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317B > Quiz 5 NEC/PDA/Pain/IEM > Flashcards

Quiz 5 NEC/PDA/Pain/IEM Flashcards

1
Q

What is NEC

A

Ischemic and inflammatory necrosis of the bowel

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2
Q

NEC morbidity

A

short bowel syndrome, TPN related liver disease, poor growth, poor neurodevelopment outcome

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3
Q

What % of NEC are term?

A

10%
gastroschisis 5%
CHD 3-7%

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4
Q

Who is at greatest risk for NEC

A

<28 weeks

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5
Q

Age of onset of NEC

A

28-33 weeks

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6
Q

Spontaneous intestinal perforation

A

Occurs earlier during first 2 weeks, isolated areas of hemmorhagic necrosis with perforation in terminal ileum

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7
Q

What is the main reason for NEC

A

immaturity of intestinal tract

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8
Q

what is the function of the toll-like receptors?

A

pattern recognition; send out signals to immune system

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9
Q

Preterm gut characteristics

A

dec GI motility; patchy mucous coating with loose junctions; decreased gastric acidity and altered circulatory regulation

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10
Q

What causes bacterial proliferation?

A

enteral feeding

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11
Q

What happens when bacteria adhere?

A

toll-like receptors are stimulated

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12
Q

Stimulation of toll-like receptors results in:

A

local inflammation and release of inflammatory mediators (PAF and TNF)

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13
Q

Inflammatory mediators result in:

A

inflammation, vasoconstriction, permeability

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14
Q

pathognomonic sign for NEC

A

pneumatosis intestinalis

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15
Q

Most frequent location for NEC

A

terminal ileum and ascending colon

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16
Q

Where is the most likely site for perforation?

A

Ileocecal valve

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17
Q

Risk factors for NEC

A

black and hispanic race, outworn, no standard feeding protocol, NPO, formula, hypertonic meds, jejunal feedings, abnormal bacterial colonization, blood transfusions

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18
Q

Stage II NEC

A

proven NEC
abd distention, absent bowel sounds, mild metabolic acidosis, thrombocytopenia, cellulitis, pneumatosis intestinalis, intestinal dilation, ileum, ascites

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19
Q

Stage III NEC

A

impending bowel perforation, hypotension, A/B’s, respiratory and metabolic acidosis, pneumoperitoneum

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20
Q

Triad of late non-specific symptoms of NEC

A

thrombocytopenia, increased lactate (metabolic acidosis), hyponatremia

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21
Q

Left lateral decubitus X-ray for NEC

A

best to detect pneumoperitoneum; place left side down so air rises over liver

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22
Q

Portal venous gas

A

hydrogen gas has gotten into the portal blood system

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23
Q

Sentinal loop

A

area that loop has gotten necrotic and nothing can pass, need serial X-rays to diagnose

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24
Q

NEC sequelae

A

recurrent NEC, strictures, malabsorption, short bowel syndrome

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25
Q

Short bowel syndrome outcome dependent on:

A

presence of ileocecal valve, residual length <10% for GA

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26
Q

When does the infants bowel double in length?

A

23-25 weeks

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27
Q

Short bowel syndrome and nutrition

A

early! Breastmilk or elecare, continuous

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28
Q

Duodenum absorption:

A

iron, Ca, Mg, ADEK

29
Q

Jejunum absorption:

A

water soluble vitamins B and C, carbs, fats, and proteins

30
Q

Ileum absorption:

A

vit B and C, carbs, fats, proteins, B12 and bile acids

31
Q

Colon absorption:

A

short chain fatty acids from fermentation, water

32
Q

Dumping syndrome

A

80%; maintain normal Na and K for growth, monitor for acidosis, refeed osmotic output through mucous fistula

33
Q

Post op gastric acid hypersecretion

A

50%; can disrupt surgical site, peptic ulceration, inactivate pancreatic enzymes. May need a few days of pepcid in TPN

34
Q

Short bowel syndrome mortality primarily due to :

A

Parenteral nutrition sequelae. Length of time = central line sepsis, steatosis (fatty liver), cholestasis (direct bili>2)

