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3rd Yr 1 Semester > GI pathology (Mid-term exam content) > Flashcards

GI pathology (Mid-term exam content) Flashcards

1
Q

What is Melena?

A

Dark-black feces because it contains blood.

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2
Q

What are the mechanical obstructive esophageal diseases?

A

Atresia Agenesis Fistula Stenosis Diverticula

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3
Q

What is the functional obstructive esophageal disease?

A

Achalasia

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4
Q

What are the mechanical obstructive esophageal disease that could be congenital or acquired?

A

Tracheoesophageal fistula

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5
Q

Where is the location tracheoesophageal fistula?

A

near the tracheal bifurcation

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6
Q

What are the causes of esophageal stenosis?

A

caused by: Epithelial damage Submucosal fibrous thickening Muscularis propria atrophy (due to inflammation and scaring.)

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7
Q

What obstructive mechanical esophageal Disease causes regurgitation?

A

Esophageal diverticula ( acid trapped in diverticula)

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8
Q

what are the triad characteristics of Achalasia?

A

Incomplete (LES) relaxation. Increase LES tone Esophageal aperistalsis.

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9
Q

What is the pathophysiology behind Achalasia?

A

Destruction of the esophageal neurons and subsequent loss of their inhibitory motor function.

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10
Q

Secondary Achalasia caused by?

A

-SIIM- 1. Infectious: like Chagas disease 2. An infiltrative tumor (malignancy): like SCC. 3. Material deposition: like Amyloidosis. 4. Systemic diseases involving the esophagus: like DM and Sarciodosis.

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11
Q

How would you diagnosis Achalasia?

A
  • presented as progressive dysphagia. - Radiologically & endoscopically: Progressive dilation of the esophagus above LES. - Manometry: Aperistalsis. - Microscopically: Absence of myenteric ganglia ± mucosal inflammation and ulceration proximal to the LES.
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12
Q

What are esophageal varices?

A

Obstruction to the flow that will lead to portal

hypertension.

Dilated tortuous veins at the distal part of the esophagus

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13
Q

What are the commonest causes of esophageal varices?

A

Liver cirrhosis, (caused by alcoholic abuse, schistosomiasis, and HCV.)

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14
Q

How would you diagnosis esophageal Varices?

A

by endoscopy (Dilated and tortuous veins) & angiography (Tortuous vein & Varices)

.

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15
Q

What will esophageal varices cause clinically?

A

massive hematemesis and even death.

1/2 hemorrhagic cases die: due to hypovolemic shock or due to the hepatic coma.

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16
Q

What is an esophageal laceration?

A

longitudinal tear in the esophageal wall usually

at the gastroesophageal junction.

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17
Q

An example of an esophageal laceration?

A

Mallory-Weiss tears (laceration due to sever stretching & vomiting.)

Associated with alcohol abuse.

Can cause hematemesis.

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18
Q

Causes of injurious esophagitis?

A
  1. Chemicals.
  2. Pill-induce.
  3. Radiotherapy.
  4. Endoscopic injury.
  5. Graft versus host disease: grafted T-cells attacking host epithelial cells.
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19
Q

How would you diagnosis Injurious Esophagitis?

A

NO specific morphology under the microscope, just by finding an inflammation.

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20
Q

What are the causes of Infectious Esophagitis?

A
  1. Viral: Cytomegalovirus & Herpes simplex virus
  2. Bacterial.
  3. Fungal: Candida (commonest), Aspergillus, and, Mucormycosis.
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21
Q

How would you diagnosis infectious esophagitis?

A

Identify the specific microorganism.

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22
Q

What are the hallmark symptoms of Infectious Esophagitis?

A

ODYNOPHAGIA, dysphasia, chest pain, and fever.

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23
Q

What are the histological features of CMV Esophagitis?

A
  • Non-specific ulcers.
  • Large cells at the base.
  • Large intranuclear inclusion.
  • Basophilic → intracytoplasmic inclusion.
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24
Q

What are the histological features of HSV Esophagitis?

A
  • vesicle or punched-out ulcer.

