Renal

Front 1

inulin is used to calculate?

Back 1

GFR = (U inulin x V)/(P inulin)

Front 2

PAH is used to calculate?

Back 2

effective renal plasma volume= (U PAH x V)/(P PAH)

Front 3

what is the formula for RBF?

Back 3

RBF = RPF/(1-Hct)

Front 4

At high arterial blood volumes, you have __ FF and ___ reabsorption.

Back 4

At high arterial blood volumes, you have low FF and low reabsorption (less albumin conc. exerted = less plasma oncotic pressure).

Front 5

At low arterial blood volumes, you have __ FF and ___ reabsorption.

Back 5

At low arterial blood volumes, you have high FF and high reabsorption (more albumin conc. exerted = more plasma oncotic pressure).

Front 6

Plasma protein will have what affect on GFR?

Back 6

More plasma protein conc. = lower GFR because you have a higher glomerular capillary oncotic pressure.

Front 7

NSAIDs have what affect on FF?

Back 7

NSAIDs will have no affect on FF because it will decrease prostaglandins and thus constict afferent arteriole.

FF = GFR/RPF (both will be decreased equally = same FF)

Front 8

Where is the kidney tubular fluid most dilute?

Back 8

Early DCT, after all the solutes (NaKCl) have been reabsorbed in the ascending tubule.

Osm in DCT = 100 mOsm

Front 9

Where is the kidney tubular fluid most concentrated?

Back 9

At the end of the descending loop of henle, because the descending loop of henle reabsorbs H20.

Osm at the end of descending loop = 1200 mOsm

Front 10

How does PTH affect nephron ion transport?

Back 10

PTH: 2 functions
1. PCT = decrease Na/PO4 cotransport (decrease PO4 reabsorption)
2. DCT = increase Na/Ca exchanger (increase Ca reabsorption) - thiazides also increase this exchanger

Front 11

Aldosterone causes K+ and H+ secretion from which cells?

Back 11

After Na+ is reabsorbed from ENaC in the principal cell, K+ is secreted by principal cell and H+ is secreted in the intercalated cell.

Front 12

which ions have a TF/P > 1

Back 12

TF/P > 1 means that water is being reabsorbed more than the solute, so it concentrates in the TF.

Ex: creatine (not reabsorbed), inulin (not secreted/reabsorbed), urea (poorly reabsorbed), Cl- (reabsorbed slower than water in DCT)

Front 13

which ions have a TF/P = 1

Back 13

TF/P = 1 means it is reabsorbed at the same rate as water

ex: Na+, K+

Front 14

which ions have a TF/P < 1

Back 14

TF/P < 1 means that solute is reabsorbed more than water.

ex: Pi, HCO3-, amino acids, glucose

Front 15

How do Beta-agonists/antagonists affect K+ balance?

Back 15

Beta agonists increase Na/K ATPase -->hypokalemia

Beta antagonists decrease Na/K ATPase --> hyperkalemia

Front 16

Signs of hypokalemia

Back 16

U waves on ECG, flattened T waves, arrhythmias, paralysis

Front 17

Signs of hyperkalemia

Back 17

Peaked T waves, wide QRS, arrhythmias

Front 18

Signs of hypercalcemia

Back 18

renal stones, abdominal groans, delirium,

Front 19

Type 1 "distal" RTA

Back 19

defect in collecting ducts ability to excrete H+. Associated with hypokalemia and calcium kidney stones.

Front 20

Type 2 "proximal" RTA

what is the primary defect?
what are 2 associated findings?

Back 20

defect in proximal tubule HCO3- reabsorption. Associated with hypokalemia and hypophosphatemic rickets.

Front 21

Type 4 "hyperkalemia" RTA

Back 21

hypoaldosteronism or lack of collecting duct response to aldosterone. Associated with hyperkalemia and inhibition of ammonium excretion in proximal tubule. Leads to decrease in urine pH due to decreased buffering capacity.

Front 22

Contrast Berger's disease and post-strep GN in:
- timing
- serum findings
- microscopic findings

Back 22

Bergers:
- 2-3 days after URI/gastroenteritis
- Increased IgA
- ICs deposit in mesangium

PSGN:
- 2-3 weeks after skin/pharyngeal GAS
- large glomeruli, hypercellular neutrophils, lumpy bumpy appearance

Front 23

diffuse proliferative glomerulonephritis

LM, EM findings?

