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MS2 GI > 10/15- Malabsorption > Flashcards

10/15- Malabsorption Flashcards

1
Q

Effects of Billroth II (gastric surgery)?

A
  • Loss of antrum -> poor grinding
  • Loss of pylorus
  • Asynchronous bile and pancreatic secretions
  • Poor mixing
  • Blind loop
  • Abnormal motility and poor mixing
  • Gastrojejunostomy
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2
Q

What are the different classes of nutrients?

A
  • Fats
  • Carbohydrates
  • Proteins
  • Vitamins
  • Minerals
  • Water
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3
Q

What is the most energy dense nutrient?

A

Fat

  • 9 kcal/g
  • Intake 60-100 g/day
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4
Q

Are TGs water soluble or insoluble?

A

TGs are NOT water soluble

  • Absorption takes the most steps:
  • Pancreatic
  • Biliary
  • Intestinal
  • Intracellular
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5
Q

What is the structure of a TG? Common fatty acids?

A

H2C-O-CO-R (3) + fatty acid

90% of the fatty acids are:

  • Palmitic (16)
  • Stearic (18:0)
  • Oleic (18:1)
  • Linoleci (18:2)
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6
Q

Describe the pancreatic phase of fat absorption

A

TG degraded by lipase into 2-monoglyceride + 2 fatty acids

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7
Q

Describe the hepato-biliary phase of fat absorption

A

Solubilization

  • Bile acid monomers can form micelles
  • Can complex with cholesterol (and phospholipid)

1. Micelle Formation

  • Physical chemical complex - spherical ~3 mm, related to detergent property of bile acids

2. Bile acids

  • Detergents (polar and non-polar ends) made from cholesterol

(Critical micellar concentration 2 - 4 mM spontaneously orient into spheres)

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8
Q

What substances can micelles carry/bind?

A
  • Fatty acids
  • Monoglycerides
  • Cholesterol
  • Fat soluble vitamins
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9
Q

Describe the mucosal/absorptive (intestinal) phase of fat absorption

A
  • Micelles disaggregate at mucosal cell surface
  • Monoglycerides and fatty acids are absorbed
  • Bile acids reform micelles
  • Bile acids absorbed in ileum and recycled (entero-hepatic circulation) for reuse (4-6 times per meal)
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10
Q

Describe the intercellular/lymphatic phase of fat absorption

A
  • Re-esterification of long-chair fatty acids and monoglycerides
  • Packaged into chylomicrons (protein-cholesterol-phospholipids)
  • Transported via lymph
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11
Q

T/F: Micelle formation is essential for fat absorption

A

False

  • Medium chain TGs do not require micelles
  • Re-esterification is not essential
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12
Q

When could one benefit from the alternate fat absorption method involving medium chain TGs

A
  • Re-esterification is not essential
  • Transported via portal vein
  • Useful in diseases associated with lymph blockage (e.g. lymphoma)
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13
Q

What enzyme breaks down starch?

  • Percentage of carb intake
A

Amylase (in the brush border)

  • Starch = 60% of carbs in diet (sucrose 30%, and lactose, 10%)
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14
Q

What enzymes break down disaccharides?

  • Breakdown products?
A
  • Maltase (maltose, maltotriose) -> glucose
  • Dextrinase (dextrins) -> glucose
  • Lactase (lactose) -> galactose + glucose
  • Sucrase (sucrose) -> glucose + fructose
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15
Q

Where does major protein absorption occur?

A
  • Jejunum (major)
  • Ileum (final absorption touches)
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16
Q

Where does protein degradation occur?

A
  • Saliva
  • Stomach: gastric acid, mixing
  • Duodenum: bile and pancreatic secretions
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17
Q

What are the typical presenting features of malabsorption?

A
  • Weight loss
  • Steatorrhea
  • Vitamin deficiencies
  • Malnutrition
  • Watery diarrhea is NOT a usual presentation
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18
Q

What is steatorrhea?

  • Creatorrhea?
A
  • Steatorrhea = fat malabsorption with large, bulky, paste-like, very foul stools
  • Creatorrhea = nitrogen malabsorption (typically fixed when fat malabsorption problem fixed)
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19
Q

Causes of weight loss (broadly)?

