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110 Cards in this Set
- Front
- Back
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Gross Features of Erythroplakia
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Red, velvety eroded area that is poorly circumscribed
Has great potential for malignancy (>50%) |
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Gross Features of Oral Hairy Leukoplakia
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White confluent fluffy or hairy hyperkerotic thickenings. Layers of keratotic squames on underlying mucosal acanthosis.
Majority have EBV infections, no malignant potential |
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Symptoms of Esophageal Atresia
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Excessive drooling in newborn. Choking and Cyanosis with first feed.
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Hiatial Hernia Clinical Symptoms
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Epigastric pain and heartburn (in the sliding type)
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Clinical Features of Aclasia/Cardiospasm
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•Dysphagia
•Odynophagia (painful swallowing) •Reflux of contents •Vomiting •Aspiration pneumonia |
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Gross Morphology of Mallory Weiss Syndrome in Endoscopy
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Can see tears in the endoscopy (appears as straight bold lines)
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Gross Appearance of Esophagus if Infected with Candida
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White plaque
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Gross Appearance of Esophagus if Infected with CMV
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Will create areas of Ischemia and Red Areas of Hyperemia around it
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Clinical Features and Complications of Reflux Esophagitis
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Clinical Features
•Dyspepsia •Burning Sensation •Water Brash (regurgitation into the mouth of fluid that may be sour or almost tasteless) •Symptoms increase after lying down or after a large meal •Nocturnal Cough Complications •Bleeding •Stricture Formation •Aspiration pneumonitis •Barrett's Esophagus and Adenocarcinoma |
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Risk Factors for Esophagitis
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•Irritants
•Infections •Allergic (Eosinophilic esophagitis) •Uremia •Anticancer therapy |
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Morphology of Reflux Esophagitis
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•Hyperemia
•Presence of inflammatory cells (eosinophils, neutrophils) •Elongation of lamina propria papillae (because of necrosis and sloughing of top layer) •Basal zone hyperplasia •Esophagus is solid red |
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Clinical Features of Barrett's Esophagus
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•Heart burn, dyspepsia (upset stomach, indigestion)
•Epigastric discomfort •Substernal discomfort •Relieved with antacids |
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Appearance of Esophageal Varices in Endoscopy
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Can see blood in endoscopy
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Etiology Factors of Squamous Cell Carcinoma of Esophagus
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Diet:
•Deficiency of Vitamin A and Riboflavin (B2) •Fungal contamination •High content of nitrites (think Japan) Life Style: •Alcohol •Tobacco Use •Urban Environment Genetic: •Tylosis (ectodermal dysplasia, hyperkeratinosis of palms and feet) •Celiac Disease •Racial factors Esophageal Disease: •Chronic Esophagitis •Achalasia •Plummer Vinson Syndrome (think Fe deficiency) |
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Stain used to analyze adenocarcinoma
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Lugol's Iodine
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Causes of Pyloric Stenosis
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•Congenital
•Acquired (chronic antral gastritis, peptic ulcers, malignancy) |
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Clinical Features of Congenital Pyloric Stenosis
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•Projectile vomiting
•Regurgitation •Palpable epigastric mass •Visible peristalsis More common in first male child, M:F 3:1 |
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Etiology of Acute Gastritis
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•NSAIDs
•Excessive alcohol consumption •Heavy smoking •Ischemia and shock •Severe stress (burns, surgery) •Cancer chemotherapy •Systemic infections •Uremia |
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Clinical Features of Acute Gastritis
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•May be asymptomatic
•Epigastric pain, vomiting, nausea •Hematemesis and malena •Bleeding can be fatal |
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Morphology of Acute Gastritis
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•Loss of surface epithelium (erosions)
