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Gastrointestinal Pathology_2 Flashcards

1
Q

what is the morphology seen in necrotizing enterocolitis?

A

terminal ileum and ascending colon (gas in intestinal walls- radiology)

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2
Q

what are the clinical features of necrotizing enterocolitis?

A

mild GI disturbance or as a fulminant illness with intestinal gangrene, perforation, sepsis, shock

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3
Q

what is collagen EC?

A

when patches of band like collagen deposits under the surface epithelium, common in middle aged and older women

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4
Q

what is the gender prevalence of collagen EC?

A

W>M

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5
Q

what happens in lymphocytic EC?

A

intraepithelial infiltrate

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6
Q

what is the gender prevalence of lymphocytic EC?

A

M=F

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7
Q

what are the clinical features of both collagen and lymphocytic EC?

A
  • endoscopy= normal • - radiology= unremarkable • - clinically= chronic watery diarrhea • - clinical course= benign in nature
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8
Q

what is another name for neutropenic colitis?

A

typhilitis

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9
Q

what happens in neutropenic colitis?

A

acute inflammatory destruction of the mucosa

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10
Q

what is an important cause of neutropenic colitis?

A

compromised blood flow

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11
Q

what is the site of neutropenic colitis?

A

cecal region

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12
Q

what is the pathogenesis of neutropenic colitis?

A

impaired mucosal immunity

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13
Q

how dangerous is Neutropenic colitis?

A

life threatening

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14
Q

what are the features of solitary rectal ulcer syndrome?

A
  • inflammation of the rectum • - impaired relaxation and sharp angulation of the anterior rectal shelf • - inflammatory polyp
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15
Q

what is the characteristic triad associated with solitary rectal ulcer syndrome?

A
  1. rectal bleeding • 2. mucus discharge from the anus • 3. superficial ulceration of the anterior rectal wall
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16
Q

what are the intestinal malabsorption syndromes?

A

celiac sprue • tropical sprue • Whipple disease • disaccharidase deficiency

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17
Q

malabsorption syndromes are characterized by what?

A

deficient absorption of fat, protein, carbohydrates, electrolytes, minerals, fat soluble vitamins, water • –> vitamin deficiency, tetani

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18
Q

malabsorption syndromes are caused by what?

A
  • deficient digestion (biliary-pancreatic disease) • - deficient absorption (small intestinal disease)
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19
Q

what are the clinical findings in malabsorption syndromes?

A

weight loss • flatulence • diarrhea with bulky, frothy, greasy stools

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20
Q

what happens in prolonged cases of malabsorption?

A

anemia • petechiae • hemorrhages • dermatitis • bone aches • latent tetany • menstrual disturbance • impotence • infertility

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21
Q

what are the common causes of malabsorption?

A

celiac sprue • chronic pancreatitis • Crohn’s • tropical sprue • Whipple’s • bacterial overgrowth • disaccharidase deficiency • abetalipoproteinemia

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22
Q

what is the geographic distribution of tropical vs celiac sprue?

A

tropical= tropics and travelers • celiac= caucasian

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23
Q

what is the etiology of tropical vs celiac sprue?

A
  1. tropical= ?infection (E coli, Hemophilus) • 2. celiac= diet: gluten–> gliadins
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24
Q

what is the site of involvement in tropical vs celiac sprue?

A

tropical= all levels of small intestine • celiac= proximal small intestine (duodenum, proximal jejunum)

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25
Q

what is the clinical presentation of tropical vs celiac sprue?

A
  1. tropical= symptoms after acute diarrheal episode • 2. celiac= after gluten diet
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26
Q

what is the treatment for tropical vs celiac sprue?

A

tropical= antibiotic • celiac= gluten free diet

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27
Q

what is the ris of malignancy in tropical vs celiac sprue?

A

tropical= no risk • celiac= yes increased risk

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28
Q

how common is Whipple’s disease?

A

rare systemic disease

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29
Q

what does Whipple’s disease involve?

A

intestines • joints • CNS

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30
Q

Whipple’s disease is caused by what?

A

Gram-positive actinomycetes Tropheryma Whippelii

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31
Q

who is affected by whipple’s disease?

A

white males (M:F=10:1), 30-50yrs

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32
Q

what are the hallmark features of Whipple’s disease?

