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Pathology > Chapter 17- The GI Tract > Flashcards

Chapter 17- The GI Tract Flashcards

1
Q

What congenital anomalies are common in the GI tract?

A

Atresia

Fistula

Stenosis

Congenital duplication cysts

Diaphragmatic hernia

Omphalocele

Gastroschisis

Ectopia

Meckel diverticulum

Congenital hypertrophic pyloric stenosis

Hirschsprung disease

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2
Q

What is the most common form of intestinal atresia?

A

Imperforate anus

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3
Q

What is esophageal atresia associated with?

A

A fistula connecting the upper or lower esophageal pouches to a bronchus or the trachea

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4
Q

Esophageal atresia causes what form of obstruction?

A

Mechanical

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5
Q

What is the most common site of intestinal fistula?

A

Esophagus-trachea

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6
Q

Stenosis is an incomplete form of what?

A

Atresia

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7
Q

What causes stenosis?

A

Fibrous thickening of the wall

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8
Q

What areas of the GI tract does stenosis commonly affect?

A

Esophagus

Small intestine

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9
Q

What are congenital duplication cysts?

A

Masses with redundant smooth muscle layers

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10
Q

What is a diaphragmatic hernia?

A

An incomplete diaphragm allows the abdominal viscera to herniate into the thoracic cavity

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11
Q

What is the difference between an omphalocele and gastroschisis?

A

Omphalocele- abdominal musculature is incomplete, viscera herniates into the ventral membranous sac

Gastroschisis- involves all the abdominal wall layers, not just the musculature, not contained

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12
Q

What is the most common form of intestinal ectopia?

A

Gastric mucosa in the upper third of the esophagus (acid production)

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13
Q

What are the features of Meckel diverticulum?

A

Blind outpouching of the GI tract

Includes all three layers of the bowel wall

Occurs in the ileum (2ft of ileocecal valve)

Tip shows ectopia tissue

Pouch is antimesenteric

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14
Q

How does Meckel diverticulum occur?

A

Failed involuntary of the vitelline duct

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15
Q

How does Meckel diverticulum differ from acquired?

A

Acquired only lacks the muscularis layer (or show diminished muscularis propria)

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16
Q

What is congenital hypertrophic pyloric stenosis?

A

Hyperplasia of the pyloric muscularis propria, obstructs gastric outflow

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17
Q

What are the characteristics of congenital hypertrophic pyloric stenosis?

A

Onset at 3-6th week

Regurgitation, nonbilious vomiting after feeding

Firm ovoid mass

Left to right hyperperistalsis during feeding

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18
Q

What increases the risk of congenital hypertrophic pyloric stenosis?

A

Male

Monozygotic twins

Turner syndrome and trisomy 18

Exposure to erythromycin and azithromycin in first 2 weeks of life

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19
Q

What is Hirschsprung disease?

A

Aganglionic megacolon (loss of bowel innervation)

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20
Q

How does Hirschsprung disease occur?

A

Neural crest cell migration from the caecum to the rectum is arrested

Distal segment lacks Meissner submucosal and Auerbach mesenteric plexus

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21
Q

What are the characteristics of Hirschsprung disease?

A

Impaired peristalsis

Functional obstruction

Dilation proximal to affected segment

Mucosal inflammation or shallow ulcers

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22
Q

What disorders can cause esophageal obstruction?

A

Spasms

Diverticuli

Mucosal webs

Esophageal/Schatzki rings

Achalasia

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23
Q

What type of obstruction is caused by esophageal spasms?

A

Functional

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24
Q

What are the different types of esophageal diverticuli and where are they found?

A

Zenker- above upper esophageal sphincter

Traction- midpoint

Epiphrenic- above lower esophageal sphincter

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25
Q

How many walls do esophageal diverticuli involve?

A

One or more

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26
Q

What are mucosal webs?

A

Ledge-like protrusions of mucosa

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27
Q

What is Plummer-Vinson syndrome?

