What is obstructive uropathy, and what 5 factors determine its severity?
Blockage of urine flow in the urinary tract. Severity is based on: location, completeness, involvement of one or both upper urinary tracts, duration, and nature/cause of the obstruction.
What the the 4 complications of upper urinary tract obstruction? Define each.
Hydoureter (dilated ureters), Hydronephrosis (dilated renal pelvis), Ureterohydronephrosis (both dilated), Tubulointerstitial fibrosis (excess extracellular matrix deposition that leads to neprhon death)
What is postobstructive diuresis and why is it dangerous?
Diuresis caused by relief of a urinary obstruction. Dangerous because it can cause fluid and elctrolyte imbalances.
What is the most prevalent risk for nephrolithiasis?
Inadequate fluid intake
What are the 4 types of kidney stones and their pecentages?
Calcium oxalate/phosphate (70–80%)
Uric acid (5–10%)
Struvite — magnesium, ammonium
phosphate (1–5%), Cystine/xanthine (genetic amino acid metabolism disorder, low urine pH).
What are staghorn calculi and how do they differ from non-staghorn calculi?
Staghorn calculi are large stones and non-staghorn vary in size and can be located in the calyces, renal pelvis or ureter
What are the 4 treatment approaches for nephrolithiasis?
Pain management, adjusting urine pH, removal of stones, and reduce formation of more stones
What is the difference between OAB and UAB?
OAB is detrusor overactivity with s/s of urgency, frequency, nocturia, urge incontinence.
UAB is reduced detrusor strength/duration that leads to weak stream, hesitancy, incomplete emptying.
What neurologic conditions cause UAB?
Spinal cord injury, stroke, multiple sclerosis, Parkinson disease, diabetic neuropathy, and aging.
Compare upper vs lower motor neuron effects on the bladder.
Upper motor neuron- detrusor hyperreflexia (overactive/spastic bladder); dyssynergia= bladder and sphincter contract simultaneously
What is a UTI and how do bacteria typically reach the urinary tract?
Inflammation of the urinary epithelium caused by
bacteria from the gut via retrograde movement through the urethra into the bladder, ureter, and kidney.
What two mechanisms make uropathogens virulent?
Ability to adhere to uroepithelium (via pili/fimbrae) and ability to resist host defenses (via biofilm formation).
What distinguishes painful bladder syndrome/interstitial cystitis from regular cystitis?
Cystitis symptoms lasting more than 6 weeks with negative urine cultures and no other known cause. Thought to be autoimmune in origin.
What the classic clinical manifestations of acute pyelonephritis?
Flank/groin pain, fever, chills, costovertebral tenderness, and UTI symptoms. Key lab finding: white blood cell casts.
What is the pathophysiology of acute glomerulonephritis?
Antibodies against an organism cross-reacts with glomerular endothelial cells that lead to complement activation that leads to immune cell recruitment that leads to decreased GFR, glomerular scarring, and thickening of the basement membrane with increased protein/RBC permeability.
Name the 5 types of glomerulonephritis and their key features.
IgA, membranous nephropathy, crescentic GN, Mesangial proliferative GNk Membranoproliferative GN
What the classic manifestations of acute glomerulonephritis?
Hematuria with RBC casts, smoky/brown urine, proteinuria > 3-5g/day, low serum albumin, edema, and oliguria (<30 mL/hour) in severe cases.
What causes diabetic nephropathy and lupus nephritis?
Diabetic nephropathy: podocyte injury + progressive thickening/fibrosis of glomerular basement membrane + mesangial expansion. Lupus nephritis: autoantibodies against double-stranded DNA- immune complex deposition in glomeruli.
Define and distinguish: renal insufficiency, renal failure, and end-stage renal failure, azotemiz, and uremia.
Renal insufficiency = 25 % function remaining. Renal failure= significant loss. End-stage=<10 % function. Azotemia= elevated BUN and creatinine. Uremia= syndrome of renal failure with azotemia + fatigue, nausea, pruritus, neurologic changes.
What are the 3 categories of AKI causes? Give the most common cause of each.
Prerenal= renal hypoperfusion (most common overall). Intrarenal= acute tubular necrosis (ATN) from ischemia (most common intrarenal). Postrenal= urinary tract obstruction (rare).
What is the intact nephron hypothesis in CKD?
As nephrons are lost, surviving nephrons compensate by sustaining normal kidney function- but over time this compensations accelerates disease progression through hyperfiltration and hypertension.
Why is glucose and insulin given in AKI with hyperkalemia?
To drive K+ into the cells, temporarily lowering serum K+ levels. Insulin facilitates K+ uptake into cells; glucose prevents hypoglycemia.
What two factors most drive CKD progression?
Proteinuria (promotes inflammation and tubulointerstitial fibrosis) and Angiotensin II (causes glomerular hypertension and tubulointertstitial fibrosis/scarring).
What happens to calcium, phosphate, and bone in CKD?
