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Anatomic Pathology > Gastrointestinal Pathology > Flashcards

Gastrointestinal Pathology Flashcards

1
Q

The GIT consists of ?

A

The mouth, esophagus, stomach, the Small intestine, colon, rectum and anus

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2
Q

Tracheo-esophageal fistula definition?

A

Congenital connection between the esophagus and trachea that’s often associated with esophageal atresia

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3
Q

How soon is TEF discovered ?

A

Soon after birth, usually due to regurgitation during feeding

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4
Q

Types of T.Esophageal Fistula?

A

Type A: isolated esophageal atresia (no fistula) - 8%
Type B: Esophageal atresia with proximal TEF - 1%
Type C: Proximal Esophageal Atresia with distal TEF - 86%
Type D: Proximal Esophageal atresia with proximal and distal TEFs (double fistula)
Type E; H-type (TEF with no atresia) - 4%

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5
Q

Atresia ?

A

Incomplete development of an organ

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6
Q

Complications of TEF ?

A

Aspiration
suffocaton
Aspiration pneumonitis
Severe fluid and electrolyte imbalance

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7
Q

Esophageal webs ?

A

Web like protrusions of the esophageal mucosa into the lumen which presents with dysphagia.

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8
Q

Esophageal web is associated with what syndrome ?

A

Plummer-Vinson syndrome in middle aged women xterized by Esophageal Webs, Iron deficiency Anaemia and increased risk of carcinoma

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9
Q

Web-like narrowings at the GEJ are called ?

A

Schatzki rings

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10
Q

Esophagus develops from which part of the foregut?

A

From the proximal part of the foregut

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11
Q

Nutcracker Esophagus is?

A

Functional obstruction of the esophagus as a result of high amplitude uncontrolled contractions of the circular and longitudinal smooth muscles of the esophagus

Esophageal dysmotility

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12
Q

Corkscrew esophagus ?

A

Diffuse esophageal spams, repititive simultaneous contractions of the distal esophageal smooth muscles. Contractions are of normal amplitude

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13
Q

Zenker diverticulum?

A

Pharyngoesophageal diverticulum, spasm of the cryopharyngeus leading to increased pressure in the distal pharynx

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14
Q

Achalasia is defined as ?

A

Triad of Incomplete LES relaxation, increased LES tone, and aperistalsis of the esophagus

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15
Q

In South America, achalasia may be caused by?

A

Chaga’s disease
Trypanosoma Cruzi infection causes destruction of myenteric plexus, failure of peristalsis, and esophageal dilatation

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16
Q

Clinical presentation of achalasia ?

A

Dysphagia to both solid and liquid feeds
- Dilated esophagus proximal to the LES

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17
Q

Barium swallow and microscopic view of achalasia shows?

A
  • Bird beak sign - Barium studies
  • Loss of ganglionic cells in the myenteric plexus - microscopic
  • Increased risk of esophageal cancer
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18
Q

Treatment of Achalasia ?

A

Lower esophageal sphincter balloon dilation
Laparoscopic myotomy
**Botulinum neurotoxin (Botox) injection to inhibit contraction

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19
Q

Mallory- weiss syndrome ?

A
  • Longitudinal mucosal lacerations at the gastroesophageal junction
  • Produced by severe prolonged vomiting secondary to acute alcohol toxicity and/or **chronic alcoholism*
  • Presents with *hematemesis and can be complicated by esophageal rupture (Boerhaave syndrome) rare
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20
Q

Boerhaave syndrome?

A

Esophageal rupture as a result of sudden increase in intraesophageal pressure (severe straining or vomiting).

  • Mediastinitis, severe chest pain, shock, tachypnea
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21
Q

Esophageal varices?

A

Dilated submucosal veins in the lower third of the esophagus, usually secondary to portal hypertension

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22
Q

LES dysfunction can be associated with what congenital syndrome?

A
  • Down syndrome
  • Triple A syndrome ( achalasia, adrenal insufficiency, alacrima )
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23
Q

Pathogenesis of esophageal varies?

A

1) Impared blood flow through the portal venous system and liver
2) increased portal venous pressure
3) Development of collateral channels
4) Collateral channels result in congestion and dilation of subepithelial and submucosal venous plexuses in the distal esophagus and proximal stomach
5) dilated vessels are called (varices)

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24
Q

Causes, complications and treatment of esophageal varices ?

A

1) Liver cirrhosis due to alcoholic liver disease
2) Hepatic schistosomiasis

  • Asymptomatic presentation with massive hematemesis when it ruptures
  • exsanguination (fatal hemorrhage) may occur
  • Treated with band ligation, sclerotherapy, balloon tamponade
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25
Q

Reflux esophagitis (GERD)?