•Erosions along with hemorrhage (acute erosive gastritis) •Hyperemia, punctate areas of hemorrhage •Edema and congestion of lamina propria •Neutrophils in the surface epithelium and lumina of glands |
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Etiology of Chronic Gastritis
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•Chronic infection with H. pylori (most important)
•Autoimmune disease (i.e. pernicious anemia) •Alcohol and smoking •Post-surgical (i.e. after antrectomy) •Radiation •Granulomatous conditions (Crohn's disease, sarcoidoisis) |
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Chronic Gastritis Clinical Features
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•Asymptomatic
•Nausea, vomiting •Epigastric discomfort •Dyspepsia •Indigestion |
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Endoscopy of Chronic Gastritis
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•Varies from normal to diffuse/patchy erythema w/ hemorrhage to boggy appearing mucosa with thick mucosal folds
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Morphology of Chronic Gastritis
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•Inflammatory infiltrate in lamina propria (lymphocytes, plasma cells)
•Neutrophils in surface epithelium and glandular lumen •Lymphoid aggregates (marker for H. pylori) •Intestinal metaplasia and glandular atrophy |
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Microscopic Features of Pernicious Anemia
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•Body looks like antrum, because autoimmune gastritis has destroyed gland (pyloric metaplasia)
•Loss of rugal folds |
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Other Features of Pernicious Anemia
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•Macrocytic Anemia
•Hypergastrinemia •Achlorhydria •ECL cell hyperplasia |
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Curling Ulcers
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Gastric Ulcer after Suffering Burns
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Cushing Ulcers
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Gastric Ulcer after Head Injury
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Gross Morphology of Acute Gastric Ulcers
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•Multiple, small, circular
•Gastric rugae are normal •Base is not indurated (hardened) •Adjacent gastric mucosa is normal |
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Gross Morphology of Peptic Ulcer Disease
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•Round to oval, punched out with straight walls
•Sharp and raised margins but not everted •Depth varies but may penetrate entire wall •Smooth and clean base •Radiating surrounding mucosal folds |
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Microscopy of Peptic Ulcers
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Active ulcer has four zones:
•Necrotic fibrinoid disease •Non-specific inflammatory infiltrate (predominantly neutrophilic) •Granulation tissue •Fibrosis and collagenous scar Typically see features of chronic gastritis in adjacent mucosa: •Loss of surface epithelium (erosions) •Erosions along with hemorrhage (acute erosive gastritis) •Hyperemia, punctate areas of hemorrhage •Edema and congestion of lamina propria •Neutrophils in the surface epithelium and lumina of glands |
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Etiopathogenesis of Peptic Ulcers
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•H. pylori
•NSAIDs •Smoking •Alcohol •Psychological Stress •Zollinger-Ellison Syndrome |
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Clinical Features and Complications of Peptic Ulcers
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Clinical Features:
•Burning epigastric pain 1-3 hours after meals •Relieved by food and alkali •Worse at night •Associated weight loss (because eating is associated with pain) •Gastric outlet obstruction Complications: •Bleeding •Perforation •Gastric outlet obstruction •Malignant transformation |
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Morphology and Etiology of Gastric Adenocarcinoma (Intestinal-type)
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•In the setting of chronic gastritis
•H. pylori associated •Neoplastic glands resemble intestinal epithelium of colon •Intestinal metaplasia is precursor lesion •More common in high-risk populations |
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Morphology and Etiology of Gastric Adenocarcinoma (diffuse type)
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•No gland formation
•Single cells, sheets, clusters •Signet ring cells •No intestinal metaplasia •E-cadherin implicated •More common in familial types with young female predominance •Linitis plastica appearance (tumor still has rugal folds, they become more prominent) |
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Clinical features of gastric adenocarcinoma
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•Most asymptomatic in early stages
•Non-specific-weight loss, anorexia, abdominal pain •Pyloric obstruction •Krukenberg tumor (bilateral metastasis to ovaries) •Virchow's lymph node swollen |
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Gross appearance of gastric adenocarcinoma
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•Tumor grows onto pylorus
