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Quiz 3 Flashcards

1
Q

What is the most common form of esophageal atresia?

A

atresia with distal fistula

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2
Q

What is the most common site of esophageal webs?

A

middle and inferior third of esophagus

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3
Q

What is the main symptom of esophageal webs?

A

odynophagia and dysphagia

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4
Q

What is one of the main causes of acquired esophageal webs?

A

plummer-vinson syndrome

iron deficiency anemia»>webs

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5
Q

T/F? all of the esophageal motility disorders may present with both solid and liquid dysphagia.

A

true

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6
Q

What is achalasia?

A

decreased tone in proximal esophagus with increased tone at LES
bird beak appearance on xray with barium

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7
Q

What is the etiology of achalasia?

A

lymphocytic infiltration of Auerbach’s plexus and destruction of ganglion cells

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8
Q

What is the appearance of achalasia histologically?

A

lymphocytes in Auerbach’s plexus

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9
Q

What is another name for diffuse esophageal spasm?

A

corkscrew esophagus

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10
Q

What is diffuse esophageal spasm?

A

contractions are uncoordinated and several segments contract simultaneously

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11
Q

What is Nutcracker esophagus?

A

contractions proceed in coordinated manner but with excessive amplitude (hard enough to crack nuts apparently)

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12
Q

What is Mallory-Weiss syndrome?

A

bleeding from tears in the mucosa at the junction of the stomach and esophagus

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13
Q

Which layers of tissue are involved with Mallory-Weiss tears?

A

mucosa and submucosa (not muscular)

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14
Q

What usually causes Mallory-Weiss tears?

A

coughing, retching, vomiting
think alcoholism and eating disorders
hiatal hernia may predispose also

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15
Q

How is Boerhaave’s syndrome different than Mallory-Weiss?

A

Here, the tears are full thickness tears (including muscular layer) or rupture of esophageal wall

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16
Q

What are the most common causes of Boerhaave’s tears?

A

retching or vomiting
perforation of esophageal ulcers
endoscopy/trauma

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17
Q

What is the most common cause of esophagitis?

A

GERD (reflux esophagitis)

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18
Q

Who is most likely to get esophageal candidiasis?

A

Immunocompromised

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19
Q

What is happening with GERD?

A

LES has insufficient tone
gastric acid reaches esophagus
mucosa is damaged
sx: heartburn

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20
Q

What is the most common type of hiatal hernia?

A

sliding HH

gastroesophageal junction moves above the diaphragm with some of the stomach

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21
Q

What is the most common ring in the esophagus?

A

B ring/Shatzki ring

usually in lower esophagus and marks proximal margin of a hiatal hernia

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22
Q

What is the cell transformation that occurs with Barrett’s esophagus?

A

squamous epithelium —> columnar epithelium

at lower esophagus

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23
Q

What most commonly causes Barrett’s esophagus?

A

GERD

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24
Q

What are the two types of columnar cells that are often found in Barrett’s esophagus?

A

gastric
colonic
often a mix of the two is found with biopsy

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25
Q

What type of Barrett’s metaplasia is associated with an increased risk of malignancy?

A

colonic columnar

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26
Q

What type of CA does Barrett’s esophagus increase risk for?

A

adenocarcinoma

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27
Q

What portion of the esophagus is affected by esophageal varices?

A

lower third

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28
Q

Which patients are most likely to develop esophageal varices?

A

Those with cirrhosis due to portal hypertension

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29
Q

What is the risk of esophageal varices?

A

severe, life-threatening hemorrhage

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30
Q

What is the most common benign esophageal tumor?

A

leiomyomas

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31
Q

What types of cells do granular cell tumors arise from?

A

schwann cells

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32
Q

T/F. granular cell tumors are always benign and can occur anywhere in the body.

A

true

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33
Q

What are the two main forms of esophageal cancer?

A

scc (upper)

adenocarcinoma (lower)

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34
Q

What are the most common causes of SCC in the esophagus?

A

alcohol and tobacco

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35
Q

What is the most common esophageal CA worldwide? In the US?

A

SCC

Adenocarcinoma (US)

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36
Q

T/F. SCC and Adenocarcinoma look grossly different/

A

Nope

need histology to see the difference

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37
Q

What does adenocarcinoma look like histologically?

A

variable nucleus size, staining and shape

mitotic figures abundant in neoplastic cells

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38
Q

What is SCC in situ?

A

This means the basement membrane is not dysplastic
metastasis is unlikely
surgery is likely effective

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39
Q

What is a life threatening complication of a congenital diaphragmatic hernia?