A

distended macrophages in lamina propria contain PAS (+) granules • - tiny rod shaped bacilli in EM

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33
Q

what are the clinical features of Whipple’s disease?

A

malabsorption syndrome • fever • joint pains • cardiac and neurologic S&S • weight loss

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34
Q

what is the most common presenting feature of Whipple’s disease?

A

weight loss

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35
Q

what is the Rx for Whipple’s disease?

A

broad spectrum antibiotic therapy

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36
Q

what is disaccharidase?

A

apical membrane enzyme that cleaves lactose

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37
Q

what happens in disaccharidase deficiency?

A

leads to accumulation of lactose in the gut lumen, exerting an osmotic purgative effect–> diarrhea and malabsorption

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38
Q

what is the presentation of the congenital forms of disaccharide deficiency?

A

infants on exposure to milk or milk products

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39
Q

what is the most common presentation of disaccharide deficiency?

A

acquired form

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40
Q

what are the features of the acquired form of disaccharidase deficiency?

A

more common • affects adults • blacks>white

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41
Q

what are the features of intestinal mucosa in disaccharidase deficiency?

A

no morphologic abnormalities

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42
Q

what is abetalipoproteinemia?

A

congenital deficiency of betalipoprotein which is required for intestinal transport of chylomicrons

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43
Q

what happens in abetalipoproteinemia?

A

the inability to synthesize apoprotein (required to assemble lipoproteins) by the enterocytes leads to accumulation of TG’s in the cells, with lipid vacuolation

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44
Q

abetalipoproteinemia results in what?

A

marked lowering of serum LDL, VLDL, and chylomicrons–> defective lipid-membranes of cells (including RBC)–> acanthocytic RBC (burr cells) and widespread cell injury

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45
Q

how does abetalipoproteinemia present?

A

in infancy with malabsorption and wasting

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46
Q

what are the idiopathic inflammatory bowel diseases?

A

Crohn’s disease • Ulcerative colitis

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47
Q

What are idiopatchic inflammatory bowel diseases characterized by?

A

a chronic relapsing inflammatory condition

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48
Q

what is the etiology of idopathic inflammatory bowel disease?

A

unknown

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49
Q

speculations as to the etiology of idopathic inflammatory bowel disease include what?

A

genetic factors • unknown infectious agents • special susceptibility factors • altered immuno-reactivity to dietary or infectious antigens and altered regulatory controls of the inflammatory responses

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50
Q

what are the 2 clinicopathologic entities into which idiopathic inflammatory bowel disease are distinguished?

A

Crohn’s disease (CD) • Ulcerative Colitis (UC)

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51
Q

what is Crohn’s disease?

A

transmural granulomatous inflammation of the bowel, with mucosal ulcerations, fissures and fistulas in young white females

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52
Q

skip lesions (cobblestone appearance) are characteristic of which idiopathic inflammatory bowel disease?

A

CD

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53
Q

what are the features of UC?

A

crypt abscesses, pseudopolyps & increased risk of carcinoma (adenocarcinoma)

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54
Q

is there gross blood in the stool in UC vs CD?

A

UC= Yes • CD= Occasionally

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55
Q

is there mucus in UC vs CD?

A

UC= Yes • CD= Occasionally

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56
Q

how often are there systemic symptoms in UC vs CD?

A

UC= Occasionally • CD= Frequently

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57
Q

how often is there pain in UC vs CD?

A

UC= Occasionally • CD= Frequently

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58
Q

is there abdominal mass present in UC vs CD?

A

UC= rarely • CD= Yes

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59
Q

is there significant perineal disease in UC vs CD?

A

UC: no • CD: Frequently

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60
Q

are there fistulas in UC vs CD?

A

UC: No • CD: Yes

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61
Q

is there small intestinal obstruction in UC vs CD?

A

UC: no • CD: Frequently

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62
Q

is there colonic obstruction in UC vs CD?

A

UC: rarely • CD: Frequently

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63
Q

is there response to antibiotics in UC vs CD?

A

UC: no • CD: yes

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64
Q

is there recurrence after surgery in UC vs CD?

A

UC: No • CD: Yes

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65
Q

is there ANCA-positive result in UC vs CD?

