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Neo Pathophys 2 > NEC > Flashcards

NEC Flashcards

1
Q

Define NEC

A

Ischemic and inflammatory necrosis of the bowel

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2
Q

When was NEC first recognized?

A

1960-1970’s-when younger babies were being saved (especially cardiac babies)

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3
Q

What was the mortality rate in 1960-1970’s?

A

Mortality >70%

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4
Q

Has the Medical or Surgical Management changed since 1970?

A

No

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5
Q

What is the Medical Management of NEC?

5 things

A
  1. NPO
  2. NG suction (replogyl to LIS)
  3. Systemic Antibiotics
  4. IV Fluids (d/t 3rd spacing)
  5. Monitoring clinical signs & X-ray findings
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6
Q

What is the surgical Management of NEC?

3 things

A
  1. Removal of Necrotic/Non-viable bowel
  2. Enterostomy Formation
  3. Reanastomosis at a later time
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7
Q

What is the current Mortality rate of NEC?

What is the Mortality rate w/Surgical NEC?

A

~30%

As high as 50% (w/surgical NEC)

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8
Q

Current Morbidity of NEC is high/low?

A

High

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9
Q

What are the Morbidities of NEC?

A
  1. Short Bowel Syndrome
  2. Parenteral Nutrition-related Liver Dz
  3. Poor Growth (they are growth restricted later on-don’t do as well)
    < 10% on Wt, Length, and OFC
  4. Poor Neurodevelopmental Outcome
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10
Q

Describe the ND outcomes of NEC

A 
1. Mental Retardation
   < 70 on MDI Mental Developmental Index
   < 70 on PDI Psychomotor Dev. Index
2. PVL/Cerebral Palsy/Motor Problems
3. Vision &amp; Hearing Impairment
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11
Q

What is one of the worst sequellae of NEC?

Which babies usually get this?

A

Poor ND outcome

Usually babies w/Surgical intervention from NEC

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12
Q

What is sometimes noted on Clinic F/U?

What can cause this?

A

Microcephaly

Gram Negative Rod Sepsis (has a predilection to cause it)

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13
Q

What causes the Microcephaly after NEC?

A

Lipopolysaccharides (LPS) release endotoxins in the outer Gram Negative cell wall.
-There are receptor sites on the Microglia in the White Matter that pick up the Endotoxins.

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14
Q

T/F: In NEC, there is Bacterial invasion of the intestinal wall?

A

True

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15
Q

With Bacterial invasion of the intestinal wall, what do the bacteria do?

A

Set up “camp” and Eat the Intestine : (

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16
Q

What metabolic by-product is produced by the invading intestinal wall bacteria?

What does this create?

A

Hydrogen gas

Creates the linear tracks of air bubbles (Pneumotosis intestinalis)

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17
Q

What does KUB stand for? (old term)

A

Kidneys, Ureters, Bladder (Abdominal X-ray)

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18
Q

What might be seen on abdominal X-ray of an infant w/NEC?

A
  1. Portal Venous Air

2. Pneumatosis Intestinales

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19
Q

What is Portal Venous Air?

What might it look like on Abdominal X-ray?

Does Portal Venous Air stay or is it transient?

A

The Hydrogen has dissected into the blood vessels and into the portal venous system & is in the Liver

  • the Liver should be white/solid, w/air it has little lines or black dots.
  • it can be Transient
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20
Q

Pneumatosis Intestinales is a ____________ sign.

A

Pathognomonic sign

sign specific to NEC

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21
Q

T/F: When Pneumatosis Intestinales is seen, you can definitively say the pt has NEC?

A

True

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22
Q

The predominant Lesion of NEC is what type?

A

Necrosis–either coagulative or ischemic

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23
Q

What is the spread of a NEC lesion?

Is there a distinct pattern?

A

Location: May be longitudinal or transmural

May be Patchy w/no pattern

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24
Q

Where are NEC lesions typically located?

A

Usually terminal ileum & ascending Colon

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25
Q

What is the most likely site for perforation?

A

Ileocecal valve

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26
Q

Is a Spontaneous Intestinal Perforation (SIP) the same as NEC?

A

No

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27
Q

Are babies w/sponatneous intestinal perf. as sick as babies w/NEC?

A

No, they are sick but not AS sick as those w/NEC (septic shock, etc).

