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Pathology > GI pathology > Flashcards

GI pathology Flashcards

1
Q
  • Diseases of the GI tract can be classified as:
A

– Developmental disorders
– Inflammatory diseases
– Functional disorders
– Circulatory disturbances
– Neoplastic diseases

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2
Q

functions of the GI

A
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3
Q

esphogeal dx’s

A

– Hiatal hernia
– Reflux esophagitis
– Barrett esophagus
– Achalasia
– Esophageal varices
– Esophageal cancer

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4
Q

stomach dx’s

A

– Acute gastritis
– Chronic gastritis
– Peptic ulcer disease
– Stomach cancer

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5
Q

SI dx’s

A

– Meckel diverticulum
– Bowel obstruction
– Herniation
– Adhesions
– Intussusception
– Volvulus
– Adenocarcinoma
– Carcinoid tumor

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6
Q

LI dx’s

A

– Pseudomembraneous colitis
– Diverticulosis
– Crohn disease
– Ulcerative colitis
– Adenomatous polyps
– Colon cancer

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7
Q

Layers of the GI

A
  • Mucosa
    – Epithelium
    – Lamina propria
    – Muscularis mucosae
  • Submucosa
  • Muscularis propria: inner circular and outer longitudinal
  • adeventitia and serosa
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8
Q

Important Clinical Symptoms and Signs Relating to the GI System

A
  • Dysphagia
  • Vomiting
  • Hematemesis
  • Hematochezia
  • Melena
  • Diarrhea
  • Constipation
  • Odynophagia
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9
Q
  • Dysphagia
  • Vomiting
A
  • Dysphagia –difficulty in swallowing
  • Vomiting –expulsion of stomach contents through the mouth
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10
Q
  • Hematemesis
  • Hematochezia
A
  • Hematemesis –vomiting of fresh, red blood
  • Hematochezia –bright, red blood in stool
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11
Q

Melena
* Diarrhea

A

Melena –black, tarry feces
* Diarrhea –frequent, loose, watery bowel movements

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12
Q
  • Constipation
  • Odynophagia
A
  • Constipation –hard feces that are difficult to eliminate
  • Odynophagia –painful swallowing
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13
Q

subspecialty and types

Fiberoptic Endoscopy

A

Gastroenterology –a subspecialty
of Internal Medicine
* Esophagogastroduodenoscopy
(EGD) –upper GI endoscopy
* Colonoscopy –lower GI endoscopy

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14
Q

esphogus layers

A
  • Mucosa
    – Epithelium
    – Lamina propria
    – Muscularis mucosae
  • Submucosa
  • Muscularis
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15
Q

Clinical Symptoms and Signs of
Esophageal Disease

A
  • Dysphagia –difficulty in swallowing
  • Odynophagia –pain on swallowing
  • Heartburn –a burning behind the sternum -GERD
  • Acid regurgitation into the mouth –a sign of GERD
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16
Q

type of disorder? dysfunction of? presentation?

Achalasia

A

a Functional (Motor) Disorder
* Dysfunction of ganglion cells of myenteric plexus (Auerbach plexus) prevents proper relaxation of lower esophageal sphincter - a motility disorder
* Presents with: Dysphagia, regurgitation, halitosis and proximal dilation

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17
Q

demo? dx? signs? increased risk for?

Plummer-Vinson Syndrome
(Paterson-Kelly Syndrome)

A
  • Scandinavian, Northern European women
  • Severe Fe-deficiency anemia
  • Mucosal atrophy - atrophic glossitis
  • Esophageal webs - dysphagia
  • Increased risk for squamous cell carcinoma
    – Esophagus
    – Oropharynx
    – Posterior Oral Cavity
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18
Q

usually form where?

Esophageal Varices due to:

A
  • Portal hypertension produces venous dilation
    usually develop in lower portion
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19
Q

leads to? mortality? advanced chirrhosis?

rupture of esphogeal varices

A
  • Rupture leads to hematemesis and massive upper GI bleed
  • Rupture of a varix is associated with high mortality
  • Rupture of a varix accounts for half of the deaths in advanced cirrhosis
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20
Q

Mallory-weiss syndrome

A
  • Mallory-Weiss tears are seen in chronic alcoholics, where violent retching causes esophageal lacerations
    and hemorrhage
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21
Q
A

mallory weiss syndrome

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22
Q

Hiatal Hernia

A
  • Diaphragmatic hernia - widened diaphragmatic hiatus allows protrusion of the stomach through the diaphragm
  • Gastroesophageal junction pulled into thorax causing GERD
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23
Q

presents with? risk for?