A

UC: Frequently • CD: Rarely

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66
Q

What are the endoscopic features of Ulcerative Colitis?

A
  1. Rectal Sparing: rarely • 2. Continuous disease: Yes • 3. Cobblestoning: No • 4. Granuloma on biopsy: No
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67
Q

what are the endoscopic features of Crohn’s disease?

A
  1. Rectal sparing: frequently • 2. Continuous disease: Occasionally • 3. Cobblestoning: Yes • 4. Granulomas on biopsy: Occasionally
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68
Q

what are the radiographic features of Ulcerative Colitis?

A
  1. Small bowel significantly abnormal: No • 2. Abnormal terminal ileum: Occasionally • 3. Segmental Colitis: No • 4. Asymmetrical Colitis: No • 5. Stricture: Occasionally
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69
Q

what are the radiographic features of Crohn’s disease?

A
  1. Small bowel significantly abnormal: Yes • 2. Abnormal terminal ileum: yes • 3. Segmental Colitis: yes • 4. asymmetrical colitis: yes • 5. Stricture: frequently
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70
Q

what are the microscopic features of CD?

A

Fissuring Ulcer • Noncaseating Granuloma

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71
Q

what are the morphologic features of UC?

A

pseudopolyp • Ulcer

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72
Q

what are the intestinal vascular disorders?

A
  1. ischemic bowel diseases • 2. angiodysplasia • 3. hemorrhoids
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73
Q

what is the extent of transmural ischemic bowel disease?

A

all layers

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74
Q

what is the extent of Mural/Mucosal ischemic bowel disease?

A

mucosa& submucosa

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75
Q

what is the cause of transmural ischemic bowel disease?

A

compression/obstruction

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76
Q

what is the cause of mural/mucosal ischemic bowel disease?

A

hypoperfusion

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77
Q

what types of thrombus are associated with ischemic bowel disease?

A

Transmural: • - arterial (common) • - venous

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78
Q

what vessels are associated with transmural ischemic bowel disease?

A

SMA>IMA

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79
Q

is gangrene associated with transmural ischemic bowel disease?

A

yes

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80
Q

is gangrene associated with mural/mucosal ischemic bowel disease?

A

no

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81
Q

is perforation associated with transmural ischemic bowel disease?

A

yes

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82
Q

is perforation associated with mural/mucosal ischemic bowel disease?

A

no

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83
Q

what is the mortality rate associated with transmural ischemic bowel disease?

A

50-75%

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84
Q

what is the mortality rate associated with mural/mucosal ischemic bowel disease?

A

very less

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85
Q

what is the differential diagnosis for transmural ischemic bowel disease?

A

acute abdomen

86
Q

what is the differential diagnosis for mural/mucosal ischemic bowel disease?

A

enterocolitis • IBD

87
Q

what is angiodysplasia?

A

tortuous dilated submucosal veins in the cecum

88
Q

angiodysplasia may cause what?

A

massive bleeding

89
Q

angiodysplasia occurs when?

A

in old age

90
Q

what are hemorrhoids?

A

dilated varicose veins of the perianal plexus

91
Q

what is the incidence of hemorrhoids?

A

affects 5% of adults

92
Q

hemorrhoids are due to what?

A

chronic constipation, pregnancy, liver cirrhosis

93
Q

what are the 2 types of hemorrhoids that can occur singly or together?

A

External • Internal

94
Q

what perianal plexus is associated with internal hemorrhoids?

A

superior hemorrhoidal plexus

95
Q

what perianal plexus is associated with external hemorrhoids?

A

inferior hemorrhoidal plexus

96
Q

which type of hemorrhoids are painful?

97
Q

what is diverticular disease?

A

multiple flask-like outpouchings

98
Q

what is the age group affected by diverticular disease?

99
Q

diverticular disease is characterized by what?

A

protruding into the appendices epiploicae, in the distal colon • - they are lined by mucosa but no muscularis propria

100
Q

diverticular disease is caused by what?

A

focal anatomic defect in the bowel wall at the site of penetration of blood vessels • - increased intraluminal pressure is a contributory factor (constipation and increased peristalsis)

101
Q

what are the complications of diverticular disease?

A

bleeding • diverticulitis • pericolic abscess • peritonitis

102
Q

which pathologies involve intestinal obstruction?

