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Gastrointestinal Flashcards

1
Q

Oral Leukoplakia

A
  • ETIOLOGY: well-defined white patch or plaque
  • Older males
  • Precancerous until proven otherwise
  • 3-7% undergo malignant transformation

• PATHOGENESIS: caused by epidermal thickening or hyperkeratosis

RISK FACTORS:
• Tobacco (pipe-smoking or chewing)
• Chronic friction: ill-fitting dentures
• HPV infection

SYMPTOMS: not removed with scraping

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2
Q

Erythroplakia

A
  • ETIOLOGY: less common than leukoplakia but more severe
  • Malignant transformation in >50% → squamous cell carcinoma

PATHOGENESIS: marked dysplasia

  • Pre-disposing factors: Alcohol and Tabacco

SYMPTOMS: red velvety eroded area

  • red plaque → Red Flag → Presence of Vascularization
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3
Q

Oral Hairy Leukoplakia

A
  • ETIOLOGY: seen in HIV patients
  • No malignant potential
  • Most common in older men and tobacco use

HISTOLOGY

  • Hyperkeratosis - Epidermal thickening of the Stratum Conreum with acanthosis ( thickening of the lower layers)
  • Increased number of inoculated layers of keratin
  • Thick toungue due to keratin

• PATHOGENESIS: EBV

• MORPHOLOGY: layers of keratotic squames on underlying mucosal
acanthosis (hyperkeratotic)
• Fluffy and raised

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4
Q

Oral Squamous Cell Carcinoma

A
  • AT RISK: chewing tobacco, alcohol, jagged teeth, HPV 16/18
  • PATHOGENESIS: loss of p53
  • MORPHOLOGY: white/yellow/red sore
  • SYMPTOMS: asymptomatic
  • Most common: (1) vermillion border of lip (2) floor of mouth (3) lateral tongue
  • Metastasis to anterior cervical lymph nodes

• DIAGNOSIS: biopsy → keratin pearls

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5
Q

Esophageal Atresia

A

• PATHOGENESIS: disruption of elongation and separation of esophagus and trachea during embryogenesis

  • SYMPTOMS: excessive drooling in newborn
  • Choking and cyanosis with first feed
  • Tracheo-esophageal fistula
  • Maternal polyhydramnios - aminotic fluid not swallowed by fetus = abdmonial distention → air in the stomach
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6
Q

Plummer-Vinson Syndrome Kelly Patterson Syndrome

A

• ETIOLOGY: genetic → females > males

  • seein in post-menopausal women who have blleding

• Web = 2 layers, Ring = 3 layers

  • concentric rings or normal esophageal tissue
  • food impaction
  • stricture
  • perforation

• PATHOGENESIS: dysphagia due to esophageal webs ( protrusion of mucosa + obstruction of the lumen) , glossitis( beefy red tounge) , and
hyprchromic iron deficiency anemia

  • SYMPTOMS:
  • Koilonychia (spoon-shaped nails)
  • Splenomegaly- due to iron deficiency
  • Hypochromic anemia
  • COMPLICATIONS: can progress to squamous cell carcinoma
  • TREATMENT: iron supplementation, endoscopic dilation
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7
Q

Hiatal Hernia

A
  • ETIOLOGY: herniation of stomach through enlarged diaphragmatic hiatus
  • Sliding type (95%) → stomach herniates into esophagus → reflux
  • Paraesophageal (rolling) type (5%) → stomach herniates beside esophagus

• PATHOGENESIS: incompetence of LES (sliding type)

  • SYMPTOMS:
  • Sliding Type: reflux of gastric contents, epigastric pain, heart burn
  • Rolling Type: volvulus, strangulation, perforation
  • bowel sounds are heard in the lower left lung field
  • fundus herniates up due to defect in diaphragm
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8
Q

Achalasia / Cardiospasm

A

• Functional esophageal obstruction

• Three main features
– Partial or incomplete relaxation of LES with swallowing
– Aperistalsis
– Increased resting tone of LES

• ETIOLOGY: incomplete relaxation of LES

  • PATHOGENESIS:
  • Primary: loss of ganglion cells in myenteric plexus and Loss of intrinsic inhibitory innervation of LES
  • Secondary: Chagas Disease, Polio, Paraneoplastic syndromes, Sarcoidosis, diabetic autonomic neuropathy
  • SYMPTOMS:
  • Dysphagia
  • Odynophagia
  • Vomiting
  • Aspiration Pneumonia
  • Progressive dilation of esophagus above LES (bird’s beak appearance)
  • Squamous cell carcinoma (5%)
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9
Q

Mallory-Weiss Syndrome

A

• Longitudinal mucosal/mural tear at the esophageal function

ETIOLOGY: frequently in alcoholics after bout of severe retching
(vomiting)

• PATHOGENESIS: inadequate relaxation of LES during vomiting

  • increase pressure from the abdomen + vasospasms of the esophagus
  • SYMPTOMS: mucosal tears at EG junction
  • alcohol → severe retching → Painful hematemesis
  • Usually heals but may be fatal
  • melena

COMPLICATIONS

  • BoerHaave Syndrome → Transmural rupture of esophagus → Severe chronic vomiting or retching
  • Air exists mediastinum
  • Air under skin in the neck → Subcutaneous emphysema
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10
Q

Esophagitis

A
  • inflammation of Squamous Mucosa
  • IRRITANTS: alcohol, acids, alkalis → reflux esophagitis → GERD
  • INFECTIONS: HSV, CMV, Candidiasis → yeast + pseudohyphae
  • ALLERGIC: eosinophilic esophagitis
  • UREMIA
  • ANTICANCER THERAPY
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11
Q

Eosinophilic Esophagitis

A

→ Allergic reaction to a unknown antigen → immune mediated

  • MORPHOLOGY: elongation of lamina propria papillae
  • Hyperemia
  • Trachealization of the esophagus (rings + white plaques)
  • Eosinophils, neutrophils
  • Basal Zone hyperplasia

PRESENTATION

  • Children → feeding intolerance & GERD symptoms
  • Adults → Food impaction & dyphagia

INVESTIGATIONS

  • endoscopy

CLASSIC

  • Dysphagia
  • Poor response to GERD treatment
  • Eosinophils on biopsy
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12
Q

Reflux Esophagitis

A
  • ETIOLOGY:
  • CNS depressants
  • Hypothyroidism
  • Alcohol
  • Nasogastric intubation
  • Tabacco
  • Pregnancy
  • Obesity
  • SYMPTOMS:
  • Dyspepsia
  • Burning
  • Water-brash
  • Exacerbation upon lying down
  • Nocturnal cough
  • PATHOGENESIS:
  • Decreased LES tone
  • Delayed esophageal clearance
  • Decreased reparative capacity of esophagus