A
  • Abnormal reflux of gastric contents into the esophagus causing chronic symptoms or mucosal damage.
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26
Q

The major cause of GERD

A
  • Transient lower esophageal sphincter relaxation
  • Abrupt increase in intra abdominal pressure (coughing, straining or bending)
  • Alcohol, tobacco use, Obesity
  • CNS depressants, pregnancy
  • Hiatal hernia
  • Delayed gastric emptying
  • Increased gastric emptying
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27
Q

Risk factors and symptoms of GERD

A
  • Age > 40yrs

Dysphasia, heart burn, regurgitation of sour tasting gastric contents postprandially

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28
Q

Effects of reflux on the esophageal mucosa lining ?

A
  • Inflammation
  • Hyperplasia of the squamous epithelial lining of the esophagus
  • Erosion/ulceration of the epithelium
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29
Q

Complications of GERD?

A
  • Barrett’s esophagus
  • Stricture due to fibrosis
  • Perforation due to erosion
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30
Q

Feline esophagus is seen where ?

A

Appearance of stacked circular rings in the esophagus.
Seen in Eosinophilic esophagitis

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31
Q

Histological features of Eosinophilic esophagitis?

A
  • Abundant intraepithelial eosinophils, superficially.
  • Not associated with an increased risk of Barrett’s esophagus
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32
Q

Gross description of GERD?

A
  • Edematous and inflamed (erythematous) esophageal mucosa
  • Erosions
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33
Q

Microscopic features of GERD ?

A
  • Basal cell hyperplasia
  • Elongated lamina propria papillae
  • Eosinophilic and neutrophilic infiltrations
34
Q

Barrett’s Esophagus

A

Generally defined as **intestinal metaplasia of the squamous epithelium lining of the esophagus.

  • reversible process
  • ## Adaptive substitution of squamous epithelial cells (sensitive to stress) with columnar epithelium with globet cells (resistant to stress)
35
Q

Complications of Barrett’s esophagus

A

Progress through low and high grade dysplasia to adenocarcinoma

Low grade dysplasia - Treated with acid suppressing absents
High grade dysplasia - indication for oesophagectomy

36
Q

Endoscopic finding of Barrett’s esophagus ??

A

Irregular GEJ, with tongues of red granular mucosa extending up into the esophagus

Histology- intestinalized epithelium with *goblet cells and columnar cells

37
Q

Mechanism behind Corrosive Esophagitis ?

A
  • Caused by ingestion of acid or alkaline material
  • leading to Mucosal injury of the mouth, pharynx, esophagus and stomach
  • severe forms; leads to full thickness mucosal necrosis, ulceration and even perforation
  • heals by fibrous stricture formation
38
Q

Causative agents in Infectious esophagitis ?

A
  • common in immunocompromised individuals (AIDS, transplant patients)
  • agents; Candida species, herpes simplex virus, Cytomegalovirus
39
Q

Role of candida in infectious esophagitis ?

A

Colonise the squamous epithelium, forms white plaques and hyperkeratosis with an inflammatory infiltrate

40
Q

Role of herpes simplex virus in infectious esophagitis ?

A

They infect squamous cells resulting in blisters and superficial ulcers
- infected cells; multi-nucleated, intranuclear viral inclusions (glassy basophilic appearance)

41
Q

Role of cytomegalovirus in infectious esophagitis?

A

Infected cells appear enlarged with prominent intranuclear inclusions
With or without basophilic intracytoplasmic inclusions

42
Q

Oesophagial tumors as regards to age and sex?

A
  • Commonly occur after age 50
  • Higher incidence in Males
43
Q

Clinical features of esophageal tumors?

A
  • Retrosternal pain
  • Anorexia
  • Weight loss
  • Melana
  • Systemic symptoms of metastasis
44
Q

Common Locations of esophageal tumors?

A

50% middle third of esophagus
30% lower third of esophagus
20% upper third of esophagus

45
Q

Common sites of metastases of esophageal tumors ?

A

The lungs and the liver

46
Q

Esophageal cancers (tumors) are either ?

A

Squamous cell carcinomas or Adenocarcinoma

47
Q

Esophageal squamous cell carcinoma ?

A
  • occurs in men > 45yrs
  • More common in rural and low income populations
  • Highest incidence in Iran, central China, Hong Kong, Brazil, and South Africa
  • Blacks > whites
48
Q

Risk factors for ESCC?