A

hernias • adhesions • intussusceptions • volvulus

103
Q

what is the most common site of intestinal obstruction?

A

small intestine

104
Q

what are hernias?

A

protrusion of peritoneal hernial sac into a defect in the abdominal wall (inguinal, femoral, umbilical, surgical scars, retroperitoneal space)

105
Q

what happens when a hernia causes viscera to become trapped?

A

incarceration • obstruction • strangulation

106
Q

what are adhesions?

A

twisting f bowel loops around peritoneal fibrous bands

107
Q

what causes adhesions?

A

previous surgery • infection • endometriosis • radiation

108
Q

what is an intussusception?

A

a segment of the gut telescopes into the distal one

109
Q

what is the cause of intussusception?

A

may be caused by tumors

110
Q

what is volvulus?

A

complete twisting of a bowel loop around its mesenteric base

111
Q

what is the most common site of volvulus?

A

sigmoid colon

112
Q

what are the two types of small intestinal tumors?

A

adenomas • adenocarcinomas

113
Q

how common are neoplasms of the small intestine?

114
Q

what is the most common benign tumor of the small intestine?

115
Q

what is the most common site of benign tumor of the small intestine?

A

ampulla of Vater

116
Q

what are the complaints associated with benign tumors of the small intestine?

A

occult blood loss/rarely obstruction orintussusceptions

117
Q

benign tumors of the small intestine are associated with which condition?

A

familial polyposis

118
Q

what is the clinical course of small intestinal adenoma?

A

premalignant

119
Q

what is the most common malignant tumor of the small intestine?

A

adenocarcinoma

120
Q

what is the most common site of malignant tumor of the small intestine?

121
Q

what is the clinical presentation of malignant tumors of the small intestine?

A

intestinal obstruction

122
Q

what is the only sign of small intestinal malignant tumor?

A

occult blood loss

123
Q

what sign is present if small intestinal malignant tumor involves the ampulla of vater?

A

cause fluctuating obstructive jaundice

124
Q

what are the risk factors associated with malignant small intestinal tumor?

A

most tumors - no identifiable factor • - Crohn’s • - celiac • - FAP • - HNPCC • - Peutz-Jeghers syndrome

125
Q

what is Peutz-Jeghers syndrome?

A

autosomal dominant genetic disease characterized by the development of benign hamartomatous polyps in the gastrointestinal tract and hyperpigmented macules on the lips and oral mucosa

126
Q

what are the benign lower intestinal tumors?

A
  1. onneoplastic polyps • 2. adenomas • 3. familial polyps
127
Q

what are the malignant lower intestinal tumors?

A
  1. colorectal carcinoma • 2. carcinoid tumor • 3. GI lymphoma • 4. miscellaneous tumors • 5. anal canal tumors
128
Q

how common are large intestine neoplasms?

129
Q

what is the most common benign tumor of the large intestine?

A

adenoma=polyp

130
Q

what is the most common site of GI polyps?

131
Q

what are the types of large intestine polyps?

A
  1. non-neoplastic: hyperplastic, inflammatory, harmtomatous • 2. neoplastic/adenomatous( tubular, villous, tubulovillus)
132
Q

with what does the malignant risk of adenomatous polyps correlate?

A
  1. polyp size (>4cm) • 2. degree of dysplasia • 3. extent of villous component (more villous= more cancerous)
133
Q

what is the frequency and age associated with non-neoplastic large intestine polyps?

A

MC (90%) • young people • mostly hyperplastic

134
Q

what is the frequency and age associated with neoplastic large intestine polyps?

A

only 10% • elderly people • mostly tubular

135
Q

what is the level of dysplasia seen in non neoplastic large intestine polyps?

A

without dyplasia

136
Q

what is the level of dysplasia seen with neoplastic large intestine polyps?

A

with dysplasia

137
Q

what is is the mechanism that underlies non-neoplastic large intestine polyps?

A

production of epithelial cells exceeds their loss

138
Q

what is the mechanism that underlies neoplastic large intestine polyps?

A

mutations in genes

139
Q

what is the complication associated with non-neoplastic large intestine polyps?

A

no risk of malignancy

140
Q

what is the complication associated with neoplastic polyps of the large intestine?

A

premalignant

141
Q

what are the types of neoplasms of the large intestine?

