GI TBP Flashcards
2 main symptoms related to pathology of the GI tract
1) Abdominal pain
2) GI hemorrhage
Most frequent category/cause of chronic abdominal pain
Functional
Landmark that separates the upper GI tract from the lower GI tract
Ligament of Treitz
Pediatric congenital malformation that most commonly presents during adulthood or may remain asymptomatic throughout life
Meckel diverticulum
Congenital pyloric stenosis: Male vs female
Male
Congenital pyloric stenosis: Associated syndromes (2)
1) Turner
2) Trisomy 18
Congenital pyloric stenosis: Associated drug
Erythromycin
Duodenal atresia: Associated congenital anomaly
Trisomy 21 (Down syndrome)
Duodenal atresia: Symptom
Bilious vomiting in the first 24 hours of life
Duodenal atresia: Appearance on plain film (2)
1) Double-bubble sign
2) Paucity of gas distal to duodenum
Hirschprung disease: Males vs females
Males
Hirschprung disease: Common associated congenital anomaly
Trisomy 21 (Down syndrome)
Hirschprung disease: Pathogenesis
Aganglionosis of intestinal segment due to dysfunctional neural crest migration
Type of Hirschrpung that involves entire colon
Long-segment
Type of Hirschrpung that involves rectum and sigmoid
Short-segment
Hirschprung disease: Complication
Toxic megacolon
Intussusception: Triad
1) Colicky abdominal pain
2) Bilious vomiting
3) Currant jelly stools
Intussusception: PE
Sausage-shaped mass on the RUQ
Intussusception: Ultrasound
Target sign
Intussusception: Both a diagnostic and therapeutic intervention
Contrast enema
Meckel diverticulum: Persistent embryologic structure
Omphalomesenteric duct
Layers that are present in a true diverticulum
All layers of wall
T/F Most Meckel diverticula remain asymptomatic
T
Meckel diverticulum: Possible presentations
1) Intussusception
2) Obstruction
3) Bleeding (20%)
Muscle layer deficient in a false diverticulum
Muscularis propria
What herniates in a false diverticulum
Mucosa
Most common cause of hematochezia in patients >60 years old
Colonic diverticulum
T/F Most diverticular bleeds are self-limited
T
Massive bleeding from a colonic diverticulum is best managed by (diagnostic and therapeutic)
Mesenteric angiography
Important rule for Meckel diverticulum (5)
Rule of Two’s
1) 2% of the population
2) 2 inches long
3) 2 feet from ileocecal valve
4) Children younger than 2 y/o
5) 2 types of tissue (ectopic stomach or pancreas)
Grossly presents as white patches of hairy hyperkeratotic thickening on the lateral surface of the tongue
Hairy leukoplakia
Grossly presents as white patch on oral mucosa that cannot be scraped off
Leukoplakia
Microscopically, hyperparakeratosis, acanthosis, and “balloon cells” in the stratum spinosum
Hairy leukoplakia
Hairy leukoplakia vs leukoplakia vs SCC of oral cavity: Associated with immunosuppression
Hairy leukoplakia
Cause of hairy leukoplakia
EBV
80% of patients with hairy leukoplakia have this infection
HIV infection
T/F Leukoplakia can be premalignant
T
Major risk factor for leukoplakia
Tobacco use
Risk factor/s of SCC of oral cavity
Alcohol and tobacco use
Histology of 95% of head and neck tumors
SCC
T/F In salivary gland tumors, the larger the gland involved, the more likely it will be malignant
F
Most common parotid gland tumor
Pleomorphic adenoma
Risk factor for pleomorphic adenoma
Radiation
3 components of pleomorphic adenoma (microscopic)
1) Ductal cells
2) Myoepithelial cells
3) Matrix (myxoid, hyaline, chondroid)
Clinical presentation of pleomorphic adenoma
1) Slow-growing
2) Painless
Benign vs malignant: Pleomorphic adenoma
Benign
Important surgical consideration for pleomorphic adenoma
High rate of recurrence if excised with no margins of neoplastic tissue
Carcinoma that can arise within a pleomorphic adenoma
Carcinoma ex pleomorphic adenoma
High vs poor: Survival rate in patients with carcinoma ex pleomorphic adenoma
Poor
Most common malignant tumor of the salivary glands
Mucoepidermoid carcinoma
65% of mucoepidermoid CA are found in what gland
Parotid
Condition whereby there is increased tone of the LES with subsequent failure to relax
Achalasia
In achalasia, there is loss of
VIP and NO inhibitory innervation of the LES
Secondary achalasia may arise from
1) Chagas disease
2) Malignancy
3) Sarcoidosis
Classic “bird’s beak” appearance
Achalasia
Dysphagia initially to solids then progressing to liquids indicates
Mechanical problem
Dysphagia initially to liquids and then to solids indicates
