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NUNP531 Applied Pathophysiology > FINAL GI > Flashcards

FINAL GI Flashcards

1
Q

Describe how layers of the GI tract are innervated. What is the name of the plexus that is dispersed throughout the walls of the GI tract?

A

A network of intrinsic nerves that controls mobility, secretion, sensation, and
blood flow is located solely within the GI tract and controlled by local and autonomic nervous system
stimuli through the enteric (aka INTRAMURAL) PLEXUS located in different layers of the GI walls

(see figure 35.2 in first edition text for a good image of this!)

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2
Q

Is salivation controlled by sympathetic or parasympathetic system?

A

Both.

Cholinergic parasympathetic fibres stimulate the salivary glands, and atropine (an anticholinergic agent)
inhibits salivation and makes the mouth dry. β-Adrenergic stimulation from sympathetic fibres also
increases salivary secretion.

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3
Q

Describe the esophagus in terms of portions that are voluntary and involuntarily controlled. How is each section innervated?

A

The pharynx and upper third of the esophagus contain striated muscle (voluntary) that is
directly innervated by skeletal motor neurons that control swallowing.

The lower two-thirds contain
smooth muscle (involuntary) that is innervated by preganglionic cholinergic fibres from the vagus nerve.

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4
Q

How is peristalsis stimulated in the esophagus?

A

Peristalsis is stimulated when afferent fibres distributed along the length of the esophagus sense
changes in wall tension caused by stretching as food passes.

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5
Q

The esophagus has both intrinsic and extrinsic innervation. Describe what this means

A

Extrinsic innervation = innervated by the vagus nerve

Intrinsic = also innervated by enteric nervous system, which is inside the walls of the esophagus. This is the same as the enteric/intramural plexus

**The enteric plexus serves as a type of secondary wave of peristalsis if the initial wave doesn’t get the food all the way to the stomach

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6
Q

When the swallowing reflex is initiated, afferent sensory information is sent to the swallowing center via 3 cranial nerves. Which 3 are they?

Efferent (motor) info is then sent back via 2 nerves…which are they?

A

Sensory:
Glossopharyngeal
Vagus
Trigeminal

Motor:
Vagus & glossopharangeal

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7
Q

What nerve is the primary control for tone of the lower esophageal sphincter?

A

Vagus! (basically, vagus for everything)

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8
Q

What are the two plexuses that constitute the enteric (intramural)
nervous system? (this is likely too detailed, but it does say that basically all of the GI tract has this intrinsic innervation)

A

myenteric plexus (Auerbach
plexus) and the submucosal plexus (Meissner plexus)

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9
Q

Sympathetic vs parasympathetic innervation of the stomach - what is responsible for each?
What nervous system

A

The vagus nerve provides parasympathetic innervation, and
branches of the celiac plexus innervate the stomach sympathetically.

the enteric (intramural)
nervous system within the stomach responds to local stimuli.

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10
Q

What is the function of bile?

A

Aids in intestinal digestion of fats. Bile salts aid in fat emulsification and absorption. Fats are broken down into fatty acids that are absorbed across the intestinal mucosa as micelles (water soluble fat products).

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11
Q

What is bile?

A

Yellow green alkaline fluid containing bile salts, cholesterol, bilirubin, electrolytes, and water. It is important in intestinal fat digestion and absorption.

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12
Q

Describe the production and flow of bile.

A

Bile is produced by the hepatocytes and moves through the liver via bile canaliculi to drain into bile ducts that eventually drain into the common bile duct. This leads to the ampulla of vater (where the bile duct and pancreatic duct meet), which empties into the duodenum called the major duodenal papilla (surrounded by the sphincter of oddi). If the spincter is closed (i.e., in periods between meals), bile backs up and is stored in the gall bladder.

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13
Q

What blood vessel returns bile salts absorbed in the terminal ileum to the liver?

A

Portal vein (enterohepatic circulation)

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14
Q

What stimulates the gallbladder to contract?

A

Food in the duodenum about 30min after eating. Contraction stimulated by the vagus nerve.

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15
Q

What stimulates the gallbladder to relax?

A

Sympathetic stimulation, vasoactive intestinal peptide, pancreatic polypeptide.

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16
Q

What is the function of the gallbladder?

A

Sac like organ on the inferior surface of the liver that stores and concentrates bile between meals. The mucosa of the gall bladder wall readily absorbs water and electrolytes, leaving a high concentration of bile salts, pigments, and cholesterol.