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Morphology of Gastrointestinal Stromal Tumors (GIST)
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•Whorls and bundles of spindle shaped cells
•CD117 is marker |
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Clinical Features and Complications of Meckel's Diverticulum
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Clinical features:
•Commonly asymptomatic Complications: •Hemorrhage and peptic ulceration •Intestinal obstruction •Diverticulitis •Perforation •Fistula |
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Clinical Features and Causes of Malabsorption
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Clinical Features:
•Chronic diarrhea •Steatorrhea •Weight loss due to decreased nutrient absorption Causes: •Scleroderma (muscle tissue replaced with complex collagen tissue) •Short Bowel Loop due to Surgical Resection (Less time for absorption) |
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Morphology of Celiac Disease
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•Changes can be seen throughout intestine but is more marked in proximal intestine (because sentinel event occurs here)
•Marked atrophy and loss of villi (decreased area for absorption because of intraepithelial lymphocytes) •Elongated and hyperplastic crypts (shorter villi) •Increased number of T lymphocytes, macrophages and plasma cells in lamina propria Endoscopy: •Flattened small intestine, lack of villi, whitish looking |
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Tropical Sprue (compared to Celiac Disease)
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•In people visiting tropics
•Symptoms appear months after visit •Pathogenesis is based on bacterial infection superimposed on preexisting small intestine injury •All parts of small intestine involved equally •Responds to antibiotics |
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Symptoms of Whipple's Disease
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•Dementia
•Arthralgia •Seizures •Hyperpigmentation of sun exposed skin •General malabsorption symptoms: bulky, greasy, yellow/grey, frothy stools |
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Morphology of Whipple's Disease
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•Mucosa has distended macrophages in lamina propria that contain PAS positive granules
•Macrophages are "foamy in appearance" |
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Appearance of Hirschsprung's Disease in X-Rays and Microscopy
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X-ray:
•Dilation of intestime and then distal to it, stenosis Microscopy: •Can see nerve cells but no ganglia (which are large dark cells) within them |
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Clinical Features of Hirschsprung's Disease
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•Delayed passage of meconium
•Constipation •Abdominal distension •Diagnosed by rectal biopsy •Complications are enterocolitis, perforation and peritonitis |
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Clinical Features of Diverticular Disease
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Diverticulosis:
•Usually asymptomatic, sometimes painless bleeding Diverticulitis •Lower abdominal pain •Constipation, diarrhea, flatulence •Fever •Can lead to perforation Remember, this is when mucosa and submucosa herniates through muscularis (Umer's slide) |
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Clinical Features of Colitis
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•Diarrhea (mucoid or bloody)
•Abdominal Pain (usually below umbilicus) •Abdominal cramps •Tenesmus (painful defecation) |
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Pseudomembrane Colitis Morphology
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•Colon (esp. rectosigmoid) shows raised yellow plaques
•Fibronopurulent-necrotic debris •Superficially damaged rypts that are distended by mucopurulent debris that looks like mushrooming cloud |
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Amoebic Colitis Morphology
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•Flask shaped ulcers that invade laterally in submucosa
•Organisms have engulfed RBCs |
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Clinical Features of Ulcerative Colitis
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•Intermittent rectal bleeding, bloody diarrhea and abdominal pain
•Typically continuous colonic involvement |
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Clinical Features of Crohn Disease
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•More variable symptoms than UC that include abdominal pain, fatigue, weight loss, fever
•Typically patchy transmural involvement |
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Clinical Features and Morphology of Infectious Colitis
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•Bloody Diarrhea
•Nausea •Vomiting •Fever •Lamina propria hemorrhage, erosion and neutrophils infiltrate lamina propria and glands |
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Clinical Features of Amebic Colitis
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•Gradual dysentry
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Clinical Features and Morphology of Typhoid
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•Fever
