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Pathoma > Gastrointestinal Pathology > Flashcards

Gastrointestinal Pathology Flashcards

1
Q

Cause of Cleft Lip and Palate

A

Due to failure of facial prominences to fuse - During early pregnancy, facial prominences (one superior, two from sides, and two from inferior) grown and fuse together to form the face; Usually CL and P occur together.

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2
Q

Aphthous Ulcer

A

Painful, superficial ulceration of the oral mucosa; arises in relation to stress; grayish base surrounded by erythema

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3
Q

Behcet Syndrome

A

Triad = Recurrent aphthous ulcers + genital ulcers + uveitis; Due to immune complex vascultiits involving small vessels

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4
Q

Oral Herpes

A

HSV-1; infection of childhood heals, virus remains dormant in ganglia of the trigeminal nerve

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5
Q

Squamous Cell Carcinoma

A

Malignant neoplasm of squamous cells lining the oral mucosa; Tobacco and alcohol are major risk factors; floor of mouth; Leukoplakia and erythroplakia are precursor lesions

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6
Q

Hairy Leukoplakia

A

White, rough patch arises on lateral tongue; immunocompromised; EBV-induced squamous cell hyperplasia; not pre-malignant.

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7
Q

Erythroplakia (red plaque)

A

Vascularized leukoplakia highly suggestive of squamous cell dysplasia

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8
Q

Type of tumor? What is a common characteristic after surgical removal?

A

Pleomorphic adenoma (#1 salivary gland tumor) High rate of recurrence; extension of small islands of tumor through tumor capsuleoften leads to incomplete resection; Benign

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9
Q

Types of salivary glands

A

Divided into major (parotid, submandibular, and sublingual glands) and minorglands (hundreds of microscopic glands distributed throughout the oral mucosa)

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10
Q

Mumps

A

Infection with mumps virus resulting in bilateral inflamed parotid glands; Orchitis, pancreatitis, and aseptic meningitis may also be present.

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11
Q

Lab findings in Mumps

A

Serum amylase is increased due to salivary gland or pancreatic involvement.

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12
Q

Risk of complications in mumps

A

Orchitis carries risk of sterility, especially in teenagers. Orchitis only in those >10 yo

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13
Q

Pleomorphic Adenoma

A

Benign tumor composed of stromal (e.g., cartilage) and epithelial tissue (biphasic); #1 salivary gland tumor; Usually arises in parotid; presents as a mobile, painless, circumscribed mass at the angle of the jaw

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14
Q

Previous surgery of salivary gland tumor; 3 years later paient presents with pain and signs of facial nerve damage

A

Pleomorphic adenoma may rarely may transform into carcinoma, which presents with signs of facial nervedamage

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15
Q

Complication of surgery of Pleomorphic adenoma?

A

_ High rate of recurrence_; extension of small islands of tumor through tumor capsuleoften leads to incomplete resection

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16
Q

SIALADENITIS

A

Inflammation of the salivary gland; Most commonly due to an obstructing stone (sialolithiasis) leading to Staphylococcus aureus infection; usually unilateral

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17
Q

Sialolithiasis

A

Obstructing stone in a salivary gland

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18
Q

WARTHIN TUMOR

A

Benign cystic tumor with abundant lymphocytes and germinal centers (lymphnode-like stroma);2nd most common tumor of the salivary gland; Almost always arises in the parotid

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19
Q

2nd most common salivary gland tumor

A

WARTHIN TUMOR

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20
Q

MUCOEPIDERMOID CARCINOMA

A

Malignant tumor composed of mucinous and squamous cells; most common malignant tumor of the salivary gland; Usually arises in the parotid; commonly involves the facial nerve

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21
Q

TRACHEOESOPHAGEAL FISTULA; most common type

A

Congenital defect resulting in a connection between the esophagus and trachea; Most common variant consists of proximal esophageal atresia with the distal esophagus arising from the trachea;

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22
Q

$ Presentation of Tracheoesophageal Fistula

A

$ Presents with vomiting, polyhydramnios (fluid can’t be swallowed), abdominal distension, and aspiration

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23
Q

ESOPHAGEAL WEB

A

Thin protrusion of esophageal mucosa, most often in the upper esophagus; Presents with dysphagia for poorly chewed food; Increased risk for esophageal squamous cell carcinoma; Part of PV syndrome

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24
Q

$ Plummer-Vinson syndrome

A

characterized by 1 severe iron deficiency anemia, 2 esophageal web, and 3 beefy-red tongue due to atrophic glossitis (blood vessels are exposed).

