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peds34 Flashcards

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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
other non-renal manifestations of alports
hearing loss that begins in childhood and is progressive; ocular abnormalities
26
management of alport
ace inhib initially; eventually renal transplant
27
multcystic renal dysplasia
most common cause of renal mass in the newborn; most often unilateral
28
autosomal recess polycystic idney disease or infantile polycystic kidney disease
uncommon; cystic kidneys with severe htn; liver involvement (cirrhosis) w portal htn can be seen
29
infants with ARPKD may have in utero hx of
oligo hydramnios, leading to pulm hypoplasia
30
prognosis of ARPKD
progressive and ultimately all patients require renal transplant
31
Aut dom PKF or adult polycystic disease
common; presents in adulthood
32
prognosis for ADPKD
sever htn and renal insuff; require transplant
33
medullary sponge kidney
occurs sporadically or may have aut dom inheritance; patient maybe symp or asymptomatic
34
nephronophthisis-medullary cystic disease complex
juvenile form is aut recessive and leads to ESRD in childhood
35
malig htn
htn associated with evidence of end organ damage
36
essential htn
htn without a clear etiology
37
most htn in kids is secondary htn or essential htn?
secondary
38
most common causes of htn in neonates
renal artery embolus after umbilical artery catheter placement; coarctation of the aorta; congenital renal disease, renal artery stenosis
39
most common causes of htn in ages 1-12 yrs
renal disease and coarctation of aorta
40
most common cause of htn in adolescents
renal disease and essential htn
41
what fundoscopic findings indicate htn?
retinal hemorrhages, papilledema, arterial-venous nicking
42
how to identify renal artery stenosis
radioisotope renal scan w administration of captopril or renal angiography
43
captopril
ACE-inhib
44
renal tubular acidosis
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
younger kids RTA presentation
growth failure and vomitting, and sometimes w life threatening metabolic acidosis
46
older kids RTA
recurrent calculi, muscle weakness, bone pain, and myalgias
47
how can you get polyuria in RTA
some forms of RTA lead to nephrocalcinosis which gives you urinary concentrating defects
48
electrolyte presentation in RTA
hyperchloremic metabolic acidosis with a normal serum anion gap
49
calculate anion gap
Na+ K+- Cl
50
when is a pos URINE anion gap seen?
distal RTA
51
distal RTA (type 1)
inability of distal renal tubules to excrete H+
52
proximal RTA (type 2)
impaired bicarb reabsoprtion y the proximal renal tubules
53
RTA type 3
variant of type 1, complicated by proximal tubular bicarb wasting during infancy
54
type 4 RTA
transient acidosis in infants and kids; hyperkalemia is the hall mark
55
treatment for RTA
type 1- small doses of oral alkali; types 2 and 3- large doses of oral alkali
56
treamtnet for type 4 RTA
furosemid to lower serum potassium, oral alkali
57
diffuse tubular disorder
manifested by hypokalemia, hypophosphatemia, and aminoacidduria, think Fanconi syndrome
58
oliguria
less than 1 mL/kg/hr
59
renal osteodystrophy
bone disease secondary to renal failure
60
nutritional management in chronic kidney disease
avoid high phosphorous, high sodium, and high potassium foods; patients need oral phosphate binder and vit D analogs to prevent renal osteodystrophy
61
when is dialysis or transplant indicated?
when GFR is 5-10% of normal
62
preferred dialysis in kids
peritoneal dialysis; but kidney transplant is the preferred treatment in kids with esrd
63
most common cause of transplant loss
acute and chronic rejection, noncompliance with meds, technical problems during surgery, and recurrent disease
64
causes of bladder outlet obstruction?
posterior urethral valves (in males), polyps, or prune belly syndrome
65
prune belly syndrome
absence of rectus muscles, bladder outlet obstruction, and, in males, cryptochoridsm
66
most common abdominal mass in newborns
multicystic dysplastic kidney, which is usually associated with atretic ureter
67
vesicoureteral refleux
urine refluxing from the urinary bladder into the ureters and the renal collecting system
68
VUR is most commonly associated with what condition?
UTIs
69
VUR genetics?
aut dom inheritance with varibale expression
70
grades of VUR
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
diagnosis of VUR
voiding cystourethrogram, in which contrast is introduced into the urinary bladder and bladder and kidneys are imaged during voiding
72
management of VUR
low dose prophylactic antibiotics until kid outgrows the VUR; kids with grade 4 or 5 reflux should be referred to urologist
73
urolithiasis
uncommon in kids; but most common stones seen in childhood are calcium, uirc acid, cystein, and mag ammonium phosphate (struvite)
74
what conditions are associated with renal stones
hypercaliuria, hyperoxaluria, distal RTA, hyperuricosuria, cystinuria, UTI, hyperPTH
75
what can cause hyperoxaluria
can be inherited or secondary to enteric malabsorption (inflamm bowel disease)
76
how can hyperuriosuria occur?
during the treatment of leukemia or lymphoma, with Lesch-nyhan syndrome, or primary gout
77
lesch-nyhan syndrome
def in an enzyme that affects how your body breaks down purines
78
UTIs and gender
more common in boys until 6 months of age, then more common in girls
79
circumcison and UTIs
before 6 months, UTIs are 10x more common in uncircumcised boys than those who are circumcised
80
proteus causign URI
associated w high urinary pH
81
urinalysis findings suggestive of UTI
leukocytes (>5-10 WBC/hpf) and a pos nitirite or leukocyte esterase on dipstick
82
who should have an imaging eval with UTI? (renal u/s and voiding cystourethrogram)
pyelonephriitis, recurrent UTI, all males, all girls less than 4 with cystitis,
83
management for uti
empiric antibiotic therapy; neonatesadmitted to hospital for IV managemen; neonates alaso get low-dose prophylactic antibitoics for at least 3 months
84
duration of treatment of UTI
10 daysl but 14 days for pyelonephritis
85
renal vein thrombosis
unilateral flank mass
86
central vs peripheral hypotonia
central is UMN; peripheral is LMN
87
associated with peripheral hypotonia
decreased fetal movements and breech presentation
88
associated with central hypotonia
seizures in the neonatal period
89
consciousness in central vs peripheral hypotonia
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
causes of hypotonia
systemic pathology (sepsis, etc.) or neural pathology
91
what imaging do you do when you suspect central hypotonia?
head CT
92
spinal muscular atrophy
anterior horn cell degeneration and infiltration of microglia and astrocytes; presents with hypotonia, weakness, and tongue fasciculations
93
second most common hereditary neuromuscular disorder
SMA
94
most common inherited neuromusc disorder
duchenne muscular dystrophy
95
types of spinal muscular atrophy
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
inheritance of spinal muscular atrophy
aut recessive
97
genetics of SMA
aut recessive, all three types caused by mutation in survival motor neuron gene (SMN1) on chrom 5
98
clinical features of SMA
weak cry, tongue fasciculations, and difficulty sucking and swallowing; bell shaped chest; frog leg poster; normal extraocular movements and norman sensory exam
99
what does muscle biopsy of kid with SMA show?
atrophy of muscle fibers that were innervated by the damaged azons
100
management of SMA
supportive

Peds (99 decks)

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