baby nelson tidbits Flashcards

1
Q

Secretory Diarrhea vs Osmotic diarrhea

A
  1. Secretory diarrhea: intestinal mucosa directly secretes fluid and lutes into the stool; result of inflammation (i.e. IBD, chemical stimulus, from hormones - i.e. vasoactive intestinal peptide by neuroendocrine tumour). Holera - stimulated by enterotoxin of vibrio cholera, causes increased ccAMP in enterocytes, secretion into small bowel
  2. Osmotic diarrhea: malabsorption of a substance, pulls water into the bowel i.e.) lactose intolerance, maldigestion (i.e. pancreatic insufficiency, intestinal injury) , PEG, Milk of Mg; fermentation of the substances can lead to gas, cramps, acidic stools, toddler’s diarrhea
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2
Q

How to decide if diarrhea is osmotic or secretory

A
  1. calculate the osmotic gap
    290- (2 x Na x K) Na and K are the measured stool Na and K
    assume the stool is always isoosmotic (omsoles of 290) since will have free water exchange across intestine
    Secretory diarrhea: osmotic gap 50 - malabsorbed substances other than electrolytes account for decal osmolarity
  2. stop feedings and give IV only - if gets better when NPO, more likely osmotic, secretary will continue to poopp (not perfect, i.e. viral will cause some damages and inflammation of the bowel)
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3
Q

tests for pancreatic insufficiency

A

oily or fatty stools, should test decal fat content or decal elastase to test for pancreatic insufficient

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4
Q

Functional constipation, definition

A

2 or fewer stools per week, voluntary withholding of stool, infrequent passage of large-diameter, often painful stools, often have “retentive posturing” and have associated decal incontinence from leakage of retained stool (aka encopresis)
Constipation : defined as 2 or fewer stools per week or passage of hard pellet like soils for at least 2 weeks

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5
Q

Differential of constipation

A
  1. functional constipation very common when tolilet training onwards; key is large caliber stools, encopresis, voluntary retaining, age of onset at potty training; normal or reduced anal sphincter tone because the big poops may have stretched it ; often have fecal impaction, can also have a large-caliber empty rectum if they just pooped
  2. Hirschprung - (see below)
  3. Anorectal and Colonic Malformation - usually confirmation from birth - anal stenosis, anteriorly displaced anus (mainly in females), imperforate anus, colonic stricture
  4. Mulridystem disease: muscular dystrophy, CF, diabetes meliitus (?), Developmental delay, celiac, hypothyroidism -
  5. Spinal cord abnomalities - history of swelling/exposed neural tissue in the lower back , history of urinary incontinence; will have lax sphincter tone; i.e. meningomyelocele, tethered cord, sacral teratoma or lipoma
  6. Drugs - narcotics, psychotropics
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6
Q

Hirschprung disease - what part of the bowel is dilated

A

narrow distal bowel - no ganglions
dilated proximal bowel
(can look on barium enema), rectal suction biopsy is the confirmatory test - no ganglion cells in the rectal submucosal plexus, lack of internal anal sphincter relaxation by anorectal manometry
delayed passage of meconium, failure of ganglions to migrate **no associated with large caliber stools or encopresis; snug anal sphincter, empty contracted rectum, may have explosive poop after examiner’s finger is withdrawn
can present in the initial stages with enterocolitis

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7
Q

common drugs that cause giginval hypertrophy

A

cyclosporine
phenytoin
calcium channel blockers

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8
Q

causes of delayed teeth eruption

A

hypopituitarism, hypothyroidism, osteopetrosis, Gaucher disease, Down syndrome, cleidocranial dysplasia, rickets

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9
Q

eosinophilic esophagitis

A

non IgE mediated allergic reactions to foods or aeroallergens
may have some familial connection
diagnosis: biopsy will show >15 eosinophils/hpf
treatment with high dose PPI to exclude that it is simply from acidic injury from reflux
barium study - may show a food impaction or esophageal stricture
presentation: young kids - oral aversion, vomiting and failure to thrive
school age: vague abdo pain o vomting
teens/adults - dysphagia/food impactions

