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NURS 373: Pediatrics > week 8: caring for child and family w CVS, neuro, and MSK dysfunction > Flashcards

week 8: caring for child and family w CVS, neuro, and MSK dysfunction Flashcards

1
Q

what are the 2 types of cardiac defects

A
  1. congenital
  2. aquired
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2
Q

what is congenital cardiac defects

A

anatomic: abnormal function

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3
Q

what is acquired cardiac defects

A

disease process
- infection
- autoimmune response
- enviro factors
- familial tendencies
- meds

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4
Q

describe congenital heart disease (CHD)

A
  • 5 to 8 per 1000 live births
  • about 2 or 3 are symptomatic in 1st year of life
  • major cause of death in 1st yr of life (after prematurity)
  • most common anomaly is ventricular septal defect (VSD)
  • often children with CHD have another recognized anomaly (trisomy 21, 13, 18, +++)
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5
Q

what are the 4 circulatory changes at birth that are normal

A
  • umbilical vein; umbilical arteries
    umbilical veins + arteries construct (CUT CORD)
    low resistance to high resistance
    no blood flowing = clotting
  • foramen ovale
    foramen ovale closes so that blood can no longer move from R atrium to L atrium by-passing pulm arteries
    baby lungs working so how blood entering L atrium and pulm arteries doing their job
  • ductus arteriosus
    closes -> ligamentum arteriosus
    so blood cannot bypass lungs
    lungs in full swing
  • ductus venosus
    b4 fuctus venous closed it was taking oxygenated blood thru umbilical vein (placenta) by passing liver
    now blood from portal vein directed into liver -> blood filtered/metabolized
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6
Q

for CHD what are the 2 altered hemodynamics

A

acyanotic and cyanotic

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7
Q

what are the classification of CHD defects

A
  • increased pulmonary blood flow
  • decreased pulmonary blood flow
  • obstruction to blood flow (out of the heart)
  • mixed blood flow (saturated and desaturated blood mix within the heart)
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8
Q

in CHD describe the defect of increased pulmonary blood flow defects

A

abnormal connection between 2 sides of heart
- septum or great vessels
- increased BV on R side of heart
- increased pulmonary blood flow
- decreased systemic blood flow

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9
Q

what are examples of CHD caused by increased pulmonary blood flow defects

A
  • atrial septal defect
  • ventricular septal defect
  • patent ductus arteriosus
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10
Q

describe CHD in particular obstructive defects

A
  • blood exiting heart meets area of anatomical narrowing (stenosis) causing obstruction to blood flow
  • increased pressure proximal to defect
  • decreased pressure distal to obstruction
  • usually occurs near valve
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11
Q

give examples for CHD caused by obstructive defects

A
  • coarctation of aorta
  • aortic stenosis
  • pulmonic stenosis
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12
Q

describe CHD caused by decreased pulmonary blood flow defects

A
  • pulmonary blood flow obstructed AND anatomical defect (ASD or VSD) between R and L sides of the heart

blood has difficulty exiting R side of heart
- pressure on R side increases
- allows desat blood to shunt R to L
(results in desat in L side of heart and systemic circulation)

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13
Q

give examples of decreased pulmonary blood flow defects causing CHD

A
  • tetralogy of fallot
  • tricuspid atresia
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14
Q

describe CHD - mixed defects

A

fully saturated systemic blood flow mixes with desaturated pulmonary blood flow
- causing relative desat of systemic blood flow

  • pulmonary congestion occurs
  • CO decreased
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15
Q

examples of CHD causing mixed defects

A
  • transposition of great arteries or vessels
  • total anomalous pulmonary venous connection
  • truncus arteriosus
  • hypoplastic L heart syndrome
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16
Q

describe CHF
(congestive heart failure)

A
  • inability of heart to pump adequate amount of blood into systemic circulation
  • R or L sided failure
  • heart muscle may become damaged if left untreated
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17
Q

treatment goals for CHF

A
  • relieve symptoms
  • decrease morbidity (including risk of hospitalization)
  • slow progression of heart failure
  • improve pt survival and quality of life
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18
Q

nursing care management for CHD

A
  • assist in measures to improve cardiac function
  • monitor afterload reduction
  • decrease cardiac demands
  • reduce rep distress
  • maintain nutritional status
  • prevent infections
  • assist in measures to promote fluid loss
  • support child and family
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19
Q

hypoxemia

A
  • can adversely affect every tissue in the body
  • state where insufficient o2 to meet metabolic demands
  • identified by decreased arterial o2 sat
    (hypoxia, cyanosis, polycythemia, clubbing)
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20
Q

describe a hypercyanotic episode

A
  • severe cyanotic episode
  • associated w TOF
  • can be spontaneous
  • can be precipitated by events associated w decreased systemic vascular resistance
  • usually self-limiting
  • knee-chest position (increases systemic vascular resistance)
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21
Q

is endocarditis congenital or acquired

A

acquired

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22
Q

describe endocarditis
1. what are the most common pathogens
2. caused by routine exposure to bacteremia associated w usual daily activities