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25
Q

ZENKER DIVERTICULUM

Location

Presentation

A
  • Outpouching of pharyngeal mucosa through an acquired defect in the muscular wall (false diverticulum);
  • Arises above the upper esophageal sphincter at the junction of the esophagus and pharynx;
  • Presents with dysphagia, obstruction, and halitosis (bad breath)
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26
Q

Air under skin surface makes rice crispy crackling sounds when pushed

A

Subcutaneous emphysema often due to rupture of the esophagus (Boerhaave syndrome)

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27
Q

subcutaneous emphysema

A

The presence of air or gas in the subcutaneous tissues.

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28
Q

MALLORY-WEISS SYNDROME

Cause

Presentation

Risks

A
  • Linear longitudinal laceration of mucosa at the gastroesophageal (GE) junction
  • Caused by severe vomiting, usually due to alcoholism or bulimia
  • Presents with painful hematemesis
  • Risk ofBocrhaave syndrome- rupture of esophagus leading to air in themediastinum and subcutaneous emphysema
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29
Q

ESOPHAGEAL VARICES

Etiology

Presentation

Risks

A
  • Dilated submucosal veins in the lower esophagus; Arise secondary to portal hypertension
    1. Distal esophageal vein normally drains into the portal vein via the left gastric
      vein.
      2. In portal hypertension, the left gastric vein backs up into the esophageal vein,
      resulting in dilation (varices).
  • Asymptomatic, but risk of rupture exists. Presents with painless hematemesis
  • Most common cause of death in cirrhosis
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30
Q

painless hematemesis

A

ruptured esophageal varice

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31
Q

painful hematemesis

A

MALLORY-WEISS SYNDROME

32
Q

Most common cause of death in cirrhosis

A

Ruptured esophageal varice

33
Q

ACHALASIA

Etiology

Clinical features

Risks

A
  • Disordered esophageal motility with inability to relax the lower esophageal sphincter (LES)
  • Due to damaged ganglion cells in myenteric plexus - important for regulating bowel motility and relaxing the LES
  • Idiopathic or secondary to known insult (Trypansoma cruzi infection in Chagas disease)
  • Clinical features; Dysphagia for solids and liquids; Putrid breath; High LES pressure on esophageal manometry; ‘Bird-beak’ sign on barium swallow study
  • Increased risk for esophageal squamous cell carcinoma
34
Q

Type of process occuring here.

A

A late complication of GERD in which lower esophageal stem cells respond to acid stress undergoing Metaplasia of lower esophageal mucosa from normal Non-Keratinized Squamous Epithelium to Nonciliated Columnar Epithelium with goblet cells; seen in 10% patients with GERD.

35
Q

GASTROESOPHAGEAL REFLUX DISEASE (GERD)

Risk factors

Clinical features

A

Reflux of acid from stomach due to reduced LES tone.

  • Risk factors - alcohol, tobacco, obesity, fat-rich diet, caffeine, hiatal hernia.
  • Clinical features - Heartburn (mimics cardiac chest pain); Asthma (adult-onset) and cough; Damage to enamel of teeth; Ulceration with stricture and Barrett esophagus are late compliations.
36
Q

BARRETT ESOPHAGUS

A

Metaplasia of lower esophageal mucosa from NK stratified squamous epithelium to nonciliated columnar epithelium with goblet cells; may progress to dysplasia and adenocarcinoma

37
Q

Most common type of hiatal hernia

A

Sliding hiatal hernia

38
Q

Hour glass appearance

A

Paraesophageal hernia - may cause lung hypoplasia

39
Q

Bowel sounds in the lung field

A

Paraesophageal hernia, may have lung hypoplasia

40
Q

Most common esophageal cancer in the Western Hemisphere

A

Adenocarcinoma

41
Q

Most common esophageal cancer Worldwide

A

Squamous cell carcinoma of the esophagus

42
Q

ESOPHAGEAL CARCINOMA

A
  • Classified as adenocarcinoma or squamous cell carcinoma
  • Adenocarcinoma - malignant proliferation of glands; arises from preexisting Barret esophagus; lower 1/3 esophagus
  • SCC - malignant proliferation of squamous cells - upper or middle third of esophagus; major risk factors - Alcohol and tobacco (most common); very hot tea, achalasia; Esophageal web (P-V syndrome); Injury (lye ingestion)
43
Q

Presentation of Esophageal Carcinoma

A
  • Late (poor prognosis)
  • Symptoms - progressive dysphagia (solids to liquids), weight loss, pain, hematemesis
  • SCC additionally presents with hoarse voice (recurrent laryngeal involvement) and ough (tracheal involvement)
44
Q

Lymph node spread in Esophageal Carcinoma

A

Depends on level of esophagus involved:

  1. Upper 1/3 - cervical nodes
  2. Middle 1/3 - mediastinal or tracheobronchial nodes
  3. Lower 1/3 - celiac and gastric nodes
45
Q

achlorhydria

A

Absence of hydrochloric acid from the gastric juice.

