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HN 320 Clinical Nutrition I > Diseases of Lower GI Tract > Flashcards

Diseases of Lower GI Tract Flashcards

1
Q

How adaptive is the small intestine?

A

Very adaptive. >50% needs to be removed to affect functional ability

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2
Q

What are the two sphincters of the lower GI tract?

A
  • Sphincter of Oddi

* Ileocecal Valve

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3
Q

Describe the Sphincter of Oddi

A

Found at the junction of the pancreatic and bile ducts to control flow from gallbladder and pancreas.

Nerve damage causes dysfunction

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4
Q

Describe the Ileocecal Valve

A

Controls flow of upper GI contents into lower GI and prevents regurgitation of bacteria from large intestine

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5
Q

What three hormones/secretions stimulate release of pancreatic and gallbladder secretion?

A

CCK, gastrin, and secretin

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6
Q

Where are most nutrients absorbed?

A

Duodenum and jejunum

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7
Q

What nutrient is only absorbed in the ileum?

A

B12

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8
Q

What is steatorrhea?

A

Diarrhea that’s high in fat; signals lipid malabsorption

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9
Q

What is absorbed in the large intestine?

A

Vitamin K, Biotin (these two endogenously produced in gut)

Na, Cl, K

SCFAs

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10
Q

Describe the anatomy of the large intestine

A

Ascending, transverse, descending, sigmoid colon

•No villi or microvilli

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11
Q

What is the last sphincter in the GI?

A

Anal sphincter

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12
Q

What are the large intestine secretions?

A
  • Goblet cells produce mucus

* Potassium and bicorbonate

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13
Q

What enzymatic digestion occurs in lg intestine?

A

None. Already done.

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14
Q

What is the primary function of the large intestine?

A

Reabsorption of water, electrolytes, and some vitamins (eg: K)

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15
Q

What is the secondary function of the large intestine?

A

Formation and storage of feces
•insoluble fiber and bilirubin
•400 species of bacteria
•fermentation of fiber and sugar alcohols

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16
Q

Describe fermentation in the large intestine

A
  • Produces SCFA and lactate
  • Energy produced used by bacteria for tissue growth in colon or used in body
  • Excess substrate results in gas
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17
Q

What are the three types of diarrhea?

A
  • OSMOTIC DIARRHEA - from lg sugar load; goes to stomach and body naturally tries to pull in fluid. Acts as a dumping syndrome. (eg: lactose intolerance)
  • SECRETORY DIARRHEA - underlying disease causes secretions - bacteria, viruses, and intestinal hormone secretion, high levels e-lytes
  • EXUDATIVE DIARRHEA - associated with mucosal damage, mucus, blood, proteins, e-lytes, water (Chron’s Disese, UC, radiation enteritis)
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18
Q

Describe the medical diagnosis of diarrhea

A
  • Diagnose underlying etiology
  • Age, hydration status, presence of blood in stool, and immunocompetency
  • Recurrence of episodes related to time of day and food intake
  • Stool cultures
  • Endoscopy
  • Osmolality and electrolyte content
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19
Q

Describe treatment for diarrhea

A
  • treat underlying disease
  • antibiotics
  • restore fluid, e-lyte, and acid/base balance
  • IV therapy, rehydration status
  • medication to treat symptoms
  • suggest prevention strategies
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20
Q

Describe the recommended nutrition therapy for diarrhea

A
  • Dairy - cut fat; buttermilk and yogurt (high in bacteria)
  • Protein - tender, well-cooked meats
  • Grains - white or refined flour (low fiber)
  • Fruits - avoid all raw fruits except banana and melons (sorbitol - prebiotic)
  • Vegetables - (low fiber) well-cooked veggies w/out seeds or skins
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21
Q

Name the primary and secondary functions of the large intestine

A

1st: Reabsorption of water, electrolytes, and some vitamins (Vit K)
2. Formation and storage of feces

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22
Q

What are the symptoms of irritable bowl syndrome?

A

Abdominal pain, alterations in bowel habits, gas, flatulence

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23
Q

What are the three possible types of IBS?

A
  • IBS-D (with diarrhea)
  • IBS-C (with constipation)
  • IBS-M (mixed)
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24
Q

What diet intervention is often used for IBS patients?

A

Fermentable oligo-, di-, and monosaccharides and polyols (FODMAP)

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25
Q

Define diverticulosis/diverticulitis. Where is it most commong?

