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Pathology II > GI Pathology > Flashcards

GI Pathology Flashcards

(105 cards)

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1
Q

Pathologies of the GI tract

A
  • Esophagitis (GERD)
  • Acute and Chronic Gastritis
  • Peptic Ulcer Disease
  • Malabsorption Syndromes
  • Idiopathic Inflammatory Bowel Disease (Chron’s, Ulcerative Colitis)
  • Colon Cancer
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2
Q

Pathology and infections of the liver

A
  • Jaundice
  • Viral hepatitis
  • Cirrhosis
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3
Q

Pathology of the exocrine pancreas

A
  • Acute and chronic pancreatitis

- Tumors of the pancreas

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4
Q

Esophagitis

A
  • Inflammation of esophageal mucosa
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5
Q

Gastric juices influence in GERD

A
  • The action of gastric juices is critical to the development of esophageal mucosal injury
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6
Q

Reflux Esophagitis

(Gastroesophageal Reflux Disease / GERD) causative factors

A
  • Decreased LES tone
  • Hiatal Hernias
  • Central nervous system depressants
  • Hypothyroidism
  • Pregnancy
  • Alcohol or tobacco exposure
  • Presence of a sliding hiatal hernia
  • Delayed gastric emptying and increased gastric volume
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7
Q

GERD complications

A
  • Hyperkeratosis
  • Erosion
  • Ulceration
  • Stricture
  • Barrett Esophagitis
  • Adenocarcinoma
  • Bad taste
  • Pneumonitis
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8
Q

Chronic GERD complications

A
  • Barrett’s Esophagitis
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9
Q

Barrett’s Esophagitis causative factors

A
  • Gastroesophageal reflux (GERD)

- Distal squamous mucosa is replaced by metaplastic columnar epithelium

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10
Q

Barrett Esophagitis diagnostic criteria

A
  • Endoscopic evidence of columnar epithelial lining above the gastroesophageal junction
  • Histologic evidence of intestinal metaplasia in the biopsy specimens from the columnar epithelium
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11
Q

Barrett Esophagitis clinicopathologic concern

A
  • Dysplasia within areas of intestinal metaplasia

Precursor of Adenocarcinoma

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12
Q

Etiologies of infectious and chemical esophagitis

A
  • Alcohol
  • Corrosive acids
  • Heavy smoking
  • Cytotoxic anticancer therapy
  • Uremia in the setting of renal failure
  • Infection following bacteremia or viremia
  • Fungal infection
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13
Q

Morphology of chemical esophagitis

A
  • Necrosis
  • Ulceration
  • Fibrosis
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14
Q

Malignant tumors of the esophagus

A
  • Squamous Cell Carcinoma

- Adenocarcinoma

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15
Q

Squamous cell carcinoma of the esophagus

A
  • Most common malignancy of the esophagus
  • Occur in adults over age 50
  • US / a disease of adult males
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16
Q

Esophageal squamous cell carcinoma etiology and pathogenesis

A
  • Dietary
  • Environmental
  • Genetic factors
  • Mutagenic compounds (alcohol, tobacco)
  • Alcoholic drinks contain carcinogens
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17
Q

Carcinogens in alcoholic drinks

A
  • Polycyclic hydrocarbons

- Fuel oils and nitrosamines

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18
Q

Esophageal squamous cell carcinoma morphology

A
  • Begin as intraepithelial neoplasm or carcinoma in situ (CIS)
  • Early lesions (small, gray-white, plaque-like elevations)
  • Lesions become tumorous masses that can encircle the lumen (months to years)
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19
Q

Three morphological patterns of esophageal squamous cell carcinoma

A
  • Protruding (60%)
  • Flat (15%)
  • Excavated (25%)
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20
Q

Esophageal squamous cell carcinoma clinical features

A
  • Dysphagia
  • Weight loss
  • Hemorrhage
  • Obstruction
  • Difficulty in swallowing
  • Aspiration
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21
Q

Esophageal adenocarcinoma

A
  • Glandular differentiation in Barrett mucosa
  • Risk factors: tobacco and obesity
  • Helicobacter pylori infection
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22
Q

