Oral Cavity & Esophagus

1. Dental & Gingival Disease

 Caries: bacterial acid → enamel/dentin demineralization.
o Fluoride → fluoroapatite → resistant to degradation by bacterial
acids.
o caused by acids generated during the fermentation of sugars by
bacteria.
 Gingivitis: plaque (biofilm of bacteria + proteins + cells) →
calculus(tartar) → inflammation.
o Reversible with hygiene.
 Periodontitis: deeper inflammation → ligament, bone, cementum
destruction → tooth loss.
 Facultative Gram-positive organisms are found at healthy sites, while
anaerobic and microaerophilic Gram-negative bacteria colonize plaque
within areas of active periodontitis
o Pathogens: Aggregatibacter actinomycetemcomitans,
Porphyromonas gingivalis, Prevotella intermedia.

2. Oral Inflammatory Lesions

 Aphthous ulcers (canker sores): painful, recurrent, associated
with IBD, celiac, Behçet.
 Most Common superficial mucosal ulcerations
 they are shallow, with a hyperemic base covered by a thin exudate and
rimmed by a narrow zone of erythema.
 HSV infection:
o Primary (children, gingivostomatitis).
o Reactivation (stress, trauma, UV, immunosuppression).
o Lesions: grouped vesicles common at (labialis, nasal
orifices,palate, gingiva).
 Oral candidiasis (thrush): Candida albicans.
o Risk: immunosuppression, diabetes, antibiotics,specific
strains of candida.
 o Pseudomembranous form: white curdlike membrane, scraped
off → erythematous base and hyperplastic

3. Oral Neoplastic Lesions

 Fibroma: benign reactive hyperplasia due to chronic irritation.
 Pyogenic granuloma: inflammatory/vascular lesion, pregnancy
tumor. Histologically -proliferation of immature vessels
 Leukoplakia: white patch, cannot be scraped → precancerous (5–
25% dysplastic).
 Erythroplakia: red, velvety, higher malignant risk than
leukoplakia.
 tobacco –mc cause for both
 Squamous cell carcinoma (SCC):
o 95% oral cancers.
o Risk: tobacco, alcohol, HPV-16.

2 types

o 1) exposure to carcinogen –mutation of TP53 and genes that

regulate cell proliferation, such as RAS. stems from chronic alcohol
and tobacco
o 2) HPV associated- overexpress p16, a cyclin-dependent kinase
inhibitor.,better prognosis.
o Concept: field cancerization ??→ multiple primaries.

4. Salivary Gland Disorders

 Xerostomia: dry mouth ,reduced or absent salivary gland(Sjögren,
radiation, drugs). → can cause -caries, candidiasis.
 Sialadenitis: inflammation.
o Viral: mumps (parotid),complication in adults - orchitis,
pancreatitis,sterility).
 oBacterial: (submandibular)S. aureus, S. viridans (often after
obstruction).by [Link] and [Link].
 Mucocele: duct rupture → saliva leakage → lower lip swelling.
 Neoplasms:
o Pleomorphic adenoma (benign, mixed epithelial (ductal)+
mesenchymal(myoepithalial),mc-site parotid, recurrence if
incomplete excision). Carcinoma arise from it is called
Carcinoma ex pleomorphic adenoma (aggressive, high
mortality).
o Mucoepidermoid carcinoma (most common malignant
salivary tumor; variable mixtures of squamous cells, mucus-
secreting cells, and intermediate cells
o Parotid tumors common but usually benign; sublingual
tumors rare but malignant.

5. Odontogenic Cysts & Tumors

derived from remnants of odontogenic epithelium present within the jaws

 Dentigerous cyst: around unerupted tooth crown. result of

degeneration of the dental follicle
 Odontogenic keratocyst: posterior mandible, locally aggressive,
high recurrence.
 Periapical cyst: inflammatory at tooth apex, due to pulpitis
(caries/trauma).
 Ameloblastoma: locally invasive, indolent.
 Odontoma: most common odontogenic tumor, deposits
enamel/dentin, cured by excision.
 “Dentigerous = crown, Keratocyst = mandible, Periapical =
apex.”

