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Gastrointestinal Pathology - Coggle Diagram

- - - - Clinical features:
        
        Polyhydramnios
        
        Distension f stomach and blind loop
        of duodenum (double bubble sign)
        
        Bilious vomiting 🤮
  - - - Failure of the vitelline
        duct to involute
        
        Rule of 2s':
        
        2% population **most common congenital GI anomaly
        
        2 inches long and located in small bowel within 2 feet of ileocecal valve
        
        Can present during the first 2 years of life with bleeding due to heterotopic gastric mucosa) volvulus, intussusception or obstruction (mimics apendicitis) MOST CASES ASYMPTOMATIC
  - - - Results in obstruction and disruption
        of the blood supply with infarction
        
        Locations:
        
        Sigmoid colon - elderly
        
        Cecum - Young adults
  - - - Associated with
        a leading edge
        (focus of traction)
        
        ADULT: Most common cause → Tumor
        
        CHILDRE:
        
        Most common cause → lymphoid hyperplasia (by rotavirus)
        
        Arises in the terminal ileum→ intussusception into the cecum
  - - - Transmural infarction → with thrombosis/embolism of the superior mesenteric artery or mesenteric vein
      - Mucosal infarction → with marked hypotension
      - Abdominal pain, bloody diarrhea, and decreased bowel sounds
  - - - Presentation: Osmotic diarrhea with ↓ stool pH
        
        Abdominal distension and diarrhea with milk products
        
        Undigested lactose is osmotically active (colonic bacteria ferment lactose)
      - Etiology:
        
        Congenital
        
        Acquired (late childhood)
        
        Temporary deficiency after infection
  - - - Gluten most pathogenic
        component is gliadin
      - Deamidated gliadin is presented
        by antigen presenting cells via
        MHC class II. Helper T cells
        mediate tissue damage
        
        Clinical Presentation: Small, herpes-like vesicles may arise on skin (dermatitis herpetiformis). Due to IgA deposition at the tips of dermal papillae; resolves with gluten-free diet. malabsorption and steatorrhea
        CHILDREN: abdominal distension, diarrhea, and failure to thrive
        ADULTS: chronic diarrhea and bloating
        
        Laboratory findings: IgA antibodies against endomysium, tTG, or gliadin; IgG also present, useful when IgA deficiency (like in celiac disease); Histology: villous atrophy, crypt hyperplasia + intraepithelial lymphocytosis.
        
        Tx: GLUTEN-FREE DIET
        If refractory symptoms → late complications like *Small bowel carcinoma and T-cell lymphoma.
  - - - Similar to celiac
        disease except
        
        Tropical regions
        
        After infectious diarrhea →responds to antibiotics
        
        More damage in jejunum and ileum (secondary vitamin B12 or folate deficiency)
        
        Duodenum is less commonly involved
  - - - Involvement
        
        Small bowel lamina propria: Macrophages compress lacteals →Chylomicrons cannot be transferred from enterocytes to lymphatics→fat malabsorption and steatorrhea
        
        Other sites: synovium of joints (arthritis), cardiac
        valves, lymph nodes, and CNS.
  - - - Malabsorption → defective chylomicron
        formation (requires B-48)
        
        Absent plasma VLDL and LDL (require B-100)
  - - - Low-grade malignancy
        
        Arise anywhere
        along the gut
        
        Often secretes
        serotonin
        
        Serotonin released into the portal circulation →metabolized by liver monoamine oxidase (MAO)→ into 5HIAA→ excreted in urine
        
        Serotonin is released into the hepatic vein and leaks into systemic circulation via hepato-systemic shunts, resulting in carcinoid syndrome and carcinoid heart disease
        
        Carcinoid syndrome: bronchospasm, diarrhea, and flushing of skin; symptoms can be triggered by alcohol or emotional stress, which stimulate serotonin release from the tumor
        
        Carcinoid heart disease is characterized by right-sided valvular fibrosis (increased collagen) leading to tricuspid regurgitation and pulmonary valve stenosis; left-sided valvular lesions are not seen due to presence of monoamine oxidase (metabolizes serotonin) in the lung
        
        Metastasis of carcinoid tumor to the liver
        allows serotonin to bypass liver metabolism
        
        Small bowel is the most common site
        Grows as a submucosal polyp-like nodule
- - - - Clasification
        
        CROHN
        
        Any portion of the GI tract, usually
        the terminal ileum and colon.
        