A
  • Inadequate intake
  • Excess loss
  • Excess need
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20
Q

What conditions fall under the category of weight loss: inadequate intake (or mal-ingestion)?

A
  • Anorexia
  • Depression
  • Inability to chew
  • No food
  • No money
  • Dysphagia, etc.
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21
Q

What conditions fall under the category of weight loss: excess loss?

A
  • GI = malabsorption
  • Urinary = diabetes
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22
Q

What conditions fall under the category of weight loss: excess need?

A

Thyrotoxicosis

23
Q

What are tests for malabsorption?

A

- Fecal fat excretion

  • Quantitative or qualitative
  • Measure of total intestinal function

- D-xylose absorption

  • Measure of proximal* intestinal function
  • No digestion required
  • Can measure in blood, urine, breath

- B12 absorption tests

  • Measure of distal* intestinal function

- Small bowel biopsy

  • Diagnose mucosal diseases, parasites, tumors

- Small bowel x-ray

- Breath tests (e.g., bile salt)

  • Screening tests for malabsorption (e.g. carbs, bile salts)

- Pancreatic function

  • Lundh test meal
  • Secretin test
  • Response to enzyme therapy
24
Q

Tests that are not of great value for malabsorption?

A
  • Serum carotene
  • Qualitative fecal fat
25
Q

Describe fecal fat test

A
  • 72 hr duration test
  • Measure amt of fat ingested (% of intake)
  • Fat intake influences fat excretion (?)
  • Evaluate effect of bowel resection
26
Q

What are the effects of ileal resection on fecal fat?

A

If > 100 cm (fixed) of ileum resected, will have increased fecal fat excretion

27
Q

Describe the bile acid breath test

A
  • Breath collected (drying tube, rubber tubing, transfer pipette) into scintillation counting vial
  • Measure breath radioactive CO2 specific activity
  • Indicates exposure of bile acids to bacteria
28
Q

What are causes of B12 absorption?

  • Describe Schilling’s test
A

Schilling’s used radioactive B12 (not done anymore)

  • Stage 1: no addition = normal IF and ileum
  • Stage 2: add intrinsic factor => pernicious anemia
  • Stage 3: add antibiotics => bacterial overgrowth
  • Stage 4: add tryspin => pancreatic insufficiency
29
Q

What are some causes of insufficient pancreatic enzyme activity?

A
  • Chronic pancreatitis
  • Pancreatic resection
  • Pancreatic carcinoma
  • Cystic fibrosis
  • Zollinger-Ellison syndrome
30
Q

What is the treatment for insufficient pancreatic enzyme activity?

A
  • Replace enzymes
  • Fix pH problems
31
Q

Describe the different protective substances that bind B12 and aid in absorptive process

A
  • R protein binds B12 in stomach
  • Trypsin in pancreatic secretions digests R protein
  • B12 binds intrinsic factor
32
Q

What are some causes of insufficient bile salt activity?

A
  • Biliary obstruction (jaundice)
  • Blind loop syndrome
  • Ileal disease or resection
  • Zollinger-Ellison syndrome
33
Q

How could you help diagnose pernicious anemia is you suspect it as the cause of B12 malabsorption?

A

Measure gastrin (should be low)

34
Q

Treatment for insufficient bile salt activity?

A
  • Remove obstruction
  • Eliminate bacteria
  • Give ox bile
  • Fix pH problems
35
Q

List of small bowel diseases (contributing to malabsorption)

A
  • Resection
  • Celiac sprue (gluten enteropathy)
  • Whipple’s disease
  • Amyloid
  • Lymphoma
  • Crohn’s disease
  • Many more
36
Q

What causes Celiac Sprue?

  • Histological finding
  • Results in
A
  • Caused by ingested toxin (gluten)
  • Loss of intestinal villi
  • Results in malabsorption
37
Q

What is seen here?

A

Normal small bowel biopsy

  • Many villi with big absorptive surface area
38
Q

What is seen here?

