Week 2 Flashcards
Obsesity, Vitamins, Diseases
3 main categories of bariatric surgery
restrictive, malabsorptive, combination
how does restrictive bypass surgery assist with weight loss
it shrinks the stomach(via resection, bypass, or gastric pouch) by reducing the caloric intake helping the pt feel full quicker
how does malabsorptive weight loss surgery assist with weight loss
it lowers the time spent absorbing food by shortening the functional small intestine (removing the pylorus and dividing both the duodenum and ileum)
whats the main restrictive bariatric procedure type in US
Roux-En-Y
what’s a sleeve gastrectomy
a type of restrictive bariatric surgery
-removes part of the stomach
what is Roux-En-Y procedure
combination restriction and malabsorption (shrinks and resection the small intestine(up to 70% weight loss))
why has the lap band procedure fallen out of favor as a bariatric surgery option in recent years
sleeve gastrectomy is a better procedure because it is easier to perform and viewed as not as drastic by patients
where is intrinsic factor produced
in the stomach
whats the role of intrinsic factor
helps absorb b12 (cobalamin) by transporting it to the ileum.
what nutrients are absorbed in the duodenum
Calcium, Iron, Phosphorus, Folate, Vit. A, D,E,K
Nutrients absorbed in the Jejunum
Vit A, D, E, K, calcium, amino acids
Absorbed in the ileum
Folate, Vit B12, D, K
what vitamin deficiency can freq. occur with a sleeve gastrectomy due to decrease parietal cells
B12(parietal cells produce intrinsic factor)
what comorbid conditions can bariatric surgery help treat
-type 2 diabetes
-hypertension
-dyslipidemia
-sleep apnea
-nonalcoholic fatty liver disease
-GERD
-arthritis
-Joint and back pain
-stress urinary incontinence
Why do water soluble vitamins not cause toxicity
because it dissolves in the water content of the body therefore its easily excreted through the kidneys via urine
B1 deficiency
Beri-Beri, Wernicke encephalopathy> Wernicke Krokoff
vitamin b6 deficiency
Seborrheic Rash
Vitamin B12
megaloblastic anemia
vitamin B3 deficiency
pellagra
what is the most common cause of thiamine deficiency
poor dietary intake. excessive tea/coffee or raw fish intake
3 components of wernickes encephalopathy
Nystagmus (eyes looking back and forth)
Ophthalmoplegia (cannot follow finger)
ataxia
what is glossitis
tongue swelling> become inflamed> turns purple or red
Ds of B3 deficiency
Dementia, Diarrhea, Dermatitis
Describe skin rash in pellagra
Looks like sunburn. In Areas around the lower arms and neck region, top of the shoulders. Normally looks brown or darker skin and is blistery and flaky looking
What patient population is Vit. b12 deficiency common in
Vegans, gastritis, autoimmune malabsorption syndrome
Symptoms of B12 deficiency
Fatigue, pale skin, neurological problems (irritable, memory loss, hallucination, ataxia, numbness in extremities, poor coordination)
why is folate recommended to pregnant women
deficiency can cause neural tube defects
symptoms on biotin deficiency b7?
hair loss, brittle nails, red scaly rash around eyes, nose, and mouth
Vitamin C deficiency
Scurvy 4H’s
Hemorhagic: bleeding gums, prolonged wound healing, nail bed
hyperkeratosis: clogged hair follicles
hypochondriasis= mental=always feeling sick
hematologic abnormalities
what are the fat soluble vitamins
A,D,K,E
what sensory functions does vitamin A deficiency impact
Eyes (nighttime blindness)
what patients pop. is at risk of vitamin A deficiency
premature infants, young children, pregnant women, individuals with low fruit and vegetable intake, malabsorptive syndromes
what major organ does vitamin A toxicity impact
liver
greatest source of vit d
sun
Severe vitamin d deficiency in children are called
Rickets
What type of infants do Rickets affect mostly
chronic malabsorption syndromes
renal disease(activate vit d)
breast feed infants
dark skinned infant (absorb UVB rays> cant absorb vit D)
what other deficiency are seen in rickets and osteomalacia
calcium and phosphorus , vitamin d
what is vitamen d deficiency in adults
osteomalacia
pathophysiology of rickets
defective bone mineralization at cartilage of growth plate> weak bone> gravity> bending of bone changes shape> caused by unmineralized bone
pathophysiology of osteomalacia
qualitative defects in the bone matrix and soft/brittle bones > weak bone> prone to fractures
clinical presentation of rickets
delay in the time of closure of fontanelles (soft spots in skull)
bowed legs (varum) knotkneed( valgum)
frontal bossing (huge forehead)
kyphoscoliosis
rib beading rachitic rosary
clinical presentation of osteomalacia
diffuse bone pain
muscle weakness
fractures
lab test in rickets and osteomalacia
Low calcium
increased PTH
decrease phosphate
decrease vit D
increased alkaline phosphate (normal in children because of growth plates
x ray findings in osteomalacia
looks fuzzy, alot of space in between bone where they are supposed to be connected
pseudofracture
management of rickets and osteomalacia
vitamin d supplement
calcium rich diet; calcium and phosphate supplementation(can correct rickets after supplements)
adequate exposure to sunlight
what lab do you order to evaluate vitamin d deficiency
25-hydroxy vitamin d test
what two major diseases does vitamin E protect against
Heart disease (cardiovascular disease), cognitive decline, liver damage
cancer= macular degeneration/cataracts
whats the major role of vitamin K
clot formation
why do we give newborns a dose of vitamin K after delivery
Vitamin K is produced in liver and their liver isnt developed fully yet to produce vitamin K
whats pagets disease
disorder of bone mineralization and remodeling that leads to bone deformities
etiology of pagets disease
genetics
linked to measles> decline in PBD because of measles vaccine
pathophysiology of pagets disease
disease is caused by excessive and disorganized bone resorption (osteoclast)> followed by abnormal bone formation (osteoblast)> bone remodeling disorganized> structurally weakened bones
how to tell the difference between osteomalacia and pagets disease
mosaic bone and labs are normal in pagets disease
clinical presentation of pagets disease
mostly asymptomatic
axial skeleton or proximal femur in 80% of cases (shoulder, hip, spine, femur)
dull aching pain
worse in weight bearing bones
palpate bone protrusion
Pagets on Xray
irregular thickening of cortical and cancellous bone
bone overgrowth
laboratory findings in pagets
Alkaline phosphatase often elevated
normal gamma-glutamyl transpeptidase
normal calcium and phosphorus in most patients
management of Pagets Disease
Reduce pain
Meds: Bisphosphonates>inhibit osteoclast> helps osteoblast take time to lay down bone carefully
calcitonin if bisphosphonates are not tolerated
surgical interventions
G6PD
inherited in a X linked recessive manner causing intravascular hemolytic anemia.
