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202A > Test #5 > Flashcards

Test #5 Flashcards

1
Q

what is the mature minors doctrine

A

a minor may consent to tx for certain procedures without informing legal guardian

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2
Q

what 2 categories fall under the mature minors docterine

A
  • at any age a person can obtain treatment or prevention of pregnancy ( except sterilization)
  • at age 12 and older- drug tx, HIV testing or tx, STI testing or tx, sexual assault diagnosis or tx does not have to have informed legal guardian
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3
Q

what qualifies a person to be an emancipated minor

A

a valid marriage
if you are in active duty in the armed services
if you have court ordered declaration of emancipation
(you have to prove you are a better support for yourself than your parents. )

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4
Q

what are the ethical consent considerations

A
  • Assent

- dissent

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5
Q

what is assent

A

the children should participate in the decision making if they are capable.
the child should be taught in age appropriate ways and make sure the child agrees to the care if possible

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6
Q

what is dissent

A

-the childs refusal to assent

if the childs treatment is not time critical or essential it can be deferred.

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7
Q

can the parent refuse treatment for their child

A

yes- it is their fundamental right
it may be related to religious or cultural beliefs or the
childs quality of life.

if you suspect is is neglect - you are a mandated reporter and the situation needs to go through the judicial system.

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8
Q

what are things to focus on with a child with an illness

A
  • they are a child -not the illness
  • focus on what they can do not what they can’t
  • pay attention to their developmental age not chronilogical age (they may be developmentally delayed.)
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9
Q

how should you handle the family with a sick child

A
  • be honest with them
  • relate to them in a therapeutic way
  • awknowledge their expertise- they may have been dealing with their childs illness for a while and know what works and what doesn’t.
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10
Q

what is the goal of therapeutic play

A

to promote coping and minimize stress on the child

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11
Q

what is a child life specialist

A

a person in the hospital that designs interventions to reduce stress
they come up with things such as
injection play- the child gets to inject a teddy bear
using a kazoo for lung expansion rather than an IS
using a paper airplane for ROM

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12
Q

what are ways to promote normalization in sick kids

A
  • include the child in decisions
  • allow the family members to be apart of care
  • apply same family rules to all children
  • help the child focus on what they can do
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13
Q

how do you support parental coping

A
  • model acceptance
  • affirm the parents strengths. let them know they are doing a good job
  • refer them to support groups

let the parent know you are there for their child and that if they want to go take a break thats ok.
build trust with the family

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14
Q

how do you support the siblings of a sick child

A
  • try to explain age appropriately the illness
  • encourage them to ask questions
  • acknowledge their feelings
  • find ways to involve them in their siblings care
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15
Q

what are the different stress points with a chronically ill child

A
  • the diagnosis
  • development/lack of development milestones
  • start of schooling (worried if their child will be cared for appropriately/worry about leaving them in the care of someone else)
  • adolescence- they are growing and going through puberty
  • future placement- what will happen when they are grown
  • death of a child
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16
Q

what is a primi’s respiratory system like

A
  • compliant chest wall
  • weak respiratory muscles
  • intercostal muscles are less developed
  • obligate nose breathers

retractions are more common in infants- their diaphragm is the major respiratory muscle

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17
Q

what is the child respiratory system like

A

-they have a small lower airway
-underdeveloped cartilage -
(these two predispose the child to infection)

  • eustachian tube is short and horizontal- causing inadequate draining causing otitis media
  • a higher respiratory rate
  • use abdominal muscles to breath
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18
Q

qhow long does alveoli develop

A

until the age of 3

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19
Q

when does a child stop being a “belly breather”

A

children use their abdominal muscles to breathe until age 5

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20
Q

what is the most common illness in pediatrics

A

respiratory illness

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21
Q

when is the highest incidence of respiratory illness in a child

A

in winter and spring

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22
Q

what increases the risk for a child to get a respiratory illness

A
  • 2nd hand smoke
  • daycare
  • fatigue/anemia
  • malnutrition
  • chronic disease
  • air pollution
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23
Q

what are the upper respiratory tract infections

A

otitis media

croup

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24
Q

what are the lower respiratory tract infections

A

RSV (respiratory syncytial virus)

Inluenza

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25
Q

what are respiratory diseases

A

asthma

cystic fibrosis

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26
Q

why are pediatric patients at such a high risk for respiratory infections

A

because they have less developed immune system

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27
Q

what are the s/s of a respiratory illness

A
  • fever 100.5 or higher (ages 6mo-3yrs)
  • tachypnea
  • stiff neck/HA (s/s resembling meningitis)
  • anorexia
  • vomitting/diarrhea
  • dehydration (from vomiting/diarrhea- not necessarily the illness)
  • abdominal pain
  • nasal discharge (causing irritated skin/ulcerations)
  • sore throat- causing dysphagia leading to anorexia
  • cough
  • adventitious lung sounds
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28
Q

what can a high fever do (what temp?)

