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Final FA review > 2/28 renal > Flashcards

2/28 renal Flashcards

1
Q

Order of metanephros, pronephros, mesonephros.

A

1-pronephros
2-mesonephros
3-metanephros

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2
Q

What does mesonephros eventually contribute to?

A

Wolffian duct

-internal male structure except prostate.

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3
Q

When does the metanephros show up?

A

5th week.

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4
Q

What does ureteric bud give rise to?

A

From collecting duct til ureter (including ureter).

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5
Q

What does Metanephric mesenchyme give rise to?

A

All of nephron until/except collecting duct.

-starting from glomerulus going til (& including) DCT.

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6
Q

Last to canalize in fetal kidney?

A

Ureteropelvic junction = most common site of obstruction (hydronephrosis) in fetus.

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7
Q
  • Cause of death in oligohydramnios?

- Causes?

A
  • pulmonary hypoplasia

- ARPKD, posterior urethral valves, bilateral renal agenesis.

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8
Q

Horseshoe kidney

  • what stops its ascent?
  • associated w/what syndrome?
  • is renal function affected?
  • which poles commonly fused?
A
  • inf mesenteric art.
  • Turners
  • no
  • inf. poles
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9
Q

Multicystic dysplastic kidney

  • cause?
  • function of kidney affected?
  • if bilateral, dont confuse w/what?
A
  • Due to abnormal interaction between ureteric bud and metanephric mesenchyme.
  • leads to non-functional kidney.
  • polycystic kidney .disease
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10
Q

Which kidney is taken during a transplant and why?

A

Left kidney, longer renal vein.

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11
Q

Renal arterial supply:

A

Ab. aorta => renal => segmental => lobar => interlobar => arcuate => interlobar => afferent => glomerulus.

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12
Q

Renal venous path:

A

glomerulus => efferent arteriole => interlobar v => arcuate => interlobar => renal => IVC

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13
Q

Ureters course:

A
  • pass UNDER uterine artery and under ductus deferens (retroperitoneal).
  • pass OVER the common/external iliac vessels.
  • “Water (ureters) under the bridge (uterine artery, vas deferens).”
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14
Q

Gynecologic procedures involving ligation of the uterine vessels: watch out not to damage what?

A

-ureter, which passes just under uterine artery.

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15
Q

What type of epithelium do ureters have?

A

-transitional

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16
Q
  • How much of total body weight is water?

- What fraction is intra & extracellular?

A
  • 60%
  • 2/3 intracellular (40% body weight)
  • 1/3 extracellular (20% body weight)
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17
Q

Extracellular fluid

-what fraction is plasma volume vs interstitial volume?

A
  • 1/4th plasma volume (5% body weight)

- 3/4th interstitial volume (15% body weight)

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18
Q

mnemonic for % of body weight for total body water/ICF/ECF.

A

60–40–20 rule (% of body weight):

  • 60% total body water
  • 40% ICF
  • 20% ECF
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19
Q
  • Whats used to measure plasma vollume?

- Whats used to measure extracell. volume?

A
  • radiolabeled albumin

- inulin

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20
Q

Normal plasma osmolarity

A

Osmolarity = 290 mOsm/L.

-about double your serum Na b/c Na has +2 charge.

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21
Q

What gives basement membrane of glomerulus a negative charge?

A

heparan sulfate

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22
Q

Renal clearance equation:

A

Cx = UxV/Px

  • Cx = clearance of X (mL/min).
  • Ux = urine concentration of X (mg/mL).
  • V = urine flow rate (mL/min).
  • Px = plasma concentration of X (mg/mL).

*-so basically: urine conc = what you take out / what you put in. Then you multiply by how fast you’re doing it. And thats clearance.

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23
Q
  • Cx < GFR:
  • Cx > GFR:
  • Cx = GFR:
A
  • net tubular reabsorption of X.
  • net tubular secretion of X.
  • no net secretion or reabsorption (like inulin)
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24
Q
  • oncotic pressure of bowmans space?

- whats normal GFR?

A
  • normally = 0

- 100ml/min

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25
Q

Is serum creatinine a sensitive indicator for renal function?

A
  • relationship btwn GFR & creatinine is NOT linear.
  • you can have normal creatinine level even w/50% loss of renal fcn.
  • So after you lose a significant amount of GFR, after that, small decreases in GFR can cause big increases in blood creatinine levels.
  • *serum creatinine is not a sensitive indicator for decreasing GFR when creatinine levels are normal.
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26
Q

Effective renal plasma flow

-estimated using what?