46
Q

Most common cause of vitamin B12 deficiency

A

Chronic autoimmune gastritis - due to autoimmune destruction of gastric parietal cells (can’t make intrinsic factor).

47
Q

Process occuring in stomach mucosa

A

Intestinal metaplasia inchronic gastritis - increased risk for gastric adenocarcinoma. Notice foviolar cells at surface which are normal. Goblet cells are a result of metaplasia.

48
Q

Gastritis involving Body and Antrum

A

Chronic Autoimmune gastritis

49
Q

Gastritis involving Antrum

A

Chronic H pylori Gastritis (90%) most common

50
Q

Organism

A

H Pylori - sit on surface of epithelium, do NOT invade, antrum most common location of gastritis

51
Q

Diagnosis?

White material?

A
  • Gastric carcinoma - diffuse type
  • Hyperplasia of fibroblasts and disproportionate formation of fibrous connective tissue, especially in the stroma of a carcinoma.
52
Q

Type of cell seen in image?

A

Signet ring cells diffusely infiltrate the gastric wall seen in Gastric Carcinoma (diffuse type); The nucleus gets pushed to the side with mucus production in the center

53
Q

GASTROSCHISIS

A

Congenital malformation of the anterior abdominal wall leading to exposure of abdominal contents

54
Q

OMPHALOCELE

Cause

How is it different from gastroschisis?

A

Persistent herniation of bowel into umbilical cord

  • Due to failure of herniated intestines to return to the body cavity during development
  • Contents are covered by peritoneum and amnion of the umbilical cord
55
Q

PYLORIC STENOSIS

Presentation

Treatment

A

Congenital hypertrophy of pyloric smooth muscle; more common in males

  • Classically presents two weeks after birth as:
  1. Projectile nonbilious vomiting
  2. Visible peristalsis
  3. Olive-like mass in the abdomen
  • Tx: myotomy - surgical division of a muscle
56
Q

ACUTE GASTRITIS

Etiology

Mucosal defenses?

A
  • Acidic damage to the stomach mucosa
  • Due to imbalance between mucosal defenses and acidic environment
  • Defenses include mucin layer produced by foveolar cells, bicarbonate secretion by surface epithelium, and normal blood supply (provides nutrients and picks up
    leaked acid).
57
Q

Curling ulcer

A

Stress ulcer - A lesion of the duodenum in a patient with extensive superficial burns, intracranial lesions, or severe bodily injury. SYN Curling ulcer

58
Q

Risk factors for Acute Gastritis

A
  1. Severe burn (Curling ulcer) - Hypovolemia leads to decreased blood supply. Blood needed for proper defences
  2. NSAIDs (decreased PGE2)
  3. Heavy alcohol consumption
  4. Chemotherapy (decreased ability to regenerate stomach cells)
  5. Increased intracranial pressure (Cushing ulcer)-increased stimulation of vagus nerve leads to increased acid production.
  6. Shock- Multiple (stress) ulcers may be seen in ICU patients.
59
Q

Cushing Ulcer

pathogenesis

A

Increased intracranial pressure (Cushing ulcer) -increased stimulation of vagus nerve leads to increased acid production. Mechanism: Increased acetylcholine binds to parietal cells stimulating acid production.

60
Q

Acid damage can result in these 3 processes in acute gastritis

A

superficial inflammation, erosion (loss of superficialepithelium), or ulcer (loss of mucosal layer).

61
Q

CHRONIC GASTRITIS

A

Chronic inflammation of stomach mucosa

  • Divided into two types based on underlying etiology: chronic autoimmune gastritis and chronic H pylori gastritis
    • Chronic autoimmune gastritis - 10%, body and fundus
    • H pylori chronic gastritis - 90%, antrum
62
Q

Chronic autoimmune gastritis

  • Diagnosis and pathogenesis*
  • Clinical features*
  • Risks*
A

Chronic autoimmune gastritis is due to autoimmune destruction of gastric parietal cells, which are located in the stomach body and fundus.

