Nephrology Flashcards

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1
Q

At what week does the PRONEPHROS degenerate?

A

4 weeks

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2
Q

What structure is the “permanent” kidney?

A

Metanephros

appears at week 5

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3
Q

What structures are derived from the ureteric bud?

A

Ureters
Pelvises
Calyces
Collecting ducts

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4
Q

The metanephric mesenchyme/ blastema gives rise to

A

glomerulus –> DCT

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5
Q

Obstruction of this structure is the most common cause of prenatal hydronephrosis

A

Ureteropelvic junction

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6
Q

Compression of the developing fetus caused by oligohydramnios –> limb deformities

A

Potter sequence (syndrome)

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7
Q

What conditions are associated with Potter sequence?

A

POTTER:

Pulmonary hypoplasia
Oligohydramnios
Twisted face
Twisted skin
Extremity defects
Renal failure
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8
Q

A condition in which the inferior poles of the kidneys fuse and are trapped under the INFERIOR MESENTERIC ARTERY. Associated with hydronephrosis.

A

Horshoe kidney

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9
Q

This is the most common cause of bladder outlet obstruction. Presents with bilateral hydronephrosis and oligohydramnios

A

posterior urethral membrane

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10
Q

Why is the left kidney used for living donor transplant?

A

because it has a longer renal vein.

The left renal vein receives 2 additional veins: left suprarenal an left gonadal

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11
Q

3 most common points of ureteral obstruction

A

ureteropelvic junction
pelvic inlet
ureterovesical junction

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12
Q

What is the effect of prostaglandin in the kidneys

A

preferentially dilates AFFERENT arteriole
(increase RPF and GFR, no change in FF)

Prostaglandin is inhibited by by NSAIDS –> constriction

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13
Q

What is the effect of ANGIOTENSIN II in the kidneys

A

Preferentially constricts EFFERENT arteriole
(decreased RPF, increased GFR and FF)

inhibited by ACE inhibs

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14
Q

Site where all glucose and amino acids, most HCO3, Na, Cl, PO4, K, H2O, and uric acid are reabsorbed. generation and secretion of NH3

A

PCT

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15
Q

Effect of PTH in PCT

A

increase PO4 EXCRETION

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16
Q

Effect of angiotensin II in PCT

A

increase Na, H2O, and HCO3 reabsorption

17
Q

This is a reabsorption defect in PCT causing proximal RTA –> hypophosphatemia, osteopenia (excretes everything PCT reabsorbs)

A

Fanconi syndrome

18
Q

This is where passive reabsorption of H2O happens. Concentrating segment –> hypertonic urine.

A

Thin descending loop of Henle

19
Q

Site of Na, K, Cl reabsorption and paracellular reabsorption of Mg and Ca

A

Thick ascending loop of Henle

20
Q

What condition affects the Na/K/2Cl cotransport in the thick ascending loop of Henle causing metabolic acidosis, hypoK, hyperCa

A

Barter syndrome

21
Q

Diluting segment of the nephron. Reabsorption of Na, Cl, Ca

A

DCT

22
Q

What is the effect of PTH in the DCT?

A

increase Na/Ca exchange –> increased Ca reabsorption

23
Q

This part of the nephron is regulated by aldosterone causing reabsorption of Na in exchange for K and H2O

A

Collecting tubules

24
Q

This is a reabsorption defect of NaCl in DCT causing metabolic alkalosis, hypoMg, hypoK, hypoCa

A

Gitelman syndrome

25
Q

Gain of function mutation causing increase Na reabsorption in collecting tubules

A

Liddle syndrome

Met alk, hypoK, HPN

26
Q

Hereditary 11B-HSD deficiency –> increase in cortisol –> increase mineralocorticoid receptor activity

A

Syndrome of apparent mineralocorticoid excess

27
Q

What activates RAAS?

A

decrease BP and NaCl delivery (macula densa)

increase sympathetic tone (B1-receptors)