A

a high fever can cause a febrile seizure in age 3-4

most occur greater than 102.2

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29
Q

what is acute otitis media

A

effusion (fluid) and inflammation of the middle ear

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30
Q

what causes AOM

A

pathogens such as s. pneumonia or h. influenza

virus’s do not cause AOM- they predispose the child for infection by altering the body immune response allowing these ear infections bacteria to grow and cause infection

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31
Q

who is at increased risk for otitis media

A

< age 3
pacifier use
bottle feeding d/t positioning and reflux of fluid
male

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32
Q

what are s/s of otitis media

A

-earache
-bulging, opaque, red tympanic membrane
-yellow/green purulent foul smelling ear drainage
fever
irritability
vomiting
anorexia
diarrhea

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33
Q

how do you diagnose AOM

A

s/s of AOM

pneumatic otoscopy- a puff of air observing the movement of the tympanic membrane

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34
Q

how do you manage non severe AOM

A

with abx or observation and follow up

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35
Q

what abx is used for AOM

A

amoxicillin if:
< or equal to 6 months AND severe sxs of AOM

or 6-23 months AND bilateral AOM without severe sxs

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36
Q

what can you do for recurring AOM

A

placement of tympanovstomy tubes

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37
Q

what is croup

A

the inflammation and edema of the larynx, trachea and bronchi.

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38
Q

what causes croup

A

usually a viral infection

however it can be bacterial

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39
Q

what does croup sound like

A

inspiratory stridor with a barking cough

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40
Q

what are the sxs of croup

A 
-barking cough
inspiratory stridor
-retractions
repsiratory distress AT NIGHT
(usually lasts for a few hours and reside in the morning occurring again the next night)
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41
Q

how do you manage croup

A

diagnose via the s/s
-humid or cool air can help alleviate sxs. (go outside at night in the cool air or in the bathroom with a steaming shower)

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42
Q

when does a croup pt need to be hosptalized

A

if the pt has asthma.

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43
Q

what is the tx for severe croup

A

hospitalization
racemic (nebulized) epinephrine
oral dexamethazone

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44
Q

what does oral dexamethasone do

A

reduces inflammation and promotes broncho dilation

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45
Q

what is RSV

A

infected epithelial cells fuse and form syncita (giant cell)
edema and mucus obstruct the bronchioles causing hyperinflation, atelectasis and hypoxia

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46
Q

how is RSV trasmitted

A

via contact

can also be spread by droplet

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47
Q

what is the duration of RSV

A

10-14 days
the first 4-7 days the pt has mild URI sxs
the next 2-3 days the pt has tachypnea, tacky, wheezing, crackles, rhonchi, retractions, nasal flaring and cyanosis
temp up to 105.8

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48
Q

How is RSV CONFIRMED

A

A nasal wash

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49
Q

What is RSV management

A 
Rest
Humidified oxygen 
Fluids
Elevate HOB
Inhaled bronchodilator
50
Q

How do you prevent RSV

A

Hand washing
Clean toys
No smoking

51
Q

Who is a high risk RSV pt

A

Infants born between 35wks

Congenital heart disease or lung diseases

52
Q

Is there to for RSV

A

No but there is prophylaxis for high risk infants

It is synagis-an immune globulin administered Iv monthly throughout RSV season

53
Q

What is cystic fibrosis

A

A chronic multi system disorder that effects the exocrine glands of bronchioles, small intestines and pancreatic bike ducts

A thick mucus obstructs the passageway of organs

54
Q

What is an autosomal recessive trait regarding cystic fibrosis

A

Meaning if both parents are carriers the child will have a 25% chance of getting cystic fibrosis

When one parent is a carrier and one has cystic fibrosis there is a 50 % chance the child will have it

55
Q

What are the respiratory sxs of CF

Early stages leading to

A 
Early- wheezing
Dry cough
Repeat pneumonia, bronchitis
Purulent copious amounts of sputum
LEADING TO:
Adventitious lung sounds 
Dyspnea 
Tachypnea
Retractions
Hypoxia
Cyanosis
56
Q