Esophageal adenocarcinoma evolution

A
  • Squamous
  • Esophagitis
  • Barrett
  • Dysplasia
  • Carcinoma
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23
Q

Esophageal adenocarcinoma morphology

A
  • Distal esophagus
  • Early lesions (flat or raised patches of intact mucosa)
  • Later (large infiltrative, nodular masses)
  • Mucin-producing glandular tumors
  • Intestinal-type features
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24
Q

Esophageal adenocarcinoma clinical features

A
  • > 40 (median age 60)
  • More common in men
  • Difficulty swallowing
    progressive weight loss
  • Bleeding, chest pain, vomiting
  • Prognosis is poor
  • Regression may occur with low-grade dysplastic lesions
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25
Acute gastritis
- Inflammation of the Gastric Mucosa | - Predominant neutrophilic infiltrate (usually transient)
26
Chronic gastritis
- Chronic mucosal inflammatory changes - Mucosal atrophy - Epithelial metaplasia - Absence of erosions
27
Acute gastritis pathogenic factors/damaging forces
- Heavy NSAID use - High EtoH consumption - Heavy smoking - Severe stress - Uremia
28
Chronic gastritis pathogenic factors/damaging forces
- Helicobacter pylori - Gastric hyperacidity - Autoimmune - EtoH
29
Acute gastritis pathology
- Intact Epithelium - Neutrophils - Superficial Erosion (severe) - Clinically presents asymptomatic to severe
30
H. pylori
- Gram neg. rod - Motile - Urease - Superficial colonization (adhesin) - Invasion
31
Symptoms associated with H. pylori chronic gastritis
- Inflammation - Mucosal changes - Metaplasia - Regeneration - Dysplasia
32
Ulcer
- Breach in the mucosa of the alimentary tract | - Extends through the muscularis mucosae into the submucosa or deeper
33
Stomach histology (layers)
- Mucosa - Muscularis mucosa - Submucosa - Muscle layer
34
Peptic Ulcer Disease (PUD)
- Gastroduodenal mucosal defense mechanisms (imbalance) | - Damaging forces
35
Peptic Ulcer Disease biological factors
- > 30yrs and older - Higher DU in blood grp O - Higher DU in EtoH cirrhosis - M:F DU 3:1 GU 2:1 - Decreasing frequency
36
Peptic Ulcer Disease locations
- Duodenum (1st portion) - Stomach (body/antrum/lesser) curvature - GE junction
37
H. pylori virulence factors
- Protease - Phospholipase - Inflammation - Neutrophil sequestration - Mucosal damage (nourishment for H. pylori)
38
Factors increasing Peptic Ulcer Disease risk
- NSAIDs - Tobacco - EtoH - Steroids
39
Duodenal ulcer factors
- Acid hypersecretion | - Rapid gastric emptying
40
Duodenal ulcer clinical]
- Pain after meal | - Relieved by food, milk antacids
41
Gastric ulcer clinical]
- Pain after meal | - Not relieved by food
42
Duodenal/gastric ulcer complications
- Hemorrhage (both) - Perforation (both) - Obstruction (DU) - Malignant change (GU)
43
Chron Disease
- Relapsing - Inflammatory - Granulomatous disease - Esophagus to anus - Often involves the small intestine and colon - Extraintestinal inflammatory manifestations
44
Extraintestinal inflammatory manifestations in Chron Disease
- Migratory polyarthritis - Pyoderma gangrenosum - Sacroiliitis - Ankylosing spondylitis
45
Chron disease pathological manifestations
- Skip lesions - Linear ulcers - Cobblestone appearance - Transmural inflammatory process with mucosal damage - Noncaseating granulomas - Fissuring with fistulas
46
Chron Disease clinical presentation
- Steatorrhea - Pernicious anemia - Stricture formation - Intestinal obstx - Fistula formation - CA
47
Chron Disease complication
- Toxic megacolon
48
Ulcerative Colitis
- Relapsing - Inflammatory - Non-granulomatous - Limited to colon - Extraintestinal inflammatory manifestations