•Headache •Abdominal pain •Rash •Diarrhea •Longitudinal Ulcers, typically over Peyer's Patches |
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Clinical Features and Morphology of Tuberculosis
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Clinical Features:
•Chronic abdominal pain •Multifocal involvement, jejenum to ileum, terminal ileum most common •Annular circular or oval ulcers, lying transversely •Large single ulcers or small numerous ulcers •Granulommatous inflammation, often necrotizing •M. bovis infection when food is not pasteurized |
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Differential between Crohn's and Ulcerative Colitis
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•CD is granulommatous inflammation that can affect any part of GI from mouth to anus. Is transmural
•UC affects colon only, is non-granulommatous. Affects mucosa and submucosa only |
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Gross Appearance and Morphology of Ulcerative Colitis
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•Serosa usually normal
•Mucosa is red, friable, granular •Broad based ulcers •Isolated islands of regenerating mucosa - Pseudopolyps! •"Bear claw" appearance in bowel •Crypt abscesses •Lymphoplasmacytosis |
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Morphology of Crohn's Disease
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•Sharply delimited and transmural involvement by an inflammatory process
•Non caseating granulomas •Mucosal fissuring with formation of fistulas •Cobblestone appearance •"String Sign" on X-ray •Creeping up of Mesenteric fat |
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Clinical Features and Morphology of Typhoid Fever
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Clinical Features
•Headache •Fever •Abdominal Pain •Rash •Diarrhea Morphology •Longitudinal Ulcers, typically over Peyer's Patches |
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Clinical Features and Morphology of Tuberculosis
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Clinical Features
•Chronic Abdominal Pain •Multifocal involvement, jejenum to ileum, terminal ileum most common •Annular circular or oval ulcers, lying transversely •Single ulcers large, multiple ulcers smaller Morphology •Granulommatous Inflammation, often necrotizing Caused by M. bovis in food that is not pastuerized |
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Morphology of Ulcerative Colitis
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•Serosa usually normal
•Mucosa is red, granular, friable •Broad based ulcers •Isolated islands of regenerating mucosa create pseudopolyps •"Bear claw" appearance in bowel •Crypt abscesses •Crypt distortion |
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Morphology of Crohn's Disease
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Microscopy:
•Sharply delimited & transmural involvement by an inflammatory process •Presence of non caseating granulomas •Mucosal fissuring with formation of fistulas Gross: •Creeping up of mesenteric fat because of fibrosis •Mesentery thickened and fibrotic •Wall is thickened due to edema, hypertrophy, fibrosis, inflammation On X-Ray: •String Sign |
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Clinical Features in Ischemic Bowel Disease
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Mucosal Type:
•Nausea •Vomiting •Bloody Stools Transmural •Severe abdominal pain •Tenderness •Gangrene •Perforation •Peritonitis •Shock •Vascular Collapse |
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Features of Chronic Ischemic Colitis
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•Common at watershed areas (i.e. splenic flexure)
•Stricture formation can be cause •Intermittent attacks of pain •Intestinal Angina •Can mimic inflammatory bowel disease |
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Clinical Features of Carcinoid Syndrome
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•Wheezing
•Flushing •Diarrhea •Increased Peristalsis Check serum for 5-HT to diagnose |
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Symptoms of Gastric MALT Lymphoma
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•Dyspepsia
•Pain in abdomen •Nausea •Vomiting •Weight Loss |
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Morphology of Juvenile Polyps
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•Rectum (distal colon) is most common site
•Lamina Propria forms the bulk and encloses abundant cystically dilated glands •Inflammatory cells can be present •Sporadic Single Polyps: NO MALIGNANT POTENTIAL •Inflammatory cells such as eosinophils will infiltrate nearby reacting to mucin Juvenile Polyposis Syndrome: Increased risk of malignancy (more than 5, 1 more than 10 cm) |
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Peutz Jeger's Polyp Morphology and Clinical Features and Features
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Features:
•Hamartomous •Autosomal Dominant •No malignant potential, but patients have higher risk of pancreas, breast, lung, overy and uterus Morphology: •Multiple Polyps in whole GIT •Arborizing network of smooth muscle extending into polyp and surrounds glands •Glands are lined by non-dysplastic epithelium rich in goblet cells Clinical Features: •Melanotic pigmentation in mucocutaneous areas (lips, perioral areas, face, genatalia, palms) |
