GI Pathology (Pathoma) Flashcards
Cleft Lip an Palate
Full-thickness defect of lip and/or palate.
*Due to failure of facial proiminences to fuse
Usually occur together.
Apthous Ulcer
Painful superficial ulceration of the oral mucosa
Arises in relation to stress. Resolves spontaneously and recurs.
Characterized by grayish base surrounded by erythema.
AKA cancer core.
Can be a part of Behcet Syndrome
Behcet Syndrome
Recurrent apthous ulcers, genetial ulcers, and uveitis.
Due to immune complex vasculitis of small vessels.
Can follow viral infx.
Oral Herpes
Vesicles involving oral mucosa that ruptures. Shallow painful, red ulcers.
HSV-1
*Primary infection in childhood –> remains dormant in the ganglia of the trigeminal (V) nerve.
Stress and sunlight cause reactivation.
AKA cold sore
Squamous Cell Carcinoma
Malignant squamous cells lining oral mucosa
Tobacco and alcohol are syntergistic risk factors.
Floor of mouth is MC location.
Leukoplakia and Erythroplakia
Precursor lesion that doesn’t scrape off (vs. candidiasis)
Can be precursor to scc —> biopsy.
Erythroplakia is vascularized leukoplakia (more commonly a precursor for SCC/dysplasia).
DDX vs. Hairy Leukoplakia is on SIDE of tongue and caused by EBV in immunocomprised pts. Hyperplasia only
Hairy Leukoplakia
White plaque on SIDE of tongue and caused by EBV in immunocomprised pts. Hyperplasia only (not dysplasia)
Mumps
Infection w/ Mumps virus
Bilateral inflamed parotid glands
Orchitis, pancreatitis, and aseptic meningitis may also be present.
- ) Serum Amylase is increased due to salivary gland or pancreatic involvement
- )Orchitis carries risk of sterility, especially in teens.
Sialadenitis
Obstruction (Sialolithiasis) causing inflammation of salivary gland secondary to infx. (S. aureus)
Usually unilateral
Pleomorphic Adenoma
Benign tumor composed of stromal (caritlage) and epithelial tissue (glands).
AKA biphasic or mixed tumor
MC tumor of salivary gland
Parotic is MC
Mobile, painless, circumscribed mass at angle of jaw. (Key sx for bengn –> no invasion)
High Rate of recurrence –> irregular margins.
Rare transformation into scc
Warthrin Tumor
Benign cystic tumor.
2nd mc tumor of salivary gland
Always parotid
Lymph tissue
Mucoepidermoid Carcinomaq
Malignant tumor composed of mucinous and squamous cells.
Usually in parotid. Commonly involves facial nerve.
TE Fistula
Congenital defect resulting in connection of esophagous and trachea.
MC = proximal esophageal atresia w/ distal fistula
Clinical findings: Vomiting, Polyhramnios, abdominal distension, and aspiration.
Esophageal Web
Thin protrusions of mucosa, most often in UPPER esophagous.
Presents w/ dysphagia of poorly chewed food.
Increased risk for esophageal SCC
Can be a part of Plummer-Vinson syndrome
Plummer-Vinsion Syndrome
Severe IDA, Esophageal web, and beefy red tongue due to atrophic glossitis.
Zenker Diverticulum
Outpouching of pharyngeal mucosa through an acquired defect in the muscular wall (false diverticulum –> not entire wall)
Arises above UES at the junction of esophagus and pharynx.
Presents w/ dysphagia, obstruction, and halitosis.
Mallory-Weiss Syndrome
Longitudinal laceration of mucosa at GE junciton.
Caused by severe vomiting (alcoholics and bulimia)
Presents w/ painful hematemesis.
Risk for Boerhaave syndrome - rupture of esophagus leading to air in mediastinum causing subcutaneous emphysema (crackling upon pressing –> Hammond’s sign).
Esophageal Varices
Dilated submucosal veins in lower esophagus
Arises secondary to portal HTN
Asx, but risk of rupture exists –> painless hematemesis (vs. Mallory Weiss)
MCC of death in cirrhosis (synergism w/ coagulopathy due to liver failure)
Achalasia
Disordered esophageal motility w/ inability to relax LES.
Dysphagia of solids and liquids (no peristalsis).
Due to damaged ganglion cells in myenteric plexus
- ) Located between inner circular and outer longitudinal muscular layers. Important for bowel motility and relaxing LES.
- ) Damage can be idiopathic or secondary to insult (i.e. Chagas)
Birdbeak sign on barium study
Presents /w dysphagia to solids and liquids, putrid breath, High LES pressure, Bird beak sign, Increased risk for SCC.
