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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

25
what stimulated renin release?
decreased renal perfusion--> hypotension, volume depletion increased sympathetic activity
26
where does ACE come from? angiotensin converting enzyme
lung endothelium
27
what does aldosterone do to the kidney?
increase Na+ reabsorption increase Cl- passively increase K+ secretion increase H+ secretion
28
what does angiotensin II do?
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
pseudohypoaldosteronism
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
causes of increased BUN
dehydration increased protein intake hypercatabolic states/hypoxia sequestered blood tissue breakdown
31
definition of hematuria
> 5 RBCs per HPF
32
cause of sediments: 1. leukocyturia 2. RBC casts 3. WBC casts 4. epithelial, granular casts 5. hyaline casts
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
lenth of kidneys on US is proportional to what?
gestational age in weeks
34
most common renal anomalies
horshoe kidney (Turner Syndrome) unilateral renal agenesis (L>R) pelvic kidney (L>R)
35
congenital nephrotic syndrome
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
renal agenesis
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
muticystic dysplastic kidney MCDK
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
ARPKD
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
Fanconi syndrome
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
Lowe Syndrome oculocerebrorenal syndrome
XR gene defect leads to an enzyme deficiency --> disrupts Golgi apparatus which helps regulate specific cell lines
41
exstrophy of cloaca sequence
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
Exstrophy of bladder sequence
primary defect of infraumbilical mesoderm at 6-7 weeks
43
risks for HTN
BPD central lines postnatal acute renal failure
44
which anti-hypertensive medication is contraindicated in neonates?
verapamil
45
most common nephrotoxic drugs
acyclovir aminoglycosides amphotericin B vancomycin
46
first choice for dialysis in a neonate
peritoneal
47
indications for dialysis in neonate
hyperkalemia hyponatremia with symptomatic volume overload hyperphosphatemia metabolic acidosis hypocalcemia uremic symptoms inability to provide adequate nutrition due to need for fluid restriction
48
GFR depends on?
1. flow in the afferent arteriole 2. transcapillary hydraulic pressure 3. colloid osmotic pressure 4. permeability of the glomerular capillaries
49
most common cause of acute renal failure in neonate
HIE
50
most common cause of prenatal hydronephrosis
no specific cause
51
cause of renal dysplasia
no interaction of the ureteric bud with undifferentiated mesoderm
52
cause of renal agenesis
ureteric bud fails to develop
53
54
plasma osmolality
55
FeNa
56
TRP Tubular Reabsorption of Phosphate
57
sodium deficit
58
congenital nephrotic syndrome
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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