1Explain Caries, Gingivitis, and Periodontitis
Dental Caries: Focal demineralization of enamel/dentin by bacterial acid (from sugar fermentation). Gingivitis: Reversible inflammation of gums/soft tissues due to plaque/calculus. Periodontitis: Irreversible destruction of periodontal ligament and alveolar bone; leading cause of tooth loss.
2Eplain the leukoplakia and erythroplakia lesions seen in the oral cavity ın terms of macroscopic and microscope aspect. Which lesion has a higher risk of malignant transformation (to squamous cell carcinoma) state the histopatholpgical reason for this.
Leukoplakia: White patch (cannot be scraped off). Micro: Hyperkeratosis to dysplasia. Erythroplakia: Red, velvety/eroded area. Micro: Severe dysplasia or Carcinoma in situ (CIS). Highest Risk: Erythroplakia (>50% malignant risk). Reason: Erythroplakia histopathologically shows much more advanced epithelial dysplasia than leukoplakia.
3Explain the two different pathways (risk factors) that play a role in the development of oral squamous cell carcinoma (SCC) and the relationship of these pathways with prognosis.
Pathway 1 (Tobacco/Alcohol): Associated with TP53 and p63 mutations. Prognosis: Poorer. Pathway 2 (HPV): Linked to HPV-16; shows p16 expression. Prognosis: Better.
4Give 3 examples each for the benign and malignant types of salivary gland tumors.
Benign: Pleomorphic adenoma, Warthin tumor, Oncocytoma. Malignant: Mucoepidermoid carcinoma, Adenoid cystic carcinoma, Acinic cell carcinoma.
5What are the most common benign and malignant tumors of the salivary glands? Explain the macroscopic and microscopic features of both.
Most Common Benign: Pleomorphic Adenoma. * Macro: Painless, slow-growing mass. Micro: Mixture of ductal/myoepithelial cells in a myxoid or chondroid (cartilaginous) matrix. Most Common Malignant: Mucoepidermoid Carcinoma. * Micro: Mix of squamous, mucus-secreting, and intermediate cells.
6What are the 3 oral Inflammatary lesions. Explain macroscopic.
Aphthous Ulcers: Shallow, painful ulcers with a yellow exudate and red rim. Herpetic Infections (HSV): Small vesicles that rupture to form shallow ulcers. Oral Candidiasis (Thrush): Gray-white "cheesy" membrane that can be scraped off to reveal a red base.
7Explain "Dentigerous Cyst" and "Periapical/Radicular Cyst" (inflammatory) in terms of their localizations, etiopathogenesis, and histopathological findings.
Dentigerous Cyst: Around the crown of an unerupted tooth (e.g., impacted wisdom tooth). Caused by follicle degeneration. Periapical (Radicular) Cyst: At the tooth apex. Caused by chronic inflammation (pulpitis) or necrosis.
8Explain the clinical symptoms and pathological findings of Reflux Esophagitis
Symptoms: Heartburn, dysphagia, sour regurgitation. Pathology: Mucosal injury/erythema caused by stomach acidile damaging the squamous epithelium.
9Explain the clinical symptoms and pathological findings of Barret Esophagitis. What is it reason. And which tumour develop at the background of the Barret Esophagitis.
Reason: Chronic GERD. Pathology: Intestinal Metaplasia (replacement of squamous cells by goblet cells). Tumor Risk: Increases risk of Esophageal Adenocarcinoma.
10Explain the underlings reasons of the peptic ulcer, Stress ulcers, Curling ulcers, and Cushing ulcers.
Peptic Ulcer: H. pylori infection or NSAID use. Stress Ulcers: Critically ill patients (shock/sepsis). Curling Ulcers: Proximal duodenum; associated with severe burns/trauma. Cushing Ulcers: Stomach/duodenum; associated with CNS injury (vagal stimulation —> high acid).
11What is the pathological cause of primary achalasia and secondary achalasia. Write the classic triad of pathophysiological and motility findings of Achalasia disease.
Pathology: Loss of inhibitory neurons in the myenteric plexus (Primary is idiopathic; Secondary is Chagas disease). Triad: 1. Incomplete LES relaxation. 2. Increased LES tone. 3. Esophageal aperistalsis.
12What are the defensive and offensive mechanisms of the stomach?
Defensive: Mucus layer, bicarbonate secretion, rich mucosal blood flow. Offensive: Gastric acid, pepsin, H. pylori, NSAIDs, alcohol.
13Compare Helicobacter pylori infection and Autoimmune Gastritis, in terms of their pathogenesis, clinical features, and characteristic properties.
H. pylori: Antrum-dominant, high acid, risk of Peptic Ulcers. Autoimmune: Body/Fundus-dominant, loss of parietal cells, Vitamin B12 deficiency (Pernicious anemia), high gastrin levels.
14Compare the microscopic and macroscopic features of "Intestinal type" and "Diffuse type" gastric adenocarcinomas.
Intestinal Type: Bulky/exophytic mass; Micro: Gland-forming cells. Diffuse Type: Thickened wall (Linitis plastica); Micro: Signet-ring cells (mucin pushes nucleus to the side).