A
  • clearance of para-aminohippuric acid (PAH).

- ERPF underestimates true renal plasma flow (RPF) by ~10%.

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27
Q
  • renal blood flow equation

- is ERPF an accurate measure of renal plasma flow (RPF)?

A

RBF = RPF/(1 - Hct) or RBF(1-hct) = RPF

-ERPF underestimates true renal plasma flow (RPF) by ~10%.

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28
Q

Filtration fraction equation:

A

FF = GFR/RPF

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29
Q

-Filtered load equation
-Excretion rate = V × Ux
.

A
  • Filtered load = GFR × Px
  • Excretion rate = V × Ux
  • Ux = urine concentration of X (mg/mL).
  • V = urine flow rate (mL/min).
  • Px = plasma concentration of X (mg/mL).
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30
Q
  • How is glucose resorbed in kidney?
  • At what plasma glucose does glucosuria begin?
  • At what plasma glucose are all transported fully saturated?
A

-Glucose at a normal plasma level is completely reabsorbed in proximal tubule by Na+/glucose
cotransport.
-200 mg/dL
-375 mg/dL

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31
Q

Glucose and amino acid resorption in pregnancy:

A

Dec. reabsorption of glucose and amino acids in the proximal tubuleŽ glucosuria and aminoaciduria.
-this is normal in pregnancy.

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32
Q

Amino acid resorption in nephron:

A

-Sodium-dependent transporters in proximal tubule reabsorb amino acids.

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33
Q

Hartnup disease:

A
  • Autosomal recessive.
  • Deficiency of neutral amino acid (ie. tryptophan) transporters in PCT and on enterocytes.
  • Leads to neutral aminoaciduria & dec. absorption from the gut
  • Results in pellagra-like symptoms; treat with high-protein diet and nicotinic acid.
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34
Q

What does the PCT secrete?

A

NH3

-buffer for secreted H+

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35
Q

PTH effect on PCT?

A
  • inhibits Na+/PO43– cotransport → PO43– excretion.

* remember, PTH inc. phosphate excretion but inc. Ca resorption. Trying to inc. free Ca.

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36
Q

AT 2 effect on PCT?

A

stimulates Na+/H+ exchange → ↑ Na+, H2O, and HCO3
- reabsorption (permitting contraction alkalosis).

  • so it inc. Na, water, and bicarb resorption in exchange for secreting H.
  • permits contraction alkalosis.
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37
Q

How much of filtered Na is resorbed in PCT?

A

-65-80%

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38
Q
  • What generates the (+) luminal potential in the Thick ascending loop of Henle?
  • What does this (+) luminal potential accomplish?
A
  • K+ backleak.
  • paracellular Mg & Ca resorption.

*thats why loop diuretics cause you to lose cations.

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39
Q

What is loop of henle accomplishing?

A

The reason you resorb water and then resorb ions in loop of henle is because there is not a way to resorb both water and ions at the same time. So the strategy
is first resorb the water to make the tubular fluid hyperosmotic, and then to resorb the ions by letting them follow their osmotic gradient.

40
Q

How much of filtered Na being resorbed in thick ascending loop of henle?

A

-10–20% Na+ reabsorbed.

41
Q

Where are the two places PTH acts?

A
  • PCT: inhibits Na/PK4 cotransport, leads to PO4 excretion.

- DCT: inc. Na/Ca exchanger. Inc. Ca resorption.

42
Q

Fanconi syndrome

  • problem?
  • what can it result in?
  • causes?
A
  • Reabsorptive defect in PCT.
  • inc. excretion of nearly all amino acids, glucose, bicarb, and phosphate.
  • May result in metabolic acidosis (proximal renal tubular
    acidosis) .
  • Wilson disease, ischemia, and nephrotoxins/drugs.
43
Q

Mnemonic for renal tubular defects & locations

A

The kidneys put out FABulous Glittering Liquid:

  • FAnconi syndrome is the 1st defect (PCT)
  • Bartter syndrome is next (thick ascending loop of Henle)
  • Gitelman syndrome is after Bartter (DCT)
  • Liddle syndrome is last (collecting tubule)
44
Q

Bartter syndrome

A
  • Reabsorptive defect in thick ascending loop of Henle. -Autosomal recessive, affects Na+/K+/2Cl– cotransporter.
  • Results in hypokalemia and metabolic alkalosis with hypercalciuria.
  • fucks up the (+) luminal potential. So you waste Ca and Mg.
  • kind of like loop diuretics.
45
Q

Gitelman Syndrome

A
  • Reabsorptive defect of NaCl in DCT.
  • Autosomal recessive. Less severe than Bartter syndrome.
  • Leads to hypokalemia and metabolic alkalosis, but without hypercalciuria.

