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peds > exam 4 > Flashcards

exam 4 Flashcards

1
Q

management of soft tissue injury

A

RICE

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2
Q

most common broken bone in childhood

A

distal forearm

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3
Q

fracture in infants

A

huge red flag for abuse
their bones are harder to fracture

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4
Q

types of fractures

A

simple/closed
open/compound
comminuted
complicated

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5
Q

growth plate injuries

A

growth plates are the weakest of long bones.
injury here may affect future bone growth

treatment may include open reduction and internal fixation

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6
Q

bone healing times

A

the younger you are the quicker it will heal

neonates: 2-3 weeks
early childhood: 4 weeks
later childhood: 6-8 weeks
adolescents: 8-12 weeks

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7
Q

goals of fracture management

A

reduction and immobilization
restoring function
preventing deformity

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8
Q

diagnosing fracture

A

xray
history

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9
Q

assessing compartment syndrome: the 6 Ps

A

pain
pallor
pulselessness
paresthesia
paralysis
pressure

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10
Q

spica cast

A

Used for pelvic to keep legs in position

bar is to keep legs at a certain position/in place

dont use bar to move pt!

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11
Q

why is traction used in children

A

relieve fatigue of muscles
position bone ends
immobilize
prevent deformity
reduce muscle spasms

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12
Q

distraction of fracture

A

process of separating opposing bone to encourage regeneration of new bone in created space

external fixation devices are commonly used

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13
Q

developmental dysplasia of the hip (DDH)

A

misplaced hip.
Congenital
more common in girls

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14
Q

s/s of DDH

A

infants:
restricted adduction of hip
unequal gluteal folds
positive ortolani test result
positive barlow test
hip joint laxity

toddlers: walking/standing may appear off

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15
Q

management of DDH

A

from birth to 6 months: plavik harness for hip adduction and flexion. prevent harness from scratching baby-use clothes

ages 6-24 months- typically not recognized until standing/walking. need closed reduction and spica cast

as child gets older (past age 4), correction gets difficult. Need operative reduction, tenotomy, osteotomy

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16
Q

club foot

A

deformity of the foot and ankle
multiple different types: talipes varus most common

correct deformity
ponseti method (serial casting)- every couple weeks cast is changed and made straighter each time

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17
Q

osteogenesis imperfecta

A

brittle bones that fracture easy due to faulty bone mineralization or abnormal bone architecture.

med- IV pamidronate Q3 months to promote increased bone density/prevent fractures

handle these pts/babies gentle!!
they should avoid contact sports

prevent osteoporosis, malalignment, weakness, contractures

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18
Q

legg-calve-perthes disease

A

Aseptic necrosis of femoral head due to disturbed circulation to femoral head.

typically only occurs in one hip but could be bilateral

most common in white boys age 4-8

dx by MRI and XRAY

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19
Q

legg-calve-perthes disease manifestations

A

pain and limp is most evident
may also have limited ROM, soreness, stiffness

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20
Q

legg-calve-perthes disease management

A

goal is to keep head of femur in acetabulum.
femoral head collapses due to blood supply loss, it does not stay where it needs to be.

containment can be done with various appliances and devices
no weight bearing initially, rest
NSAIDs
surgery may be needed

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21
Q

slipped capital femoral epiphysis (coxa vara)

A

femoral head slips off spontaneously in a posterior-inferior direction

develops shortly before puberty
bilateral half of the time

treated by surgery

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22
Q

scholiosis

A

inward curvature of spine

most common spinal deformity

could be congenital or develop in childhood
typically idiopathic cause
generally noticeable after growth spurt

dx by XRAY and assymetry

treated by brace is not severe or surgery - rods and fusion, if severe

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23
Q

osteomyelitis

A

infection of bone

most commonly caused by staph

s/s begin abruptly, resemble arthritis and leukemia

bone scans for dx. bone cultures done for abx

ABX and good nutrition (protein) needed!
Pain management is important

may get sent with picc line for long term abx

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24
Q

cerebral palsy

A

non-progressive brain disorder affecting movement/motor skills.
causes growth and development issues as well as intellectual disabilities.

most common motor disability with childhood.

could occur prenatally or postnatal

multiple types

severity ranges person to person

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25
Q

causes of prenatal cerebral palsy

A

hypoxia
radiation
infection

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26
Q

causes of postnasal cerebral palsy

A

CNS infection
head trauma
hypoxia

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27
Q

spastic CP

A

Most common type
We see contractures. Really jerky and stiff movements due to hypotonia muscles. Muscles are flexed
Foot drop may. Sometimes will walk on tip toes if can walk, scissor legs, newborn refluxes stay throughout life

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28
Q

s/s of CP

A

pain
sleep disorders
difficulty taking PO if spasticity
communication difficulties
intellectual disabilities
hearing/vision problems
seizures
GERD
constipation/incontinence
contractures
scoliosis