Barrett Esophagus

A
  • Gastric metaplasia of lower esophageal mucosa - columnar epithelium replaces stratified squamous epithelium
  • Presents with: Odynophagia, ulceration, hemorrhage
  • at risk for Adenocarcinoma (now glandular tissue not squamous)
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24
Q

forms of esphogeal cancer

A
  • Squamous cell
    carcinoma
  • Adenocarcinoma -
    Barrett esophagus
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25
Q

esphogeal cancer may present with

A
  • Dysphagia due to
    narrowing of lumen or
    interference with
    peristalsis
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26
Q

Esophageal Squamous Cell Carcinoma
* demo? prognosis?
* common? US?
* where is esphogus?
* risk factors?

A
  • Older adults, geographical variation,
    poor prognosis
  • Squamous cell carcinoma most
    common world-wide, but
    adenocarcinoma of esophagus is
    more common in the United States
  • Most common in middle third
  • Alcohol and tobacco, Plummer-
    Vinson syndrome, diet influence
    incidence
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27
Q
A

SCC of LE

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28
Q

Esophageal Adenocarcinoma
* where?
* risk factor?
* More common in US?

A
  • Lower segment
  • Barrett esophagus is a risk factor
  • More common than squamous carcinoma in United States
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29
Q

progression of esphogeal adenocarcinomma

A
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30
Q

from lower portion esphogus

A

adenocarcinoma

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31
Q

stomach portions

A
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32
Q

cardia cell types

A

mucous cells

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33
Q

fundus cells

A

paritel, cheif and endocrine

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34
Q

body cells

A

paritel, cheif, endo

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35
Q

pylorus cells

A

mucus, endo, d cells

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36
Q

parietal cells release

A

HCL and IF (B12)

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37
Q

chief cells release

A

pepsinogen

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38
Q

endocrine/G cells release?

A

gastrin

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39
Q

Gastritis

A
  • Inflammation of the
    gastric mucosa
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40
Q
  • Acute gastritis –
A

erosive, due to irritants
and NSAIDs

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41
Q
  • Chronic gastritis –
A

erosive or non-erosive infectious or autoimmune

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42
Q

Acute Erosive Gastritis
* presentation
* erosions?
* causes?
* One of the major causes
of what in alcoholics?

A
  • Epigastric burning, pain, nausea, vomiting
  • Shallow erosions
  • Causes: Asprin, NSAIDs, alcohol, stress, shock, sepsis
  • One of the major causes of hematemesis in alcoholics
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43
Q

infectious chronic gastritis

A

the most common form of chronic gastritis is due to infection by Helicobacter pylori

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44
Q

AI chronic gastritis

A

autoantibodies to parietal
cells

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45
Q

Helicobacter Pylori Gastritis can lead to:

A
  • Peptic ulcer disease
  • Adenocarcinoma
  • MALT Lymphoma (H. pylori is a potential human carcinogen)
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46
Q

gram/shape? biopsy/stain? breath test? Ab test?

H pylori

A
  • Gram negative s-shaped rods
  • Biopsy and silver stain
  • Urea breath test
  • Antibody test for H. pylori
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47
Q

additional path formed?

AI atrophic gastritis

A
  • Autoantibodies against gastric parietal cells causes Gastric mucosal atrophy
  • No intrinsic factor, low serum vitamin B12, pernicious anemia
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48
Q

erosion depth? due to?

Gastric Stress Ulcers

A
  • Deeper than erosions, may extend to
    muscularis
  • Severe stress - ICU patients (shock,
    trauma, burns, sepsis)
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49
Q

solitary? mainly occur where?

peptic ulcer dx

A
  • Most peptic ulcers are generally solitary lesions
  • Most occur in the duodenum - 98% are located in the duodenum and stomach
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50
Q

demarcaation? base? chronic ones may exhibit what?

Characteristics/appearence? of Peptic Ulcers

A

Sharply-demarcated ulcer with a clean, smooth base
* Chronic lesions may exhibit puckering due to fibrosis

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51
Q
A

peptic ulcer

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52
Q

blood loss? signs? major cause of death?

Clinical Course of Peptic Ulcer Disease

A
  • Acute/chronic blood loss
  • Nausea, vomiting, hematemesis, melena/ heamtocheza
  • Perforation - major cause of death in PUD
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53
Q

immeadiate and delayed pain relative to ulcer location

A

Immediate pain – gastric ulcer
Delayed pain - duodenal ulcer

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54
Q

Etiology of Peptic Ulcers
* factors? result?
* Infection by ?
* Drugs?
* Neuroendocrine?