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28
Q

Describe Spontaneous Intestinal Perforation

A
  • Occurs earlier (1-2 wks of life)
  • A/W: Indomethicin, Steroids, Umb. Catheters
  • ISOLATED AREA of hemorrhagic necrosis often w/perforation in Terminal Ileum
  • Generally less morbidity/mortality than NEC
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29
Q

Up to 10% of babies who develop NEC are _____.

A

Term

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30
Q

What types of babies (generally term) are at High Risk of NEC?

Why?

A

Gastroschesis–5% incidence
Cong. Heart Dz–3-7% Incidence

The risk is from perfusion problems

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31
Q

Is Preterm NEC different than Term NEC?

A

Yes

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32
Q

Which Preemies are at greatest Risk of NEC?

A

< 1000 gms & < 28 wks

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33
Q

The age of onset of NEC varies ________ with ____.

A

Inversely w/ GA

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34
Q

What is the Mean Postmenstrual Age of NEC?

A

29-32 wks

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35
Q

The younger GA at birth, the ______the onset of NEC may be.

A

later

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36
Q

What is the usual time babies develop NEC?

A

When they are just about up to full feedings

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37
Q

What is the Biggest Problem with a Preemies GI system, leaving them vulnerable to NEC?

A

The Immaturity of the Intestinal Tract

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38
Q

Name the 6 things of a premature Intestinal Tract.

A
  1. Decreased GI Motility–>bacterial overgrowth
  2. Patchy Protective Mucus coat
  3. Not tight junctions in intestinal wall structure
  4. Immature Immune system
  5. Decreased gastric acidity (increased pH)
  6. Altered Circulatory Regulation (dilation/vasoconstriction)
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39
Q

What does decreased gastric acidity (increased pH) do?

A

Alters Bacterial Flora

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40
Q

What medications are A/W NEC?

A

H2 Blockers—absolute no-no

i.e. Pepcid, Zantac

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41
Q

One study found a ___ - fold increase in NEC when H2 blockers were used.

A

6.6 x’s

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42
Q

The intestinal Avascular Area (watershed area) depends on what?

A

Vessels coming across Avascular Area to perfuse it

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43
Q

If you stretched out the Surface area of Microvilli of a term baby, it would be the size of what?

A

1/2 a Tennis Court

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44
Q

The Microvilli are ___ cells deep.

They measure ____-____ in Length.

A

1

0.5-1.6mm in Length

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45
Q

The Intestinal Epithelium is a single layer of _________.

A

Enterocytes

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46
Q

How do the single Enterocyte cells move along the Villus?

A

They move up as other cell die via Apoptosis

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47
Q

Each Villi has a ______, _______, & _______.

A

Vein, Artery, & Lymphatic vessel

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48
Q

What sits on top of the Enterocyte that works on protein recognition of pathogens?

A

TLR’s (Toll-Like Receptors)

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49
Q

What is the principal sensor of infection?

A

TLR’s (toll-like receptors)

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50
Q

TLR’s are _______ Receptors.

What do TLR’s do?

A

Signaling receptors.

They Recognize pathogens & Activate the immune system

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51
Q

When TLR’s recognize a pathogen, and the immune system is activated, what happens next?

Is this beneficial?

What happens to this system in a preemie?

A

This sets up an inflammatory reaction

Yes, it’s beneficial as long as it is CONTROLLED.

The premature body can’t regulate the inflammatory reaction well.

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52
Q

What does an inflammatory reaction produce?

A

heat
increased blood flow
WBC’s

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53
Q

What is the Proposed Mechanism of NEC?

A
  1. Intestinal wall immaturity
  2. Enteral feeding = bacterial proliferation (microbial dysbiosis)
    - Abnormal Colonization
    - Low Microbiota Diversity
  3. Bacterial Adhesion (TLR’s stimulated)
  4. Inflammatory cascade triggered (Macrophages and Polyneutrophils arrive–>Release of inflammatory mediators)
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54
Q

What is an essential component of NEC?

A

Bacteria

  • can be Bacteria, Virus, Fungus
  • can be normal flora or probiotic (lactobacillus sepsis)
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55
Q

Preemies are a set up for NEC from inappropriate colonization with pathogenic organisms due to?

A
  1. Lack of contact with mother
  2. Exposure to NICU environment
  3. Exposure to Antibiotics
  4. Exposure to H2 Blockers
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56
Q

Preemies have a ______ in development of commensal bacteria (normal flora)

A

Delay

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57
Q

Preemies have an increase/decrease colonization of potential pathogenic bacteria.

