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peds30 Flashcards

1
Q

treatment for anaphylaxis

A

epinephrine acutely; systemic antihistamines, steroids, beta ags are also used

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2
Q

allergic shiners

A

dark circles nder the eyes caused by venous congestion

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3
Q

dennie’s lines

A

creases under the eyes as a result of chronic edema; seen in allergic rhinitis

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4
Q

allergic salute

A

when patient uses palm of hand to elevate tip of nose to relieve itching

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5
Q

nasal smear in allergic rhinitis

A

more than 10% eosinophils suggests allergic rhinitis; lots of PMNs suggests infectious cause

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6
Q

most effective drugs for rhinitis

A

intranasal steroids; antihistamiens, intransala cromolyn sodium; decongestants

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7
Q

difference between first and second generatio antihistamines

A

second are safer and better tolerated but not any more effective

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8
Q

how does cromolyn sodium work?

A

prevents mast cell degranulation

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9
Q

side effects of decngestants

A

pseudoephedrine; insomnia, nervousness, and rebound rhinitis

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10
Q

immunotherapy

A

repeated injections of the allergen lead to better tolerance over time

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11
Q

atopic dermatitis

A

eczema; dry skin and lichenification; pruritis leads to scratching

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12
Q

when does eczema first present

A

usually in infancy; almost always before 5 yo

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13
Q

fam hx of eczema

A

yes

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14
Q

clinical features of atopic dermatiits

A

pruritis; erythema, weeping and crusting; lichenification; pigmentary changes; secondary infection is common

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15
Q

infantile eczema presentation

A

truncal and facial areas, along with the scalp; extensor surfaces more common than flexor

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16
Q

early childhood eczema

A

flexural surfaces are more severely affectd and lichenification; chronic itching

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17
Q

late childhood eczema

A

disease more localized or tendency towards remission

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18
Q

diagnosis of eczema

A

three of four critera: pruritis, personal or family hx of atopy, typical morpology and distribution, and relapsing or chronic dermatitis

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19
Q

atopy

A

predisposition toward allergies

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20
Q

treatment for eczema

A

steroids, antihistamines, baths, avoid known triggers

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21
Q

exclusive breastfeeding for the first 6 mos may decrease food allergies

A

and atopic dermatitis

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22
Q

radioallergosorbent tests (RAST)

A

identify serum IgE antibodies to spec food antigens

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23
Q

acute vs chronic urticaria

A

acute is ppt by something; chronic is greater than 6 mos and may be associated with underlying condition like malignancy or thyroid disease

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24
Q

common causes of drug allergies

A

penicillin, aspirin and other NSAIDs, and narcotics

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25
Q

most common immune def

A

igA def

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26
Q

clinical symptoms of IgA def

A

both infections and autoimmune diseases amd allergies

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27
Q

treatment of IgA def

A

igA cannot be replaced, so tx by managing infections

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28
Q

common variable immunoef

A

group of disorders characterized by hypogammaglobulinemia;

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29
Q

clinical features of common variable immunodef

A

infections and autoimmune disorders and incr risk of malignancy; normal numbers of B and T cells but T cell dysfunction

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30
Q

treatment of common variable immunodef

A

monthly IVIG; chronic diarrhea management; aggressive management of infection

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31
Q

Severe combined immunodef Disease

A

SCID; profoundly defective T and B cell function

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32
Q

clinical features of SCID

A

incr susceptibility to infection int eh first year of life; chronic diarrhea and FTT

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33
Q

diagnosis of SCID

A

persistent lymphopenia; decr T cells; severe hypogammaglobinemia; T cell response to mitogens and antigens is depressed

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34
Q

management of SCID

A

monthly IVIG; blood products should be irradiated to prevent GVH disease; PCP prophylaxis; BMT can be curative

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35
Q

ataxia telangiectasia

A

aut recessive; combined immunodef, cerebellar ataxia, oculocutaneous telangiectasia, and predisposition to malignancy

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36
Q

genetics of ataxia telangiectasia

A

utation of long arm of chrom 11; aut recess;

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37
Q

immunoglobulins in ataxia telangiectasia

A

IgE def in 85% and igA def in 75%; diminshed T cell proliferation

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38
Q

management of ataxia telangiectasia

A

treat neuro complications, treat infectiosn, monitor for malignanciesl avoid ionizing radiation