A

Abnormal presence of outpockets or pouches on surface of SI or colon/ inflammation of

Most common in Western and industrialized countries

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26
Q

What are some risk factors for diverticulosis/diverticulitis?

A

Obesity, sedentary, steroids, alcohol and caffeine intake, cigarette smoking

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27
Q

Give the pathophysiology of diverticulosis/diverticulitis

A
  • Fecal matter trapped, excessive pressure against walls of colon
  • Development of pouches
  • Diverticulitis: pouches become inflamed
  • Bleeding abscess, obstruction, fistula, perforation
28
Q

What are the symptoms for diverticulosis? For diverticulitis? How is it diagnosed?

A
  • Diverticulosis: typically asymptomatic
  • Diverticulitis: fever, abdominal pain, GI bleeding, elevated WBC

Diagnosed by radiology testing (thickened walls, abscess, inflammation)

29
Q

Give three similarities of Crohn’s Disease and Ulcerative Colitis

A

Both:
• Are classified as Inflammatory Bowel Disease (IBD)
• Have environmental/inflammatory triggers
• Are autoimmune disorders

30
Q

Give the etiology and pathophysiology of IBD

A

Genetic predisposition + environmental trigger -> inflammatory response -> Damage to cells of small and/or lg intestine with malabsorption, ulceration, or stricture -> symptoms

31
Q

What are some symptoms of IBD?

A
  • Diarrhea
  • Weight loss
  • Poor growth
  • Hyperhomocysteinemia (related to B vitamins)
  • Partial GI obstructions
32
Q

Where in the body is affected by Crohn’s Disease?

A
  • Distal ileum and colon - 50-60% of cases
  • Small intestine - 25% only in SI or colon
  • Can affect any part of GI (mouth -> anus)
33
Q

How can you spot Chron’s disease on an endoscope?

A

Inflammatory polyps give a “cobblestone” appearance to the mucosa

34
Q

Give some symptoms of Crohn’s disease

A
  • abdominal pain in LRQ
  • diarrhea
  • rectal bleeding
  • weight loss
  • fistulas
  • fever
  • bleeding -> leading to anemia
35
Q

How can Crohn’s disease be diagnosed using blood work/body samples?

A
  • Blood tests for anemia
  • Check WBC count- if elevated sign of inflammation in body
  • Test stool sample for bleeding or infection in the intestines
36
Q

Give two common complications of Crohn’s

A
  • Strictures of the intestine - thickened intestinal wall with swelling and scar tissue, narrowing passage
  • Fistulas - abnormal connection between two organs or organ and skin. Can become infected and fuse together when healed (forming fistula)
37
Q

What are the three goals of Crohn’s treatment?

A
  • Control inflammation
  • Correct nutritional deficiencies
  • Relieve symptoms
38
Q

What does Crohn’s treatment look like?

A

Includes drugs, nutrition supplements, surgery, or a combo

Can help control, but THERE IS NO CURE

39
Q

What deficiency is common in UC? Why?

How is it treated?

A

Iron-deficient anemia due to blood losses

Iron supplements and iron-rich foods + Vitamin C (for absorption)

40
Q

What diet would you recommend to someone during a CD flareup?

A
  • Minimal residue diet with small, frequent, lactose-free meals
  • MCTs may be used to add calories
  • Avoid foods assoc with gas, reflux, bloating
41
Q

Compare Low Residue vs Low Fiber diets

A

**All low residue diets are low fiber diets; not all low fiber diets are low residue
• Low residue limits fiber as well as lactose, mannitol and xylitol, fructose, lots of sucrose, caffeine, and alcohol (basically anything that would increase motility)

42
Q

When the colon and rectum are removed, the surgeon performs a _________

A

ileostomy

43
Q

Describe a COLOSTOMY

A

When the rectum is surgically removed

Colon is attached to stoma

44
Q

Describe colostomy irrigation

A

Purpose is to stimulate peristalsis and get BM going; gives freedom to not wear a bag

45
Q

Describe MNT for colostomy patients

A
  • Begin with clear liquids low in simple sugar (lower osmolality) post-op
  • Progress to low-fiber nutrition therapy with adequate calories and protein for patient
  • Avoid high fiber foods for 2-4 weeks post-op then slowly added back in (water-soluble then insoluble)
  • Avoid odor and gas-producing foods
46
Q

When would we use MCT oil?

A

For fat malabsorption patients.

