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Systems Path > Gastro-Intestinal System > Flashcards

Gastro-Intestinal System Flashcards

1
Q

Define: Leukoplakia

A

White plaque - keratin precursors in mucous membranes

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2
Q

What are the 2 types of precancerous lesions for mouth and lips?

A
  • leukoplakia

- dysplasia

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3
Q

What causes thrush?

A

Candida (yeast)

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4
Q

Most common mouth cancer?

A

Exposed lower lip

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5
Q

Which cancer has a better prognosis: lower lip or tongue?

A

Lip - 90%

Tongue - 33%

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6
Q

Infection causing inflammation of salivary glands?

A

Mumps

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7
Q

Define: xerostomia

A

Dry mouth

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8
Q

Define: pleomorphic adenoma

A

Mixed tumor of salivary origin (parotid most common, small salivary glands more risky)

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9
Q

Where are salivary tumors most common? Which salivary tumors are most likely to be malignant?

A

Most common = parotid gland

Most malignant = small / sublingual salivary glands

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10
Q

What parts of the esophagus are most vulnerable to pathological lesions?

A

Constrictions:

  • cricoid
  • tracheal bifurcation
  • esophageal hiatus
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11
Q

Define: dysphagia

A

Difficulty swallowing (subjective condition)

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12
Q

Define: odynophagia

A

Painful swallowing (associated with acute esophageal inflammation)

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13
Q

Define: achalasia

A

Motor dysfunction related to the esophagus

  • incomplete relaxation OR increased resting tone of lower esophageal sphincter
  • decreased peristalsis
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14
Q

Degeneration or dysfunction of which nerve(s) may lead to achalasia and/or dysphagia?

A

Vagus nerve or esophageal myenteric plexus.

General neurodegenerative changes from a variety of disease processes (like demyelination) may also be a factor)

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15
Q

What is a hiatal hernia?

A

When a portion of the stomach pushes through the esophageal hiatus in the diaphragm.

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16
Q

What are the two types of hiatal hernias, which is more common, and what do they include?

A

Common (90%)
Sliding hernia — gastroesophageal junction shifted above hiatus

Paraesophageal or Rolling hernia — portion of fundus is reflected upward along the esophagus.
*this is less common and less complicated.

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17
Q

Is acute or chronic esophagitis more common? What are the causes??

A

Chronic esophagitis is more common.

Causes: chronic reflux, immunodeficiency, achalasia

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18
Q

What are the changes associated with chronic esophagitis?

A
  • inflammation
  • erosions
  • ulcers

May lead to metaplasia known as Barrett’s esophagus.

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19
Q

What is the primary cause of esophageal varacosities?

Why are they dangerous?

A

Portal hypertension due to cirrhosis

Danger = up to 50% are fatal on first rupture. Asymptomatic before first rupture.

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20
Q

What are the major risk factors for esophageal carcinoma?

A
  • alcohol abuse
  • smoking
  • dietary nitrates and aflatoxins
  • HPV?

*prognosis is poor

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21
Q

Recall: define hematemesis

A

Bloody vomit

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22
Q

Which bacteria is most commonly implicated in mucosal disruption of the upper GI tract?

A

Helicobacter pylori

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23
Q

Motility disruptions contribute to ulcers where?

  • delayed gastric emptying
  • premature emptying
A

Delayed - stomach ulcers

Premature - duodenal ulcers

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24
Q

Define: gastritis

A

Mucosal inflammation, with accompanying:

  • discomfort
  • indigestion
  • vomiting
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25
Q

What are the features of acute gastritis?

A
  • erosive
  • variable in severity
  • reversible
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26
Q

What are the general features of chronic gastritis?

A
  • non-erosive
  • non-hemorrhagic
  • range of severity
    • superficial / mild
    • atrophic / moderate
    • gastric atrophy / severe
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27
Q

What are the two classifications of chronic gastritis?

A

Type A: fundic

  • loss of parietal cells in peptic regions
  • pernicious anemia
  • more likely autoimmune

Type B: antral

  • more common*
  • mucosal atrophy of antrum
  • more likely to involve H pylori
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28
Q

Define: dyspepsia

A

Indigestion - burning, bloating, gassiness, nausea after starting to eat

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29
Q

Describe acute peptic ulcers

A

Rapid onset of multiple small lesions that are shallow with ragged edges.

