module 11 pediatric

Question 1

children more susceptible to airway issues

Answer 1

infant trachea has more mucus producing glands
trachea lumen, bronchi and bronchioles are narrower
- inc. risk obstruction
- higher resistance to air flow
increased work of breathing required for ventilation
- large volume of dead space
- immature alveoli and smaller number of alveoli
- ventilation primarily done by diaphragm and abd.
infants nose breathers

Question 2

anatomical differences in peds

Answer 2

process of alveolar development continues through age 8
collateral ventilation not well developed -> inc. risk of atelectasis
lung tissue very compliant and prone to over-distention

Question 3

bronchiectasis

Answer 3

obstructive and suppurative (pus forming) disease
dilation of bronchi
acquired or congenital
peds inc risk d/t: small, soft elastic bronchi
-> easily damaged from inflammation/infection

Question 4

3 types of bronchiectasis

Answer 4

saccular: cavity like dilations
cylindrical: widening of bronchial walls
fusiform: combo of both

Question 5

bronchiectasis pathogenesis

Answer 5

inflammation -> destruction of walls in central bronchi and obliteration of peripheral bronchi/bronchioles
most common cause: H. influenza

Question 6

bronchiectasis s/s

Answer 6

chronic productive cough
copious amounts of purulent, foul, yellow/green sputum 
hemoptysis
fever
night sweats
moist crackles
rhonchi
bad breath
skin pallor

Question 7

bronchiectasis complications

Answer 7

malnutrition
recurrent pneumonia
RV failure
secondary visceral abscesses

Question 8

bronchiolitis

Answer 8

widespread inflammation of bronchioles, production of thick mucus -> airway obstruction, atelectasis and hyperinflation
RSV, influenza virus, bacteria, occasionally allergic reactions

Question 9

bronchiolitis s/s

Answer 9

wheezing r/t bronchospasm
crackles
dec. breath sounds
retractions
inc. sputum 
dyspnea 
inc. RR
low fever

Question 10

bronchiolitis pathogenesis

Answer 10

causal agent -> proliferation and necrosis of bronchiolar epithelium -> obstruction and inc. mucus production -> airway obstruction, atelectasis, hyperinflation

Question 11

bronchiolitis 3 mechanisms of obstruction

Answer 11

development of inflammatory exudate, displaces surfactant
chemical mediators -> bronchiolar constriction
inflammation -> fibrosis and narrowing

Question 12

cystic fibrosis

Answer 12

autosomal recessive disorder of exocrine glands
most common genetic lung disease
classified as either obstructive or suppurative
dysfunction of CFTR gene

Question 13

CFTR gene

Answer 13

encodes a membrane chloride channel in sweat glands, lungs, pancreas, and intestinal tract
with cystic fibrosis
- alteration in chloride and water transportation across epithelial cells
-> dehydrated mucus, hypersecretion of thick mucus that is hard to clear

Question 14

pathogenesis of cystic fibrosis

Answer 14

mucus producing glands enlarge

• excessive secretion in GI tract
• plug the glands and duct of pancreas acini and gallbladder -> dilation and fibrosis, dec. pancreatic enzymes for digestion -> inc. fat and protein in stool
• thick, tenacious mucus in bronchopulmonary system -> airway obstruction, atelectasis, hyperinflation, dec. ciliary action -> mucus stasis -> infection

Question 15

cystic fibrosis s/s

Answer 15

causes infertility in males
cough
thick sputum 
recurrent infections/bronchitis
RSHF
exercise intolerance
dyspnea
clubbing (late)
inc. retractions
unequal breath sounds/crackles
barrel chest and hyperresonant 
pancreatic insufficiency
cirrhosis of liver
DM
gallstones
nasal polymps 
fatty stools

Question 16

cystic fibrosis dx

Answer 16

ABG: hypoxemia, hypercapnia
PFT: dec. VC, flow rate, and TV. Inc. resistance, FRC
sputum cx
CXR: patchy atelectasis, bronchiectasis, obs. emphysema, cystic lung fields, peribronchial thickening
stools for fat
pilocarpine iontophoresis (sweat test)
genetic testing
72 hr stool collection w/ diet hx to determine fat absorption and fecal fat rate

Question 17

complications of cystic fibrosis

Answer 17

anorexia

dec. growth rate
dec. midarm indices

Question 18

acute tracheobronchial obstruction

Answer 18

foreign body
trauma
tumors 
swelling
malpositioned ET tube
larynogospasm
epiglotitis
post-surgical blood clot
- requires immediate tx
- w/ inhaled foreign bodies R. side affected > than left d/t angle of anatomic extension of R. main bronchus