3M:

  • Multinucleated squamous cells. (dark eosinophilic + intranuclear inclusions)
  • Molding nuclei.
  • Marginal chromatin.
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25
Q

What are the histological/endoscopic features of Candida Esophagitis?

A

fungal hyphae and inflammatory cells.

endoscopic: gray-white pseudomembrane with an underlying erythematous mucosa.

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26
Q

What are the protective mechanisms of the esophagus?

A
  1. The continuous peristaltic movement of the esophagus.
  2. Continuous LES tone.
  3. Submucosal glands secretions: bicarbonate and mucus.
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27
Q

What diseases will occur due to the progressive condition of reflux esophagitis (GERD)?

A

Barrett Esophagus and eventually carcinoma.

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28
Q

What can cause a decrease in LES tone leading to GERD?

A
  • Hiatal hernia.
  • CNS depressants
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29
Q

What can cause an increase in abdominal pressure leading to GERD?

A
  1. Oral intake: e.g (alcohol, tobacco, fatty meals, & soft drinks.)
  2. Obesity.
  3. Pregnancy.
  4. Delayed gastric emptying.
  5. increased gastric volume.
  6. Increase acid production: Zollinger–Ellison syndrome. (tumors form in your pancreas or the duodenum.)
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30
Q

How would you diagnosis Reflux Esophagitis (GERD)?

A

Endoscopically: hyperemia. (In the lower esophagus part)

Microscopically, there is NO single histologic diagnostic criterion had been made.

In severe cases we can see the triad:

  1. Spongiosis with elongated lamina propria papillae.
  2. Thickened basal layer: > 15% of epithelial thickness.
  3. intra-epithelial T-cell lymphocytes, eosinophils, & neutrophils.
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31
Q

What is the treatment of Reflux Esophagitis (GERD)?

A

Antihistamine, Proton pump inhibitors (omeprazole), or surgery.

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32
Q

What is the difference between Eosinophilic Esophagitis and GERD?

A

characterized by eosinophilic infiltration without any explanation.

Presence of epithelial infiltration by large numbers of eosinophils that are away from the GEJ (mid-esophagus).

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33
Q

What is the treatment of Eosinophilic esophagitis?

A

steroids.

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34
Q

How would you diagnosis Barrett Esophagus (endoscopic + microscopic.)?

A

(salmon-pink velvety mucosa) above GEJ proved by a biopsy to be intestinal metaplasia.

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35
Q

What disease is associated with Barrett Esophagus?

A

BE associated with an increase risk of adenocarcinoma.

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36
Q

What is the pathogenesis of Barrett Esophagus?

A

Recurrent GERD → inflammation of mucosa → healing by ingrowths of stem cells that give columnar epithelium (instead of squamous) due to the effect of abnormal environmental pH level.

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37
Q

What are the histological features Barrett Esophagus?

A
  • Goblet cell.
  • Glands with abnormal hyperchromatism,
  • Enlargement, crowding, and stratification of nuclei of the columnar lining cells.
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38
Q

What is the treatment of Barrett Esophagus & low-grade dysplasia? and the treatment of High-grade dysplasia & intramucosal carcinoma?

A
  • BE & low-grade dysplasia: treat the GERD + periodic

endoscopy with biopsy every 6 months until two consecutive negative results.

  • High-grade dysplasia & intramucosal carcinoma:

Endoscopic mucosal resection or esophagectomy.

39
Q

What are the cells in the cardia and antrum and what do the produce?

A

Both cardia and antrum lined by chief cells which

produce mucin and pepsin.

The antrum also contains neuroendocrine cells (G-cells) that release Gastrin.

40
Q

What are the cells in the fundus and body and what do they produce?

A

Both fundus and body are lined by chief & parietal cells. Parietal cells secret HCl and (IF).

41
Q

What is the pH of gastric juice?

A

Strongly acidic (pH almost 1)

42
Q

What are the acidity protective mechanisms for the gastric mucosa?

