First-aid - GI - Pathology

Aphthous ulcers are aka what

Canker sores

What are aphthous ulcers

Common oral lesions that appear as painful, shallow, round to oval ulcers covered with a yellow-ish exudate

Diagnosis:

Patient presents with painful oral lesions, upon examination, you note that they are covered by a white-yellow exudate

Aphthous ulcers - Canker sores

Recurrent Aphthous Stomatitis

Recurrent Aphthous Ulcers, associated with:

• Behcet Syndrome

• IBD

• Celiac Disease

• HIV

• SLE

Mnemonic: BICHS

Squamous Cell Carcinoma of the Oral Cavity Presentation

Usually affects the tongue, and presents as a nonhealing ulcer with irregular margins and raised borders

Leukoplakia may also be noted and
Erythroplakia are precursor lesions

What is the most common malignancy of the oral cavity

Squamous cell carcinoma

Squamous Cell Carcinoma of the Oral Cavity Associations

• Tobacco

• Alcohol

• HPV-16

Sialothiasis - Definition

Stone formation in major salivary gland ducts (= Parotid, submandibular, sublingual)

Sialothiasis - Pathophysiology

Why Do the stones form?

Salivary stasis due to dehydration or trauma (fibrosis → obstruction)

Most common in submandibular gland duct because:

1. Saliva is more alkaline + more mucus

2. Saliva has to travel a bit uphill → Stasis

3. The duct is narrower

Why is the pain pre/periprandial?

Because we start secreting saliva at the moment we start smelling or imagining food, which is before we start eating the food, and all throughout the meal

Sialothiasis - Presentation

Pre/peri-prandial pain and swelling in the affected area

Sialadenitis - Definition

Inflammation of the salivary glands due to:

• Obstruction

• Infection (S. aureus/ mumps)

• Immune-mediated mechanisms (Sjögren syndrome)

Describe how you can get from Sialothiasis to Sialadenitis

Obstruction → Stasis → S. Aureus overgrowth → Sialadenitis

Discuss general Salivary gland tumor Benignity and Malignancy (Likelihood stuff)Wh

Salivary gland tumors are usually benign.

Most commonly found in the parotid gland (Most benign ones)

Tumors found in the submandibular/ sublingual and other minor glands are more likely to be malignant

What is the classic presentation for benign salivary gland tumors

They typically present as a painless mass or painless swelling

What symptoms are more suggestive of malignant involvement of salivary gland tumors

Facial paralysis and painful masses

Pleomorphic Adenoma - General + Histology

Most common salivary gland tumor

It’s a benign mixed tumor, composed of chondromyxoid stroma and epithelium

It may undergo malignant transformation

Recurrence of Pleomorphic Adenoma after treatment

Only recurs if incompletely excised or if ruptured intraoperatively

Other name for Warthin Tumor

Papillary cystadenoma lymphomatosum

Warthin tumor - Description + Associations

Benign cystic tumor with germinal centers, may be bilateral or multifocal. Typically found in smokers

Mnemonic: Warriors from Germany love smoking

Mucoepidermoid carcinoma - Description

Most common malignant tumor. Mucinous and Squamous components

List the main causes of acute gastritis

• Chronic NSAIDs use (Especially in alcoholics and those who take NSAIDs daily like in Rheumatoid arthritis)

• Burns (Hypovolemia)

• Brain injury (Increased vagal tone)

How can chronic NSAID use cause acute gastritis

NSAIDs → COX inhibition → ↓ PGE₂

Normally, PGE₂:

• ↑ mucus

• ↑ bicarbonate

• ↑ mucosal blood flow

Therefore:

↓ PGE₂ → ↓ mucosal protection → gastric erosions

How can Burns cause acute gastritis (Curling ulcers)

Burns cause severe hypovolemia due to massive fluid loss → Decreased gastric perfusion → Severe mucosal ischemia that causes loss of mucosal integrity → Erosions and ulcers - Curling ulcers

A 45-year-old obese woman presents with dysphagia, chronic intermittent cough, and chest burning for several months. Her symptoms are worse after large meals or lying down. Her diffculty swallowing has intensifed recently, which prompted her to schedule an appointment. Tums helped with the burning sensation in the past, but her symptoms are getting worse. She has not lost weight. She recently started verapamil for hypertension. On physical exam, oropharynx is clear without erythema or exudates, lungs are clear to auscultation, and she has mild tenderness to palpation in the epigastric region.

