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NSG 401 > Exam 1 > Flashcards

Exam 1 Flashcards

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1
Q

DiGeorge Syndrome (complete or partial)

A

T cell disorder caused by chromosome deletion

  • hypocalcemia with tetany after birth
  • cardiac defects
  • low set ears
  • Complete DiGeorge –> need thymus transplant
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2
Q

Severe Combined Immunodeficiency Disease (SCID)

A

T cell/B cell immunity is deficient or absent

  • infection, pneumonia, oral ulcers, FTT, dermatitis
  • “Bubble Boy Disease”
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3
Q

Systemic Lupus Erythematosus (SLE)

A
  • AI disease of connective tissues and BVs
  • genetic component
  • fever, wt loss, fatigue, anemia, leukopenia, thrombocytopenia
  • Sx mild to life-threatening: arthritis, nephritis, vasculitis
  • RENAL DISEASE = most common cause of morbidity/mortality
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4
Q

SLE - Criteria for Diagnosis (must have four)

A
  1. renal d/o
  2. neurologic disorders
  3. hematologic disorders
  4. immunologic disorders
  5. antinuclear antibodies
  6. butterfly rash
  7. discoid rash
  8. photosensitivity
  9. oral ulcers
  10. arthritis
  11. serositis
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5
Q

Juvenile Idiopathic Arthritis (JIA)

A

early onset = better prognosis
inflammation > scar tissue > limited ROM of joints
early closure of epiphyseal plates > altered growth
90% of children have NEGATIVE rheumatic factor

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6
Q

s/s of JIA

A

(exacerbation/remission)

  • stiffness, loss of motion, swelling, pain
  • fever, rash
  • lymphadenopathy, splenomegaly, hepatomegaly
  • loss of mobility in affected joints
  • warmth to touch, usually without erythema
  • Sx worsen with stressors
  • delayed growth
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7
Q

JIA Diagnostics

A
  • ESR & CRP determine amount of inflammation
  • antinuclear antibodies are common, but not specific to JIA
  • leukocytosis and anemia during exacerbations
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8
Q

Pharmacologic Management of JIA

A
  • NSAIDS
  • DMARDs (disease modifying antirheumatic drugs)
  • SAARDs (slow-acting antiarthritic drugs)
  • Corticosteroids
  • cytotoxic agents
  • immunologic modulators
  • biologic response modifiers
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9
Q

Other Management of JIA

A

DON’T massage - risk of emboli
DON’T immobilize - risk of loss of function
DON’T elevate - does not help pain

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10
Q

Hypersensitivity Response: anaphylaxis

A

within seconds to minutes of exposure

  • IgE
  • most common type of allergy = BEE STING/POLLEN
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11
Q

Hypersensitivity Response: cytotoxic reaction

A

within 15-30 min of exposure

  • cell surface antigens (blood)
  • antigen/antibody binding activates complement
  • includes transfusions, Rh incompatibility, ITP, and AI hemolytic anemia
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12
Q

Hypersensitivity Response: immune complex disease

A

generally peaks at 6 hours

  • excess antigen/antibody complexes in circulation deposit into tissues
  • results in local inflammation
  • includes SLE, rheumatic fever, glomerulonephritis, rheumatoid arthritis
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13
Q

Hypersensitivity Response: delayed hypersensitivity

A

takes 24-27 hours to fully develop

  • antigen processed by macrophages and presented to T cells
  • sensitized T cells release lymphokines
  • includes contact dermatitis, poison ivy, tuberculin
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14
Q

foods to avoid with latex allergy

A

bananas, kiwis, avocados

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15
Q

IVIG

A

used to treat immune thrombocytopenic purpura (ITP), Kawasaki disease, primary immunodeficiency d/o’s, hemolytic anemia, AIDS, etc.