A
  1. Acid activation.
  2. Bicarbonate production.
  3. Mucin production.
  4. Rich blood supply to the stomach.
  5. Continuous rapid epithelial regeneration capacity.
  6. Localized prostaglandin E2 & I2 synthesis.
43
Q

What are the causes of the gastric defense mechanisms disruption that can lead to gastritis?

A
  1. NSAIDs.
  2. Increase production of urea.
  3. Decrease mucin &/or bicarbonate production.
  4. Hypoxemia and decreased oxygen delivery.

Direct injury to epithelial and stromal cells by chemical ingestion (alcohol consumption & chemotherapy)

44
Q

What are the histopathological Types of Gastritis? and what are their differences?

A
45
Q

What can an acute gastritis endoscope/microscope show?

A

Endoscopically: erosions, ulcers, & hemorrhage (as dark punctate in hyperemic mucosa).

Microscopically: intraepithelial neutrophils, cryptitis, &/or crypt abscesses.

46
Q

What can a reactive gastropathy microscope show?

A
  1. Foveolar hyperplasia: elongated tortuous gastric pits.
  2. Elongation of muscularis propria: arising from the muscularis mucosa and extending through the lamina propria up to the epithelial surface.
  3. Edema & vascular congestion.
  4. Minimal inflammatory cells.
47
Q

What diseases can cause (stress-Related Mucosal diseases)?

A

trauma, extensive burns, intracranial disease, major surgery, or serious medical diseases.

48
Q

What can Stress-Related Mucosal Diseases show endoscopically?

A

75% of critically ill patients develop gastric ulcers during the first 3 days of their illness.

49
Q

Stress-Related Mucosal Diseases Tx?

A
  1. PPI prophylaxis.
  2. Determine underlying condition and treat it.

(ulcers heal within days to weeks after removing the causative agent.)

50
Q

What are the specific names of ulcers given to Stress-Related Mucosal Diseases?

A
  1. Stress ulcers: shock, sepsis, or severe trauma.
  2. Curling ulcers: proximal duodenum and severe burns or trauma.
  3. Cushing ulcers: in esophagus, stomach, or duodenum. (Intracranial disease cause activation of vagal nuclei causing hypersecretions of acid)
51
Q

What is the different pathogenesis of Stress-Related Mucosal Diseases?

A
  1. Local ischemia. (stress-induced vasoconstriction)
  2. Stimulation of vagal nuclei. (Cushing ulcers)
  3. Systemic acidosis. (lowering the intracellular pH of mucosal cells causing mucosal injury)
52
Q

What is the morphology of Stress-Related Mucosal Diseases?

A
  1. Ranges: shallow erosions - deeper ulcers.
  2. Rounded (less than 1cm diameter).
  3. The ulcer base is stained brown to black by acid-digested extravasated RBCs.
  4. Acute stress ulcers are multiple and found anywhere in the stomach.
  5. They are sharply-demarcated.
  6. NO scarring or thickening of blood vessels (in contrast to chronic peptic ulcers).
  7. Healing with complete re-epithelialization occurs days or weeks after the injurious factors are removed.
53
Q

What are the causes of reactive Gastropathy “chemical gastritis”?

A

Bile reflux, NSAIDs, & alcohol.

54
Q

What is shown under a microscope in Reactive Gastropathy?

A
  1. Foveolar hyperplasia: elongated tortuous gastric pits.
  2. Elongation of muscularis propria: arising from the muscularis mucosa and extending through the lamina propria up to the epithelial surface.
  3. Edema & vascular congestion.
  4. Minimal inflammatory cells.
55
Q

What are the causes of Stress-Related Mucosal Diseases?

A

severe physical/psychological stress as severe trauma, extensive burns, intracranial disease, major surgery, or serious medical diseases.

56
Q

What is shown under a microscope/histology in Stress-Related Mucosal Diseases?

A

Endoscopically visible gastric ulcers during the first 3 days of their illness.

Histologic evidence of gastric mucosal damage.

57
Q
A
58
Q

How can H.pylori cause GIT diseases?