What are the late stages of CF

A 
Emphysema 
Atelectasis
Cod pulmonale 
Chf 
Pneumothorax 
Hemotysis

Death from respiratory failure

57
Q

What are the digestive sxs of CF

A

Blockage of the pancreatic duct prevents secretion of trypsin, amylase and lipase into sm intestine
(Therefore protein cho and fats are poorly absorbed)
Leading to steatorrhea and azotorrhea

Malnutrition d/t the decreased absorption causing underweight, protuberant abdomen, barrel chest, wasted butt , thin extremities

Deficiency in vit ADEK

Meconium ileus
Rectal prolapse
Intussusception

58
Q

What may develop d/t the digestive complications of CF

A

Type one diabetes due to the damage to the pancreas

59
Q

What is exocrine problems with CF

A

The movement of salt in and out of cells is impaired

Causing a risk for hyponatremia, hypochloremia and dehydration during hot weather

60
Q

What is a sign of exocrine dysfunction related to CF

A

Very salty sweat

61
Q

What happens to the reproductive system with CF

A

Thick cervical mucus can affect the reproductive organs blocking the Soren from entering the cervix

They cause sterility in 95%males

62
Q

How is CF diagnosed

A

positive sweat chloride test on 2 occasions

DNA testing and positive newborn screens

63
Q

what are the therapy goals for CF

A

Prevent and treat pulmonary infections
maintain nutritional balace
promote psychological adjustment
hospitalize during acute pulmonary infections for IV abx and vigorous chest physical therapy

64
Q

how do you manage the respiratory problems with CF

A

percussion and postural drainage multiple times daily
forced exhalation and positive expiratory devices
inflatable best performing high frequency chest wall oscillation

65
Q

what drugs are good for CF

A

mucolytic agents
bronchodilators
anti inflammatory
abx

66
Q

why is oxygen therapy used with caution in CF pts

A

because the children are at risk for oxygen induced carbon dioxide narcosis

67
Q

what type of diet should a CF pt have

A

A high caloric, high protein diet
with pancreatic enzymes with every meal or snack.
(fats are not restricted unless steatorrhea occurs)
obtain water miscible forms of vit ADEK

extra salt in hot weather or vigorous exercise

68
Q

what other meds should a person take to protect the intestines in CF

A

H2 blockers or PPIs

69
Q

in a normal heart which side has more pressure

A

the left side of the heart has more pressure

70
Q

in a fetus where does oxygenation take place

A

in the placenta

71
Q

where does the blood from the umbilical cord go to

describe blood flow through the fetal circulation

A

a small portion goes to perfuse the liver and the remainder goes through he DUCTUS VENOSUS to the inferior vena cava
into the R atrium
through the foramen oval to the left atrium
to the left ventricle to the body

a small amount goes from the rt atrium to the rt ventricle to the pulmonary arteries- off of the pulmonary arteries, blood flows through he ductus arteriosus to the aorta to the rest of the body.
a small amount of blood stays in the pulmonary arteries and goes to the lungs for perfusion.

72
Q

explain the fetal transition to neonatal circulation

A

the lungs inflate with the first breath causing pulmonary resistance to fall
this increases pulmonary blood flow
the right side heart pressure falls

the increasing uptake of O2 by the lungs will cause the ductus arteriosus to constrict

as the pressure on the left side increases and the right side decreases the foramen oval will close

73
Q

when does the ductus venosus close

A

when the cord is clamped

74
Q

why is a pediatric heart have a fixed stroke volume

A

because the heart doesn’t have the ability to distend in the same way a mature heart does.

75
Q

how does a pediatric heart keep up with cardiac output

A

it has to pump faster because it isn’t compliant to increase pressure to increase output.

76
Q

what are early s/s of pediatric HF

A

tachypnea at rest
poor feeding
slow wt gain
lethargic

77
Q

what does left sided HF produce?

RT sided?

A

LEFT: Pulmonary edema because the blood gets clogged up and pushed back in the lungs

RIGHT: systemic congestion because it backs up in the right side of the heart pushing back out to the rest of the body
right sided will produce JVD and periorbital edema

78
Q

what med improves cardiac function and how

A

digoxin
it strenghtens the force of contractions
and
slows the heart rate to allow more time to fill

79
Q

besides digoxin, what are managements of HF

A

remove fluids with diuretics
restrict fluids (Not in infants)
low Na+ diet

vasodilate with ace inhibitors
decrease cardiac demand by keeping them calm, HOB elevated, holding them up while feeding
monitor temp - cold or fever promotes tachycardia
improve perfusion with O2
optimize nutritional intake - give small amounts more frequently and allow them to burp