GERD
Due to relaxed LES tone.
Risk factors: alcohol, tobacco, obesity, fat-rich diet, caffeine, and hiatal hernia (sliding type is MC –> hour glass stomach. Paraesophageal hernia is also possible –> less common and bowel sounds in lung field w/ possible lung hypoplasia).
Clinical features:
- ) Heartburn (mimics cardiac chest pain
- )Asthma (adult onset) and cough
- ) Damage to enamel of teeth
- )Ulceration with stricture (fibrosis and narrowing)) and Barrett esophagus (metaplasia) are late complications.
Barrett’s Esophagus
Metaplasia of lower esophageal mucosa from stratified squamous epithelium to nonciliated columnar epithelium w/ goblet cells; seen in 10% of GERD patients.
Response of lower esophageal stem cells to acidic stress.
May progress to dysplasia and adenocarcinoma.
Esophageal Carcinoma
Sublassified as adenocarcinoma or SCC.
Adenocarcinoma is a malignant proliferation of glands; MC type of esophageal carcinoma in the West. –> After Barrett’s and in lower 1/3.
SCC is a malignant proliferation of squamous cells; most common esophageal worldwide.
1.) Usually arises in upper or middle third of esophagous.
Major risk factor is IRRITATION
- ) Alcohol and Tobacco (MC)
- )Very hot tea (China and Iran)
- ) Achalasia
- ) Esophageal Web
- ) Esophageal injury (lye injestion)
Presents late (poor prognosis)
- ) Progressive dysphagia (solids and liquids), weight loss, pain, and hematemesis
- ) SCC may additionally present w/ hoarse voice (recurrent laryngeal nerve) and cough (tracheal involvement.
Location determines lymph node/spread:
- ) Upper 1/3 = cervical
- ) Middle 1/3 = Mediastinal or tracheobronchial
- ) lower 1/3 = celiac or gastric
Gastroschisis
Congenital malformaiton of abdominal wall –> exposure of abdominal contents.
Omphalocele
Pesistent herniation of bowel into umbilical cord.
Due to failure of herniated intestines to return to body cavity during development.
Contents are covered by peritoneum and amnion (in bubble vs. gastroschisis)
Pyloric Stenosis
Hypertrophy of pyloric smooth muscle.
More common in males.
Results in stenosis of pyloric sphincter.
*Normal at birth, and develops 2 weeks after birth.
Projectile nonbilious vomiting. Can see intense peristalsis on PE. Can palpate olive-like structure.
Rx = myotomy
Acute Gastritis
Acidic damage to mucosa due to:
- ) Increase in acid production or
- )Decreased protection of mucosa.
Risk factors:
- ) Severe burn (Curling ulcer) –> secondary to severe hypovolemia
- ) NSAIDs –> lack of PGE2 which decrease acid produciton, increase mucosal blood flow, and increase bicarb/mucus production
- ) Heavy Alcohol consumption
- ) Chemotherapy - death of regenerating cells
- ) Increased ICP (Cushing ulcer) –> increased vagal stimulation –> increased Ach stimulation of parietal cells –> increased acid production
- ) Shock (same as mech as Curling ulcer) - also known as stress ulcer –> usually multiple –> PPI if in ICU
Acid damage results in:
- )Superficial inflammation
- )Erosion of epithelium
- ) Ulcer (loss of mucosal layer)
Chronic Autoimmune Gastritis
Autoimmune destruction of the parietal cells *(fundus and body esp.)
T-cell mediated (Type 4 HS) –> creates ABs in blood vs. parietal cells.
Clinical features:
- )Atrophy of mucosa, 2.)Achlorhydria w/ increased gastrin levels and antral G-cell hyperplasia,
- )Megaloblastic (pernicious) anemia due to lack of IF –> no B-12 absorbtion in ileum. MCC of B-12 deficiency.
Increased risk for gastric adenocarcinoma –> Chronic inflammation induces intestinal metaplasia (goblet cells)
Chronic H. Pylori Gastritis
H pylori-induced acute and chronic inflammation; MC form of gastritis
H pylori ureases and proteases and inflammation weaken mucosal defenses.
Antrum is most common site (vs. autoimmune)
Presentation -
- )Epigastric abdominal pain
- ) Increased risk for ulceration, gastric adenocarcinmoa, and MALT lymphoma (B cell lymphoma in stomach wall)
Rx: Triple Therapy = Amoxocillin or Clarithromycin + Metronidazole + Omeprazole (for three complication). Resolves gastritis/ulcer, and reverses intestinal metaplasia. Negative urea breath test and lack of stool antigen confirm eradication.