Back 23

Most common cause of death in SLE
LM: wire looping of capillaries
EM: subendothelial DNA-anti-DNA ICs

Front 24

what are the 5 types of nephritis syndromes

Back 24

1. Post strep
2. RPGN
3. Diffuse proliferative GN (SLE's nephritic presentation)
4. Berger's disease
5. Alport's syndrome

Front 25

what are the 6 types of nephrotic syndromes

Back 25

1. minimal change
2. membranous
3. amyloidosis
4. diabetic nephropathy
5. MPGN
6. FSGS

Front 26

what are the two types of MPGN?

Back 26

type I: tram track appearance due to GBM splitting caused by mesangial ingrowth. Caused by HBV, HCV

type II: "dense deposits" associated with C3 nephritic factor.

Front 27

which kidney stones are radioopaque and which are radiolucent?

Back 27

radioopaque: calcium, ammonium magnesium phosphate, cystine

radiolucent: uric acid

Front 28

what infectious are associated with "staghorn" ammonium magnesium phosphate stones?

how do you treat these stones?

Back 28

urease positive stones (proteus, staph, klebsiella)

Rx = acidify the urine

Front 29

what is the treatment for uric acid and cystine stones/

Back 29

Rx: acetazolamide, pyridoxine (alkalinize the urine)

Front 30

what are 4 known risk factors for transitional cell carcinoma?

Back 30

phenacetin
smoking
aniline dyes
cyclophosphamide

Front 31

Contrast Berger's disease and post-strep GN in:
- timing
- serum findings
- microscopic findings

Back 31

Bergers:
- 2-3 days after URI/gastroenteritis
- Increased IgA
- ICs deposit in mesangium

PSGN:
- 2-3 weeks after skin/pharyngeal GAS
- large glomeruli, hypercellular neutrophils, lumpy bumpy appearance

Front 32

diffuse proliferative glomerulonephritis

Back 32

Most common cause of death in SLE
LM: wire looping of capillaries
EM: subendothelial DNA-anti-DNA ICs

Front 33

what are the 5 types of nephritis syndromes

Back 33

1. Post strep
2. RPGN
3. Diffuse proliferative GN (SLE's nephritic presentation)
4. Berger's disease
5. Alport's syndrome

Front 34

what are the 6 types of nephrotic syndromes

Back 34

1. minimal change
2. membranous
3. amyloidosis
4. diabetic nephropathy
5. MPGN
6. FSGS

Front 35

what are the two types of MPGN?

Back 35

type I: tram track appearance due to GBM splitting caused by mesangial ingrowth. Caused by HBV, HCV

type II: "dense deposits" associated with C3 nephritic factor.

Front 36

which kidney stones are radioopaque and which are radiolucent?

Back 36

radioopaque: calcium, ammonium magnesium phosphate, cystine

radiolucent: uric acid

Front 37

what infectious are associated with ammonium magnesium phosphate stones?

Back 37

urease positive stones (proteus, staph, klebsiella)

Rx = acidify the urine

Front 38

what is the treatment for uric acid and cystine stones/

Back 38

Rx: pyridoxine (alkalinize the urine)

Front 39

what are 4 known risk factors for transitional cell carcinoma?

Back 39

phenacetin
smoking
aniline dyes
cyclophosphamide

Front 40

what are the 3 events during acute tubular necrosis?

Back 40

1. inciting event: ischemia, MI, hemorrhage
2. maintenance: oliguria within 12-24hrs- causes edema, hyperkalemia, anion gap metabolic acidosis, hyperphosphatemia, muddy brown casts, low urinary Osm (but high Na+)
3. recovery (within 2-3 weeks): vigorous diuresis

Front 41

renal papillary necrosis is associated with 4 known risks?

Back 41

renal papillary necrosis = sloughing of renal papillae --> gross hematuria, proteinuria

1. diabetes
2. acute pyelonephritis
3. chronic phenacetin use (and acetaminophen)
4. sickle cell anemia

Front 42

what is the BUN/Cr for prerenal, renal, postrenal failure?

Back 42

Prerenal: BUN/Cr >20 (maximal BUN reabsorption to conserve volume0
Renal: BUN/Cr <15 (unable to reabsorb)
Postrenal: BUN/Cr >15 (back up causes more BUN reabsorption0

Front 43

what are the 3 mechanisms how loops and thaizide diuretics cause alkalosis?

Back 43

1. volume contraction - increase ATII causes increase Na/H exchange in DCT
2. K+ loss leads to K+ exiting cells, and swapping with H+, which go inside cells.
3. In a low K+ state, H+ is exchanged for Na+ in the collecting duct.