80
Q

what is the cause of a murmur

A

defective valve or an abnormal heart passage

81
Q

what are the classifications for congenital heart disease

A 
increased pulmonary blood flow
decreased pulmonary blood flow
obstructive defect
acyanotic
cyanotic
82
Q

what are the conditions of increased pulmonary blood flow

A

atrial septal defect
ventricular septal defect
patent ductus arteriosus

83
Q

what are the conditions of decreased pulmonary blood flow

A

tetralogy of ballot
hypoplastic LT heart syndrome
transposition of great vessels

84
Q

what are the conditions of obructive defects

A

coarctation of aorta

85
Q

what CHD are acyanotic

A

atrial septal defect
ventricular septal defect
coarctation of aorta

86
Q

what CHD are cyanotic

A

tetralogy of fall
hypoplastic lt heart syndrome
transposition of great vessels

87
Q

what are the risk factors of CHD

A

the first 8 wks of life

maternal factors:
Rubella ETOH use
pregnant after age 40
type 1 diabetes

genetics:
chromosomal abnormalities
parents or siblings with CHD
down syndrome

88
Q

what is atrial septal defect

and its classification

A

increased pulmonary blood flow
acyanotic

an abnormal opening between the atria such as:
patent foramen ovale
the blood in the left atrium flows to the right atrium and back up to the lungs.
the body is not getting enough blood flow and the lungs are getting too much

prognosis is good

89
Q

possible s/s of atrial septal defect

A

systolic murmur

heart failure

90
Q

what is the management of atrial septal defect

A

manage if HF is present

small may close without tx.
an occlusive device can be placed via cardiac catheterization

can be surgically closed with sutures or patch

91
Q

what is a patent ductus arterioles and what calssification

A

increased pulmonary flow and acyonotic

it is the failure of the ductus arterioles to close and produces a LT to RT shunt
the blood comes into the RT atrium to the RT ventricle to the lungs to LT atrium to LT ventricle to aorta
from there the blood will flow back through the ductus arterioles back to the pulmonary artery

92
Q

what is the management of patent ductus arteriosus

A

manage if HF is present

surgically: ligation
medical: indomethacin (prostaglandin inhibitor) to constrict ductus

93
Q

what is coarctation of the aorta and what is the classification

A

it is an obstructive defect and an acyanotic defect

it is a narrowing of the aorta that restricts blood flow to the lower part of the body
causing blood to flow up the LT subclavian vein b/c it has less pressure

94
Q

what are s/s of coarctation of the aorta

A 
HA
nosebleeds
blurred vision
Arms-High BP
legs- Low BP
leg pain/cramps-claudication
LT sided HF
stroke

*may present as pulmonary edema d/t the LT side of the heart not pumping properly

95
Q

what is the management of coarctation of the aorta

A

manage HF if present

surgery: end to end anastomosis (cut out the stricted part and put the two ends together)
bypass- bypass the stricture with a graft

nonsurgical: ballon dilation with stent placement

96
Q

what is tetralogy of Fallot and classification

A

decreased pulmonary blood flow- cyanotic defect

it is the combination of 4 cardiac abnormalities:
pulmonary valve stenosis-pulmonary valve makes it hard for blood to leave, RT heart has to work harder = increased pressure

ventricular septal defect: there is a hole in between the RT and LT ventricle pushing blood LT to RT

overriding aorta: aorta sitting over the ventricular septum getting blood from both sides

rt ventricular hypertrophy: rt side works so hard it hypertrophies and the rt will have higher pressure and move blood right to left ventricle

97
Q

s/s of tetralogy of fallow

A
  • cyanosis
  • hyper cyanotic episodes (TET spells)- blue skin nails and lips after a sudden drop in O2 in the blood

-compensetory squatting- children may instinctively squat when they feel SOB, squatting improves pulmonary blood flow

fatigue
poor growth/weight gain
harsh systolic murmur
clubbing of the nails

polycythemia- increase in RBCs because the prolonged hypoxemia stimulates the kidneys to secrete erythropoietin causing production of more RBCs

98
Q

what is the management of tetralogy of fallot

A

preop management of hypoxemia and polycythemia

surgery: successful in the 1st yr of life
- patch the ventricular septal defect
- replace the pulmonary valve
- widen the pulmonary artery

99
Q

what can be done for a child with tetralogy of fallot who is not strong or big enough for surgery

A

a placement of a palliative shunt that copies the ductus arterioles that connects the subclavian to the pulmonary artery