A

the hernia may compress the lungs

usually Asx though

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40
Q

Which congenital diaphragmatic hernia is most common?

A

Bochdalek/left-sided

small and large bowel + solid organs into thoracic cavity

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41
Q

When does congenital hypertrophic pyloric stenosis usually present?

A

2-3 weeks after birth

vomiting and regurg.

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42
Q

What is the histologic presentation of congenital hypertrophic pyloric stenosis?

A

elongated, branched, mildly distorted pits

abundant lamina propria that is edematous

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43
Q

What usually infiltrates mucosa in acute gastritis?

A

neutrophils

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44
Q

What is most strongly associated with duodenal peptic ulceration?

A

H. pylori

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45
Q

What kind of organism is H. pylori?

A

spirochete, gram neg

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46
Q

Besides, duodenal peptic ulcer, what else is strongly associated with H. pylori?

A

gastric ulceration and gastric CA

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47
Q

What do benign peptic ulcers look like compared to malignant ulcers?

A

Smooth, regular, round edges, flat and smooth base

Malignant are irregular margins, nodular, protrudes into stomach lumen

48
Q

What are the top two causes of peptic ulcers?

A

h.pylori

NSAID use

49
Q

What type of ulcer is most common?

A

duodenal

50
Q

What are the complications of PUD?

A

GI bleed
perforation of gastric/duodenal wall
scarring/swelling that could lead to obstruction
develops into CA

51
Q

What is the triad of Zollinger-Ellison syndrome?

A

gastric acid hypersecretion
severe peptic ulceration
non-beta cell islet tumor of the pancreas (gastrinoma)

52
Q

What is occurring in Zollinger-Ellison syndrome?

A

increased gastric causes stomach to produce too much HCL

53
Q

Where is the gastrinoma usually found in Zollinger-Ellison syndrome?

A

pancreas

duodenum

54
Q

what else is noted in most Zollinger-Ellison syndrome pts.?

A

peptic ulcers

55
Q

What is Menetrier’s Disease?

A

marked enlargement of the gastric folds
= increased amounts of mucus from gastric mucosa and atrophy of gastric glands
= decreased acid secretion and loss of protein (decreased plasma protein)

56
Q

When does Menetrier’s Disease usually occur in children?

A

after an infection

57
Q

When does Menetrier’s Disease usually occur in adults?

A

over expression of transforming growth factor alpha

(TGF-alpha) protein

58
Q

What is the process that occurs in atrophic gastritis?

A

chronic inflammation of stomach mucosa leads to loss of gastric glandular cells, which are replaced by fibrous tissues
stomach can’t secrete HCl, pepsin and IF as well

59
Q

What two conditions usually cause atrophic gastritis?

A

h. pylori

AI destruction of gastric lining (more likely to develop achlorhydria and gastric carcinoma)

60
Q

What is the result of impair IF in atrophic gastritis?

A

impaired B12 absorption = megaloblastic anemia

61
Q

What will atrophic gastritis look like histologically?

A

decreased number of gastric glands

inflammation, neutophils

62
Q

What is AMAG?

A

autoimmune metaplastic atrophic gastritis
inherited
immune response directed toward parietal cells and IF

63
Q

What are characteristic findings of AMAG?

A

serum antibodies to parietal cells and IF

64
Q

In AMAG, hypochlorhydria induces what type of hyperplasia? What can it lead to?

A 
G cell (gastrin producing)
hypergastrinemia
65
Q

What do the neoplastic glands of gastric adenocarcinoma look like histologically?

A

signet ring cell pattern: cells filled with mucin vacuoles that push the nucleus to one side

66
Q

In which gastric CA does the stomach wall turn into leather-like scar tissue that cannot swell or contract as it should and results in disrupted digestion and inadequate metabolism of vital nutrients?

A

Linitis plastica

67
Q

What does MALT stand for?

A

malignant lymphoma of mucosa associated lymphoid tissue (a gastric lymphoma)

68
Q

What does MALT look like histologically?

A

atypical lymphoid cells
lymphoepithelial lesions
H.pylori

69
Q

What types of cells do carcinoid tumors arise from?

A

enterochromaffin cells

70
Q

Where are carcinoid tumors most commonly found?

A

gi tract

71
Q

What is the most common type of gastric carcinoid tumors?

A

Type 1

72
Q

What do carcinoid tumors look like histologically?

A

“endocrine pattern” (nets of cells separated by thin walled vessels)
low mitoses
cells and nuclei are uniform
no necrosis

73
Q

What other condition does duodenal atresia have a strong association with?