Esophagus
6. Esophageal Mechanical Obstruction
  Atresia/fistula: congenital, regurgitation at birth, aspiration risk.
 Stenosis: can be congenital or acquired (GERD, caustics,
radiation).
 Functional obstruction (achalasia):
o Triad: ↑ LES tone, incomplete relaxation, aperistalsis.
o Primary: idiopathic (loss of inhibitory neurons).
o Secondary: Chagas disease (T. cruzi destroys myenteric
plexus). � Achalasia = “Bird’s beak” on barium swallow.

7. Esophageal Varices
 Portal HTN → collateral veins dilate in distal esophagus.
 50% cirrhotics develop varices.
 Rupture → massive hematemesis, 50% mortality first bleed.

8. Esophagitis
 Mallory-Weiss tears: mucosal lacerations at GE junction, after
severe vomiting → hematemesis.
 Boerhaave syndrome: transmural rupture → mediastinitis,
catastrophic.
 Chemical injury: alcohol, hot fluids, pills (bisphosphonates,
doxycycline).
 Infectious: HSV (punched-out ulcers), CMV (shallow ulcers,
nuclear/cytoplasmic inclusions), Candida (white
pseudomembrane). �Mallory-Weiss = mucosal, Boerhaave = full
thickness.

9. GERD & Barrett Esophagus

 GERD: reflux due to ↓ LES tone or ↑ abdominal pressure (obesity,
pregnancy, alcohol, tobacco).
o Symptoms: heartburn, regurgitation, dysphagia, chest pain.
o Complications: ulcer, stricture, Barrett esophagus.
  Barrett esophagus: intestinal metaplasia (goblet cells) in distal
esophagus.
o Risk: adenocarcinoma.
o Surveillance with biopsy for dysplasia. Mnemonic: “Barrett
= Goblet cells in esophagus.”

10. Esophageal Tumors

 Adenocarcinoma:
o Arises from Barrett + GERD.
o Distal esophagus.
o Risk: obesity, tobacco, radiation.
o Histology: mucin-producing glands.
 Squamous cell carcinoma:
o Risk: alcohol, tobacco, poverty, caustics, achalasia,
Plummer-Vinson, hot drinks.
o Location: middle third (50%).
o Spread: upper → cervical nodes; middle → mediastinal;
lower → gastric/celiac.
o Clinical: dysphagia, weight loss, cachexia, hemorrhage.
Mnemonic: “Adeno = Acid reflux, Squamous = Smoking +
Spirits.”

keys
 Dental triad: Caries → Gingivitis → Periodontitis.
 Oral precancer: Leukoplakia (white), Erythroplakia (red, riskier).
 Salivary tumors: Parotid = benign, Sublingual = malignant.
 Achalasia triad: ↑ LES tone, ↓ relaxation, aperistalsis.
 Varices: portal HTN → fatal bleed.
 Esophagitis: Mallory-Weiss (mucosal), Boerhaave (transmural).
 Barrett: goblet cells → adenocarcinoma risk.
 Esophageal cancer Adeno = distal, GERD; Squamous = middle,
alcohol/tobacco.
Small & Large Intestines
1. Congenital Anomalies
 Meckel’s diverticulum
 Most common congenital anomaly of GIT
o Failure of vitelline duct involution → true diverticulum.
o Rule of 2’s: 2% population, 2 inches long, within 2 feet of
ileocecal valve, presents before age 2.
o Complications: bleeding, ulceration (ectopic gastric mucosa),
intussusception, perforation.
 Hirschsprung disease (Congenital aganglionic megacolon)
o Arrest of neural crest migration → aganglionosis (no
ganglion cells in submucosa/myenteric plexus).
o Always involves rectum → proximal colon dilates
(megacolon).
o Clinical: neonate fails to pass meconium, constipation, risk of
enterocolitis, perforation.
o Genetics: RET mutations.