A

Constellation of mucosal webs, IDA, glossitis and Cheilosis

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28
Q

What is another name for Plummer-Vinson syndrome?

A

Paterson-Brown-Kelly syndrome

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29
Q

How do esophageal rings differ from mucosal webs?

A

Rings are thicker and circumferential

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30
Q

What are the two types of esophageal rings and what are their characteristics?

A

A- squamous epithelium above the gastroesophageal junction

B- gastric cardiac mucosa at the squamocolumnar junction

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31
Q

What is achalasia?

A

Triad of incomplete LES relaxation, increased LES tone and esophageal aperistalsis

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32
Q

What causes primary achalasia?

A

Failure of distal esophageal neurons to induce LES relaxation or degenerative changes in neuron innervation

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33
Q

What can cause secondary achalasia?

A

Chaga’s

Disorders of vagaries dorsal motor nuclei

Diabetic autonomic neuropathy

Infiltrative disorders

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34
Q

What are the chief symptoms of esophagitis?

A

Pain

Dysphagia

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35
Q

What can cause esophagitis?

A

Lacerations (Mallory Weiss tears)

Chemicals

Infections- HSV, CMV, candida

Reflux

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36
Q

How do the ulcers in esophagitis caused by HSV and CMV differ?

A

HSV- punched out

CMV- shallower

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37
Q

What is the most common cause of esophagitis?

A

Reflux

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38
Q

What causes reflux?

A

Decreased LES tone

Increased abdominal pressure

Hiatal hernia

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39
Q

What are the characteristics of esophagitis caused by reflux?

A

Ulceration, hematemesis, melena, stricture, Barrett esophagus

Nasal zone hyperplasia

Elongation of lamina propria papillae

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40
Q

What are the characteristics of eosinophilic esophagitis?

A

Dysphagia and feeding intolerance (GERD-like symptoms)

Large number of superficial intraepithelial eosinophils

Mostly atopic

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41
Q

What are esophageal varices?

A

Congested subepithelial and submucosal venous plexi

Tortuous, dilated veins within the submucosal of the distal esophagus and proximal stomach

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42
Q

What types of patients are esophageal varicies seen in?

A

Cirrhotic patients (hypertension)

Alcoholic liver disease

Schistomiasis infections

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43
Q

Barrett esophagus is a complication of what?

A

Chronic GERD

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44
Q

What is Barrett esophagus?

A

Intestinal metaplasia within the esophageal mucosa (glandular tissue replaces squamous)

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45
Q

What is Barrett esophagus a precursor lesion to?

A

Esophageal adenocarcinoma

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46
Q

What is required for the diagnosis of Barrett esophagus?

A

Endoscopic evidence of metaplastic columnar mucosa above the gastroesophageal junction

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47
Q

What is the gross morphology of Barrett esophagus?

A

Tongues of velvety red mucosa extending upwards from the gastroesophageal junction

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48
Q

The majority of esophageal tumours are what kinds?

A

Adenocarcinoma

Squamous cell carcinoma

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49
Q

What is the most common form of benign esophageal tumours?

A

Leiomyomas

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50
Q

Adenocarcinoma in the esophagus normally evolves from what?

A

Barrett esophagus

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51
Q

Where is SCC often found in the esophagus?

A

Middle third

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52
Q

What is the pathology of acute gastritis?

A

Neutrophils present

Mechanisms that protect the mucosa are overwhelmed/defective

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53
Q

What are causative agents of acute gastritis?

A

NSAIDS
Alcohol
Bile
Stress-induced injury

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54
Q

What are the types of ulcers associated with acute gastritis and when do they occur?

A
  1. Stress- shock, sepsis, severe trauma
  2. Curling- in the proximal duodenum after severe burns or trauma
  3. Cushing- in the esophagus, duodenum and stomach of patients with intracranial disease
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55
Q

How do NSAIDS cause ulcers?

A

Inhibit COX-dependent synthesis of PGE2 and I2 (stimulate defence mechs)

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56
Q

What is the morphology of stress-related ulcers?

