GI 4 Flashcards
why does dereased sleep lead to more obesity
decreased glucose tolerance and insulin sensivitiy (glucocorticoids and sympathetic activity)
Genetic and Endocrind disorders related to obesity
Endocrine: Cushing, GH deficiency, hyperinsulin, hypothyroid, pseudohypoparathyroid
Genetic: Prader-Willi, Turner, Down (a tone of others)
Comorbidities of obesity
- increased CV disease
- type 2 diabetes, hypertension, hyperlipidemia, nonalcoholic fatty liver disease (in 10-25% of teens, can progress to cirrhosis)
- Mechanical complications: OSA, orthopedic complications (Blount disease (tibia vara, look bow legged) and SCFE)
- Mental health: (possibly bidirectional) : may have lower self-esteem, some association with depression, co-occurence of eating disorders and obesity
When to worry about endocrine causes of obesity?
short and fat - usually eating to much should lead to increased linear growth
Labs in obese kids:
fasting plasma glucose, TG, LDL and HDL, LFTs for initial evaluation
overweight with family history of diabetes or signs of insulin resistance should have a fasting plasma glucose
how much screen time
no more than 2 hour/day for >2 year old
children <2 year old should not watch TV
anti obesity drugs that can use as adjunct
- sibutramine - nor epi and Serotonin reuptake inhibitor
2. Orlistate - intestinal lipase inhibitor
when can you consider bariatric surgery in teens?
- complete/near complete skeletal maturity
- BMI>40
- medical complication from obesity
after they failed 6 months of multiD weight management program
which vitamin commonly associated with toxicity with excess intake
vitamin A
vitamin A deficiency symptoms
- maintain epithelial function - i.e. GI (diarrhea) , resp (bronchial obstruction), bladder (pyuria/hematuria)
- eye lesions - most characteristic, usually after age 2 ->poor night vision to night blindness, photophobia, xerophthalmia (dark layers); Bitot spots
- poor growth
- susceptibility o infections
- anemia
- apathy
- MR
- increased ICP (wide separation of cranial bones)
zinc deficiency can increase chance of vitamin A deficiency
mainly in developing world
diagnosis of vitamin A deficiency
vitamin A level <20 ug/dL in deficiency
retinol level is NOT useful
treatment of vitamin A deficiency: 1400 ug
hypervitaminosis A - from excessive ingestion of vitamin A
from chronic ingestion 1. skin lesions 2.bony abnormalities - hyperostosis 3. hypercalcemia 4. liver cirrhosis can also have increased ICP (similar to pseudotumor) , neuro sx, desquamation
excess carotenoids associated with toxicity?
no, not with toxicity but skin can get yellow and the colour can get reduced if intake is reduced
Thiamine deficiency B1
occurs in malnourished states (i.e. malignancy, after surgery) iwhtin 2-3 months of deficiency intake
early: non specific fatigue, irritability, drowy etc
specific
1. peripheral neuritis, decreased DTRs, loss of vibration sense, cramping of leg muscles, CHF, psychic disturbances, ptosis
hoarseness or aphonia
muscle atrophy and tenderness of the nerve trunks
later: increased ICP, meningismus and coma
can get fluid overlaid from unclear mechanism 9wet type)
death from cardiac involvement
True of false - wernicke encephalopathy occurs commonly from thiamine deficiency in kids
false - rare in kids, wernike is mental status changes, ocular signs, ataxia
Diagnosis of thiamine deficiency
ETKA - erythrocyte transketolase activity
thiamine pyrophosphate effect
Prevention of thiamine deficiency
ensure good intake - with meat and enriched cereals, polished rice does not provide enough thiamine
Treatment of thiamine efficiency
can give thiamine orally, if having severe manifestations then IM followed by PO
riboflavin (vitamin B2) deficiency
causes: malnourished and malabsorption, certain drubs (probenicid, phenothiazine, OCP), complex 2 deficiency (mitochondrial disease)
clinicaL:
cheilosis, glossitis, keratitis, conjunctivitis, photophobia, lacrimation, corneal vascularization, seborrheic dermaititis
angular chelosis in malnourished child, which vitamin to think of
vitamin B2 (riboflavin)
reponds to riboflavin
need to eat enough milk, eggs to prevent
Pellagra, what is it and which vitamin deficiency is it associated with?
diarrhea, symmetric scaly dermatitis, neurological symptoms of disorientation and delirium
vitamin B3 (aka niacin)
(table 46-1 is good summary)
usually clinical diagnosis
treatment to replace vitamin and improve diet
which vitamin to think about in infants with seizures without clear cause?
