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
What is the result of increased Na delivery to the collecting duct?
increased K excretion
26
What are the effects of aldosterone?
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
What are the two stimuli for ADH release?
hyperosmolarity volume loss
28
What does ADH act on in the collecting duct?
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
How is urea recycled by the nephron?
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
What are the important components of the JG apparatus?
* 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
Key functions of angiotensin II
stimulate sympathetic system renal Na/Cl reabsorption arteiolar vasoconstriction adrenal aldosterone secretion pituitary ADH secretion
32
What are the stimulators of renin release?
low perfusion pressure (sensed by JG cells) low NaCl delivery (sensed by macula densa) sympathetic activation
33
How does angiotensin II increase Na/water reabsorption?
capillary effect in the proximal tubule increased proximal tubule resorption via Na/H exchange stimulates aldosterone release
34
explain the capillary effect
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
What are the potassium sparing diuretics? MOA?
triamterene / amiloride inhibit ENaC
36
What are the effects of PTH in the kidney?
* increase Ca resorption (DCT) * decrease PO43- resorption (PCT) * increase vitamin D production
37
What cells product erythropoietin?
interstitial cells in the peritubular capillary
38
What are the characteristics of rapidly progressive glomerulonephritis?
_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
What auto-antibodies are seen in goodpasture syndrome?
anti-glomerular basement membrane syndrome alpha 3 chain of type IV collagen
40
What is a renal crescent?
\>2 layers of proliferating cells w/in Bowman's space initiation of the coagulation cascade promotes depostion of large quantities of fibrin
41
Cause of urgency incontinence & treatment
uninhibited bladder contraction B3 receptor agonist (mirabegron)- causes detrusor smooth muscle relaxation antimuscarinics (oxybutynin)- prevent detrusor contractions
42
What is patiromer therapy? AE?
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
SLE can cause what kind of kidney problems? appearnce w/ light microscopy & elecron microscopy?
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
SIADH can be casued by what medications?
carbamezapine (antiepileptic), chlorpropramide (antidiabetic) NSAIDS, SSRIs, MDMA
45
What are granular urinary casts composed of? Associated condtion?
(muddy brown) sloughed tubular epithelial cells w/ pigmented granules acute tubular necrosis
46
Identify the composition & associated condition for each of the following types of urinary casts: hyaline fatty waxy wbc rbc
* 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
What are the characteristics of nephrotic syndrome?
generalized edema, heavy proteinemia, hypoalbuminemia
48
What are the urinary buffers?
titratable acids ammonia
49
What are the possible inciting events for minimal change disease?
respiratory infections, immunizations, insect sting/bite
50
Infection by a urease producing bacteria can result in what type of kidney stone?
magnesium ammonium phosphate (struvite)
51
What is normal arterial HCO3- PCO2 pH
* HCO3- * 24 * PCO2 * 40 * pH * 7.4