A

Increase Colonization

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58
Q

Preemies have increased/reduced microbiota diversity

A

Reduced
-Preemies who develop NEC may show altered microbiota several weeks before Dx (they usually only have a few types of normal flora, and an increased build up of certain ones)

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59
Q

The ability to _____ pain comes before the ability to _________ pain.

Preemies have an Increased/Decreased pain sensation vs. Term. Why?

A

Feel
Modulate

Increased pain sensation b/c they can’t suppress any of it.

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60
Q

T/F: Preemies are skewed toward UNbalanced pro-inflammatory (injury vs/ repair) response

A

True.

-The balance between the 2 happens later in development

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61
Q

Name the 2 Inflammatory Mediators involved in NEC

A
  1. PAF-Platelet Activating Factor

2. TNF-Tumor Necrosis Factor

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62
Q

Inflammatory Mediators PAF & TNF lead to increased what? (3 things)

A
  1. Inflammation
  2. Vasoconstriction
  3. Permeability
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63
Q

When the intestinal barrier is broken, injury/repair balance is altered favoring ___________ leading to ______ _______.

A 
Vasoconstriction
Tissue Injury (via hypoxia &amp; ischemia-->tissue necrosis)
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64
Q

The vasoconstriction that happens after intestinal barrier is broken is ____ of ______.

A

Out of Control

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65
Q

Inflammatory and vasoconstrictive prostanoids result in:

A

Increased production of Nitric Oxide

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66
Q

Low levels of NO = ?

High levels of NO = ?

A

Vasodilatory & Beneficial

Injure intestinal epithelium (what you get with a preemie from vasoconstrictive prostanoids)

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67
Q

Injury to intestinal epithelium—>_____ _____—>__________ ________—>________.
If it continues, —>_______—>_____ _____

A

Bacterial Invasion–>Pneumotosis Intestinales–>Necrosis–>Septicemia–>Septic Shock

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68
Q

Name 10 Risk factors for NEC

A
  1. Black and Hispanic race (vs. Caucasian)
  2. Outborn
  3. NICU NEC rate
  4. Abnormal bacterial colonization
  5. H2 Blockers/PPI’s/Jejunal feedings
  6. Hypertonic formula/meds (osmolarity)
  7. No standardized feeding protocol
  8. NPO Status
  9. Non-Human Milk
  10. Blood transfusions (or anemia?)
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69
Q

What is the osmolarity of term formula?
Breastmilk?
Fortified Breastmilk?

A

275-295 miliosmols
~ 300
> 400

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70
Q

What is the 1 thing we KNOW can prevent NEC?

A

Maternal Breastmilk

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71
Q

What standard feeding protocol is best?

A

Any (is better than none)

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72
Q

What items should be included in a standardized feeding protocol?

A

When to start feeds
When to advance feeds
When to add fortifier
When to hold feeds

73
Q

Can NEC happen in UNfed infants?

A

Yes, but rare

74
Q

NPO can be BAD to the gut, why?

A
  1. Intestinal Atrophy
  2. Cellular Death
  3. Increased Permeability of Intestine
  4. Bacterial Translocation
75
Q

Do early trophic feedings decrease NEC?

A

No, not specifically but they do have many benefits

76
Q

What are the benefits of early trophic feeds?

A

Increased:

  • Digestive Hormone release
  • Intestinal blood flow
  • GI Motility
  • Feeding Tolerance
  • Growth

Decreased:

  • Sepsis
  • Hospital Stay
77
Q

A study conducted by Henri Ford MD showed that mice fed Formula in a hypoxic state had what compared to their breastmilk fed counterparts?

A

Apoptotic Enterocytes

78
Q

Is the incidence of NEC higher or lower in breastmilk fed babies vs formula?

A

Lower.
formula = highest
formula + breastmilk = lower
breastmilk only = lowest

79
Q

In breastmilk fed infants with NEC, what is the course like?

A

less fulminant course

80
Q

In a study done by Lucas et. al, in Lancet, any addition of human milk did what?

The more human milk, the ________

A

helped and protected the babies

better

81
Q

What % of NEC follows a blood transfusion?

Is there a proven pathogenic pathway?

What is the consensus on what to do about blood transfusion associated NEC?

A

25-35%

No

None

82
Q

Anemia itself could be the pathway to NEC instead of the blood transfusion, what is the thought behind this?

A

In Anemia, there is reperfusion injury w/transfusion.

Maybe we should transfuse earlier

83
Q

Any condition that causes hypoperfusion-hypoxia is a ________ risk factor

A

secondary

84
Q

After what GA are feedings able to be advanced faster?