A

Small, diffuse

Stained brown/black

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57
Q

How does intracranial injury cause ulcers?

A

Stimulates vagal nuclei (hypersecretion of gastric acid)

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58
Q

What is the most common cause of chronic gastritis?

A

H. pylori

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59
Q

Where does H. pylori most often cause chronic gastritis?

A

Antrum (increased acid production)

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60
Q

What is the gross morphology associated with gastritis caused by H. pylori?

A

Erythmatous, coarse, nodular mucosa

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61
Q

Chronic gastritis due to H. pylori can progress to what?

A

Multifocal atrophic gastritis

Intestinal metaplasia

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62
Q

Chronic gastritis not caused by H. pylori is the result of?

A

Autoimmune disorder or peptic ulcer disease

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63
Q

Autoimmune gastritis normally spares what area of the stomach?

A

The antrum

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64
Q

What is autoimmune gastritis associated with?

A

Hypergastrinemia

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65
Q

What is the gross morphology of autoimmune gastritis?

A

Rugal folds lost

Diffuse mucosal damage in body and fundus

Inflammatory infiltrate

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66
Q

What is PUD?

A

Chronic mucosal ulceration

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67
Q

What is the morphology of PUD?

A

Solitary ulcers with punched out defects and a clean base

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68
Q

What is the cause and morphology of hypertrophic gastropathies?

A

Epithelial hyperplasia linked to excessive GF production

Giant enlargement of rugal folds

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69
Q

What are two forms of hypertrophic gastropathies?

A
  1. Menetrier disease

2. Zollinger-Ellison syndrome

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70
Q

What is the pathology of Menetrier disease?

A

Folveolar cell hyperplasia in body and fundus

Protein losing enteropathy (hypoproteinemia)

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71
Q

What is the pathology of Zollinger-Ellison syndrome?

A

Gastronomes in the small bowel or pancreas increase gastric release

Increased number of gastric parietal cells and HCl production

Ulcers and/or diarrhea

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72
Q

What are the different types of benign gastric polyps and what are their characteristics?

A

Inflammatory and hyperplastic- less than 1cm, multiple lesions, can have surface ulceration

Fundic gland- single or multiple smooth, well circumscribed lesions

Gastric adenoma- usually solitary and greater than 2cm

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73
Q

What percentage of gastric adenomas harbour carcinoma?

A

30%

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74
Q

What is the most common form of gastric malignancies?

A

Adenocarcinoma

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75
Q

What is important for the oncogenesis of adenocarcinoma?

A

Loss of intracellular adhesion (E-cad)

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76
Q

Adenocarcinoma affects what areas of the stomach most?

A

Antrum > lesser curve > greater curve

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77
Q

Gastric adenocarcinoma is associated with what?

A

H. pylori

N-nitro compounds

Benzo-alpha-pyrene

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78
Q

What are the two forms of gastric adenocarcinoma and their characteristics?

A
  1. Intestinal- bulky, exophytic masses with glandular structures and flat dysplasia
  2. Diffuse- signet ring cells, no glands with flat desmoplastic response (thickened wall/linitus plastic)
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79
Q

What does the prognosis of gastric adenocarcinoma depend on?

A

Depth of invasion

Node involvement

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80
Q

Extranodal lymphoma is common where?

A

The stomach

81
Q

What cells do carcinoid tumours arise from?

A

Endocrine

82
Q

What is the morphology of carcinoid tumours in the stomach?

A

Yellow-tan intramural or submucosal masses forming polyploid lesions

Scant cytoplasm, stippled nuclei, positive for chromogranin A and synaptophysin

83
Q

What are two types of gastric carcinoid tumours and their characteristics?

A

Zollinger-Ellison syndrome- gastrin carcinoids

Carcinoid syndrome- cutaneous flushing, bronchospasm, bowel motility, RS cardiac valance thickening

84
Q

What is the most important prognostic factor of carcinoid tumours?

A

Primary site

85
Q

What is the prognosis for carcinoid tumours in the fore-, mid- and hindguts?