        Morphology: Transmural inflammation→ fistulas. Cobblestone mucosa, creeping fat, bowel wall thickening (“string sign” on small bowel follow-through), linear ulcers, fissures.
        
        Histology: Noncaseating granulomas, lymphoid aggregates
        
        Symptoms: Diarrhea that may or may not be bloody
        
        Extraintestinal: Kidney stones (usually calcium oxalate), gallstones. May be ⊕ for anti-Saccharomyces cerevisiae antibodies (ASCA).
        
        Complications: Fistulas (eg, enterovesical fistulae, which can cause recurrent UTI and pneumaturia), phlegmon/abscess, strictures (causing obstruction), perianal disease.
        
        Tx: Glucocorticoids, azathioprine, antibiotics (eg,ciprofloxacin, metronidazole), biologics (eg,infliximab, adalimumab).
        
        Skip lesions, rectal sparing.
        
        CUCI
        
        Continuous colonic lesions,
        always with rectal involvement.
        
        Morphology: Mucosal and submucosal inflammation only. Friable mucosa with superficial and/or deep ulcerations (compare normal B with diseased). Loss of haustra → “lead pipe” appearance on imaging.
        
        Histology: Crypt abscesses/ulcers, bleeding, no granulomas
        
        Symptoms: Bloody diarrhea (usually painful).
        
        Extraintestinal: 1° sclerosing cholangitis. Associated with MPOANCA/ p-ANCA.
        
        Complications: Fulminant colitis, toxic megacolon, perforation
        
        TX: 5-aminosalicylic acid preparations (eg,mesalamine), 6-mercaptopurine, infliximab, colectomy.
        
        Colitis = colon inflammation
- - - - Oral leukoplakia and erythroplakia
        are precursor lesions
        *often biopsied to rule out carcinoma.
        
        Leukoplakia: white plaque that cannot be scraped away; often represents squamous cell dysplasia
        *is distinct from oral candidiasis (thrush) and hairy leukoplakia
        
        Oral candidiasis is a white deposit on the tongue, which is easily scraped away; usually seen in immunocompromised states
        
        Hairy leukoplakia is a white, rough ('hairy') patch that arises on the lateral tongue. It is usually seen in immunocompromised individuals (AIDS) and is due to EBY-induced squamous cell hyperplasia; not pre-malignant
        
        Erythroplakia (red plaque) represents vascularized leukoplakia and is highly suggestive of squamous cell dysplasia.
      - LOCALIZATION: Floor of mouth
  - - - Primary infection occurs in childhood; lesions heal, but virus remains dormant in ganglia of the trigeminal nerve
      - Stress and sunlight cause reactivation of the virus, leading to vesicles that often arise on the lips
  - - - Due to immune complex vasculitis involving small vessels
      - Can be seen after viral infection, but etiology is unknown
  - - - Arises in relation to stress and resolves spontaneously
        
        Grayish base surrounded by erythema
  - - - Due to failure of facial prominences to fuse:
        
        Normally:facial prominences (one from superior, two from the
        sides, and two from inferior) grow and fuse together to form the face
        
        Cleft lip and palate usually occur together; isolated cleft lip or palate is less common
- - - - Risk of Boerhaave syndrome:
        Rupture of esophagus→ air in the
        mediastinum and subcutaneous emphysema
      - Symptoms: Painful hematemesis
  - - - Arise secondary to
        portal hypertension
        
        Asymptomatic
        -BUT! risk of rupture
        
        RUPTURE:
        Painless hematemesis
        Most common cause of death in cirrhosis
      - Portal hypertension: left gastric vein backs up
        into the esophageal vein →dilation (varices
  - - - Etiology: Damaged ganglion
        cells in the myenteric plexus
        
        Can't regulate bowel motility
        and relaxing the LES
        
        Clinical features:
        1. Dysphagia for solids and liquids
        2. Putrid breath
        3. High LES pressure on esophageal manometry
        4. 'Bird-beak' sign on barium swallow study
        5. Increased risk for esophageal squamous cell carcinoma
        