A

34 wks

85
Q

NEC can present with ____ to _____ symptoms

A

mild to severe

86
Q

NEC courses can vary from what to what?

A

slow & paroxysmal

rapid & fulminant

87
Q

Name the 8 non-specific signs of NEC

A
  1. temp instability
  2. A & B’s
  3. Lethargy
  4. Mild GI problems
  5. Increased residuals
  6. Low PCV (% of RBC’s)
  7. Low Platelets (unless mom had PHTN, low plts can be a sign of NEC)
  8. Metabolic Acidosis
88
Q

What is the only non-specific sign that can be an actual sign of NEC?

A

Low platelets

89
Q

Name 7 more specific signs of NEC

A
  1. Abdominal tenderness
  2. Abdominal distension
  3. Decreased or Absent bowel sounds
  4. Emesis
  5. Frank or occult blood in stools
  6. Visible loops of bowel
  7. Discoloration of abdomen
90
Q

In a term baby w/CHD, what sign can herald NEC?

A

Frank or occult stools

91
Q

There are lots of late non-specific symptoms of NEC. What are the triad of signs?

A
  1. Thrombocytopenia
  2. Increased Lactate
  3. Hyponatremia
92
Q

Why is oliguria a late non-specific sign?

A

they 3rd space and have decreased blood flow to kidneys

93
Q

Why is hyperkalemia a late non-specific sign?

A

K+ is released from dead cells

94
Q

In Diagnosing NEC severity what criteria is used (in general).
Has it changed much since 1978?

A

Modified Bells staging criteria

No, it has not changed much

95
Q

What is blood in stool usually caused from? What can be used for it?

A

From an anal fissure

Vaseline

96
Q

Stage 1 NEC is __________

Stage 2 is ______ by ____

A

Suspected

Definite by x-ray

97
Q

What % NEC can be Medically managed?

A

50-75%

98
Q

What is the 1st thing that should be done to medically manage NEC?
Why?

A

Replogyl tube to LIS

Gastric Decompression–try to prevent perforation

99
Q

When would it be ok to use a feeding tube vs/replogyl?

A

on transport

-connect fdg tube to syringe

100
Q

What does Medical Management of NEC involve?

A
  1. Blood Gas
  2. Blood Culture
  3. CBC, diff, plts
  4. CRP
  5. Electrolytes
  6. Vanc/Gent/Flagyl
  7. NPO 10-14 days after normal x-ray
  8. Ventilator support PRN
  9. Volume expanders
  10. Pressors
  11. TPN/IL
  12. Pain meds
  13. Serial x-rays
  14. Surgical consult
101
Q

How often are serial X-rays done w/NEC?

A

every 6-8 hours

102
Q

What abnormal gas patterns are looked for on the AP w/NEC?

A 
Dilated loops of bowel
Bowel wall edema
Sentinel loop (fixed loop of bowel)
Pneumatosis intestinales
Portal venous air
Football sign
Pneumoperitoneum
103
Q

With the Left lateral decubitus view, why do we use this?

How do you position baby?

A

Best film to detect pneumoperitoneum

Left side down

104
Q

“Soap bubbles” is a term used to describe what condition?

A

CF, not NEC

air mixed w/mec

105
Q

On abdominal x-ray you might see:

A 
Bowel wall edema
Grossly dilated loops
Pneumatosis intestinales-"railroad track sign"
Portal venous gas
Sentinel loop 
Footbal sign - Falciform ligament
Pneumoperitoneum
106
Q

What i the “railroad track” sign caused from?

A

Coalesced Hydrogen gas.

The tracks are in the bowel walls themselves.

107
Q

What is a Sentinel Loop?

A

Seen on every serial x-ray, the same loop is noted. It means the area is necrotic and gas can’t pass the area.

108
Q

What is the Football sign a/w the falciform ligament?

A

The faliciform ligament sticks the liver to the anterior intestinal wall. You can visualize the ligament when air is surrounding it on x-ray.

109
Q

Ultrasound can be very helpful in Dx NEC. What can it detect?

A
  • ID loculated/absscessed areas consistent w/walled off perforation
  • ID and quantify ascites (a gasless abdomen is not good either = fluid/blood in peritoneum)
  • May be better at identifying pneumatosis and portal venous air than x-ray

(US w/doppler):

  • Detects absence of flow in intestinal wall–>possible ischemia
  • Detects increased vascularization–>inflammatory process
110
Q

T/F: the timing of surgery is controversial

A

True (too early vs. too late)

111
Q

What is the traditional surgical management?

