USMLE Step 2CK Genitourinary
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Kidney Bx w/ dense deposits within glomerular basement membrane
Immunofluorescence positive for C3
Negative for Immunoglobulins
1) What is it?
3) Clinical presentation?
1) Membranoproliferative Glomerulonephritis, Type 2
2) IgG ab's against C3 convertase (alt. pathway) --> persistent activation of complement --> kidney damage
3) Pitting edema, dark urine, fatigue, creatinine and vitals normal.
UA: 4+ protein (nephrotic range), microhematuria
Pathophysiology of kidney findings in Goodpastures
List the [circulating] immune complex-mediated glomerulopathies
2) Post-streptococcal glomerulonephritis
3) IgA nephropathy (?)
Pathophysiological mechanism of Idiopathic Crescentic Glomerulonephritis
Name two nephropathies that result from Non-immunologic kidney damage.
1) Diabetic Nephropathy
2) Hypertensive Nephropathy
Site of lesion in initial (beginning-stream) hematuria with or without clots
Site of lesion in terminal (end-stream) hematuria, with or without clots
Bladder or prostatic damage.
Next step is cystoscopy to eval for bladder cancer.
Site of lesion in Total hematuria (throughout entire void)
Kidney or Ureters
Hematuria with clots rules out which cause?
Renal. Clots come from ureters or below
Presenting symptoms of Polycystic Kidney disease?
- 1) Abdominal or flank pain
- 2) microscopic or gross hematuria
(Must distinguish from stones).
PKD is most common heritable cause of renal disease in adults
GU symptoms of UTI?
Hematuria is possible (micro or gross)
muddy brown casts
(either toxic, or because of hypovolemic shock, e.g. blood loss from trauma w/ hypotension)
- a) Interstitial nephritis
- b) pyelonephritis
(WBC casts definitively mean that the WBCs came from the kidney)
made of protein, pass unchanged along the urinary tract.
- Asymptomatic individuals
- Patients w/ pre-renal azotemia
Broad and Waxy casts
Chronic Renal Failure
(Broad casts come from dilated tubules in hypertrophied nephrons resulting from reduced viable renal mass. Waxy casts are shiny and translucent)
Lab features of ATN
BUN:Cr < 20:1
Urine osmolality 300-500, never less than 300.
Urine Na+ > 20 mEq/L
FENa > 2%
1st Generation Antihistamines and their side-effects, both generally and specifically re: GU
- 1st Gen H1-antihistamines are Anticholinergic: block ACh's effect on Parasympathetic Muscarinic receptors.
- -->Dryness of the eyes/ mucosae/ respiratory passages, urinary retention and dysuria, due to preventing detrusor contraction (controlled by parasympathetic pelvic splanchnic nn.)
Occurs w/ neurological disease. It's when detrusor contracts (parasympathetic), but the urethral sphincter contracts instead of relaxing. What a dick.
Why are the GU side effects of anticholinergic drugs especially troublesome in older males?
They probably already have some degree of BPH-related urinary obstruction, which, when combined with detrusor paralysis makes it really hard to pee.
Cause of isolated mild-to-moderate proteinuria in a middle aged adult with renal insufficiency and longstanding diabetes?
Diabetic glomerulosclerosis, secondary to diabetic microangiopathy.
(which is the result of endothelium being constantly glycosylated in the setting of hyperglycemia, as Goljan would point out.)
Time-line of progressive renal disease in diabetics, (and how many get it?)
50% of Type 1 and 2 diabetics eventually develope moderate-to-severe proteinuria.
- Timeline is:
- Microalbuminuria (detectable within a few years of DM onset)
- --> Proteinuria on Dipstick (12 to 22 years after onset.)
- --> CRF and ESRD (4-5 years after appearance of proteinuria)
Normal postvoid residual volume
50cc or less
Greater than 50cc is too much
Contrast-induced nephropathy: Definition, mechanism, and risk factors
Def: a spike in creatinine within 24 hours of contrast administration, returning to baseline w/in 5-7 days.
Path: renal vasoconstriction and direct tubular injury
Risk factors: Diabetes, elevated baseline creatinine
Prophylaxis for contrast-induced nephropathy
Adequate pre-scan IV hydration w/ normal saline or isotonic bicarb. Begin prior to scan and continue for several hours after.
Acetylcysteine as an adjuvant.
Effect of diuretics on likelyhood of getting contrast-induced nephropathy?
Doesn't help, and Lasix can make it worse!
NSAIDs and contrast-induced nephropathy.
Discontinue NSAIDs prior to contrast administration, because they too cause renal vasoconstriction (by inhibiting prostaglandin production). You can continue Clopidogrel.
Varicocele that fails to empty when patient is recumbent.
What do you do?
Raises suspicion for Renal Cell Carcinoma.
(obstruction of gonadal vein where it enters the renal vein).
CT Abdomen makes the diagnosis.
Presenting symptoms of Renal Cell Carcinoma
1) Classic triad & frequency
2) Most common symptom
3) 2nd MC constellation of symptoms
4) Two unique symptoms
- Classic triad in only 10% of pts, indicates advanced/metastatic dz.
- 1) Flank pain
- 2) Hematuria
- 3) Palpable abdominal/renal mass
Hematuria in 40% (MC)
Varicocele (predom. L-sided) in <10%
Constitutional sx in 20% (fever, night sweats, anorexia, weight loss, fatigue)
Polycythemia & thrombocytosis from increased erythropoietin (due to incr kidney mass)
Plain film doesn't show kidney stones. Possibilities?
- 1) Uric acid stones (radiolucent)
- 2) Small stones (<3mm)
- 3) non-stone cause (obstruction by clot/tumor)
US or CT to diagnose.
Flank pain, negative plain film for stones, no infection, and low urine pH.
Uric acid stones (radiolucent to plain film but visible to CT and US)
- Account for 10-15% of stones.
- Tx is hydration, then:
- alkalinization of urine to >pH 6.5 with oral KCitrate or KBicarb (they like low pH, but alkaline urine dissolves them)
Then low-purine diet w/ or w/o allopurinol (if hyperuricosuric)
What type of stones are treated w/ HCTZ? Why?
HCTZ decreases excretion of Calcium, so use it for recurrent hypercalciuric stones. (CaOx or CaPhos)
Role of Furosemide (Lasix) in Tx of stones?
None!!! Lasix can increase calcium excretion, making Ca stones more likely to form.
Role of Calcium-restricted diet in prophylaxis against stones?
None! Calcium restriction would just cause increased absorption of Oxalate, leading to relative hyperoxaluria and more stones.
Patient w/ creatinine > 1.5 and/or DM nevertheless needs a contrast CT. What do you use? How do you prophylax?
Use a Non-ionic contrast agent. Give plenty of fluids (NS or isotonic bicarb) and acetylcysteine as prophylaxis. Stop NSAIDs.
Patient starts IV acyclovir, three days later creatinine has spiked to 3.4 mg/dL. What happened? How to prevent?
Acyclovir-nephrotoxicity occurs in 5-10% of high-dose IV patients.
- It is a crystalline nephropathy. Acyclovir is excreted via glomerular filtration and tubular excretion. If the urine in the collecting ducts becomes super-saturated with Acyclovir, it crystallizes and causes tubular damage.
- Prevent it by administering adequate hydration and by slowing the IV rate if it starts to happen. It is usually transient even if it does occur.
Rx prophylaxis of tumor-lysis-associated urate crystal nephropathy:
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