B6 aka pyridoxine
can replace with the vitamin in seizure management (100 mg IV /IM)
causes include prolonged treatment with INH, penilliamine, OCPs
presentation: irriabtiliy, convulsions, hypochromic anemia, FTT, oxaluria
food sources: human milk, infant formula, fortified cereals, meat, fish poultry, banns rice veggies
which are the water soluble vitamins?
thiamine (B1), riboflavin (B2), niacin (B3), pyridoxine (B6), biotin, pantothenic acid (B 5), folic acid , cobalamin (vitamin B12), ascorbic acid (vitamin C)
Biotin deficiency
- scaly periorifical dermatitis
- conjunctivitis
- hair thinning
- alopecia
- CNS: lethargy, hypotonia, withdrawn behaviour
Folate defiiency
megaloblastic anemia, growth retardation, glossitis, neural tube defects
causes: malnutrition, malabsorption, malignancy, hemolytic anemia, anticonvulsant therapy
dx: low folate levels
treatment: 0.5-1.0 mg daily
B12 deficiency
human breast milk can provide enough if mom has good B12 levels
Causes; vegan diet, pernicius anemia (intrinsic factor deficiency) ileal resections, Crohn disease
1. heme manifestations: megaloblastic anemia
2. neuro findings; sensory, parasthesia, peripheral neuritis
3. hyperpigmented knuckles and palms
treament: give vitamin B12
patient presents with irritability, tender and swelling legs, bleeding gums, petechiae, ecchymoses, follicular hyperkeratosis and poor wound healing, what vitamin deficiency to think of?
scurvy (vitamin C deficiency)
predominantly non human milk diets or severe malnutrition
not stored in the body
breast milk contains vitamin C
most common cause of rickets
vitamin D deficiency
differential of causes:
1. vitamin D deficiency - includes nutritional, congenital, secondary to malabsorption/from decreased liver 25 OHD, vitamin D dependent (1 and 2), chronic renal failure
2. calcium deficiency - low intake from diet, prems, malabsorption or from dietary malabsorption
3. phosphorus deficiency - inadequate intake (from perms, from aluminum containing antacids)
4. renal losses (X linked hypophosphatemic rickets, disal RTA, fancony, overproduction of phosphatonin (in tumor, McCune-Albright, epidermal nevus, neurofibromatosis)
Clinical manifestations of rickets
craniotabes (can also get frontal bossing, delayed fontanel closure, delayed dentition dn craniosynostosis)
rachitic rosary
growth plate widening - metaphysics loses its sharp border -fraying; concave metaphysics - aka cupping , get widening of the metaphysis
Harrison Groove (also predisposes to atelectasis and pneumonia)
diagnosis usually made on X ray findings as well as labs
Differential for craniotabes
ping pong skull
rickets, OI, hydrocephalus, syphilis, can be normal in newborns but should disappear in a few months
rickets with significant changes in lower extremity (i.e. coxa vara/bowing of tibia and femur/windswept deformity. What type of rickets most likely to have lower limb involvement?
X linked hypophosphatemic rickets
a
types of rickets with low Ca
can have seizures/tetany/stridor from laryngeal spasm in these
types are: vitamin D deficiency, Vit D dependant rickets type 1 and 2, chronic renal failure , dietary Ca deficiency (can also have normal Ca in these types)
Evaluation of kid with rickets
- dietary history - vitamin D and Ca; soy formula does not have vitamin D or minerals
- cutaneous synthesis - time outside, sunscreen use and clothing; season, skin colour
- material risk factors for vitamin D deficiency (esp if breastfed)
- calcium intake - also, fiber can interfere with calcium absorption
- medication: phenobarbital, phenytoin, aluminum containing antacids can interfere with absorption of phosphate
- malabsorption of vitamin D - by history of liver or intestinal disease - if having GI symptoms should think about this (i.e. diarrhea) - also think about other fat soluble vitamins (ADEK)
- renal disease - chronic renal failure can cause rickets; can also get polyuria
rickets with alopecia
vitamin D dependant rickets type 2
labs in kid with rickets
calcium, phosphorus, ALP, PTH, 23 OHD, 1,25 OHD, creatinine, electrolytes
urinalysis - look for glycosuria and aminoaciduria (positive protein dipstick) (i.e. see in in Fanconi syndrome )
best measure of vitamin D status
25 OHD
vitamin D becomes 25 OHD in the liver
why low phosphate in nutritional rickets
high PTH makes you pee out your phosphate, also lower intestinal absorption
almost never get normal PTH with nutritional vitamin D deficiency, suggests primary phosphate disorder
treatment of nutritional vitamin D deficiency
vitamin D treatment -
1. Stoss therapy 300 000-600000 IU of vitamin D po or IM as 2-4 doses over 1 day
ideal when adherence is an issue
2. daily high dose vitamin D 2000-5000IU/day over 4-6 weeks
after this do 400IU/day if 1 year
ensure enough calcium and phosphorus
calcitriol can help with hypocalcemia in the acute phase
may need acute calcium for symptomatic hypocalcemia
bone malformations can often heal dramatically
Causes of secondary vitamin D deficiency
- . inadequate absorption
- decreased hydroxylation in the liver
- increased degradation
- systemic illness decreasing absoprtion: cholestatic liver disease, defect in bile acid metabolism, CF (other pancreatic disease), celiac, Crohn, intestinal lymphangiectasia
- medications: phonobarb/phenytoin/anti TB (isoniazid or rifampin)
Treatment of secondary vitamin D deficiency
malabsorption: 25 vitamin D - dose based on 25 vitamin D levels; alternatively can be treated with 125 D or parenteral vitamin D
vitamin D dependant rickets, where is the problem
type 1 - problem with 1alpha hydroxyls (low 125 OHD)
type 2 - problems in vitamin D receptor (high 125 D)
treat with calcitriol for type 1 (since need the active form
What is the phosphate in rickets from chronic renal failure?