15What are the 3 main complications of Chronic Gastritis.
Peptic ulcer disease. Mucosal atrophy and intestinal metaplasia. Epithelial dysplasia (cancer precursor).
16Where do carcinoid tumors located in the gastrointestinal tract originate from?
Origin: Neuroendocrine cells (like G-cells). Micro: Small uniform cells with a "salt-and-pepper" chromatin pattern; arranged in nests or trabeculae.
17Describe the microscopic structural features of the carcinoid tumors.
Patterns: Cells grow in nesting (organoid), trabecular, or insular arrangements. Cell Type: Small, uniform cells with round nuclei and moderate eosinophilic cytoplasm. Chromatin: Features a characteristic "salt-and-pepper" (finely granular) chromatin pattern. Markers: Cells are immunohistochemically positive for Chromogranin A and Synaptophysin.
18Explain the morphological, and clinical features of Gastrointestinal Stromal tumors.
Morphology: Spindle-shaped cells; originates from interstitial cells of Cajal. Clinical: Often associated with c-KIT (CD117) mutations.
19Explain what Hirschsprung's Disease is? Pathogenesis and treatment.
What: Congenital absence of ganglion cells in the colonic wall. Pathogenesis: Failure of neural crest cell migration. Treatment: Surgical resection of the aganglionic segment.
20What is the Abdominal Hernia and write down the types and complications.
Types: Inguinal, femoral, umbilical, or incisional. Complications: Incarceration (trapped) and Strangulation (loss of blood supply/infarction).
21Explain what Hemorrhoid is, and mention their grading system and treatment.
What: Dilated ****/perianal venous collaterals. Treatment: Sclerotherapy, rubber band ligation, or surgical removal.
22Write the effects of Cholera, C. Enterocolitis, Shigellosis, E. coli, and Salmonella pathogens on the enteric system individually.
Cholera: Secretory diarrhea ("rice-water" stools). C. jejuni: Common traveler’s diarrhea; may lead to Guillain-Barré. Shigella: Bloody diarrhea (dysentery). E. coli: ETEC (watery diarrhea); EHEC (O157:H7, bloody diarrhea/HUS). Salmonella: Nontyphoid (gastroenteritis); Typhi (Typhoid fever, "rose spots").
23Explain Ulcerative colitis and crohn Disease possible pathogenesis. Write histopathological findings.
Pathogenesis of IBD (UC and CD) Both result from inappropriate mucosal immune activation. The immune system reacts abnormally to the normal gut microbiota. External triggers such as stress, diet, and smoking (especially for CD) can reactivate the disease. Histopathological Findings Crohn Disease: Transmural inflammation involving the submucosa and serosa. Noncaseating granulomas (the hallmark). Haphazard crypt organization from repeated injury and regeneration. Ulcerative Colitis: Inflammation limited to the mucosa and submucosa only. Continuous involvement starting from the rectum. Absence of granulomas.
24Compare ulcerative colitis and Crohn's disease according to Table 15.5 (in terms of 10 characteristics).
Crohn’s (Deep & Patchy) Where: Skip lesions, Frequent Ileum, Sometimes Rectum. Wall: Transmural (full depth), Thickened, Creeping fat (fat wrapping). Injury: Deep knife-like ulcers, Common Strictures/Fistulas/Sinuses, No dilation. Micro: Granulomas (35%), Marked Lymphoid/Fibrosis/Serositis. Clinical: Yes Malabsorption, Common Recurrence, Increased Cancer Risk. Ulcerative Colitis (Surface & Continuous) Where: Continuous, Always Rectum, Rare Ileum (Backwash ileitis). Wall: Mucosal/Submucosal, Normal thickness, No fat wrapping. Injury: Superficial broad-based ulcers, Common Pseudopolyps, Toxic Megacolon (dilation). Micro: Absent Granulomas, Moderate Lymphoid, Minimal/Absent Fibrosis/Serositis/Fistulas.
25 24) What are Colonic Polyps, write their types.
Non-neoplastic: Inflammatory, Hamartomatous (e.g., Juvenile), and Hyperplastic. Neoplastic (Adenomas): Tubular, Villous (highest risk), and Sessile serrated.
26Explain the clinical significance of serological markers (HBsAg, HBeAg, Anti-HBc IgM/IgG, Anti-HBs) detected in the blood during the course of Hepatitis B virus (HBV) infection and their predictive roles in the development of chronicity.
HBsAg (Surface Antigen): First marker; means infection is present. HBeAg (Envelope Antigen): Means active replication and high infectivity. Anti-HBc IgM: Means acute infection (recent). Anti-HBc IgG: Means past or chronic infection. Anti-HBs: Means immunityecovery (after infection or vaccine). Chronicity Prediction: Definition: HBsAg persists for >6 months. Risk: The younger the patient (e.g., infants), the higher the risk of becoming chronic.
273 List and define the types of liver failure.
Acute Liver Failure: Encephalopathy (brain dysfunction) within 6 months of injury. Fulminant: Within 2 weeks of jaundice. Sub-fulminant: Within 3 months of jaundice. Chronic Liver Failure: Slow progression; usually the end-stage of Cirrhosis. Acute-on-Chronic: Sudden, life-threatening crash in a patient with stable chronic disease.