2. Enterocolitis & Diarrhea

 Diarrhea types
o Secretory (isotonic,persists with fasting): cholera, rotavirus,
villous adenoma.
o Osmotic (abates with fasting): lactase deficiency, laxatives,
lactulose therapy.
 o Exudative (bloody, purulent, persists with fasting): Shigella,
Salmonella, IBD.
o Motility disorders: surgical shortening, hypermotility or
hypomotility.

� Exam trick: If diarrhea stops with fasting → osmotic. If it *continues

→ secretory/exudative.

3. Malabsorption Syndromes
 Hallmark: steatorrhea (bulky, greasy stools).
 Causes:
o Defective digestion: pancreatic insufficiency.
o Mucosal defects: celiac disease, disaccharidase deficiency.
o Reduced surface area: Crohn’s, surgical resection.
o Lymphatic obstruction: lymphoma, TB.
o Infections: tropical sprue, Whipple disease.
 Celiac disease
o Gluten → immune reaction (anti-TTG, anti-gliadin,
anti-endomysial antibodies).
o Histology: villous atrophy, crypt hyperplasia, intraepithelial
lymphocytosis.
o Complications: ↑ risk of T-cell lymphoma & small bowel
adenocarcinoma
o Most common cause of malabsorption in developed country
o Child failure to thrive,abdominal distension and severe
diarrhea
 Lactase deficiency
o Congenital (rare, autosomal recessive) → explosive watery
diarrhea after milk.
o Acquired (common in African, Asian, Native American
populations).
o Stops when milk avoided.

4. Infectious Enterocolitis
  Cholera (Vibrio cholerae)
o Toxin → ↑ cAMP → chloride secretion → massive watery
diarrhea (“rice-water stools”).
o Can reach 1 L/hour → shock, death if untreated.
o Mortality 50–70% untreated, but fluid replacement saves
>99%. �Secretory diarrhea prototype.

5. Idiopathic Inflammatory Bowel Disease (IBD)

 Crohn disease (CD)
o Anywhere GI tract, esp. terminal ileum & colon.
o Transmural inflammation, skip lesions, cobblestone mucosa,
creeping fat,stricture
o Histology: non-caseating granulomas (50%).
o Complications: fistulas, strictures, malnutrition, ↑ cancer risk.
Mnemonic: “Crohn’s = Cobblestone, Creeping fat, Cracks
(fissures), Cancer risk.”
 Ulcerative colitis (UC)
o Limited to colon & rectum, continuous lesions.
o Mucosa & submucosa only.
o Features: bloody diarrhea, crypt abscesses, pseudopolyps,
toxic [Link],lower abdominal pain releaved by
defecation
o Complication: ,pancolitis,colorectal carcinoma. Primary
sclerosis cholangitis(beading of f bile duct)

�Key distinction: CD = skip lesions, transmural, granulomas. UC =

continuous, mucosal, no granulomas.

6. Vascular Disorders
 Ischemic bowel disease
o Causes: arterial thrombosis, embolism, venous thrombosis,
hypoperfusion (shock, CHF,MI).
 o Severity: mucosal → mural → transmural infarction(if major
mesenteric vessel).
o Acute occlusion : celiac, superior mesenrtic or inferior mesentric => infarction
of several meters of intestine
o Clinical: severe abdominal pain, bloody diarrhea,
[Link] peristaltic sound(due to paralytic ileus)
o Mortality: 50–75%. Mnemonic: “3 layers of infarction:
Mucosa → Mural → Transmural.”

�Hemorrhoids
 Definition: Variceal dilations of the anal and perianal venous plexuses.
 Causes/Predisposing factors:
o Elevated venous pressure (constipation with straining, pregnancy).
o Portal hypertension (collateral venous channels).