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17
Q

Define cholelithiasis

A

Formation of gallstones

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18
Q

Describe the epidemiology of cholelithiasis

A

More prevalent in developed countries and Indigenous populations
More common in women than men
Risk factors include obesity, middle age, pregnancy, use of oral contraception, rapid weight loss, genetic predisposition, and gallbladder, pancreatic, or ileal disease

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19
Q

True or false: gall stones are always symptomatic

A

False- can be asymptomatic for months to years. Symptoms result if gallstones become lodged in the cystic or common duct during contraction of the gallbladder.

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20
Q

What is the most common type of gallstone?

A

Cholesterol

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21
Q

What do all gallstones contain?

A

Cholesterol, unconjugated bilirubin, bilirubin calcium salts, fatty acids, calcium carbonate and phospates, and mucin glycoproteins

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22
Q

True or false: many gallstones can fill the entire gallbladder

A

True

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23
Q

When do gallstones become symptomatic?

A

When they become lodged in the cystic duct (or any part of bilirary tract), obstructing flow of bile out of the gallbladder, causing pain and inflammation

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24
Q

What are the two types of inflammatory bowel disease?

A

Crohn’s Disease and Ulcerative Colitis

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25
Q

Outline the epidemiology of IBD.

A

Age of onset 10 – 40 (CD 10-30; UC 10-40)

Equal prevalence between men and women

Higher prevalence in Caucasians, Ashkenazi Jewish populations

Family history/genetic susceptibility

DIFFERENCE: smoking/nicotine increases risk of CD but reduces risk of UC

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26
Q

True or false, IBD is an autoimmune disease?

A

True

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27
Q

What kind of pain is characteristic of gallstones

A

Epigastric, right hypochondrium (RUQ), intolerance to fatty foods are cardinal manifestations
Pain occurs 30 min to hours after eating a fatty meal, and may be constant or intermittent.
May also have vague symptoms like heartburn, flatulence, epigastric pain, discomfort

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28
Q

Where does the inflammation occur in the two types of inflammatory bowel disease?

A

In Crohn’s Disease – begins in intestinal submucosa and spreads discontinuously. Small bowel involved, right sided colonic involvement, rectum usually not involved. Bowel wall affected asymmetrically and segmentally with skip areas, patchy inflammation with ulcerations extending transmurally (throughout the layers of organ wall)

Ulcerative Colitis – lesion begins with the base of the crypt of Lieberkuhn in large intestine. Starts with the rectum and may extend to entire colon. Bowel wall affected symmetrically with uninterrupted pattern, inflammation is uniform and diffuse, affects mucosal layer

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29
Q

What is the time course of IBD?

A

Age of onset 10 – 40 (CD 10-30; UC 10-40)

Chronic disease with remissions and exacerbations

Incurable

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30
Q

Jaundice indicates a gallstone is lodged in the _______________duct

A

common bile

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31
Q

Describe the signs and symptoms in Crohn’s disease

A

Lesions from mouth to anus (terminal ileum and colon most common)

Lesions discontinuous

Entire intestinal wall inflamed

Transmural granulomata are common – cobblestone appearance

Ulcerations are deep fissures, fistula common

Narrow lumen and obstruction common

Small intestine malabsorption common

Abdo pain – classically RLQ, moderate-severe

Diarrhea/constipation/vomiting

+ many extraintestinal symptoms

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32
Q

Describe the signs and symptoms of ulcerative colitis

A

Continuous lesions in the large intestine

Mucosal layer inflammation

Ulcerations superficial crypt abscesses

Abdo pain – mild-severe

Diarrhea common, frequent small volume, mucous, severe urgency (tenesmus)

Bloody stool common

+ many extraintestinal symptoms

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33
Q

What is the laboratory stool test which can differentiate IBS from IBD?

A

Fecal calprotectin – indicates migration of neutrophils to intestinal wall.

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34
Q

What other diagnostic testing would be beneficial with IBD?

A

Labs related to inflammation, nutritional status and anemia

Stool studies to rule out other causes such as cdiff, parasites

Imaging: abdo xray (bowel wall thickening, obstruction, toxic megacolon, perforated bowel); Barium enema (colon xray, shows mucosal patterns differentiating CD from UC). US, CT and MRI more limited use.