• Increased gastric volume

  • COMPLICATIONS:
  • Bleeding
  • Aspiration pneumonia
  • Barrett Esophogus
  • Adenocarcinoma
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13
Q

Barrett Esophagus

A

• ETIOLOGY: replacement of esophageal squamous mucosa with
metaplastic columnar epithelium with goblet cells
• Long standing esophageal reflux (GERD)

  • Men > women
  • White people

• PATHOGENESIS: proliferation of stem cells in lower 1/3 of
esophagus which differentiate into columnar cells (more resistant to acid injury)

• MORPHOLOGY: salmon pink patches above EG junction

  • SYMPTOMS:
  • Heart burn - worst when lying down
  • Dyspepsia
  • Epigastric pain
  • Substernal discomfort
  • Relived with antacids
  • 30-40x increased risk for adenocarcinoma
  • Waterbrash - metallic taste of acid in the mouth

• DIAGNOSIS: serial endoscopic biopsies

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14
Q

Esophageal Varices

A
  • ETIOLOGY: dilated, tortuous vessels in mucosa and submucosa of lower esophagus
  • Alcoholics
  • portal hypertension → back up into liver
  • the distal esophageal vein drains into portal vein via left gastic vein
  • left gastic vein backs up into esophageal vein causing dilation
  • dilated tortuous collaterals in the lower esophagus + proximal stomach
  • PATHOGENESIS: portal hypertension due to liver cirrhosis
  • increased association with decompensated cirrohsis and hepatocellular carcinoma
  • SYMPTOMS: usually asymptomatic until rupture
  • Non-painful hematemesis

• Cause of death in 50% of patients with
advanced cirrhosis

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15
Q

Esophageal Squamous Cell Carcinoma

A
  • ETIOLOGY: adults >50 years old
  • Black people
  • Males > females
  • Central Asia, Northern China

•Vitamin deficiency, Thiamine

  • LOCATION:
  • 20% upper 1/3 of esophagus
  • 50% middle 1/3 of esophagus
  • 30% lower 1/3 of esophagus
  • PATHOGENESIS:
  • Long standing esophagitis
  • Achalasia
  • Plummer-Vinson Syndrome

Celiac disease

Ectogermal dysplasia - begins as in-situ lesion in the form of squamous dysplasia

  • MORPHOLOGY:
  • Exophytic
  • Diffusely infiltrative
  • Ulcerated / excavated
  • DIAGNOSIS: barium swallow - obstruction of lumen
  • HISTOLOGY → Keratin Pearls
  • METASTASIS: adjacent mediastinal structures (trachea, heart)
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16
Q

Adenocarcinoma

A

Gland forming tumor - infiltrates basement membrane

  • ETIOLOGY: precursor lesion = Barrett esophagus + GERD
  • Lower 1/3 of esophagus
  • 50 years old
  • White males
  • PATHOGENESIS: multistep process through dysplasia
  • Reflex esophagitis → Barrett Esophagus → Dysplasia → Adenocarcinoma
  • COMPLICATIONS
  • Melena →DIC
  • Tracheoesophageal fistula →Aspriation pnemonia→ Lung Abscesses
  • invades heart→ Pericarditis→ Pericardial Effusion
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17
Q

Pyloric Stenosis

A

• ETIOLOGY:

  • M:F→ 3:1
  • Congenital: more common in first male child→ associated with Tuner Syndrome, Trisomy 18, and Esophageal Atresia
  • Acquired: chronic antral gastritis, peptic ulcers, malignancy
  • PATHOGENESIS: concentric hypertrophy of circular muscle coat • SYMPTOMS:
  • Regurgitation
  • Projectile vomiting→ Non billious
  • Palpable epigastric mass→ Olive-like
  • Visible peristalsis • TREATMENT: myotomy
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18
Q

Acute Gastritis

A
  • ETIOLOGY: acute erosive gastritis
  • NSAIDs
  • Alcohol
  • Ischemia / shock
  • Severe stress (burns, surgery)
  • PATHOGENESIS: loss of surface epithelium due to erosions
  • Full thickness mucosal injury: ulcer
  • Erosions and hemorrhage seen on endoscopy
  • Acute mucosal process of transient nature
  • Inflammation associated with hemorrhage and in severe cases erosion lading to GI bleed
  • MORPHOLOGY: hyperemia, punctate areas of hemorrhage
  • Edema / congestion of lamina propria
  • Neutrophils in surface epithelium (secondary to epithelial necrosis)
  • Transmural = Erodes all layers
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19
Q

Chronic Gastritis

A
  • ETIOLOGY: chronic mucosal inflammation
  • Chronic H.pylori infection
  • Autoimmune
  • Alcohol + smoking

• MORPHOLOGY: mucosal atrophy and metaplasia

  • SYMPTOMS: asymptomatic
  • Nausea
  • Vomiting
  • Epigastric discomfort
  • Dyspepsia (acid reflux)
  • Indigestion
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20
Q

H.Pylori Gastritis

A
  • PATHOGENESIS: urease and phospholipase
  • Pain is relieved after you eat
  • Never becomes malignant
  • MALToma
  • Antro-pyloric region of lesser curvature

• MORPHOLOGY:
• Lymphocytes and plasma cells in lamina propria
• PMNs in surface epithelium (indicates currently
active inflammation)

• Reactive lymphoid aggregates - chronic inflammatory infiltrates

  • DIAGNOSIS:
  • Invasive: rapid urease test, biopsy, PCR
  • Non-invasive: urea breath test( NH3 + CO2 → which is measured), serology, PCR
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21
Q

Autoimmune Gastritis

A
  • ETIOLOGY: anti-parietal cell or anti-intrinsic factor antibodies
  • Mainly involves body and fundus

• PATHOGENESIS: gland oxyntic destruction → atrophy → loss of acid
production + loss of IF (oxyntic cells)→ Vit B12 deficiency

  • Chronic inflammation
  • Gastric atrophy
  • Intestinal metaplasia
  • SYMPTOMS
  • Achlorhydria (low HCl)
  • Pernicious anemia
  • Increased gastrin levels
  • No relief with antacids
  • Long term risk of gastric carcinoma
  • Risk factor for carcinoid tumors
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22
Q

Acute Gastric Ulcers

A

• ETIOLOGY: severe trauma, major surgeries, extensive burns (curling
ulcers), head injuries (cushing ulcers)