Question 19

acute trachobronchial obstruction s/s

Answer 19

complete:
- no air movement on auscultation, may have chest movement
- inability to talk
- inc. HR
- cyanosis
- LOC
partial:
- stridor
- retractions
- wheezing
- nasal flaring
- inc. RR
- dyspnea
- inc. HR
- cyanosis (late)

Question 20

epiglottitis

Answer 20

cellulitis of epiglottis and adjacent soft tissues

• rapid and potentially fatal inflammation/ swelling and airway obstruction
• pain w/ swallowing out of proportion for physical findings
• inability to swallow saliva -> drooling
  causative:
• HIB
• pneumococci
• strep
• staph

Question 21

epilottitis s/s

Answer 21

acute respiratory distress
drooling
dysphagia
rapid onset fever
dysphonia
inspiratory stridor
retractions
oropharynx edematous and cherry red

Question 22

croup

Answer 22

acute viral and inflammatory disease of the larynx, trachea, and bronchi
causative: 
- influenza
- parainfluenza 1,2, 3
- adenovirus
- mycoplasma pneumonia
seen more in fall and winter
6mo-3yrs 
infectious agent -> edema formation in subglottic area

Question 23

croup s/s

Answer 23

hx uri
barky cough
stridor
low grade/absent fever
retractions
cyanosis

Question 24

IRDS: infant respiratory distress syndrome

Answer 24

restrictive lung disease, also known as hyaline membrane disease
charachterized by
- hemorrhagic pulmonary edema
- patchy atelectasis
- hyaline (glassy) membranes
- hallmark: hypoxemia refractory to inc. O2 supplementation

Question 25

high risk factors for IRDS

Answer 25

earlier than 25 wk gestation
- 60% in 30 wk gestation w/out antenatal steroids
- 30% in those who received steroids 
advanced gestational age
poorly controlled DM in mom
delevery afer antepartum hemorrhage
c-section w/out antecedent labor
perinatal asphyxia
multiple births
previous infant with IRDS
Rh factor incompatibility

Question 26

normal labor process

Answer 26

dec. secretion of fetal lung liquid and inc. in absorption of liquid
release of surfactant
inc. catecholamine release

Question 27

pathogenesis of IRDS

Answer 27

lack of surfactant -> inc. alveolar surface tension and dec. lung compliance

• must generate high intrathoracic pressure to maintain patent alveoli
• • infants have soft compliant chest: hard to get pressure where needed
• > inc. WOB amd dec/ ventilation -> atelectasis, inc. pulmonary vascular resistance, hypoxemia, acidosis

Question 28

IRDS and type 2 alveolar cells

Answer 28

type 2 alveolar cells produce surfactant: inc. in quantity after 32 weeks gestation

• also maintains pulmonary fluid balance
• • alteration -> leakage of proteinaceous fluid into alveoli (fibrin, debris) -> hyaline membrane formation

Question 29

secondary cause of IRDS

Answer 29

• immaturity of capillary blood supply -> V/Q mismatch -> hypoxemia and metabolic acidosis
• progressive damage to basement membrane and respiratory epithelial cells
• > edema and loss of cells -> patchy areas of atelectasis

Question 30

IRDS s/s

Answer 30

shallow resps
retractions
dec. breath sounds
nasal flaring
hypoTN
peripheral edema
low temp
oliguria
inc. RR (60-120)
dec. HR
late:
- frothy sputum
- central cyanosis
- expiratory grunting
- paradoxal respirations

Question 31

inspired O2 with IRDS

Answer 31

maintain between 85-94%

Question 32

changes in resp. system in children

Answer 32

overproduction of mucus in trachea
smaller diameter of trachea
narrow diameter of bronchi and bronchiolies
- inc. risk airway obstruction
flexible rib cage with less elastic recoil
-> external muscles elevate ribs, ventilation done by diaphragm, inc. WOB, inc. RR
glottis higher in throat
high bifurcation of trachea
larynx higher in neck
- inc. risk aspiration -> infection -> inc. WOB -> inc. RR

Question 33

changes in resp system in geriatrics

Answer 33

dec. elastin and inc. collagen
-> dec. lung elastic recoil/stiffer chest wall
-> dec. expiratory rate, dec. VC
enlargement of alveoli
-> inc. dead space and dec. surface area
-> inc. risidual volume and V/Q mismatch
-> dec. PaO2 and inc. WOB
hypertrphy of bronchial mucus glands
-> V/Q mismatch
dec. respiratory muscle strength and dec. number and motility of cilia
-> dec. effectiveness of cough
-> dec. PaO2 -> inc. WOB