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Clinical Features of Colonic Adenoma
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•Clinically most are asymptomatic
•May have features of anemia due to occult blood loss •Villous adenoma may present with hypokalemia and hypoproteinemia due to loss of electrolytes and proteins and fluid •Rarely intussusception •All are considered potentially malignant |
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Gardner's Syndrome
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FAP with:
•Multiple osteomas •Desmoid tumors •Epidermal cysts •Fibromatosis |
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Turcot's Syndrome
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FAP along with:
•CNS Gliomas |
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FAP
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•apc gene involved
•Over 100 polyps is magic number •Early age of presentation •Tubular polyps |
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Clinical Features of Colonic Carcinoma
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•Asymptomatic
•RIGHT SIDED: fatigue, weakness, iron deficiency anemia •LEFT SIDE: changed bowel habits •Iron deficiency anemia in elderly man is due to GI malignancy unless proven otherwise |
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Morphology of Colonic Carcinoma
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•Proximal Colon: obstructions and exophytic lesions uncommon
•Distal Colon: Annular, napkin-ring encircling constrictions. Apple core appearance on X-ray Microscopy: •Neoplastic glands invading submucosa and muscularis propria Spreads to regional lymph nodes, systemic liver, lung, bones |
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Morphology of HNPCC
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•aka Warthin Lynch Syndrome
•Mucinous histology •Increased number of tumor infiltrating lymphocytes Associated with carcinomas of biliary tract, endometrium, ovaries, stomach, small intestine |
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Morphology of Appendicitis
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•Edema
•Inflammation •Neutrophils |
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Clinical Features of Liver Disease
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•Right upper quadrant pain
•Anorexia •Yellowish discoloration of skin (Jaundice) •Pruritus •Fever •Mental confusion •Easy bruising |
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Signs of Liver Disease (Acute and Chronic)
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Acute:
•Icterus (Jaundice) •Hepatomegaly •Tenderness in right hyochondrium •Peripheral edema Chronic: •Splenomegaly •Palmar erythema •Spider angiomas •Gynecomastia and testicular atrophy •Dupuytren contracture •Parotid enlargement •Clubbing •White nails (leukonychia) •Muscle wasting |
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ALT and AST levels in alcoholic liver disease and viral hepatitis
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•Alcoholic liver disease: AST/ALT > 2
•Viral hepatitis: AST/ALT < 1 |
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General Morphological Features of Hepatic Injury
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1.Degenerations
a.Balloning degeneration- irregularly clumped cytoplasm b. Feathery degeneration- fine foamy cytoplasm because of detergent action of bile salts 2. Steatosis - macro and microvesicular 3.Necrosis: focal, bridging massive or submassive 4. Apoptosis- Councilman’s bodies/ Acidophil bodies 5. Inflammation- commonly caused by T cells 6. Regeneration – thickening of hepatocyte cords, mitosis and some disorganization 7. Fibrosis |
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Causes of Macro and Microvesicular Liver
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Macro:
•Alcohol •NASH •Malnutrition Micro: •Reye's Syndrome •Drugs •Acute Fatty Liver of Pregnancy |
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Morphology of Cirrhosis
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•Bridging fibrous septa
•Parenchymal nodules created by regeneration •Architectural disruption •Conversion of normal architecture into structurally abnormal nodules •No central vein •Liver becomes green-ish due to bile •Nodules of regenerative epithelium |
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Morphology of Pseudomyxoma peritonei
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▪ Entirely mucinous (No epithelium)
▪ Abundant mucin (Scant low grade neoplastic epithelium) ▪ Abundant malignant epithelial cells (Signet ring cells and infiltrating columnar epithelium) |
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Morphology of Alcoholic Liver Disease
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▪Hepatic steatosis
▪Alcoholic hepatitis (Inflammation and steatohepatitis) ▪Variable amount of fibrosis to cirrhosis ▪Mallory hyaline/ bodies (tangled skeins of intermediate filaments, seen as eosinophilic cytoplasmic inclusions) Alcoholic Cirrhosis: ▪Initially enlarged yellow fatty liver which progresses to fibrotic, fatty and shrunken ▪Mainly micronodular, macronodulesmay be formed at a later stage |
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Characteristics of Hemochromatosis
