, disorders associated w/ acute urinary tract obstruction
Prerenal AKI
- Most common cause; reduction in arterial blood flow causing hypoperfusion w/ and elevated BUN and Cr, GFR eventually decreases due to decrease in filtration pressure
- Multiple factors can play a role: artery thrombosis, hypotension, hypovolemia, hemorrhage, renal vasoconstriction, microthrombi, sepsis
Intrarenal AKI
- exposure to radiocontrast dye, abx, acute glomerulonephritis, DIC, allograft rejection, interstitial disease-drug allergy, infection, or tumor growth
- Oliguria and anuria are common w/ intrarenal AKI; increased Cr w/ decreased GFR
Post renal AKI
- Rare-occurs w/ renal obstruction that affeccts both kidneys; BPH, neurogenic bladder, tumor.
- Increase in intraluminal pressure upstream from obstruction and a decrease in GFR; flank pain and anuria followed by polyuria
AKI initiation phase
- Reduced perfusion or toxicity, during which renal injury is evolving
- Usually lasts 24-36 hours
- Prevention of injury is possible
AKI maintenance or oliguric phase
- Period of established renal injury and dysfunction after the initiating event has been resolved
- May last from wks to months
- Urine output is lowest and serum Cr, BUN, and serum K increase, metabolic acidosis develops, and salt and water overload occurs
AKI recovery phase
- renal injury is repaired and normal renal function is reestablished
- GFR returns toward normal but the regenerating tubules cannot concentrate the filtrate
- Diuresis is common, w/ a decline in Cr and urea and increase in creatinine clearance
- Polyuria can result in excessive loss of Na, K, and water
AKI prevention and Tx
- Maintenance of fluid volume before and after surgery or diagnostic procedures or when nephrotoxic drugs or contrast agents are used
- Tx: correct fluid and electrolytes, manage BP, prevent and treat infections, maintain nutrition, remember certain drugs can be toxic
TX hyperkalemia
- restrict sources of K
- use non-K sparing diuretic agents or use cation-ion exchange resins
- administer glucose and insulin or Na bicarb to drive K into the cells
- Administer Ca
- May need dialysis
CKD: Factors that contribute to progression of disease
- glomerular HTN
- Hyperfiltration
- tubulointerstitial inflammation
- Fibrosis
CKD manifestations
- affects every body system
- uremic syndrome
- Epistaxis
- sallow pigmentation
- Pruritic excoriations
- bruising
- amenorrhea
- myopathy
- peripheral neuropathy
- Edema
- frost, red eye
- anorexia, n/v
- htn, pericarditis, HF
Uremic syndrome
- proinflammatory state w/ accumulation of urea and other nitrogenous compounds
- Toxins
- Alterations in fluid and electrolyte and acid-base balance
CKD and endocrine and reproductive systems
- decrease in circulating sex steroids
- Decreased libido
- insulin resistance
- low thyroid hormone levels
CKD tx
- management of protein intake
- supplement vit D
- maintenenace of Na and fluid
- restriction of K
- maintenance of adequate caloric intake
- Mangement of dyslipidemias
- erythopoietin as needed
- ACE inhibitors or receptor blockers: controls systemic HTN and provide renoprotection, particularly in the presence of diabetes mellitus
- Dialysis, transplant