Small Bowel Dz Flashcards

1
Q

Impaired breakdown of nutrients to absorbable split-products

A

Maldigestion

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2
Q

Defective mucosal uptake and transport of adequately digested nutrients including vitamins and trace elements.

A

Malabsorption

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3
Q

What do carbohydrates normally breakdown into?

A

Mono, Di or Oligosaccharides

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4
Q

What do amino acids break down into?

A

Oligopeptides

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5
Q

What do Fatty Acids break down into?

A

Monoglycerides

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6
Q

In this phase of absorption nutrients are hydrolyzed and solubilized. Digestion is accomplished by pancreatic enzymes such as amylase, lipase/colipase, trypsin, chymotrypsin, elastase, etc. Also, bile salts are secreted to facilitate emulsification and absorption. Guess where else enzymes come from!? THE BRUSH BORDER WOOT WOOT WOOT.

A

This is the Luminal Phase. Lots happen here, and its a place where malabsorption can occur.

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7
Q

In this phase of absorption, further processing takes place at the brush border with transfer into the cell and across the membrane.

A

Mucosal Phase

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8
Q

In this phase of absorption, nutrients are moved from the epithelium to the portal venous or lymphatic circulation.

A

Transport Phase

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9
Q

The three phases of absorption are the sites where malabsorptive issues can occur.

A

If you don’t know, now you know.

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10
Q

What are 4 basic mechanisms for maldigestion to occur?

A
  1. Gastric Motility
  2. Exocrine Pancreatic Insufficiency
  3. Bile Salt Deficiency
  4. Mucosal Dz
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11
Q

What are three causes of Gastric Motility Related Maldigestion?

A
  1. Subtotal Gastrectomy (Biliroth I and II)
  2. Vagotomy
  3. Dumping Syndrome
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12
Q

This is the partial removal of the stomach including the antrum. Can cause gastric dysmotility and maldigestion

A

Subtotal Gastrectomy

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13
Q

This is a condition that causes gastric motility related maldigestion where food may enter the small intestine too rapidly for proper mixing with digestive enzymes to occur. This can also cause iron deficiency anemia and osteomalacia.

A

Vagotomy

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14
Q

Why does Vagotomy cause Iron deficiency Anemia and Osteomalacia?

A
  1. Iron Deficiency Anemia – gastric acid is required for iron absorption, with it moving too fast you aren’t absorbing adequately.
  2. Osteomalacia – decreased calcium absorption due to the speed of movement.
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15
Q

This is a condition that causes gastric motility related maldigestion where rapid gastric emptying of hypertonic fluids into the small bowel occur.

A

Dumping Syndrome

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16
Q

What are some systemic effects of Dumping Syndrome?

A
  1. Decreased blood volume as fluids are pulled through the bowel
  2. Osmotic diarrhea within an hour
  3. Large carbohydrate meal can cause an excessive insulin surge and hypoglycemia.
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17
Q

This can cause maldigestion if 90+% acinus dysfunction or ductal obstruction occurs.

A

Exocrine Pancreatic Insufficiency

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18
Q

What would you see in labs for a patient with exocrine pancreatic insufficiency?

A
  1. Decreased lipase causing steatorrhea and decreased ADEK absorption.
  2. Decreased amylase causing increased starch fermentation in the gut
  3. Decreased protease causing azotorrhea
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19
Q

What the treatment for exocrine pancreatic insufficiency?

A

Enzyme replacement

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20
Q

This cause of maldigestion has to do with the gall bladder (vague, I know I’m sorry, will you ever forgive me?)

A

Bile Salt Deficiency

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21
Q

When you have a Bile Salt Deficiency, what could be happening?

A
  1. Decreased production via Chronic liver dz
  2. Decreased delivery due to biliary obstruction
  3. Drugs that bind bile salts like cholestyramine
  4. Impaired reabsorption int he terminal ileum
  5. Altered bile salt structure (SIBO) can cause deconjugation leading to free bile acids which are less effective and less soluble

** Remember that bile salts are normally found in micelles for lipid absorption.

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22
Q

This cause of maldigestion occurs via the loss of terminal stages of digestion such as the loss of the enterocyte brush border enzymes (maltase, lactase, sucrase)

A

Mucosal Disease

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23
Q

What can mucosal dz (enterocyte damage) cause?

A
  1. Decreased CCK –> Decreased Gall Bladder Contraction –> Decreased Pancreatic Secretions
  2. Decreased Enteropeptidase secretion into the lumen –> pancreatic zymogens don’t get activated (trypsinogen)
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24
Q

What are five main causes of malabsorption?

A
  1. Decreased intestinal surface area (most common)
  2. Decreased circulation and lymphatic drainage
  3. Mucosal infiltration with abnormal cells
  4. Transport protein mutations
  5. Impaired motility
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25
Q

Where is the majority of absorption occurring in the body?

A

Duodenum/Proximal Jejunum

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26
Q

Where is iron and calcium absorbed proximally?

