Gastrointestinal Pathology

Question 1

Cause of Cleft Lip and Palate

Answer 1

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.

Question 2

Aphthous Ulcer

Answer 2

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

Question 3

Behcet Syndrome

Answer 3

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

Question 4

Oral Herpes

Answer 4

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

Question 5

Squamous Cell Carcinoma

Answer 5

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

Question 6

Hairy Leukoplakia

Answer 6

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

Question 7

Erythroplakia (red plaque)

Answer 7

Vascularized leukoplakia highly suggestive of squamous cell dysplasia

Question 8

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

Answer 8

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

Question 9

Types of salivary glands

Answer 9

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

Question 10

Mumps

Answer 10

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

Question 11

Lab findings in Mumps

Answer 11

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

Question 12

Risk of complications in mumps

Answer 12

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

Question 13

Pleomorphic Adenoma

Answer 13

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

Question 14

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

Answer 14

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

Question 15

Complication of surgery of Pleomorphic adenoma?

Answer 15

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

Question 16

SIALADENITIS

Answer 16

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

Question 17

Sialolithiasis

Answer 17

Obstructing stone in a salivary gland

Question 18

WARTHIN TUMOR

Answer 18

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

Question 19

2nd most common salivary gland tumor

Answer 19

WARTHIN TUMOR

Question 20

MUCOEPIDERMOID CARCINOMA

Answer 20

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

Question 21

TRACHEOESOPHAGEAL FISTULA; most common type

Answer 21

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;

Question 22

$ Presentation of Tracheoesophageal Fistula

Answer 22

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

Question 23

ESOPHAGEAL WEB

Answer 23

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

Question 24

$ Plummer-Vinson syndrome

Answer 24

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

Question 25

ZENKER DIVERTICULUM Location Presentation

Answer 25

* 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)

Question 26

Air under skin surface makes rice crispy crackling sounds when pushed

Answer 26

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

Question 27

subcutaneous emphysema

Answer 27

The presence of air or gas in the subcutaneous tissues.

Question 28

MALLORY-WEISS SYNDROME Cause Presentation Risks

Answer 28

* 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

Question 29

ESOPHAGEAL VARICES Etiology Presentation Risks

Answer 29

* 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_

Question 30

painless hematemesis

Answer 30

ruptured esophageal varice

Question 31

painful hematemesis

Answer 31

MALLORY-WEISS SYNDROME

Question 32

Most common cause of death in cirrhosis

Answer 32

Ruptured esophageal varice

Question 33

ACHALASIA Etiology Clinical features Risks

Answer 33

* 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

Question 34

Type of process occuring here.

Answer 34

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.

Question 35

GASTROESOPHAGEAL REFLUX DISEASE (GERD) Risk factors Clinical features

Answer 35

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.

Question 36

BARRETT ESOPHAGUS

Answer 36

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

Question 37

Most common type of hiatal hernia

Answer 37

Sliding hiatal hernia

Question 38

Hour glass appearance

Answer 38

Paraesophageal hernia - may cause lung hypoplasia

Question 39

Bowel sounds in the lung field

Answer 39

Paraesophageal hernia, may have lung hypoplasia

Question 40

Most common esophageal cancer in the Western Hemisphere

Answer 40

Adenocarcinoma

Question 41

Most common esophageal cancer Worldwide

Answer 41

Squamous cell carcinoma of the esophagus

Question 42

ESOPHAGEAL CARCINOMA

Answer 42

* 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)

Question 43

Presentation of Esophageal Carcinoma

Answer 43

* 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)

Question 44

Lymph node spread in Esophageal Carcinoma

Answer 44

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

Question 45

achlorhydria

Answer 45

Absence of hydrochloric acid from the gastric juice.

Question 46

Most common cause of vitamin B₁₂ deficiency

Answer 46

_Chronic autoimmune gastritis_ - due to autoimmune destruction of gastric parietal cells (can't make intrinsic factor).

Question 47

Process occuring in stomach mucosa

Answer 47

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

Question 48

Gastritis involving Body and Antrum

Answer 48

Chronic Autoimmune gastritis

Question 49

Gastritis involving Antrum

Answer 49

Chronic H pylori Gastritis (90%) most common

Question 50

Organism

Answer 50

*_H Pylori_* - sit on surface of epithelium, do NOT invade, antrum most common location of gastritis

Question 51

Diagnosis? White material?

Answer 51

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

Question 52

Type of cell seen in image?

Answer 52

_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

Question 53

GASTROSCHISIS

Answer 53

_Congenital_ malformation of the anterior abdominal wall leading to _exposure of abdominal contents_

Question 54

OMPHALOCELE Cause How is it different from gastroschisis?

Answer 54

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

Question 55

PYLORIC STENOSIS Presentation Treatment

Answer 55

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

Question 56

ACUTE GASTRITIS Etiology Mucosal defenses?

Answer 56

* 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).

Question 57

Curling ulcer

Answer 57

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

Question 58

Risk factors for Acute Gastritis

Answer 58

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.

Question 59

Cushing Ulcer *pathogenesis*

Answer 59

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.

Question 60

Acid damage can result in these 3 processes in acute gastritis

Answer 60

_superficial inflammation_, _erosion_ (loss of superficialepithelium), or _ulcer_ (loss of mucosal layer).

Question 61

CHRONIC GASTRITIS

Answer 61

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

Question 62

Chronic autoimmune gastritis * Diagnosis and pathogenesis* * Clinical features* * Risks*

Answer 62

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)

Question 63

Chronic H pylori gastritis * pathogenesis* * presentation* * treatment* * confirmation of eradication*

Answer 63

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.

Question 64

PEPTIC ULCER DISEASE Etiology Presentation

Answer 64

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. 3. May rupture leading to bleeding from the gastroduodenal artery (posterior ulcer) or acute pancreatitis (posterior ulcer)

Question 65

Differential diagnosis of ulcers must include Difference between benign and malignant gastric carcinoma?

Answer 65

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.

Question 66

GASTRIC CARCINOMA

Answer 66

* Malignant proliferation of surface epithelial cells (adenocarcinoma) * Subclassified into intestinal and diffuse types

Question 67

Gastric Carcinoma - Intestinal type

Answer 67

``` 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) ```

Question 68

Risk factors for intestinal type of gastric carcinoma (4)

Answer 68

Intestinal metaplasia (e.g., due to _H pylori_ and _autoimmune_ gastritis), nitrosamines in _smoked foods_ (Japan), and _blood type A_.

Question 69

Diffuse type Gastric Carcinoma

Answer 69

* 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

Question 70

Presentation of Gastric Carcinoma Mets

Answer 70

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)

Question 71

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

Answer 71

Diffuse type GC

Question 72

$ Hallmark of Ulcerative Colitis (UC)

Answer 72

Inflammation involving **Crypt abscesses with neutrophils**

Question 73

$ Hallmark of Crohn Disease?

Answer 73

Inflammation - **Lymphoid aggregates with granulomas (40% of cases)** Note the noncaseating granuloma

Question 74

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

Answer 74

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)**

Question 75

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

Answer 75

**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)