A
  • Multifactorial disease, decreased mucosal resistance
  • Infection by H. pylori
  • Drugs –aspirin, NSAIDs
  • Neuroendocrine –hormonal hypersecretion syndromes
    – Cushing Syndrome –corticosteroids
    – Zollinger-Ellison Syndrome –gastrin
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55
Q

peptic ulcer formation diagram

A
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56
Q

bleedings (types and signs)? perforation? stenosis? pancreas?

Complications of Peptic Ulcer Disease

A
  • Minor hemorrhage –melena, iron deficiency anemia
  • Major hemorrhage -hematemesis
  • Perforation - peritonitis
  • Stenosis and obstruction
  • Penetration into pancreas
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57
Q

Zollinger-Ellison Syndrome

A

Gastrin-secreting tumor in pancreas or duodenum (“gastrinoma”)
* Hypergastrinemia causes hypersecretion of gastric acid
* Severe peptic ulcer disease with multiple ulcers in unusual locations

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58
Q

demo/prognosis? dietary? predepositions to this?

gastric adenocarcinoma

A
  • Older individuals, poor
    prognosis
  • Smoked fish –nitrosamines
  • Predispostion to gastric
    cancer
    – H. pylori infection
    – Chronic atrophic gastritis
    – Gastric adenomatous polyps
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59
Q

Gastric Adenocarcinoma location

A
  • Lesser curve of antro-
    pyloric region
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60
Q

types of gastric adenocarcinomas

A

intestinal and diffuse

61
Q
  • Intestinal type gastric adenocarcinoma
A

bulky tumors composed of glandular structures

62
Q
  • Diffuse type gastric adenocarcinoma
A
  • Diffuse type -infiltrative growth of poorly-differentiated cells (linitis plastica)
63
Q

Krukenberg Tumor

A
  • Metastatic adenocarcinoma to
    ovaries
  • Bilateral ovarian metastases
  • Frequently of gastric origin - mucus-
    producing cells
64
Q

mainly? types?

Gastrointestinal Tract Lymphoma

A

Mainly Non-Hodgkin Lymphoma
* Primary lymphomas -MALT-omas and other NHLs
* Secondary lymphomas - extranodal spread to GI

65
Q

associated with what infection? tx?

Gastric MALT Lymphoma

A
  • MALT lymphomas - B cell lymphomas of Mucosa-Associated Lymphoid
    Tissue
  • Associated with Helicobacter pylori infection –may regress with H. pylori treatment
66
Q

most common site of extranodal lymphomas in the GI

67
Q

SI structure

68
Q

Meckel Diverticulum

A
  • Developmental defect of ileum - a blind pouch containing all layers
  • “Left-sided appendix” -may produce symptoms similar to appendicitis
69
Q

from left side of ileum

A

meckel diverticulum

70
Q

possible bowel obstructions at SI

A

herniation
intussception
adhesions
volvulus

71
Q

due to? possible locations?

herinations

A

Weakness in peritoneum, outbulge of intestines that will be strangled=infarct
* Inguinal
* Femoral
* Umbilicus
* Incisional

72
Q
A

umbilcal hernia

73
Q

inguinal/scrotal hernia

A

herniation thru inguinal canal

74
Q

Adhesions
* They are usually
sequelae of?

A
  • Fibrotic bridges of
    peritoneum
  • May trap and kink
    bowel segments
  • They are usually
    sequelae of prior
    surgery or infection
75
Q
76
Q

Intussusception
* possible cause?

A
  • Small intestine invaginates into itself -
    intussusceptum becomes necrotic
    unless everted
  • Small pedunculated tumors carried by
    peristalsis may pull forward the loop to
    which it is attached
77
Q

most common location? result?

Volvulus

A
  • Rotation of a loop of intestine about
    its own mesenteric root
  • Most common in small intestine and
    sigmoid colon
  • Volvulus undergoes necrosis
78
Q

adenocarcinomas in SI?

79
Q

grade? app? cells? where/most commonly? may produce?

carcinoid tumor of SI

A
  • A low-grade malignancy of neuroendocrine cells, appearing as mucosal nodules
  • May occur throughout gastrointestinal tract but are most common in appendix
  • May produce hormones, such as serotonin
80
Q

Carcinoid Syndrome
* Caused by?
* result?

