Digestivo Flashcards
Findings en gastropatía reactiva
Mucosa en sacacorchos y lámina propia con infiltrado inflamatorio.
Tipos y clasificaciones de pólipos
Reparativo:
- Hiperplásicos
-
Neoplásico:
Células de goblet en estómago sugieren
Metaplasia intestinal
País donde son más comunes los adenocarcinomas
Japón
Most common site of gastric ectopia in the GI tract
Upper aesophagus
Site of Meckel diverticulum
Ileum
Rule of 2’s for Meckel diverticula (5)
2% of the population
Within 2 feet of the ileocecal valve
2 inches long
twice common in males
Symptomatic by age 2
Side of the small bowel in which the meckel diverticulum is located
Antimesenteric side
Meckel diverticulum
Drugs that ingested in the first 2 weeks of life are related with pyloric stenosis
Erythromycin and azithromycin
Layer of the stomach with hyperplasia in pyloric stenosis
Pyloric muscularis propria
Result of abdominal contents incursion to the chest in diaphragmatic hernia.
Pulmonary hypoplasia
Disease of the colon with aganglionosis, from failed migration from cecum to rectum or premature death.
Hirschprung disease
Extraembryonic gut failure to return to abdominal cavity, abdominal musculature.
Omphalocele
Main mutation that causes the majority and 15% of sporadic Hirschprung disease cases
TK RET receptor
Extraembryonic viscera due to a lack of all the layers of the abdominal wall.
Gastroschisis
Ganglion cell component stained when looking for a Hirschprung with immunohistochemistry
Acetylcholinesterase
Result of ectopic pancreatic tissue in the pylorus
Inflammation and scarring that lead to obstruction
Genetic conditions associated with pyloric stenosis
Turner’s and Trisomy 18
Clinical finding in pyloric stenosis in 90% of cases
Firm, ovoid, 1-to-2-cm abdominal mass
Cells lacking in pyloric stenosis and their function
Interstitial cells of Cajal (ICC), produce hemeoxygenase-2, produce CO to relax muscle.
Pyloric stenosis manifestation in adult
Mymic of the gastric mucosa
Development above LES due to wall stress in esophageal dysfunction.
Small diverticula
Cause of benign esophageal stenosis
Fibrous thickening of the submucosa, atrophy of the muscularis propria
Ledge-like esophagic mucosal protrusions in women +40 associated with reflux.
Esophageal mucosal webs
Circumferential protrusions in the aesophagus that include mucosa, submucosa and muscularis propria.
Schatzki rings and A rings and B rings
Clinical condition associated with gastric contents reflux to the esophagus due to epithelium sensitivity to acid.
GERD
Major cause of GERD
LES relaxation
Indication for endoscopy in GERD
Refractory response to PPIs
Histologic findings in GERD
Basal zone hyperplasia and elongation of lamina propria papilae
Characteristic of Barret esophagus
Intestinal metaplasia in squamous mucosa
Group with higher risk of Barret’s esophagus
White men 40-60 years
Type of cancer caused by Barret’s
Esophageal adenocarcinoma
Mucosa appearance in Barret’s
Tongues of red, velvety mucosa
Classification of Barret’s with higher risk of dysplasia and carcinoma
Long segment ≥3 cm
Endoscopic evidence in Barret for diagnosis
Metaplastic columnar mucosa above gastroesophageal junction
Diagnostic cells for Barret
Goblet cells
A multifocal high-grade dysplasia in Barret has the risk of progressing to
Intramucosal or invading carcinoma
Condition shown
Barret esophagus, normal mucosa on the left with metaplasia on the right
Grade of the dysplasia
Low grade, nuclei on the base and architecture preserved
Grade of the dysplasia
High grade, miss-arranged nuclei and loss of architecture
Most common esophageal cancers
Adenocarcinomas and squamous cell carcinoma
Only benign tumor of the aesophagus that does not arise from mesenchyma and is not within the esophageal wall.