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29
Q

diagnosis of CP

A

MRI and CT to role out brain damage

dx via clinical manifestations
milestones not met is common, but dont assume this is case when they arnt met

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30
Q

treatment of CP

A

give muscle relaxers and botox
most common med: Baclofen

speech therapy, OT, PT

laxatives for constipation

maximize coordinate movement, decrease pain, prevent complications

surgeries- G tube, nissen fund, spinal fusions, etc….

educate on importance of immunizations, support family

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31
Q

neural tube defects- spina bifida

A

meningocele- involves only meninges
myelomenigocele- involves meninges and spinal cord

sac could be intact or ruptured

dx by manifestations. could also be dx in utero with prenatal care

surgery will be done in 12-18 hours for best prognosis. ruptured sac is prioritized due to high infection risk

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32
Q

nursing care at birth for spina bifida

A

apply sterile dressing soaked in NS
assess/prevent infection
prevent pressure on back. keep them on stomach or side

33
Q

what are spina bifida babies commonly allergic too

A

latex

34
Q

spinal muscular atrophy (SMA)

A

1 genetic disorder that is lethal in children under 2 years of age

Degenerative disorder causing weakness and atrophy of skeletal muscles

3 types. The worst is wernig hoffman disease

NO CURE. care is supportive: mobility, nutrition, respiratory, developmental

dx by genetic analysis

35
Q

wernig-hoffman disease (SMA)

A

begins in utero or by 6 months of age

Baby cannot lift head, has trouble sucking/swallowing, loss of DTR, fasciculations of tongue, weak resp muscles

death occurs due to resp compromose

36
Q

Duchenne muscular dystrophy (DMD)

A

Due to absence of the protein dystophin, which causes muscle deterioration over time

typically dx btwn ages 3 and 7

no cure
corticosteroid meds given for clinical trial

these patients can live until they are 30, but will eventually develop cardio and resp issues

37
Q

DMD s/s

A

Pelvic weakness, waddle, clumsy, lordosis, calf muscles look tight but its just fatty buildup

gowers maneuver- use hands pushing on thighs to get up because they are so weak

38
Q

goals for treatment for DMD

A

maintain function, prevent contractures
resp care
cardiac assessment
family support

39
Q

blood flow thru heart

A

vena cava- right atrium- tricuspid valve- right vent- pulmonary valve- pulmonary artery- lungs- pulmonary vein- left atrium- mitral valve- left ventricle- aortic valve- aorta

40
Q

right side of heart

A

goes to pulmonary

only needs to pump to lungs so easy going

41
Q

left side of heart

A

goes to body

work horse of the heart

42
Q

L to R shunt heart

A

Blood from left side going to lungs, but o2 also going to body so sats are fine

pulmonary over load occurs

acryanotic

42
Q

types of congenital heart diseases

A

Patent ductus arteriosus
atrial septal defect
ventricular septal defect
tetrolgy of fallot
transposition of the great arteries (TGA)
hypoplastic left heart syndrome (HLHS)

43
Q

Patent ductus arteriosus (PDA)

A

L to R shunt
pulmonary overload

sats are normal, lungs are congested

if not treated can lead to CHF
systolic murmur may be heard

44
Q

how to treat PDA

A

indomethacin (prostaglandin inhibitor) can be successful in premies and some newborns

coil occlusion in cath lab

surgery may be needed if cant repair in cath lab- a clip on ductus would be needed which would be done through left thoracotomy

45
Q

Atrial Septal Defect (ASD)

A

left to right shunt

their is a whole in the septum which divides the atrium of heart

usually asymptomatic. referred to by murmur
exercise intolerance may be seen

unrepaired adults could have atrial dysrhythmias, emboli, etc

46
Q

ASD treatment

A

depends on size

could be closed in cath lab

surgical repair- pericardial patch. this is much more invasive and is open chest surgery. Surgical repair typically happens between age 2-5 unless symptomatic

47
Q

Ventricular Septal Defect (VSD)

A

Whole in septum between ventricles.