        Damage: Idiopathic or secondary to a known
        insult (Trypanosoma cruzi infection in Chagas disease
      - Located between the inner circular and outer longitudinal
        layers of the Fibromuscular propria
  - - - Arises→ above the upper esophageal sphincter;
        at the junction of the esophagus and pharynx
      - Dysphagia, obstruction, and halitosis (bad breath)
  - - - 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 complications.
  - - - Increased risk for esophageal
        squamous cell carcinoma
        
        Plummer-Vinson syndrome:
        severe iron deficiency anemia,
        esophageal web, and beefy-red
        tongue due to atrophic glossitis
      - Symptoms: dysphagia for
        poorly chewed food
  - - - 10% of patients
        with GERD
      - Response of lower esophageal
        stem cells to acidic stress
        
        May progress to dysplasia
        and adenocarcinoma
  - - - Most common variant:
        proximal esophageal atresia-distal esophagus
        arising from the trachea
      - Vomiting, polyhydramnios,
        abdominal distension, & aspiration
  - - - Adenocarcinoma
        
        Malignant proliferation of glands
        
        Arises from preexisting Barrett esophagus
        in the lower one-third of the esophagus
        
        Most common type of esophageal
        carcinoma in the West
      - Squamous cell
        carcinoma
        
        Malignant proliferation
        of squamous cells
        
        Arises in upper or middle
        third of the esophagus
        
        Major risk factors:
        
        Alcohol & Tobacco (most common)
        
        Very hot tea
        
        Achalasia
        
        Esophageal web (Plummer-Vinson Sx)
        
        Esophageal injury (lye ingestion)
        
        Additional Symptoms:
        
        Hoarse voice (recurrent laryngeal nerve involvement)
        
        Cough (tracheal involvement)
        
        Most common esophageal
        cancer worldwide
- - - - Failure of herniated intestines to return
        to the body cavity during development
        
        Contents are covered by peritoneum
        and amnion of the umbilical cord
  - - - Classically presents two weeks after birth as:
        
        Projectile non bilus vomiting 🤮
        
        Visible peristalsis
        
        Olive-like mass in the abdomen
      - Tx: Myotomy
  - - - Acid damage→superficial inflammation + erosion (loss of superficial epithelium), or ulcer (loss of mucosal layer).
        
        Severe burn (Curling ulcer) - Hypovolemia leads to decreased blood supply.
        
        NSAIDs (decreased PGE).
        
        Heavy alcohol consumption.
        
        Chemotherapy
        
        Increased intracranial pressure (Cushing ulcer) -Increased stimulation of vagus nerve leads to increased acid production.
        
        Shock - Multiple (stress) ulcers may be seen in ICU patients.
  - - - 2 types based
        on underlying etiology
        
        Chronic autoimmune gastritis
        
        Autoimmune destruction
        of gastric parietal cells.
        
        Pathogenesis is mediated by T cells
        (type IV hypersensitivity)
        
        Clinical
        features:
        
        Atrophy of mucosa with intestinal metaplasia
        
        Achlorhydria with increased gastrin levels and antral G-cell hyperplasia
        
        Megaloblastic (pernicious) anemia due to lack of intrinsic factor
        
        Increased risk for gastric adenocarcinoma (intestinal type)
        
        Autoantibodies (T-cell induced) to the
        H+/K+-ATPase on parietal cells and to intrinsic
        factor. ↑ risk of pernicious anemia; useful for diagnosis
        
        In body and fundus
        
        Chronic H pylori gastritis
        
        H pylori-induced acute
        and chronic inflammation
        
        H pylori ureases and proteases along
        with inflammation weaken mucosal defenses
        creates alkaline enviroment so survive in acidic
        
        Clinical
        findings:
        
        Epigastric abdominal pain
        
        Increased risk for peptic ulcer, gastric adenocarcinoma (intestinal type), and MALT lymphoma (oncogenic microbe)
        
        Tx → Triple therapy: amoxicillin (metronidazole if penicillin allergy) + clarithromycin + proton pump inhibitor. Bismuth-based quadruple therapy if concerned about macrolide resistance
        
        Resolves gastritis/ulcer and reverses intestinal metaplasia
        
        Negative urea breath test and lack of stool antigen confirm eradication of H pylori.
        