A

Celiac disease

  • Big crypts; no villi
39
Q

What is seen here?

A

Celiac disease: “scalloping”

40
Q

What is seen here?

A

Celiac disease: “scalloping”

  • Mosaic pattern (50% sensitive; 95% specific)
41
Q

What is seen here?

A

Characteristics of Celiac Sprue

  • Absent villi
  • Fissuring
  • Scalloping
  • Mosaic pattern
  • Fissuring and ulcer
42
Q

What causes celiac disease

  • Pathogenesis
  • Immune response centers on what
  • Where is it most severe
A

Genetically determined, specific immune response to antigens present in the wheat protein, gluten

  • Most severe in proximal bowel (because allergy)

Pathogenesis:

  • Gluten -> deamidated gluten -> activates APC -> activates Th cell
  • > activates plasma cell to produce antibodies
  • IgA vs. TG2 and anti-deamidated gluten
  • Immune response is focused on limited portion of alpha-gliadin
  • Production of epitopes recognized by CD4 T cells
  • Requires deamidation by tissue transpeptidase producing a 33 mer resistant to further digestion
43
Q

How is celiac disease diagnosed?

A
  • Stool fat
  • D-xylose
  • Serologic (antibody) tests
  • Anti-gliadin
  • Anti-endomysial (EMA) (EMA-IgA)
  • Anti-tissue transglutaminase (tTG) (tTG-IgA)
  • Small bowel biopsy***
44
Q

Process of diagnosing/documenting celiac disease?

A
  • Demonstrate impaired mucosal function
  • Document mucosal lesion
  • Improvement with gluten withdrawal
  • Clinical - rapid
  • Histologic - slower
45
Q

What causes variability in celiac disease?

A
  • Key = length of bowel involved
  • Proximal only: selective iron deficiency anemia unresponsive to oral iron therapy
  • Iron reabsorbed in duodenum!!
  • Large amount: pan malabsorption
  • Diarrhea, weakness, weight loss, anemia, tetany, bleeding (vitamin K deficiency), etc.
46
Q

What key nutrients are absorbed in:

  • Dudodenum
  • Jejunum
  • Ileum
A
  • Duodenum: Iron (Fe)
  • Jejunum: folate
  • Ileum: Vit B6

(double check?)

47
Q

Therapy for celiac disease?

A

- Gluten free diet

  • No: wheat, rye, barley
  • Yes: rice, oats, corn

- Replace vitamins

48
Q

What causes lactase deficiency

  • Mechanism
  • Genetic?
A
  • Lack of brush border disaccharidase
  • Congenital
  • Acquired
  • Ethnic
  • Mucosal disease (e.g., viral gastroenteritis)
49
Q

How to diagnose lactase deficiency?

A
  • History (e.g., can not drink milk)
  • Lactose tolerance test
  • Symptoms after large lactose drink: diarrhea, cramps, gas, borborygmi; no rise in blood glucose
  • Breath hydrogen test
  • Increase after lactose ingestion as lactose gets to colon
50
Q

Lactose is normally broken down into what products?

  • What about in lactase deficiency?
A
  • Normally -> glucose + galactose and absorbed in small intestine
  • In lactase deficiency, converted into lactic acid and other products (H2 and CO2) by bacteria in the colon; osmotic diarrhea as well (fluid pulled into colon)
51
Q

What does someone have if they think they are allergic to mushrooms?

A

Trehalase (a disaccharidase) deficiency!

52
Q

Bacterial overgrowth:

  • Causes/predispositions
  • Pathogenesis
  • Result
A

Causes:

  • Diverticula
  • Motor abnormalities of the small bowel
  • Surgical bypass, etc.

Pathogenesis

  • Bacterial compete for luminal contents (Vitamin B12, bile acids [deconjugate])

Results in: Malabsorption

  • Caused by abnormal populations of bacteria in the small intestine (stasis is implied)
53
Q

Test for bacterial overgrowth?

A
  • Schilling test before and after antibiotics
  • Fecal fat before and after antibiotics
  • Bile salt breath test
  • D-xylose breath test
  • Response to antibiotic therapy

MS2 GI (26 decks)

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