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Peds > peds22 > Flashcards

peds22 Flashcards

1
Q

pityriasis alba

A

hypopigmented dry scaly patches, most commonly on the cheeks; treat with moisturizers and mild steroids

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2
Q

vitiligo

A

complete loss of skin pigment in patchy area; caused by melanocyte desruction; no treatment but psoralen with UV light might help

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3
Q

oculocutaneous albinism

A

genetic defect in melanin synthesis. White skin and hair, blue eyess and other eye findings; no treatment

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4
Q

tuberous sclerosis

A

ash-leaf spots (hypopigmented macules under woods light); adenoma sebaceum; shagreen patch; ungual fibromas

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5
Q

neurofibromatosis type 1

A

cafee-au-lait spot, axillary or inguinal freckling, plexiform neurofibroma or skin neurofibroma

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6
Q

CNS findings in tuberous sclerosis

A

seizures, infantile spasms, intracranial calcifications

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7
Q

CNS findings in NF-1

A

optic glioma, intracranial calcifications, CNS neurfibromas

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8
Q

systemic findings in TS

A

renal cysts, cardiac rhabdomyomas (number 1 cause of neonatal cardiac tumors), retinal astrocytomas or hamartoma; mental retardation

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9
Q

systemic findings in NF-1

A

oseeous lesions; sphenoid dysplasia; scoliosis, hypertension; learning problems

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10
Q

congenital nevi

A

first detected before 6 months of age; all have increased risk of malignancy but giant nevi have a 6-7% ifetime risk of maig melanoma; you excise giant nevi

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11
Q

acquired nevi

A

aka moles; peak ages 2-3 yo and 11-18 yo incr in size and number after puberty and pregnancy or in sun; most are junctional nevi; risk of malignancy is lower

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12
Q

alopecia

A

autoimmune lymphocyte mediated injury to the hair follicle; complete hair loss in certain areas without scalp inflamm;

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13
Q

alopecia can be associated with what nail finding

A

pitting of nails

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14
Q

alopecia totalis vs alopecia universalis

A

totalis is loss of all scalp hair; universalis is loss of all scalp and body hair

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15
Q

management of alopecia

A

most patients regrow hair in 1 year without treatment; topical or injected corticosteroids may help accelerate growth

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16
Q

tinea capitis is a common cause of hair loss

A

right

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17
Q

trichotillomania

A

hair loss due to conscious or unconscious pulling or twisting of the hair

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18
Q

traction alopecia

A

hair loss caused by constant traction (tight braids); thinned, small hairs but few broken hais

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19
Q

telogen effluvium

A

acutely stressful event (pregnancy, surgery) that converts hairs from a growing phase (anagen) to final resting phase (telogen); excessive hair loss 2 months after event

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20
Q

most common skin disease

A

acne

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21
Q

noninflamm acne

A

open comedones (black heads) and closed comedones (white heads)

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22
Q

inflamm acne

A

erythematous papules, pustules, nodules and cysts

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23
Q

systemic isotretinoin (Accutane)

A

highly effective for all kinds of acne (inflamm and noninflam); women must be tested for pregnancy before treatment and use BC

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24
Q

lisch nodules

A

nf1

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25
Q

murphys sign

A

palpation of the RUQ during inspir elcits pain; means inflamed gall bladde

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26
Q

when is cholecystectomy indicated?

A

not in all cases of cholecystitis; only if disease progresses or peritonitis develops

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27
Q

chronic abdominal pain

A

abdominal pain that occurs each month for at least 3 consec months

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28
Q

h pylori screening should be reserved for kids with sx of dyspepsia

A

because the asymp carrier rate is very hgih

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29
Q

lactose breath hydrogen testing

A

to rule out lactose intolerance

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30
Q

long term prognosis of fuctional abdom pain

A

poor; only 50% complete symptom resolution during childhood; 25% still have sx into adulthood

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31
Q

encopresis

A

developmentally inapp release of stool; it almost always asso with severe constip; seen predom in males

