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Neonatology Boards > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Bartter syndrome

A

Renal tubular salt wasting disorder in which the kidneys cannot reabsorb sodium and chloride in the thick ascending limb of the loop of Henle
Hypertrophy and hyperplasia of renal juxtaglomerular apparatus

Decreased Na, K, Cl
Increased HCO3, Calcium
Nephrocalcinosis

Severe polyhydramnios
Looks like being on lasix

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2
Q

Calcitonin

A

Secretion: parafollicular/C cells of thyroid in direct response to Ca levels

Inhibits osteoclasts bone resorption
Enhances renal Ca excretion
Modulates prolactin secretion

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3
Q

Vitamin D

A

Crosses placenta (vit d and 25 vit d)

1,25- active form- does NOT cross placenta
Placenta and kidney make 1,25

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4
Q

Calcium control in fetus versus neonate

A

Fetus: high calcitonin, low PTH

Neonate: PTH takes control after birth, stimulated by fall of calcium after birth- nadir 24-48 hrs
Vitamin D INDEPENDENT mechanism

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5
Q

Normal calcium levels

A

Ionized: 1.1-1.3
Serum: 8.8- (10-12)
Hypocalcemia <7 IF normal albumin

Total calcium falls 0.8mg/dL for every 1g/dL decrease in serum albumin

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6
Q

contraction alkalosis from diuretics

A
  1. Reduction in ECF volume
  2. Increase Na+ reabsorption
  3. Increased renal K+ and H+ secretion
  4. HCO3- reabsorption increases to maintain neutrality
  5. Volume depletion
  6. Stimulated renin
  7. Increases aldosterone
  8. Promotes further Na+ reabsorption and K+/H+ secretion
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7
Q

acidosis effect

A

for every 0.1-unit reduction in arterial pH, thre is approxx 0.6mEq/L increase in plasma K+

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8
Q

How to treat hyperkalemia

A
  1. REMOVE ALL EXOGENOUS K SOURCES
  2. 10% calcium gluconate
  3. glucose: D10W + insulin (increases intracellular update of K+ by direct stimulation of Na/K ATPase)
  4. furosemide
  5. NaHCO3
  6. Kayexalate
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9
Q

acidosis effect on K

alkalosis effect on K

A

hyperkalemia (0.1 dec ph = 0.6 inc K)

hypokalemia

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10
Q

major extracellular buffer system

A

CO2 crosses into brain –> decreases pH –> stimulates chemoreceptors –> increases respiratory drive –> eliminating CO2

H+ crosese cell membrane to reach buffer systems using 3 methods
1. Na+/H+
2. K+/H+
3. HCO3-/Cl

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11
Q

intracellular buffer systems

A

bone apatite
hemoglobin
organic phosphates

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12
Q

reabsorption of HCO3-

A

60-80% occurs in PROXIMAL TUBULE

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13
Q

anion gap metabolic acidosis

A
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14
Q

hypochloremic metabolic alkalosis

A

PYLORIC STENOSIS
cystic fibrosis
Bartter syndrome
diuretic therapy

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15
Q

type 1 RTA
distal or classic RTA

A

cannot secrete H+ in distal tubule
renal bicarb threshold is normal

urine pH > 6.2 –> CANNOT acidify urine
increased risk of renal stones –> minimize calcium excretion in urine

treat with bicarb or citrate

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16
Q

type 2 RTA
proximal

proximal think preemie

A

decreased/absent proximal tubular HCO3- reabsorption
reduced renal bicarb reabsorption threshold
normal distal acidification

large urine loses of bicarb–> urine pH < 5.3
normal urine concentrating ability
substantial K+ losses (instead of H+)

treat with bicarb or citrate, +/- phos, vitamin d

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17
Q

how does RTA cause growth issues?

A

blunts growth hormone axis and release

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18
Q

when does urine production occur?

A

10-12 weeks

major constituent of amniotic fluid production, increases with age

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19
Q

renal blood flow

A

25 weeks: 20ml/min
full term: 60ml/min

renal blood flow only accounts for 2-3% of cardiac output in utero

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20
Q

FENa

A

< 1% normal
1-2.5% = pre-renal
> 3% = intrinsic renal failure

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21
Q

Nephrogenesis

A

deep nephrons formed first
number increases until 34-35 wks then size of nephrons increases
at birth, juxtaglomerular nephrons more mature than superficial nephrons

FGR reduces number of nephrons

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22
Q

renal concentrating ability

A

fetal urine is hypotonic
osmolality increases with gestational age

max osm:
premature 500mOsm/L
term 800mOsm/L
adult ability reached at 6-12 mo: 1200osm/kg

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23
Q

why do preemies have a reduced concentrating ability?

A

tubule insensitivity to vaspressin
short loop of Henle
low osmolality of medullary interstitium –> limited Na+ reabsorption in thick ascending limb
low serum urea

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24
Q

renin-angiotensin system

A
25
Q

what stimulated renin release?

A

decreased renal perfusion–> hypotension, volume depletion

increased sympathetic activity

26
Q

where does ACE come from?

angiotensin converting enzyme

A

lung endothelium

27
Q

what does aldosterone do to the kidney?

A

increase Na+ reabsorption
increase Cl- passively
increase K+ secretion
increase H+ secretion

28
Q

what does angiotensin II do?