  • PATHOGENESIS:
  • Systemic acidosis and hypoxia

• Vagal stimulation (intracranial lesions)

  • SYMPTOMS: Usually multiple small circular ulcers, but asymptomatic
  • Normal gastric ruggae

• May present with upper GI bleed

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23
Q

Peptic Ulcer Disease

A
  • ETIOLOGY:
  • H.pylori
  • NSAIDs: inhibit PGE synthesis
  • Smoking: impairs mucosal blood flow
  • Alcohol
  • Psychological Stress
  • Zollinger-Ellison syndrome (multiple ulcers)

Gastronemia→ îgastrin→ îacid = ulcers

  • LOCATION: (1) duodenum, (2) stomach, (3) GE junction
  • MORPHOLOGY: round / oval, punched out with ”spoke-like ruggae”
  • 4 main zones:
  • 1) Necrotic fibrinoid debris
  • 2) Non-specific inflammatory infiltrate (PMNs)
  • 3) Granulation tissue
  • 4) Fibrosis + collagenous scar
  • SYMPTOMS:
  • Burning epigastric pain 1-3 hours after meals
  • Relieved by food and alkali - due to CCK + Bicard reaction in lumen
  • Worse at night (no food at night to help buffer acid)
  • Associated weight loss
  • Complications: bleeding, perforation, malignant transformation
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24
Q

Reactive Gastropathy

A

• ETIOLOGY: patients with painful, chronic inflammatory conditions

• PATHOGENESIS: chronic NSAID use → inhibition of PGE/COX → weak
gastric mucosa →

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25
Q

Gastric Adenocarcinoma

A
  • ETIOLOGY: highest occurrence in Japan and South Korea
  • Pylorus/Antrum: 50-60%
  • TYPES:
  • Intestinal: chronic gastritis due to H.pylori → metaplasia is precursor
  • Older patients
  • Sister Mary Joseph nodule
  • Diffuse: E-cadherin mutation → no gland formation or metaplasia
  • Young females
  • Signet ring cells
  • Leather-bag appearance (linitis plastic appearance)
  • GROWTH PATTERNS:
  • Exophytic
  • Flat
  • Endophytic (Excavated)

• SYMPTOMS:
• Early Carcinoma: confined to mucosa and submucosa
• Advanced Carcinoma: Krukenberg tumor, Virchow’s lymph node (left
supraclavicular lymph node)

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26
Q

GI Stromal Tumors (GIST)

A
  • ETIOLOGY: previously misdiagnosed as leiomyomata
  • Submucosal
  • PATHOGENESIS: Cells of Cajal (pacemaker cells of enteric plexus)
  • CD117 tumor marker

• c-Kit mutation in exon 11

  • MORPHOLOGY: whorls and bundles of spindle shaped cells
  • Kit mutations (Imatinib = Kit inhibitor)
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27
Q

Meckel’s Diverticulum

A
  • ETIOLOGY: Rule of 2’s
  • 2% of normal population
  • First 2 years of life
  • 2 feet from ileo-cecal valve
  • 2 inches long
  • 2 types of tissue: gastric + pancreatic
  • PATHOGENESIS: incomplete involution of the vitelline duct
  • True diverticulum: includes all layers of the GIT

• LOCATION: anti-mesenteric border

  • SYMPTOMS: asymptomatic
  • Painless rectal bleeding
  • Meckel’s Diverticulitis (mimic’s appendicitis)
  • Perforation
  • Fistula
  • Peptic ulver
  • Hemorrhage
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28
Q

Celiac Sprue

A
  • ETIOLOGY: common in whites, 1-10 years old
  • HLA DQ2/DQ8
  • PATHOGENESIS: atrophy and loss of villi (reduced SA)
  • Proximal part of intestine
  • MORPHOLOGY:
  • Increased intraepithelial lymphocytes

– Typical: Villous atrophy
• Elongated and hyperplastic crypts (for compensation)
• Increased immune cells in lamina propria

  • SYMPTOMS: chronic diarrhea (w/ steatorrhea)
  • Iron deficiency anemia
  • Long-term risk of T-cell lymphomas
  • DIAGNOSIS:
  • Anti-gliadin / Anti-endomysial antibodies
  • Anti-tissue transglutaminase (tTG) antibodies

• TREATMENT: reversal of epithelium changes after gluten-free diet

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29
Q

Tropical Sprue

A

• ETIOLOGY: people living or visiting tropical areas → contract diarrheal illness

• PATHOGENESIS: bacterial infection superimposed on pre-existing
small intestine injury
• Diffuse throughout intestine

  • Damage to brush border→ failure of reabsoprtion of micelles
  • secondary folate + Vit B12 deficiency
  • SYMPTOMS: appear months or years after visit
  • TREAMENT: responds to antibiotics + Supplemental Folate
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30
Q

Whipple Disease

A
  • ETIOLOGY: systemic → intestines, joints, CNS
  • Males > females
  • PATHOGENESIS: gram positive actinomycete → Tropheryma whippelii
  • Macrophages try to digest bacteria
  • Accumulation of macrophages causes congestion in lamina propria
  • Compression of lacteals (→ abnormal fat absorption)
  • MORPHOLOGY: distended macrophages in lamina propria
  • Possible granulomatous inflammation
  • SYMPTOMS: malabsorption and steatorrhea
  • DIAGNOSIS: PAS–positive granules containing bacteria
  • Mucosa laden with distended macrophages in lamina propria-contain PAS positive granules
  • TREATMENT: responds to antibiotics
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31
Q

Giardia

A

• Protozoan gut pathogen with flagellum
– Trophozoites and cysts are shed
• Usually acquired from drinking water contaminated with cysts
– Poor sanitation and crowded living conditions predispose to infection
• Immunosuppression increases risk

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32
Q
A
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33
Q

Cryptosporidium

A
  • Self-limited infection in a normal host
  • Chronic diarrhea in AIDS
  • Intracellular but appears at top of cell microscopically
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34
Q

Luminal Obstruction

A
  • Food bolus: macaroni, sauerkraut, fruit or vegetable
  • Therapeutic agents: barium sulfate, antacid gels
  • Bezoars: ingested hair
  • Parasite: Ascaris lumbricoides (round worms)
  • Tumors
  • Swallowed foreign bodies: dentures, bones, pins, coins, screws, nails
  • Endogenous origin:
  • Meconium ileus in infants (Cystic Fibrosis)
  • Gallstone ileus: stone >2.5cm
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35
Q