Gold standard for diagnosis: Colonoscopy

May also require flexible sigmoidoscopy

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35
Q

What are some pharmacological management options with IBD?

A

5-aminosalicylate (higher efficacy in UC)

Corticosteroids

Immunosuppressants

Monoclonal antibodies/Anti- tumor necrosis factor (TNF) therapies

Antibiotics for infections

Symptomatic treatment with analgesics, antidiarrheals, iron supplements, anticholinergics for cramps

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36
Q

What are some non-pharmacological management options with IBD?

A

Fecal transplant

Probiotics

Diet changes

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37
Q

Describe the treatment of gallstones

A

Oral bile acids may dissolve stones
Dietary modifications may prevent development of gallstones (reducing intake of poly and mono unsaturated fat and caffeine; increasing fibre intake)
Endoscopic removal of gallstones
Lithotripsy of large stones

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38
Q

What role does surgery often play in crohns/UC?

A

Surgery is not curative, indicated for failed medical therapy, recurrent disease, fistula, abdominal abscess, stricture, malignancy, acute obstruction, peritonitis, perforation, toxic megacolon, major hemorrhage.

Goal to remove grossly involved bowel and spare as much normal bowel as possible

Crohn’s - 80% require surgery at some point in disease

UC – 20% require surgery at some point in disease

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39
Q

Define cholecystitis

A

Inflammation of gallbladder or cystic duct

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40
Q

Describe epidemiology of cholecystitis

A

Affects 16-18% of Canadians. Predisposing factors include increasing age (above 40), obesity, gallstone disease, female, prolonged fasting, use of cholesterol lowering drugs, bile acid malabsorption

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41
Q

Describe the pathophysiology of cholecystitis.

A

Acute or chronic inflammation of the gall bladder wall.
Acute caused by gallstones lodged in cystic duct- causes the gallbladder to become distended and inflammed. Pressure against the distended gallbladdder wall decreases blood flow and may result in ischemia, necrosis, and perforation.

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42
Q

What are signs and symptoms of ACUTE cholecystitis

A

Abrubt, severe, constant RUQ epigastric pain that may radiate to back or shoulder. Similar pain to gallstones that is worse following 30 min ingestion of fats. Fever, leukocytosis, rebound tenderness, abdo guarding, nausea, and vomitting may occur in severe cases.

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43
Q

What are signs and symptoms of chronic cholecystitis

A

Vague symptoms or biliary colic prior to cholecystitis; exaccerbation and remission pattern

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44
Q

Describe diagnosis of cholecytisits

A

Positive Murphys signs (tenderness to R subcostal area with palpation during deep inspiration- don’t press hard or you may rupture the gallbladder!)
CBC- leukocytosis, elevated CRP, poss elevated liver enzymes and bilirubin
CT or gallbladder US to confirm diagnosis.
*Differentiate from pancreatitis, MI, pyelonephritis

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45
Q

Describe management of acute cholecystitis

A

Symptom management/ pain control/ antiemetics
Antibiotics for infection in severe cases
May require cholecystectomy

*chronic attacks treated with low fat diets and potential cholecystectomy in the future

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46
Q

Irritable bowel syndrome is a disorder of the ______ - _______ axis

A

The brain-gut axis

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47
Q

Describe the prevalence and risk factors of IBS

A

Higher prevalence during youth and middle age – 50% occurs before age 35

North American prevalence 10-15%

Higher prevalence in females

Underdiagnosed – estimated 40% undiagnosed

Risk factors: previous gastroenteritis, stress, genetics, Associated with fibromyalgia, chronic fatigue syndrome, GERD, functional dyspepsia, non-cardiac chest pain, anxiety and depression

48
Q

What are some of the general theories of the contributing patho mechanisms in IBS?

A

Patho is not clear; presentations vary widely, and multiple factors seem to play a role. Note there are no micro or macroscopic abnormalities

-changes in gastrointestinal motility – increased or decreased

-visceral hypersensitivity

-intestinal inflammation

-postinfectious gut changes

-fecal flora alterations/bacterial overgrowth

-food sensitivities/intolerances

-psychosocial factors: early trauma, abuse, emotional stress

49
Q

Is IBS acute or chronic?

A

IBS is characterized by chronic symptoms with severity variation over time

50
Q

What are the signs and symptoms of IBS?