A

Duodenum/Proximal Jejunum

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27
Q

Where are Vitamin B12 and Bile Salts Absorbed?

A

Terminal Ileum

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28
Q

What factors can cause less surface area and therefore malabsorption?

A
  1. Surgical Resection
  2. Bypasses
  3. Diffuse Mucosal Dz
29
Q

Surgical resections are possible because?

A

40% of the small bowel is expendable and the body compensates by hyperplasia or hypertrophy. This does not bring back the lost surface area completely!

30
Q

Natural or Formerly completed bypasses can also decrease the surface area. What ways does this happen.

A
  1. Jejunal-ileal bypass (no longer completed)
  2. Gastrocolic fistula (Crohns dz, ulcers)
  3. Duodenocolic fistula (Crohns dz, ulcers)
31
Q

What can cause diffuse mucosal dz that can lead to malabsorption due to less surface area available?

A

Celiac Dz! (Gluten-sensitive enteropathy – immune destruction of villi)

32
Q

What factors can cause impaired circulation/lymph drainage and therefore malabsorption?

A
  1. Chronically impaired drainage in heart failure
  2. Congential Lymphangiectasia
  3. Tumor/Infection Blocking Ducts

— These all cause mucosal edema and dilated lacteals and protein loss.

33
Q

What factors can cause mucosal infiltration and therefore malabsorption?

A
  1. Lymphoma
  2. Radiation Enteritis
  3. Whipple’s Dz
34
Q

What is the bacteria involved in Whipple’s Dz?

A

Tropyrema Whipplei

35
Q

What does this bacteria do?

A

Causes malabsorption but can affect the heart, lungs, brain, joints, skin and eyes.

36
Q

What are the symptoms of Whipple’s Dz?

A

Diarrhea
Abdominal Pain
Weight Loss
Joint Pains (can happen before GI symptoms)

37
Q

What is the most commonly inherited tefect in transport proteins that can cause malabsorption?

A

Congenital beta-lipoprotein deficiency

38
Q

If suspecting malabsorption, what is more important: proving malabsorption is occurring or ruling out other dz?

A

Ruling out other dz

39
Q

What are the clinical manifestations of malabsorption?

A
  1. Diarrhea (Hallmark due to inc. osmotic load)
  2. Steatorrhea
  3. Weight Loss
  4. Flatulence and Abdominal Distension
  5. Edema/Ascites
  6. Anemia (microcytic in Celiac) (macrocytic in Vit B12 deficiency – Crohn’s)
  7. Bleeding Disorders (low PT)
  8. Pathologic fracture or secondary hyper-parathyroidism
  9. Electrolyte Disturbances
  10. Vitamin Malabsorption
40
Q

What test can you do to determine a decreased in calcium/magnesium?

A

Chvostek’s Sign

41
Q

Common Vitamin Deficiency Symptoms/Signs (could be due to malabsorption)

A
  1. Motor Weakness (Pantothenic Acid = Vit B5 and D)
  2. Peripheral Neuropathy (Thiamine)
  3. Loss of Vibratory and Proprioception (Vit. B12)
  4. Night Blindness (Vit. A)
  5. Seizures (biotin = Vit. B7)
42
Q

What is an important thing to get when investigating suspected malabsorption?

A

PMH and FamHx!!!

43
Q

What are pertinent past medical history questions to ask when suspecting malabsorption?

A
  1. Previous Surgery (gastric or pancreatic)
  2. Chronic Pancreatitis
  3. Chronic Cholestasis
  4. History of XRT (Radiotherapy)
44
Q

What are pertinent family hx questions to ask when suspecting malabsorption?

A
  1. Celiac’s Dz
  2. Crohn’s Dz
  3. CF
  4. Lactase Deficiency
45
Q

How do you diagnose malabsorption?

A
  1. Check the routine labs for abnormalities in things like carotene, folic acid, iron, calcium, magnesium, total protein, albumin, cholesterol, PT
  2. Fecal Fat! Qualitative Test first with a Sudan Stain THEN 72 hour Quantitative Test. If positive, then D-xylose Testing
  3. Test Exocrine Pancreatic Function (Stool Elastase, Chymotrypsin, Serum Trypsinogen, CT Pancreas for calcifications, Secretin Stimulation Test)
  4. D-xylose Test
46
Q

After testing a patient, you get results that show an increase in fecal fat, normal D-Xylose excretion and normal duodenal/jejunal biopsy. What would you think?

A

Maldigestion due to Pancreatic Insufficiency

47
Q

After testing a patient, you get results that show an increase in fecal fat, decreased D-Xylose excretion and abnormal “flat” duodenal/jejunal biopsy. What would you think?

A

Malabsorption – Celiac Sprue?

48
Q

How does the D-Xylose Test work?

A

D-Xylose is transported largely by passive diffusion across the BBM.
SO
The patient ingests 25 grams of d-xylose and urine is collected over a 5 hour span

49
Q

Healthy subjects will secrete about how much D-xylose in their urine each hour?