Intramural Obstruction
→

A

• Congenital atresias

  • Inflammatory conditions:
  • Crohn’s Disease
  • Tuberculosis - causes transmural granulomatous inflammation of intestine with makred congestion, edema + fibrinoud adhesions → eventually replaced with scar tissue
  • Drug-induced stenosis
  • Ischemic strictures
  • Radiation damage
  • Polypoid neoplasms
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36
Q

Extramural Obstruction

A

•Mechanical→ involement of entire segment

  • Diseases of peritoneum:
  • Congenital mesenteric/omental bands
  • Peritoneal tumors
  • Peritoneal adhesions - bands of adhesion tissue→ fibrinious bridges within which bowels are trapped
  • Hernias
  • Intussusception: telescoping of proximal bowel segment into distal
  • Often in adults due to tumor

lymphoid hyperplasia in children→ strong association with adenovirus infections

• Volvulus: twisting of bowel loop

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37
Q

Infections of the Small Intestine

A
  • Enteric Fever
  • Salmonella typhi → lymphoid aggregates → ulceration → perforation
  • Longitudinal ulcers
  • Tuberculosis
  • Caseation → necrosis → ulceration → healing → fibrosis → obstruction
  • Terminal ilium most common
  • Annular, circular or oval ulcers lying transversely

Ischemia of the Small Intestine

Acute - villi become tin and detach from basement membrane

Chronic - crypt atrophy and lamina propria fibrosis
• Volvulus

  • Strangulated hernia
  • Gangrene
38
Q

Acute Appendicitis

A
  • ETIOLOGY: inflammation of the appendix
  • Underlying obstruction of the lumen in 50-80% of cases

• PATHOGENESIS:
• Obstruction → continued secretion → increased intraluminal pressure →
collapse of draining veins → ischemia → bacterial proliferation → inflammation + edema

  • SYMPTOMS:
  • Periumbilical pain → RLQ
  • Nausea, vomiting, anorexia, fever
  • McBurney’s Point tenderness
  • Complications: perforation, peritonitis, abscess
  • INVESTIGATION
  • CBC→ Increased Nuetrophils
  • DDX
  • Meckels Diverticulitis
  • Ectopic Pregnancy
  • Chron’s Disease
39
Q

Pseudomyxoma Peritonei

A

• ETIOLOGY: peritoneal studding by mucinous implants

  • MORPHOLOGY
  • Entirely mucinous: no epithelium
  • Abundant mucin: scant low grade neoplastic epithelium
  • Abundant malignant cells: Signet ring cells, infiltrating columnar epithelium
40
Q

Hirschsprung Disease

A
  • ETIOLOGY: most common cause of congenital intestinal obstruction
  • Congenital megacolon: dilation and hypertrophy proximal to aganglionic segment
  • Association with Down Syndrome
  • M:F is 4:1
  • Rectum is always affected
• Dilatation and hypertrophy proximal to
aganglionic segment (congenital megacolon)

• PATHOGENESIS: absence of ganglion cell migration to Meissner/Aurbach’s
plexus

  • SYMPTOMS:
  • Delayed passage of meconium
  • Constipation
  • Abdominal distention
  • Enterocolitis
  • Perforation / peritonitis
41
Q

Diverticular Disease

A
  • ETIOLOGY: diverticulosis
  • Western world
  • Most common: sigmoid colon
  • >60 years
  • Diverticulosis = false diverticulum

• PATHOGENESIS: lack of dietary fiber leads to
sustained bowel contractions and increased intraluminal pressure
• Herniation of colonic wall at sites of focal defects

• decreased fiber→ sustained bowel contraction & increased intraluminal pressure→ herniation of the colonic wall

• MORPHOLOGY: flask-like structures of
mucosal outpouchings from lumen through the
muscular layer (95% sigmoid colon)
  • SYMPTOMS: lower abdominal pain, constipation, fever, painless bleeding
  • Usually asymptomatic, can cause painless bleeding
  • Diverticulitis – Lower abdominal pain – Constipation, diarrhea, flatulence – Fever
  • Can be complicated by perforation – Fistula
42
Q

Ulcerative Colitis

A
  • ETIOLOGY: ulcero-inflammatory disease limited to colon
  • White people
  • 20-25 years old
  • HLA-DRB1 association
  • MORPHOLOGY: mucosa is red, granular and friable
  • No skipped lesions → continuous → curable by surgery
  • Broad based ulcers
  • Regenerating mucosal bulges create pseudopolyps
  • Lead-pipe appearance on barium enema (loss of haustra)
  • Crypt Abscess + cryptitis

• No Granulomas

  • SYMPTOMS: begins in rectum and extends proximally to involve whole colon
  • Inflammatory diarrhea
  • 10% of cases → backwash ileitis
  • Associated with Primary Sclerosing Cholangitis → p-ANCA

PRESENTATION: LLQ abdominal Pain

43
Q

Crohn’s Disease

A
  • ETIOLOGY: terminal ileitis, regional ileitis, granulomatous colitis
  • Adolescents / young adults
  • Females > males
  • Jews
  • HLA-DR7, DQ4

• PATHOGENESIS: mesenteric fat wraps around bowel serosa
(creeping fat)

•Bacteria in lamina propria→ dendritic cells presentation to TH1→ release of TNFa & INF-Y→ activates macrophages→ Transmural inflammation

  • MORPHOLOGY: mesentery thickened and fibrotic (transmural)
  • Cobblestone appearance (gross morphology)
  • Intestinal wall thickened: edema, hypertrophy, fibrosis, inflammation
  • Transmural fibrosis = (String Sign)
  • Non-caseating granulomas
  • Mucosal fissuring with fistula formation
  • Skip-lesions (not continuous)
  • Linear Ulcers
  • SYMPTOMS: malabsorption ( Vit B12 + Bile Salts), fever, weight loss, diarrhea
  • Migratory polyarthritis
  • Ankylosing spondylitis
  • Erythema nodosum
44
Q

Amoebic Colitis

A

• ETIOLOGY: following travel to the tropics

  • PATHOGENESIS: Entamoeba histolytica
  • Cyst → 4 nuclei
  • Trophozoite → 1 nuclei w/ RBCs inside

• MORPHOLOGY: flask-shaped ulcer

  • SYMPTOMS: abdominal pain, mucoid/bloody diarrhea
  • Hypoalbuminemia
  • Hypokalemia
  • Perforation
  • Liver abscess
  • DIAGNOSIS: stool assay for cysts
  • Complications
  • perforation→ peritonitis→ E.coli sepsis→ DIC
  • Abscesses→ liver,lungs, brain
45
Q