A

Gastrointestinal:

Recurrent abdominal pain/discomfort which improves with bowel movements

Altered bowel habits (diarrhea, constipation)

Flatulence, bloating, nausea

Sense of incomplete emptying

Symptoms do not interfere with sleep

Extraintestinal:

Dysmenorrhea

Urinary frequency, urgency and incomplete bladder emptying

Impaired sexual functioning

Fibromyalgia

51
Q

There are 4 different classifications of IBS, what are they?

A

IBS with predominant constipation (IBS-C): Small, hard, pellet-like stools >25% of the time and loose stools<25% of the time

IBS with predominant diarrhea (IBS-D): Loose stools (small volume, pasty/mushy or watery) >25% of the time and hard stools<25% of the time

IBS with mixed bowel habits: Alternating constipation and diarrhea; Constipation and diarrhea each>25% of the time

IBS unclassified: Meet IBS criteria but do not fit above classifications.

52
Q

What is the key diagnostic test to diagnose IBS?

A

Trick question! There are no definitive diagnostic tests for IBS, testing is done to rule out differential diagnoses. It is a diagnosis of exclusion

53
Q

What might initial evaluation include for a patient presenting with IBS symptoms

A

All Classifications: complete CBC, Age-appropriate colorectal cancer screening

IBS-D: Fecal calprotectin or fecal lactoferrin, Stool testing for giardia, Celiac disease serology

IBS-C: Abdo x-ray

54
Q

Patients without alarm features receive only initial evaluation for IBS. Additional evaluation is indicated if alarm features are present. What are some alarm features?

A

Onset after age 50

Rectal bleeding/melena

Nocturnal symptoms

Progressive abdo pain

Unexplained weight loss

Lab abnormalities (iron deficiency anemia, increased CRP, fecal calprotectin/lactoferrin)

Family history of IBD or colorectal Ca

55
Q

What types of additional evaluation may be required for alarm features in IBS?

A

Colonoscopy

Abdominal CT

Abdominal U/S

56
Q

Once underlying organic disease has been ruled out the Rome IV criteria are used to diagnose IBS. What are the criteria?

A

Recurrent abdominal pain, on average, at least one day per week in the last three months, associated with two or more of the following:

Related to defecation

Associated with a change in stool frequency

Associated with a change in stool form (appearance)

(Criteria fulfilled for the last 3 months with symptom onset at least 6 months prior to diagnosis)

57
Q

Management of IBS can start with a trial of diet and lifestyle modifications. What are some of these modifications?

A

Psyllium (soluble fiber) improves both constipation and diarrhea

Low FODMAP diets

Possible lactose or gluten avoidance

Regular meal pattern

Avoid large meals

Reduced intake of fat, insoluble fibers, caffeine and gas-producing foods (ex. Beans, cabbage, onions

Adequate fluid intake

Physical activity

Stress management: counselling, meditation, yoga

58
Q

IBS that is Moderate-severe/ unresponsive to lifestyle/dietary modifications can require pharmacologic therapies, what are some examples?

A

Polyethylene glycol (PEG) first line for constipation

Antidiarrheals (loperamide)

Antispasmodics (Hyoscyamine, Dicyclomine)

Prosecretory medications

Low-dose antidepressants (amitriptyline, nortriptyline)

Visceral analgesics

Serotonin agonists or antagonists

59
Q

What are some alternative therapies for the management of IBS?

A

Prebiotics, probiotics

Hypnosis

Acupuncture

CBT

60
Q

What is a peptic ulcer? Where in the GI tract does it occur (3) and which is most common?

A

break or ulceration in the protective mucosal lining of the lower esophagus, stomach, or duodenum.

DUODENAL ulcers are most common!

61
Q

What are the primary causes of peptic ulcers

A

Ulcers develop when mucosal protective factors are overcome by erosive factors
commonly caused by NSAIDs and H. pylori infection.

62
Q

Is H pylori infection common? Which population in Canada is particularly affected?

A

Very! In Canada, it is estimated that 8 to 10 million people are infected with H. pylori. In First Nations
communities, approximately 75% of people are infected with H. pylori.

63
Q

are young or old more likely to be infected with H pylori?

A

Older
The infection rate for 30-year-olds is 1 in 5 people. The infection rate for people 80 years or older is 1 in 2 people.