A
  1. Flagella.
  2. Urease production.
  3. Adhesins.
  4. Toxins: inflammation/tumor formation.
59
Q

Best micro-environment for H.pylori?

A

The antrum, bc it doesn’t have parietal cells and doesn’t produce acid.

60
Q

What is the gold standard for diagnosing H.pylori Gastritis?

A

Biopsy (1. Histopathological identification. 2. Rapid urease test. 3. Culture. 4. PCR.)

61
Q

What will a biopsy microscopically of H.pylori Gastritis show?

A
  1. H.pylori Bacilli.
  2. Inflammation: Plasma cells, lymphocytes, and neutrophils.
  3. Neutrophils: in lamina propria, intraepithelial cryptitis and crypt abscesses.
  4. Lymphocytic aggregation with germinal center formation.

(LOOK for Intestinal metaplasia, dysplasia, and tumors).

62
Q

H.pylori Gastritis Tx?

A

Triple therapy for 2 weeks (2 antibiotics + 1 PPI).

63
Q

Complications of H.pylori Gastritis?

A
  1. Ulcers: in the gastric &/or duodenum.
  2. Intestinal metaplasia & dysplasia.
  3. Tumors: in the stomach/duodenum. (adenocarcinoma, lymphoma (MALT lymphoma), or carcinoid tumor.)
64
Q

What is Autoimmune Gastritis?

A

a type of gastritis caused by the production of auto-Ab against parietal cells and IF.

65
Q

What is the pathogenesis of Autoimmune Gastritis?

A
66
Q

What is shown endoscopically/Microscopically in Autoimmune Gastritis?

A

Endoscopically

Diffuse damage to the body-type mucosa with atrophy (i.e. thinning & loss of rugal)

Microscopically:

  • Antralization (body & fundus).
  • Lymphocytes & plasma cells infiltration.
  • chief cells loss.
67
Q

Complications of Gastritis?

A
  1. Gastric erosions and Ulcers.
  2. Gastric Perforation.
  3. Gastric Bleeding & Anemia.
  4. Gastric tumors (adenocarcinoma, lymphoma, and carcinoid tumor)
68
Q

Malabsorption is the result of disturbance of what?

A
  1. Intraluminal digestion.
  2. Terminal digestion.
  3. Transepithelial transport.
  4. Lymphatic transport of absorbed lipids. (Obstruction of lymphatic)
69
Q

What are the major causes of malabsorption in Celiac disease?

A

Severe villous abnormality and crypt hyperplasia (grooves elongated in intestinal lining) have celiac sprue.

70
Q

What is the pathogenesis of coeliac disease?

A
71
Q

What is the diagnosis of coeliac disease?

A
  1. Biopsy taken from 2nd portion of duodenum or proximal jejunum.
  2. ↑ Intra-epithelial CD8+ T lymphocytes In histology.
  3. ↑Plasma cell, mast cells, eosinophils in lamina propria.
  4. Loss of mucosal & brush border surface area accounts for malabsorption.
72
Q
A
73
Q

What are the clinical features of coeliac disease?

A
74
Q

What is the skin feature of coeliac disease?

A

A pruritic blistering skin lesion called Dermatitis Herpetiformis.

75
Q

What is the most sensitive test for coeliac disease?

A

IgA antibodies to tissue transglutaminase.

IgA to - IgG antibodies to deamidated gliadin.

76
Q

What is the highly specific test for coeliac disease?

A

Antiendomysial antibodies are highly specific

77
Q

What is the guideline in diagnosing coeliac disease?

A
78
Q

What is the complications of coeliac disease?

A

Enteropathy-associated T cell lymphoma.

Adenocarcinoma of the small intestine.

79
Q

What is Whipple disease? (Causal organism, Affects, Microscopally, and Clinical features)

A

The causal organism is Tropheryma whippelii.

Affects the intestine, CNS, and joints.

Microscopically: periodic acid-Schiff (PAS) positive and macrophages in the lamina propria.

