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Neonatal-Perinatal Boards Review > Renal, Water/Electrolytes and GU > Flashcards

Renal, Water/Electrolytes and GU Flashcards

1
Q

Clinical triad in renal vein thrombosis

A

Hematuria

Flank mass

Thrombocytopenia

Can propagate from origin in small renal veins to IVC

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2
Q

Mechanism of hypertension in renal artery thrombosis

A

Release of renin as a response to renal hypoperfusion from the clot

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3
Q

Initial trigger for renin release

A

Decreased renal perfusion pressure

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4
Q

Renin ultimately stimulates ___ in the lungs to make more ____

A
  1. ACE— throughout body, but highest in vascular endothelium of lungs.
  2. Angiotensin II—potent vasoconstrictor
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5
Q

Effects of angiotensin II (immediate and if sustained)

A

Vasoconstriction

Vascular hyperplasia and hypertrophy

(Reason ACEI can help with preventing long term sequelae if vascular injury/hypertension is prolonged)

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6
Q

Two downstream proteins after Angiotensin II and their effects

A

Angiotensin III—aldosterone secretion, increases sodium retention and therefore blood volume/fluid overload

Angiotensin IV—increases blood viscosity

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7
Q

ACEI mechanisms

A
  1. Decreases ACE activity (lungs)—less angiotensin II that causes vasoconstriction
  2. Less angiotensin II/III: less aldosterone and decreased vasoconstriction
  3. Less bradykinin/kallidin activity (vasoactive peptides)
  4. Long-term, prevents vascular remodeling
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8
Q

Beta blocker mechanisms

A
  1. Decreased HR
  2. Decreased stroke volume
  3. Decreases renin secretion
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9
Q

Spironolactone mechanism

A

Blocks aldosterone receptor

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10
Q

Location of:

  1. Angiotensinogen synthesis
  2. Conversion to Angiotensin I
  3. Conversion to Angiotensin II
A
  1. Liver
  2. Kidneys (in response to renin)
  3. Lung (high concentration of ACE in pulmonary vascular endothelium)
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11
Q

Most common abdominal mass in female neonates

A

Simple ovarian cyst

“Simple” can have >1 THIN-walled septated region

Thick walls or heterogenous echogenecity means it’s complex (potential torsion/necrosis)

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12
Q

Potter’s sequence findings

A

Oligohydramnios, arthrogryposis, pulmonary hypoplasia, face with beaked nose, wide-set eyes, low-set ears

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13
Q

Triad of Eagle-Barrett Syndrome

A

I.e. prune belly syndrome

Absent/hypoplastic abdominal musculature

Cryptorchidism

Renal dysplasia with megaureter and poorly contractile, distended bladder

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14
Q

Ultrasound findings in posterior urethral valve

A

Megaureters with a thickened, trabeculated bladder (because it’s been pushing against the dysfunctional urethral valve)

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15
Q

Which of the congenital cystic kidney disorders carries the worst prognosis?

A

Autosomal recessive polycystic kidney disease (ARPKD)

70% survival in neonatal period

50% develop renal failure in childhood

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16
Q

Findings in renal artery thrombosis

A

Hypertension (if mild/moderate)

Conjugated hyperbilirubinemia

Thrombocytopenia

Hematuria

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17
Q

Which has a higher morbidity/mortality, renal artery or vein thrombosis?

A

Renal artery thrombosis–10-20% mortality if involves aorta, hypertension common

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18
Q

Treatment for renal artery vs. renal vein thromboses

A

RAT–systemic heparinization (when moderate/severe)

RVT–supportive care (electrolyte corrections, avoidance of further injury)

(RAT treatment is intensive because outcomes if persists are worse)

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19
Q

Definition of stage 3 AKI (acute kidney injury)

A

Serum creatinine >3x baseline and/or urine output (UOP) = 0.3ml/kg/h

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20
Q

FeNa and types of renal injury

A

FeNa (fraction excreted Na)= (uNa x sCr) / (sNa x uCr)

Prerenal: FeNa <1% (because kidneys can still concentrate and hold onto Na)

Acute tubular necrosis (ATN): >2%

uNa goes on top because it’s the fraction in your urine that you’ve peed out

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21
Q

Location and mechanism of action of furosemide

A

Thick ascending loop of Henle (Na-K-2Cl symporter)

Causes decreased Na, K, Cl (Mg and Ca) reabsorption

Less hypertonic medulla, more water excretion

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22
Q

Location and mechanism of action of thiazides

A

Distal convoluted tubule (the Na-Cl cotransporter)

Causes decreased Na, K and Cl reabsorption but INCREASED Ca++

Leads to smaller osmotic gradient so don’t reabsorb water

23
Q

Most common palpable abdominal mass in neonates

A

Hydronephrosis

24
Q

Studies to consider in multicystic dysplastic kidney (MCKD/MKD)

A
  1. Postnatal ultrasound (30-50% have contralateral renal anomaly)–should be done at 48-72h to decrease false negatives
  2. DMSA (dimercaptosuccinic acid/radionuclide scan) if other kidney’s also abnormal
  3. Annual renal ultrasound
25
Q

Similar to autosomal recessive polycystic kidney disease (ARPKD), posterior urethral valves often results in end-stage renal disease by ____

A

10 years

ARPKD is the most severe of the cystic kidney diseases

PUV is the most severe of the obstructive uropathies

26
Q

Frequent concomitant finding with posterior urethral valves (PUV)