64
Q

T/F H pylori is considered to be a carcinogen

A

True, because it is associated with stomach cancer

65
Q

Risk factors for development of a peptic ulcer

A
  • Infection of the gastric and duodenal mucosa with Helicobacter pylori
  • Chronic use of nonsteroidal anti-inflammatory drugs
  • Alcohol
  • Smoking
  • Advanced age
  • Chronic diseases, such as emphysema, rheumatoid arthritis, cirrhosis, obesity, and diabetes
  • Type O blood
  • Psychological stress
66
Q

What is the difference between an erosion and an ulcer in terms of layers they damage?

A

Superficial ulcerationsare called erosions because they erode the mucosa but do not penetrate the muscularis mucosae

True ulcers extend through the muscularis mucosae and damage blood vessels, causing hemorrhage, or perforate the GI wall.

67
Q

What is the difference between an erosion and an ulcer in terms of layers they damage?

A

Superficial ulcerationsare called erosions because they erode the mucosa but do not penetrate the muscularis mucosae

True ulcers extend through the muscularis mucosae and damage blood vessels, causing hemorrhage, or perforate the GI wall.

68
Q

In duodenal ulcers, commonly we see ________ and ______production/secretion is increased

A

Acid & pepsin

69
Q

How does H Pylori infection lead to an ulcer?

A

The host response to H. pylori infection
is activation of T and B lymphocytes (T and B cells) with infiltration of neutrophils
–> Release of
inflammatory cytokines damages the gastric epithelium.
–> some other cytotoxins released by H pylori causes apoptosis of gastric epithlelial cells & promotes inflm

70
Q

S&S of PUD. What might a patient report around mealtime?

A

Pain -aching, boring, gnawing, or burning feeling.
- Epigastric pain (RUQ or LUQ)
- Pain that awakens the client at night or in early morning.

Patient reporting of epigastric abdominal pain, early satiety, and fullness following a meal raise suspicion of PUD. .

Perforated peptic ulcer presents with a sudden onset of severe sharp abdominal pain.

Other S&S:
Asymptomatic, GI distress one to three hours after a meal- on an empty stomach, Pain relieved by food, antacids, or vomiting, Nausea and vomiting, Haematemesis, Chest discomfort, Blood in stools, “grape jelly-” or maroon-coloured stools, Loss of appetite or weight, Weight gain.

71
Q

How do gastric and duodenal ulcers differ in terms of pain following a meal?

A

Duodenal: The pain begins 2 or 3 hours after eating, when the stomach is empty. Pain is relieved rapidly by ingestion of food or antacids, creating a typical pain-food-relief pattern.

Gastric: The same pattern of pain is common but the pain of gastric ulcers also occurs immediately after eating

72
Q

Complications of PUD?

A
  • Upper gastrointestinal bleeding

· Gastric outlet obstruction

· Perforation

· Penetration

· Gastric cancer

73
Q

How does obstruction result in PUD?

A

may be the result of edema from inflammation or scarring from chronic injury

74
Q

T/F duodenal ulcers typically resolve on their own and reccurenace is rare

A

false

Duodenal ulcers often heal spontaneously but recur within months without treatment.
Exacerbations tend to develop in the spring and fall.

75
Q

Diagnosis of PUD

A

History & physical exam

Labwork: Complete blood count (CBC), Stool for occult blood, Coagulation studies
*Testing for H. pylori:
1) Endoscopy with biopsy is the most accurate test.
2. Rapid urease test is the diagnostic test of choice
3. Urea breath test (UBT) is preferred.
4. Serum test for H. pylori antibodies.
5. Stool H. pylori antigen testing—more accurate than antibody testing and less expensive.

Radiography with barium

Mucosal biopsy, after GI consultation, to rule out cancer.

Fasting gastrin level (screen for Zollinger–Ellison syndrome).

Esophagogastroduodenoscopy (EGD): Patients over 50 years of age and new onset of dyspeptic symptoms should get evaluated by an EGD. Anyone with the presence of alarm symptoms should undergo EGD irrespective of age. Lesions less than 5 mm in diameter are termed erosions, whereas lesions greater than 5 mm in diameter are termed ulcers.

Barium swallow: It is indicated when EGD is contraindicated.

76
Q

What part of the stomach do gastric ulcers most often develop in?