GERD

How can Brain injury cause acute gastritis

Brain injury can cause a Cushing ulcer due to high vagal stimulation which will lead to Increased Acetylcholine production → Increased H+ production

*Note: vagal stimulation can make it so there’s acid secretion even when there’s no food in the GI Tract

Achalasia etiology and pathophysiology

Failure of LES to relax due to degeneration of NO and VIP-secreting neurons in the Auerbach/Myenteric Plexus of the esophageal wall

Achalasia presentation

Progressive dysphagia to solids and liquids

*Note: Achalasia and diffuse esophageal spasm, which present with simultaneous solid and liquid dysphagia.

A 35-year-old woman presents with progressive difficulty swallowing both solids and liquids. Her symptoms have worsened over the past 5 years. She initially only had symptoms with solids, and she progressively has had symptoms with liquids. She also notes regurgitation of undigested food. She denies weight loss. In the past, she has had multiple trials of PPIs without improvement of her symptoms.

Achalasia

Achalasia Risk Factors

• Chagas disease (Trypanosoma Cruzi)

• Extraesophageal Malignancies
  
  

• Can be Idiopathic tho

Achalasia potential complications

Achalasia is associated with an increased risk of esophageal cancer.

How do you diagnose achalasia

Manometry: Will reveal uncoordinated peristaltic movements with increased LES resting pressure.

Barium Swallow: Will show dilated esophagus with area of distal stenosis (“bird’s beak”)

Achalasia Treatment

Surgery, endoscopic procedures (e.g. Botulinum toxin injection)

GERD etiology

It’s due to a transient decrease in LES tone

GERD classic presentation

Classically presents as: Heartburn, Regurgitation, Dysphagia

Symptoms of laryngopharyngeal reflux

In laryngopharyngeal GERD, patients may also present with: Chronic cough, lump in throat sensation, constant throat clearing, hoarseness

GERD complications

• Erosive esophagitis

• Esophageal strictures

• Barett Esophagus

Esophagitis presentation

Odynophagia and/or Dysphagia

List the different types of Esophagitis

• Reflux/Errosive Esophagitis

• Pill Esophagitis

• Infectious Esophagitis

• Corrosive Esophagitis

• Eosinophilic Esophagitis

What condition commonly arises secondary to GERD

Reflux/Erosive esophagitis

List pills that cause Pill esophagitis

Bisphosphonates, tetracyclines, NSAIDs, ferrous

sulfate, potassium chloride

Infectious causes of Esophagitis

• Candida (most common) - white pseudomembranes

• CMV

• HSV-1 - punched out ulcers

All associated with immunosuppression

Plummer-Vinson syndrome presentation

Plummer DIES

• Dysphagia

• Iron-deficiency anemia

• Esophageal webs

• Increased risk for esophageal SCC

Name a condition associated with Plummer-Vinson syndrome associated

Glossitis (It’s due to the iron-deficiency causing atrophy of the tongue’s mucosa)

Mallory-Weiss syndrome etiology

Partial thickness, longitudinal lacerations of the gastroesophageal junction
- Confined to mucosa/submucosa, due to severe vomiting

Mallory-Weiss presentation

• Hematemesis

• Abdominal/back pain (±)

Mallory-Weiss risk factors

• Alcohol use

• Bulimia nervosa

Esophageal varies etiology

Dilated submucosal veins in lower 1/3 of esophagus 2° to portal hypertension

Esophageal varices presentation and cause

Presents as hematemesis. Secondary to cirrhosis

Distal esophageal spasm etiology

Spontaneous, no peristaltic (uncoordinated) contractions of the esophagus with normal LES pressure