A

Fore- resection cures

Mid- multiple and aggressive

Hind- benign, found incidentally

86
Q

Gastrointestinal stromal tumours (GISTs) arise from what cells?

A

Interstitial cells of Cajal (peristaltic cells)

87
Q

What is the morphology of GIST?

A

Solitary, well circumscribed, fleshy masses

Up to 30cm

Epitheloid or spindle cell shaped

88
Q

75% of GIST patients have what mutation?

A

C-KIT

89
Q

What is the Carney Triad?

A
  1. Nonhereditary syndrome with GIST
  2. Paraganglioma
  3. Pulmonary chondromas
90
Q

What part of the intestine is most commonly involved in obstruction?

A

Small intestine

91
Q

What are the most common causes of intestinal obstruction and what are their characteristics?

A

Hernia- defect in peritoneal wall permits peritoneal sac protrusion

Adhesions- healing from inflammation causes fibrous bridging between viscera

Volvulus- complete twisting of a bowel loop about its mesenteric base

Intrassusception- segment telescopes into the immediate distal segment of intestine

92
Q

What areas of the intestine are most vulnerable to hypoperfusion?

A

Watershed zones

93
Q

What cells are most susceptible to damage due to hypoperfusion and why?

A

Epithelial cells

Tips of villi

Located in lumen (furthest from blood supply in mesentary)

94
Q

What are the phases of ischemic bowel injury?

A
  1. Initial hypoxic injury

2. Reperfusion injury

95
Q

Differentiate intestinal mural and trans mural infarctions.

A

Mural- complete mucosal necrosis, no serositis

Transmural- involves entire wall thickness, segments are hemorrhagic, serositis, coagulation necrosis with perforation, wall fibrosis, sometimes stricture formation

96
Q

What is angiodysplasia?

A

Tortuous, ectatic dilations or mucosal and submucosal vessels

97
Q

What are the most common locations of angiodysplasia?

A

Caecum

Right colon

98
Q

What is steatorrhea and what is it associated with?

A

Excessive fecal fat

Malabsorption

99
Q

What is the pathogenesis of malabsorption?

A

Disturbances in intraluminal digestion, terminal digestion, transepithelial support and lymph transport

100
Q

What is celiac disease?

A

Immune mediated, diarrheal disorder triggered by the ingestion of gluten

101
Q

What protein in gluten causes celiac disease? How does it exert its effects?

A

Alpha gliadin

Induces epithelial IL-15 expression with CD8 activation and binds APCs to activate CD4 cells

Cytokine mediated epithelial damage

102
Q

What is the morphology of celiac disease?

A

Diffuse, flattened, atrophic villi and elongated crypts

103
Q

Where is severity greatest in celiac disease?

A

Proximal intestine

104
Q

10% of celiac patients have what skin disorder?

A

Dermatitis herpetiforms

105
Q

Celiac disease increases the risk for what?

A

T-cell lymphoma

Small intestine adenocarcinoma

106
Q

Where is severity greatest in patients with tropical sprue?

A

Distal small bowel

107
Q

What are the characteristics of autoimmune enteropathy?

A

X-linked disorder of children

Persistent diarrhea

108
Q

How does lactase deficiency cause diarrhea and malabsorption?

A

Unabsorbed lactose exerts osmotic pull

109
Q

What are the characteristics of abetalipoproteinemia?

A

Lipids are unable to leave absorptive cells

Failure to thrive, diarrhea, steatorrhea, absence of apolipoprotein B lipids

Acanthocytes, lipid vacuolation

110
Q

What is the mutation is abetalipoproteinemia?

A

Microsomal trig transfer protein (MTP)

111
Q

What are examples of bacterial causes of infectious enterocolitis?

A 
Cholera
Campylobacter enterocolitis
Shigellosis
Salmonellosis
Yersinia
E. coli
Pseudomembranous colitis
Whipple disease
112
Q

What is indicative of cholera?