A

Antrum (adjacent to acid-secreting mucosa)

77
Q

Duodenal ulcers tend to follow a pattern of remissions and exacerbations. Do gastric ulcers tend to follow the same path?
What symptoms might you see in gatric ulcers more than duodenal that can lead to weight loss?

A

Gastric ulcers tend to be chronic rather than alternating between periods of remission and exacerbation and
cause more anorexia, vomiting, and weight loss than duodenal ulcers.

(because you have pain immediately after eating with gastric, I imagine this makes it much less appealing to eat!)

78
Q

Treatment of PUD?

A

If p. pylori infection, needs abx treatment to eradicate it.

PPIs are the most potent inhibitors of gastric acid secretion. Once-daily dosing is generally sufficient for acid inhibition (best before breakfast); however, a second dose may be necessary and should be given before the evening meal.

An H2 antagonist could be given at bedtime for breakthrough symptoms after a morning dose of a PPI.

Sucralfate is not recommended for H. pylori or NSAID ulcers.

Misoprostol is effective for peptic ulcers caused by NSAID use

Eliminating NSAIDs if applicable and appropriate.

Lifestyle

Advise the client to avoid alcohol, coffee (including decaffeinated), and other caffeine containing beverages, because they stimulate acid secretion.

Smoking cessation, stress reduction

79
Q

What is GERD? General causes (not specific)?

A

is the reflux of acid and pepsin or bile salts from the stomach
into the esophagus that causes esophagitis

Causes: Abnormalities in LES function, esophageal motility, and gastric motility or emptying

80
Q

Risk factors for GERD?

A

older age
obesity
hiatal hernia
medications or chemicals that relax the LES (anticholinergics, nitrates, calcium channel blockers, nicotine)
pregnancy

81
Q

Patho of GERD

A

Dysfunctional lower esophageal sphincter leads to loss of tone to the sphincter due to weakening or from transient lower esophageal sphincter relaxation (most common). This results in stomach contents refluxed back up to the esophagus.

The esophagus is exposed to the refluxed chyme containing acids and enzymes, causing mucosal injury, inflammation with hyperemia (increased blood flow to the tissues), which causes increased capillary permeability of the mucosa, edema, tissue fragility, and erosion (fibrosis and thickening may develop)

82
Q

How long does GERD take to heal? What complications can it develop into?

A

GERD may take weeks to heal, depending on efficacy of treatment.

In the long term (depending on exposure intensity and timing) precancerous lesions such as Barrett esophagus can develop. This can further progress to adenocarcinoma.

Complications:
Esophageal: Barret’s esophagus, esophageal stricture, esophageal adenocarcinoma
Extraesophageal: chronic laryngitis, asthma exacerbation

83
Q

What two respiratory conditions/symptoms are associated with GERD?

A

1) asthma exacerbation
2) chronic cough

84
Q

What is Barretts esophagus?

A

Barrett’s esophagus occurs when the lining of the esophagus heals abnormally and changes from cells that look like skin to cells that look like intestinal cells. Hence, Barrett’s esophagus is suspected by the appearance of the esophageal lining (salmon pink color compared to normal white color) and is confirmed by the microscopic examination of cells. It is defined in the United States as intestinal metaplasia.

85
Q

What is “functional heartburn”

A

have symptoms of reflux disease but no visible esophageal mucosal injury. Occurs In nonerosive reflux disease (NERD)

86
Q

What is the fancy term for heartburn?

A

Pyrosis

87
Q

What do you call reflux that doesn’t cause symptoms?

A

Physiologic reflux

88
Q

When is heartburn usually worsened in those with GERD?

A

The symptoms worsens if the patient is lying down, or during activity where they increase their intra-abdominal pressure: coughing, vomiting, straining stool

Heartburn discomfort usually occurs after meals or can waken patients in the middle of the night or exacerbated by emotional stress.

89
Q

What is chest pain described in GERD?

A

squeezing or burning, located in the middle of the sternum and may radiate to the back neck, jaw, or arms. The pain can last from minutes to hours, and spontaneously resolve or resolve with the use of antacids.

90
Q

How does GERD result in dysphagia?

A

Edema, strictures narrowing the esophagus, esophageal spasm, or decreased esophageal motility may lead to problems with swallowing (dysphagia), which usually results in weight loss

91
Q

Dx of GERD

A

Diagnosis is based on the patient’s history and their clinical manifestations (above).