Leiomyomas
Epidemiology of esophageal adenocarcinomas
Caucasian | Men x7
Genes associated with adenocarcinoma
Early: TP53, CDKN2A
Late: + EGFR, ERBB2, MET, cyclin D1 and E
Most common location of esophageal adenocarcinoma and squamous cell carcinoma
Adenocarcinoma: distally
SCC: Mid-esophagus
Epidemiology of squamous cell carcinoma
+45 and males x4
Type of esophageal cancer associated with consumption of very hot beverages
Squamous cell carcinoma
Organization pattern of squamous cell carcinoma
Nests of malignant cells that reorganize squamous epithelium
Infection associated with development of squamous cell carcinoma in high-risk regions
HPV
Genes associated with squamous cell carcinoma
SOX2, cyclin D1, TP53, CDH1 and NOTCH1
Factor that has increased the incedence or esophageal squamous cell carcinoma in Kenya
Consumption of traditional fermented milk mursik, it has carcinogen acetaldehyde
Early lesions of squamous cell carcinoma
Small, gray-white, plaque-like thickening
When neutrophils are present in inflammation of gastric mucosa it is called
Acute gastritis
pH of gastric lumen
Close to 1
Prostaglandins that contribute to normal defense mechanisms of the stomach
E2 and I2
Histologic finding in gastrophathy and mild acute gastritis
Foveolar cell hyperplasia with corkscrew profiles and epithelial proliferation
Corkscrew epithelial injury without inflammation
Most common cause of chronic gastritis
H. pylori
Main age group for H. pylori infection
+65
Manifestation of H. pylori infection
Antral gastritis with normal or increased acid production
Effect of H. pylori
Reduces parietal cells, less acid secretion, increased gastrin production
Effect of decreased acid secretion in H. pylori with atrophy
Reduces the risk of gastric and duodenal ulcers
Histologic characteristic of H. pylori gastritis
Lymphoid aggregates with germinal centers and abundant subepithelial plasma cells within surface of lamina propria
H. pylori infection is associated with the next types of cancer:
MALT and adenocarcinoma
H. pylori gastritis
Mutated genes that lead to sporadical appearance of fundic gland polyps
APC gene and MUTYH
Difference between inflammatory and hyperplastic polyps
Hyperplastic are ovoid and smooth surface
Inflammatory have superficial erosions
Chronic gastritis characteristics for the development of gastric adenomas
Atrophy and intestinal metaplasia
Epidemiology of gastric adenoma
50-6o years, males 3x
Risk of adenoma becoming an adenocarcinoma
> 2 cm in diameter
Most common malignancy of the stomach
Adenocarcinoma
Types of adenocarcinoma
Intestinal type: bulky mases
Diffuse type: infiltrates and thickens gastric wall
Countries where adenocarcinoma is most common
Japan, Chile, Costa Rica and Eastern Europe
Sites of common metastases in adenocarcinoma
Virchow node (supraclavicular)
Sister Mary Joseph nodule (periumbilical)
Krukenberg tumor (ovary)
Left axillary node and puch of Douglas
Typical cells found in diffuse adenocarcinomas
Signet-ring cells
Main gene associated with gastric cancer, mainly in diffuse
CDH1 which encodes for E-cadherin
Pathway related with intestinal gastric adenocarcinomas
Wnt pathway
Main adenocarcinoma gene mutated in high-risk regions like Japan
adenomatous polyposis coli (APC) tumor suppresor gene
Desmoplastic reaction in diffuse gastric cancer that stiffens the gastric wall
Linitis plastica
Clinical features for intestinal-type gastric cancer
55 y/o, males x2, previous lesions, high-risk areas
Clinical features for diffuse-type gastric cancer
Uniform across countries, no previous lesions, same males and females
Cause for gastric lymphomas in transplant patients
Oral immunosuppresants have more action in stomach T-cell function
Site where extranodal marginal zone B-cell lymphomas arise
Chronic inflammation sytes, preexisting MALT (H.pylori)
Gene translocations associated with extranodal marginal zone B-cell lymphomas
t(11;18)(q21;q21)
Factor on which B cell translocations depend for activation in extranodal marginal zone B-cell lymphomas
NF-KB