        Antrum is the most common affected site
        
        Most common form
        of gastritis (90%)
  - - - DUODENAL ULCER
        Proximal duodenum
        90%
        
        Etiology:
        H pylori (> 95%)
        ZE syndrome
        
        Clinical findings:
        
        Epigastric pain that improves with meals
        
        If arises in posterior duodenum → rupture →bleeding from gastroduodenal artery or acute pancreatitis.
        
        DX: Endoscopic biopsy →ulcer with
        hypertrophy of Brunner glands
        
        Duodenal carcinoma
        is extremely rare
      - GASTRIC ULCER
        Distal stomach 10%
        
        Etiology:
        
        Etiology: H pylori (75%
        NSAIDs & Bile reflux
        
        Clinical findings:
        
        Epigastric pain that worsens with meals
        
        Ulcer located on the lesser curvature of the antrum
        
        Rupture carries risk of bleeding from left gastric artery
        
        Benign peptic ulcers are usually small(< 3 cm), sharply demarcated ("punched-out"), and surrounded by radiating folds of mucosa
        
        Gastric carcinoma
        (intestinal subtype)
        
        Malignant ulcers are large and
        irregular with heaped up margins
        
        Biopsy is required for definitive Dx.
  - - - Intestinal type
        (more common)
        
        large, irregular ulcer
        with heaped up margins
        
        Risk factors:
        
        Intestinal metaplasia (due to H pylori and autoimmune
        gastritis)
        
        Nitrosamines in smoked foods (Japan)
        
        Blood type A
        
        Metastasis: Periumbilical region
        (Sister Mary Joseph nodule
        
        Curvature of the antrum
        (similar to gastric ulcer
      - Diffuse type
        
        Signet ring cells that diffusely
        infiltrate the gastric wall
        
        Not associated with H pylori, intestinal
        metaplasia, or nitrosamines
        
        Metastasis: Bilateral ovaries
        (Krukenberg tumor)
        
        Desmoplasia results in thickening
        of stomach wall (linitis plastica)
- - - - Periumbilical pain, fever, and nausea; pain eventually localizes to right lower quadrant (McBurney point).
        
        Rupture results in peritonitis that presents with guarding and rebound tenderness.
        
        Periappendiceal abscess is a common complication.
- - - - Related to wall stress
        
        Associated with constipation, straining, and low-fiber diet; commonly seen in older adults (risk increases with age)
        
        Arise where the vasa recta traverse the muscularis propria (weak point in colonic wall); sigmoid colon is the most common location
      - Usually asymptomatic
        
        Complications:
        
        Rectal bleeding (hematochezia)
        
        Diverticulitis - due to obstructing fecal material; presents with appendicitis-like symptoms in the left lower quadrant
        
        Fistula - Inflamed diverticulum ruptures and attaches to a local structure.Colovesicular fistula presents with air (or stool) in urine.
  - - - Arises in the cecum and right colon due to high wall tension
        
        Rupture classically presents as hematochezia in an older adult
  - - - Rupture presents as bleeding.
  - - - Congenital failure of ganglion cells (neural crest-derived) to
        descend into myenteric and submucosal plexus
        
        Clinical features are
        based on obstruction
        
        Failure to pass meconium
        
        Empty rectal vault on digital rectal exam
        
        Massive dilatation (megacolon) of bowel proximal
        to obstruction with risk for rupture
        
        Dx: Rectal suction biopsy reveals
        lack of ganglion cells.
        
        Tx: resection of the involved bowel;
        ganglion cells are present in the bowel
        proximal to the diseased segment
      - Myenteric (Auerbach) plexus: between the inner circular and outer longitudinal muscle layers of the muscularis propria and regulates motility.
        