May reflect collateral anastomatic channels as a result of portal hypertension

 Types:
o Internal hemorrhoids: Superior hemorrhoidal plexus, above anorectal line.
o External hemorrhoids: Inferior hemorrhoidal plexus, below anorectal line.

o Thin-walled, dilated submucosal varices protruding beneath mucosa.
o Pain, bleeding, swelling.
o Complications: ulceration, infection, thrombosis, strangulation.

� Diverticular Disease
 Definition: Blind pouch leading off GI tract, lined by mucosa communicating with
lumen.
 Types:
o Congenital diverticula: All three layers present (Meckel diverticulum).
o Acquired diverticula: Usually lack muscularis propria (common in sigmoid
colon).
o Rare under age 30.
o Common in left colon, especially sigmoid.
o Multiple diverticula → diverticulosis.
o Small, flask-like outpouchings (0.5–1 cm).
 Pathogenesis:
o Focal weakness in colonic wall + increased intraluminal pressure.
o Exaggerated peristaltic contractions.
o Low-fiber diet → reduced stool bulk → increased peristaltic activity.
o sensation of never being able to completely empty the rectum
7. Intestinal Obstruction
Small intestine most often involved

 Causes (80%): hernias, adhesions, intussusception, volvulus.

o Hernia → Weakness or defect in the wall of the peritoneal cavity
may permit protrusion of a pouch like, serosa lined sac of
peritoneum ,incarceration, strangulation.
o Adhesions → fibrous bridges post-surgery/[Link]
common cause of obstruction
o Intussusception → telescoping bowel (children: rotavirus;
adults: tumor or intraluminal mass).
o Volvulus →complete twisting, esp. sigmoid colon. Clinical:
pain, distension, vomiting, constipation, no flatus.

8. Tumors
 Polyps
o 1) Non-neoplastic are most common

 Hyperplastic Polyps

decreased epithelial cell turnover and accumulation of mature cells on the surface

 No malignant potential.
 Exception: Hyperplastic polyposis syndrome → multiple polyps, dysplastic cells → ↑
carcinoma risk.

 Hamartomatous Polyps

 Malformations of glands + stroma.

 Juvenile polyps:cyctically dilated crypts filled with mucin and inflammatory
debris,mc-in chldrens
 Juvenile (Familial) Polyposis syndrome:
o Numerous polyps.
o ↑ risk of adenoma & adenocarcinoma.
 Peutz-Jeghers polyps:
o Multiple polyps + mucocutaneous pigmentation.

 Inflammatory Polyps (Pseudopolyps)

  Islands of inflamed, regenerating mucosa surrounded by ulceration.
 Seen in (IBD).
 No inherent malignant potential, but background IBD increases cancer risk.
o 2) Neoplastic
o benign-adenomas(adenomatous polyps) at ampulla of vater—
precrsors of cancer, result of epithelial proliferative dysplasia):
types: tubular(most common), villous ↑ cancer risk,
tubulovillous.
o malignant – adenocarcinoma at deodenum, carcinoid tumor, anal
zone cancer
o Sessile – without a definable stalk • Pedunculated - with a stalk

 Colorectal carcinoma
o 98% [Link]-site rectosigmoid
o Risk factors: low fiber, high red meat and cholesterol ,
refined carbs, obesity.
o Right-sided: exophytic, iron-anemia.
o Left-sided: annular, obstructive, bleeding.
o Spread: direct etension,lymph nodes, liver, lungs, bone.
o Mnemonic: “Right = anemia, Left = obstruction.”
 Carcinoid tumors
o Neuroendocrine origin, indolent course.
o Appendix most common site.
o May secrete hormones → carcinoid syndrome (flushing,
diarrhea, bronchospasm).

Gastrointestinal Lymphoma
o Accounts for 1–4% of all GI malignancies.
o Mc-site -ileum
o No liver, spleen, or bone marrow involvement at diagnosis.
 Risk Groups:
o Helicobacter gastritis.
o Mediterranean natives.
o Congenital immunodeficiency states.
o HIV infection.
o Immunosuppressive therapy.
o Patients with sprue.
 -nonspecific GI symptoms depending on site.