*kind of like thiazide effect.

46
Q

Liddle Syndrome

A
  • Inc. Na+ reabsorption in distal and collecting tubules (activity of epithelial Na+ channel).
  • Autosomal dominant.
  • Results in hypertension, hypokalemia, metabolic alkalosis, dec. aldosterone.
  • Treatment: Amiloride.

*Aldo inserts eNaC channels. These channels are increased in Liddle syndrome, so you get the effect of high aldo, without the high aldo.

47
Q

Liddle syndrome

-Tx:

A

amiloride

48
Q

Exact action of Aldo:

A

-↑ Na + channel and Na + /K + pump insertion in principal
cells.
-Enhances K + and H + excretion (upregulates principal cell K + channels and intercalated cell H + ATPases).

49
Q
  • Does AT2 stimulate release of ADH?

- Does AT2 have any effect on hypothalamus?

A
  • yes

- yes, stimulates thirst.

50
Q

What does AT2 do to PCT?

A
  • inc. PCT Na/H exchanger.
  • inc. resorption of Na, bicarb, water.
  • allows for contraction alkalosis.
51
Q

what is contraction alkalosis?

A

-Inc. in pH as a result of fluid loss.

52
Q

So if AT2 causing vasoconstriction, wont you have reflex brady?

A

AT2 affects baroreceptor function; limits reflex bradycardia, which would normally accompany its pressor effects. Helps maintain blood volume and blood pressure.

53
Q

How does ANP relax smooth muscle?

A

inc. cGMP.

54
Q

Where is EPO released from?

A

-Interstitial cells in the peritubular capillary bed in response to hypoxia.

55
Q

Where is 1α-hydroxylase in kidney?

-whats it regulated by?

A
  • PCT cells

- up reg by PTH.

56
Q

IgA nephropathy + extra-renal symptoms =

A

Henoch-Schonlein purpura.

57
Q

IgA nephropathy vs RSGN

A
  • IgA nephropathy shows up a few days after the infection.
  • PSGN shows up a couple weeks after the infection.
  • complement levels are normal in IgA nephropathy, but C3 is low in PSGN.
  • Mesangial prolif is not seen in PSGN.
58
Q

Whats name of active vitamin D?

A
  • calcitriol

- 1,25 - OH - D3

59
Q
  • Which rib overlies left kidney?

- Which ribs overlie spleen?

A
  • 12th

- 9, 10, 11th

60
Q

Do pts w/chronic renal insufficiency require higher or lower doses of diuretics for a good therapeutic response?

A
  • higher.

- may be counter intuitive. you may think that less is excreted so you need less, but thats not the case.

61
Q

Ototoxic agents:

A

-aminoglycosides, loop diuretics, cisplatin, salicylates.

62
Q

Do renal tubules secrete glucose?

A

-no

63
Q

Vasopressin action & urea

A
  • vasopressin produces a V2-mediated inc. in permeability to water and urea at inner medullary collecting duct.
  • will decrease excretion of free water and urea.
  • also inc. water perm in corticol collecting duct.

*as free water is resorbed, the conc. of urea inc. Vasopressin adds more urea channels so urea can be passively resorbed down its conc. gradient.

64
Q

Aldo promotes secretions of

  • K, from which cell?
  • H, from which cell?
A
  • K secreted from principal cell.

- H secreted from intercalated cell.

65
Q

Foscarnet

-toxicity

A
  • chelates calcium, induces renal wasting of Mg, reduces PTH secretion which leads to hypocalcemia.
  • hypocalcemia & hypomagnesemia = can lead to seizures.
  • can cause acute tubular necrosis.

-watch out for drug interaction w/pentamidine (Tx pneumocystis jirovecci) = both cause hypocalcemia.

66
Q

Tx for wilson’s disease

A

-penicillamine or trientene.

67
Q

Acute tubular necrosis

  • is it reverisible?
  • what are the 3 phases?
A
  • yes

- initiation, maintenance, recovery

68
Q

Nephrotic syndrome s/p URI?

