renal and urologic systems Flashcards
S&S of polycystic kidney disease
cysts found in liver and spleen, gross hematuria, pain, infected cysts (ascending UTIs), hypertension, aneurysms (late)
diagnosis and treatment of polycystic kidney disease
total kidney volume (TKV) to measure cyst expansion, manage hypertension and make lifestyle modifications (low sodium, no NSAIDS, hydrate, no smoking)
S&S of hydronephrosis
UTI (microorganism overgrowth), pain, complete bilateral obstruction, partial obstruction (polyuria, nocturia), hypertension
diagnosis and treatment of hydronephrosis
early diagnosis is key, use ultrasound, treatment is cause dependent
S&S of renal calculi
pain; renal colic (acute/intermittent, flank pain upper right quadrant), noncolic (dull, deep, flank, back, mild-severe, exaggerated by drinking large amounts of fluids). pain and vomiting
diagnosis and treatment of renal calculi
based on symptoms, run diagnostic tests such as urinalysis and nonspiral contrast CT, strain urine and test stone
S&S of UTIs
frequent urinations, lower abdominal/back discomfort, burning and pain (dysuria), cloudy/foul smelling urine.
SPECIAL POPULATIONS: symptoms absent to typical UTI, change in mental status, anorexia, fatigue, weakness, classic signs (fever, chills, flank pain) may be absent!!
what renal and urologic conditions are caused by disease or injury?
describe manifestations of acute kidney injury
sharp decrease in urine output (early sign), elevation BUN related to serum creatinine levels
prerenal AKI
hemorrhage reduces golmerular filtration rate which leads to tissue ischemia, impaired perfusion due to heart failure/cardiogenic shock, decreased vascular filling due to increased vascular capacity, vasoactive mediators/drugs/diagnostic agents stimulate intrarenal vasoconstriction
intrarenal AKI
ischemia from prerenal AKI leads to intrarenal vasoconstriction, decreased hydrostatic pressure in glomeruli, toxic/ischemic insult to tubular structures of nephron, acute pyelonephritis, acute glomerulonephritis
postrenal AKI
obstruction of urine outflow from kidneys, retrograde pressure in tubules/nephrons leads to damage, prostatic hyperplasia
both ureters must be obstructed to induce renal failure
postrenal obstruction
ureter; stones and strictures
bladder; neurogenic bladder, cancer
urethra; prostatic hyperplasia
describe the azotemia and fluid/acid base balance manifestations of chronic kidney disease
-BUN elevates with progression (normal is 20mg/dl)
-uremia leads to weakness/fatigue/nausea which leads to vomiting/lethargy/confusion, leading to coma
and death without dialysis/transplant
-dehydration or fluid overload leads to altered Na+/H20 balance and progressive inability to regulate Na+ excretion
-salt wasting
- hyperkalemia through increased excretion in remaining nephrons and GI
-impaired hydrogen ion secretion
-impaired Na+ and HCO3- reabsorption
-loss of ammonia production results in metabolic acidosis
describe the skeletal manifestations of CKD
PO4- levels rise with impaired kidney excretion
PO4- rise and Ca++
Ca++ decreases, stimulating PTH and increasing bone resorption, compromising the bone structure over time
reduced calcitriol and active viamin D elevates PTH, less vitamin D means less Ca++ absorbed from GI
secondary hyperparathryroidism develops
describe the blood and cardiac manifestations of CKD
-anemia
-epistaxis, menorrhagia, GI bleeding, subcutaneous bruising, platelet function impaired
-hypertension
-left ventricular hypertrophy
-congestive heart failure and pulmonary edema
-pericarditis (ckd stage 5)
describe the GI and neuromuscular manifestations of CKD
- anorexia
- nausea, vomiting, early morning nausea
- ulcerations/bleeding GI mucosa
- PNS function impaired (peripheral neuropathy, sensory and motor function is impaired, restless leg syndrome at rest)
- CNS system function impaired (uremic encephalopathy, reduced alert/aware, loss of recent memory, can’t ID people/objects, reduced fine motor movements and asterixis)
describe the skin and immune manifestations of CKD
- high levels or urea/metabolic wastes
- decreased granulocyte count
- impaired humoral/cell mediated immunity
- active inflammatory and delayed hypersensitivity responses impacted
- may not have fever
- pallor skin
- sallow, yellow brown skin
- dry skin
- subcutaneous bruising
- pruritis
describe CKD treatment
- treat UTIs quickly
- avoid nephrotoxic medications
- treat OG cause
- manage BP
- no smoking
- manage blood sugar
- dialysis/transplantation if appropriate
- diet management (restrict protein, fluid and electrolyte balance, restrict K+ when needed, limit dietary phosphorus)
describe the pathophysiological mechanisms of chronic kidney disease
GFR < 60mL/min/1.73m squared >or= 3 months
permanent loss of nephrons leads to the progressive decreased ability to filter, concentrate urine, and fulfill endocrine function
causes include diabetes, hypertension, glomerulonephritis, SLE, polycystic kidney disease
nephron changes to compensate, leading to structural and functional hypertrophy to meet the need
stage 1: 90% function
stage 2: 60-89% function
stage 3: 30-59% function
stage 4: 15-29% function
stage 5: <15% function, kidneys can no longer keep up with removing waste products and extra water