A

1) Lifestyle;
Alcohol and tobacco use
poverty
2) Esophageal disorders
- Caustic esophageal injury
- Achalasia
- Plummer-Vinson syndrome
- long standing esophagitis
3) Dietary factors
- Diets that are deficient in thiamine, VIT A and C, Zinc
- Frequent consumption of very hot beverages
4) Genetic predispositions
- Celiac disease
- Previous radiation to the mediastinum
- ectodermal dysplasia

49
Q

Esophageal adenocarcinoma ?

A
  • Typically arises in the background of Barrett esophagus and long-standing GERD 10% of B.E develop this.
  • Genetic alteration of metaplastic mucosa ——> low grade dysplasia ——> high grade dysplasia ——> carcinoma In situ ——-> invasive carcinoma
  • Men (7folds) & whites and Hispanics commonly
  • usually occurs in the distal third of
    the esophagus     and may invade the adjacent gastric cardia
50
Q

Symptoms of Esophageal adenocarcinoma??

A
  • pain or difficulty in swallowing, progressive weight loss, hematemesis, chest pain, or vomiting
  • By the time symptoms appear, the tumor has often spread to submucosal lymphatic vessels. As a result, overall 5-year survival is less than 25%.
51
Q

Pyloric stenosis?

A
  • Congenital stenosis of the pylorus due to marked muscular hypertrophy of the pyloric sphincter, resulting in gastric outlet obstruction
  • male infants > females
  • treatment is surgical
52
Q

Pyloric stenosis is associated with which syndromes?

A

Turner syndromes
Edwards syndromes

Presentation; onset of regurgitation and vomiting in the second week of life
Waves of peristalsis are visible on the abdomen and palpable oval abdominal mass

53
Q

Congenital diaphragmatic hernia ?

A
  • Occurs when a congenital defect is present on the diaphragm, resulting In the herniation of abdominal organs into the thoracic cavity
  • Stomach (commonly)
  • Associated with intestinal malrotation
54
Q

Congenital diaphragmatic hernia may be complicated by?

A

Significant Lung hypoplasia —> respiratory compromise

55
Q

Two examples of Hypertrophic gastropathy associated diseases ??

A

Menetrier disease
Zollinger-Ellison syndrome

56
Q

Menetrier disease

A
  • Disease of middle aged men characterized by enlarged fugal folds in the body and fundus
  • Due to hyperplasia of the surface mucous cells that’s accompanied by glandular atrophy
  • symtoms; protein losing Enteropathy, decreased acid production and increased gastric cancer risk
  • Gross; marked hypertrophy of rugal folds
  • histology; **foveolar hyperplasia with elongated and focally dilated glands
57
Q

Acute gastritis;

A

Transient mucosal inflammatory process that may be asymptomatic or cause variable degrees symptoms **secondary to breakdown of the mucosal barrier and acid response injury **

58
Q

Clinical symptoms of acute gastritis;

A

Epigastric abdominal pain, gastric hemorrhage, hematemesis and melena

59
Q

Etiology of Acute gastritis;

A

Chronic use of aspirin or NSAIDs
Alcohol and smoking
Recent surgery, burns, stress
Ischemia, uremia, chemotherapy

60
Q

Protective factors in the development of gastritis ?

A
  • surface mucin secretion
  • Bicarbonate secretion into mucus
  • Mucosal blood flow
  • Epithelial barrier function
  • Epithelial regenerative capacity
  • Elaboration of prostaglandins
61
Q

What are gastric stress ulcers ?

A

Multiple, small, round, superficial ulcers of the stomach and duodenum

high incidence in ICU patients and may be complicated by bleeding.

62
Q

Predisposition factors to gastric stress ulcers?

A
  • NSAID use
  • severe stress
  • sepsis
  • shock
  • Severe burns or trauma (curling ulcer)
  • raised intracranial pressure (Cushing ulcers)
63
Q

Macroscopic and microscopic feature of gastric stress ulcers

A

Macroscopic; multiple, small (<1cm), superficial defects with a blood stained base
Microscopic; superficial erosion of surface epithelium which may extend deeper to become full thickness mucosal ulceration

64
Q

Chronic gastritis includes ?

A
  • Autoimmune gastritis (FUNDIC type A)
  • Helicobacter pylori associated gastritis (ANTRAL type B)
  • Menetrier disease
65
Q

Autoimmune gastritis is associated with what type of cells

A

parietal cells and/or Intrinsic factor

Autoimmune atrophic gastritis that involves the body and the fundus

66
Q

Characteristics of Autoimmune gastritis?