A

Laparotomy w/resection & stoma formation

112
Q

What is the goal of Surgical Management for NEC?

A

Save as much intestine as possible

113
Q

Do they keep the “Leopard Skinning” parts of the intestine during surgery?

A

Yes, some-they think it will heal

114
Q

Stomas are very ____________.

A

hypervascular

115
Q

Risk of postoperative complications is ____-____%

A

20-40%

116
Q

Name 4 surgical wound complications

A
  1. Infection
  2. Dehiscense
  3. Abscess
  4. Fistula
117
Q

Name 3 Stoma complications

A
  1. Retraction
  2. Prolapse
  3. Hernia
118
Q

Preterms have ________ tissue strength

Preterms have ________ immune response

A

Decreased
Decreased
-they don’t heal well, depends on nutrition

119
Q

Bedside peritoneal drainage was originally what?

A

Palliative procedure–used to stabilize infants too sick for immediate laparotomy

120
Q

What % babies actually get better with peritoneal drainage?

A

~50%

121
Q

Is peritoneal drainage used as primary tx vs. surgery?

A

yes, sometimes

122
Q

What does bedside peritoneal drainage eliminate?

A
  1. Stress of transfer to OR

2. Use of general anesthesia

123
Q

Bedside peritoneal drainage uses Local/General anesthesia?

A

Local

124
Q

What does bedside peritoneal drainage do?

A
  1. Decompresses pertoneal cavity of gas, necrotic debris, & stool
  2. Peritoneal cavity can be irrigated w/NS/antibiotics
125
Q

If there is no improvement or is deterioration in 12-48 hrs of peritoneal drainage, what is the course of action?

A

Taken to OR for Laparotomy and Resection

126
Q

What would be 2 signs of worsening NEC w/drain in place?

A

Decreasing Plts

Decreasing B/P, etc.

127
Q

50% babies post-op have Gastric Acid hypersecretion. What can this do?

What might be used in this situation, for how long?

A

Disrupt surgical site
Cause Peptic ulcer
Inactivate Pancreatic Enzymes

H2 blocker might be used for a few days

128
Q

Name 4 NEC Sequelae

A
  1. Recurrent NEC 5%
  2. Strictures 10-30%
  3. Malabsorption (d/t bacterial overgrowth)
  4. Short Bowl Syndrome
129
Q

How is Malabsorption from bacterial overgrowth treated?

A

Rotating courses of enteral antibiotics

Tapering of bowel (Bianchi procedure-at about 1 yr for max intestinal growth)

130
Q

Determining Short Bowel Syndrome depends on what?

A

What segments were removed
Presence of Ileocecal valve
FUNCTION of remaining bowel

131
Q

Poor outcomes of Short Bowel Syndrome are associated w/?

A

Residual length <10% for GA

132
Q

How much small intestine does a Term infant have?

A

240-300 cms

133
Q

A 23 wkr’s small intestine doubles in length by what GA?

A

35 wks

134
Q

The small intestine doubles in length from Birth to ____

A

1 yr

135
Q

The small intestine has the ability to ______ by increasing the _____ ___ as much as 4 x’s

A

Adapt

Surface Area

136
Q

When does compensatory hyperplasia begin?

A

At time of resection and continues for 3-4 years.

137
Q

Mortality from short bowel syndrome is primarily due to what?

A

Parenteral Nutrition sequelae

138
Q

Length of time on parenteral nutrition matters. Usually don’t want them on it longer than ______.

A

5 years

139
Q

What are the side effects of long-term parenteral nutrition?

A

Central line sepsis
Steatosis (fatty Liver)
Cholestasis (persistent direct bili >2 mg/dL)

140
Q

How can Cholestasis be prevented?

A

20-30% parenteral nutrition

141
Q

How is Cholestatsis treated?

A

Actigall
Omegaven-life saving in some situations
Cycling TPN-Liver rest

142
Q

Early ____ _______ is very important w/short bowel syndrome.

Why?

A

Enteral nutrition

Prevent Atrophy of the gut

143
Q

Traditional centers wait ___ - ____ days to restart feeds

A

10-14 days

144
Q

Centers of Excellence start feeds around ____ days post-op

A

~4 days–may be able to start as early as 12 hrs

145
Q

Semi-elemental formula (elecare) is more trophic than breastmilk but may not provide a ________ _______

A

Functional workload

146
Q

What is theoretically the best method for feeds w/short bowel syndrome?