A

increasea Na+, H2O reabsorption by direct tubular stimulation
arteriolar vasoconstriction
stimulates release of ADH
stimulates release of aldosterone
activates vitamin D by PTH
activates erythropoietin

29
Q

pseudohypoaldosteronism

A

XR

unresponsiveness of renal tubule to aldosterone
Labs: decreased Na, increased K, metabolic acidosis, increased aldosterone, increased renin

Presentation:
prenatal: increased UOP, polyhydramnios
2-3 mo: dec feeding, vomiting, FTT

rule out CAH
give Na/Cl, indomethacin to reduce UOP

30
Q

causes of increased BUN

A

dehydration
increased protein intake
hypercatabolic states/hypoxia
sequestered blood
tissue breakdown

31
Q

definition of hematuria

A

> 5 RBCs per HPF

32
Q

cause of sediments:
1. leukocyturia
2. RBC casts
3. WBC casts
4. epithelial, granular casts
5. hyaline casts

A
  1. UTI, obstructive uropathy, glomerulonephritis
  2. glomerular injury
  3. infection, renatl interstitial/tubular injury
  4. dehydration, renal interstitial/tubular injury
  5. severe proteinuria, dehydration
33
Q

lenth of kidneys on US is proportional to what?

A

gestational age in weeks

34
Q

most common renal anomalies

A

horshoe kidney (Turner Syndrome)
unilateral renal agenesis (L>R)
pelvic kidney (L>R)

35
Q

congenital nephrotic syndrome

A

PROTEINURIA, hypoproteinemia, hyperlipidemia, edema

Finnish: Chr 19- NPHS1 (nephrin), AR;
- 90% sxs by 1 mo, dx by 3 mo
- large placenta, increased alpha-fetaprotein, ? hydrops
- SGA, premature
- complications: infection, thromboemboli –> urinary losses of IgG and coag proteins

Diffuse mesangial sclerosis:
later onse, normal placenta/alpha-feto/BW
- rapidly develop renal insufficiency
- early-onset hypertension

36
Q

renal agenesis

A

1/10,000
recurrent risk: 3-5%
40% stillborn or die shortly after birth

Associations:
- oligohydramnios sequence
- pulmonary hypoplasia
- Potter’s syndrome
- single umbilical artery

37
Q

muticystic dysplastic kidney
MCDK

A

M>F
L>R
sporadic

cysts: unilateral > bilateral, multiple, non-communicating, “grape-like” clusters
GU anomalies (90%)

bilateral disease in neonatal period- severe clinical presentation- oligo, life-threatening secondary complications

38
Q

ARPKD

A

INFANTILE!

M=F
PKHD1 - encodes fibrocystin/polyductin
CILIA related disorder

Neonates: kidney > liver
Child: liver > kidney

severe HTN - ACEi or loop diuretics
INCREASED RISK: hepatic fibrosis, biliary dysgenesis, portal hypertension

39
Q

Fanconi syndrome

A

RARE, AD, sporadic
proximal tubule dysfunction leading to excess urinary losses of AA, glucose, phos, bicarb
polyuria with increased risk for dehydration, rickets
labs: dec phos/TRP, metabolic acidosis, hypokalemia, normal glomerular function

40
Q

Lowe Syndrome
oculocerebrorenal syndrome

A

XR
gene defect leads to an enzyme deficiency –> disrupts Golgi apparatus which helps regulate specific cell lines

41
Q

exstrophy of cloaca sequence

A

primary defect of early mesoderm
leads of failure of cloacal septation and the ureters/ileum/rudimentary hindgut connected to common cloaca

associated with omphalocele

42
Q

Exstrophy of bladder sequence

A

primary defect of infraumbilical mesoderm at 6-7 weeks

43
Q

risks for HTN

A

BPD
central lines
postnatal acute renal failure

44
Q

which anti-hypertensive medication is contraindicated in neonates?

A

verapamil

45
Q

most common nephrotoxic drugs

A

acyclovir
aminoglycosides
amphotericin B
vancomycin

46
Q

first choice for dialysis in a neonate

A

peritoneal

47
Q

indications for dialysis in neonate

A

hyperkalemia
hyponatremia with symptomatic volume overload
hyperphosphatemia
metabolic acidosis
hypocalcemia
uremic symptoms
inability to provide adequate nutrition due to need for fluid restriction

48
Q

GFR depends on?

A
  1. flow in the afferent arteriole
  2. transcapillary hydraulic pressure
  3. colloid osmotic pressure
  4. permeability of the glomerular capillaries
49
Q

most common cause of acute renal failure in neonate

A

HIE

50
Q

most common cause of prenatal hydronephrosis

A

no specific cause

51
Q

cause of renal dysplasia

A

no interaction of the ureteric bud with undifferentiated mesoderm

52
Q

cause of renal agenesis

A

ureteric bud fails to develop

53
Q
A
54
Q

plasma osmolality

A
55
Q

FeNa

A
56
Q

TRP
Tubular Reabsorption of Phosphate

A
57
Q

sodium deficit

A
58
Q

congenital nephrotic syndrome

A

large hypoechoic kidneys on prenatal US
elevated maternal serum AND amniotic fluid alpha fetoprotein

presentation: edema, wide cranial sutures, large open fontanelle, premature, SGA

UA = proteinuria

Dx with genetic testing: NPHS1/S2, WT1, PLCE1

Neonatology Boards (19 decks)

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