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Clin. Med 1 > Week 2 > Flashcards

Week 2 Flashcards

Obsesity, Vitamins, Diseases (83 cards)

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1
Q

3 main categories of bariatric surgery

A

restrictive, malabsorptive, combination

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2
Q

how does restrictive bypass surgery assist with weight loss

A

it shrinks the stomach(via resection, bypass, or gastric pouch) by reducing the caloric intake helping the pt feel full quicker

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3
Q

how does malabsorptive weight loss surgery assist with weight loss

A

it lowers the time spent absorbing food by shortening the functional small intestine (removing the pylorus and dividing both the duodenum and ileum)

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4
Q

whats the main restrictive bariatric procedure type in US

A

Roux-En-Y

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5
Q

what’s a sleeve gastrectomy

A

a type of restrictive bariatric surgery
-removes part of the stomach

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6
Q

what is Roux-En-Y procedure

A

combination restriction and malabsorption (shrinks and resection the small intestine(up to 70% weight loss))

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7
Q

why has the lap band procedure fallen out of favor as a bariatric surgery option in recent years

A

sleeve gastrectomy is a better procedure because it is easier to perform and viewed as not as drastic by patients

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8
Q

where is intrinsic factor produced

A

in the stomach

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9
Q

whats the role of intrinsic factor

A

helps absorb b12 (cobalamin) by transporting it to the ileum.

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10
Q

what nutrients are absorbed in the duodenum

A

Calcium, Iron, Phosphorus, Folate, Vit. A, D,E,K

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11
Q

Nutrients absorbed in the Jejunum

A

Vit A, D, E, K, calcium, amino acids

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12
Q

Absorbed in the ileum

A

Folate, Vit B12, D, K

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13
Q

what vitamin deficiency can freq. occur with a sleeve gastrectomy due to decrease parietal cells

A

B12(parietal cells produce intrinsic factor)

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14
Q

what comorbid conditions can bariatric surgery help treat

A

-type 2 diabetes
-hypertension
-dyslipidemia
-sleep apnea
-nonalcoholic fatty liver disease
-GERD
-arthritis
-Joint and back pain
-stress urinary incontinence

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15
Q

Why do water soluble vitamins not cause toxicity

A

because it dissolves in the water content of the body therefore its easily excreted through the kidneys via urine

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16
Q

B1 deficiency

A

Beri-Beri, Wernicke encephalopathy> Wernicke Krokoff

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17
Q

vitamin b6 deficiency

A

Seborrheic Rash

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18
Q

Vitamin B12

A

megaloblastic anemia

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19
Q

vitamin B3 deficiency

A

pellagra

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20
Q

what is the most common cause of thiamine deficiency

A

poor dietary intake. excessive tea/coffee or raw fish intake

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21
Q

3 components of wernickes encephalopathy

A

Nystagmus (eyes looking back and forth)
Ophthalmoplegia (cannot follow finger)
ataxia

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22
Q

what is glossitis

A

tongue swelling> become inflamed> turns purple or red

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23
Q

Ds of B3 deficiency

A

Dementia, Diarrhea, Dermatitis

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24
Q

Describe skin rash in pellagra

A

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

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25
What patient population is Vit. b12 deficiency common in
Vegans, gastritis, autoimmune malabsorption syndrome
26
Symptoms of B12 deficiency
Fatigue, pale skin, neurological problems (irritable, memory loss, hallucination, ataxia, numbness in extremities, poor coordination)
27
why is folate recommended to pregnant women
deficiency can cause neural tube defects
28
symptoms on biotin deficiency b7?
hair loss, brittle nails, red scaly rash around eyes, nose, and mouth
29
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
30
what are the fat soluble vitamins
A,D,K,E
31
what sensory functions does vitamin A deficiency impact
Eyes (nighttime blindness)
32
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
33
what major organ does vitamin A toxicity impact
liver
34
greatest source of vit d
sun
35
Severe vitamin d deficiency in children are called
Rickets
36
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)
37
what other deficiency are seen in rickets and osteomalacia
calcium and phosphorus , vitamin d
38
what is vitamen d deficiency in adults
osteomalacia
39
pathophysiology of rickets
defective bone mineralization at cartilage of growth plate> weak bone> gravity> bending of bone changes shape> caused by unmineralized bone
40
pathophysiology of osteomalacia
qualitative defects in the bone matrix and soft/brittle bones > weak bone> prone to fractures
41
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
42
clinical presentation of osteomalacia
diffuse bone pain muscle weakness fractures
43
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
44
x ray findings in osteomalacia
looks fuzzy, alot of space in between bone where they are supposed to be connected pseudofracture
45
management of rickets and osteomalacia
vitamin d supplement calcium rich diet; calcium and phosphate supplementation(can correct rickets after supplements) adequate exposure to sunlight
46
what lab do you order to evaluate vitamin d deficiency
25-hydroxy vitamin d test
47
what two major diseases does vitamin E protect against
Heart disease (cardiovascular disease), cognitive decline, liver damage cancer= macular degeneration/cataracts
48
whats the major role of vitamin K
clot formation
49
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
50
whats pagets disease
disorder of bone mineralization and remodeling that leads to bone deformities
51
etiology of pagets disease
genetics linked to measles> decline in PBD because of measles vaccine
52
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
53
how to tell the difference between osteomalacia and pagets disease
mosaic bone and labs are normal in pagets disease
54
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
55
Pagets on Xray
irregular thickening of cortical and cancellous bone bone overgrowth
56
laboratory findings in pagets
Alkaline phosphatase often elevated normal gamma-glutamyl transpeptidase normal calcium and phosphorus in most patients
57
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
58
G6PD
inherited in a X linked recessive manner causing intravascular hemolytic anemia.
59
etiology of G6PD
mutation in the coding region of G6PD gene
60
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
61
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
62
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)
63
management of G6PD
avoid oxidative stressors (infections, drugs, fava beans) -splenectomy but RARE
64
PKU(phenylketonuria)
increase in phenylalanine levels in body due to inability to metabolize this amino acid
65
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
66
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)
67
diagnosis (labs)
heel prick 1st week of life (PKU test) genetic testing
68
management PKU
dietary modifications and medication/supplementation regular blood testing to evaluate phenylalanine in blood diet
69
lactose intolerance
deficiency is lactase> causing problems with ingestion of lactose
70
why isnt lactose intolerance not seen in children under 6
because of breast milk (lactase activity in milk)
71
Primary lactase deficiency
overtime development of lactose intolerance
72
secondary lactase deficiency
gut injury(intestinal injury)
73
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
74
Clinical presentation lactose intolerance
bloating, gas, diarrhea
75
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)
76
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
77
celiac disease
gluten allergy (autoimmune reaction to gliadin)
78
celiac disease is most seen in what age groups
8-12 months of age 3rd to 4th decade of life 30-40
79
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
80
clinical presentation of celiac disease
steatorrhea(bulky, foul smelling, floating stool) dermatitis herpetiformis(causes itchy blistering rash)=bullae, vesicles, pruritic papules
81
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)
82
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
83

Clin. Med 1 (2 decks)

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