Usually self limiting and reversible.

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30
Q

Describe chronic peptic ulcers. Where do more than 98% of chronic peptic ulcers occur?

A

Usually solitary lesions in areas exposed to peptic acid.

Distinct punched out mucosal defects with smooth margins. Repair is scar tissue. Tend to be recurring (relapsing/remitting)

98% in stomach or duodenum

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31
Q

When are ulcers painful in the stomach? Duodenum??

A

Stomach = during a meal (highest HCl production)

Duodenum = 2 to 4 hours after a meal (at the time of gastric empty

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32
Q

H pylori is likely to cause which kind of uclers?

A

Chronic ulcers in the duodenum (less likely in the stomach)

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33
Q

What are the major complications of chronic ulcers?

A
  • bleeding (30%)

- perforation (5%)

34
Q

Define: leiomyoma

A

Smooth muscle tumor, usually benign

35
Q

What is one possible test to DDX stomach cancer from gastric ulcer?

A

Antacids should provide relief to ulcers but NOT to tumors / malignancies

36
Q

Like all cancer, late-diagnosis for stomach cancer has a poor prognosis. Why is late diagnosis common?

A

Stomach cancer is usually asymptomatic until it is fairly advanced. Advanced sx include:

  • weight loss
  • abdominal pain (may mimic ulcer but not respond to antacids)
  • nausea
  • blood loss
37
Q

What is pyloric stenosis?

What are the causes?

A

Hypertrophy of pylorus leads to obstruction —> results in projectile vomiting after meals.

Congenital - usually develops 2-4 wks
Acquired - scarring or tumors

38
Q

Inflammatory bowel diseases common characteristics:

A
  • chronic
  • remitting / relapsing
  • stress is a trigger
  • familial
  • young adult onset, and then early retiree spike in onset
  • autoimmune implications
  • rare in developing countries
39
Q

What and where are the lesions of Crohn’s?

A

Skip lesions - multiple granulomatous lesions with “garden hose” thickening of affected segments in the distal ileum

40
Q

What happens to the mucosa in Crohn’s?

A

Cobblestone effect —> focal ulcerative defects with fissures creating a cobblestone like texture

41
Q

Cobblestone effect and skip lesions are part of what condition?

A

Chron’s disease

42
Q

What is the medical name for Chron’s disease?

A

Regional enteritis

43
Q

Leukoplakia and dysplasia are part of what condition?

A

Cancer of the mucous membranes of the mouth and lips

44
Q

What are the words for these types of esophageal dysfunction:

  • difficulty swallowing
  • painful swallowing
  • motor dysfunction
A
  • dysphagia
  • odynophagia
  • achalasia
45
Q

Fundic and antral are the subtypes of what condition?

A

Chronic gastritis

46
Q

“Punched out” describes the lesions for what condition?

A

Chronic peptic ulcers

47
Q

Where in the bowel will Crohn’s and UC appear?

A 
Crohn’s = distal ileum 
UC = recto-sigmoid region
48
Q

What and where are the lesions in ulcerative colitis?

A

Continuous lesions originating in crypt abscesses in the small intestine that form extensive ulcers.

Commonly arising in the rectal-sigmoid area. Extends through small intestine, may enter ileum.

49
Q

What are pseudopolyps in UC?

A

Inflamed, hyperplastic areas of mucosal tissue that remain between extensive ulcers / scars. These heavily secrete mucous

50
Q

Define: steatorrhea

A

Diarrhea

51
Q

What is non-tropical sprue?

A

Gluten-sensitive enteropathy, aka Celiac disease:

Atrophy of villi and columnar cells of small intestine and malabsorption relating to a pathological immunosensitivity to gliadin (glycoprotein in wheat, barley, and rye)

52
Q

What is tropical sprue?

A

Malabsorptive disease common in tropical regions —> acute intestinal illness following bacterial infection (often E.coli)

Requires antibiotics and folic acid

53
Q

What is the common name of intestinal lipodystrophy?

A

Whipple’s disease

54
Q

What is whipple’s disease?