A

minimal change disease

69
Q

Is nephrotic syndrome a high or low renin state?

A

High renin b/c low albumin so all the fluid in ur vasculature leaves and goes to interstitum. This dec. perfusion to kidneys and you get high renin. Just exacerbates the volume overload/edema.

*no HTN b/c the fluid is in interstitum, not in the vascular.

70
Q

Clear cell carcinoma (renal cell carcinoma) arises from which cells?

A

-cells of PCT.

71
Q

Transitional cell carcinoma

-most commonly arises from where?

A

-renal pelvis

72
Q

Why is ethylene glycol bad for kidneys?

A

-converted to glycolic acid which is toxic to renal tubules.
-also converted to oxalic acid, which can form calcium
oxalate crystals.

-you’ll get high anion-gap metabolic acidosis.

73
Q

insulin action on potassium

A
  • shifts potassium into cells

- may cause hypokalemia.

74
Q

β-adrenergic agonist

-can they cause hypo or hyperkalemia?

A
  • hypokalemia.

- they inc action of Na+/K+ ATPase, so K shifts into cells.

75
Q

Hypokalemia

-ECG

A

-U waves on ECG, flattened T waves, arrhythmias, muscle weakness.

76
Q

Hyperkalemia

-ECG

A

-Wide QRS and peaked T waves on ECG, arrhythmias, muscle weakness.

77
Q

Does renal failure result in metabolic acidosis or aklalosis?

A

-acidosis b/c you’re not excreting organic acids.

78
Q

Winters formula

A

Pco2 = 1.5 [HCO3–] + 8 +/- 2

*The predicted respiratory compensation for a simple metabolic acidosis can be calculated using the Winters formula. If the measured Pco2 differs significantly from the predicted P co2, then a mixed acid-base disorder is likely present.

79
Q

pneumothorax: does it lead to resp. alkalosis or acidosis?

A

-resp. alkalosis b/c you shunt blood to ventilated areas and you hyperventilate.

80
Q

Anion gap

  • equation
  • normal anion gap?
A
  • Anion gap = Na – (Cl + HCO3)

- normal: 8−12 mEq/L

81
Q

Mnemonic for inc. anion gap metabolic acidosis

A 
MUDPILES:
Methanol (formic acid)
Uremia
Diabetic ketoacidosis
Propylene glycol
Iron tablets or INH
Lactic acidosis
Ethylene glycol (oxalic acid)
Salicylates (late)
82
Q

Mnemonic for normal anion gap metabolic acidosis

A 
HARD-ASS:
Hyperalimentation
Addison disease
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
83
Q
  • Renal tubular acidosis

- why hyperchloremic?

A
  • A disorder of the renal tubules which leads to non-anion gap hyperchloremic metabolic acidosis.
  • hyperchloremic b/c you’re spilling bicarb so you have to save your other major anion by resorbing more of it.
84
Q

Where in nephron do you find the lowest pH levels?

A

-DCT & collecting duct.

85
Q

Does uric acid precipitate into crystals in normal, acidic, or basic pH?

A

-acidic.

86
Q

How do you reduce risk of tumor lysis syndrome?

A

-urine alkalinization & hydration.

87
Q

If a solute is “freely filtered” what does that tell you abuot its filtration rate?

A

-filtration rate will = GFR which = inulin clearance.

88
Q

Does drug induced lupus often affect the kidney?

A

-no

89
Q

“Brisk diuresis” think what

A

-furosemide/loops.

90
Q

Alport vs goodpasture

A
  • alport = mutation in type 4 collagen.

- goodpasture = auto-ab against type 4 collagen.

91
Q

Henoch Schonlein Purpura

-Sxs:

A
  • GI: intermittent, severe GI pain, risk of intussuseption.
  • Kidneys: IgA nephropathy = nephritic
  • Skin: palpable purpura
  • Joints: migratory arthralgias.
92
Q

Nephrotic syndrome

-hyper ror hypocoaguable state?

A

-hypercoaguable b/c you can spill anti-thrombin 3.

93
Q

Why are pts w/nephrotic syndrome susceptible to infections, especially pneumococcal infections?

A

-b/c you spill immunoglobulins as well.

94
Q

Why is spironolactone added to a CHF pt’s drug regiment?

A

b/c aldosterone is inc. in CHF and aldo known to cause ventricular remodeling leading to cardiac fibrosis.

95
Q

Where in the renal tubule is the most dilute?

A

-DCT

Final FA review (52 decks)

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