Left to right shunting.
can result in CHF, enlarged LV

size varies. it may close spontaneously if small

THIS IS FREQUENTLY ASSOCIATED WITH OTHER CARDIAC DEFECTS

48
Q

what septal defect is worse

A

ventricular because left ventricle is very powerful

49
Q

VSD treatment

A

complete surgical repair is procedure of choice. This is almost always the case

could be closed in the cath lab, but this is not common

50
Q

s/s of pulmonary congestion

A

tachypnea
may be sweaty due to breathing so fast
cough, wheezing, grunting
resp distress
poor feeding/growing
decreased exercise tolerance
pulmonary edema

51
Q

R to L shunt

A

decreased blood flow to the lungs, body not getting good o2

52
Q

Tetrology of Fallot

A

4 aspects:
VSD
right ventricular outflow tract obstruction (blocking blood from getting out of RV to get to lungs)
overriding aorta (misplaced)
RV hypertrophy (pumping hard due to obsruction)

53
Q

when do tet spells occur

A

crying, feeding

they exhibit blue skin

54
Q

what to do in a tet spell

A

***knee to chest position- prevents blood from circulating to lower body, changes pressure in heart
calm child
100% o2
morphine
IV fluids

55
Q

repair of TET

A

complete repair:
patch VSD
resect stenosis
enlarge RV

palliative shunt

56
Q

transportation of great arteries

A

aorta comes off right ventricle
pulmonary artery comes off left ventricle

death will occur without repair

57
Q

what to do with TGA- repair

A

we want PDA to stay open- use prostaglandins.
if it closes prior to finding out about this, we need to get a whole in the heart

surgery will then be needed to place the arteries in the right place

58
Q

obstructive congenital heart diseases

A

coarctoin of the aotra
pulmonary stenosis
aortic stenosis

59
Q

Coarc of the aorta

A

a kink/blockage of the aorta that interrupts bloodflow to the body. typically on the aorta arch

60
Q

coarc of aorta s/s

A

BP will be drastic changes from upper body to lower body because blood flow isn’t good to lower extremities due to coaction, but very high in upper extremities due to high pressure

CHF may occur when PDA closes

61
Q

treatment of coarc of the aorta

A

surgical repair- cut out coarction and sew aorta back together

balloon angioplasty may be done

manage HTN

evaluate upper and lower BP after surgery to evaluate if worked

62
Q

Kawasaki disease

A

vasculitis of small/medium sized blood vessels (coronary highest risk)

usually seen in children ages 5 and under- unknown causes, noncongenital

63
Q

s/s of Kawasaki disease

A

high persistant fever for 5 days
swelling of conjuctiva
inflamed mouth
rash
swollen red hands and feet
cervical lymphaenopathy

64
Q

Kawasaki treatment

A

IVIG to reduce incidence of cardiac abnormalities
aspirin
IVF
mouth care

65
Q

hypopituitarism

A

deficient secretion of pituitary hormones: GROWTH HORMONES, TSH, corticotropin, gonadotropin

inhibits somatic growth and development of secondary sex characteristics

66
Q

GH deficiency clinical manifestations

A

normal growth for the first year, then slowed growth curve after first year
appear overweight due to short size

67
Q

stim testing

A

kid will fast, we will give clonidine or glucagon to excrete GH, drawl blood frequently (15-30 mins) to see how much hormone is excreted, if it is not as much as we anticipated, than we know they have a deficiency

68
Q

diagnosing GH deficiency under age 3

A

do a skeletal survey (take a Xray of most of body) to decide what bones look like from a developmental standpoint

69
Q

diagnosing GH deficiency over age 3

A

we would take a x-ray of their left hand. They are looking at the growth plates. They will compare to bones of other ages.

70
Q

what are we looking for in a hand xray for GH

A

advancing bone age (older than chronological age)=less time to help them

or

younger bone age than chronological age = more time we can help them

or

normal bone age for chronological age

71
Q

Growth Hormone replacement

A

we cant help if growth plates are closed

GH replacement is done at home and is synthetic. There is not a lot of side effects. Daily injections, done sub cut. It is very successful. It is best to do these GH at night because that is when kids grow.

Changes typically take a few months. Feet grow first. An appetite increase also occurs

therapy is ended when growth rates are less than a inch/year. this is around age 14 for girls and 16 for boys, but could be different depending on bone age

72
Q

pituitary hyperfunction

A

excess GH before closure of growth plates

patients may get VERY tall.
weight is typically normal

treatment depends on cause. it is most commonly due to tumor

73
Q

acromegaly

A

excess GH after growth plate closure

bones cant grow anymore since plates are closed so it typically causes facial overgrowth

this doesnt occur until late adolecents after growth plates are closed

psychosocial support will be needed

74
Q

precocious puberty

A

sexual development before age of 9 in boys and 8 of girls

if its younger than 7 in white girls and 6 in african american girls we need to fix the underlying cause

75
Q

types of precocious puberty

A

central (CPP)- most common, caused by gonodotropin

peripheral- caused by any other hormone than gonodotropin

76
Q

management of precocious puberty

A

leuprolide (lupron)
med that slows pubertal growth, but does not reverse it.
If girls have started their periods than we dont give this

77
Q

diabetes mellitus 1

A

Born with a predisposition of this than a autoimmune process kicks in causing the pancreas to make no insulin

not revirsable

teach carb counting

78
Q

type II DM

A

more common in adults but can happen in kids

caused by insulin resistance, revirsable

peds (4 decks)

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