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▪Micronodular cirrhosis
▪Diabetes mellitus ▪Skin pigmentation Common in males, uncommon before age 40, increased Fe absorption |
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Morphology of Hemochromatosis in Heart, Skin, Pancreas
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Pancreas
▪Intensely pigmented ▪Diffuse interstitial fibrosis ▪Hemosiderin in both acinar and Islet cells ▪Diabetes mellitus Heart ▪Hemosiderin in myocardial fibres (Cariomyopathy) ▪Delicate interstitial fibrosis Skin ▪Slate gray coloration ▪Iron in dermal melanophages ▪Increased melanin production |
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Characteristic Findings in Wilson's Disease
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▪Presentation is rare before 6 years of age
▪Characterized by accumulation of toxic levels of Cu in Liver, Brain and Eyes Brain: ▪Deposited in basal ganglia Eyes: ▪Deposits of copper in Descemet’s membrane of corneal limbus a.k.a. Kayser Fleischer ring ▪In some sun flower cataracts Blood: ▪hemolysis (intravascular) ▪Heinz bodies |
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Morphology and Investigations for Wilsons Disease
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In liver variable morphology
• Fatty change • Acute hepatitis • Chronic hepatitis-Ultimately cirrhosis • Rarely massive necrosis • Glycogenated nuclei, see blank areas around nucleus because glycogen does not stain in H&E. Also seen in NASH. Investigations • Decreased serum ceruloplasmin levels • Increased hepatic Cu (>250μgm/gm dry weight of liver is diagnostic) • Increased urinary copper excretion |
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Morphology of Alpha-1 Antitrypsin Deficiency
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•Neonatal hepatitis with or without cholestasis
•Smoldering chronic inflammation •Cirrhosis at early age •PAS (+) granules •"constipated hepatocyte" - granules accumulate in cytosol of liver •Can lead to Hepatocellular carcinoma •Liver transplantation is the only treatment |
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Morphology of Primary Biliary Cirrhosis
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•Chronic, progressive and can progress to cirrhosis
•Non suppurative, granulomatous destruction of medium sized bile ducts •Death usually occurs because of liver failure •"Florid duct lesion" •Associated with primary biliary cirrhosis •Very high ALP, GGT, somewhat high ALT, AST •Edema, acute inflammation |
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Morphology of Primary Sclerosing Cholangitis
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ASSOCIATED WITH ULCERATIVE COLITIS
•Onion skin fibrosis that obstructs and does not permit bile flow •Beaded appearance of biliary tree •p-ANCA in 80% cases (p-ANCA is also in Churgh-Strauss syndrome) •Inflammation, fibrosis and dilatation of intra and extra hepatic ducts |
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Hepatoblastoma Clinical Presentation
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•Usually occurs at ~ 18 months (birth to 40 mths)
•Slight male predominance •Hepatomegaly or abdominal mass, jaundice rare •AFP elevated in 80-90% |
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Hepatoblastoma Morphology
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Epithelial:
▪Fetal (Small uniform cells in cords ▪Embryonal and fetal (Fetal components with sheets of round, fusiform cells. Arranged in rosettes, cords and ribbons) Combined epithelial-mesenchymal components ▪Epithelial with mesenchymal elements (Fibrous tissue. Osteoid or cartilaginous differentiation) |
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Liver Cell Adenoma Clinical Presentation
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Acute (about 50%, Mortality 20%) or Incidental (acute below):
▪ Pain abdomen ▪ Shock and hemorrhage (Hemorrhage into tumor or peritoneal cavity) ▪ Episodic pain or discomfort ▪Associated with birth control pills and anabolic steroids. ▪Can be malignant ▪Normal serum AFP!!! |
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Focal Nodular Hyperplasia in Liver Morphology
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▪Central scar that looks like whitish-like fibrosis
▪Can have no central vein with big scar ▪Hyperplasia of hepatocytes |
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Hepatocellular Carcinoma Morphology
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Can be Unifocal, Multifocal or Diffuse infiltrative
▪Are usually paler than surrounding hepatic parenchyma ▪Strong propensity for invading vascular channels (portal vein, IVC) ▪See 3-4 hepatocytes between sinusoids instead of just one ("3-4 cell liver plate") ▪Reticulin stain ▪Increased nuclear/cytosolic ratio ▪Cirrhosis in adjacent liver parenchyma Fibrolamellar Variant ▪Single hard tumor with fibrous bands through it ▪Well differentiated polygonal cells in cords/nests, separated by fibrous septae ▪Better prognosis ▪"Lamellar fibrosis with eosinophilic cytosol and pale bodies" |
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Clinical Features of HCC
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▪Usually younger patients, age 2=35 or less. Only one at young age.