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10
Q

Treatment and prognosis of eosinophilic esophagitis

A

avoid the causative antigens - but can be hard to identify, since the typically allergy testing (skin prick, RAST and imunocap assay will only identify IgE mediated antigen)
atopic patch testing might be better
one approach: eliminate cow’s milk, soy, wheat, eggs, peanuts and fish/shellfish (since most common causes)
may need repeat endoscopy
elemental diet
steroids can help with symptoms but can’t do long term because of complications
endoscopy - can be used for food impactions and to dilate esophageal strictures

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11
Q

esophageal foreign body - when do you need to remove them

A

don’t need to remove if small and in the stomach already
need to remove if
1. - threaten the airway - (need to intubate and do GA)
2. symptoms
3. disc batter in esophagus or multiple magnets

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12
Q

what are pill ulcers

A

when certain meds (i.e. tetracycline, nSAIDS) are swallowed without sufficient liquids, allow prolonged direct contact of the pill with the esophageal mucosa
presents with odynophagia and dysphagia as well as chest pain

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13
Q

caustic injury (ie kid swallows a clearner) what to do?

A

CXR to rule out aspirations dn look for mediastinal air
hospital, keep NPO with fluids until endoscopy
can get subsequent strictures, also might not see the whole burn initially
NG tube can be placed over a guide wire at the time of the initial endoscopy - provides a route for feeding and to stent the esophagus
steroids don’t help reduce strictures
treatment of esophageal strictures: treat with endoscopic dilation; can have a risk of perforation during dilation

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14
Q

Peptic ulcer disease in kids, name some risk factors

A
  1. H pylori **plays a significant role, but not as much as in adults, RFs are lower SES and poor sanitation
  2. drugs - HSAIDS (including aspirin) tobacco use, bispohophonates, potassium supplements, family history, sepsis, head trauma, burn injury, hypotension
  3. family history
  4. sepsis
  5. head trauma
  6. burn injury
  7. hypotension
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15
Q

true or false - non ulcer dyspepsia is associated with H pylori

A

false - non ulcer dyspepsia - which are upper abdo symptoms 9pain, bloating, nausea, early satiety) in the absence of gastric or duodenal ulceration are not associate diwth H pylori

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16
Q

which ulcers have pain relieved by eating and which are worse with eating?

A

duodenal - better with eating

gastric - worse with eating - result in weigh gloss

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17
Q

diagnosis of ulcers

A

endoscopy
can do empiric therapy with H2 blockers or PPI
can test for H pylori with biopsy during scope or can do non invasive tests 13C urea breath test/H. pylori decal antigen

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18
Q

patients with ulcers and H. pylori (positive) how to treat

A

PPI
amoxicillin
clarithromycin
or PPI, amoxicillin, metronidazole or omeprazole/clarithromycin/flagyl
2x daily for 1-2 weeks
if no H pylori, then H2
most will heal in 3- 8 weeks in at least 80% of patients; esophagitis takes longer to heal 4-5 months

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19
Q

treatment of cyclic vomiting syndrome

A

acute episode - hydration, dark, quiet environment, and anti emetics such as ondansetron
abortive treatment - NSAIDS/triptans
if frequent - can try prophylactic (similar to migraine meds 0 cyproheptadine, TCAs, beta blockers or topiramate

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20
Q

Associated anomalies with omphalocele

A

cardiac
Beckwith-Wiedemann
intestinal complications

21
Q

Anorectal malformations

A
  1. low lesions - often have fistula that drain meconium on the perineum, also have fistulas between bowel and bladder, vagina or urethra, may need a colostomy with subsequent reconstruction
  2. high lesions - internal sphincter muscle functionally absent - continence can be hard to achieve
22
Q

what test to do in all kids with imperforate anus

A

MRI of lumbosacral spinal cord - high incidence of tethered spinal cord

23
Q

extraintestinal manifestations of celiac disease

A
osteoporosis
pulmonary hemorrhage
seizures/encephalopathy
dermatitis herpetiformis
erythema nodosum
24
Q

biopsy findings in celiac

A

villous atrophy
crypt hyperplasia
increased numbers of intraepithelial lymphocytes

