baby nelson tidbits Flashcards
Secretory Diarrhea vs Osmotic diarrhea
- 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
- 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
How to decide if diarrhea is osmotic or secretory
- 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 - 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)
tests for pancreatic insufficiency
oily or fatty stools, should test decal fat content or decal elastase to test for pancreatic insufficient
Functional constipation, definition
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
Differential of constipation
- 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
- Hirschprung - (see below)
- Anorectal and Colonic Malformation - usually confirmation from birth - anal stenosis, anteriorly displaced anus (mainly in females), imperforate anus, colonic stricture
- Mulridystem disease: muscular dystrophy, CF, diabetes meliitus (?), Developmental delay, celiac, hypothyroidism -
- 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
- Drugs - narcotics, psychotropics
Hirschprung disease - what part of the bowel is dilated
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
common drugs that cause giginval hypertrophy
cyclosporine
phenytoin
calcium channel blockers
causes of delayed teeth eruption
hypopituitarism, hypothyroidism, osteopetrosis, Gaucher disease, Down syndrome, cleidocranial dysplasia, rickets
eosinophilic esophagitis
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
Treatment and prognosis of eosinophilic esophagitis
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
esophageal foreign body - when do you need to remove them
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
what are pill ulcers
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
caustic injury (ie kid swallows a clearner) what to do?
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
Peptic ulcer disease in kids, name some risk factors
- H pylori **plays a significant role, but not as much as in adults, RFs are lower SES and poor sanitation
- drugs - HSAIDS (including aspirin) tobacco use, bispohophonates, potassium supplements, family history, sepsis, head trauma, burn injury, hypotension
- family history
- sepsis
- head trauma
- burn injury
- hypotension
true or false - non ulcer dyspepsia is associated with H pylori
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
which ulcers have pain relieved by eating and which are worse with eating?
duodenal - better with eating
gastric - worse with eating - result in weigh gloss
diagnosis of ulcers
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
patients with ulcers and H. pylori (positive) how to treat
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
treatment of cyclic vomiting syndrome
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
Associated anomalies with omphalocele
cardiac
Beckwith-Wiedemann
intestinal complications
Anorectal malformations
- 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
- high lesions - internal sphincter muscle functionally absent - continence can be hard to achieve
what test to do in all kids with imperforate anus
MRI of lumbosacral spinal cord - high incidence of tethered spinal cord
extraintestinal manifestations of celiac disease
osteoporosis pulmonary hemorrhage seizures/encephalopathy dermatitis herpetiformis erythema nodosum
biopsy findings in celiac
villous atrophy
crypt hyperplasia
increased numbers of intraepithelial lymphocytes
treatment of intusseption
pneumatic enema (best success 90% if t get reduction then need surgery
Main causes of neonatal cholestatic jaundice
- biliary atresia - usually in first few weeks of life, need surgery by 2 months or will have liver failure
- 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
- 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
- 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
treatment of metabolic causes of cholestasis
- vitamins adek
2. formula with medium -chain triglyceride
fulminant liver failure
severe liver disease with onset of hepatic encephalopathy within 8 weeks after initial symptoms, in absence of chronic liver disease
causes of fulminant liver failure
viral hepatitis metabolic disorders autoimmune hepatitis ischemia neoplastic disease toxins
clinical features of fulminant liver failure
- hepatic encephalopathy (has stages)
- respiratory compromise
- hypoglycemia
- renal failure - hepatorenal syndrome - low u/o, azotemia, low urine Na
- ascites from hypo albumin
- increased infection risk
- esophageal varices
8 . hypersplenism from portal hypertension - can lead to thrombocytopenia
treatment of liver failure
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
Chronic liver disease - features
- portal hypertension
- hepatocellular function impaired
- cholestasis
Causes of pancreatitis in kids
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)
pancreatic insufficiency - labs
decal fat
fecal elastas int eh stool (can also measure the other pancreas enzymes)
what are the enzymes made by thte exocrine pancreas
they are inactive proenzymes
trypsin, chymotrypsin, carboxypeptidase
amylase and lipase in pancreatitis
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)
management of pancreatitis
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
Which drugs are contraindicated in breastfeeding
radioactive compounds antimetabolites lithium certain antithyroid drugs (see the CPS statement)
Marasmus features
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
Kwashiorkor, what is the weight
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
Treatment of malnutrition
- 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
- antiinfective therapy if needed - for ova and parasites
increase caloric intake very gradually, monitor for lute problems, poor cardiac function, edema or feeding intolerance
What are the electrolyte abnormalities in referring syndrome?
hypophosphate
hypomagnesemia
hypokalemia
What is catch-up growth?
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
true or false- should give iron supplements early in nutritional rehab for malnourished kids
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
name some complications of malnutrition
- infectino - esp sepsis, pneumonia, gastro
- hypoglycemia
- hypothermia -
- bradycardia and poor cardiac output - increase chance of heart failure
- micronutrient deficiencies -
- growth stunting
- delayed development
- social deprivation with malnutirtion->can further impair development and cognitive function
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?
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
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
B1 - aka thiamine cuses: alcoholics teens with bariatric surgery protein-calorie malnutrition mom's with thiamine deficiency unsupplemented hyperalimentation fluid boiled milk
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
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