49
Ulcerative Colitis pathological characteristics
- Ulceroinflammatory Disease (mucosa, submucosa) - Continuous extension from rectum - No granulomas
50
Ulcerative Colitis complications
- Pseudopolyps - Friable mucosa - Serosa not involved - Backwash ileitis - Toxic megacolon
51
Ulcerative Colitis microscopic presentation
- Mononuclear inflammatory cell infiltrate - Crypt abscesses - Submucosal fibrosis - Dysplasia
52
Ulcerative Colitis clinical features
- Bloody mucoid diarrhea | - Tenesmus
53
Colorectal carcinoma polyps morphological types
- Hyperplastic Polyps | - Adenomatous Polyps
54
Hyperplastic polyps (colorectal carcinoma)
- Abnormal mucosal maturation - Inflammation - Architecture - No malignant potential
55
Adenomatous polyps (colorectal carcinoma)
- Epithelial proliferation - Exhibit dysplasia - Precursors of carcinoma
56
Adenomatous polyps precursors of carcinoma
- Tubular adenomas: tubular glands - Villous adenomas: villous projections - Tubulovillous adenoma: mixture of the above
57
Adenoma --> Carcinoma sequence supporting evidence
- Similar distribution patterns (between adenomas and colorectal cancer) - Invasive carcinoma surrounded by adenomatous tissue
58
Colorectal carcinoma molecular pathogenesis
- Abnormalities in tumor suppressor genes - Genes responsible for repairing DNA - Structural changes in DNA - Activation of oncogenes - Loss of cell cycle regulator genes
59
Colorectal cancer etiology and epidemiology
- Peak 60 to 79 - Highest death rate - USA - Excess energy intake - Diet low in fiber - Diet high in carbohydrates - Red meat
60
Colorectal carcinoma distribution
- High percentage in the sigmoid colon
61
Colorectal carcinoma proximal tumors
- Polypoid - Exophytic - No obstruction - Easily bleed - Fecal occult blood - Anemia
62
Colorectal carcinoma distal tumors
- Annular - Encircling - Napkin ring constriction - Change in bowel habits - Hematochezia
63
Colorectal carcinoma microscopic findings
- Adenocarcinoma - Differentiation - Can produce mucin - Invasive - Desmoplastic
64
Colorectal carcinoma clinical/diagnosis
- Asymptomatic - Occult blood in stool - Fe Deficiency - Barium study - Colonoscopy - Biopsy - Carcinoembryonic antigen (CEA)
65
Astler-Collier Classification for colorectal cancer
- Stg A - 100% 5yr survival | - Stg C2 - 23% 5yr survival
66
Hepatobiliary tree anatomy
- Bile Canaliculi - Bile Ductules - Bile Duct - Intrahepatic Ducts - L and R hepatic Ducts - Common Bile Duct
67
Hepatic panel
- SGOT (AST) - SGPT (ALT) - Alkaline Phosphatase - GGT - Serum Bilirubin (total, direct, indirect)
68
Jaundice
- The equilibrium between bilirubin production and clearance is disturbed - Unconjugated bilirubin (Insoluble) - Conjugated bilirubin (Soluble)
69
Unconjugated bilirubin (insoluble)
- Tightly complexed to Serum Albumin | - Not excreted in urine
70
Conjugated bilirubin (soluble)
- Loosely bound to Serum Albumin | - Excreted in urine
71
Causes of jaundice
- Overproduction - Reduced uptake - Impaired conjugation - Excretion impaired - Obstruction
72
Jaundice versus Icterus
- Jaundice = yellow discoloration of the skin | - Icterus = yellow discoloration of the sclerae (retention of pigmented bilirubin)
73
Neonatal jaundice levels
- [UC Bilirubin] < 2mg/dL | - [Serum Bilirubin] < 12 to 15mg/dL
74
Neonatal jaundice causes
- Immature conjugating machinery | - Transient unconjugated hyperbilirubinemia
75
Kernicterus
- Hemolytic disease of the newborn
76
Kernicterus serum UC bilirubin levels
- Serum UC bilirubin > 20 mg/dL
77
Jaundice serum UC bilirubin levels
- Serum UC Bilirubin > 2.0 to 2.5 mg/dL
78
Hereditary hyperbilirubinemias
