Misc Flashcards
Mutations occur in which genes for
AD-PKD
AR-PKD
AD-PKD: POLYcystin
AR-PKD: FIBROcystin
Other organs that can be involved:
AD-PKD
AR-PKD
AD-PKD
- cardiac, pancrease, CNS (wall defects)
AR-PKD
- lungs: pulmonary hypoplasia due to secondary oligohydramnios
- liver: fibrosis (not cystic). Can manifest as portal HTN, splenomegaly/esophageal varices
Histology of RCC
papillary finger-like projections
high N-C ratio
RCC which areas of the nephron do they affect?
- Clear cell
- Papillary
- Chromophobe
- Collecting Duct (Bellini)
- Clear cell: Prox tubule
- Papillary: Distal tubule
- Chromophobe: Collecting duct
- Collecting Duct (Bellini): Collecting duct
Classic triad of RCC
3 Ps
palpable mass
pain
pee blood
all 3 are observed in 10% of pts
most common neoplasm of renal pelvis/ureter/bladder
urothelial carcinoma
absence of crystals in UA tells you what?
blood is not related to urinary stones
but are not ruled out by absence of crystals
Exophytic vs endophytic lesions
exophytic (papillary): finger like extensions of epithelium surround fibrovascular core
- potential for invasive growth
endophytic (flat): dysplastic growth is invasive w.o exophytic component
Cyclophosphamide is a toxic risk factor for which cancer?
urothelial carcinoma (but dat smoking doh . . . 80% of cases)
Could you biopsy if you suspect wilms tumor for dx?
NO. run risk of rupture of lesion
Most common cause of abdominal mass in newborns?
Most common kidney tumor when detected at birth?
multicystic dysplastic kidney
congenital mesoblastic nephroma
Burning bush pattern
IgA nephropathy
burning bush indicates mesangeal changes, not linear GBM deposition
Describe which diseases correlate with location of deposits in either EM/LM
- Subepithelial
- Basement membrane
- Subendothelial
- Mesangial
- Subepithelial
- Membranous N
- PSGN - Basement membrane
- Goodpasteur - Subendothelial
- MPGN, SLE - Mesangial
- IgA N
What are strongly suggestive of nephrotic syndromes?
proteinuria
hypoalbuminemia
edema
Gold, penicillamine, NSAIDS, captopril are pathogenic for which disease?
membranous nephropathy (MN - usually in adults - minimal change is in kids)
Would pts with SLE have high or low C3?
Low C3 indicating that disease is active, being consumed
WHO classification of SLE
Class I: mesangial minimal/no prolif Class II: mesangial proliferative Class III: Focal proliferative glomerulonephritis Class IV: Diffuse proliferative Class V: Membranous
pts with IgA neph. should be treated with what?
ACEI
and maybe steroids
if pt has proliferative lupus what should you give them?
mofetil or cyclophos
Why does cerebral edema happen if you correct serum osmolality too quickly?
brain adapts to hyperosmolar serum by increasing its own osmolarity to prevent water movement out of cells
water gets pulled into the brain
In nephrotic syndrome, What would happen to TBW, ECF, CVP, PP, EABV
TBW and ECF increases due to decreased oncotic P in interstitium
CVP, PP, EABV decreases
Why is giving starving people food when they are K+ depleted dangerous?
If they were K+ deficient, they are probably also insulin suppressed.
Suddenly giving them food–> shoots up their insulin –> transcellular shift –> further K+ depletion –> death
Emergency therapy for hyperkalemia
CBIGK
calcium HCO3 Insulin Glucose Kayexalate
How do Beta blockers affect K+ levels?
they prevent activation of Na/K pump –> decrease K+ uptake by Na/K channels
–> increase K+ levels
How does digoxin affect K+ levels?
They increase K+ levels
They inhibit Na/K pump
What increases CO or TPR for indiv with essential HTN? why
initially CO increases
- Na excretion
Then there is an increase in autoregulation (increase TPR)
What increases CO or TPR for indiv with CRF? why
TPR
- increase in sympathetic and AII activity
What increases CO or TPR for indiv with hyperaldosteronism? why
initially CO increases
- due to increased salt and water retention
Aldosterone escape after sev. days –> chronic increase in TPR
What increases CO or TPR for indiv with pheochromocytoma ? why
increase in TPR from catecholamines
Why do vasodilators lead to resistance with chronic use?
may initially control BP but overtime . . .
lots of renal sodium reabsorption with volume expansion and increase in CO
Ways to treat high aldosterone (due to aldosteronoma)
remove
spirinolactone: aldo antagonist
How do kidneys in chronic renal failure handle Na and K balance?
Both of their fractional excretion INCREASES
- Na gets reabsorbed LESS
- K+ gets secreted MORE
How do kidneys in chronic renal failure handle phosphate and Ca2+ balance?
RF → ↓PO4 excretion → ↓ Ca2+ → ↑ PTH → ↑PO4 excretion → ↑ Ca2+
- calcium and pO4 are maintained at the expense of higher circulating PTH
What lab findings would diff between chronic and acute kidney failure?
chronic:
- small kidney
- K is low, bc kidney has responded
- high phosphate
- high PTH
How does ANP work?
Decreases ADH release
Decreases Renin and therefore aldosterone release
A 65 yo patient with a history of HTN and previous myocardial infarction has a blood pressure of 150/95. What stage of HTN is he in, how should you treat this patient, and what should the goal BP be?
Stage 1 HTN, Thiazide diuretic, 130/80
Difference between aldosterone producing adenoma and idiopathic adrenal hyperplasia
aldosterone producing adenoma: high aldosterone unilaterally
idiopathic adrenal hyperplasia: high aldosterone bilaterally (one side higher than other)
Most common cause of CKD
diabetic nephropathy
states of Kidney disease
Stage 1: /= 90 Stage 2: 60-89 Stage 3: 30-59 Stage 4: 15-29 Stage 5: 15
papillary carcinoma is often _____
papillary = multifocal
Multicystic Dysplastic Kidney Disease. results from what
abnormal induction of metanephric blastema by the ureteral bud