A
  • Caused by a serotonin-producing carcinoid tumor that is asymptomatic until metastasis to the liver
  • The serotonin that is no longer metabolized by the liver causes cramping, diarrhea, flushing and
    bronchospasm
81
Q

what cells are abundant with carcinoid SI tumors?

82
Q

acute ischemic bowel dx

A

ischemia of Aa that can effect dif layers of intestine
mucosal infarct: only mucosa
mural infarction: mucosa and submucosa
transmural infarct: all layers

83
Q

colon vs SI app

84
Q

NS in colon

A
  • Enteric nervous system - myenteric
    (Auerbach) and submucosal plexus
    (Meissner)
85
Q

colon is colonized by?

A

Colonized by non-pathogenic strains of bacteria

86
Q

presentation? tx?

hirschsprung dx

A

congenital megacolon
* Developmental defect of enteric nervous system - agangliosis of
terminal colon (myenteric plexus)
* Chronic constipation, proximal dilation
* Resection of aganglionic segment

87
Q

associated with? may become?

Diverticulosis

A
  • Consist of out-pouchings of mucosa and submucosa through muscular layer of colon
  • Associated with a low bulk diet, straining during defecation
  • May become inflamed (diverticulitis)
88
Q
A

diverticulosis

89
Q

Intestinal Polyps types

A

neoplastic and. non-neoplastic

90
Q

neoplastic polyps

A

adenomatous polyps/ adenomas
– Tubular adenoma
– Villous adenoma

91
Q

types of?

non-neoplastic polyps

A

– Hyperplastic polyp –most common
– Hamartomatous polyp -
Peutz-Jeghers Syndrome

92
Q

Hyperplastic Polyp

A
  • Non-neoplastic hyperplasia of epithelium, most common
  • Not pre-malignant
93
Q
A

hyperplastic polyp

94
Q

app? assoiated with? risk for? malignant?

Hamartomatous Polyp

A
  • Large, pedunculated polyp, consisting of all layers of the mucosa
  • May be associated with Peutz-Jeghers syndrome
  • Risk for intussusception
  • No malignant change
95
Q
A

hamartomatous polyp

96
Q

Peutz-Jegher Syndrome
* iheritence?
* Pigmented macules where?
* polyps?
* Increased risk for?

A
  • Autosomal dominant
  • Pigmented macules of oral mucosa and perioral skin
  • Hamartomatous polyps of bowel
  • Increased risk for adenocarcinoma outside GI tract - pancreas, breast, lung, ovary, uterus
97
Q
A

peutz-jhager

98
Q

tubular adenomas

A
  • tubular glands, frequently
    pedunculated
    neoplastic polyp
99
Q

villus adenoma

A

villous projections, frequently
sessile
neoplastic polyp

100
Q

most common neoplastic polyp

101
Q

tubular polyp malignant transformation

102
Q

tx tubular adenomas

A

endoscopic polyectomy

103
Q
A

tubular adenoma

104
Q
A

tubular adenoma

105
Q

Villous Adenoma
commonality?
malignant transformation?
endoscopic removal?
tx?

A
  • Least common neoplastic polyp
  • 50% malignant transformation
  • Endoscopic removal often not possible
    often colon resection
106
Q
A

villus adenoma

107
Q
  • Third most common cause of cancer death
A

colonic adenocarcinoma

108
Q

demo of colonic adenocarcinoma

A
  • Older adults, unless predisposing condition (ulcerative colitis, hereditary colon cancer syndrome –Gardner syndrome)
109
Q
  • Dietary risk factors of colonic adenocarcinoma
A
  • high caloric intake, high fat, red meat, high refined carbohydrates, low fiber
110
Q

mutations of what genes?

Adenoma - Carcinoma Sequence

A

Accumulation of mutations in tumor supressor genes and proto-oncogenes

111
Q

most common site colonic adenocarcinoma

A

sigmoid colon

112
Q

left side adenomcarcinoma

A
  • circumferential, napkin-ring lesion producing narrowing of
    lumen
113
Q

right side colonic adenocarcinoma

A
  • exophytic, polypoid, crater-like ulcerations with rolled
    borders
114
Q

where else could an adenocarcinoma occur

A

rectal adenocarcinoma, easy to detect

115
Q

can colonic adenocarsinomas metastisize

116
Q

Staging of Colon Cancer

A

Stage is most important prognostic indicator, based on layers involved

117
Q

Hereditary Colonic Cancer Syndromes inheritence

A

–Autosomal Dominant

118
Q

Hereditary Colonic Cancer Syndromes

A
  • Familial Adenomatous Polyposis Coli (garner syndrome)
  • Hereditary Non-Polyposis Colorectal Cancer (HNPCC)
119
Q

presentation? malignant?