etiology of G6PD
mutation in the coding region of G6PD gene
pathophysiology of G6PD
G6PD makes NADPH> reduce glutathione> needed to neutralize free radicals> increase oxidative damage
NADPH is needed for RBCs for energy
decrease in G6PD> no NADPH> no energy to RBC> increase oxidative stress> denature hemoglobin and cause intravascular hemolysis
clinical presentation of G6PD
history of a trigger for oxidative stress (fava beans, sulfas (bactrum), Aspirin/NSAIDs
Pallor
Jaundice (heme> indirect bilirubin)
Hemoglobinuria(RBC lysis> hemoglobin excreted)
tachy
Diagnoses (lab test)
decrease hemoglobin, haptoglobin
increase reticulocytes, LDH, and bilirubin
blood smear=Heinz Bodies>denature Hg precipitates. Bite cells> spleen removes heinz bodies (damaged parts)
management of G6PD
avoid oxidative stressors (infections, drugs, fava beans)
-splenectomy but RARE
PKU(phenylketonuria)
increase in phenylalanine levels in body due to inability to metabolize this amino acid
pathophysiology of PKU
mutation of phenylalanine hydroxylase> needed to convert phenylalanine to tryptophan> increase phenylalanine levels cause damage to white matter tracts and myelin> neurological deficits
clinical presentation of PKU
newborns do not present with symptoms takes time
-fair skin due to lack of melanin (tyrosine>dopa>melanin)
musty odor (urine and skin)
developmental delay
behavioral problems (social problems, anxiety, depression)
diagnosis (labs)
heel prick 1st week of life (PKU test)
genetic testing
management PKU
dietary modifications and medication/supplementation
regular blood testing to evaluate phenylalanine in blood
diet
lactose intolerance
deficiency is lactase> causing problems with ingestion of lactose
why isnt lactose intolerance not seen in children under 6
because of breast milk (lactase activity in milk)
Primary lactase deficiency
overtime development of lactose intolerance
secondary lactase deficiency
gut injury(intestinal injury)
pathophysiology of lactose intolerance
increase in lactate>fermented in the gut> causing gas (hydrogen, carbon dioxide and methane)> undigested lactose>osmotic load that pull water and electrolytes into bowel> watery diarrhea
Clinical presentation lactose intolerance
bloating, gas, diarrhea
how to diagnose lactose intolerance
lactose hydrogen breath test=give 50g of lactose orally and sample breath hydrogen at baseline and every 30 mins for 3-4 hrs
Small bowel biospy (rare)
management of Lactose intolerance
reduce dairy intake
lactaid tablets (lactase enzyme prep
if they stop consuming diary increase consumption of calicum and vitamin d supplements
celiac disease
gluten allergy (autoimmune reaction to gliadin)
celiac disease is most seen in what age groups
8-12 months of age
3rd to 4th decade of life 30-40
pathophysiology of celiac disease
gliadin>release tTG> deamidate gliadin> T cell >plasma activation> plasma release anti-tTG etc
t helper cells> cytokine release> intestinal destruction, including loss of the brush border, crypt hyperplasia, and villous atrophy> causes impaired absorption of fat, fat soluble vitamins and minrals> malabsorption
clinical presentation of celiac disease
steatorrhea(bulky, foul smelling, floating stool)
dermatitis herpetiformis(causes itchy blistering rash)=bullae, vesicles, pruritic papules
diagnosis of celiac disease
1st screen = autoantibodies= tissue transglutaminase IgA (98% sensitivity and specificity)
2nd= gold standard small bowel biospy> duodenum may be atrophic, with loss of folds and villi(crypt hyperplasia)
Management of celiac disease
life long gluten free diet(better after 2 weeks)
repeat IgA anti-tissue transglutaminase antibody at 6 and 12 month after diagnosis
