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Peds > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

A&P Respiration

A

diaphragmatic breathers (stomach rises & falls), ribs & sternum too pliable for intercostal muscles, less alveoli which increases exponentially, paradoxical chest movement, increased O2 consumption; biggest difference = airway is size of straw

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2
Q

Respiration – S/S

A

1 sign of change in oxygenation = restlessness

LOC, alteration in perfusion (color change, cap refill, decreased pulse ox, cool skin, mottling), increased HR & RR, nasal flaring, decreased urine output, dyspnea, grunting, retractions, stridor, wheezing, clubbing, intercostal bulging

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3
Q

Respiration – Assessment

A

LOC & response to environment, RR, resp effort (use of accessory muscles & work of breathing), color of skin/mucous membranes, lung sounds; hx including urine output, activity level

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4
Q

Retractions

A

usually starts lower & moves up (higher is worse); subcostal (below ribs), substernal, intercostal, suprasternal, clavicular

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5
Q

Respiratory distress

A

stridor (high pitched noisy respiration indicating upper airway narrowing), wheezing, grunting (body’s attempt to create PEEP), retractions (sinking in of soft tissue indicates use of accessory muscles to improve respiration

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6
Q

Resp distress – Moderate to Severe

A

anxious/restless, more retractions, color changes, wheezing/stridor, O2 going down w/ HR going up, head bobbing

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7
Q

Resp distress – Mild

A

mild retractions that start low, maybe a little pale, not much nasal flaring, responding to environment

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8
Q

O2

A

use nasal cannula but don’t go above 4L on little guys; only use mask if really need a higher O2% (kids will fight it)

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9
Q

Asthma

A

hyperresponsiveness of the airway = inflammation, constriction & mucus secretion

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10
Q

Asthma Peak Flow – Green

A

80-100% of kid’s personal best; no symptoms, continue maintenance tx

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11
Q

Asthma Peak Flow – Yellow

A

50-79%; acute exacerbation may be occurring, may need to increase maintenance tx, call Dr if kid stays here

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12
Q

Asthma Peak Flow – Red

A

less than 50%; medical alert b/c severe airway narrowing may be occurring, short-acting bronchodilator & notify Dr immediately if doesn’t come up to yellow or green

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13
Q

Croup

A

named by location of inflammation/infection (acute epiglottis/supraglottis, acute laryngotracheobronchitis (LTB), acute spasmodic laryngitis, acute tracheitis

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14
Q

Croup – S/S Acute Tracehitis

A

cough (brassy or barky sounds like a seal) & varying degrees of inspiratory stridor & resp distress (d/t inflammation/obstruction of larynx)

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15
Q

Croup – S/S Acute Epiglottis (Supraglottis)

A

more acute rapid onset w/ high fever, toxic looking, tripod position (w/ drooling); no throat inspection w/o prep to intubate

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16
Q

Croup – Tx Acute Epiglottis

A

IV antibiotics & corticosteroids

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17
Q

Croup – S/S Acute LTB

A

slower onset, less of a temp, usually a little older kids, usually viral & preceded by URI, most common form; tx by maintaining airway w/ cool mist (outside in winter), nebulized epinephrine (bronchodilate & open airways), steroids

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18
Q

Pneumonia – viral

A

supportive (fluids, cool mist, antipyretics, O2) & is more frequent than bacterial vs. bacterial = give antibiotics on time, antipyretics, O2, hydration, possibly thoracentesis (if pleural perfusion) teaching family w/ antibiotics

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19
Q

Suctioning

A

0.5-1cm beyond end of trach
babies 80 - 100 mmHg
2-3 = 100 mmHg
older kids 100-120 mmHg

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20
Q

CF – path and S/S

A

common organisms that cause infection are pseudomonas, streptococcus & pneumococcus; expect manifestations of long-term hypoxia (ie barrel chest & clubbing); increased risk for infection d/t depressed immune system & thick pulmonary secretions

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21
Q

CF – diet

A

high protein, low-moderate carbs & mod-high fat; need pancreatic enzymes before any meals/snacks; need fat-soluble vitamins

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22
Q

CV – health Hx

A

maternal rubella during PG, maternal ETOH or drugs, family hx of CHD (congenital heart defect), chromosomal abnormalities, presence of murmurs & age 1st detected, feeding problems (fatigue, FTT, diaphoresis during feedings), resp difficulties (tachypnea, DOE, SOB, cyanosis, frequent URIs), chronic fatigue/activity intolerance

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23
Q

CV – physical findings in child

A

FTT w/ minimal fat, cyanosis/dusky/pallor, periorbital & peripheral edema, pulse alterations, tachypnea & use of accessory muscles, hypotension or unequal BP b/w upper & lower extremities (coarctation of aorta), engorged neck veins, murmurs/bruits/thrills, abdominal distension, hepatomegaly, splenomegaly, decreased activity, diaphoretic