25
Q

treatment of intusseption

A

pneumatic enema (best success 90% if t get reduction then need surgery

26
Q

Main causes of neonatal cholestatic jaundice

A
  1. biliary atresia - usually in first few weeks of life, need surgery by 2 months or will have liver failure
  2. neonatal hepatitis - ill-appearing, enlarged liver and jaundice, no specific diagnostic test; liver biopsy - hepatocyte giant cells; need to rule out CMV< HSV and syphilis; HIDA - slow hepatic uptake with eventual exertion of isotope into the intestine; usually have spontaneous resolution
  3. alpha1-antitrypsin deficiency - looks like neonatal hepatitis; 20-30% develop chronic liver disease ; life-threatening in 3-5% of affected patients ; leading metabolic disorder needing transplant
  4. Alagille syndrome: chronic cholessticy, paucity of bile ducts on liver biopsy; associated abnormalities includes peripheral pulmonic stenosis or other cardiac; hypertelorism; unusual facies with deep-set eyes, prominent forehead and a pointed chin; butterfly vertebrae; defect of the ocular limbus ; uncommon to progress to end-stage liver disease; sometimes get transplant to help with pruritus
27
Q

treatment of metabolic causes of cholestasis

A
  1. vitamins adek

2. formula with medium -chain triglyceride

28
Q

fulminant liver failure

A

severe liver disease with onset of hepatic encephalopathy within 8 weeks after initial symptoms, in absence of chronic liver disease

29
Q

causes of fulminant liver failure

A
viral hepatitis
metabolic disorders
autoimmune hepatitis
ischemia
neoplastic disease
toxins
30
Q

clinical features of fulminant liver failure

A
  1. hepatic encephalopathy (has stages)
  2. respiratory compromise
  3. hypoglycemia
  4. renal failure - hepatorenal syndrome - low u/o, azotemia, low urine Na
  5. ascites from hypo albumin
  6. increased infection risk
  7. esophageal varices
    8 . hypersplenism from portal hypertension - can lead to thrombocytopenia
31
Q

treatment of liver failure

A

management should be in ICU at a liver transplant centre
Treatment of fulminant liver failure (pg 448)
1. hepatic encephalopathy - avoid sedatives, give lactulose via NG tue, neomycin, enemas if constipated, mechanical ventilation if stage 3 or 4
2. coagulopathy - FFP if active bleeding, monitor coats, transfuse platelets as needed
3.hypoglycemia - IV glucose as needed
4. ascites - fluid restrict to 50-60% maintenance, restric sodium to 0.5-1 meq/kg/day, monitor CVP
5. renal failure - maintain volume, diuretics, vasoconstrictors, dialysis or exchange or liver transplant ultimate

32
Q

Chronic liver disease - features

A
  1. portal hypertension
  2. hepatocellular function impaired
  3. cholestasis
33
Q

Causes of pancreatitis in kids

A

idiopathic
meds
CF, hypertriglycerdiemia, biliary microlithiasis, trauma, viral infection
collagen vascular disorders
parasite infestations
(in adults alcohol or gallstone are the most common)
(long list on pg 452)

34
Q

pancreatic insufficiency - labs

A

decal fat

fecal elastas int eh stool (can also measure the other pancreas enzymes)

35
Q

what are the enzymes made by thte exocrine pancreas

A

they are inactive proenzymes

trypsin, chymotrypsin, carboxypeptidase

36
Q

amylase and lipase in pancreatitis

A

as progresses amylase declines faster than lipase
lipase a good choice for later in the illness
other tests to do - US important to look for edema, as is CT if US no work
also want to rule out gallstones (even though not as common in kids as adults)

37
Q

management of pancreatitis

A

NPO
acid blocking drug
NG suction
fluid resuscitation because of vomiting and third space losses
pain relief - often use opioids
nutritional support early if patient will be NPO for extended periods
feedings can begin once pain subsides
can also consider feeds after the duodenum (i.e. NJ feeds)
less complications with NJ feeds vs TPN
antibiotics if febrile, pancreatic necrosis or infection

38
Q

Which drugs are contraindicated in breastfeeding

A
radioactive compounds
antimetabolites
lithium
certain antithyroid drugs
(see the CPS statement)
39
Q

Marasmus features

A

body’s response to inadequate calories and nutrient -
loss of muscle mass and subcutaneous fat stores
head might look big, but is usually proportional to the body length
edema usually is absent
skn is dry and thin; hair may be thin, sparse and easy to pull out
apathetic, weak, may be irritable
bradycardia and hypothermia - severe/life-threatening
can get stunting eventually from combo of malnutrition and recurrent infections