Esophageal endoscopy – shows hyperemia, edema, erosion, and strictures

Endoscopy is not required to make a diagnosis, but it can help detect esophageal manifestations of GERD (such as Barrett’s metaplasia, erosive esophagitis)

  • Tissue biopsy – to rule out Barrett esophagus (it will show dysplastic changes)
  • Esophageal impedance pH monitoring: measuring the pH of the stomach contents and the acidity of the refluxate

Barium x-ray à to visualize the esophagus and stomach and locate areas of inflammation.

92
Q

Non-pharm treatment of GERD?

A

Avoid food that contains acid: citrus fruits, alcohol (these types of food can trigger symptoms)

Avoid fried or fatty foods, spicy foods, gassy foods or high in fiber (these types of food can trigger symptoms)

Avoid smoking, maintain healthy body weight, eat small meals, don’t eat before bed

Weight reduction, smoking cessation, elevation of the head of bed to at least 15cm, avoiding tight clothing

93
Q

How does delayed gastric emptying lead to GERD? What causes delayed gastric emptying?

A

By (1) lengthening the period during which reflux is
possible and (2) increasing gastric acid content.

Disorders that delay emptying include gastroparesis,
gastric or duodenal ulcers, which can cause pyloric edema and strictures that narrow the pylorus.

94
Q

What is eosinophilic esophagitis

A

is an idiopathic inflammatory disease of the esophagus characterized by
infiltration of eosinophils associated with atopic disease, including asthma and food allergies. It occurs in
adults and children. Dysphagia, food impaction, vomiting, and weight loss are common symptoms.
Endoscopy with biopsy identifies the eosinophilc infiltration and differentiation from GERD. Treatment is
symptomatic, including elimination diets and steroids.

95
Q

What is gastritis? Acute or chronic? What part of the stomach does it affect?

A

Gastritis is an inflammatory disorder of the gastric mucosa. It can be acute or chronic and affect the
superficial mucosa of the fundus or antrum, or both.

96
Q

What causes acute gastritis?

A

Acute gastritis is caused by injury of the protective mucosal barrier caused by medications, chemicals,
or Helicobacter pylori infection.

97
Q

How do NSAIDs lead to gastritis?

A

Inhibit prostaglandin synthesis (which normally stimulates the secretion of mucus)

98
Q

With acute gastritis, what S&S do we see? Time course?

A

The clinical
manifestations of acute gastritis can include vague abdominal discomfort, epigastric tenderness, and
bleeding. Healing usually occurs spontaneously within a few days. Discontinuing injurious medications,
using antacids, or decreasing acid secretion with H2 receptor antagonists facilitates healing.

99
Q

What is chronic gastritis? What changes are occuring here?

A

Chronic gastritis tends to occur in older adults and causes chronic inflammation, mucosal atrophy, and epithelial metaplasia.

Although the term “gastritis” is often used to describe endoscopic or radiologic characteristics of abnormal-appearing gastric mucosa, a diagnosis of gastritis requires histopathologic evidence of inflammation.

100
Q

Which type of chronic gastritis occurs primarily in the antrum of the stomach and which in the fundus?
Which is considered immune and nonimmune?

A

Type A = fundal, immune
Type B = antral, nonimmune

101
Q

What are types AB and C of chronic gastritis?

A

TYPE AB → when both types occur (aka “pangastritis”) → antrum more severely involved.

TYPE C → associated with reflux of bile and pancreatic secretions into stomach ⇒ causing chemical injury.

102
Q

Causes of type A and B chronic gastritis? Which is rare, and which is more common?

A

A = Chronic immune (fundal) gastritis is the rarest form of gastritis and is associated with loss of T
lymphocyte (T cell) tolerance and development of autoantibodies to gastric H+–K+ ATPase.
** associated with other autoimmune disorders

B = Chronic nonimmune (antral gastritis) generally involves the antrum only and is more common than
fundal gastritis. It is caused by H. pylori bacteria and it also is associated with use of alcohol, tobacco, and
NSAIDs. There are high levels of hydrochloric acid secretion with an increased risk for duodenal ulcers.

103
Q

What type of anemia can result from chronic immune gastritis?