**but provide no essential fatty acids

47
Q

Describe Ulcerative Colitis

A
  • An IBD that causes inflammation and ulcers in lining of lg intestine
  • Usually occurs in rectum and lower part of colon
  • Inflammation causes rectal bleeding or bloody diarrhea
48
Q

Name 4 ways UC is different from Chron’s?

A
  • UC affects only large intestine (colon) and rectum; Crohn’s can affect anywhere in GI
  • UC only in continuous stretches; Crohn’s occurs in patches
  • UC only the innermost lining; Crohn’s deep layers of tissues
  • UC can be cured through surgical removal of colon; Chron’s is incurable and surgery doesn’t always work
49
Q

What are the most common symptoms of UC?

A

Abdominal pain and bloody diarrhea

50
Q

When does short bowel syndrome occur (SBS)?

A

After resection of small intestine

••severity of problems dependent on what section is removed and health of remaining bowel (eg: ileum causes more deficiencies)

51
Q

What parts of small bowel are best to keep to avoid SBS?

A

Proximal duodenum, prox jejunum, distal ileum and ileocecal valve and ascending colon

52
Q

Why is the ileocecal valve important?

A
  • Prolongs intestinal transit time and prevents ileal contamination with colonic bacteria
  • If removed it results in severe diarrhea
53
Q

What happens if duodenum is removed?

A

Compromised absorption of Ca++, Mg++, and feSo4 (severe hypocalcemia and anemia)

54
Q

Why is removal of the ileum problematic?

A

• Bile salts and B12 are absorbed at terminal end (if cannot reabsorb bile salts

  • liver can’t compensate –> steatorrhea)
  • B12 defic. can cause megaloblastic anemia ~4-5 years

• Reduced absorption of fat soluble vits

  • night blindness (Vit A)
  • hypoprothrombinemia (Vit K)
  • osteomalacia, osteopenia (Vit D)
55
Q

SBS patients are prone to kidney stones. Explain.

A
  • Decreased colonic absorption of oxalate
  • Oxalates normally bind calcium and can’t be absorbed; with low bile salts the FFA and calcium bind instead; unbound oxalates are absorbed and excreted by kidney where they’re bound to Ca++ and form calcium oxalate stones
56
Q

Describe the main goal of nutrition therapy in SBS

A

Aim to prevent malnutrition and dehydration (may include oral eating, enteral nutrition, and parental nutrition - just depends on how bad it is)

57
Q

What are the general dietary guidelines with SBS patients with colon?

A
  • Low fat, high carbohydrate diet –> fat divided equally between meals
  • Chopped, ground, or well-chewed nutrient rich foods
  • Small, frequent meals (~6-8/day)
  • Fluids between meals
  • No concentrated sweets
  • Low oxalate foods to avoid kidney stones (spinach, bran flakes, beets, potato chips)
  • Multivitamin/mineral supplement
  • Lactose restricted
58
Q

Describe gastric hypersecretion in SBS. What does it cause and what is the treatment?

A

Loss of small bowel segments results in change in levels of CCK, secretin, and gastrin), resulting in continued acid secretion
• Increased acid load causes: erosion of gut lining, diarrhea, altered pancreatic enzymes
• Treatment: H2 blockers, PPIs

59
Q

What are the two functions of bile secretions?

A
  • Emulsifying agent

* Absorption - formation of micelles

60
Q

What is the pH of food entering the duodenum?

A

Should be pH 4-5

61
Q

Describe CHOLESTASIS

A

A condition where little/no bile is secreted or bile flow into GI is obstructed

62
Q

What stimulates bile secretion and pancreatic juices?

A

Food entering duodenum and CCK

63
Q

Name and describe some risk factors for gallstones

A
  • High dietary fat, low fiber intake - constant bile synthesis for fat digestion
  • Rapid weight loss (gastric, fasting, etc)
  • Central obesity, insulin resistance, diabetes
64
Q

What are four causes of gallstones?

A
  1. too much water absorption from bile
  2. too much absorption of bile acid from bile
  3. too much cholesterol in bile
  4. inflammation of epithelium
65
Q

What is CHOLELITHIASIS?

A

Presence or formation of gallstones in the gallbladder or bile ducts

66
Q

Describe the nutrition intervention for cholelithiasis

A
  • Low fat, modest protein
  • Small, frequent meals
  • Inactive during acute attacks - NPO
  • Post surgery - high fiber

HN 320 Clinical Nutrition I (10 decks)

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