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Peds > peds34 > Flashcards

peds34 Flashcards

1
Q

how does hypercholesterolemia happen in NS?

A

reduced plasma oncotic pressure induces increased hepatic production of plasma proteins, including lipoproteins; plasma lipid clearance is reduced because decr lipoprotein lipase in adipose tissue

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2
Q

clinical features of NS

A

edema following an URI; patients are predisposed to thrombosis;

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3
Q

patients with NS at risk for what?

A

thrombosis and infection with encapsulated organisms (strep pnumona) so may present with bacterial peritonitis, pneumonia, or sepsis

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4
Q

what does CBC show in NS

A

elevated hematocrit as a resut of hemoconcentration due to decr protein; platelet count may be elevated

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5
Q

why would you get a metabolic acidosis in NS?

A

renal tubular acidiosis

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6
Q

NS on renal u/s

A

enlarged kidneys

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7
Q

management of NS?

A

IV infusions of albumin to treat edema; no salt diet; steroids (or cyclophosphamide or cyclosporine if don’t respond); if child is febrile, do blood and urine culture and IV antibiotic if needed

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8
Q

prognosis of NS

A

mortality about 5%, usually from infection or thrombosis; mortality in kids who are steroid-resistant;

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9
Q

ESRD in NS kids?

A

the majority of kids who are steroid-resis develop but the majority of kids who are steroid sens do not develop

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10
Q

Hemolytic uremic syndrome

A

acute renal failure in the presence of microangiopathic hemolytic anemia and thrombocytopenia

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11
Q

two diff subtiypes of HUS

A

shiga toxin asociated and atypical HUS

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12
Q

most common HUS subtype seen in kids

A

shiga-toxin associated

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13
Q

most common pathogen to cause shiga-txin HUS

A

e coli

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14
Q

how does shiga toxin cause HUS

A

vascular endothelial injury, leads to platelet thrombi formation and renal ischemia

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15
Q

clinical features of shiga toxin hus?

A

diarrheal prodrome (often bloody and may be severe) followed by suden onset of hemolytic anemia, thrombocytopenia and acute renal failure

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16
Q

management of shiga toxin HUS

A

mostly supportive; transfusion for severe anemia and thrombocytopenia; anitbiotics not indicated

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17
Q

prognosis for shiga toxin HUS

A

generally good but poor prognostic indicators are high WBCs and prolonged oliguria;

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18
Q

if patients do die from shiga HUS, what do they die of?

A

complications of colitis lke toxic megacolon or from CNS complications like cerebral infarction

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19
Q

causes of atypical HUS

A

drugs (OCPs, cyclosporine, tacrolmus); inherited

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20
Q

clinical features of atypical HUS

A

same as shiga HUS but no diarrhe

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21
Q

treatment of atypical HUS

A

supportive

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22
Q

prognosis of atypical HUS

A

some patients have a chronic relapsing course; all patients with atypical HUS have a higher risk of progression to ESRD than shiga HUS

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23
Q

alport’s syndrome

A

progressive nephritis secondary to defects in type 4 collagen within the glomerular basement membrane

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24
Q

inheritance of alport

A

x linked dome

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25
Q

other non-renal manifestations of alports

A

hearing loss that begins in childhood and is progressive; ocular abnormalities

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26
Q

management of alport

A

ace inhib initially; eventually renal transplant

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27
Q

multcystic renal dysplasia

A

most common cause of renal mass in the newborn; most often unilateral

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28
Q

autosomal recess polycystic idney disease or infantile polycystic kidney disease

A

uncommon; cystic kidneys with severe htn; liver involvement (cirrhosis) w portal htn can be seen

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29
Q

infants with ARPKD may have in utero hx of

A

oligo hydramnios, leading to pulm hypoplasia

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30
Q

prognosis of ARPKD

A

progressive and ultimately all patients require renal transplant

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31
Q

Aut dom PKF or adult polycystic disease

A

common; presents in adulthood

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32
Q

prognosis for ADPKD

A

sever htn and renal insuff; require transplant

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33
Q

medullary sponge kidney

A

occurs sporadically or may have aut dom inheritance; patient maybe symp or asymptomatic

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34
Q

nephronophthisis-medullary cystic disease complex

A

juvenile form is aut recessive and leads to ESRD in childhood

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35
Q

malig htn

A

htn associated with evidence of end organ damage

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36
Q

essential htn

A

htn without a clear etiology

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37
Q

most htn in kids is secondary htn or essential htn?