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39
Q

DiGeorge syndrome

A

immunodef, cardiac defect, abnormal facies, thymic hypoplasia, cleft palate, and hypocalcemia because of deletion on chrom 22q11

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40
Q

CATCH-22

A

digeorge syndrome; cardiac defects, abnormal facies, thymic hypoplasic, cleft palate, hypocalcemia; also immunodef

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41
Q

wiskott-aldrich syndrome

A

x-linked disorder characterized by combined immunodef, eczema, and congenital thrombocytopenia with small platelets

42
Q

immune system in wiskott-aldrich

A

decr igM; antibody response to polysach antigens is defective; cellar immune function is defective and anergy is present; no antigen-spec cytotoxic T cells; but normal number of T cells

43
Q

management of wiskot-aldrich syndrome

A

bone marrow transplant is the therapy of choice; IVIG; splenectomy cures thrombocytopenia

44
Q

x-linked (bruton’s) agammaglobulinemia

A

severe hypogammaglobulinemia and paucity of mature B cells with normal T cell number

45
Q

genetics of x-linked (bruton’s) agammaglobulinemia

A

mutation in the bruton’s tyrosine kinase gene on the x chrom; it is critical to normal B cell ontogeny

46
Q

clinical features of x-linked agammaglobinemia

A

increased susceptibility to infections with encapsulated bacteria

47
Q

diagnosis of x linked agammaglobinemia

A

decr in all ig subtypes; B cells absent; T cells present; mutation in the BTK gene

48
Q

treatment for x linked agammaglobinemia

A

monthly IVIG

49
Q

chronic granulomatous disease

A

defective neutrophil oxidative metabolism as a result of defects in NADPH system; severely impaired intracellular killing of catalase pos bacteria and some fungal pathogens

50
Q

diagnosis of chronic granulomatous disease

A

NBT test demonstrates defecetive neutrophil oxidative burst

51
Q

management of chronic granulomatous disease

A

abscesses drained and antibiotics; prophylactic bactim, itraconazole, interferon gamma, BMT is curative

52
Q

chronic granulomatous disease classic feature

A

abscess formation

53
Q

schwachman-diamond syndrome

A

decr neutrophil chemotaxis, cyclic neutropenia, and panc exocrine insuf; recurrent soft tissue infection, chronic diarrhea, and FTT

54
Q

chediak-higashi syndrome

A

variable neutropenia and thrombocytopenia; patients have partial oculocutaneous albinism

55
Q

complement def

A

genetic; most aut recessive

56
Q

deficiencies of the early components of the classical pway

A

associated with autoimmune disease, like SLE

57
Q

def of the late components of the classic pway

A

associated with increased susceptibility to meningococcal and gonoccocal infectins

58
Q

def of C1 esterase inhib causes

A

hereditary angioedema; swelling of body parts; hands, feet, bowel, airway

59
Q

CH-50

A

total serum hemolytic complement; normal means all components of complement system are present and functional

60
Q

management of complement disorders

A

management of autoimmune disease; therapy with fibrinolysis inhib and attenuated androgens (danazol) for hereditary angioedema

61
Q

henoch-schonlein purpura

A

igA mediated vasculitis

62
Q

who does H-S affect?

A

kids less than 10; median age is 5 yo; males more likely to be affected

63
Q

clinical features of H-S

A

viral or URI infection; distinctive skin, GI, and joint manifestations

64
Q

skin manifestations of H-S

A

petechiae and palpable purpuric lesions on the butt and lower exremities; edema of hands, feet, scrotum; Gi or joint symptoms may precede the diagnostic rash in 30% of patients

65
Q

joint manifestations of H-S

A

arthalgia or arthritis; knees and ankels most commonly involved

66
Q

GI manifestations of HS

A

colicky abdominal pain, GI bleeding, incr risk of intussusception

67
Q

renal manifestations of H-S

A

from mild hematuria to gross hematuria, nephrotic syndrome, and ESSRD

68
Q

H-S what do you see in lab

A

increased igA; platelet counts are normal despite the presence of petechiae and purpura (i.e. the skin rash is nonthrombocytopenia purpura)

69
Q

management of H-S purpura

A

pain control and hydration; steroids may be effective for relief of abdominal painadn arthritis

70
Q

prognosis for H-S purpura

A

most patients recover within 4 weeks; recurs in 50% of patient; long term morbidity depends on severity of nephritis

71
Q

kawasaki disease

A

acute febrile vasculitis of childhood of unknown origin; affects multiple organ systems

72
Q

most common cause of acquired heart disease in kids in the US

A

kawasaki disease

73
Q

mean age at presentation of kawasaki disease?