A

neoplastic or adenomatous (Tubular, Villous, Tubulo-Villous)

142
Q

Are neoplasms of the large intestine true neoplasms?

143
Q

Neoplasms of the large intestine cause what?

A

occult bleeding, anemia, protein loss, obstruction

144
Q

what is FAP syndrome?

A

100 polyps and 100% malignant risk

145
Q

what are the features of FAP syndrome?

A
  • Autosomal dominant inheritance • - innumerable polyps (100=1000) in the colon & other parts of the GIT • - 100% risk of progression to adenocarcinoma in 10-15 years (indication for pancolectomy) • - onset in adolescence (bleeding and anemia)
146
Q

What is Gardner’s syndrome?

A

FAP syndrome associated with abnormal dentition, epidermal cysts, desmoid tumors, osteomas, duodenal and thyroid cancers

147
Q

what is Turcot’s syndrome?

A

FAP syndrome associated with CNS gliomas

148
Q

how common is colorectal carcinoma?

A

one of the most common malignancies

149
Q

what is the peak age for colorectal carcinoma?

A

60-70yo for sporadic cases • 30-40yo for FAP syndromes

150
Q

where do colorectal carcinomas arise?

A

preexisting adenomas

151
Q

what is the etiology/pathogenesis of colorectal carcinoma related to?

A

1 - genetic factors • 2 - Diet: • - rich in carbs and fat • - low in veg, fruit, Vit A,C,E

152
Q

what is the site of colorectal carcinoma?

A

distal colon

153
Q

what type of tumors are colorectal carcinomas?

A

all are invasive adenocarcinomas

154
Q

what is the clinical presentation of colorectal carcinoma?

A
  • IDA (occult bleeding) • - abdominal discomfort • - progressive bowel obstruction • - weight loss • - liver metastases
155
Q

what does the prognosis of colorectal carcinoma depend on?

A

clinical stage

156
Q

what is the staging system for colorectal carcinoma?

A

Astler-Coller modification of Duke’s staging system

157
Q

What are the features of Astler-Coller stage A LI tumors?

A

limited to mucosa

158
Q

what are the features of Astler-Coller stage B1 LI tumors?

A

Extending to (not penetrating) muscularis propria; no LN’s

159
Q

what are the features of Astler Coller stage B2 LI tumors?

A

Penetrating the muscularis propria, but with no LN’s

160
Q

what are the features of Astler-Coller stage C1 LI tumors?

A

Extending t (not penetrating) muscularis propria + LN’s

161
Q

what are the features of Astler-Coller stage C2 LI tumors?

A

penetrating through muscularis propria + LN’s

162
Q

what are the features of Astler Coller stage D LI tumors?

A

distant metastatic spread

163
Q

what is the only hope for cure of LI tumors?

164
Q

what is the prognosis for Astler Coller stage A LI tumors?

165
Q

what is the prognosis for Astler-Coller stage B1 LI tumors?

166
Q

what is the prognosis for Astler-Coller stage C1 LI tumors?

167
Q

what is the prognosis for Astler- Coller stage C2 LI tumors?

168
Q

what is the most common site of carcinoid Gi tumors?

169
Q

what fraction of small intestinal malignancies are carcinoid tumors?

170
Q

what is the peak age for carcinoid tumors?

A

6th decade

171
Q

what do carcinoid tumors do?

A

arise from neuroendocrine cells and secrete active amines or peptides

172
Q

what happens with a carcinoid tumor secretes gastrin?

A

Zollinger-Ellison Syndrome

173
Q

what happens when a carcinoid secretes insulin?

A

hypoglycemia

174
Q

what happens when a carcinoid secretes ACTH?

A

Cushing’s

175
Q

what happens when a carcinoid secretes serotonin?

A

carcinoid syndrome

176
Q

how often do appendiceal and rectal carcinoids metastasize?

177
Q

how often do ileal, gastric & colonic carcinoids metastasize?

178
Q

what is the prognosis for carcinoid GI tumors?

A

5 years: • - 90% without mets • - 50% with mets

179
Q

What is the implication for carcinoid tumor with liver mets?

A

will develop carcinoid syndrome

180
Q

what are the pathologies of the appendix?

A

acute appendicitis • tumors

181
Q

in what age group is acute appendicitis most common?

