Renal/GU Flashcards

1
Q

what is a patent urachus?

A

a urinary connection from the bladder to the umbilical cord

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2
Q

Where does ADH act on kidney?

A

acts on late distal tubule, as well as cortical and medullary collecting ducts.

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3
Q

Whey to Caesin Ratio of following:
Colostrum
Mature Milk
Casein Formulas
Whey Formulas

A

Colostrum 80:20
Mature milk 55:45
Casein formulas 20:80
Whey formula 80:20

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4
Q

Why are newborns predisposed to Vitamin K deficiency?

A

lack of GI microorganisms that synthesize Vitamin K
immature newborn liver
some maternal medications
(some breastfed infants have lower vitamin k, than cow milk formula)

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5
Q

Why do amino acid solutions have decreased tyrosine and cysteine?

A

because they both have decreased solubility

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6
Q

Why is CHO requirement higher in preterm infant?

A

increased brain-to-body weight ratio, decreased fat stores, increased total enery requirements

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7
Q

what medical management is necssary for myelomeningocele for gu pathology?

A

intermittent bladder catheterization

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8
Q

When do you do ultrasound and karyotyping for hypospadias?

A

when it is complex (no descended testes), or if it is posterior hypospadias?

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9
Q

ADH is synthesized how early in fetus?

A

11 weeks

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10
Q

AKI more common in oliguric, or non-oliguric patients?

A

non-oliguric

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11
Q

Angiotensin II acts on what to stimulate release of Aldosterone?

A

on the adrenal cortex

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12
Q

Are renin levels increased or decreased in fetus?

A

decreased

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13
Q

Bigger increase in stones in RTA 1 or 2?

A

in Type 1
increased CA excretion due to bone mobilization due to attempts at buffering

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14
Q

Difference between UPJ and UVJ obstruction?

A

do not have dilated ureter in UPJ obstruction

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15
Q

Do loop of henle and distal tubule play role in urinary acidification?

A

No

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16
Q

How and Why is Renin released?

A

released by juxtaglomular cells
stimulated by decreased renal perfusion, and increased sympathetic activity

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17
Q

How do Antenatal Steroids affect Kidney?

A

Antenatal corticosteroids improve Na handling and by increasing Na+,K+-ATPase and Na/H+ exchanger

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18
Q

How do Prostaglandins affect kidney?

A

mediator of renal vascular tone and renin secretion

inhibition of prostaglandin increases fetal vascular resistance and can decrease UOP

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19
Q

how do you treat Barter Syndrome

A

potassium supplementation, thiazide diuretics, indomethacin

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20
Q

how do you treat renal vein thrombosis?

A

supportive care if not extending to IVC

anticoagulation for 3 months if extends to IVC

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21
Q

How do you treat RTA?

A

HCO3 or citrate (usually more HCO3 required to treat proximal, because of constant HCO3 wasting compared to distal RTA)

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22
Q

How does renal vein thrombosis present?

A

flank mass, hematuria, thrombocytopenia

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23
Q

Is effect of catecholamines (noriepi) more or less pronounced in fetuses or newborns?

A

less pronunced

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24
Q

Is MDKD or PCKD associated with Vacterl?

A

multicystic dysplastic kidney disease

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25
Q

Males or females more likely to have vesicoureteral reflux?

A

females x 2
but males present earlier due to shorter ureteres

26
Q

Management of Prerenal AKI vs intrinsic

A

volume resuscitation in prerenal
fluid restriction in intrinsic

27
Q

Multicystic Dysplastic kidney disease unilateral or bilateral?

A

unilateral

28
Q

Polycystic kidney disease inheritance pattern

A

Autosomal recessive (Infantile)
Autosomal dominant (adult)

29
Q

true or false preterm infants can dilute urine as much as term kids?

