Misc Flashcards

1
Q

Mutations occur in which genes for
AD-PKD
AR-PKD

A

AD-PKD: POLYcystin

AR-PKD: FIBROcystin

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2
Q

Other organs that can be involved:
AD-PKD
AR-PKD

A

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
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3
Q

Histology of RCC

A

papillary finger-like projections

high N-C ratio

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4
Q

RCC which areas of the nephron do they affect?

  • Clear cell
  • Papillary
  • Chromophobe
  • Collecting Duct (Bellini)
A
  • Clear cell: Prox tubule
  • Papillary: Distal tubule
  • Chromophobe: Collecting duct
  • Collecting Duct (Bellini): Collecting duct
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5
Q

Classic triad of RCC

A

3 Ps
palpable mass
pain
pee blood

all 3 are observed in 10% of pts

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6
Q

most common neoplasm of renal pelvis/ureter/bladder

A

urothelial carcinoma

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7
Q

absence of crystals in UA tells you what?

A

blood is not related to urinary stones

but are not ruled out by absence of crystals

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8
Q

Exophytic vs endophytic lesions

A

exophytic (papillary): finger like extensions of epithelium surround fibrovascular core
- potential for invasive growth

endophytic (flat): dysplastic growth is invasive w.o exophytic component

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9
Q

Cyclophosphamide is a toxic risk factor for which cancer?

A
urothelial carcinoma
(but dat smoking doh . . . 80% of cases)
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10
Q

Could you biopsy if you suspect wilms tumor for dx?

A

NO. run risk of rupture of lesion

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11
Q

Most common cause of abdominal mass in newborns?

Most common kidney tumor when detected at birth?

A

multicystic dysplastic kidney

congenital mesoblastic nephroma

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12
Q

Burning bush pattern

A

IgA nephropathy

burning bush indicates mesangeal changes, not linear GBM deposition

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13
Q

Describe which diseases correlate with location of deposits in either EM/LM

  1. Subepithelial
  2. Basement membrane
  3. Subendothelial
  4. Mesangial
A
  1. Subepithelial
    - Membranous N
    - PSGN
  2. Basement membrane
    - Goodpasteur
  3. Subendothelial
    - MPGN, SLE
  4. Mesangial
    - IgA N
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14
Q

What are strongly suggestive of nephrotic syndromes?

A

proteinuria
hypoalbuminemia
edema

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15
Q

Gold, penicillamine, NSAIDS, captopril are pathogenic for which disease?

A
membranous nephropathy
(MN - usually in adults - minimal change is in kids)
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16
Q

Would pts with SLE have high or low C3?

A

Low C3 indicating that disease is active, being consumed

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17
Q

WHO classification of SLE

A
Class I: mesangial minimal/no prolif
Class II: mesangial proliferative
Class III: Focal proliferative  glomerulonephritis
Class IV: Diffuse proliferative
Class V: Membranous
18
Q

pts with IgA neph. should be treated with what?

A

ACEI

and maybe steroids

19
Q

if pt has proliferative lupus what should you give them?

A

mofetil or cyclophos

20
Q

Why does cerebral edema happen if you correct serum osmolality too quickly?

A

brain adapts to hyperosmolar serum by increasing its own osmolarity to prevent water movement out of cells

water gets pulled into the brain

21
Q

In nephrotic syndrome, What would happen to TBW, ECF, CVP, PP, EABV

A

TBW and ECF increases due to decreased oncotic P in interstitium

CVP, PP, EABV decreases

22
Q

Why is giving starving people food when they are K+ depleted dangerous?

A

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

23
Q

Emergency therapy for hyperkalemia

A

CBIGK

calcium
HCO3
Insulin
Glucose
Kayexalate
24
Q

How do Beta blockers affect K+ levels?

A

they prevent activation of Na/K pump –> decrease K+ uptake by Na/K channels
–> increase K+ levels

25
Q

How does digoxin affect K+ levels?

A

They increase K+ levels

They inhibit Na/K pump

26
Q

What increases CO or TPR for indiv with essential HTN? why

A

initially CO increases
- Na excretion

Then there is an increase in autoregulation (increase TPR)

27
Q

What increases CO or TPR for indiv with CRF? why

A

TPR

- increase in sympathetic and AII activity

28
Q

What increases CO or TPR for indiv with hyperaldosteronism? why

A

initially CO increases
- due to increased salt and water retention

Aldosterone escape after sev. days –> chronic increase in TPR

29
Q

What increases CO or TPR for indiv with pheochromocytoma ? why

A

increase in TPR from catecholamines

30
Q

Why do vasodilators lead to resistance with chronic use?

A

may initially control BP but overtime . . .

lots of renal sodium reabsorption with volume expansion and increase in CO

31
Q

Ways to treat high aldosterone (due to aldosteronoma)

A

remove

spirinolactone: aldo antagonist

32
Q

How do kidneys in chronic renal failure handle Na and K balance?

A

Both of their fractional excretion INCREASES

  • Na gets reabsorbed LESS
  • K+ gets secreted MORE
33
Q

How do kidneys in chronic renal failure handle phosphate and Ca2+ balance?

A

RF → ↓PO4 excretion → ↓ Ca2+ → ↑ PTH → ↑PO4 excretion → ↑ Ca2+

  • calcium and pO4 are maintained at the expense of higher circulating PTH
34
Q

What lab findings would diff between chronic and acute kidney failure?

A

chronic:
- small kidney
- K is low, bc kidney has responded
- high phosphate
- high PTH

35
Q

How does ANP work?

A

Decreases ADH release

Decreases Renin and therefore aldosterone release

36
Q

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?

A

Stage 1 HTN, Thiazide diuretic, 130/80

37
Q

Difference between aldosterone producing adenoma and idiopathic adrenal hyperplasia

A

aldosterone producing adenoma: high aldosterone unilaterally

idiopathic adrenal hyperplasia: high aldosterone bilaterally (one side higher than other)

38
Q

Most common cause of CKD

A

diabetic nephropathy

39
Q

states of Kidney disease

A
Stage 1: /= 90 
Stage 2: 60-89 
Stage 3: 30-59 
Stage 4: 15-29 
Stage 5: 15
40
Q

papillary carcinoma is often _____

A

papillary = multifocal

41
Q

Multicystic Dysplastic Kidney Disease. results from what

A

abnormal induction of metanephric blastema by the ureteral bud