A

Vesicoureteral reflux (VUR) from malpositioned/ectopic ureteral insertion

27
Q

Non-renal finding associated with autosomal recessive polycystic kidney disease (ARPKD)

A

Hepatic fibrosis

28
Q

Non-renal findings associated with autosomal dominant polycystic kidney disease (ADPKD)

A

Cysts in other organs (e.g. spleen and pancreas)

29
Q

Synonym for arginine vasopressin and its location of synthesis

A

Antidiuretic hormone (ADH)

Posterior pituitary (precursor made in hypothalamus)

Acts mainly on collecting duct and increases aquaporins

30
Q

Primary hormonal determinant of water excretion

A

ADH (ie. vasopressin)

Synthesized in hypothalamus but stored in posterior pituitary

Acts mainly on collecting duct (also DCT) and increases aquaporins

31
Q

Two locations of the V2 receptors

A
  1. DCT
  2. Collecting ducts (CD)

V2R is predominantly in kidneys, V1R is throughout (vascular smooth muscle, liver, etc)

V2R is robust in neonates, even preemies

32
Q

Reason for neonatal poor response to ADH

A

Immaturity of renal ADH-specific adenylate cyclase [in both DCT and collecting ducts]

Neonates (even preemies) have many ADH (aka V2) receptors, just can’t respond

(ADH and AVP are synonyms)

33
Q

Mechanism of action of ADH at the DCT and collecting duct

A

Stimulates adenylate cyclase–increased cAMP–increased translocation of aquaporins–more water reabsorptive capacity

34
Q

Mechanism of action of ADH at Loop of Henle

A

Stimulates adenylate cyclase–increased cAMP–active transport of Na into renal medulla–increased osmotic gradient drives water reabsorption

35
Q

Bladder extrophy is more common in ____ and usually associated with ____

A

Males Inguinal hernia

36
Q

Primary location of sodium reabsorption in the kidney

A

Proximal tubule (70%)

(Followed by 25% in thick ascending limb of loop of Henle, only 5-10% is in DCT and collecting ducts)

37
Q

Primary reason for decreased sodium reabsorption in preemies

A

Decreased number of Na-K-ATPase and ion-specific transporters (everywhere)

Even if aldosterone has a normal concentration (which normally is), preemie kidneys have limited transporters to respond (would normally upregulate number as well as activate them)

38
Q

Renin is made in the ___

Angiotensinogen is made in the ___

Angiotensinogen is converted to Angiotension I in the ___

Angiotensin II is made in the ____

Aldosterone is made in the ___ and acts at the _____

A

Kidneys

Liver

Plasma

Lung vasculature (by ACE)

Adrenals

Cortical collecting ducts (CCD) and DCT

39
Q

Hormonal reason for late (2-6 weeks of age) hyponatremia in preemies

A
  1. Poor response to aldosterone (decreased number but normal function of Na-K-ATPase and other transporters) so increase urine loss
40
Q

Classic laboratory urine findings in premature infants with hyponatremia

A

High urine sodium and FeNa Kidney can’t hold onto Na (and that’s aldosterone’s job)

41
Q

Primary role of aldosterone

A

Upregulates and activates sodium transporters in distal tubule (DCT) and collecting duct (CCD)

(Important even though PCT and Loop of Henle both are more responsible for Na reabsorption than DCT and CCD)

42
Q

Aldosterone is made in the ____, primarily acts at the ____ by upregulating and activating ____

A
  1. Adrenals
  2. Cortical collecting ducts (CCDs) and distal convoluted tubules (DCTs)
  3. Na-K-ATPase (pumps) and ENaC channels (cause Na reabsorption)
43
Q

Hormonal reason for early hypernatremia in preemies

A

Poor response to ADH (adenylate-cyclases in kidneys are present but immature) so lose too much water

44
Q

Which RTA causes a non-anion gap acidosis and a normal (acidic) urine pH

A

RTA Type II: decreased bicarbonate reabsorption in the proximal tubule

You _P_ee 2 much HCO3

45
Q

What is the issue in RTA I

A

Cannot secrete H+ in DCT (distal)

(Since you can’t secrete acid, your urine is alkaline)

46
Q

Type IV RTA is caused by _______ deficiecy

A

Aldosterone deficiency

Think of CAH–salt wasting, hyperkalemia, acidosis

47
Q

Draw the nephron, which parts do what, and key associations

A
48
Q

FeNa indicative of intrinsic renal injury

A

FeNa >2-2.5% (depends on source)

Because point of kidney is reabsorption, so if injured can’t pull Na+ back in

49
Q

If you are highly suspicious of posterior urethral valves, what is the first step in management postnatally

A

Placement of a foley catheter to relieve the obstruction

(Would be suggested by bilateral hydronephrosis, hydroureters, and a thickened/trabeculated bladder)

50
Q

What sodium transporters/channels does aldosterone effect?

A

DCT: Na-Cl transporter (apical AKA urine side)

CCD: ENaC (apical)

Both DCT and CCD: Na/K ATPase (bloode side)

51
Q

What is the AT2 receptor most important for?

A

Found in fetal/preemie kidneys, promotes nephrogenesis (via angiotensin II)

52
Q

The class of antihypertensives to be avoided in preterm infants (and those with acute renal failure)

A

Angiotensin-converting enzyme inhibitors (ACEI)

53
Q

Nephrogenesis occurs until ____ (GA or PMA)

A

36 weeks

Neonatal-Perinatal Boards Review (11 decks)

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