A

Associated with parietal cells or Intrinsic factor
- Achlorhydria, Pernicious anemia, Autoimmune disease - chronic thyroiditis and Addison’s disease
- Associated with aging, partial gastrectomy, gastric ulcer and gastric carcinoma

67
Q

Function type A gastritis

A

-Autoimmune gastritis involving the body and the fundus
- autoantibodies directed against parietal cells and IF
- megaloblastic anemia, pernicious anemia, increased serum gastrin, decreased acid production.
- intestinal metaplasia, lymphocytic infiltrates
- loss of rugal folds in the body and fundus
- increased risk of gastric carcinoma

68
Q

Helicobacter associated gastritis

A
  • Most common form of chronic gastritis
  • increased gastric acid secretion occurs
  • adenocarcinoma of the stomach , maltoma,
  • production of urease breakers down urea to CO2 and ammonia, vacuolating cytotoxic A, phospholipases (help in epithelial cell damage)
  • blood group o antigens
69
Q

Duodenal peptic ulcer

A
  • Associated with H pylori infection (100%)
  • Blood group O
  • MEN type 1
  • Zollinger Ellison syndrome
  • Cirrhosis and copd
  • located in the anterior wall do the proximal duodenum
  • burning epigastric pain 1-3hours after eating, relieved by food
70
Q

Gastric peptic ulcer ?

A

H pylori (75%)
- Located in the lesser curvature of the antrum (transition between antrum and body)
- Small, sharply demarcated, solitary ulcers, round or oval shaped, overhanging margins, radiating mucosal folds
- Burning epigastric pain that worsens when eating

71
Q

Stomach carcinoma

A
  • common after 50 years of age
  • increased incidence in men
  • more frequent in person with blood group A
  • high incidence in Japan, Finland and Iceland
72
Q

Etiology of gastric cancer

A
  • H pylori
  • Nitrosamine (canned food preservatives, smoked fish and meat
  • excessive salt intake
  • low fiber diet
  • Achlorydia
  • chronic gastritis w/ pernicious anemia
  • blood type A
  • subtotal gastrectimy
  • Menetrier disease
73
Q

Characteristics of stomach cancer and Adenocarcinoma

A
  • almost always adenocarcinoma (>90%)
  • low incidence in UK, US, NZ, Canada
  • distal stomach, lesser curvature of the antrum or pre pyloric region
  • 50% arise in antrum and pylorus, 25% cardia
  • tumor cells contain abundant mucin (signet ring cells - displace the nucleus to one side)
74
Q

Metastasis of gastric Adenocarcinoma

A

-virchow node; left supreclavicular lymph node involvement
- Krukenberg tumor- bilateral involvement of the ovaries
- sister Mary Joseph node - periumbilical subcutaneous metastasis
- Liver

75
Q

Morphological variants of stomach carcinoma ?

A

1) Intestinal type
- fungating (polypoid) - H.pylori, gastric atrophy and intestinal metaplasia, chronic gastritis
- ulcerating base, raised margins
2) Infiltrating or diffuse carcinoma (signet-ring type)
- not associated with h pylori or chronic gastritis
- thickens rigid stomach wall
- from diffuse infiltration of tumor cells
- extensive fibrosis

76
Q

Infiltrating or diffuse carcinoma (signet-ring type)?

A
  • Gastric type mucous cells that don’t form glands
  • they permeate mucosa as signet cell
  • leather bottle appearance - linitis plastic
  • thickened gastric wall and rugal folds are partially lost
  • female predominance at younger age
77
Q

Gastric lymphomas

A
  • May regress after taking antibiotics
  • arise from B Cells
  • Mucosa associated lymphoid tissue lymphoma
  • better prognosis than adenocarcinoma
  • account for 4% of malignant gastric tumors
  • untreated, can progress to diffuse large B cell lymphoma
  • lymphoid infiltration do the stomach
78
Q

Gastrointestinal stromal tumors (GIST)

A
  • mesenchymal tumors derived from pacemaker cells of cajal (interstitial cells of cajal)
  • most common in the sub mucosa of the stomach (70%), 20% small intestine, 10% esophagus
  • most cases are indolent
  • metastasis to the liver
  • arose beneath mucosa and protrude into the lumen
  • overlying mucosa may ulcerate leading to blood loss
  • CKIT oncogene CD117
  • PDGR alpha-
79
Q

Volvolus

A
  • Twisting of segment of bowel on its vascular mesentary
    Site
  • sigmoid colon - elderly
  • small bowel - children
    Complications
  • infarction and peritonitis
80
Q

Intussusception

A
  • Telescoping of proximal segment of bowel into the distal segment
  • most common in infants and children (meckel diverticulum, viral)
  • may be associated with a mass or tumor in adults
  • intestinal obstruction, abdominal pain, currant jelly stools
  • complication - infarction

Anatomic Pathology (12 decks)

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