Distal esophageal spasm presentation

Dysphagia & Angina-like chest pain

Distal esophageal spasm Diagnostics

Barium swallow will reveal Corkscrew Esophagus

Manometry is diagnostic

Distal esophageal spasm treatment

Nitrates and CCBs

Esophageal smooth muscle atrophy and fibrosis with weakened LES pressure and distal motility

Scleroderma esophageal involvement

Scleroderma esophageal involvement

Complications of Esophageal involvement in scleroderma

• Acid reflux → Dysphagia and Stricture

• Barret esophagus and aspiration

Etiology of esophageal perforation

Most commonly, following esophageal instrumentation, but can also be due to spontaneous rupture, foreign body ingestion, trauma, and malignancy

Esophageal perforation findings

Pneumomediastinum & Subcutaneous emphysema

(signs include crepitus in the neck region or chest wall) can indicate dissecting air.

Boerhaave syndrome

transmural, usually distal esophageal rupture due to violent retching (from vomiting)

Hematemesis DDx

What is Barrett esophagus

Intestinal metaplasia characterized by replacement of nonkeratinized stratified squamous epithelium with intestinal epithelium

What is the known cause of Barett esophagus, and what are its complications

Cause: Chronic GERD

Complication: Highly associated with development of esophageal adenocarcinoma

Dumping syndrome

Hyperosmolar food (often sugary) moves too quickly from the stomach to small intestine. Typically occurs after stomach or esophageal surgery

How does esophageal cancer present, and what makes it an agressive cancer

It typically presents with progressive dysphagia to solids and then to liquids and weight loss.

It’s aggressive due to the lack of serosa in the esophageal. Patients also typically present with advanced disease

In which part of the esophagus is squamous cell carcinoma typically observed

Upper 2/3

Esophageal squamous cell carcinoma risk factors

Alcohol, hot liquids, caustic strictures, smoking, achalasia, nitrosamine-rich foods (processed meats, smoked fish, and certain alcoholic beverages, particularly beer)

Esophageal adenocarcinoma risk factors

Chronic GERD, Barrett esophagus, obesity, tobacco smoking

In which part of the esophagus is adenocarcinoma typically observed

Lower 1/3

Which esophageal cancer is more common worldwide, and which is more common in America

SSC → Worldwide

Adeno → America

What is chronic gastritis

Mucosal inflammation, often leading to atrophy (hypochlorhydria → hypergastrinemia) and intestinal metaplasia (→ risk of gastric cancers)

Classic causes of chronic gastritis

H. Pylori

Autoimmune (Anti-IF and Anti-H+/K+ ATPase)

H pylori chronic gastritis basic rundown

Affects antrum first and spreads to body of stomach.

Peptic Ulcer disease

H. pylori is associated with which cancer

MALT lymphoma

Autoimmune chronic gastritis

Anti-IF, and Anti-H+/K+-ATPase on parietal cells → *Increased risk of Pernicious anemia

*Affects body/fundus

Autoimmune gastritis affects which part(s) of the stomach

Affects body/fundus

What is Menetrier disease

Hyperplasia of gastric mucosa p hypertrophied rugae (“wavy” like brain gyri). Causes excess mucus production with resultant protein loss and parietal cell atrophy with r acid production.

Menetrier disease presentation

Weight loss, Anorexia, Vomiting, Epigastric pain, Edema (due to protein loss; “WAVEE”).

---

Protein loss because too many amino acids are used in mucin production + Increased permeability of gastric mucosa → loss of protein into stomach)

Parietal cell atrophy is because increased mucin in stomach compresses parietal cells → Atrophy

Common gastric tumors

• Gastric adenocarcinoma

• Gastric lymphoma

• GI stromal tumors (KIT or PDGFRA)

• Carcinoid tumors

Gastric cancer classical symptoms

• Weight loss

• Early satiety

• Abdominal Pain

• Obstruction

• Sudden-onset Acanthosis Nigricans or Leser-Trélat sign (Sometimes)

---

WEAPON

Intestinal-type Gastric Adenocarcinoma pathophysiology

Chronic H. pylori infection → Chronic mucosal injury (Atrophy/achlorhydria) → Intestinal metaplasia → Dysplasia → Adenocarcinoma