Pseudomembranous Colitis

A
  • ETIOLOGY: Clostridium difficile infection secondary to chronic antibiotic treatment
  • PATHOGENESIS: exotoxin
  • MORPHOLOGY: raised yellowish / grey membrane
  • Fibropurulent-necrotic debris

– Surface epithelium denuded
– Superficially damaged crypts distended by mucopurulent
exudate which erupts to form a mushrooming cloud

– Coalescence of these clouds leads to pseudo membrane
formation

• SYMPTOMS: diarrhea, fever, abdominal pain

• DIAGNOSIS: exotoxin in stool assay
• NO COLONOSCOPY → will perforate the membrane
and bowel

46
Q

Ischemic Bowel Disease

A
  • ETIOLOGY: venous or arterial insufficiency
  • Common in elderly

• PATHOGENESIS: transmural
• Occlusive (Arterial thrombosis, arterial embolism,
venous thrombosis)

• Non-occlusive (cardiac failure, shock, dehydration)

  • SYMPTOMS:
  • Absent bowel sounds
  • Severe abdominal pain
  • Gangrene, perforation, peritonitis
  • Shock / vascular collapse
  • High mortality
47
Q

Chronic Ischemic Colitis

A
  • ETIOLOGY: stricture formation
  • Common at watershed areas
  • Splenic flexure

• MORPHOLOGY: chronic inflammation and fibrosis

  • SYMPTOMS: can mimic inflammatory bowel disease
  • Intestinal angina

• Intermittent attacks of pain

48
Q

Eosinophilic colitis

A
  • Allergy: ow’s milk protein allergy
  • Parasites

• Iatrogenic
Drugs, radiation

• Collagen vascular diseases
Rheumatoid arthritis, Churg-Strauss syndrome

• Inflammatory bowel disease

• Tumor or tumor-like conditions
- Leukemia/lymphoma

  • Hypereosinophilic syndrome
49
Q

Juvenile Polyp

A
  • ETIOLOGY: common in children <5 years
  • Rectum is most common site
  • No malignant potential if single polyp
  • MORPHOLOGY: 1-3cm, lobulated with stalk
  • Lamina propria forms the bulk
  • Dilated glands
  • PTEN mutation

Histologically:
• Expanded lamina propria
• Abundant cystically dilated glands
• Inflammatory cells may be present

  • Usually 1-3 cm, lobulated with stalk
  • Juvenile polyposis syndrome→ leads to increased risk of malignancy

•associated: Cowden and Bannayan-Ruvacalba-Riley
syndromes

50
Q

Peutz-Jegher Polyp

A

• ETIOLOGY: hamartomatous polyp

• MORPHOLOGY: arborizing network of smooth
muscle extending into the polyp and surrounds
glands
• Glands are lined by non-dysplastic epithelium rich in
goblet cells

• SYMPTOMS: no malignant potential

  • Peutz-Jegher Syndrome: autosomal dominant
  • Multiple polyps
  • Melanotic (black) pigmentation in lips, face, genitalia
51
Q

Adenomas

A
  • ETIOLOGY: epithelial proliferative dysplasia
  • 90% in the colon
  • Precursor lesions of carcinomas
  • Malignant risk increases with: polyp size, Severity of dysplasia ,Villous architecture, 3 or more adenomas

• MORPHOLOGY: adenomatous epithelium is
severity of dysplasia tall, hyperchromatic and disordered
• Tubular
• Villous
• Tubulovillous

  • SYMPTOMS: asymptomatic
  • Anemia (occult blood loss)
  • Villous adenoma → dehydration, hypoproteinemia, hypokalemia

• Intussusception

52
Q

Familial Adenomatous Polyposis

A
  • ETIOLOGY: genetic defect in APC gene (5q21) - requires 2 hits plus p53 and KRAS
  • Young people

• Bright, red bloody, & mucoid diarrhea

  • MORPHOLOGY: tubular type in left (descending colon)
  • Typically 500-2500 mucosal adenomas
  • Minimum required for diagnosis is 100
  • SYMPTOMS:
  • Gardener Syndrome: tubular adenomas with multiple osteomas, desmoid tumors, and epidermal cysts

• Turcot Syndrome: adenomas and CNS gliomas

53
Q

Colorectal Carcinoma

A
  • ETIOLOGY: elderly individuals
  • Young individuals if history of ulcerative colitis and polyposis syndromes

• RISK FACTORS: obesity, low fiber diet, diet rich in animal fat •

PATHOGENESIS: Iron deficiency, Blood in stool
• Chromosomal Instabilities (90%): APC, p53, KRAS
• MSI Pathway (10%) : MLH1/MSH2

  • MORPHOLOGY: neoplastic glands invading submucosa and beyond
  • Proximal Colon: exophytic polypoidal lesions
  • Distal Colon: annular, encircling napkin ring constrictions
  • SYMPTOMS: asymptomatic
  • Right Sided: fatigue, weakness, iron deficiency anemia
  • Left Sided: altered bowel habits
  • Spread to liver, lung, and bones

• DIAGNOSIS: CEA

54
Q

Hereditary Non-Polyposis Colorectal Cancer

A

• Warthin-Lynch Syndrome

  • ETIOLOGY: MLH1/MSH2 mutation - DNA repair Gene
  • Microsatellite instability
  • MORPHOLOGY: ascending colon more common
  • Large, sessile - Villious Adenocarcinoma ( no benign polyps)
  • Less polyps than FAP
  • SYMPTOMS: occult bleeding - Fatigue and Iron deficiency , anemias due to blood loss
  • Associated with carcinomas of other abdominal sites
55
Q

Carcinoid Tumor

A
  • ETIOLOGY: derived from endocrine cells
  • MORPHOLOGY: nested and organized - Salt pepper appearance

• STOMACH:
• Type 1: gastric atrophy and achlorhydria →
hypergastrinemia leads to ECL cell hyperplasia •

Type 2: Gastrinoma (Zollinger-Ellison Syndrome) →
MEN1 syndrome, hypergastrinemia

• Type 3: Sporadic (most aggressive)

  • SMALL INTESTINE + APPENDIX: most common site
  • Carcinoid syndrome → wheezing, diarrhea, flushing

• DIAGNOSIS: 5HT elevated→ may lead to right sided heart failure

56
Q

Primary Gastrointestinal Lymphomas

A
  • ETIOLOGY: lymphoma presenting with the main bulk of disease in the GI tract
  • SITES: stomach > small intestine > colon/rectum
  • B-CELL:
  • MALT-type
  • High grade DLBCL
  • Mantle Cell lymphoma
  • Burkitt Lymphoma
  • Follicular lymphoma
  • T-CELL:
  • Enteropathy Associated (EATL)
  • Hepatosplenic T-cell lymphoma
  • Angioimmunoblastic-type T cell lymphoma
57
Q