A

secondary

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38
Q

most common causes of htn in neonates

A

renal artery embolus after umbilical artery catheter placement; coarctation of the aorta; congenital renal disease, renal artery stenosis

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39
Q

most common causes of htn in ages 1-12 yrs

A

renal disease and coarctation of aorta

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40
Q

most common cause of htn in adolescents

A

renal disease and essential htn

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41
Q

what fundoscopic findings indicate htn?

A

retinal hemorrhages, papilledema, arterial-venous nicking

42
Q

how to identify renal artery stenosis

A

radioisotope renal scan w administration of captopril or renal angiography

43
Q

captopril

A

ACE-inhib

44
Q

renal tubular acidosis

A

inability of the kidney to maintain normal acid/base balance because of defects in biacrb conservation or bc of defects in excretion of H ions

45
Q

younger kids RTA presentation

A

growth failure and vomitting, and sometimes w life threatening metabolic acidosis

46
Q

older kids RTA

A

recurrent calculi, muscle weakness, bone pain, and myalgias

47
Q

how can you get polyuria in RTA

A

some forms of RTA lead to nephrocalcinosis which gives you urinary concentrating defects

48
Q

electrolyte presentation in RTA

A

hyperchloremic metabolic acidosis with a normal serum anion gap

49
Q

calculate anion gap

A

Na+ K+- Cl

50
Q

when is a pos URINE anion gap seen?

A

distal RTA

51
Q

distal RTA (type 1)

A

inability of distal renal tubules to excrete H+

52
Q

proximal RTA (type 2)

A

impaired bicarb reabsoprtion y the proximal renal tubules

53
Q

RTA type 3

A

variant of type 1, complicated by proximal tubular bicarb wasting during infancy

54
Q

type 4 RTA

A

transient acidosis in infants and kids; hyperkalemia is the hall mark

55
Q

treatment for RTA

A

type 1- small doses of oral alkali; types 2 and 3- large doses of oral alkali

56
Q

treamtnet for type 4 RTA

A

furosemid to lower serum potassium, oral alkali

57
Q

diffuse tubular disorder

A

manifested by hypokalemia, hypophosphatemia, and aminoacidduria, think Fanconi syndrome

58
Q

oliguria

A

less than 1 mL/kg/hr

59
Q

renal osteodystrophy

A

bone disease secondary to renal failure

60
Q

nutritional management in chronic kidney disease

A

avoid high phosphorous, high sodium, and high potassium foods; patients need oral phosphate binder and vit D analogs to prevent renal osteodystrophy

61
Q

when is dialysis or transplant indicated?

A

when GFR is 5-10% of normal

62
Q

preferred dialysis in kids

A

peritoneal dialysis; but kidney transplant is the preferred treatment in kids with esrd

63
Q

most common cause of transplant loss

A

acute and chronic rejection, noncompliance with meds, technical problems during surgery, and recurrent disease

64
Q

causes of bladder outlet obstruction?

A

posterior urethral valves (in males), polyps, or prune belly syndrome

65
Q

prune belly syndrome

A

absence of rectus muscles, bladder outlet obstruction, and, in males, cryptochoridsm

66
Q

most common abdominal mass in newborns

A

multicystic dysplastic kidney, which is usually associated with atretic ureter

67
Q

vesicoureteral refleux

A

urine refluxing from the urinary bladder into the ureters and the renal collecting system

68
Q

VUR is most commonly associated with what condition?

A

UTIs

69
Q

VUR genetics?

