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BOARD PREP > Renal > Flashcards

Renal Flashcards

1
Q

What is the most common renal malignancy of young children?

D/t what mutation?

A

Wilm’s Tumor

proliferation of metanephric blastema (WT1 gene)

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2
Q

A child born with one kidney may develop what condition later in life?

A

focal segmental glomerular sclerosis

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3
Q

What is the difference between primary & secondary vesicoureteral flow?

A

primary: abnormal closure ureteralvesical junctions (associated w/ duplex ureters)
secondary: high bladder pressure, seen w/ posterior urethral valves

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4
Q

Influence on GFR, FF, & RPF with dilation of the affarent & constriction of the efferent arteriole?

A
  • afferent (dilation)
    • GFR increases
    • FF & RPF same
  • efferent (constriction)
    • GFR increases
    • RPF decreases
    • FF increases
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5
Q

angiotensin preferentially constricts what arteriole?

A

efferent

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6
Q

Impact of ACE inhibitors on GFR, RPF, FF?

A
  • decrease GFR
  • increase RPF
  • decrease FF
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7
Q

Clincal features of postinfectious glomerulonephritis:

Electron microscopy

A

gross hematuria (tea-colored)

edema (periorbital)

hypertension

electron dense sub-epithelial deposits (humps)

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8
Q

What process occurs early in acute tubular necrosis?

This lead to..

A

loss of epithelial cell polarity d/t alterations in the actin skeleton, which is very susceptible to ischemia

leads to loss of cell-cell adhesions, redistribution of integrins & Na-K-ATPase from basolateral membrane to apical membrane

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9
Q

patient who has postprandial pain, lost 10lbs, & has multiple risk factors for atherosclerosis - likely diagnosis?

A

chronic mesenteric ischemia

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10
Q

Marked unilateral kidney atrophy is suggestive of what diagnosis?

A

renal artery stenosis

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11
Q

Symptoms of salicylate overdose:

A

tinnitus

hyperventilation

nausea & vomiting

hyperthermia that causes an increase in lactic acid, which causes primary metabolic acidosis w/ anion gap

altered mental status

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12
Q

Upon starting an ace inhibitor, you may see a rise in what substance?

A

creatinine - if the patient has bilateral atherosclerosis

this is because you will see a decrease in the GFR

but b/c the glomeruli & the renal tubules are otherwile unremarkable, urinalysis is usually unremarkable

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13
Q

What diuretic can help prevent calcium oxlate stone formation?

A

thiazide diuretic

b/c decrease urine Ca2+ excretion

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14
Q

What segment of the nephron absorbs 100% of glucose & amino acids?

A

proximal tubule

also, 2/3 of water, bicarb & NaCl are absorbed here

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15
Q

Explain the transport mechanisms that establish the ion concentration gradients in the proximala tubule

A

Na/K ATP pump on the basolateral membrane (interstitium/blood) maintains a low concentraion of Na in the cell & a high concentration of K outside the cell

d/t this concentration gradient, Na/glucose can diffuse along their concentration gradient into the cell from the lumen

d/t the high conc. of K inside the cell, it travels along its gradient into the blood/interstitium via a K/Cl co-cotransporter

d/t the K/Cl cotransporter, the concnetration of Cl inside the cell is low, which establishes the gradient for Cl to enter via a Cl/anion antiporter, which excretes anions (OH, formate, oxalate, sulfate) into the lumen

also, d/t the low conc. of Na+ in the blood, NaCl & water can be reabsorbed via the paracellular route

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16
Q

At what blood glucose level will it start to appear in the urine?

At what level are all the transporters saturated?

A

160mg/dl- appear in urine

350mg/dl- all transporters saturated

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17
Q

What is the clinical presentation & mutation seen in Hartnup disease?

A

skin rash resembling pellegra w/ amino acids in urine

no tryptophan transporter in the proximal tubule, so patients will have a tryptophan deficiency

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18
Q

What is Fanconi syndrome?

symptoms?

common causes?

A

loss of proximal tubule functions

Symptoms: polyuria, polydypsia (w/ normal blood glucose levels), non-anion gap acidosis (loss of bicarb), hyopkalemia (increased nephron flow), hypophosphatemia, amino acids in urine

inherited form associated w/ cystinosis (lysosomal storage disease that leads to accumulation of cystine)

lead poisoning, multile myeloma, drugs

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19
Q

General function of the thin descending loop of henle?

A

impermeable to NaCl, but absorbs water

so, concentrates urine

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20
Q

What solutes are responsible for maintaining the high osmolarity of the medulla?

A

Na, Cl, Urea

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21
Q

What is the permeability of the ascending loop of henle?

A

impermeable to water

permeable to NaCl

22
Q

Explain the transporters located in the thick ascending loop of henle that establish the necessary concentrations.

A

Na/K ATPase on the basolateral membrane that pumps Na into the blood and K into the cell

the low concentration of Na in the cell established by the transporter provides the gradient for a Na/K/2Cl transporter into the cell from the lumen

d/t the high concentration of K in the cell, some leaks out into the lumen creating a + charge in urine - this is important b/c it drives the reabsorption of other cations (Mg & Ca) via paracellular transportation & also into the blood

23
Q

Explain the transporters of the distal tubule

A

Na/K ATPase pump - pumps Na out of cell into blood & K into cell from blood

this gradient allows Na/Cl co-transporter on the apical side to absorb these ions

Cl- diffuses out of the cell & into the blood

Ca can also enter the cell from the lumen via a channel & then it can reabsorbed by the blood in exchange for Na

24
Q

What are the cells of the collecting ducts?