H. pylori and Gastric MALT Lymphoma

A
  • ETIOLOGY: 60 years (mean)
  • MALToma cell proliferates in-vitro with heat killed H.pylori

• SYMPTOMS: dyspepsia, abdominal pain, nausea, vomiting, weight
loss

  • TREATMENT:
  • Antibiotic treatment for H.pylori
58
Q

Morphology of Hepatic Injury

A
  • DEGENERATION:
  • Ballooning: irregularly clumped cytoplasm
  • Feathery: fine foamy cytoplasm → detergent action of bile salts

• STEATOSIS

  • MACROVESICULAR: single fat vacuole displaces nucleus to periphery
  • Alcohol
  • MICROVESICULAR: multiple vacuoles, central nucleus
  • Acute fatty liver of pregnancy
  • Reye’s Syndrome
  • Drugs
  • NECROSIS: focal, bridging, or massive/sub-massive
  • APOPTOSIS: Councilman’s Bodies, Acidophil Bodies

• REGENERATION: Thickening of hepatocyte cords, mitosis, and some
disorganization

• FIBROSIS

59
Q

Cirrhosis

A
  • ETIOLOGY: diffuse liver process with fibrosis and conversion of normal architecture into structurally abnormal nodules
  • Alcoholic liver disease
  • Viral hepatitis
  • Hemochromatosis
  • A1AT Deficiency
  • Wilson’s Disease
  • Budd-Chiari Syndrome
  • MORPHOLOGY:
  • Bridging fibrous septa

• Parenchymal nodules created by regeneration

– Diffuse involvement of liver

• Architectural disruption

Based on nodule sized, often classified as:
– Micronodular < 3mm nodules – Macronodular > 3 mm nodules

  • PATHOGENESIS:
  • Chronic inflammation + cytokines + toxins stimulate Ito cells
  • Deposition of collagen I and III in Space of Disse
  • Loss of fenestrations, new vascular channels in septa, obstruction of biliary channels
  • Impaired hepatic secretions, shunting of blood, jaundice
  • SYMPTOMS:
  • Portal hypertension • Liver failure • Increased risk for HCC
60
Q

Portal Hypertension

A

• PATHOGENESIS: increased resistance to portal blood flow

• SYMPTOMS:
• Ascites
• Portosystemic shunts: esophageal varices, gastric varices, hemorrhoids,
caput medusae

  • Congestive splenomegaly
  • Hepatic encephalopathy
61
Q

Viral Hepatitis

A

• ETIOLOGY: most common infectious disease of the liver

• HEPATITIS A – SsRNA
• Does not cause chronic hepatitis • Common in children • Fecal-oral route • Diagnosis- IgM anti-HAV at onset
of disease
• HEPATITIS B: Enveloped DNA Virus
• Propensity for chronicity • Transfusion of blood, sexual intercourse, IV drug abuse, homosexuals, needle sticks
• HEPATITIS C: SsRNA
• Most important cause of transfusion-associated hepatitis • Inherently unstable → no vaccine • Persistent infection + chronicity
• HEPATITIS D: Replication Defective RNA Virus
• Infective only when encapsulated by HBsAg • Co-infection of super-infection
• HEPATITIS E: Unenveloped single stranded RNA virus
• Transmitted as endemics • No chronicity • Self-limited • Severe cholestasis • High mortality in pregnant females

62
Q

Autoimmune Hepatitis

A

• ETIOLOGY: common in females

  • PATHOGENESIS:
  • Type I: Anti-nuclear antibodies (ANA), Anti-smooth muscle antibodies (ASMA)
  • Type II: Anti LKM antibodies (liver kidney microsomal)
  • DIAGNOSIS: high IgG titers
  • TREATMENT: immunosuppressive therapy

HISTOLOGY - clusters of lymphocytes and plasma cells in the interface of portal tracts and hepatic lobules

COMPLICATIONS - liver cirrohsis

63
Q

Alcoholic Liver Disease

A
  • ETIOLOGY:
  • Hepatic steatosis
  • Alcoholic hepatitis
  • Fibrosis → cirrhosis

• MORPHOLOGY: initially enlarged fatty liver with progresses to
fibrotic, fatty, and shrunken
• Mallory Hyaline Bodies: tangled intermediate filaments (eosinophilic
inclusions)

INVESTIGATIONS : AST > ALT & increased GGT

64
Q

Primary Biliary Cirrhosis (Cholangitis)

A
  • ETIOLOGY: disease of middle aged women
  • PATHOGENESIS: anti-mitochondrial antibodies
  • MORPHOLOGY: granulomatous destruction of medium sized (intrahepatic) bile ducts
  • Dense lymphoid infiltration with florid duct lesion
  • SYMPTOMS: death occurs due to liver failure
  • Secondary Biliary Cirrhosis: due to partial or total bile duct obstruction
  • Tumors, strictures, gallstones
65
Q

Primary Sclerosing Cholangitis

A

• ETIOLOGY: inflammation, fibrosis, and dilation of intra and extra
hepatic ducts

Median age is 30 years and most commonly in male

  • Inflammatory destruction of Extrahepatic and large intrahepatic ducts
  • Periductal inflammation and fibrosis – “onion skin” lesions
  • P-ANCA (80%)
  • SYMPTOMS: associated with chronic ulcerative colitis
  • DIAGNOSIS: ERCP → dilating and beading of the biliary tree

• Associated with ulcerative colitis

67
Q

Hemochromatosis

A
  • ETIOLOGY: excessive accumulation of iron
  • Males <40yrs.
  • Liver fibrosis, eventually cirrhosis (micronodular)
  • PATHOGENESIS: HFE gene
  • Increased Fe absorption

• Parenteral iron overload
– Repeated blood transfusions
– Iron dextran injections

• Ineffective erythropoiesis
– β thalassemia
– Other chronic hemolytic anemias

• Increased oral intake
– Bantu disease

• Chronic liver disease
– Alcohol, hepatitis C

  • Common in males
  • Rarely manifests before 40
  • SYMPTOMS:
  • Micronodular cirrhosis
  • Diabetes mellitus
  • Skin pigmentation
  • Cardiomyopathy

• PANCREAS – Hemosiderin in both acinar and Islet cells → Diabetes mellitus

• HEART
– Hemosiderin in myocardial fibers (cardiomyopathy)
• SKIN
– Iron in dermal melanophages
– Increased melanin production