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24
Q

Murmurs

A

organic (CHD or acquired heart defect w or w/o physiologic abnormality)

innocent (no anatomic or physiologic abnormality)

functional (no cardiac defect but physiologic eg anemia)

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25
Q

Syndromes with high CHD

A

Trisomy 13, 18 & 21

26
Q

Eisenmenger Syndrome

A

left to right shunt becomes right to left shunt = cyanosis which increases pulmonary vascular resistance (PVR); occurs after prolonged period of increased pulmonary blood flow & can lead to death

27
Q

Increased pulmonary blood-flow (acyanotic)

A

ASD VSD PDA

28
Q

ASD

A

left to right shunt so some of oxygenated blood goes back to r. side of heart & lungs; s/s: activity intolerance, fatigue & orthopnea, also resp issues (ie infections b/c lungs working harder)

29
Q

ASD Tx

A

often spontaneous closure, supportive tx w/ diuretic until old enough for closure

30
Q

VSD

A

most common, left to right shunt

s/s – overactive precordium, harsh systolic murmur, increased ventricular & pulmonary artery pressure, FTT, HF, dyspnea, frequent URIs, small = asymptomatic

31
Q

VSD Tx

A

~1/2 spontaneously close, lg = managed w/ Dig & diuretics, sx closure before irreversible pulmonary disease (periodic caths to check pressures until repair d/t risk of Eisenmenger)

palliative tx – pulmonary artery banding (multiple VSDs or complex heart anatomy): assess for tightening of band

32
Q

PDA

A

lg channel b/w pulmonary artery & descending aorta supposed to close at birth, increased incidence in premies (increased prostaglandins keep it open, may also have lung disease); sometimes w/ major defect must keep this open intentionally

s/s – sm may be asymptomatic, frequent URIs, premies present sooner, older kids slight growth retardation & activity intolerance

33
Q

PDA Tx

A

some close spontaneously, admin Indomethacin to premie will close it, sx closure w/ ligation or VATS, nonsx w/ coils in cath lab

34
Q

Decreased pulmonary blood-flow (cyanotic)

A

Tetraology of Fallot

Tricuspid atresia

35
Q

TOF – patho

A

VSD
Overriding Aorta
Pulmonary Stenosis
R. Ventricular Hypertrophy

36
Q

TOF – S/S

A

cyanosis, clubbing, dyspnea, thrill, resp distress during feedings, polycythemia (imp to prevent dehydration); infants = intense cyanosis when PDA closes, severe DOE, syncope, limpness, convulsions; older kids = squatting position

37
Q

TOF – Tx

A

O2, Propranolol, Morphine, newborns get Inderal (BB) until sx repair (complex defects like this are staged repairs that start w/ palliative sx to get more blood to lungs

38
Q

Hypercyanotic episode

A

intense cyanosis, extreme fussiness, pallor, tachypnea, flaccidity, possible LOC, common in AM, precipitated by crying, defecation & feeding (increases R-L shunting); can lead to seizures, CVA & death

39
Q

Hypercyanotic episode – Tx

A

be calm & place sm kids & infants in knee-chest position (reduces desaturated venous return from legs & increases systemic vascular resistance which diverts more blood to pulmonary artery & lungs to get oxygenated)

40
Q

Obstruction of blood-flow from heart (acyanotic)

A

Coarctation of Aorta, Aortic Stenosis/Atresia, Pulmonic Stenosis/Atresia; big issue is CHF

41
Q

COA

A

narrowing of aorta near ductus arteriosus = increased pressure proximal & decreased pressure distally; s/s – high BP & bounding pulses in upper extremities, weak/absent pulses in lower extremities, BP difference 8-10mmHg b/w upper & lower needs to be evaluated, O2 sat differences b/w upper & lower extremities, present w/ s/s of CHF, infants present w/ near death state (severely acidotic & hypotensive), older kids present w/ dizziness, h/a, fainting & epistaxis

42
Q

Mixed Blood Flow – patho

A

major heart defects

transposition of the great vessels (TGV), hypoplastic left heart syndrome (HLHS), truncus arteriosus

43
Q

Mixed Blood Flow – Tx

A

O2 is of little benefit, may enlarge or create ASD for more mixing, Nitric Oxide (decrease PVR, increase pulmonary bloodflow & reduce cyanosis), Prostoglandin to dilate ductus arteriosus, sx (arterial switch – put the 2 great vessels where they’re supposed to go)

44
Q

CHF – causes

A 
CHD
increased pulmonary blood-flow
obstruction of blood-flow from heart 
also
Cardiomyopathies
Arrhythmias
Hypertension
Pulmonary Embolism or Chronic Lung Disease
Severe Hemorrhage or Anemia
45
Q

Right Ventricular Heart Failure

A

Less blood is oxygenated

Pressure increases in the right atrium and systemic venous circulation, which leads to edema of the extremities