28Draw the histological structure of the liver. Indicate the directions of blood flow and bile flow. Label the components of the structure.
Unit: Hexagonal Lobule. Center: Central vein. Periphery: Portal Triad (Hepatic Artery, Portal Vein, Bile Duct). Blood Flow: From Periphery →→ Center (Triad to Central Vein). Bile Flow: From Center →→ Periphery (Canaliculi to Bile Duct). Key Cells: * Hepatocytes: Form plates/sheets. Kupffer Cells: Specialized macrophages in sinusoids. Stellate Cells: Store Vitamin A; cause fibrosis when activated.
29Detail the types of necrosis in the liver along with their morphological findings.
Centrilobular (Zone 3): Necrosis around the central vein (Ischemia/Acetaminophen).
Periportal (Zone 1): Necrosis near portal tracts (Toxins).
Mid-zonal (Zone 2): Necrosis between zones (Yellow fever).
Interface (Piecemeal): Erosion of hepatocytes at the portal tract edge (Autoimmune Hepatitis).
Bridging: Necrotic bands linking portal-to-portal or portal-to-central areas.
Massive: Complete collapse of lobules or the entire liver.
30Write the manifestations of acute liver failure.
Jaundice: Yellowing of skin and sclera. Hepatic Encephalopathy: Brain dysfunction (confusion to coma) due to toxin buildup. Coagulopathy: Easy bleeding; high PT/INR (liver cannot make clotting factors). Cerebral Edema: Brain swelling; the most common cause of death.
31Write the manifestations of chronic liver failure.
Portal Hypertension: Leads to Ascites (fluid in belly), Esophageal Varices, and Splenomegaly. Hyperestrogenism: Spider angiomas, palmar erythema, and gynecomastia (in males). Hypoalbuminemia: Leads to peripheral edema.
32Discuss the pathogenesis of hepatic encephalopathy.
The liver fails to clear Ammonia (\$NH_3\$) (produced by gut bacteria). Ammonia crosses the Blood-Brain Barrier. High ammonia causes Astrocyte swelling and neurotoxicity, leading to cognitive impairment and coma.
33Write the clinical and laboratory findings of the Hepatitis B carrier state.
Clinical: Asymptomatic; patient feels healthy but is infectious. Laboratory: HBsAg (+) for >6 months, Anti-HBs (-), and Normal ALT/AST (no active liver cell damage).
34Write the clinical and laboratory findings of autoimmune hepatitis, and describe the morphological findings observed in liver biopsy.
Clinical/Lab: Mostly females; ANA (Antinuclear) or ASMA (Anti-smooth muscle) antibodies (+); High IgG levels. Morphology: Plasma cell infiltrates and Interface hepatitis (piecemeal necrosis).
35Write the patterns of liver injury caused by drugs or toxins.
Predictable: Dose-dependent (e.g., Acetaminophen causing Zone 3 necrosis). Idiosyncratic: Unpredictable; host-dependent (e.g., Isoniazid). Patterns: Steatosis, Cholestasis, Hepatitis, or Massive Necrosis.
36What are the morphological findings of alcoholic liver disease?
Steatosis: Reversible macrovesicular fat accumulation. Alcoholic Hepatitis: Hepatocyte ballooning, Mallory-Denk bodies (tangled protein), and Neutrophil infiltrate. Cirrhosis: Final, irreversible micronodular stage.
37Write the hereditary metabolic liver diseases along with their causes.
Hemochromatosis: HFE gene mutation --> Iron overload.
Wilson Disease: ATP7B gene mutation--> Copper overload (Kayser-Fleischer rings).
Alpha-1 Antitrypsin (A1AT) Deficiency: Protein misfolding --> Cirrhosis + Lung emphysema.
38What are the causes of non-alcoholic fatty liver disease (NAFLD)?
Associated with Metabolic Syndrome: Obesity Type 2 Diabetes Mellitus Dyslipidemia (High triglycerides) Insulin resistance
39List the liver diseases that cause cholestasis
Primary Biliary Cholangitis (PBC). Primary Sclerosing Cholangitis (PSC). Biliary Atresia (Neonatal). Choledocholithiasis (Stones in the bile duct).
40Compare Primary Biliary Cholangitis (PBC) and Primary Sclerosing Cholangitis (PSC) in terms of the bile duct diameters they affect, associated autoantibodies, and radiological appearances.
PBC: Small intrahepatic ducts; AMA antibody (+); Normal radiology.
PSC: Large and small ducts; p-ANCA antibody (+); "Beaded" radiology.
41List the hereditary hyperbilirubinemia disorders and explain their mechanisms.
Gilbert: Decrease UGT1A1; mild/stress jaundice (Unconjugated).
Crigler-Najjar: Zero UGT1A1; fatal (Unconjugated).
Dubin-Johnson: MRP2 defect; Black Liver (Conjugated).
Rotor: OATP defect; similar, no black liver (Conjugated).