68
Q

Wilson’s Disease

A

• ETIOLOGY: accumulation of toxic levels of copper in liver, brain, eyes •

MORPHOLOGY:
• Fatty change in liver
• Acute hepatitis

PATHOGENESIS

  • due to lack of Cu transporters into bile
  • Defective Cu incorporation into Ceruloplasm Carrier→ Cu into the Blood
  • Copper is toxic via Fenton Reaction→ Free Radical Damage to Hepatocytes
  • SYMPTOMS:
  • Deposition of copper in basal ganglia
  • Kayser-Fleischer rings
  • DIAGNOSIS:
  • Decreased serum ceruloplasmin levels
  • Increased hepatic Cu
  • Increased urinary copper excretion
69
Q

Alpha-1 !ntitrypsin (α 1 -AT) Deficiency

A
  • Autosomal recessive disorder
  • Markedly low levels of α 1 AT (protease inhibitor that is a glycoprotein encoded by the PiMM gene on Chr14)
  • Synthesized mainly by hepatocytes

• Homozygosity for mutant variant (PiZZ) leads to retention of
mutant protein in cells

  • Cytoplasmic globules in hepatocytes
  • Lung disease (emphysema) can be present → Liver transplantation is the only treatment

• Clinical presentation
– Neonatal hepatitis with or without cholestasis
– Chronic hepatitis
– Cirrhosis

• Hepatocellular carcinoma

70
Q

Non-Alcoholic Fatty Liver Disease (NAFLD / NASH)

A

• ETIOLOGY: changes like in alcoholic liver disease in non-drinkers

  • RISK FACTORS:
  • Obesity
  • Insulin resistance
  • Hyperlipidemias

• MORPHOLOGY: steatosis with or without hepatitis

  • SYMPTOMS: usually asymptomatic
  • Mild elevation of serum transferases
  • May lead to cirrhosis
71
Q

Hemangioma

A

Tumor composed of vascular space often filled with thrombus

  • ETIOLOGY: commonest liver tumor
  • Females > males

• DIAGNOSIS: incidental on CT scan

  • TREATMENT: depends on the following factors
  • Bleeding
  • Location
  • Size
  • Platelet consumption
72
Q

Liver Cell Adenoma

A

Benign tumor of hepatocytes

• ETIOLOGY: associated with oral contraceptive pill or anabolic steroids

  • SYMPTOMS:
  • Abdominal pain
  • Shock/hemorrhage
  • May be fatal during pregnancy
  • DIAGNOSIS: normal serum AFP
  • TREATMENT: stop causative medication
73
Q

Focal Nodular Hyperplasia (FNH)

A
  • ETIOLOGY: females > males
  • DIAGNOSIS: central scar on CT, MRI

HISTOLOGY

  • Composed of multiple spherical aggregates of hepatocytes held together in a fibrosis meshwork + central stellate Scar
  • NON- Neoplastic - localized vascular abnormalities
  • Normal Liver and Spleen Scan
74
Q

Hepatoblastoma

A
  • ETIOLOGY: most common liver tumor in neonates and children
  • ~18 month
  • Associated with Down Syndrome, Beckwith-Wiedemann syndrome
  • MORPHOLOGY:
  • Small uniform cells in cords with rapid growth
  • SYMPTOMS:
  • Hepatomegaly
  • Abdominal mass
  • Spread to lungs and peritoneum

• DIAGNOSIS: AFP elevated

75
Q

Hepatocellular Carcinoma (HCC)

A
  • ETIOLOGY: global distribution strongly related to prevalence of HBV
  • Highest frequencies in Taiwan, Mozambique and China
  • Hepatitis B+C
  • Hemochromatosis
  • Alcoholic cirrhosis
  • Alpha-1-antitrypsin deficiency
  • Aflatoxin
  • MORPHOLOGY: unifocal or multifocal
  • Paler than surrounding hepatic parenchyma
  • Propensity for invading vascular channels (portal vein/IVC)
  • Trabecular, sinusoidal or pseudoacinar pattern

– Bile production by tumor cells, cytoplasmic inclusions

– Usually cirrhosis in adjacent liver parenchyma

  • SYMPTOMS:
  • RUQ pain
  • Fatigue
  • Cachexia
  • Masked by underlying liver disease

• DIAGNOSIS: AFP, FNAC, biopsy

76
Q

Fibrolamellar Variant of HCC

A

• ETIOLOGY: no association with HBV or cirrhosis

  • chimeric Proteins

• MORPHOLOGY: single hard tumor with fibrous bands traversing
through
• Well-differentiated polygonal cells in cords or nests, separted by fibrous
septa

• SYMPTOMS: better prognosis

  • INVESTIGATION → Normal AFP
77
Q

Liver Metastasis

78
Q

Acute Cholecystitis

A

• Acute Inflammation of gallbladder wall resulting in ischemia and

• Pathogenesis:
– Chemical irritant and inflammation in the setting of obstruction to flow → mucosal phoshpholipase convert lecithin to lysolecithin which causes → Damage to glycoprotein layer of the mucosa which results in → increased release of prostaglandin from the mucosa.
– Cumulatively leads to mucosal and mural inflammation → Gall bladder dysmotility and increased intraluminal
pressure →superimposed bacterial contamination

• Presentation:
– Pain in the right hypochondrium/ epigastrium
– May become surgical emergency
– Associated fever, nausea, vomiting –> Most patients recover
– Positive Murphy’s sign:
• Examiner presses on RUQ and asks patient to deeply inspire –> patient stops inspiration d/t to pain

  • Will be negative if there is only bile duct obstruction and not inflammation (cystitis)
  • Complications: rupture and perforation

• Chronic Cholecystitis
– Sequelae of repeated acute cholecystitis
– More common: no antecedent attacks of acute cholecystitis → Starts off as chronic!
– HALL MARK: PORCELAIN GALL BLADDER Appearance →high association with carcinoma due to the extensive
dystrophic calcfication – The role of gallstones with chronic cholecystitis is unclear

– Micro-organism can be cultured from bile in 1/3rd of patients

– Rokitanksy Aschoff Sinus : increased pressure in I the gall bladder causing diverticuli (dilated cysts)
• Herniation of gall bladder mucosa in to the muscularis

80
Q

Cholangiocarcinoma

A
  • ETIOLOGY: carcinoma of bile duct origin
  • Normal serum AFP

RISK FACTORS: Sclorising cholangitis, parastic infection, cyctic dilation, gall stones