A

true
but they cannot concentrate urine same way term infant does

30
Q

What are 3 states of renal development? (mesodermic structures)

A

Pronephros
Mesonephros
Metanephros

31
Q

What are characteristics of nephrotic syndrome

A

hypoproteinemia, proteinuria, and hyperlipidemia

32
Q

What are classic lab findings in RTA Type IV?

A

hyperkalemic with hyperchloremic metabolic acidosis

33
Q

What are some major problems you see with polycystic kidney disease?

A

severe HTN, hepatic fibrosis, biliary dysgensis, potter sequence

34
Q

what are some problems with multicystic dysplastic kidney disease?

A

frequently have other GU anomalies
(Vacterl)

35
Q

what are urine findings in RTA type 2?

A

large losses of HCO3
urine can have ph < 5.3
substantial K losses due to K excretion instead of H

36
Q

What causes posterior urethral valves?

A

congenital membrane obstructs urethra

37
Q

what causes UPJ obstruction?

A

abnormal muscle development at UPJ

38
Q

what contributes to RTA in preterm infants?

A

preterm infants have lower concentrate HCO3 threshold in proximal tubule, greater loss in urine once this threshold is exceeded

39
Q

what do you see on ultrasound of Polycystic kidney disease?

A

snowstorm appearance

40
Q

What does Angiotensin II do?

A

Acts on adrenal to stimulate release of aldosterone

41
Q

What happens in Barter syndrome?

A

increased renin, increased aldosterone, hypokalemic metabolic alkalosis, normal parathyroid hormone

42
Q

what happens in nephrotic syndrome? What happens with proteinuria?

A

Proteinuria leads to albuminuria, hypoalbuminemia, and edema.

Hyperlipidemia is due to the increased lipoprotein synthesis secondary to hypoalbuminemia, which causes increased platelet aggregation and thrombosis.

The loss of minerals and vitamins predisposes to malnutrition and infections.

43
Q

What happens to GFR if creatinine doubles?

A

GFR falls by about 50%

44
Q

What is Barter Syndrome?

A

hypertrophy and hyperplasia of juxtaglomerular apparatus

45
Q

What is difference between hydronephrosis and Pyelectasis?

A

Hydronephrosis is dilation or renal pelvis
Pyelectasis is mild enlargement of renal pelvis (can see in aneupleouidy)

46
Q

What is inheritance pattern of pseudohypoaldosteronism?

A

x-linked recessive

47
Q

what is major risk factor for developing renal artery thrombosis?

A

UAC

48
Q

What is management of prune belly syndrome?

A

non-operative management, no clear benefit of surgery in preserving renal function in most patients

49
Q

What is more likely to resolve RTA 1 or RTA 2?

A

RTA 2 (recovery usually expected in 2-3 years)

50
Q

what is most common cause of congenital hydronephrosis?

A

UPJ obstruction

51
Q

What is primary inheritance pattern of RTA type 2

A

Autosomal recessive

52
Q

What is RTA Type IV?

A

Abnormal Aldosterone production or change in sensitivty to aldosterone
5 subtypes
1,4,5 most common
1&4 with NACL wasting
5 NACL normal (due to aldosterone insensitivity)

53
Q

What is urinary ph in RTA type 1?

A

ph > 6.2 (cannot acidify urine)

54
Q

What is usual genetic inheritance pattern of RTA 1?

A

Primary autosomal dominant
on occasion autosomal recessive (associated with deafness)

55
Q

What other electrolyte abnormalities do you see in hypernatremia?

A

elevated BUN, elevated potassium, hyperglycemia

56
Q

What percentage of cardiac output do fetal kidneys receive?

A

25%
falls to about 5% after birth

57
Q

What staging/grade VUR do you see renal scarring

A

stage IV and V reflux

58
Q

What trisomy do you see renal dysplasia/ hypoplasia?

A

trisomy 13, 18, and 21

59
Q

Where does RTA 2 take place?

A

takes place in proximal tubules
(absent proximal HCO3 reabsorption)

60
Q

Where is RTA Type I located?

A

distal tubules