Describe their respective transporters

A
  • Principal cell
    • Na/K ATPase on basolateral membrane
    • ENaC
      • Na & water in; K out
      • regulated by aldosterone
  • Intercalated cell
    • ATP driven protone pump that pumps H+ into the lumen
25
Q

What is the result of increased Na delivery to the collecting duct?

A

increased K excretion

26
Q

What are the effects of aldosterone?

A

increases Na/K/ATPase proteins

increases Na (ENaC) channels of principal cells

promotes K secretion in principal cells

promotes H secretion in intercalated cells

increase sodium/water resorption (increases effective circulating volume), increases K & H excretion

27
Q

What are the two stimuli for ADH release?

A

hyperosmolarity

volume loss

28
Q

What does ADH act on in the collecting duct?

A

V2 receptors on principal cells in the collecting duct (G protein CAMP second messenger system)

endosome insertion into cell membrane - they contain aquaporin 2 water channels that increase the permability of cells to water

29
Q

How is urea recycled by the nephron?

A

medullary collecting duct is permeable to urea - urea enters medullary interstitium & can be reabsorbed via transporters in the thin descending limb

ADH increases urea reabsorption

30
Q

What are the important components of the JG apparatus?

A
  • JG cells - modified smooth muscles of afferent arteriole
    • secrete renin
  • macula densa
    • part of distal convoluted tubule
    • important for triggering the release of renin
31
Q

Key functions of angiotensin II

A

stimulate sympathetic system

renal Na/Cl reabsorption

arteiolar vasoconstriction

adrenal aldosterone secretion

pituitary ADH secretion

32
Q

What are the stimulators of renin release?

A

low perfusion pressure (sensed by JG cells)

low NaCl delivery (sensed by macula densa)

sympathetic activation

33
Q

How does angiotensin II increase Na/water reabsorption?

A

capillary effect in the proximal tubule

increased proximal tubule resorption via Na/H exchange

stimulates aldosterone release

34
Q

explain the capillary effect

A

d/t efferent arteriole constriction

decrease hydrostatic pressure from less blood flow

increased oncotic pressure from more H2O filtered

net effect: increased NaCl resorption

35
Q

What are the potassium sparing diuretics? MOA?

A

triamterene / amiloride

inhibit ENaC

36
Q

What are the effects of PTH in the kidney?

A
  • increase Ca resorption (DCT)
  • decrease PO43- resorption (PCT)
  • increase vitamin D production
37
Q

What cells product erythropoietin?

A

interstitial cells in the peritubular capillary

38
Q

What are the characteristics of rapidly progressive glomerulonephritis?

A

nephritic syndrome

hypertension, edema, acute renal failure, hematuria, proteinuria

on biopsy- light microscopy (crescent formation); immunofluorescence (linear deposits of IgG and C3 on GBM)

alveolar hemorrhage & increase in DLCO d/t hemogloblin in the alveoli

39
Q

What auto-antibodies are seen in goodpasture syndrome?

A

anti-glomerular basement membrane syndrome

alpha 3 chain of type IV collagen

40
Q

What is a renal crescent?

A

>2 layers of proliferating cells w/in Bowman’s space

initiation of the coagulation cascade promotes depostion of large quantities of fibrin

41
Q

Cause of urgency incontinence & treatment

A

uninhibited bladder contraction

B3 receptor agonist (mirabegron)- causes detrusor smooth muscle relaxation

antimuscarinics (oxybutynin)- prevent detrusor contractions

42
Q

What is patiromer therapy?

AE?

A

non-absorbable cation exchange resin that binds colonic potassium in exchange for calcium, trapping potassium w/in the resin where it is then excreted in the feces

AE: GI disturbance, hypokalemia, hypercalcemia, hypomagnesemia

43
Q

SLE can cause what kind of kidney problems?

appearnce w/ light microscopy & elecron microscopy?

A

membranous nephropathy

caused by immune complex deposition in subepithelial portion of glomerular capillary wall

light microscopy: diffuse thickening of glomerular basement membrane w/o increase in cellularity

electron microscopy: irregular, electron dense immune deposits located btw GBM & epithelial cells (resembles spikes & domes w/ silver stain)

44
Q

SIADH can be casued by what medications?

A

carbamezapine (antiepileptic), chlorpropramide (antidiabetic) NSAIDS, SSRIs, MDMA

45
Q

What are granular urinary casts composed of?

Associated condtion?

A

(muddy brown)

sloughed tubular epithelial cells w/ pigmented granules

acute tubular necrosis

46
Q

Identify the composition & associated condition for each of the following types of urinary casts:

hyaline

fatty

waxy

wbc

rbc

A
  • hyaline
    • Tamm-Horsfall protein
    • nonspecific, concentrated urine
  • fatty
    • lipid droplets
    • nephrotic syndrome
  • waxy
    • degenerated hyaline casts
    • chronic kidney disease
  • wbc
    • white blood cells
    • pyelonephritis, interstitial nephritis
  • rbc
    • red blood cells
    • glomerulonephritis
47
Q

What are the characteristics of nephrotic syndrome?

A

generalized edema, heavy proteinemia, hypoalbuminemia

48
Q

What are the urinary buffers?

A

titratable acids

ammonia

49
Q

What are the possible inciting events for minimal change disease?

A

respiratory infections, immunizations, insect sting/bite

50
Q

Infection by a urease producing bacteria can result in what type of kidney stone?

A

magnesium ammonium phosphate (struvite)

51
Q

What is normal arterial

HCO3-

PCO2

pH

A
  • HCO3-
    • 24
  • PCO2
    • 40
  • pH
    • 7.4

BOARD PREP (17 decks)

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