Firecracker II

Question 1

4 K+ sparing diuretics

Answer 1

Spironolactone
Eplerenone
Amiloride
Triamterene

Question 2

PTH stimulates the production of [WHAT?] in the kidney which catalyzes the conversion of 25-OH-vitamin D → active 1,25-(OH)2-vitamin D.

Answer 2

1-α-hydroxylase

Question 3

Remember that hypovolemia and hypokalemia can exacerbate metabolic alkalosis. How?

Answer 3

Hypovolemia → contraction alkalosis

Hypokalemia → transcellular shift of K and H → H+ goes from ECF to ICF to maintain electrical neutrality → alkalosis.

Question 4

Which side effects of furosemide can exacerbate metabolic alkalosis?

Answer 4

Hypovolemia and hypokalemia

Question 5

Glomerulonephritis on microscopy

Answer 5

Scarred glomeruli w/ blue staining collagen on trichome in and between glomeruli
Atrophic tubules
Hyaline arteriolsclerosis 2ndary to HTN
Lymphocytic infiltrate

Question 6

What does aldosterone do?

Answer 6

Na reabsorption and ↑ K secretion in principal cells; also ↑ H secretion in intercalated cells

Question 7

PKD1 encodes polycystin-1: a transmembrane protein important for

Answer 7

connective tissue cohesion between renal tubular epithelial cells (esp. the distal nephron).

Question 8

Where is glomerulotubular balance maintained?

Answer 8

PCT!
Glomerulotubular balance maintains a constant fraction (normally 2/3rds, or ~67%) of filtered Na+ and H2O reabsorption in the PCT. It is regulated by Starling forces in the peritubular capillaries

Question 9

Paraneoplastic syndrome from ectopic hormone production occurs in 20% of RCC patients:

Answer 9

• PTHrP → hypercalcemia
• EPO → polycythemia
• ACTH → ↑ cortisol → Cushing syndrome
• Renin → hypertension

Question 10

With what is IgA nephropathy associated? (Besides HSP)

Answer 10

• Celiac sprue—IgA-mediated bowel disease (anti-gliadin IgA) & Dermatitis herpetiformis—grouped vesicles on extensor surfaces

Question 11

What type of infection precedes PSGN?

Answer 11

URI or skin infection with a nephritogenic strain of group A β-hemolytic Streptococcus pyogenes (especially serotype M12, M4, or M1)

Question 12

How long after the URI/skin infection do you get PSGN?

Answer 12

1-4 weeks to make antibodies (↑ anti-DNAse B) and form immune complexes

Question 13

What type of hypersensitivity reaction is PSGN?

Answer 13

Type III hypersensitivity in glomeruli (renal tubular function (concentrating ability) remains largely intact)

Question 14

Where are the immune complexes deposited in PSGN?

Answer 14

Subepithelial (subpodocyte)

Question 15

What happens immediately after the immune complexes are deposited in PSGN?

Answer 15

Alternative complement activation

Question 16

Describe alternative complement activation –> glomeruonephritis after subepithelial immune complex deposition in PSGN?

Answer 16

C5a recruits neutrophils → glomerular damage/inflammation with large hypercellular glomeruli due to WBC infiltrate & proliferation of mesangial and endothelial cells

Question 17

What recruits the neutrophils to the glomeruli in PSGN?

Answer 17

C5a

Question 18

What cells in the glomerulus proliferate w/ PSGN?

Answer 18

mesangial and endothelial cells (plus WBC infiltrate)

Question 19

How does an increase in plasma protein affect RBF?

Answer 19

It doesn’t!

Question 20

How old is the typical patient w/ PSGN?

Answer 20

6-10

Question 21

Name some URIs and skin infections (dz process not bug!) that could set off PSGN in 1-4 weeks

Answer 21

pharyngitis,

impetigo, erysipelas, scarlet fever

Question 22

What are the 6 S/Sx of nephritic syndrome present in PSGN?

Answer 22

1. Hematuria
2. Proteinuria
3. Oliguria
4. Azotemia
5. Mild to moderate HTN
6. Periorbital edema

Question 23

Besides s/sx of nephritic syndrome, child with PSGN presents w/

Answer 23

Sudden development of fever, nausea, malaise,

Question 24

What does light microscopy of a urine sample show in a patient with calcium oxalate stones?

Answer 24

colorless octahedral crystals (square crossed by a diagonal line in 2-dimensional view).

Question 25

Describe the gross appearance of a kidney with acute pyelonephritis

Answer 25

Patchy pale abscesses on the cortex and medulla

Question 26

What happens with increased RAAS and ADH secretion? (3 things)

Answer 26

1. efferent arteriole vasoconstrition
2. increased reabsorption of urea by ADH
3. Increased reabsorption of Na and H2O –> oliguria

Question 27

1 and #2 causes of chronic glomerulonephritis

Answer 27

1. RPGN

2. FSGN

Question 28

Treatment for cysteine stones?

Answer 28

Hydration and alkalinization of the urine

Question 29

4 causes of oxalate stone formation in kidney

Answer 29

1. hypercalcinuria
2. hypocalcemia
3. Crohn’s dz
4. Ethylene glycol ingestion