Nephrology Flashcards
Most common form of Nephrotic Syndrome - key features + x2 complications
Minimal change disease = <6 years old at presentation, no HTN, normal renal function + complement, no hematuria
- Peritonitis (S. pneumo, E.coli), hyper-coagulable
x5 criteria for SIADH
- HypoNa with reduced serum osmolality
- Urine osmolality elevated (compared to serum)
- Urinary Na concentration excessive for extent of hypoNa
- Absence of volume depletion
- Normal renal, adrenal, and thyroid function
Causes and investigations for urolithiasis
Causes: HyperCa, hypocitraturia, hyperoxaluria, infection, polycystic kidneys, RTA, endo (hypothyroidism, hyperparathyroid, excess adrenocorticoid), drugs (loop diuretics, excess vitamin D), bone metabolism (rickets, immobilization)
Imaging: US/CT/XR, lytes, renal function, UA +/- UCx, 24 urine collection, stone analysis, TSH/PTH/vit D
x3 types of RTA and characteristics
Type I: Distal. Inability to secrete H+. HypoK, urine pH >5.5.
Type II: Proximal. Decreased ability to reabsorp bicarb. HypoK, urine pH <5.5.
Type IV: Aldosterone deficiency. HyperK, urine pH <5.5.
When to consider RTA (clinical signs/symptoms/acid-base result)?
- HyperCl metabolic non-AG acidosis
- Growth failure
- Emesis, dehydration
- Polyuria, polydipsia
- think DKA but not
Differences between primary and secondary adrenal insufficiency - clinical presentation, hormones
Primary: Abnormality of adrenal gland = dec cortisol, inc ACTH (hyperpig), +/- mineralocorticoid deficiency (hypoNa, hyperK).
Secondary: Hypothalamic + pituitary dysfunction = dec cortisol, N/low ACTH (no hyperpig), normal mineralocorticoid.
SIADH vs cerebral salt wasting
SIADH = Intravascular euvolemic or overload. Fluid restriction leads to increase in serum Na. CSW = Intravascular volume depletion. Fluid restriction will NOT increase Na and will further impair intravascular volume.
DI - clinical presentation (no Ix)
Dehydration, polyuria, nocturia, polydipsia
Glomerular hematuria - history, exam, and UA
- Hx: tea/coca-cola urine, flank pain, systemic c/o (edema, fatigue, pharyngitis, fever, rash, arthralgia), recent infection, fmhx (hearing loss, renal failure)
- PEx: HTN, edema, systemic features, sx of infection
- UA: brown/tea/cola urine, proteinuria, dysmorphic RBCs, red cell casts
Causes (x2) of heme positive UA but RBC absent
Free hemoglobin - hemolysis
Myoglobin - rhabdomyolysis
Most common cause of hereditary type 2 RTA?
Cystinosis
Most common type of stone
Calcium carbonate
Eagleton Barrett Syndrome - classic triad?
Minimal abdo muscles, undescended testes, CAKUT
IgA nephropathy - natural history of initial presentation
-Synpharyngitic hematuria –> following URTI by 1-2 days
Glomerulonephritis with low C3 (x5)
- Post-infectious GN
- Membranoproliferative GN
- Lupus nephritis
- C3 glomerulopathy
- aHUS
Nephrotic syndrome - classic 4 features
- Proteinuria
- Hypoalbuminemia
- Edema
- Hypercholesterolemia
Pollakuria - what is this, typical age range, most common cause?
=extraordinary daytime urinary frequency (up to 50x/day)
- in 5-6 years olds typically
- context of recent death or life-threatening event
- benign or self-limited (lasting ~6 months)
Bladder capacity - equation and amount for >12 yo
= 30 + (age x 30)
-390mL
Nocturnal enuresis - prevalence
- 5 yo = 20%
- 7 yo = 10%
- Resolves at rate of 15% per year
- 15 yo = 1-2 %
- M>F
Nocturnal enuresis - causes/theories
- Delayed maturation
- Decreased secretion of ADH at night
- Genetic influence
- Small bladder capacity
- Difficulty waking from deep sleep
Nocturnal enuresis - treatment options
- Dry bed training + lifestyle modifications
- Enuresis alarms
- Desmopressin
Causes of hyperK
- Increased intake: IV fluids
- Abnormal excretion: pseudohypoaldosteronism (CAH, adrenal insufficiency, drugs), renal impairment, decreased circulating volume, impaired tubular excretion
- Intracellular shifts: metabolic acidosis, B blockers, cellular damage (hemolysis, rhabdo, TLS)
- PseudohyperK: hemolyzed sample, leukocytosis/thrombocytosis
Treatment options for hyperK
- Stabilize cardiac membrane: Ca gluconate
- Intracellular shifts: sodium bicarb, ventolin, insulin
- Increased removal: kayexylate, diuretics
Causes of hypoNa
- Hypovolemic: low urine Na (GI losses, pancreatitis, skin losses, lung losses), high urine Na (RTA, diuretics, adrenal insufficiency)
- Euvolemic: SIADH, DI, adrenal insufficiency
- Hypervolemic: low urine Na (cirrhosis, CHF, renal failure), high urine Na (renal failure)