A

~90% (4.5 grams)

50
Q

What would an abnormal D-xylose test indicate?

A

Mucosal Disruption due to resection or Celiac Sprue or SBBOG (SBBOG is discussed later)

51
Q

To identify if the abnormal D-Xylose Test as malabsorption vs. SBBOG, what do we do?

A

Treat with antibiotics. If the antibiotics work, then we know it’s SBBOG and not true malabsorption

52
Q

What does the Schilling Test test for?

A

Vitamin B12 Deficiency

53
Q

How does the Schilling test work?

A

After saturating hepatic B12 receptors with unlabeled B12, give radiolabeled B12 to see if it is absorbed.

Should be > 5% in urine, unless impaired absorption.

54
Q

How do you proceed if you get an abnormal Schilling Test?

A
  1. Repeat test after giving oral IF. If absorption is now normal, you have Pernicious anemia (lack of IF).
  2. If still abnormal, it’s malabsorption due to celiac disease, biliary disease, Whipple’s disease, fish tapeworm infestation (Diphyllobothrium latum) or liver disease.)
  3. Repeat test after antibiotics (r/o SBBOG)
  4. Repeat test after pancreatic enzymes (r/o pancreatic insufficiency)
55
Q

What is SBBOG?

A

Small Bowel Bacterial Overgrowth (mostly coliform bacteria)

56
Q

What can SBBOG cause by extension?

A

Mucosal Inflammation and Nutrient Malabsorption

57
Q

True/False: Patients with SBBOG are asymptomatic.

A

False. They can be asymptomatic, but they can also present with bloating, abdominal discomfort, diarrhea, dyspepsia, and in severe cases weight loss.

58
Q

What causes SBBOG to happen?

A
  1. Obstruction (stricture, adhesion dz)
  2. IBS-C/Chronic Constipation (impaired intestinal motility)
  3. Gastrocolic or duodenocolic fistulae (Crohn’s, PUD)
  4. Blind lops or diverticula in the proximal gut (Congenital diverticulitis, afferent loop of Billroth II)
59
Q

What does SBBOG do to the body?

A
  1. Competes for nutrients. Particularly B12
  2. Bacteria produces folic acid (inc. plasma folate)
  3. Hydroxylation of Fatty Acids leading to osmotic diarrhea.
60
Q

How do you treat SBBOG?

A
  1. Repair anatomic defect when possible (close fistuale)
  2. Treat dysmotility (Erythromycin, Domperidone, Reglan)
  3. Antibiotics!!!
  4. Replace Vitamin B12 (parenterally) where affected
61
Q

What antibiotics are used in treating (or ruling out SBBOG from other dzs)?

A
  1. Rifaximin
  2. Augmentin
  3. Metronidazole and Ciprofloxacin
  4. Norfloxacin
62
Q

This is a disorder that is characterized by small bowel intestinal mucosal injury resulting from immunologic damage caused by exposure to dietary gluten (wheat, barley, and rye) in persons genetically predisposed to this dz.

A

Celiac Dz (Gluten Sensitive Enteropathy or Non-Tropical Sprue)

63
Q

How would someone with Celiac Dz present?

A
  1. Diarrhea/Constipation
  2. Abdominal Discomfort
  3. Weight loss
  4. Anemia
  5. Infertility
  6. Premature Osteoporosis
  7. Loss of teeth
  8. Extraintestinal Symptoms
64
Q

How do you diagnose Celiac Dz?

A
  1. Serologic Testing and Upper Endoscopy can be used
  2. Biopsies indicate the spectrum of changes that can range from normal villi with inc infiltration of lymphocytes to abnormal or total villus flattening (bad absorption) – essentially biopsies can give us a gauge of how bad it is
    * **Intestinal Biopsy is gold standard, but not 100%

Labs:

  1. Tissue transglutaminase IgA antibody
  2. If positive, then confirm with Anti-endomysial Ab
65
Q

What are COMMON examples of Extraintestinal Symptoms?

A
  1. Dermatitis Herpetiformis (intense pruritic rash)

2. Iron Deficiency Anemia (common and may be the only sign)

66
Q

What labs can you do to identify Celiac Dz?

A
  1. Tissue Transglutaminase (tTG) Ab, IgA and IgG
  2. Anti-endomysial Ab, IgA
  3. Anti-gliadin Ab, IgA, and IgG
  4. Deamidated Gliadin Peptide (DGP) Ab, IgA (relatively new test that may be positive with Celiac’s who have tTg that is negative.
67
Q

Can you genetically test for Celiac’s?

A

Yes
HLA testing can help decided a difficul case.
99% patients have DQ2 or 8

68
Q

How do you treat Celiac’s Dz?

A
  1. Strict lifelong adherence to a gluten-free diet is the ONLY treatment.
  2. Nutritional supplementation should be provided to correct deficiencies (iron, vitamins and calcium)
69
Q

True/False: Long-term prognosis is excellent for Celiac patient who adheres to the diet.

A

True