A

Rice water stools

113
Q

What is the most common cause of bloody diarrhea?

A

Shigellosis

114
Q

What organisms cause typhoid fever?

A

S. typhi and paratyphi

115
Q

What is the morphology of typhoid fever?

A

Mucosal ulceration due to lamina propria inflammation

Lymphoid nodules in the liver

116
Q

What species of Yersinia cause GI infections?

A

entercolitica and psuedotuberculosis

117
Q

Symptoms of Yersinia infections mimic what?

A

Appendicitis

118
Q

What are the different strains of E. coli and their characteristics?

A

Enterotoxigenic- traveller’s diarrhea

Enterohemorrhagic- shigella toxin, 0157:H7

Enteroinvasive- invades epithelial cells, acute limited colitis

Enteroaggregative-toxin with nonbloody diarrhea

119
Q

What is pseudomembranous colitis often associated with?

A

Antibiotic use

120
Q

What organism often cause pseudomembranous colitis?

A

C. difficile

121
Q

What organism causes whipple disease?

A

Tropheryma whippelii

122
Q

What is the morphology of whipple disease?

A

Shaggy mucosa (villi expansion)

Foamy macrophages stuffed with bacteria in the lamina propria

123
Q

What are examples of viral causes of infectious enterocolitis?

A

Norovirus

Rotavirus

Adenovirus

124
Q

What virus is commonly responsible for sporadic gastroenteritis in developing countries?

A

Norovirus

125
Q

Rotavirus selectively infects and destroys what cells?

A

Mature enterocytes

126
Q

What do small intestine biopsies of adenovirus reveal?

A

Epithelial degeneration or nonspecific villous atrophy and compensatory crypt hyperplasia

127
Q

What are examples of parasitic causes of infectious enterocolitis?

A 
Ascaris lumbricoides
Strongyloides
Negatory and Ancylostoma duodenale 
Enterobius vermicularis
Trichuris trichuria
Schistosomiasis
Intestinal cestodes 
Entamoeba histolytica
Giardia lamblia
Cryptosporidium
128
Q

Strongyloides causes what kind of infection?

A

Autoinfection

129
Q

What is the morphology of hookworms (Necator and Ancylostoma)?

A

Erosions and hemorrhage of the intestine

130
Q

Trichuris infections cause what pathology?

A

Bloody diarrhea

Rectal prolapse

131
Q

Where do the worms reside in Schistomiasis infections?

A

Mesenteric veins

132
Q

What type of immune reaction is cause by Schistosomiasis infections?

A

Granulomatous

133
Q

What do cestode infections not normally cause?

A

Eosinophilia

134
Q

What is the morphology of ulcers produced in Entamoeba infections?

A

Flask-shaped

135
Q

How do Cryptosporidium invade their hosts?

A

Organelle attaches to brush border and the enterocyte engulfs the organism

Lives in endocytic vacuole within the microvilli

136
Q

How is IBS described?

A

Chronic, relapsing abdominal pain

Bloating

Changes in bowel habits

Normal gross and micro evaluation

137
Q

What is IBD described as?

A

Chronic inappropriate mucosal immune activation

138
Q

What are the two types of IBD and how are they differentiated?

A
  1. Crohn disease-affects ileum and/or colon, skip lesions with transmural inflammation, wall is thick
  2. Ulcerative colitis- only involves the colon, continuous lesions, mucosal inflammation, thin wall
139
Q

Risk for developing colitis associated neoplasia is greater with what form?

A

Pancolitis

140
Q

What are two causes of chronic colitis (besides IBD)?

A
  1. Diversion colitis- blind distal segment after ostomy surgery
  2. Microscopic colitis
141
Q

What are the characteristics of diversion colitis?

A

Mucosal erythema and friability

Lymphoplasmacytic inflammation

Lymphoid follicular hyperplasia

142
Q

What are the forms of microscopic colitis?

A
  1. Collagenous colitis

2. Lymphocytic colitis

143
Q

What is the most common finding in the intestine in GVHD?