▪Left side of liver ▪Ill defined upper abdominal pain, fatigue, cachexia ▪Raised alpha fetoprotein levels in 60-75% (markedly increased) |
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What kind of cancer is cholangiocarcinoma?
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adenocarcinoma of bile duct epithelium
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Morphology of Cholangiocarcinoma
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▪Extensive fibrosis
▪Adenocarcinoma ▪Cut surface - firm and gritty ▪Large bile duct proximal to stricture ▪aka "extrahepatic bile duct cancer" |
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Cholangiocarcinoma Clinical Symptoms
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▪Malaise
▪Weight loss ▪Jaundice ▪Cholangitis ▪Charcot’s triad: Jaundice, fever, chills ▪Reynold’s pentad:(Charcot) + hypotension, confusion ▪Clinically silent for long periods ▪More likely to spread beyond liver than HCC ▪Prognosis is poor: death within 6 months |
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Acute cholecystitis
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▪Pain right hypochondriumor epigastrium
▪May appear like surgical emergency ▪Associated fever, nausea and vomiting ▪Rarely jaundice if obstruction of CBD ▪Most patients recover ▪Pain |
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Morphology of Chronic Cholecystitis
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Rarely can see dystrophic calcification along walls of gall bladder, leading to "porcelain gall bladder"
(Increased risk of cancer) |
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Clinical Symptoms of Acute Pancreatitis
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▪Acute inflammation
▪Abdominal pain ▪Elevated pancreatic enzymes in serum ▪Self-limiting, if not fatal ▪Pain can vary from mild to very severe ▪Usually severe epigastric pain with nausea and vomiting ▪Constant, intense and is referred to upper back ▪Release of enzymes, toxins and cytokines in circulation leads to activation of systemic inflammatory response ▪Leucocytosis ▪DIC ▪Hemolysis ▪Peripheral vascular collapse shock with ATN, ARDS ▪Hypocalcemia, tetany ▪Raised amylase levels in first 24 hours ▪Followed by lipase with in 72-96 hours ▪Complications: ARDS, ATN, pancreatic abscess |
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Clinical Symptoms of Chronic Pancreatitis
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▪Chronic inflammation
▪Chronic abdominal pain ▪Progressive loss of pancreatic endocrine and exocrine function ▪Repeated attacks of moderately severe pain ▪Or persistent abdominal and back pain ▪Later on pancreatic insufficiency and diabetes may develop ▪Features of malabsorption, corrected by pancreatic enzyme supplements ▪Diagnosed by high degree of suspicion ▪X ray and CT- calcifications ▪Pseudocysts in 10% ▪Moderately increased risk of carcinoma (Alcohol) |
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Morphology of Acute Pancreatitis
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▪Focal areas of fat necrosis in pancreas and peripancreatic tissues and abdominal cavity
▪Ca++ deposition in these areas- appear radiopaque on radiographs ▪Severe cases–necrosis of pancreatic tissue (acini, ducts and islets) with hemorrhage (Hemorrhagic pancreatitis) |
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Clinical features of carcinoma of the pancreas
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▪Remain silent till late
▪Pain is usually first symptom (because of invasion posterior abdominal wall and nerves ▪Obstructive jaundice ▪Trousseau’s sign (migratory thrombophlebitis) in 10%(because of release of platelet activating factors and procoagulants from tumor and its necrotic products) ▪No single specific marker ▪Raised levels of CA 19-9 ▪Very bad prognosis |
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Morphology of Acinar Cell Carcinoma
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Subcutaneous fat necrosis and panniculitis due to lipase
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Morphology of Mucinous Cystic Neoplasms
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▪Tall columnar mucin secreting cells
▪Characteristic feature is ovarian type stroma |
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Morphology of Intra-ductal Papillary Mucinous Neoplasm
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▪Tall columnar mucin secreting cells
▪lack ovarian type stroma |