  • Familial Adenomatous Polyposis Coli (FAP)/ garner syndrome
A

multiple tubular adenomas, 100% malignant transformation

120
Q

oral/skin presentations

garner syndrome

A

a variant of FAP with multiple supernumerary teeth, jaw bone densities, multiple osteomas, fibromatosis, epidermal inclusion cysts

121
Q

presentation? increased risk of cancer outside GI?

  • Hereditary Non-Polyposis Colorectal Cancer (HNPCC) -
A

colonic cancer unrelated to adenomas
– Increased risk of endometrial and ovarian cancers

122
Q

colostomy

A

removal and resection of colon in response to colonic cancer

123
Q

Inflammatory Bowel Diseases

A

Two chronic, relapsing inflammatory disorders of unknown etiology
* Crohn Disease
* Ulcerative Colitis

124
Q

IBS immune response

A
  • Exaggerated and unregulated local immune respose in genetically susceptable individuals
125
Q

where? from of inflamm? granulomas? signs?

chrons disease

A
  • Any level of GI tract, mouth to anus, most often distal ileum and colon
  • Transmural inflammation, thickened intestinal wall
  • Sarcoid-like non-caseating
    granulomas
  • Pain, diarrhea, fissure and
    fistula formation
126
Q
A

transmural inflammation-chrons

127
Q
A

granulomatous inflammation- LI= chrons

128
Q

mucosa of chrons

A

cobblestoned and thickened mucosa

129
Q

chrons disease fistula

A

perianal fistulas form
Fistula –an abnormal channel between two hollow organs or between a hollow organ and the skin surface

130
Q

malabsorption and addtional patholgy associated w chrons

A

Malabsorption may occur =vitamin K-dependent clotting factor deficiency/ bleeding diathesis

131
Q

Oral Manifestations of Crohn Disease

A
  • Aphthous-like lesions
  • Granulomatous nodules
132
Q

picture

A

Oral granulomatous nodules of chrons

133
Q
A

apthous-like lesion of chrons

134
Q

increased risk of? thinning of? location? symptoms?

Ulcerative Colitis

A

Chronic inflammatory disease with
increased risk of malignancy
* Thinning of intestinal wall, limited to
colon and rectum
* Relapsing diarrhea, pain

135
Q

inflammtion of ulcerative colitis

A

not transmural, limited to mucosa

136
Q

abcesses of ulcerative colitis

A
  • Crypt abscesses- accumulation of neutrophils within colonic crypts are signs of active inflammation
137
Q
A

crypt abcess of ulcerative colitis

138
Q

pseudopolyps

A

seen in ulcerative colitis-Remnants of colonic mucosa surrounded by ulceration

139
Q

Pyostomatitis Vegetans

A
  • Oral lesions of ulcerative colitis
  • Small, yellow superficial pustules
140
Q
A

Pyostomatitis Vegetans- ulcerative colitis

141
Q

Crohn Disease vs Ulcerative Colitis
Region
Distribution,
Wall
Inflammation
Ulcers
Granulomas
Fistulae
Malabsorption
Malignant risk

142
Q

complications?

appendicitis

A
  • An acute bacterial infection of appendix
  • Complications may include rupture and peritonitis
143
Q

Appendicitis –Obstruction of Lumen mechanisms

A
  • Fecalith- inspissated fecal material
  • Reactive lymphoid hyperplasia – response to viral infection
  • Neoplasm –carcinoid tumor
144
Q

inflam? ulceration? affected layers? complications?

Acute Appendicitis

A

Acute inflammation, mucosal ulceration
* Transmural inflammation
* Serositis
* Peritonitis

145
Q

signs of acute appendicits

A
  • Right lower quadrant pain, rebound
    tenderness
  • Leukocytosis, fever, nausea, vomiting
146
Q

cause?

Hemorrhoids

A
  • Varicose dilation of hemorroidal venous plexus at anorectal junction
  • Increased venous pressure may be associated with pregnancy, chronic
    constipation, portal hypertension
147
Q

hemrroid treatment

A

surgical reapir

148
Q

malabsorption and addtional patholgy associated w chrons

A

malabsorption=vita K def causing def of K dependent clotting factors

Pathology (20 decks)

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