NK-KB for B-cell and T-cell activation depends on…
BCL-10 and MALT1
MALTome histologic finding
Dense lymphocytic infiltrate in the lamina propria
MALTomas evolve to aggressive diffuse large B-cell lymphoma
Richter transformation
More common GI part where neuroendocrine tumors are found
Small intestine (ileum)
A firm yellow mass in the GI tract is a
Neuroendocrine neoplasm
Nucleous characteristic of neuroendocrine tumors
Salt and pepper chromatin pttern
IHC markers of neuroendocrine tumors
Synaptophysin and chromogranin A
Mutation of neuroendocrine tumors
TP53 and RB
Layer where neuroendocrine tumors grow
Submucosa, desplazan la mucosa
Syndrome produced by a gastrin-producing neuroendocrine tumor
Zollinger-Ellison Sx
Pronostic factors of a neuroendocrine tumor
Mitotic rate, histological differentiation and Ki-67 proliferative index
Part of GI tract where neuroendocrine tumors are more aggresive
Midgut (jejunum and ileum)
Cells from which gastrointestinal stromal tumor (GIST) arises
Interstitial cells of Cajal
Important epidemiology of GIST
60 y/o
Children with Carney triad
Neurofibromatosis type 1
Cause of GISTs
Gain of function mutations in KIT Tyrosine Kinase receptor
Most useful diagnosis marker for GISTs
KIT (CD 117)
Most frequent cause of intestinal obstruction worldwirde.
Hernias
Most common cause of intestinal obstruction in children younger than 2 years
Intussusception
Vaccine associated to intestinal intussusception
Rotavirus
Causes of acute obstruction of intestinal irrigation
Thrombosis or embolism
Most important risk factor for thrombosis
Severe atherosclerosis
Watershed zones
Splenic flexure, sigmoid colon and rectum
Disease in which there is transmural necrosis of small and large intestine.
Necrotizing enterocolitis
Part of gluten that contains most of the disease-producing components.
Alcohol-soluble fraction of gluten: gliadin
IL expression induced by gliadin
IL-15
APC with which gliadin interacts
HLA-DQ2 and HLA-DQ8
Ages of celiac disease
30-60
Celiac disease
Celiac disease with positive serology and villous atrophy without symptoms
Silent celiac disease
Celiac disease with positive serology without viollous atrophy
Latent celliac disease
Skin manifestation in celiac disease
dermatitis herpetiformis
Malignancy for which celiac people have higher risk
Enteropathy-associated T-cell lymphoma
Celiac disease has a CD of
CD30
Strongest risk gene for Crohn
NOD2
Location of Crohn’s
Anywhere in the GI tract. Ileum, ileocecal valve and cecum
Disease with skip lesions
Crohn’s
Earliest lesion in Crohn’s
Aphtous ulcer
Mucosal appearance in Crohn
Cobblestone
Layers involved in Crohn’s
All
Type of granulomas in Crohn
Noncaseating granulomas
Parts in which ulcerative colitis develops
Colon and rectum only
Granular, extensive, broad-based ulcers happen in
Ulcerative fuse
Mucosal bridges in ulcerative colitis are formed by
Pseudopolyps tips that phuse
Toxic megacolon happens in:
Ulcerative colitis
Crypt abscesses occur in
Ulcerative colitis
Symptoms partially relieve after smoking in
Ulcerative colitis
Four major cases of intestinal obstruction
Herniation
Adhesion
Volvulus
Intusseption
Most often place of volvulus
Large redundant loops of sigmoid colon
Most important cause of acute obstruction in bowel ischemic disease
Thrombosis or embolism
Most important risk factor for BID thrombosis
Atheroesclerosis
Women >70 presents to the ER with sudden onset of cramping on lower left quadrant, desire to defecate and bloody diarrhea.
Acute ischemia, ischemic disease
Disorder of the small and large intestine with transmural necrosis
Necrotizing enterocolitis
Immune cells present in intraepithelial lymphocytosis in celiac disease
CD8+
Most sensitive test for celiac disease
IgA ntibodies against tissue transaglutaminase
Immune response only present in UCD and not Crohn’s
Th2
Typical pathology of Crohn
Skip lesions in ileum, ileocecal valve and/or cecum, that started as an aphtous ulcer. Mucosa with a cobblestone appearance, fissures that become fistulas and fibrosing strictures.