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32
Q

stool frequency during first week of life

A

4x/day

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33
Q

stool freq by 1 year of life

A

2x/day

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34
Q

stool freq by 4 years

A

1x/day

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35
Q

breastfed infants defecate more frequently during the first month

A

but by 4 mos, they and formula fed are at about the same rate

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36
Q

most common form of fecal retention in kids

A

functional fecal retention; results from inapprop constriction of the anal sphincter

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37
Q

organic causes of fecal retention

A

hirschsprung (most common)

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38
Q

management of FFR

A

stool evacuation, mineral oil to soften the stool, eduaction

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39
Q

age of onset is bimodeal

A

peak at 15-20 years and a second pekak after 50 year

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40
Q

inflamm in UC

A

diffuse, limited to mucosa, localized to the colon; begins in the rectum and extends proximally

41
Q

toxic megacolon

A

complication of severe UC in which disruption of the mucosal barrier allows bacteria to enter and you get colonic dilation and fever and septic shock

42
Q

UC gives you incr risk for what type of cancer

A

colon cancer

43
Q

crohns disease inflamm

A

any segment of the GI tract but usually distal ileum; skip lesions; transmural inflamm (may get fistulas, sinus tracts)

44
Q

perianal disease in crohns?

A

yes, often preceds the development of intestinal disease and presents with skin tags, fissures, fistulas, and abscesses

45
Q

drugs for IBD

A

sulfasalazine (for mild disease), corticosteroids, immunosupp agents, metrondazole (for CD, esp perianal involvement)

46
Q

serologic testing for UC

A

antineutrophil cytoplasmic antibody pos in 80%

47
Q

serologic testing for crohns

A

anti-saccharaomyces cerevisiae pos in 70%

48
Q

hematochezia

A

bright red blood passed per rectum

49
Q

melena

A

dark, tarry stools; often indicates upper GI bleed proximal to ligament of treitz

50
Q

ligament of treitz

A

suspensory muscle that marks the division between duodenum and jejunum;

51
Q

false pos guiac test

A

ingested iron, rare red meats, beets, and foods w high peroxidase content

52
Q

flase neg guiac test

A

large ingested doses of vit C

53
Q

mallory-weiss tear

A

mechanical injury to the mucosa from vomitting

54
Q

varices

A

as a result of portal hypertension or vascular malformations are uncommon but possible causes of upper GI bleeds

55
Q

how to assess ongoing upper GI bleeding

A

nasogastric tube aspirate

56
Q

elevated BUN suggests what

A

GI bleed

57
Q

octreotide

A

vasopressin; can be used to vasoconstrict varices

58
Q

newborn with rectal bleeding, feeding intolerance, or abdom distension

A

consider NEC

59
Q

hemolytic uremic syndrome

A

infection triggers hemolytic anemia, kidney failure, thrombocytopenia; most common in kids

60
Q

henoch-schonlein purpura

A

preceded by infection; palpable purpura on skin and kidney involvement; triad is purpura, athritis and abdominal pain

61
Q

most common cause of signif lower Gi bleed beyond infancy

A

juvenile polyps; bleeding is painless, intermittent, and often streaky

62
Q

allergic collitis

A

from sensitization to protein antigens in milk

63
Q

infectious enterocolitis caused by what

A

salmonella, shigella, campylobacter, yersinia, and e coli

64
Q

meckels diverticulum

A

outpouching of the bowel in the terminal ileum; important cause of lwer GI bleeding in infants and kids; the diverticulum contains ectopic gastric mucosa that produces acid

65
Q

painless acute rectal bleeding

A

classic for meckels diverticulum

66
Q

treatment for meckels diverticulum

A

use nuclear scan to identify the ectopic gastic mucosa and then resect it surgically

67
Q

hemolytic uremic syndrome

A

vasculitis characterized by microangiopathic hemolytic anemia, trombocytopenia, and acute renal failure; intestinal ulceration and infarction of the bowel causes bleeding

68
Q

henoch-schonlein purpura

A

igA mediated vasculitis with palpable purpura on the butt and loweer extremities, large joint arthralgias, renal involvement, and GI bleeding from complications like intussusception and bowel perforation

69
Q

how does H-S purpura cause GI bleeding

A

intussusception can be a complication, as can GI perforation

70
Q

how can a gall bladder issue cause increased liver enzymes?