Functional/motility problem
2 non-neoplastic disorders of the oesophagus associated with alcohol use
1) Mallory-Weiss tears
2) Esophageal varices
Risk factors for Mallory-Weiss tears (2)
1) Alcoholism
2) Hiatal hernia
Syndrome resulting from Mallory-Weiss laceration characterised by complete rupture of the esophagus
Boerhaave syndrome
Clinically presents as hematemesis after prolonged vomiting
Mallory-Weiss tears
Veins vs arteries: Esophageal varices
Veins
Mucosal vs submucosal: Esophageal varices
Submucosal
Refers to inflammation of the esophageal mucosa as a result of reflux of stomach contents
Reflux esophagitis or GERD
Complication of GERD that provides resultant risk of adenocarcinoma
Barrett esophagus or glandular metaplasia
Columnar glandular epithelium with goblet cells found in the esophagus
Barrett esophagus
Eosinophils, basal zone hyperplasia, and elongation of lamina propria papilla
GERD
Most common nonbacterial causes of esophagitis
1) CMV
2) HSV
3) Candida albicans
Common risk factor present in patients who have nonbacterial esophagitis
Decreased immune function
CMV vs HSV vs Candida albicans: Linear ulcers
CMV
CMV vs HSV vs Candida albicans: Punched out ulcers
HSV
CMV vs HSV vs Candida albicans: White plaque
Candida albicans
Glandular metaplasia that occurs in the distal esophagus as a result of chronic reflux of gastric acid into esophagus
Barrett esophagus
T/F: Glandular metaplasia in the oesophagus may be reversible
T
Lifetime risk for development of oesophageal adenoma in patients with Barrett esophagus
10%
Nonbacterial esophagitis seen microscopically as squamous cells with intranuclear inclusions with a clear halo
HSV
Microscopic finding in HSV infection described as squamous cells with intranuclear inclusions with a clear halo
Cowdry type A HSV inclusions
T/F Esophageal webs are always congenital
F
Syndrome associated with esophageal webs
Plummer-Vinson
Tetrad of Plummer-Vinson syndrome
1) Esophageal webs
2) IDA
3) Glossitis
4) Cheilosis
T/F Plummer-Vinson syndrome carries a risk for malignancy
T
Esophageal ring located above the squamocolumnar junction
Type A
Type B esophageal ring is also known as
Schatzki ring
Esophageal ring located at the squamocolumnar junction
Type B
Clinical presentation of webs and rings
Intermittent dysphagia
Type of false esophageal diverticula: Located at the proximal esophagus
Zenker
Type of true esophageal diverticula: Located at mid esophagus
Traction
Type of true esophageal diverticula: Located near the GE junction
Epiphrenic
Autoimmune disease that can cause oesophageal stenosis
Scleroderma
Most common type of esophageal CA worldwide
SCC
Male vs female: SCC of esophagus
Male
SCC of esophagus: Most common location
Middle 3rd (Robbin’s)
SCC of esophagus: Risk factors
1) Smoking and alcohol use
2) Dysphagia
3) Plummer-Vinson syndrome
4) Vitamin A deficiency
SCC of esophagus: Upper third SCC spreads to
Cervical LN
SCC of esophagus: Middle 3rd SCC spreads to
Mediastinal, paratracheal, and tracheobronchial LN
SCC of esophagus: Lower 3rd SCC spreads to
Gastric and celiac LN
AdenoCA of esophagus: Male vs female
Male
AdenoCA of esophagus: Whites vs African Americans
Whites
SCC of esophagus: Whites vs African Americans
African Americans
AdenoCA of esophagus: Occurs almost exclusively with
Barrett esophagus
AdenoCA of esophagus: Most common location
Distal esophagus
AdenoCA of esophagus: Rare source
Submucosal glands
T/F In esophageal neoplasms, by the time symptoms are present, most tumours are incurable
T
Role of prostaglandin in gastric mucosal integrity
1) Mucus production
2) Bicarbonate secretion
2 main type of chronic gastritis
1) Type A or fundal
2) Type B or antral
Etiology of fundal chronic gastritis
Autoimmune disease
Etiology of antral chronic gastritis
H. pylori
Mechanisms by which H. pylori damages gastric mucosa
1) IL-8 (chemotaxin)
2) Urease (urea->ammonia->buffers HCl)
3) Enhancement of gastric acid and impairment of HCO3
4) Epithelial adherence and secretion of phospholipases and proteases
5) VacA (passive urea transporter causing vacuolization)
In H. pylori infection, VacA requires the presence of
CagA gene
Extensive loss of parietal cells: H. pylori gastritis vs autoimmune gastritis
Autoimmune
Achlorhydria: H. pylori gastritis vs autoimmune gastritis
Autoimmune
Noninvasive testing for H. pylori (3)
1) Serology
2) Urea breath test
3) Stool Ag test