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16
Q

Cancer: most common malignancies in PEDS

A
  • leukemia
  • meduloblastoma
  • astrocytomas
  • ependymoma
  • gliomas
  • neuroblastoma
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17
Q

neuroblastoma

A

most commonly occurring tumor outside the cranium (IN THE NERVE TISSUE)
commonly a smooth, hard, non-tender mass that can occur anywhere along the SNS chain (commonly abdominal, adrenal, thoracic, and cervical)

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18
Q

Wilm’s tumor (nephroblastoma)

A

!!DO NOT PALPATE!!
intrarenal tumor (common abdominal tumor)
-associated with congenital anomalies: aniridia (no iris), hemohypertrophy (abnormal growth of half the body or a structure), GI anomalies, nevi, hemartomas
-possible genetic link

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19
Q

“bubble boy disease”

A

severe combined immunodeficiency disease (SCID)

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20
Q

Which cardiac defect has a machine-like murmur?

A

PDA

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21
Q

In which defect are peripheral pulses diminished in the LOWER extremities?

A

coarctation of the aorta

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22
Q

Treatment for Kawasaki’s Disease

A

IVIG

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23
Q

Kawasaki’s can cause what in relation to the heart?

A

vasculitis (inflammation of BV’s) – can l/t ANEURYSMS

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24
Q

Indomethacin: watch for _______

A

decreased platelets, decreased urinary output, and necrotizing enterocolitis

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25
Prostaglandin E1 is used for ?
to keep ductus arteriosus OPEN
26
Respiratory SE of Prostaglandin E1
apnea --> infants must be on ventilators
27
Digoxin
Tx for CHF
28
Legs-Calves-Perthes Disease [avg duration]
can take up to 3-4 years to resolve
29
Ex of when COMPARTMENT SYNDROME can occur?
with fractures/injuries to bones
30
Fractures: NURSING ALERT!!
- Pain unrelieved by meds 1 hr after administration - Swelling - Discoloration (pallor, cyanosis) of exposed parts - Decreased pulses - Decreased temp of extremities - Inability to move distal parts
31
bone healing: neonates
2-3 weeks
32
bone healing: early childhood
4 weeks
33
bone healing: later childhood
6-8 weeks
34
bone healing: adolescence
8-12 weeks
35
keystone Sx of DDH in infant
unequal gluteal folds when infant is prone
36
talipes varus
bending inward
37
talipes valgus
bending out
38
talipes equinus
plantar flexion, toes lower than heel
39
talipes calcaneus
dorsiflexion, toes above the heel
40
osteogenesis imperfecta (OI)
group of heterogeneous inherited CONNECTIVE TISSUE disorders
41
Manifestations of OI
- excessive fragility - bone defects - reduced cortical thickness of bones - hyperextensibility of ligaments
42
Classifications of OI: Type I
mild fragility, blue sclera, some cases abnormal dentition
43
Classifications of OI: Type II
* *LETHAL [stillborn or die in early infancy] - severe bone fragility w/ multiple fractures at birth - autosomal recessive inheritance
44
Classifications of OI: Type III
- severe bone fragility l/t severe progressive deformities - blue sclera - marked growth failure - most die in childhood d/t cardio-respiratory failure
45
Classifications of OI: Type IV
- mild to moderate bone fragility - normal sclera - some cases abnormal dentition - short stature - variable deformity - autosomal dominant
46
Therapeutic Management of OI
- primarily supportive care - bone marrow transplant for severe OI (experimental) - Drugs are of limited benefit
47
NSG Care Management of OI
- caution w/ handling to prevent fractures - family edu. - occupational planning and genetic counseling - maximize independence and minimize fracture risks - OI Foundation as resource
48
Muscular Dystrophies