  • Associated with antibodies against parietal cells and/or intrinsic factor; usefulfor diagnosis, but pathogenesis is mediated by T cells (type IV hypersensitivity)
  • i. Atrophy of mucosa with intestinal metaplasia (Fig. 10.11)
    ii. Achlorhydria with increased gastrin levels and antral G-cell hyperplasia
    iii. Megaloblastic (pernicious) anemia due to lack of intrinsic factor (#1 cause B12 deficiency
    iv. Increased risk for gastric adenocarcinoma (intestinal type)
63
Q

Chronic H pylori gastritis

  • pathogenesis*
  • presentation*
  • treatment*
  • confirmation of eradication*
A

Chronic H pylori gastritis is due to H pylori-induced acute and chronicinflammation; most common form of gastritis (90%)

  • H pylori ureases and proteases along with inflammation weaken mucosal defenses; antrum is the most common site
  • Presents with epigastric abdominal pain**; increased risk for **ulceration** (pepticulcer disease), **gastric adenocarcinoma** (intestinal type), and **MALT lymphoma
  • Treatment involves triple therapy.i. Resolves gastritis/ulcer and reverses intestinal metaplasia
    ii. Negative urea breath test and lack of stool antigen confirm eradication of
    H pylori.
64
Q

PEPTIC ULCER DISEASE

Etiology

Presentation

A

Solitary mucosal ulcer involving proximal duodenum (90%} or distal stomach (10%}

  • Duodenal ulcer is almost always due to H pylori(> 95%); rarely, may be due to ZE syndrome
    1. Presents with epigastric pain that improves with meals
    2. Diagnostic endoscopic biopsy shows ulcer with hypertrophy of Brunner glands.
  1. May rupture leading to bleeding from the gastroduodenal artery (posterior ulcer)
    or acute pancreatitis (posterior ulcer)
65
Q

Differential diagnosis of ulcers must include

Difference between benign and malignant gastric carcinoma?

A

CARCINOMA

  1. Duodenal ulcers are almost never malignant (duodenal carcinoma is extremely
    rare) .
  2. Gastric ulcers can be caused by gastric carcinoma (intestinal subtype).
  • Benign peptic ulcers are usually small (< 3 em), sharply demarcated (“punched-out”), and surrounded by radiating folds of mucosa
  • Malignant ulcers are large and irregular with heaped up margins
  • Biopsy is required for definitive diagnosis.
66
Q

GASTRIC CARCINOMA

A
  • Malignant proliferation of surface epithelial cells (adenocarcinoma)
  • Subclassified into intestinal and diffuse types
67
Q

Gastric Carcinoma - Intestinal type

A 
Intestinal type (more common) presents as a large, irregular ulcer with heaped upmargins; most commonly involves the lesser curvature of the antrum (similar to
 gastric ulcer)
68
Q

Risk factors for intestinal type of gastric carcinoma (4)

A

Intestinal metaplasia (e.g., due to H pylori and autoimmune gastritis), nitrosamines in smoked foods (Japan), and blood type A.

69
Q

Diffuse type Gastric Carcinoma

A
  • Diffuse type is characterized by signet ring cells that diffusely infiltrate the gastricwall ; desmoplasia results in thickening of stomach wall (linitis plastica,
  • Not associated with H pylori, in:estinal metaplasia, or nitrosamines
70
Q

Presentation of Gastric Carcinoma

Mets

A

Gastric carcinoma presents late with weight loss, abdominal pain, anemia, and early satiety; rarely presents as acanthosis nigricans or Leser-Trelat sign

Spread to lymph nodes can involve the left supraclavicular node (Virchow node).

  1. Intestinal - Periumbilical region (Sister Mary Joseph nodule);
  2. Diffuse - Bilateral ovaries (Krukenberg tumor)
71
Q

Gastric carcinoma not associated with H pylori, intestinal metaplasia, or nitrosamines

A

Diffuse type GC

72
Q

$ Hallmark of Ulcerative Colitis (UC)

A

Inflammation involving Crypt abscesses with neutrophils

73
Q

$ Hallmark of Crohn Disease?

A

Inflammation - Lymphoid aggregates with granulomas (40% of cases)

Note the noncaseating granuloma

74
Q

What are the black arrows pointing to? What disease is this?

A

Transmural Crohn disease with submucosal and serosalgranulomas (arrows)

$ Hallmark of Crohn disease is inflammation marked by Lymphoid aggregates with granulomas (seen in 40% of cases)

75
Q

Compare and contrast the wall invovlement, location, and gross appearance of UC vs Crohn disease

A

Wall involvement

  • UC - Mucosal and submucosal ulcers
  • CD - Full-thickness inflammation with knife-like fissures

Location

  • UC - always begins rectum,
  • CD - anywhere mouth to anus, most common location is terminal ileum

Gross Appearance

  • UC - Pseudopolyps; loss of haustra, lead pipe sign on imaging
  • CD - Cobblestone mucosa, creeping fat, strictures (string sign on imaging)

Pathoma (8 decks)

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