  • PATHOGENESIS:
  • Gallstones
  • Chemicals: benzamine, nitrosamines
  • Parasites: Clonorchis sinesis, Opisthorchis viverini
  • MORPHOLOGY: adenocarcinoma with extensive fibrosis (desmoplastic)
  • Most commonly at hilum of liver
  • Upper 1/3 → 60%
  • Middle 1/3→ 20%
  • SYMPTOMS:
  • Malaise
  • Weight loss
  • Jaundice
  • Charcot Triad: jaundice, fever, chills
  • Raynaud Pentad: Charcot triad + hypotension + mental changes
  • Poor prognosis
81
Q

Cholelithiasis (Gall Stones)

A
  • ETIOLOGY:
  • Cholesterol stones → cholesterol monohydrate (80%) (obesity) → Yellow

• Pigment stones → bilirubin calcium salts (20%) (chronic hemolytic anemia) → Black

  • RISK FACTORS:
  • Cholesterol stones: advancing age, female, OCP, obesity, hyperlipidemia • Pigment stones: Asians, hemolytic syndromes, biliary infections
  • PATHOGENESIS:
  • Mucosal phospholipase convert lecithin to lysolecithin • GB hypomotility promotes precipitation of cholesterol from bile • Mucus hypersecretion traps crystals and promotes aggregation
  • SYMPTOMS:
  • Empyema • Perforation • Cholecystitis • Pancreatitis • Porcelain gall bladder (rarely dystrophic calcification, high association w/ cancer)
  • DIAGNOSIS:
  • Cholesterol Stones = radiolucent on Ultrasound, X-ray • Pigment Stones = radio-opaque on Ultrasound, X-ray
82
Q

Carcinoma of the Gall Bladder

A

Chronic inflammation of the gall bladder

  • ETIOLOGY: females > males, 7th decade
  • MORPHOLOGY: exophytic - growin into lumen at irregular cauliflower mass invading underlying wall
  • PATHOGENESIS:
  • Squamous: p53
  • Adenocarcinoma: KRAS + Cholelithiasis
  • COMPLICATIONS: metastasis to the liver by the time of diagnosis
  • Poor prognosis
83
Q

Acute Pancreatitis

A
  • ETIOLOGY: 80% cases associated with gallstones and alcoholism → causes contraction of the sphincter of Oddi → damage to pancrease→premature activation of enzymes
  • Infections: Mumps, Coxsackie, Mycoplasma
  • Acute ischemia
  • Hyperlipoproteinemias
  • Drugs: diuretic, azathioprine, estrogens
  • MORPHOLOGY:
  • Focal fat necrosis in pancreas and peripancreatic tissues
  • Ca2+ deposition
  • SYMPTOMS:
  • Abdominal (epigastric pain) - upper back
  • Elevated pancreatic enzymes → amylase (24-48hrs) then lipase (72-96hrs)
  • Leukocytosis
  • Hypocalcemia (due to saponification), tetany
  • Complications: ARDS, ATN, pancreatic abscess → DIC
84
Q

Chronic Pancreatitis

A

• ETIOLOGY: repeated bouts of mild to moderate pancreatic inflammation with loss of pancreatic parenchyma and its replacement by fibrosis

– Progressive loss of pancreatic endocrine and exocrine function
• Middle aged alcoholics

  • SYMPTOMS:
  • Back pain
  • Persistent abdominal pain
  • Malabsorption
  • Pancreatic pseudocyst: enzymes + fibrous scar + dystrophic calcifications
  • Diabetes (if islet is damaged)
  • Pleural effusion
  • DIAGNOSIS: X-Ray or CT → calcifications
85
Q

Carcinoma of the Pancreas

A

• ETIOLOGY: association with smoking

  • LOCATION:
  • Head (60-70%)
  • Tail (10-15%)
  • Body (5-10%)
  • MORPHOLOGY:
  • Ductal-type adenocarcinomas
  • Dense stromal fibrosis (desmoplasia)
  • Perineural invasion

• SYMPTOMS: pain usually first symptom (invasion of posterior abdominal
wall)
• Trousseau’s Sign (migratory thrombophlebitis) → PAF + procoagulants + mucin
• Obstructive jaundice (if in head of pancreas)

  • DIAGNOSIS: CA19-9
  • GOLD STANDARD = biopsy
86
Q

Insulinomas

A
  • ETIOLOGY: usually benign, solitary
  • PATHOGENESIS: arise from beta-cells

• SYMPTOMS:
• Hypoglycemia (especially by fasting)
• May manifest as Whipple triad (low blood glucose, presence of symptoms,
resolution when blood glucose is normalized)

• Increased insulin

87
Q

Gastrinomas

A
  • ETIOLOGY: gastrin-producing endocrine tumors
  • Associated with MEN-1 mutation

• PATHOGENESIS: hypergastrinemia

  • SYMPTOMS: multiple ulcers
  • Results in Zollinger-Ellison Syndrome
  • Multiple duodenal peptic ulcers
  • Prominent gastric rugal golds due to increased oxyntic gland mass
  • Steatorrhea
88
Q

Acinar cell carcinoma

A
  • 1-2% of all exocrine neoplasms
  • 40-81 Y (62Y)
  • M:F = 2:1
  • Whites > Blacks
  • Subcutaneous fat necrosis and panniculitis (16%) due to lipase
  • Aggressive tumors, can metastasize to liver
89
Q

Intraductal Papillary Mucinous Neoplasm (IPMN)

A
  • Arise within the ductal system
  • Majority in the head
  • Dilated duct filled with mucin

• Cysts can be multiloculated; lined by tall columnar
mucin secreting cells (papillary/pseudopapillary/flat)

• Histologic features
– Noninvasive: Low-Grade/High-Grade tumor cells confined to duct lumen

– Invasive: extension of tumor cells beyond the pancreatic duct into stroma

– Lacks ovarian type stroma

90
Q

Mucinous cystic neoplasms (MCN)

A
  • 2-5% of all exocrine neoplasms, mostly tail
  • 20-82 Y (49Y)
  • Almost exclusively in women
  • Not connected to the ductal system

• Histologic features
-Tall columnar mucin secreting cells

  • Noninvasive with low grade/high grade cytology
  • Invasive component can be present
  • Characteristic feature: ovarian-type stroma
91
Q

Pancreatic neurondocrine tumors (NET)

A

• Islet cell tumors, make islet cell type hormones
– Functional (Insulinomas, Gastrinoma, Glucagonoma)

– Non-functional

• Behavior difficult to predict reliably
– All are potentially malignant
– NET Grading based on size and mitotic activity
– Less common: neuroendocine carcinoma, small cell or large cell

Pathology (3 decks)

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