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Flashcards in peds22 Deck (99):
1

pityriasis alba

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

2

vitiligo

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

3

oculocutaneous albinism

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

4

tuberous sclerosis

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

5

neurofibromatosis type 1

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

6

CNS findings in tuberous sclerosis

seizures, infantile spasms, intracranial calcifications

7

CNS findings in NF-1

optic glioma, intracranial calcifications, CNS neurfibromas

8

systemic findings in TS

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

9

systemic findings in NF-1

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

10

congenital nevi

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

11

acquired nevi

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

12

alopecia

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

13

alopecia can be associated with what nail finding

pitting of nails

14

alopecia totalis vs alopecia universalis

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

15

management of alopecia

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

16

tinea capitis is a common cause of hair loss

right

17

trichotillomania

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

18

traction alopecia

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

19

telogen effluvium

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

20

most common skin disease

acne

21

noninflamm acne

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

22

inflamm acne

erythematous papules, pustules, nodules and cysts

23

systemic isotretinoin (Accutane)

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

24

lisch nodules

nf1

25

murphys sign

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

26

when is cholecystectomy indicated?

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

27

chronic abdominal pain

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

28

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

because the asymp carrier rate is very hgih

29

lactose breath hydrogen testing

to rule out lactose intolerance

30

long term prognosis of fuctional abdom pain

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

31

encopresis

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

32

stool frequency during first week of life

4x/day

33

stool freq by 1 year of life

2x/day

34

stool freq by 4 years

1x/day

35

breastfed infants defecate more frequently during the first month

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

36

most common form of fecal retention in kids

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

37

organic causes of fecal retention

hirschsprung (most common)

38

management of FFR

stool evacuation, mineral oil to soften the stool, eduaction

39

age of onset is bimodeal

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

40

inflamm in UC

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

41

toxic megacolon

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

UC gives you incr risk for what type of cancer

colon cancer

43

crohns disease inflamm

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

44

perianal disease in crohns?

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

45

drugs for IBD

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

46

serologic testing for UC

antineutrophil cytoplasmic antibody pos in 80%

47

serologic testing for crohns

anti-saccharaomyces cerevisiae pos in 70%

48

hematochezia

bright red blood passed per rectum

49

melena

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

50

ligament of treitz

suspensory muscle that marks the division between duodenum and jejunum;

51

false pos guiac test

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

52

flase neg guiac test

large ingested doses of vit C

53

mallory-weiss tear

mechanical injury to the mucosa from vomitting

54

varices

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

55

how to assess ongoing upper GI bleeding

nasogastric tube aspirate

56

elevated BUN suggests what

GI bleed

57

octreotide

vasopressin; can be used to vasoconstrict varices

58

newborn with rectal bleeding, feeding intolerance, or abdom distension

consider NEC

59

hemolytic uremic syndrome

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

60

henoch-schonlein purpura

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

61

most common cause of signif lower Gi bleed beyond infancy

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

62

allergic collitis

from sensitization to protein antigens in milk

63

infectious enterocolitis caused by what

salmonella, shigella, campylobacter, yersinia, and e coli

64

meckels diverticulum

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

painless acute rectal bleeding

classic for meckels diverticulum

66

treatment for meckels diverticulum

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

67

hemolytic uremic syndrome

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

68

henoch-schonlein purpura

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

how does H-S purpura cause GI bleeding

intussusception can be a complication, as can GI perforation

70

how can a gall bladder issue cause increased liver enzymes?

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

71

AST vs ALT

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

72

LDH

elevation is nonspec for liver disease

73

alk phos

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

74

GGTP and 5NT

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

75

how is bilirubin conjugated in the liver

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

76

how is synthetic function of the liver assessed

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

77

cholestatic jaundice

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

cholestasis gives you direct or indirect hyperbilirubinemea?

direct

79

conjugated (direct) hyperbilirubnemia most commonly caused by what?

neonatal hepatitis or biliary atresia

80

how does jaundice appear

cranially, then extends caudally

81

inspissated bile syndrome

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

82

UDP-glucuronyl trasnsferase def

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

83

gilberts syndrome

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

84

crigler-najjar type 1

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

85

crigler-najjar type 2

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

86

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

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

87

clinical features of cholesstasis

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

88

why do you get bleeding in cholestasis

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

89

most common cause of cholestasis in the newborn

neonatal hepatitis; it is idopathic; male predisposition

90

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

jaundice and hepatomegaly; FTT occurs later

91

course of neonatal jaundice

slef-liited, with full recovery in 70%

92

management of neonatal hepatitis

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

93

biliary atresia

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

94

clinical features of biliary atresia

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

kasai portoenterostomy

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

worrisome complication of kasai

cholangitis

97

only give urso acid when?

once bile flow is re-established

98

alagille syndrome

aut dom; paucity of intrahep bile ducts and multiorgan involvement

99

facial features in alagille sydnrome

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