Crypt abscesses, distortion of mucosal gland and non caseating granulomas.
Women presents interrupted right lower quadrant pain, fever and bloody diarrhea, every month. Has cutaneous granulomas, uveitis and clubbing of the fingertips.
Crohn disease
Light mucosal irritation of the ileum in ulcerative colitis
Backwash ileitis
Typical pathology of ulcerative colitis
Involvement of rectum extending proximally.
Multiple ulcers that can form polips and mucosal bridges.
Colon wall not thickened, mucosa and submucosa involvement. Can have toxic megacolon due to MP and nmj dysfunction. Granulomas not present.
Women presents with attacks of bloody diarrhea, lower abdominal pain and cramps relieved by defecation, with symptoms lasting weeks-months. Had a similar episode 10 years ago.
Ulcerative colitis
Tipos de pólipos neoplásicos
Inflamatorios, hamartomatosos e hiperplásicos
Características de los pólipos hiperplásicos
Left colon (rectum and sigmoid), smooth and nodular 5 mm, mature goblet and absortive cells with cerrated surface.
Type of polyp that forms as pat of the solitary rectal ulcer syndrome.
Inflammatory polyps
Inflammatory polyps triad
Rectal bleeding, mucous production, inflammatory lesion in anterior rectal wall
Histological features of inflammatory polyps
Erosion and epithelial hyperplasia with prolapse-induced lamina propria fibromuscular hyperplasia
Smooth surface polyps located in the rectum that happen in younger than 5 years of age and have a mutation in SMAD4, may cause severe hemorrage.
Juvenile polyps
11 year old patients presents with intussusception. Has loss of function mutation in STK11, mucosal hyperpimentation suggesting Paul-Jeghers. Location of the polyps and characteristics.
Small intesting, can be in stomach and colon. Arborization involving all layers.
Polyp presented from 45 to 65, screened 10 years before appearance in family member, related to western diet.
Adenocarcinoma
Classification of colorectal adenomas and their severity.
Tubular, tubulovillous and villous. Most risky are villous adenomas.
Types of architecture of a tubulovillous adenoma
Sessile serrated lesions and intramucosal carcinoma
Type of colorectal adenoma that lacks typical cytologic features of dysplasia.
Sessile serrated lesions tubulovillous colorectal adenoma.
Size of colorectal adenomas associated with higher risk of malignancy.
4 cm
Teenager presents with hypertrophy of retinal pigment epithelium and 100+ polyps corresponding to familial adenomatous polyposis. Most probable mutation and mutation if it had <100 polyps
APC
<100 polyps: MUTYH mutation
Variants of familial adenomatous polyposis
Gardner syndrome and Turcot syndrome
Most common age for FAP polyps becoming colorectal adenocarcinoma in untreated patients
Often <30 and nearly always by age 50
Genetic error in Lynch Syndrome
Mismatch repair deficiency and microsatellite instability (MSI)
Genes associated to hereditary non-polyposis colorectal cancer (HNPCC)
MSH2 and MLH1
NSAIDs correlation to colorectal adenocarcinoma
Inhibit COX2, necessary for synthesis of prostaglandin E2, which promotes epithelial proliferation.
Age of higher incidence in adenocarcinoma
60-70
Pathways involved in colonic adenocarcinoma
APC/B catenin pathway
MSI pathway
Difference between carcinomas in the proximal colon and distal colon.
Proximal: polypoid exophytic masses that don’t cause obstruction.
Distal: annular lesions that produce “napkin-ring” constrictions and luminal narrowing
First clinical manifestation of cecal and right colon cancers
Fatigue and weakness due to iron deficiency anemia
Clinical maxim of underlying cause of iron deficiency anemia in older men and postmenopausal women
GI cancer until proven otherwise
Left-sided colon adenocarcinomas manifestations
Occult bleeding, changes in bowel habits, cramping and left lower quadrant discomfort.