100
Q

what is central cyanosis

A

bluish coloration of the lips, skin, nails and mucus membranes

101
Q

what does central cyanosis depend on

A

the absolute concentration of Desaturated hgb (3-5g.dL)

in a normal hgb cyanosis occurs around 85%
in an anemic pt cyanosis will occur at a lower O2 %
in a polycythemia pt they will appear cyanotic at a higher O2 sat

102
Q

what are hypoxemia interventions

A

-calm the infant
-place in a knee chest position- this mimics squatting and promotes pulmonary blood flow
-administer O2
-administer morphine- to slow HR and RR- prevents hyperpnea and hyperventilation ultimately preventing metabolic alkalosis
IV hydration

103
Q

why does a hypoxemic infant need IV hydration

A

because d/t the polycythemia
the IV fluids will help decrease the viscosity of the blood
increase the circulatory volume and reduce the risk of stroke

104
Q

what is polycythemia and what is the cause

A

overproduction of RBCs
caused by chronic hypoxemia

there is an abnormal high H&H
blood viscosity is increased

105
Q

what HCT is life threatenting

A

55%

106
Q

what does polycythemia increase the risk for

A

thromboembolism or stroke

hypo perfusion- d/t the viscosity of the blood- it is moving slower throughout the body

107
Q

what are the s/s of polycythemia

A

dyspnea
Ruddy (dusky or very red appearance)
lethargy

108
Q

what is the treatment for polycythemia

A

exchange transfusion

take 10-20mLs of the infants blood and replace it with NS

109
Q

what is hypo plastic LT heart syndrome and its classification

A

decreased pulmonary blood flow
cyanotic defect

when the left side of the heart does not develop completely, the LT side is unable to send blood to the body and the RT side is doing double duty.
there is LT to RT shunting via ASD
as the shunt begins to close the s/s become apparent

110
Q

what are the s/s of hypo plastic LT heart syndrome

A

progressive cyanosis
HF
difficulty eating
lethargy

111
Q

what is the management of hypo plastic LT heart syndrome

A

reconstructive sx - will give the pt a single ventricle

heart transplant

112
Q

what is the transposition of the great vessels and what is the classification

A

decreased pulmonary blood flow
cyanotic defect

a condition in which the pulmonary artery and the aorta are reversed
the aorta is coming off of the RT ventricle and the pulmonary artery is coming off the LT

the oxygenated blood from the LT ventricle then enters the pulmonary artery and goes back to the lungs to the LT atria to LT ventricle and around again
the deoxygenated blood from the body enters the Rt atria to the RT ventricle out the aorta to the body back to the RT atria never going to the lungs to be oxygenated.

113
Q

what are the signs and symptoms of the transposition of the great vessesl

A

cyanosis, acidosis, HF

114
Q

what is the management of transposition of the great vessels

A

prostaglandins to maintain the ductus arterioles and foramen ovale

correct via arterial switch sx in the 1st month of life

115
Q

what is Kawasaki disease

A

acute inflammation of the blood vessels
more often in boys than girls under the age of 5

it is the leading cause of acquired heart disease

116
Q

what causes Kawasakis?

A

unknown

it is not contagious

117
Q

how do you diagnose Kawasakies disease

A

based on the sxs- first 10days

need at least 4 to diagnose:

  • high fever 4-5 days duration
  • non purulent conjunctivitis
  • cracked, dry, fissured mucus membranes
  • red lips, strawberry tongue
  • swollen hands/feet
  • red palms/soles
  • generalized erythematous rash
  • enlarged cervical lymph nodes
  • tachycardia
  • *Extreme Irritability
118
Q

what are complications of Kawasakis disease

A

Coronary artery aneurysm

Myocardial infarction

119
Q

what happens in the sub acute phase of kawasakies disease

A

days 11-25- most of earlier sxs disappear

  • desquamation of fingers and toes
  • arthritis
  • HF
  • Arrythmias
  • coronary artery aneurysm develops
120
Q

how is Kawasakis disease managed

A 
High dose IV gamma globulin (IVIG) - to prevent coronary artery damage
High dose aspirin therapy 
promote hydration and comfort:
-popsicles and ice
-cool cloths
-lubricate lips,
-sponge bath,
-lotion
-quiet calm environment
-support parent
121
Q

what is the high dose aspirin for

A

anti-inflammatory: 80-100mg/kg/day until fever resolves

3-5 mg/kg/day up to 8 wks for antiplatelet aggregation

202A (5 decks)

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