A

Epithelial apoptosis

144
Q

GVHD follows what kind of transplant?

A

Hematopoietic stem cell transplant

145
Q

Why is sigmoid diverticulitis not considered true diverticuli?

A

Not invested in all three colonic wall layers

146
Q

Sigmoid diverticulitis with no symptoms is termed what?

A

Diverticulosis

147
Q

What is the morphology of sigmoid diverticulitis?

A

Flask-like outpouchings within a thin wall of flattened mucosa

Compressed submucosa

Attenuated/absent muscularis propria

148
Q

What causes sigmoid diverticulitis?

A

Structure of colonic muscularis propria (taenia coli) and elevated intraluminal pressure in sigmoid colon

Exaggerated peristaltic contractions increases pressure

149
Q

Where in the intestine are polyps most common?

A

Colo-rectal region

150
Q

What is thought to be the cause of hyperplastic polyps?

A

Reduced epithelial cell turnover and delayed shedding

Goblet and absorptive cells “pile up”

151
Q

Hyperplastic polyps resemble what other lesion?

A

Sessile serrated adenoma

152
Q

Why must hyperplastic polyps and sessile serrated adenomas be distinguished?

A

Polyps don’t have malignant potential but the adenoma does

153
Q

What are the histological features of inflammatory polyps?

A

Mixed inflammatory infiltrates

Erosion and epithelial hyperplasia

Lamina propria fibromuscular hyperplasia

154
Q

Why may inflammatory polyps form?

A

Chronic cycles of injury and healing

Part of rectal ulcer syndrome

155
Q

What is the triad of rectal ulcer syndrome?

A
  1. Rectal bleeding
  2. Mucus discharge
  3. Inflammatory lesion of the anorectal sphincter
156
Q

What is the morphology of juvenile hamartomatous polyps?

A

Pedunculated, smooth, reddish lesions with cystic spaces

Dysplasia rare

157
Q

What increases the risk of developing cancer in juvenile hamartous polyps?

A

Autosomal dominant form with 3-300 lesions

158
Q

What is Puetz-Jeghers syndrome and what are the characteristics?

A

Form of hamartomatous polyps

Multiple lesions

Mucocutaneous hyperpigmentation

Macules on lips, nostrils, buccal mucosa, palms, genitals and perianal region

Large, pedunculated polyps

159
Q

How is Peutz-Jeghers syndrome differentiated from juvenile polyps?

A

Arborization

Presence of smooth muscle intermixed with lamina propria

160
Q

What mutation causes Peutz-Jeghers syndrome?

A

Heterozygous loss of function in STK11

161
Q

Neoplastic polyps are precursors to the majority of what disorders?

A

Colorectal adenocarcinomas

162
Q

What is the most common neoplastic polyp?

A

Colonic adenoma

163
Q

The risk of malignancy in neoplastic neoplasms is correlated to what?

A

Size

164
Q

How are neoplastic polyps classified?

A

Tubular
Tubulovillous
Villous

165
Q

What are two forms of neoplastic polyps and what are their characteristics?

A
  1. Sessile serrated adenomas- lack cytologic dysplasia, serrated architecture throughout gland
  2. Intramucosal carcinoma- dysplasia cells invade BM into lamina propria or muscularis mucosa
166
Q

Which form of neoplastic polyps has little malignant potential?

A

Intramucosal carcinoma

167
Q

What are the two kinds of familial polyploid syndromes?

A
  1. Familial adenomatous polyposis (FAP)

2. Hereditary nonpolyposis colorectal cancer (HNPCC)/Lynch syndrome

168
Q

How many polyps are required for the diagnosis of FAP?

A

100

169
Q

What mutation causes FAP?

A

In adenomatous polyposis coli gene

170
Q

Untreated, what is the risk of FAP developing into colon cancer by 30 years?

A

100%

171
Q

What are two variants of FAP and what cancers are they associated with?