A

adolescents and young adults

182
Q

acute appendicitis is characterized by what?

A
  1. obstruction of lumen • 2. raised intraluminal pressure • 3. Ischemic injury and bacterial invasion
183
Q

what is the morphology of acute suppurative appendicitis?

A

hyperemia • edema • PML infiltration of all layers of all layers of the wall to the peritoneum

184
Q

what is the morphology of acute gangrenous appendicitis?

A

thrombosis of appendicular vessels–> gangrene–> diffuse septic peritonitis

185
Q

what is the morphology of localized or generalized peritonitis?

A

when the peritoneum becomes covered by fibrino-purulent exudate

186
Q

what is notable about the clinical features of acute appendicitis in old age?

A

deceptively minimal

187
Q

what are the complications associated with acute appendicitis?

A

perforation • pylephlebitis • liver abscess

188
Q

what are the 3 types of tumor of the appendix?

A
  1. mucocele • 2. carcinoid • 3. carcinoma
189
Q

mucocele of the appendix is characterized by what?

A

distension of the appendiceal lumen by mucinous secretion

190
Q

what is the non-neoplastic cause of mucocele of the appendix?

A

mucosal hyperplasia

191
Q

what is the benign neoplastic cause of mucocele of the appendix?

A

mucinous cystadenoma

192
Q

what is the malignant neoplastic cause of mucocele of the appendix?

A

mucinous cystadenocarcinoma (fatal)

193
Q

what are the complications of mucinous cystadenocarcinoma of the appendix?

A

may rupture–> peritoneal implants–> produce pseudomyxoma peritonei

194
Q

what is the most common tumor of the appendix?

195
Q

are carcinoid tumors of the appendix malignant or benign?

A

almost always benign and discovered accidentally on appendectomy (curative)

196
Q

what are the features of carcinoma of the appendix?

A

adenocarcinomas, identical to their intestinal counterparts

197
Q

what are the types of peritonitis?

A
  1. sterile peritonitis • 2. septic peritonitis • 3. sclerosing retroperitonitis
198
Q

what causes sterile peritonitis?

A
  1. chemical irritation by bile, pancreatic juice, endometriosis (blood) • 2. ruptured ovarian cyst (dermoid) • 3. introduction of chemical substances for diagnostic (laparoscopy, salpingography) or therapeutic procedures (peritoneal dialysis)
199
Q

what causes septic peritonitis?

A

bacterial infection of the peritoneum from: • - acute appendicitis • - ruptured PU • - acute cholecystitis • - diverticulitis • - bowel strangulation • - acute salpingitis • - evacuation of ascitic fluid • - peritoneal dialysis

200
Q

what is the clinical course of septic peritonitis?

A

localized (loculated abscesses) and may heal by fibrous adhesions–> chronic obstruction

201
Q

what are the potential causes of idiopathic sclerosing retroperitonitis?

A
  • may be related to anti-migraine drugs (methysergide) • - may be autoimmune
202
Q

sclerosing retroperitonitis is characterized by what?

A

excessive fibrous tissue proliferation (fibromatosis)

203
Q

what are the complications associated with sclerosing retroperitonitis?

A

compromising retroperitoneal structures

204
Q

what happens when ureters are compromised by sclerosing retroperitonitis?

A

hydronephrosis

205
Q

what is the cause of mesenteric cysts?

A

blocked lymphatics • enteric diverticula • postinfectious cysts • postpancreatitis pseudocysts • neoplastic cysts

206
Q

how common are primary peritoneal tumors?

207
Q

what is an example of primary peritoneal tumor and its cause?

A

mesothelioma= related to past asbestos exposure, identical to its counterpart in the pleura

208
Q

how common are secondary peritoneal tumors?

A

very common

209
Q

where do secondary peritoneal tumors come from?

A

advanced cancer of any abdominal viscera: • stomach, colon, small intestine, pancreas, liver, gallbladder, uterus, breast

210
Q

in secondary peritoneal tumor, diffuse seeding of the peritoneal cavity leads to what?

A

malignant effusions (mainly ovarian)

211
Q

how can secondary peritoneal tumors be detected?

A

cancer cells can be detected in the peritoneal fluid by cytological examination

► Med Notes (62 decks)

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