A
  1. staphylococcus aureus, streptococcus, fungus
  2. dental work, invasive procedures involving resp tract; GI/GU tract, cardiac surgery, central lines, IV drug use
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23
Q

how does endocarditis manifest clinical (s/s)

A
  • unexplained fever, malaise, wt loss
  • janeway lesions
  • osler nodes
  • roth spots
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24
Q

describe janeway lesions

A
  • nontender erythematous macules on palms and soles
  • more common in acute
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25
Q

describe osler nodes

A
  • tender subq violet nodules mostly on pads of fingers and toes
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26
Q

roth spots

A

exudative, edematous hemorrhagic lesions of the retina w pale centers

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27
Q

treatment of endocarditis

A
  • antibiotics
  • prophylaxis in high risk pt
  • surgery
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28
Q

nursing care for endocarditis

A
  • education
  • med admin
  • assessments
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29
Q

what is hypertrophic cardiomyopathy

A
  • one of the most common forms of inherited cardiomyopathy
  • hypertrophy of L ventricle
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30
Q

what is cardiomyopathy

A

refers to abnormalities of myocardium in which the ability of muscle to contract is impaired
- familial or genetic cause
- infection
- deficiency states
- metabolic abnormalities
- collagen vascular disease
- idiopathic

31
Q

clinical manifestations of cardiomyopathy (how would they present to ER)

A
  • s/s of HF - most common <1yr
  • may be asymp
  • may present w chest pain, syncope, palpitations, HF symptoms, and/or sudden cardiac arrest
  • physical exam may be normal
32
Q

cardiomyopathy diagnosis

A

ECG, exercise testing, cardiac MRI, genetic testing

33
Q

cardiomyopathy treatment

A
  • based on symptoms
  • correct the cause; if unable, aim at managing CHF and dysrhythmias
  • beta blockers - 1st line
  • cautious use of diuretics
  • implantable cardioverter/defib
  • may need heart transplant
34
Q

nursing care for cardiomyopathy

A

education + supportive care

35
Q

systemic hypertension
1. primary
2. secondary

A
  1. no identifiable cause
  2. identifiable cause - may be curable
36
Q

pediatrics systemic hypertension

A

hypertension generally secondary to structural abnormality or underlying pathology
- renal disease
- cardiovascular disease
- endocrine or neurological disorders

37
Q

clinical manifestations of HTN

A

increased BP
sympt in children - headaches, dizziness or lightheadedness, fatigue, blurred vision, chest pain, nosebleeds, SOB

38
Q

treatment of HTN

A

underlying cause
pharm and nonpharm

39
Q

nursing care for HTN

A

education
monitoring

40
Q

kawasaki disease + cause

A
  • AKA - mucocutaneous lymph node syndrome
  • acute systemic vasculitis affecting medium sized arteries, especially coronary arteries
  • unknown cause: self limiting, w fever and manifestations of acute inflammation lasting for 12 days w/o therapy
41
Q

what is the diagnostic criteria for Kawasaki Disease

A

requires > or equal days of fever plus > or equal of following 5 criteria:
- bilateral bulbar conjunctival injection
- oral mucous membrane changes, including injected or fissured lips, injected pharynx, or strawberry tongue
- peripheral extremity changes, including erythema of palms and soles, edema of hands and feet (acute phase), and periungual
- polymorphous rash
- cervical lymphadenopathy (> or equal 1 lymph node >1.5 cm in diameter)

42
Q

kawasaki disease 3 phases

A
  • acute: onest of high fever, unresponsive to antibiotics and antipyretics
  • subacute: resolution of fever and lasts until all clinical signs disappear
  • convalescent - clinical signs resolved but lab values are not normal

increased risk of coronary artery aneurysm long term

43
Q

kawasaki disease treatment

A

treat disease within 10 days w appearance of sympt
- IVIG
- Aspirin

44
Q

kawasaki disease nursing care

A
  • monitor
  • fluid balance
  • nutrition
45
Q

what are the 3 types of shock

A
  • hypovolemic
  • distributive
  • cardiogenic
46
Q

3 stages of shock

A
  • compensated shock
  • decompensated shock
  • irreversible or terminal shock
47
Q

3 managements for shock

A

ventilation
fluids
improvement of cardiac function

48
Q

cerebral palsy

A
  • group of permanent disorders of the development of movement and postures, causing activity limitations that are attributed to non-progressive disturbances that occured in the developing fetal or infant brain
  • characterized by abnormal muscle tone and coordination
  • 1.5-3 per 1000 live births
  • most common permanent physical disability in childhood
  • 15-60% of these children will also have epilepsy
49
Q

etiology of CP

A

prenatal brain abnormalities
- 80% are caused by unknown brain abnormalities
- intrauterine exposure to chorioamnionitis
- 12% of infants born prior to 36 wks
- periventricular leukomalacia
- results of shaken baby syndrome