A

Multi system disorder that begins in the intestines:

  • macrophages cannot kill T.whipplei due to missing enzyme —> results in foam cells that accumulate, distend villi in small intestine, and block lacteals, leading to malabsorption.

Other organs including heart, liver, lung, and CNS may eventually be affected.

55
Q

What different sx are expected with a high intestinal obstruction vs a low one?

A 
High = vomiting 
Low = abdominal distention and decreased bowel activity
56
Q

3 causes of functional (not mechanical) obstruction:

A
  • vascular disease
  • congenital megacolon - Hirschsprung’s disease
  • adynamic (paralytic) ileum
57
Q

How does vascular disease lead to reduced peristalsis?

A

Ischemia —> infarcts —> eventually necrotic segments = reduced peristalsis

  • necrotic sections may rupture
  • more likely in diabetics
58
Q

What is Hirschsprung’s disease?

A

Congenital megacolon:

missing sections of myenteric plexus, most commonly in recto-sigmoid region. No peristalsis without it

59
Q

What is adynamic ileus?

A

Disruption of peristalsis in the ileum due to severe infection, surgery (temporary), shock, or UC

60
Q

When should you hear peristalsis on an abdominal exam?

A

Always.

Especially if pt has recently eaten. Stomach silence is bad.

61
Q

Mechanical causes of bowel obstruction:

A
  • hernia, incarceration (entrapped segment)
  • hernia, strangulation
  • strictures or adhesions
  • volvulus (looped around self)
  • intussusception (segment slides into another segment)
62
Q

What is intussusception?

A

When one segment of bowel slides into another segment.

Due to straining around an obstruction that cannot be moved (adults) or hyperperistalsis (kids)

63
Q

What is volvulus?

A

A loop of intestine twisting around itself

64
Q

What is an incarceration hernia?

A

When a herniated bowel segment becomes trapped

65
Q

What is a “true” diverticulum?

A

A wall pouch that contains all layers of GI tract. Congenital defect.

66
Q

What is a “false” diverticulum?

A

An acquired defect in which mucosa herniates out through muscular layers of GI tract

67
Q

What is meckel’s diverticulum?

A

Remnant of yolk sac stalk located in distal ileum

68
Q

Where are false diverticulum most common?

A

Colon, especially sigmoid

69
Q

What population is most likely to get diverticulum?

A

Elderly (present in >50% of people over 80)

70
Q

How can one distinguish appendicitis pain and diverticulitis pain?

A

Diverticulitis = lower left quadrant abdominal pain

Appendicitis = lower right quadrant abdominal pain

71
Q

Acute LBP and a distinct lack of peristalsis sounds could mean what condition?

A

Spinal fracture —> send to ER for possible abdominal CT

72
Q

Define: carcinoid

What cells / organs affected?

A

Carcinoma in “slow motion”

Slowly progressing growth with late metastasis affecting argentaffin cells most commonly in the appendix and the ileum

73
Q

What is the most common location for benign polyps of the large intestine?

A

Recto-sigmoid region of adults over 50

74
Q

What are the two types of intestinal polyps?

A

Pedunculated - tubular adenoma = have stalk, stick out from the wall

Sessile - villous adenoma = broad base of attachment to the wall with villous projections

75
Q

Which kind of intestinal polyps are more common? Which are more likely to become malignant?

A

Pedunculated (tubular adenoma) = more common

Sessile (villous adenoma) = more likely to be malignant —> usually because they are larger and the more something grows the more likely it becomes cancer

76
Q

What kind of polyps are most likely to become cancer?

A

Multiple familial polyposis —> virtually all untreated subjects end up with cancer

77
Q

Where is colon cancer most likely to appear?

A

Recto-sigmoid region

78
Q

Who is at the highest risk for colon cancer?

A

People over 50 in developed countries

79
Q

What are the major risk factors for colon cancer?

A
  • multiple familial polyposis
  • ulcerative colitis
  • low fiber / high animal fat diet
80
Q

Colon cancer, like stomach cancer, generally has a poor prognosis. Why?

A

Asymptomatic until late in the disease, and by then it’s too late.

Systems Path (5 decks)

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