GI misc Flashcards

(35 cards)

1
Q

Food allergy v. food intolerance?

A

IgE-mediated

difficulty digesting or metabolizing a food

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2
Q

MC food allergies?

A

fish/seafood & peanuts/tree nuts

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3
Q

Presentation of food intolerance?

A

Gas
Bloating
Abdominal pain
Diarrhea

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4
Q

Presentation of food allergy?

A

usually immediate

Pruritis, urticarial, flushing, swelling of lips/face/throat,

N/V/D, abd cramping

wheezing, lightheadedness, syncope, hypotension

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5
Q

PE findings seen in pt w/ food allergy?

A

Urticaria
Angioedema
Resp, CV, GI, ENT, derm

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6
Q

Dx of food allergies?

A

H&P

trial of elimination of food x 2 wk +/- food challenge

labs-test for IgE mediated food allergy

  • skin testing
  • IgE immunoassays
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7
Q

Tx for food allergies?

A

Epinephrine autoinjector

Food avoidance

Allergist referral

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8
Q

What is lactose intolerance? Epidemiology?

A

Intolerance to lactose containing food

Lowest: European and European American

Highest: African American, Hispanic, Asian, Asian American, Native American

prevalence increases w/ age

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9
Q

Normal lactose physio??

A

lactase breaks down lactose –> glucose & galactose, absorbed by small intestine, passes into colon, converted to fatty acid & hydrogen gas in the colon

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10
Q

Pathophys of lactose malabsorption?

A

lactose malabsorption

-lactase deficiency

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11
Q

Clinical presentation of lactose intolerance?

A
Abdominal pain
Bloating
Flatulence
Diarrhea 
Borborygmi 

sxs affected by diet, varies

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12
Q

Dx of lactose intolerance?

A

Sxs after lactose ingestion

Sxs resolve with avoidance of lactose

Lactose hydrogen breath test

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13
Q

Tx for lactose intolerance?

A

Lactose-free diet or lactose restrictions

Enzyme replacement – lactase (Lactaid)

Monitor calcium, vit D

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14
Q

What is Glucose-6-phosphate dehydrogenase deficiency?

A

Genetic defect in G6PD, a RBC enzyme that generates NADPH and protects RBCs from oxidative injury

X-linked disorder

lots of varying degrees of enzyme deficiency

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15
Q

G6PD deficiency is assoc. with?

A

hemolytic anemia

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16
Q

Presentation of G6PD deficiency?

A

Usually asxs until a trigger causes acute hemolysis

Jaundice, pallor, dark urine, abdominal pain, back pain

17
Q

What triggers G6PD deficiency?

A

meds, food, acute illness/infx

18
Q

Labs seen in pt w/ G6PD deficiency?

A

Normochromic, normocytic anemia

Peripheral smear: “bite cells”, Heinz bodies (denatured globin chains attached to the RBC membrane)

19
Q

Tx of G6PD deficiency?

A

spontaneous resolution and reversal of anemia

Avoidance of oxidative stress to RBCs

Removal of offending agent

Hydration

Transfusion for severe anemia

20
Q

What is Paget disease of bone
(Osteitis deformans)?

A

Localized area of increased bone turnover causing overgrowth of bone

21
Q

Patho of paget disease of bone?

A

Increased osteoclast activity lytic lesions in the bone > increased osteoblast activity > disorganized bone formation > abn. bones with enlarged skeletal deformity

22
Q

What are the MC locations of paget disease of bone?

A

pelvis, vertebrae, femur, humerus, skull

Can be polyostotic or monostotic

23
Q

Presentation of paget disease of bone?

A

Usually asxs & discovered incidentally

Elevated serum alk phos (then isoenzyme to dif. bone v. liver)

x-ray: Osteolytic lesions

24
Q

Paget disease of the bone is usually discovered incidentally, however, how might a pt present if they were sxs?

A

Pain – aching, deep, worse at night and with weight bearing

Bone changes: bowed tibias, kyphosis, “chalkstick” fxs with minimal trauma, increased hat size, HA

25
Dx studies for paget's disease of the bone?
Bone turnover markers Serum calcium Serum 25-OH vitamin D Bone scintigraphy
26
Tx of paget disease of bone?
Asxs: monitor ``` Bisphosphonates: IV zoledronate (preferred but can use any) ```
27
recurrence rate of paget disease of bone?
12-60%
28
comps of paget disease of bone?
``` Hypercalcemia Renal calculi High output HF Arthritis CN palsies Vascular steal syndrome Radiculopathy or paralysis Bone tumors (sarcoma, giant cell tumors) -rare ```
29
What is rickets?
Deficiency in calcium or phosphate leading to altered bone growth and mineralization
30
Typical locations affected by rickets?
distal forearm, knee, and costochondral junctions
31
Etiology of rickets?
Decreased intake, malabsorption, or increased excretion of calcium, phosphate, or vitamin D
32
Clinical presentation of rickets?
Bowing of weight-bearing extremities Skeletal fxs Proximal myopathy
33
Labs seen in rickets?
Alk phos – elevated Serum phosphorus – low Serum Ca – low or normal PTH – elevated in calcipenic rickets 25-hydroxyvitamin D
34
Radiology findings seen in rickets?
Widened growth plate at long bones and costochondral junction Decreased radiopacity of long bones If occurs after growth plate closure – decreased cortical thickness, relative radiolucency of skeleton
35
Tx of rickets?
Treat underlying disorder Vitamin D replacement Calcium supplementation