50
Q

3 types of CP

A
  1. spastic
  2. dyskinetic
  3. ataxic
51
Q

spastic CP

A

increased muscle tone, poor control of posture, balance and coordinated movements

52
Q

dyskinetic CP

A
  • slow, worm-like movements of extremities, trunk, face, and tongue
53
Q

ataxic CP

A

rapid repetitive movements; wide gait, unable to hold objects

54
Q

diagnostic evaluation of CP

A
  • infants @ risk warrant careful assessment during early infancy
  • neurologic examination and history
  • neuroimaging
  • metabolic and genetic testing
55
Q

possible signs of CP

A
  • poor head control after age 3 mo
  • stiff or rigid limbs
  • arching back/pushing away
  • floppy tone
  • unable to sit w/o support at age 8 mo
  • clenched fists after age 3 mo
56
Q

possible behavioural signs of CP

A
  • excessive irritability
  • no smiling by age 3 mo
  • feeding difficulties: persistent tongue thrusting, frequent gagging or choking w feeds
57
Q

CP and IQ

A
  • wide variation
  • 30%-50% of CP pts are cognitively impaired
  • difficult to assess
  • rigid, atonic, and quadriparetic CP have highest incidence of profound impairment
58
Q

Goals of therapy CP

A
  • to establish locomotion, communication, and self-help skills
  • to gain optimal appearance and integration of motor functions
  • to correct associated defects as effectively as possible
  • to provide educational opportunities adapted to the child’s capabilities
  • to promote socialization experiences
59
Q

therapeutic management of CP

A
  • ankle foot braces may be worn
  • ortho surgery to correct spastic deformities
  • pharma agents to treat pain related to spasms and seizures
  • oral antispastic meds - general spasms
  • botulinum A injections - localized spasticity
  • baclofen - implanted pump - severely affected who have side effects w oral drugs
  • dental hygiene
  • physical/occupational therapy
60
Q

nursing care for CP

A
  • assist family
  • med admin
  • safety
  • ADL assistance
  • rec activities
61
Q

what is spina bifida

A
  • aka myelomeningocele
  • failure of osseous spine to close
  • commonly associated w hydrocephalus
62
Q

2 types of spina bifida

A
  1. spina bifida occulta
    - not visible externally
  2. spina bifida cystica
    - visible defect
    - saclike protrusion
63
Q

describe muscular dystrophies in children

A
  • largest group of muscular diseases in children
  • all have genetic origin w gradual degeneration of muscle fibers, progressive weakness, and wasting of skeletal muscle
  • all have increasing disability and deformity w loss of strength
64
Q

Duchenne Muscular Dystrophy (DMD)

A
  • aka pseudohypertrophic muscular dystrophy
  • most severe and most common
  • X-linked inheritance pattern; 1/3 are fresh mutations
  • 1 in 3500 male births
65
Q

characteristics of DMD

A
  • onset btwn 2-7 yrs
  • progressive muscle weakness, wasting, and contractures
  • calf muscles hypertrophy in most pts
  • progressive generalized weakness in adolesence
  • death from resp or cardiac failure
66
Q

5 diagnostic evals for DMD

A
  1. creatine kinase
    - elevated 1st 2 yrs of life (b4 clinical sympt)
  2. EMG
    - record electrical pattern in muscle when it is contracting
  3. muscle biopsy
    - most reliable way to dx DMD - shows what is happening inside the cell
  4. DNA test
    - leads to exact genetic info
  5. display of usual characteristics of the disease
67
Q

clinical manifestations of DMD

A
  • waddling gait, frequent falls, gower sign
  • lordosis
  • enlarged muscles, especially thighs and upper arms
  • profound muscular atrophy in later stages
  • varying degrees of mild cognitive impairment
68
Q

therapeutic management of DMD

A
  • no effective treatment established
  • primary goal: maintain function in unaffected muscles as long as possible
  • ROM, bracing, performance of ADLs, surgical release of contractures prn
  • physio
  • keeping kid active
  • genetic counseling for fam
69
Q

nursing care management

A
  • help child and fam cope w chronic, progressive, debilitating disease
  • design program to foster independence and activity as long as possible
  • teach kid self-help skills
  • appropriate health assistance
70
Q

describe spinal cord injuries

A
  • usually from indirect trauma
  • motor collisinos w/o child restraints
  • vertebral compression from blows to the head or butt (diving, surfing, falls from horses)
  • birth injuries from traction force on spinal cord during breech delivery
  • surgeries
71
Q

4 levels of spinal cord injuries

A
  • higher injury: more extensive damage
  • paraplegia: complete or partial paralysis of lower extremities
  • tetraplegia: lacking functional use of all 4 extremities (formerly called quadriplegia)
  • high cervical cord injury affects phrenic nerve, paralyzes diaphragm -> vent dependent
72
Q

therapeutic management of spinal cord injury

A

stabilization and transport
functional electrical stim

73
Q

nursing care management of spinal cord injury

A
  • stabilization, careful assessment, prevention of complications, maintain max function
  • rehab: evaluation and support

NURS 373: Pediatrics (16 decks)

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