� Appendicitis
 Pathogenesis:
o Obstruction → mucinous fluid accumulation → ↑ pressure → venous collapse
→ ischemia → bacterial proliferation.
o neutrophilic infiltration of the muscularis propria CM
 Morphology:
o Early acute appendicitis: neutrophils in mucosa, submucosa, muscularis; dull ,
granular, red serosa.
o Suppurative appendicitis: abscesses, ulceration, suppurative necrosis.
o Gangrenous appendicitis: hemorrhagic green ulceration, transmural necrosis,
rupture → peritonitis.
 CF
o Common in adolescents & young adults, slight male predominance.
o Lifetime risk ~7%.
o periumbilical pain.
 Complications:
o Perforation → peritonitis.
o Abscess formation.
o Sepsis if untreated.
 Appendiceal Tumors:
o Carcinoid tumor (most common, distal tip).
o Mucocele (mucinous cystadenoma).
o Mucinous cystadenocarcinoma.

keys
 Meckel’s Rule of 2’s
 RET mutation → Hirschsprung
 Diarrhea classification: Secretory vs Osmotic vs Exudative vs
Malabsorption
 Celiac = villous atrophy + antibodies (TTG, gliadin,
endomysial)
 Crohn vs UC: skip vs continuous, transmural vs mucosal
 Ischemia: mucosal → mural → transmural
 Obstruction causes: (Hernia, Adhesion, Volvulus,
intussusception)
 Colorectal cancer: Right = anemia, Left = obstruction
Liver & Biliary Tract
1. Normal Liver Basics
 Location: RUQ, fixed by ligaments (falciform, teres).
 Weight: ~1500 g (↑ = hepatomegaly).
 Dual blood supply: Portal vein (2/3) + hepatic artery (1/3).
 Functional units:
o Lobule (structural).
o Acinus (physiologic, based on blood supply).
o Canaliculi → bile duct → canal of Hering → right and left hepatic duct → common
hepatic duct + biliary (cystic duct) duct → common bile duct + pancreatic duct → opens
in ampulla of Vater in the duodenum

2. Patterns of Hepatic Injury

 Degeneration: - change in the cell without death,reversible swelling
(ballooning, foamy change in cholestasis, fatty change in
steatosis(abnormal fat accumulation)).
 Steatosis can be
o Microvesicular: Reye’s, tetracycline, pregnancy. (no displacement
of nucleus)
o Macrovesicular: alcohol, DM, malnutrition(Kwashiorkor). (Nucleus
is displaced)
 Necrosis: zonal distribution (centrilobular, midzonal,periportal,
bridging, massive and submassive,focal(scattered)).
 Fibrosis: stellate (Ito) cells deposit collagen (types I & III).
 Regeneration: nodules within fibrous septa.
 Mnemonic: “Damage → Death → Defense → Deposit →
Division).

3. Liver Function Tests (LFTs)

 ALT/AST: hepatocellular necrosis.
 GGT + ALP: liver injury.
 Albumin ↓: edema.
  PT ↑: bleeding risk.
 Bilirubin ↑: jaundice. � Always interpret ALP with GGT to
confirm hepatic origin.

4. Jaundice & Bilirubin Metabolism

 Pathway: Heme(senescent-aged) → biliverdin → unconjugated
bilirubin (albumin bound) → conjugated by UGT → excreted →
urobilinogen.
 jaundice occurs when the equilibrium b/n production and clearance is
disturbed by
for unconjugated

o ↑ Production: hemolysis.
o ↓ Uptake: drugs.
o ↓ Conjugation: newborn, Crigler-Najjar.
 for conjugated
o ↓ Excretion: Dubin-Johnson.
o ↓ Flow: intra/extrahepatic obstruction.
 Unconjugated: lipid-soluble, toxic (kernicterus in infants).
 Conjugated: water-soluble, excreted in urine.
 Both can cause jaundice

5. Cholestasis
 Systemic Retention of bile + solutes → pruritus, xanthomas,
fat-soluble vitamin deficiency.
 result from hepatocellular dysfunction or intrahepatic or extrahepatic Biliary obstruction
 Morphology: bile lakes(focal destruction of parenchyma), foamy
hepatocytes, portal fibrosis.