46
Q

Left Ventricular Heart Failure

A

Left Ventricle is unable to pump blood into systemic circulation
Pressure increase in the Left Atrium and the Pulmonary Veins
Lungs become congested with blood which leads to increased pulmonary pressure and pulmonary edema

47
Q

CHF Nx

A

dig, antiHTN ie ACEIs (monitor BP), diuretics, fluid & Na restriction, decrease cardiac demands (neutral thermal environment, tx any infections, reduce effort of breathing, sedate fussy baby w/ Chloral hydrate, cluster care), improve oxygenation (used carefully in kids w/ complex heart defects b/c O2 is a vasodilator = decrease PVR = increased bloodflow to lungs)
Fluid restriction – may be on ½ maintenance d/t fluid retention to prevent further overload

48
Q

Digoxin

A

ECG should be done before initial dose is given & always check for bradycardia; good for peds d/t rapid onset & short half-life

infants very rarely receive more than 1mL (50mcg) in 1 dose anything higher is warning of an error

49
Q

Digoxin – good

A

inotropic
chonotropic
diuretic – inc renal perfusion = pee more

50
Q

Rheumatic fever

A

systemic inflammatory disease caused by Group A Beta-Hemolytic Strep (GABHS) & Carditis is the big issue; s/s – carditis (tachycardia which is higher than would be expected w/ fever), arthritis, GI issues, thrombocytopenia, h/a, tinnitus; tx – lifelong antibiotic prophylaxis, anti-inflammatory (ASA), digoxin

51
Q

SVT

A

HR 200-300; s/s – palpitations, dizziness, diaphoresis, infants: poor feeding, pallor & extreme fussiness; tx – vagal maneuvers (coughing, face in ice cold H2O), adenosine, cardioversion, propranolol, amiodarone, ablation (NPO & explain procedure)

52
Q

Fe deficiency anemia

A

– s/s – fatigue, pallor, decreased O2, decreased Hgb/Hct, decreased SIC & increased TIBC; starting cow’s milk too early or too much (milk baby); tx – oral ferrous sulfate, Vit C, O2 by nasal cannula, Fe fortified formula & rice cereal

53
Q

Digoxin alert

A

A decrease in serum potassium level enhances the effects of Digoxin, increasing the risk of digoxin toxicity.
An increase in serum potassium levels diminish digoxins’ effect – CHECK FOR HYPOKALEMIA
Therefore serum potassium levels (normal range 3.5-5.5) must be carefully monitored

54
Q

Enemas

A

use NS; infant 120-240mL insert 1”, 2-4yrs 240-360mL insert 2”

55
Q

Esophageal atresia & tracheoesophageal fistula

A

excessive mucus, continuous or sporadic resp distress, repeated regurgitations; 3 C’s of T-E fistulas = coughing, choking & cyanosis
Preop – NPO w/ frequent mouth suctioning, antibiotics, fluids & O2

56
Q

pyloric stenosis

A

normal 1st 2 weeks of life then start vomiting or regurgitation initially progressing to projectile vomiting (hallmark symptom), vomit may occur during/right after feeding or be delayed & then infant will be very hungry

57
Q

GERD – S/S

A

usually start during 1st week of life, chronic vomiting or regurgitation, cardiorespiratory symptoms, hematemesis; doesn’t become GERD until complications such as FTT, bleeding or dysphagia develop

58
Q

GERD – Dx and Tx

A

dx – barium esophogram, esophageal pH monitoring, scintigraphic studies (radioactive nucleotide added to formula)
Tx – sm/slow feedings, frequent burping while feeding, formula thickened w/ rice cereal, upright prone (holding on shoulder), supine or side lying 1hr after heating, HOB elevated (reflux harness); antacids or H2 antagonists, PPIs, prokinetics (ie Reglan & Bethenechol

NISSEN

59
Q

Calculating dehydration

A

Pre-illness weight in grams - illness weight in grams / pre-illness weight in Kgs = mls/kg loss

Mild Fluid Loss/Dehydration is < 50 mls/Kg
Moderate Fluid Loss/Dehydration is 51-99 mls/Kg
Severe Fluid Loss/Dehydration is > 100 mls/kg

60
Q

Two Major Manifestations – CHD

A

Cyanosis
Becomes apparent when there is venous arterial shunting or obstruction of blood flow to the lungs

Congestive Heart Failure (CHF)
Occurs when Cardiac Output (C.O.) is unequal to body requirements. Blood dams up in the heart and the pulmonary vasculature become engorged

61
Q

ACE

A

ACE Inhibitors block the conversion of Angiotensin I to Angiotensin II – So vasodilation occurs as opposed to vasoconstriction

62
Q

ACE – effects

A

Decreased PVR, SVR and BP,
Reduction in Afterload
Decreased Right and Left Atrial Pressures

less preload and afterload

Peds (2 decks)

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