35
Q

Cholestasis may be prevented with:

A

20-30% enteral nutrition, actigall, omegaven, cycling TPN

36
Q

Surgical procedures to improve short bowel outcome:

A

stricture resection, bowel tapering, bowel lengthening

37
Q

Procedures for lengthening bowel

A

bianchi and STEP procedure

38
Q

Preventative measures for NEC

A

breastmilk, standardized feeding protocols, holding feeds during blood transfusions, pre/probiotics

39
Q

Which immunoglobulin correlates with a decrease in bacterial translocation?

A

IgA (closes enterocyte gaps)

40
Q

What are inborn errors of metabolism?

A

disorders caused by deficiency of one or more enzymes involved in a biochemical pathway

41
Q

What are the consequences of an enzyme deficiency?

A

won’t be able to break down that particular thing

42
Q

Acute inborn errors of metabolism:

A

metabolic disease of the newborn

43
Q

Progressive

A

organomegaly, developmental delay (develops slowly over several years)

44
Q

Chronic

A

Failure to thrive, mental retardation

45
Q

Late

A

first indication in adults

46
Q

What is an important red flag in diagnosing metabolic disease?

A

Developmental delay

47
Q

Labs for Fatty acid oxidation defect:

A

HYPOGLYCEMIA WITH ABSENT KETONES

48
Q

gluconeogenesis (fatty acid oxidation pathway)

A

takes fats and converts them to glucose

49
Q

why does fatty acid oxidation not get noticed till 3-5 months?

A

doesn’t get to catabolic phase until feeds have lengthened when baby is sleeping through the night. presents with hypoglycemia

50
Q

Labs for Urea cycle defects:

A 
High ammonia (300-2000 range). No acidosis or hypoglycemia
normal ammonia (40-70)
51
Q

Test for urea cycle defects

A

plasma amino acids

52
Q

Labs for Organic acidemias

A

ACIDOSIS, HIGH ANION GAP, KETONES, HYPOGLYCEMIA, INCREASED AMMONIA

53
Q

Galactosemia

A

1/60,000

must have lactose feeding prior to screening

54
Q

Galactosemia clinical signs

A

vomiting, diarrhea, jaundice, hepatomegaly, gram negative sepsis, liver dysfunction

55
Q

Galactosemia treatment

A

galactose/lactose restriction

56
Q

Phenylketonuria

A

1/15,000

must have protein intake prior to screening

57
Q

Phenylketonuria clinical signs

A

mental retardation, autism, seizures, hypopigmentation, eczema

58
Q

Phenylketonuria treatment

A

low phenylalanine diet, tx for life

59
Q

Pinprick studies

A

1941, greater response as GA increases

60
Q

1985 first event

A

Jeffrey Lawson PDA ligation without anesthesia

61
Q

1985 second event

A

Dr. Anand in United Kingdom proved that infants do feel pain. Sufentanyl vs control

62
Q

Cutaneous sensory receptors

A

7 weeks - face
11 weeks - palms and soles
15 weeks - trunk and proximal arms and legs
20 weeks - cutaneous and mucous surfaces
Synapses begin at 6 weeks, neurotransmission begins before 13-14 weeks, completes by 30 weeks

63
Q

C-polymodal fibers

A

unmyelinated; transfer pain even more than delta A fibers which are thinly myelinated

64
Q

Pain pathways to brain and hypothalamus are completely myelinated by when

A

30 weeks

65
Q

consequences of unmanaged pain

A

increased HR and BP, decreased O2 sat, dec GI motility, dec UO

66
Q

Repeated production of cortisol from the adrenal cortex does what to the immune system?

A

suppresses the immune system, production of ACTH and cortisol persist and increased risk of infection

67
Q

Secretion of human growth hormone and thyroid hormone

A

increases rate of protein synthesis in cells, mobilizes fatty acids from adipose tissue

68
Q

Hypoglycemia leads to secretion of what:

A

human growth hormone and thyroid hormone

317B (2 decks)

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