A

damage to the biliary system causes retention of bile enzymes that damage the bilary tree and hepatocytes

71
Q

AST vs ALT

A

AST is sens but nonspecific, since also found in muscle, RBCs, and heart; ALT is very specific

72
Q

LDH

A

elevation is nonspec for liver disease

73
Q

alk phos

A

can be elevated in biliary disease and for lots of different reasons like rapid growth in a kid

74
Q

GGTP and 5NT

A

elevated in biliarydisease. 5NT is more specific than GGTP for biliary tract disease

75
Q

how is bilirubin conjugated in the liver

A

unconjugated bili is combined with glucuronide by the enzyme UDP-glucuronyl transferase in the liver to form mono and di conjugates

76
Q

how is synthetic function of the liver assessed

A

evaluating protein production (prealbumin, albumin, and prothrombin time), serum chemistries (glucose, cholesterol), and toxic clearance (lactate, ammonia)

77
Q

cholestatic jaundice

A

retention of bile within the liver; occurs when the direct component of bilirubin is greater than 2 mg/dl or 15% of total bili

78
Q

cholestasis gives you direct or indirect hyperbilirubinemea?

A

direct

79
Q

conjugated (direct) hyperbilirubnemia most commonly caused by what?

A

neonatal hepatitis or biliary atresia

80
Q

how does jaundice appear

A

cranially, then extends caudally

81
Q

inspissated bile syndrome

A

cause of indirect hyperbilirubinema; associated with hemolysis or large hematoma; conjugated hyperbilirubinemia happens later as liver meets demand

82
Q

UDP-glucuronyl trasnsferase def

A

def of enzyme that conjugates the bilirubin; seen in Gilberts syndorme, crigler-najjar syndrome type 1 and type 2

83
Q

gilberts syndrome

A

50% of enzyme activity of UDP-glucuronyl transferase is absent; mild unconjugated bilirubinemia

84
Q

crigler-najjar type 1

A

aut recessive; 100% of enzyme activity of UDP-glucuronyl transferase activity is absent; kernicterus occurs

85
Q

crigler-najjar type 2

A

aut dom; 90% of enzyme activity of UDP-glucuronyl transferase act is absent; lower likelihood of kernicterus

86
Q

causes of cholestasis (retention of direct bili in the liver)

A

infections, extrahep obstruction, intrahep obstruction, a1-antitrypsin def, TPN-associated disease

87
Q

clinical features of cholesstasis

A

jaundice, acholic or light stools, dark urine, hepatomegaly, bleeding, FTT

88
Q

why do you get bleeding in cholestasis

A

prolongation of prothrombin time as a result of diminished hepatic synthetic function

89
Q

most common cause of cholestasis in the newborn

A

neonatal hepatitis; it is idopathic; male predisposition

90
Q

presenting features in the first week of life in babies with neonatal hepatitis

A

jaundice and hepatomegaly; FTT occurs later

91
Q

course of neonatal jaundice

A

slef-liited, with full recovery in 70%

92
Q

management of neonatal hepatitis

A

nutritional support with fat soluble vitamins; TPN may be needed; also give ursodeoxycholic acid (bile acid) ; liver transplant in severe failure

93
Q

biliary atresia

A

progressive fibrosclerotic disease that affects the EXTRAhepatic bilary tree; etiology is unknown

94
Q

clinical features of biliary atresia

A

most present between the ages of 4 and 6 weeks with jaundice, dark urine, and pale stools; bili is slightly elevated; progression of disease is rapid; hepatosplenomegaly

95
Q

kasai portoenterostomy

A

roux en y intestinal loop attached directly to the porta hepatis treatment of choice to establish bile flow in biliary atresia; works best if performed by 50-70 days of age

96
Q

worrisome complication of kasai

A

cholangitis

97
Q

only give urso acid when?

A

once bile flow is re-established

98
Q

alagille syndrome

A

aut dom; paucity of intrahep bile ducts and multiorgan involvement

99
Q

facial features in alagille sydnrome

A

broad forehead, deepset wide spaced eyes, saddle nose with bulbous tip; pointed chin and large ears

Peds (99 decks)

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