Increase feeds ________ & ______

A

Continuous drip feeds–saturates the whole gut

Carefully & slowly

147
Q

Breastmilk provides a _______ _______ stimulating adaptation

A

Functional workload

148
Q

Presence of Lactose, Complex fats, Protein in Breastmilk can lead to _______ _________

A

Feeding Intolerance

149
Q

____% babies with short bowel syndrome will have Dumping Syndrome.

What needs to be monitored carefully (depends a lot on where the stoma is)

A

80%

Na & K (growth)
Acidosis

150
Q

To “grow your baby” refeed ostomy output through the ______ _______.

A

Mucus fistula

151
Q

What Vitamins are deficient in Short Bowel Syndrome?

A 
Fat-soluble vits A,D,E,&amp; K
Vit B12 (absorbed in distal ileum)
152
Q

What can deficiency of fat soluble vits cause?

A

Anemia
Bleeding
Rickets

153
Q

The ileum can compensate for loss of _______ but not the other way around.

A

loss of Jejunum

154
Q

Nothing can compensate for loss of the _____

A

Ileum

155
Q

Name 3 surgical procedures to improve outcome of short bowel syndrome

A
  1. Stricture Resection
  2. Bowel Tapering
  3. Bowel Lengthening
156
Q

The Bianchi Procedure does what?

A

Dissects the length of bowel into 2 sections

157
Q

The STEP procedure provides what?

What area is it typically used for?

A

Lengthening and tapering
(serial transverse enteroplasty)

A very dilated area to increase the surface area and prevent stasis of food

158
Q

Intestinal transplants have ____ 1 yr survival , ____ 3 yr survival

A

~87% 1 yr

~75% 3 yr

159
Q

What is the only known preventive measure for NEC?

A

Human Breast Milk

160
Q

T/F: KC is very beneficial for GI colonization

A

True

161
Q

What cells are noted in breastmilk?

A

Neutrophils
Lymphocytes
Macrophages

162
Q

What enzyme in breastmilk is Anti-Inflammatory?

A

Lysozyme

163
Q

What 3 immunoglobulins are in breastmilk?

Which is correlates with decrease in bacterial translocation?

A

IgG, IgM, IgA

IgA (it’s like a paint brush for the GI system–>protects it, pathogens can’t get through easily & it encourages intestinal growth)

164
Q

What antibacterial/antiviral in high concentrations in colostrum is 1/3 protein?

A

Lactoferrin

165
Q

What 2 growth factors are in breastmilk?

A

Insulin-like growth factor

Epidermal growth factor

166
Q

________ encourages replication of Bifidobacteria and decreases colonization w/lactose-fermenting bacteria (that produce H gas and pneumatosis)

A

Oliogofructose

167
Q

Oligofructose is a ____biotic

A

Pre-biotic

168
Q

What do Prebiotics do?

A

Feed normal bacteria already in our bodies

169
Q

What do Probiotics do?

A

Colonize GI tract w/normal bacteria

  • limit # of pathogenic bacteria
  • compete for binding sites & nutrition

Produce acid environment hostile to bacteria

Fortify mucosal barrier

170
Q

Multiple studies show decreased _________ & ________ of NEC when using probiotics

A

Incidence & severity

171
Q

Which 2 probiotics look promising?

A

Lactobacillus & Bifidobacteria

172
Q

Must probiotics be FDA regulated?

A

Yes, they are considered a treatment now not a food supplement so they are FDA regulated.

173
Q

What might be the best balance?

A

Use of Prebiotics and Probiotics

174
Q

What are we hoping will happen with the Human Microbiome project?

A

Find the actual genome that causes NEC

ID microbial patterns prior to developing NEC

ID microbes that currently can’t be cultured

175
Q

Sensitivity =

A

Ability of a test to correctly identify those w/the disease (True Positive)

176
Q

Specificity =

A

Ability of a test to correctly identify those w/o the disease (True Negative rate)

177
Q

Name 4 potential biomarkers of NEC

A
  1. High-risk colonization patterns
  2. Serum proteins
  3. Urine proteins (enterocyte damage)
  4. Fecal Bile salts (more in babies who develop NEC)
178
Q

Synthetic Amniotic-like fluid has been trialed and used to do what?

A

Prevent atrophy of the gut

Neo Pathophys 2 (20 decks)

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