40
Q

Kwashiorkor, what is the weight

A

weight can be normal or near normal
it results from inadequate protein intake in the presence of fair to good caloric intake
hypoalbumin - pitting edema - rising
other factors: infection, toxic, micronutrient or amino acid imbalances
Clinical manifestations:
maintenance of sc tissue, marked atrophy of muscle mass
edema
sparse hair, can get discolouration of hair
nutritional repletion will restore the hair colour
skin changes: hyperpigmeneted hyperkeratosis to erythematous macular rash - aka pellagrous on the trunk
most severe - get desquamation over pressure surfaces - angular cheilosis, atrophy of the filiform papillae, monilial stomatitis
abdo: enlarged abdo, can get atrophy of LN and tonsils

41
Q

Treatment of malnutrition

A
  1. slow nutritional rehab - oral rehydration better than IV fluids- avoid excessive fluid and solute load to rehydrate; calories should be 20% above current intake, if not sure then use 50-75% of nomal energy requirements; often use high calory oral solutions in developing countries
  2. antiinfective therapy if needed - for ova and parasites
    increase caloric intake very gradually, monitor for lute problems, poor cardiac function, edema or feeding intolerance
42
Q

What are the electrolyte abnormalities in referring syndrome?

A

hypophosphate
hypomagnesemia
hypokalemia

43
Q

What is catch-up growth?

A

gaining weight at >50th percentile for age
may need 150% or more of the recommended calories for an age-matched, well-nourished child
rule is usually 100-120 kcal/kg based on ideal weight for age for kids up to age 3
also give increased proteins - since needs increase as anabolism begins, may need extra vitamins
most cases use cow’s milk based formulas

44
Q

true or false- should give iron supplements early in nutritional rehab for malnourished kids

A

false - don’t give iron during the acute rehab phase - especially kwashiorkor - ferritin often high
iron causes an oxidative stress, iron supplementation is associated with higher mobility and mortality

45
Q

name some complications of malnutrition

A
  1. infectino - esp sepsis, pneumonia, gastro
  2. hypoglycemia
  3. hypothermia -
  4. bradycardia and poor cardiac output - increase chance of heart failure
  5. micronutrient deficiencies -
  6. growth stunting
  7. delayed development
  8. social deprivation with malnutirtion->can further impair development and cognitive function
46
Q

baby is irritable, has bone tenderness with swelling and pseudo paralysis, has only been drinking cow’s milk until age 7months, what vitamin is deficient?

A

vitamin C - SCURVY
has 2 forms - ascorbic acid and dehydroascorbic acid
causes are if only cow’s milk and if no fruits/veggies
progresses to subperiosteal hemorrhage, bleeding gums and petechiae, hyperkeratosis of hair follicles and mental changes

47
Q

2 month old baby of alcoholic mom who is breastfed, presents with polyneuropathy, calf tenderness, heart failure, edema, opthalmoplegia , aphonic cry , what vitamin is deficient

A
B1 - aka thiamine
cuses: 
alcoholics
teens with bariatric surgery
protein-calorie malnutrition
mom's with thiamine deficiency
unsupplemented hyperalimentation fluid
boiled milk
48
Q

Old question:
fat absorption in childhood - which is true
a) fat exclusively digested by pancreatic lipase
b) medium chain TG require solubilization
c) triglycerides require tryptic predigestion
d) triglycerides require hydrolysis to free fatty acids
e) lipolysis enhanced by gastric acid

A

i think d )

big Nelson says:
Fat absorption in 2 phases
phase 1) dietary triglyceride broken into monoglycerides and FFAs by pancreatic lipase and colipase
phase 2) FFAs subsequently emulsified by bile acids, make micelles with phospholipid and other fat-soluble substances and transported to the cell membrane - where they are absorbed->make chylomicrons that go to the thoracic duct via intestinal lymphatics

medium chain fats absorbed more efficiently, can directly enter the cell
next they go to the liver via the portal system
fat absorption can be affected at any stage - decreased enzymes - CF; poor bile salt production in cholestatic liver disease; celiac disease - reduces mucosal surface area; abnormal chylomicron in abetalipoproteinemia; intestinal lymphangiectasia - affects transport of the chylomicrons
fat absorption less efficient in neonate compared to older people
infants with malabsorption of fat usually fed with formulas that have more medium chain triglyceride - which are absorbed independently of bile salts