A

down’s syndrome

74
Q

What are the 2 most common types of intestinal atresia?

A
  1. duodenal

2. ileal

75
Q

What is another name for Hirshsprung’s dz?

A

congenital aganglionic megacolon

76
Q

What causes Hirshsprung’s dz?

A

failure of the neural crest cells to migrate completely during fetal development of the intestine

77
Q

What is the result of Hirshsprung’s dz?

A

constipation and eventual bowel obstruction

78
Q

When is Hirshsprung’s dz suspected?

A

When an infant has not passed meconium within 48 hours of delivery

79
Q

How does one dx Hirshsprung’s dz?

A

biopsy

80
Q

Where is the most common site to be affected by Hirshsprung’s dz?

A

large intestine (Auerbach’s plexus is involved)

81
Q

What is intestinal volvulus?

A

complete twisting of a loop of intestine around it’s attachment site

82
Q

T/F. Volvulus is usually a congenital condition and is most common in infants.

A

False.

usually acquired and can occur at any age

83
Q

What is intussusception?

A

when a part of the intestine has migrated into another section of intestine. Telescoping

84
Q

T/F. usually, in intussusception, the proximal bowel is migrating into the distal bowel.

A

true

85
Q

What is the sx triad for intussusception?

A

colicky pain
bilious vomiting
red currant jelly stool

86
Q

What is the risk with volvulus and intussusception?

A

ischemia and necrosis

87
Q

What is Meckel’s diverticulum?

A

out pouching from the intestine located in the distal ileum

88
Q

Meckel’s diverticulum is a vestigial remnant of which structure?

A

vitelline duct

89
Q

What makes a diverticulum true?

A

all layers of the structure are involved (including muscular and propria)

90
Q

What layers are involved in a false diverticula?

A

submucosa and mucosa

91
Q

What is the difference between diverticulosis and diverticulitis?

A

Diverticulosis is the condition of having multiple diverticula

Diverticulitis is when one or more diverticula is inflamed

92
Q

What is the most common site for a diverticula?

A

sigmoid colon (increased pressure)

93
Q

t/f. diverticular disease is relatively common before the age of 40.

A

false

94
Q

What two factors contribute to the formation of diverticula?

A

focal weakness of the bowel wall

increased pressure

95
Q

What are the complications of diverticulitis?

A

abscess

perforation

96
Q

What is the classic triad for diverticulitis?

A

LLQ pain
fever
elevated WBC count

97
Q

Where can intestinal obstruction occur?

A

any level distal to duodenum

98
Q

What conditions can result in an obstruction?

A 
hernias
adhesions
intussusception
volvulus
diverticular dz
infectious colitis
CA
99
Q

What might you see on an xray of someone with intestinal obstruction?

A

multiple air fluid levels

100
Q

Where can volvulus occur?

A 
stomach 
small intestine
cecum
transverse and sigmoid colon
(various sites, not an exhaustive list)
101
Q

What protein do patients with celiac disease have Abs to?

A

gliadin (a gluten protein)

102
Q

Which enzyme modifies gliadin, resulting in the immune system cross reacting with small-bowel tissue?

A

tissue transglutaminase

103
Q

What is the result of celiac disease (when folks are eating gluten)?

A

villous atrophy = inhibited nutrient absorption

104
Q

What does celiac dz look like histologically?

A

blunting and flattening of villi

105
Q

Which antigen does over 95% of celiac patient’s express?

A

DQw2 histocompatibility antigen

106
Q

What differentiates Crohn’s and UC?

A

location and the nature of inflammatory changes

107
Q

What part of the GI does Crohn’s affect?

A

anywhere from mouth to anus

most often, terminal ileum

108
Q

What part of the GI does UC affect?

A

colon and rectum

109
Q

What layers do Crohn’s and UC affect?

A

Crohn’s: whole bowel wall

UC: mucosa

110
Q

What is the term used to describe the Crohn’s lesion’s affect on the entire wall of the bowel?

A

transmural lesions

111
Q

How is dx of IBD done?

A

colonoscopy with biopsy of lesions

112
Q

T/F. Crohn’s is considered to have granulomatous inflammation.

A

true

113
Q

What is the term used to describe the intermittent pattern Crohn’s lesion’s?

A

skip lesions

114
Q

What is the pattern of UC inflammation?

A

continuous

115
Q

What is the characteristic mucosal alteration in UC?

A

crypt abscess

116
Q

What does UC pose an increased risk for developing?

A

adenocarcinoma

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