6. Hepatic Failure
 the end point of progressive damage to the liver
 Requires loss of 80–90% function.
 Causes:
  chronic disease most common cause(alcohol, viral), end point of
relentless chronic hepatitis or alcoholic liver disease
 massive necrosis (fulminant hepatitis(acute liver failure), drugs),
 dysfunction without necrosis (Reye’s, fatty liver of pregnancy).
 Clinical features: jaundice, hypoalbuminemia, coagulopathy,
encephalopathy (↑ ammonia due to abnormal NT), hepatorenal
syndrome..

7. Cirrhosis
 bridging fibrous septa + regenerative nodules + disrupted
architecture.
 Types: micronodular (<3–5 mm, alcohol), macronodular (>5 mm,
post-necrotic), mixed.
 Pathogenesis: stellate cells deposit collagen type 1and 3 →
progressive fibrosis → nodules.
 Deposition of collagen may come from

-Cytokines from inflammatory cells and endogenous cells (kupfer

cells, endothelial cells..)

-disruption of intracellular matrix

-direct stimulation of stellate cells by toxins

 Etiology
  Alcoholic liver disease  Viral hepatitis  Biliary disease  α1- antitrypsin deficiency
 Cryptogenic cirrhosis(unknown)
 Complications: portal HTN, HCC, hepatic failure

8. Portal Hypertension
 Causes:
o Prehepatic: portal vein thrombosis.
o Intrahepatic: cirrhosis, schistosomiasis.
o Posthepatic: RHF, Budd-Chiari.
  Consequences: Ascites, varices (esophageal, hemorrhoids, caput
medusae), splenomegaly, encephalopathy. Mnemonic: “AVE S” =
Ascites, Varices, Encephalopathy, Splenomegaly.

9. Viral Hepatitis
 HAV: fecal-oral, self-limited, no chronicity.
 HBV: DNA virus, multiple outcomes (acute, chronic, carrier,
fulminant, cirrhosis, HCC).
o Antigens: HBsAg (surface), HBcAg (core), HBeAg
(replication).
o Anti-HBs = recovery/vaccine.
o Ground glass appearance ,,
o lead to chronic infection
 HCV: RNA virus, high chronicity (>50%), cirrhosis, HCC.
 HDV: defective RNA virus, needs HBV (coinfection or
superinfection).
 HEV: fecal-oral, high mortality in pregnancy, no chronicity.
Mnemonic: “A = Acute only, B = Broad spectrum, C = Chronic, D
= Dependent, E = Expectant mothers fatal.”

10. Drug & Toxin Injury

 Predictable (dose-dependent): acetaminophen.
 Idiosyncratic (immune): halothane hepatitis.
 Reye’s syndrome: aspirin in viral illness → microvesicular
steatosis, encephalopathy. � Always think acetaminophen
overdose → centrilobular necrosis.

11. Alcoholic Liver Disease

 Spectrum:
o Steatosis (reversible).
o Alcoholic hepatitis (Mallory bodies, neutrophils, fibrosis).
o Cirrhosis (irreversible).
  Complications: hepatic coma, GI bleed, infection, hepatorenal
syndrome, HCC. Mnemonic: “SAM” = Steatosis, Alcoholic
hepatitis, Macronodular cirrhosis.

12. Inborn Errors of Metabolism

 Hemochromatosis: iron overload (genetic or transfusion).
o Iron deposition in liver, pancreas, heart → cirrhosis, diabetes,
cardiomyopathy, bronze skin. Mnemonic: “Bronze diabetes”
= Hemochromatosis.

 A = acute, B = broad, C = chronic, D = dependent, E = expectant

mothers fatal
Hereditary diffuse gastric carcinoma—mutation of e-cadherin

Mrtastatic carcinoma –most common malignant tumor of liver