        Submucosal (Meissner) plexus:in the submucosa and regulates blood flow, secretions, and absorption.
  - - - Atherosclerosis of SMA is the most common cause.
      - Presents with postprandial pain and weight loss;
        infarction results in pain and bloody diarrhea
  - - - Tipos
        
        Adenomatous polyps →neoplastic proliferation of glands
        
        2nd most common
        
        Benign BUT premalignant; may progress via adenoma-carcinoma sequence
        
        Adenoma-carcinoma sequence →molecular progression from normal colonic mucosa to adenomatous polyp to carcinoma
        
        APC (adenomatous polyposis coli gene) mutations (sporadic or germline) ↑ risk for formation of polyp
        
        K-ras mutation → formation of polyp
        
        p53 mutation and increased expression of COX→progression to carcinoma; aspirin impedes progression from adenoma to carcinoma
        
        Hyperplastic polyps →hyperplasia of glands
        
        'Serrated' appearance on microscopy
        
        Most common
        
        Located in the left colon (rectosigmoid)
        
        BENIGN no malignant potential
      - On colonoscopy, hyperplastic and adenomatous polyps look identical →all polyps are removed and examined microscopically
        IF > 2cm, sessile growth, and villous histology carcinoma by 40 years of agGreatest risk for progresion adenoma-carcinoma
      - Screening by colonoscopy & fecal occult blood;
        polyps are usually clinically silent, but can bleed
        → Goal is to remove adenomatous polyps before
        progression to carcinoma
  - - - Colon and rectum are
        removed prophylactically
        
        Gardner syndrome is FAP with
        fibromatosis and osteomas:
        -Fibromatosis: Non-neoplastic fibroblast proliferation in retroperitoneum (desmoid) → locally destroy tissue
        -Osteoma: benign bone tumor (usually skull)
        
        Turcot syndrome is FAP with CNS tumors
        (medulloblastoma and glial tumors)
      - All patients
        →Carcinoma by 40 years
  - - - Sporadic Hamartomatous (benign) polyp
        
        Arises in children(< 5 years)
        
        Multiple juvenile polyps in the stomach and colon
        
        Large numbers → ↑ risk of progression to carcinoma
  - - - ↑↑ risk for colorectal, breast, and gynecologic cancer
  - - - 2nd most important molecular
        pathway is microsatellite instability
        → mismatch repair
        
        Increased risk for colorectal, ovarian, and endometrial carcinoma
        
        Colorectal carcinoma arises de novo (not from adenomatous polyps) at a relatively early age; usually right-sided
        
        Screening by colonoscopy & fecal occult blood since 50years
        
        Carcinoma can develop anywhere along entire length of colon:
        
        Left-sided carcinoma usually grows as a 'napkin-ring' lesion; presents with decreased stool caliber, left lower quadrant pain, and blood-streaked stool
        
        Right-sided carcinoma usually grows as a raised lesion; presents with iron deficiency anemia (occult bleeding) and vague pain.
        **An older adult with iron deficiency anemia has colorectal carcinoma until proven otherwise.
        
        Staging:
        T - depth of invasion; tumors limited to the mucosa generally do not spread due to lack of lymphatics in the mucosa.
        N - spread to regional lymph nodes
        M - distant spread; most commonly involves the liver
- - - - Obstructing stone (sialolithiasis unilateral)
        → Staphylococcus aureus infection
    - - Benign tumor composed of
        stromal (cartilage) + epithelial tissue
        
        Mobile, painless, circumscribed
        mass at the angle of the jaw
        
        High rate of recurrence due to extension of small islands of tumor through tumor capsule often leads to incomplete resection
        
        Rarely may transform into carcinoma, which presents with signs of facial nerve damage (facial nerve runs through parotid gland)
        
        Most common tumor
        of the salivary gland
      - Most common tumor
        of the salivary gland
    - - Benign cystic tumor with abundant
        lymphocytes and germinal
        centers (lymph nodelike stroma)
        
        2nd most common tumor of the salivary gland
        
        Almost always arises in the parotid
    - - Infection with mumps virus →
        bilateral inflamed parotid glands
        
        Orchitis, pancreatitis, and aseptic
        meningitis may also be present
        
        Serum amylase↑↑↑ due to salivary
        gland/pancreatic involvement
        
        Orchitis → sterility specially in teenagers
    - - Malignant tumor composed of
        mucinous and squamous cells
        
        Arises in the parotid
        
        Commonly involves the facial nerve
      - Most common malignant tumor
        of the salivary gland