- Crigler-Najjar Syndrome Type I - Crigler-Najjar Syndrome Type II - Gilbert Syndrome - Dubin-Johnson Syndrome
79
Cirrhosis of the liver
- Bridging fibrous septa - Parenchymal nodules - Total disruption of liver architecture
80
Liver cirrhosis etiology
- EtoH ingestion - Chronic Viral Hepatitis - Primary Biliary Cirrhosis - Extrahepatic biliary obstruction - Hemochromatosis - Wilson’s Disease - Cystic Fibrosis
81
Central pathogenic process in cirrhosis
- Progressive fibrosis
82
Major source of excess collagen in cirrhosis
- Perisinusoidal hepatic stellate cell
83
Pathogenesis of liver cirrhosis
- Perisinusoidal hepatic stellate cell - Inflammatory mediators - Cytokines - Disruption of extracellular matrix - Toxins (EtOH)
84
Components of Alcoholic Liver Disease
- Acetaldehyde - Ethanol - Lipid Accumulation - Cell membrane damage - Cellular component damage
85
Pathogenesis of alcoholic liver disease
- Interrelationships vs normal liver - Hepatic Steatosis - Alcoholic Hepatitis - Alcoholic Cirrhosis
86
Liver cirrhosis major clinical features
- Hepatorenal Syndrome - Hepatic Encephalopathy - Ascites - Splenomegaly
87
Liver cirrhosis general features
- Hypoalbuminemia - Gynecomastia - Spider Angiomata
88
Pathology of the Exocrine Pancreas
- Acute and Chronic Pancreatitis | - Tumors of the Pancreas
89
Acute pancreatitis is characterized by
- Acute onset of abdominal pain resulting from enzymatic necrosis and inflammation of the pancreas
90
Acute pancreatitis pathogenesis (EtOH)
- Pancreatic Duct Obstruction - Duct obstruction / edema - Blood flow impairment - Ischemia develops - Enzyme release upon acinar cells - Tissue damage results
91
Primary acinar cell injury
- Alcohol activation intracellular or extracellular enzymes - Tissue damage - Defective intracellular transport of proenzymes within acinar Cells - Defect in lysosomal enzyme packaging
92
Acute pancreatitis etiology
- EtOH
93
Acute pancreatitis patholoy
- Interstitial edema - Hemorrhage - Parenchymal necrosis - Fat necrosis
94
Acute pancreatitis clinical presentation
- Increases in serum lipase and amylase - DIC - Fluid sequestration - Respiratory distress syndrome - Peripheral vascular collapse - Shock - Acute renal tubular necrosis
95
Chronic pancreatitis is characterized by
- Repeated bouts of mild to moderate pancreatic inflammation, with continued loss of pancreatic parenchyma and replacement by fibrous tissue
96
Chronic pancreatitis etiology
- EtOH consumption | - Hyperlipidemia
97
Chronic pancreatitis pathology
- Ductal obstruction/stones - EtoH oxidative stress / necrosis - Interstitial fibrosis
98
Chronic pancreatitis clinical presentation
- EtOH - Abdominal pain - Jaundice - Pseudocyst - Mild increased amylase, lipase - Calcification
99
Pancreatic cancer risk factors
- Cigarette smoking - EtoH - Chronic pancreatitis
100
Pancreatic cancer progression
- Non-neoplastic epithelium to invasive carcinoma | - Precursor Lesions: “Pancreatic Intraepithelial Neoplasias” (PanIN)
101
Molecular pathology of pancreatic cancer
- p53 Tumor Suppressor Gene Inactivation
102
Pancreatic cancer morphology
- Adenocarcinomas - Secrete mucin - Desmoplastic reaction - Grey-white gritty tissue mass - Infiltrate
103
Pancreatic cancer clinical presentation
- Courvoisier Sign (Palpable distended gallbladder) - Trousseau Sign (Migratory Thrombophlebitis) - Metastasis
104
Pancreatic cancer diagnosis
- Computed topography scan (CT scan) | - Tumor markers (CEA, C19-9)
105
Green discoloration of skin is possible if
- Biliverdin can spill over into circulation from the RES

Pathology II (7 decks)

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