high phosphate - unlike other causes of vitamin D deficiency because not peeing out the phosphate
mechanism of rickets - decreased activity of 1alph hydroxyls in chronic renal failure
therapy is calcitriol (which is active vitamin D) and can suppress the parathyroid gland as well as help absorb calcium
normalizing phosphate is important - since high phosphate will stimulate PTH (use dietary phosphate restriction as well as binders)
most common genetic disorder that causes rickets due to hypophosphatemia?
X linked hypophosphatemic rickets
pee out phosphate ->low phosphate normally stimulates PTH but in this case the PTH and Calcium are inappropriately normal
therefore need to give calcitriol as well as phosphate supplementation
characterized by poor growth and lower extremities and rickets, as well as delayed dentition and tooth abscesses
hypervitaminosis D presentation
usually from excess vitamin d intake
symptoms from hypercalcemia: i.e. n/v, poor feeding, constipation, abdo pain, pancreatitis
cardiac findings: HTN, decreased QT, arrythmias
CNS: lethargy, hypotonia, confusion, disorientation, depression, psychosis, hallucinations and coma
can lead to renal polyuria, dehydration and hypernatremia
can also get acute renal failure, nephrolithiasis, nephrocalcinosis
usually arrythmias and dehydration lead to death
lab: high calcium, elevated 25 D, hyperphosphatemia, usually normal 1,25 D levels (surprisingly!)
PTH is decreased
might get nephrocalcinosis, anemia
DDx for hypervitaminosis D
other causes of hypercalcemia
- hyperPTH - should have hypo phosphate **makes sense (key difference since excess vitamin D will cause high phosphate)
- Williams
- SC fat necrosis
- familial benign hypocalciuric hypercalcemia
- hypercalcemia of malignancy
Treatment of hypervitaminosis D
control hypercalcemia rehydration consider loop diuretic sometimes use steroids calcitonin is an adjunct bisphosphonates also sometimes help eliminate excess sources (ie vitamins and foods, avoid sun) can be fatal or lead to renal failure
vitamin K deficiency
occurs in infants
vit K factors are @@, VII, IX and X
types of vitamin K deficiency bleeding
- early - 1-14 days of age classic hemorrhagic disease of the newborn ; because of low storage of vitamin K at birth, also don’t make in the gut
occurs mosly in breast fed infants due to the low vitamin K of breast milk, delayed feeding another risk factor
bleeding is GI, mucosa and cutaneous, umbilical stump, post circumcision site (IC bleeding less common) - Late VKDB: 2-212 weeks of age (can occur up to 6 months) ->almost all are in breasted, malabsorption (i.e. CF and liver disease) are the other RFs . Most common site is intracranial
- at birth or shortly after - from maternal meds (i.e. warfarin, phenobar, phenytoin)
- from fat malabsoprtion at any age: cholestatic liver disease, pancreatic disease, intestinal disorders (celiac, IBD, shot bowel)
- prolonged diarrhea
- CF
beyond infancy - low dietary intake never causes vitamin K deficiency
labe in vitamin K deficiency
prolonged PT, PTT usually prolonged but can be normal early on
if milk, measure PIVKA
Treatment of Vitamin K deficient bleeding
1 mg of parenteral vitamin K
vitamin E deficiency
prolonged vitamin E deficiency - can get ataxia, severe progressive neurological disorder
in prems - can get hemolysis from vitamin E deficiency in 2nd month of life
Selenium deficiency
can cause cardiomyopathy
selenium is in soil and in the food
Copper deficiency
Menkes disease - is when the body doesn’t absorb copper
microcytic anemia, osteoporosis, neurologic symptoms, neutropenia, depigmentation of hair and skin
zinc deficiency
chronic: dwarfism, hypogonadism, dermatitis, and T cell immunodeficiency
Iodine deficiency
hypothyroid and goitre