Appearance of Intestinal-type gastric adenocarcinoma

It looks like an ulcer with raised margins

Intestinal-type gastric adenocarcinoma Risk factors

• H. pylori

• Chronic gastritis

• Nitrosamines

• Tobacco smoking

• Achlorhydria

• Chronic gastritis

Diffuse-type gastric adenocarcinoma etiology

It involves E-Cadherin mutations → Cells don’t stick together → They individually infiltrate the gastric wall

These cells also tend to accumulate mucin and become known as Signet-ring cells due to their appearance

Findings in Diffuse-type gastric adenocarcinoma

• Signet-ring cells

• Stomach wall grossly thickened and leathery = Linitis plastica

  • Tumor infiltration + fibrosis → Stiff non-compliant stomach = Early Satiety

Discuss possible sites of gastric cancer metastasis

• Virchow node = Metastasis from stomach to left supraclavicular nodes

• Krukenberg tumor = Metastasis to ovaries (In Diffuse-type gastric cancer, since it’s common to find signet ring cells)

• Sister Mary Joseph Nodule: Subcutaneous periumbilical metastasis

• Blumer Shelf: Palpable mass of DGE, suggesting metastasis to pouch of Douglas

Typical causes for gastric ulcers

• H. pylori (70%)

• NSAIDs

Due to decreased mucosal protection against gastric acid

Typical causes for duodenal ulcers

• H. pylori (90%)

• Zollinger-Ellison syndrome

Due to decreased mucosal protection or due to increased gastric acid secretion

Gastric and duodenal ulcers risk of malignancy

• Gastric: High risk, should be biopsied to rule out malignancy

• Duodenal: Generally benign

Gastric vs duodenal ulcer pain characteristics

• Gastric: Pain greater with food → Weight loss

• Duodenal: Pain decreases with meals → Weight gain (food buffers acid

Ulcer complications

• Hemorrhage

  • If on lesser curvature = Bleed from left gastric artery

  • If on posterior wall of duodenum = Bleed from gastroduodenal artery

• Obstruction: Pyloric outlet obstruction, from fibrosis, can also be duodenal obstruction

• Perforation; Anterior duodenal ulcers more common, will see:

  • Pneumoperitoneum

  • Referred shoulder pain due to phrenic nerve irritation

How are GI bleeds classified as Upper or Lower

Depends on if above or below the ligament of Treitz

Upper vs Lower GI bleeds symptoms

Upper: Hematemesis/ melena

Lower: Hematochezia

What symptoms should make you think of malabsorption syndromes

• diarrhea

• steatorrhea

• weight loss

• weakness

• vitamin and mineral deficiencies

Screening tests if you suspect malabsorption syndromes

Screen for fecal fat with Sudan stain

Use D-Xylose test if you suspect abnormal absorption

Which allelic variants is Celiac disease associated with?

HLA-DQ2 & HLA-DQ8 (Northern-European descent)

I ate [8] too [2] much gluten at [D]airy [Q]ueen

In celiac, the intolerance is against which protein

Gliadin (gluten protein found in wheat, barley, rye)

Which parts of the intestines are affected in Celiac Disease

Distal duodenum and/or proximal jejunum → malabsorption and steatorrhea.

Celiac disease potential Complications/Associations

• Dermatitis herpetiformis

• Decreased bone density

• Iron-deficiency anemia

• Increased risk for malignancy (T-cell lymphoma)

Celiac disease Serology

Serology: ⊕ IgA anti-tissue transglutaminase (IgA tTG), anti-endomysial, and anti-deamidated gliadin peptide antibodies.

Celiac disease Histology

Histology: Loss of Villi, mucosal atrophy, Crypt hyperplasia, intraepithelial lymphocytosis

Lactose Intolerance etiologies

1. Lactase deficiency

2. 2ndary lactose intolerance = If severe gastroenteritis -> Damage to villi, and lactase sits on villi tip -> temporary lactose insufficiency (Secondary Intolerance)