- group of inherited diseases characterized by muscle fiber degeneration and muscle wasting - starts from LE and moves up the body * *Most common form: Duchenne (x-linked)
49
Manifestation of MD
(vary w/ type) - generalized weakness and hypotonia - difficulty sucking/swallowing - some ocular problems - in childhood, parents may notice child tripping, toe walking, enlarged calf muscles
50
MD progression up the body
can potentially cause scoliosis, musculoskeletal conditions, cardiomyopathy, difficulty ingesting foods, respiratory distress
51
Management of MD
steroids can help preserve walking and pulmonary function for longer -HIGH fiber, HIGH protein, LOW calorie diet
52
Legg-Calve-Perthes Disease
- self limiting - idiopathic - more common in males age 4-8 - avascular necrosis of femoral head --> disturbed circulation to the femoral head with ischemic aseptic necrosis
53
Definitive Dx of Legg-Calve-Perthes Disease
MRI
54
Slipped Capital Femoral Epiphyses
- spontaneous displacement of the proximal femoral epiphyses in a posterior and inferior direction - EMERGENCY ; requires early Dx and Tx (surgery) - seen most often in males and obese children - bedrest initially - Sx: hip/thigh/knee pain
55
osteomyelitis
- inflammation and infection of bony tissue - marked leukocytosis - Dx: bone scans - Increased ESR and CRP due to inflammation - ANY organism can cause osteomyelitis
56
types of osteomyelitis
exogenous: infectious agent invades bone following penetrating wound, open fracture, etc. hematogenous: PREEXISTING INFECTION spreads to bone
57
Tx for osteomyelitis
prompt, vigorous, IV ABX for 3-4 weeks or up to several months [may need central line for LT ABX]
58
Tx for PDA
Indomethacin - CLOSES ductus arteriosus
59
Four Parts of TET of Fallot
1. Pulmonic Stenosis: narrowing of pulmonary valve which prevents BF from RV to pulmonary artery 2. Right ventricular hypertrophy: heart muscle thickens bc RV is pumping against high pressure 3. Ventricular septal defect: hole in the ventricular septum 4. Overriding of the aorta: aortic valve enlarged and looks like it arises from both RV and LV
60
TET spells
rapid drop in O2 that l/t cyanosis; can occur after feeding, crying, having a BM, or kicking legs upon walking **knee-to-chest position is best for the child
61
Therapeutic Management of Congestive HF
- take apical pulse for 1 min. and listen to heart sounds - I&O - provide rest periods - daily weights - frequent, small meals - high calorie snacks - change positions frequently - low sodium diet - Meds: digoxin, ACE-I, BB, Lasix
62
Complications of Kawasaki's Disease
- Vasculitis ; can l/t aneurysms - inflamed coronaries, heart muscle, heart lining/valves, and outer membrane of heart - arrhythmias and abnormal function of the heart valves can develop
63
Sickle Cell Anemia
- genetic mutation (hereditary) - Autosomal recessive - sickle cells obstruct the BV's so normal RBC's cannot get through > ischemic pain > chronic pain (round the clock pain meds for pts) - avascular necrosis of bone marrow = extreme pain
64
Management of SCA
HYDRATION AND OXYGENATION OF SICKLED CELLS
65
Thalassemias Pathophysiology
anemia results from defective synthesis of Hgb, structurally impaired RBCs, and shortened life of RBCs -CHRONIC hypoxia
66
Alpha Thalassemia
- occurs in Chinese, Thai, African, and Mediterranean descent - usually results in "hydrops fetalis" - build up of bodily fluids in neonates
67
Beta Thalassemias
- occurs in Greeks, Italians, and Syrians - most common - Complications: RBCs fragile and easily destroyed (body tries to increase production of fetal Hgb) - As hemolysis increases, deposits in the skin l/t bronze skin color; LT may see liver failure, endocrine complications, HF
68
Complications of Beta Thalassemias
- frequent transfusions: hemosiderosis and alloimmunization - cardiac complications are LEADING CAUSE OF DEATH in these pts. - Chelating drugs (Desferal) allows Fe to be excreted in the urine - blood transfusions q2-4 weeks to maintain normal Hgb levels

NSG 401 (1 decks)

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