Clinical features: Triad of diarrhea, weight loss, and arthralgia and Extraintestinal symptoms: arthritis, arthralgia, fever, lymphadenopathy, and neurologic, cardiac, or pulmonary disease. Also, smelly stool.

80
Q

What layers of the epithelium does ulcerative colitis effect?

A

The mucosa and submucosa.

81
Q

What layers of the epithelium does crohn disease effect?

A

Involve any area of the gastrointestinal tract and transmural.

82
Q

What are the gross pathological characteristics of Crohn’s disease?

A
  1. skip lesions.
  2. cobblestone appearance.
  3. Fissuring, fistulae formation.
  4. Strictures.
  5. Thickened intestinal wall and fibrosis.
  6. Creeping fat.
83
Q

Which disease has a continuous colonic involvement starting with the rectum?

A

Ulcerative colitis.

84
Q

What disease has a psudopolyp characteristic?

A

Ulcerative colitis.

85
Q

What are the causes of IBD’s?

A
  1. Genetics.
  2. Mucosal immune responses.
  3. Epithelial defects.
  4. Microbiota.
86
Q

What genes are involved in Crohn’s disease? 🧬

A
  1. NOD2 (nucleotide oligomerization binding domain 2).
  2. ATG16L1.
  3. IRGM.
87
Q

What is the pathogenesis of Crohn’s disease?

A

A frameshift mutation in NOD2/ATG16L1/IRGM. Excessive inflammatory response → tissue damage.Unknown immune response trigger → Th1 cells release cytokines IFN γ, TNF α → inflammatory response → cytokines recruit macrophages → proteases, PAF, free radicals released → further inflammation → healthy tissue destroyed → inflammatory cells invade intestinal mucosa → ulcer, granuloma form → transmural inflammation → intestinal lumen; fistula formation, narrowing.

  • Paneth cell granules, which contain antimicrobial peptides that can affect the composition of the luminal microbiota, are abnormal in patients with Crohn disease carrying ATG16L1 mutations
88
Q

What are the histological features of Crohn’s disease?

A
  1. Mucosal inflammation with extensive neutrophilic inflammation leading to cryptitis and crypt abscess.
  2. Ulceration.
  3. Transmural inflammation affecting all layers
  4. Distortion of mucosal architecture.
  5. No uniform shape of the crypt!
  6. Non-caseating granulomas.
  7. Other mural changes (thickening, irregularity, and fibrosis)
89
Q

What are the clinical features of Crohn’s disease?

A
  1. Mild to bloody diarrhea.
  2. Right lower quadrant pain.
  • (Asymptomatic intervals that last for weeks to many months.)
  • May mimic acute appendicitis or bowel perforation.
90
Q

What are the extraintestinal manifestations of Crohn’s disease?

A
  1. Uveitis.
  2. Migratory polyarthritis.
  3. Sacroiliitis.
  4. Ankylosing spondylitis.
  5. Erythema nodosum.
  6. Clubbing of the fingertips.
  7. Pericholangitis. (Common in UC)
  8. primary sclerosing cholangitis. (Common in UC)
91
Q

What are the complications of Crohn’s disease?

A
  1. Fistula formation.
  2. Abdominal abscesses.
  3. Peritonitis.
  4. Intestinal stricture leading to obstruction.
  5. Gallstones. (Disease in Ileum → bile salts poor reabsorption → deficient bile salts and gallstones.)
  6. Colonic carcinoma.
92
Q

What are the Non-specific and specific histological features of Ulcerative colitis?

A
  • Non-specific:
    1. Edematous in lamina propria.
    2. infiltrate of neutrophils.
    3. Cryptitis & crypt abscesses.
  • Specific:
    1. Distorted crypt architecture.
    2. Crypt atrophy.
93
Q

What are the complications of Ulcerative colitis?

A
  1. Toxic Megacolon.
  2. Colonic Carcinoma.
94
Q

What are the clinical features of ulcerative colitis?

A
  1. Bloody diarrhea with mucus.
  2. Lower abdominal pain relieved by defecation.
  3. Symptoms: persist for days, weeks, or months.

3rd Yr 1 Semester (5 decks)

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