A

18-24 monhts

74
Q

diagnostic criteria for kawasaki

A

fever greater than 102 lasting over 5 days; four of the five clinical signs of kawasaki

75
Q

what are the five clinical signs of kawasaki

A

bilateral conjunctivitis without exudate; oropharyngeal changes (red, cracked, swollen lips); cervical adenopathy; rash; changes in distal extremities

76
Q

what kinds of changes in distal extremities do you see in kawasaki?

A

early (first 7-10 days) you see brawny edema and induration of the hands and feet with red plams and soles; later (7-10 days after fever) peeling around nails or of the distal extremitis

77
Q

other clinical features of kawasaki

A

cardiovascular manifestations, urethritis, aseptic meningitis, hydrops of the gallbladder, arthritis, anterior uveitis,

78
Q

cardiovascular manifestations in kawasaki

A

coronary artery aneurysm occur in 20% of untreated; myocarditis, CHF, arrythmias; aneurysms of the brachial arteries

79
Q

hydrops of the gallbladder

A

seen in kawasaki; acute RUQ abdominal pain

80
Q

time course of kawasaki disease

A

acute phase 1-2 weeks; subacute phase weeks to month; convalescent phase (weeks to years)

81
Q

management of kawasaki

A

IVIG wit aspirin within 10 days of onset of fever; acute phase- high dose ASA for anti-inflamm; subactute ohase- low dose ASA for antiplatele t effect; steroids if unrespons to IVIG

82
Q

prognosis for kawasaki

A

if no coronary artery disease, no long term sequealae; mortality less than 1% even with CAD; risk of atherosclerotic disease in adulthood

83
Q

juvenile rheumatoid arthritis

A

chronic joint inflamm in kids; mean age 1-3 years; more common in females

84
Q

male v female predom in JRA

A

females are more likely to have JRA EXCEPT equally likely to have systemic-onset JRA and males more likely to have late onset pauciarticular JRA

85
Q

three categories of JRA

A

pauciarticular, polyarticular, systemic-onset

86
Q

pauciarticular JRA

A

less than 4 joints involved; early onset (female predom) present at 1-5 yo; pos ANA, high risk from chronic uveitis; late-onset (male predom) present over 8 yo; HLA-B27 pos with invovlement of sacral and iliac joint s

87
Q

polyarticular

A

greater than 4 joints involved; rheum factor pos presents in kids over 8 and is more severe; rheum fact neg presents both early and late

88
Q

rheumatoid factor

A

IgM molecule against IgG

89
Q

polyarticular JRA- what joints?

A

both large and small

90
Q

systemic onset JRA

A

aka Still’s disease; high spiking fevers, transient rash, hepatosplenomegaly, lymphadenopathy; systemic features may overshadow joint sx

91
Q

descirbe the fevers of stills disease (systemic JRA)

A

occur in the late afternoon and subsequently return to baseline

92
Q

rash of stills disease

A

transient salmon colored; found on trunk and prox extremities, esp during febrile episodes; rash is evanescent (occurs with fever and then fades) and is nonpruritic

93
Q

lab findings in JRA

A

microcytic hypochromic anemia (consistent w anemia of chronic disease); rheum factor negative in most patients; ANA present in some;

94
Q

ANA in JRA

A

ANA is present in most with early onset pauci JRA; half of patients with polyart JRA; not present in kids with systemic onset JRA and late pauci

95
Q

management of JRA

A

NSAIDS, immunomodulators for more severe sx; physical therapy

96
Q

diagnostic criteria for JRA

A

age of onset less than 16 years; arthritis in at least one joint; duration of disease greater than 6 weeks; exclusion of other causes of arthritis

97
Q

age of onset SLE

A

adolescence

98
Q

most frequent cardiac manifestation of lupus

A

pericarditis

99
Q

lab findins in SLE

A

elevated ESR, anemia of chronic disease, leukopenia, thrombocytopenia, proteinuria, ANA pos; RF may be pos; anti-DS DNA antibodies; anti-smith antibodies;

100
Q

which antibodies can be used as a measure of disease progression in SLE

A

anti-DS DNA (not anti-smit)

Peds (99 decks)

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