A

Pernicious (and i suppose others if you had significant bleeding…but point here is we have breakdown of the stomach wall, so loss of intrinsic factor production)

104
Q

Describe the epidemiology of celiac disease

A

Usually presents between ages 10-40

Prevalence 1%

Estimated 75% underdiagnosed

105
Q

What are Risk Factors for the development of celiac disease

A

First and second-degree relatives with Celiac disease

High association with type I diabetes mellitus, auto immune thyroiditis, Down syndrome, Turner syndrome

Selective IgA deficiency

Dietary introduction of gluten before 4 months old

Infectious diarrheal episode

106
Q

Briefly outline the patho of celiac disease

A

Triggered by foods containing gliadin (a peptide in gluten), including wheat, barley, rye and oats

In duodenum secretory IgA binds to gliadin,

IgA-gliadin complex travels into lamina propria, immune cascade causes B and T cell activation resulting in inflammatory response and tissue destruction

Causes atrophy and flattening of villi and crypt hyperplasia in upper small intestine and results in malabsorption

107
Q

Is celiac disease acute or chronic?

A

Chronic life-long condition which requires permanent removal of gluten from the diet

Most people see symptom resolution with removal of gluten

108
Q

What are the GI symptoms of celiac disease?

A

On microscopy: villous atrophy, mucosal inflammation and crypt hyperplasia

Abdominal pain, distention

Chronic diarrhea/steatorrhea, vomiting, anorexia, constipation

Lactose intolerance – secondary to CD, may improve as CD controlled

109
Q

What are the extraintestinal symptoms of celiac disease? What is the common cause of most extraintestinal symptoms?

A

Malabsorption of nutrients causes most extraintestinal symptoms

Failure to thrive, delayed puberty (children)

Weight loss, Fatigue, Hair loss

Dermatitis herpetiformis – circulating IgA antibodies attack dermal papillae causing generalized rash, Aphthous stomatitis

Osteoarthritis, osteoporosis, fractures

Peripheral neuropathy

Iron-deficiency anemia

110
Q

What are the varied presentations of celiac disease we may encounter?

A

Classic CD: Diarrhea and/or evidence of malabsorption (steatorrhea, weight loss, other signs of nutrient deficiencies)

Atypical CD: May have minor GI symptoms but lack malabsorption symptoms. Usually demonstrate extraintestinal symptoms such as anemia, dental enamel defects, osteoporosis, arthritis, infertility. Usually have duodenal villous atrophy

Subclinical/Asymptomatic: Asymptomatic patients incidentally diagnosed during endoscopy for other purpose or by serologic screening. Once eliminating gluten patients often recognize retrospectively symptoms of CD that they accepted as normal. Villous atrophy present.

Potential CD: Test positive for serum antibodies but have normal duodenal biopsies and no symptoms. Should be monitored for risk for developing CD

111
Q

What are the main diagnostic tests for celiac disease?

A

Serology (IgA anti-tissue transglutaminase (tTG) antibody with total IgA levels)

Endoscopy with duodenal biopsy

112
Q

Can patients be tested for celiac disease if they are already on a gluten-free diet?

A

HLA genotyping – if HLA DQ2/DQ8 negative, CD excluded.

If HLA positive, perform gluten challenge for 2-8 weeks as tolerated, then perform serology and endoscopy

113
Q

What other investigations should be done when celiac disease is suspected?

A

CBC and electrolyte panel

PTT – may be prolonged due to malabsorption of vit K

Iron, transferrin, ferritin

Vit B12, folate

Thyroid screen

Stool culture, ova and parasites

Colonoscopy if bloody stools/signs of colitis

114
Q

Outline treatment for celiac disease

A

Lifelong gluten-free diet

Identify and treat nutritional deficiencies

Long term follow-up by multidisciplinary team

Pharmacology: Corticosteroids can be prescribed for rapid control of symptoms, nutrient supplements, bisphosphonates for osteoporosis.

115
Q

What are some considerations for patient education with celiac disease?

A

Foods containing gluten. Mnemonic: Grains are BROWn – Barley, Rye, Oats and Wheat. (Although some oats are gluten free)

Read labels carefully

May experience secondary lactose intolerance, avoid lactose products if aggravating and attempt to reintroduce once CD controlled

In poorly controlled or refractory CD medication absorption may be lessened – oral birth control may be less effective in these patient

116
Q

S&S of chronic gastritis

A

Is often include vague symptoms: anorexia, fullness, nausea,
vomiting, and epigastric pain. Gastric bleeding may be the only clinical manifestation of gastritis.

NUNP531 Applied Pathophysiology (24 decks)

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