A

aut dom inheritance with varibale expression

70
Q

grades of VUR

A

grade 1- reflux into distal ureter; grade 2- into renal pelvis and calyces w/o dilation; grade 3 is into calyces w dilateion; grade 4 clubbed calyces; grae 5 gross dilation of entire system

71
Q

diagnosis of VUR

A

voiding cystourethrogram, in which contrast is introduced into the urinary bladder and bladder and kidneys are imaged during voiding

72
Q

management of VUR

A

low dose prophylactic antibiotics until kid outgrows the VUR; kids with grade 4 or 5 reflux should be referred to urologist

73
Q

urolithiasis

A

uncommon in kids; but most common stones seen in childhood are calcium, uirc acid, cystein, and mag ammonium phosphate (struvite)

74
Q

what conditions are associated with renal stones

A

hypercaliuria, hyperoxaluria, distal RTA, hyperuricosuria, cystinuria, UTI, hyperPTH

75
Q

what can cause hyperoxaluria

A

can be inherited or secondary to enteric malabsorption (inflamm bowel disease)

76
Q

how can hyperuriosuria occur?

A

during the treatment of leukemia or lymphoma, with Lesch-nyhan syndrome, or primary gout

77
Q

lesch-nyhan syndrome

A

def in an enzyme that affects how your body breaks down purines

78
Q

UTIs and gender

A

more common in boys until 6 months of age, then more common in girls

79
Q

circumcison and UTIs

A

before 6 months, UTIs are 10x more common in uncircumcised boys than those who are circumcised

80
Q

proteus causign URI

A

associated w high urinary pH

81
Q

urinalysis findings suggestive of UTI

A

leukocytes (>5-10 WBC/hpf) and a pos nitirite or leukocyte esterase on dipstick

82
Q

who should have an imaging eval with UTI? (renal u/s and voiding cystourethrogram)

A

pyelonephriitis, recurrent UTI, all males, all girls less than 4 with cystitis,

83
Q

management for uti

A

empiric antibiotic therapy; neonatesadmitted to hospital for IV managemen; neonates alaso get low-dose prophylactic antibitoics for at least 3 months

84
Q

duration of treatment of UTI

A

10 daysl but 14 days for pyelonephritis

85
Q

renal vein thrombosis

A

unilateral flank mass

86
Q

central vs peripheral hypotonia

A

central is UMN; peripheral is LMN

87
Q

associated with peripheral hypotonia

A

decreased fetal movements and breech presentation

88
Q

associated with central hypotonia

A

seizures in the neonatal period

89
Q

consciousness in central vs peripheral hypotonia

A

central has an altered level of consciousness and incr DTRs, often w ankle clonus; perip- consciousness not affected but decr DTRs and muscle bulk

90
Q

causes of hypotonia

A

systemic pathology (sepsis, etc.) or neural pathology

91
Q

what imaging do you do when you suspect central hypotonia?

A

head CT

92
Q

spinal muscular atrophy

A

anterior horn cell degeneration and infiltration of microglia and astrocytes; presents with hypotonia, weakness, and tongue fasciculations

93
Q

second most common hereditary neuromuscular disorder

A

SMA

94
Q

most common inherited neuromusc disorder

A

duchenne muscular dystrophy

95
Q

types of spinal muscular atrophy

A

type 1 is infantile form with onset less than 6 mos; type 2 or intermediate form is onset 6-12 mos; type 3 or juvnile form with onset greater than 3 years

96
Q

inheritance of spinal muscular atrophy

A

aut recessive

97
Q

genetics of SMA

A

aut recessive, all three types caused by mutation in survival motor neuron gene (SMN1) on chrom 5

98
Q

clinical features of SMA

A

weak cry, tongue fasciculations, and difficulty sucking and swallowing; bell shaped chest; frog leg poster; normal extraocular movements and norman sensory exam

99
Q

what does muscle biopsy of kid with SMA show?

A

atrophy of muscle fibers that were innervated by the damaged azons

100
Q

management of SMA

A

supportive

Peds (99 decks)

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