A
  1. Gardner syndrome- osteomas, fibromatosis, epithelial cysts, duodenal and thyroid cancers
  2. Turcot syndrome- medulloblastomas
172
Q

What mutation is responsible for HNPCC and what does it cause?

A

In MSH 1 and 2 (responsible for DNA replication errors)

Microsatellite instability

173
Q

What is the most common syndromic form of colon cancer?

A

HNPCC

174
Q

What factors increase risk of developing HNPCC?

A

MMR mutations

CRC and endometrial cancers

175
Q

What is the most common GI tract malignancy?

A

Adenocarcinoma

176
Q

What is an uncommon site for adenocarcinoma in the GI tract?

A

Small bowel

177
Q

What molecular events can lead to the colonic form of adenocarcinoma?

A

APC/beta catenin pathway and microsatellite instability pathway- beta cat aggregation activates genes that promote proliferation

Late K-RAS and p53 mutations promote growth and prevent apoptosis

SMAD mutations reduce TGF-B signalling (promote cell cycle)

Telomerase reactivation

178
Q

What are the types of morphologies associated with colonic adenocarcinomas and what areas are they found in?

A

Proximal- polypoid, exophytic/bulky masses

Distal- anular/ring-like

Adenomas- tall columnar cell’s that resemble dysplastic epithelium

179
Q

Invasive adenocarcinomas in the GI tract elicit what kind of response?

A

Strong desmoplastic/fibrotic response

180
Q

Tumours that produce what substance have a worse prognosis?

A

Mucin

181
Q

How are colonic tumours detected?

A

Cecal and right side- fatigue and weakness (IDA)

Left side- occult bleeding, changes in bowel habits/cramping, LLQ discomfort

182
Q

What are the two most important prognostic factors in colonic adenocarcinomas?

A

Depth of invasion

Lymph node mets

183
Q

What is the most common site of mets in colonic adenocarcinomas?

A

Liver

184
Q

How do you differentiate between primary cancer and mets in the liver?

A

Mets- multiple lesions

Primary- one or two

185
Q

What are the different forms of anal canal tumours and where are they found?

A

Upper third- columnar rectal epithelium (glandular)

Middle third- transitional epithelium (basaloid)

Lower third- stratified squamous epithelium (squamous)

186
Q

Pure squamous cell is associated with what virus?

A

HPV

187
Q

What are haemorrhoids?

A

Variceal dilations of anal and perianal submucosal venous plexi

188
Q

What can cause rectal haemorrhoids?

A

Constipation

Venous stasis

189
Q

What is the difference between external and internal rectal hemorrhoids?

A

External- ectasia of inferior hemorrhoid plexus below anorectal line

Internal- ectasia of superior hemorrhagic plexus above anorectal line

190
Q

What does acute appendicitis present as?

A

Periumbilical pain

Migrated to RLQ

Nausea

Mild fever

Leukocytosis

191
Q

What is the most common abdominal condition requiring surgery?

A

Acute appendicitis

192
Q

The majority of acute appendicitis cases are associated with what?

A

Lumen obstruction

193
Q

What are the characteristics of early and advanced acute appendicitis?

A

Acute- scant exudate, dull, granular and red serosa

Advanced- fibropurulent exudate, luminal abscess, ulceration, suppurative necrosis

194
Q

What is the most common form of appendix tumours?

A

Carcinoid

195
Q

Mucocele dilation of the appendix lumen can be caused by?

A

Benign obstruction

Adenoma

Adenocarcinoma

196
Q

What is mucinous cystadenocarcinoma?

A

Appendiceal wall invasion by neoplastic cells which can lead to peritoneal implants

197
Q

What is sclerosing retroperitonitis/Ormond disease?

A

Dense fibrosis of retroperitoneal tissue

198
Q

Are peritoneal tumours benign or malignant?

A

Virtually all malignant

199
Q

What are the causes of primary and secondary peritoneal tumours?

A

Primary- mesothelioma and desmoplastic small round cell tumour

Secondary- derived from any cancer (ovarian and pancreatic adenocarcinoma)

Pathology (25 decks)

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