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6. HDS GI Repro > Intestinal Disorders > Flashcards

Intestinal Disorders Flashcards

1
Q

Small Intestine

Characteristics

A
  • Three portions: duodenum, jejunum and ileum
  • Four wall layers: mucosa, submucosa, muscularis propria, serosa
    • Villous:Crypt ratio ranges 3:1 to 5:1
  • Cell types:
    • Enterocyte (columnar absorptive cell)
    • Goblet cell
    • Endocrine cell
    • Paneth cell
    • Undifferentiated crypt cell
  • Function:
    • Terminal digestion and absorption of food
    • Secretion of IgA
    • Uptake of macromolecules (e.g., B12)
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2
Q

Large Intestine

Characteristics

A
  • Regions: Cecum, ascending, transverse, descending, sigmoid colon (100-150cm), rectum (15-18cm)
  • Diameter: Cecum 8cm, sigmoid 2-3cm
  • Four wall layers: mucosa, submucosa, muscularis propria, serosa
  • Gross Appearance: test tube shaped pits
  • Cell types:
    • Colonocyte (absorptive cell)
    • Paneth cell (R colon)
    • Goblet cell
    • Endocrine cell
    • Undifferentiated crypt cell
  • Function: Fluid absorption, fecal storage, defecation
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3
Q

Intestinal

Congenital Abnormalities

A
  • Atresia/stenosis
    • Most common in duodenum
    • Appears as string-like segment or diaphragm
    • Pathogenesis: failure to develop, in utero vascular accident or intussception
    • Imperforate anus: failure of cloacogenic diaphragm to rupture
  • Heterotopia: Presence of tissue that belongs elsewhere
    • Pancreatic
    • Gastric
  • Other: Duplication, malrotation, omphalocele, gastroschisis
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4
Q

Meconium Ileus

A
  • Failure to pass meconium during the neonatal period
  • Obstructive sx
  • Associated w/ Cystic Fibrosis
  • Meconium seen as brown material inspissated in the colon
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5
Q

Meckel’s Diverticulum

A
  • Etiology: failure of involution of omphalo-mesenteric (vitelline) duct
    • Connects gut to yolk sac in utero
  • Located in small intestine on anti-mesenteric side within 30 cm of ileocecal valve
  • Contains all wall layers (true diverticulum)
  • May contain gastric or pancreatic heterotopia (50%)
  • Complications: ulceration, intussception, incarceration, perforation
  • Incidence: 2% of population, more in males
    • 4% will be symptomatic, usually before age 2
    • Most common small intestine congenital anomaly
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6
Q

Hirschsprung Disease

Pathogenesis

A

Congenital Aganglionic Megacolon

  • Abnormality: Absence of ganglion cells in myenteric plexus (Meissner & Auerbach plexus)
    • Due to either premature arrest of normal migration of neural crest cells from cecum to rectum or premature death of ganglion cells
    • Always involves rectum w/ variable proximal extension (results in distal obstruction)
  • Associations: Down’s syndrome (10%), other neurologic problems (5%)
    • Some genetic component (4% of siblings affected)
    • Majority of familial and 15% of sporadic cases show heterozygous loss-of-function mutations in receptor tyrosine kinase RET
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7
Q

Hirschsprung Disease

Clinical Characteristics

A
  • Incidence: 1/5-8k live births
    • M:F 4:1
  • Presentation: fail to pass meconium, constipation to life threatening obstruction depending on length of agalionic segment
  • Treatment: resect aganglionic segment
  • Diagnosis: intra-operative frozen section analysis to confirm presence of ganglion cells @ anastomotic margin, gross ID of aganglionosis difficult
  • Complication: progressive dilation of proximal innervated colon (megacolon), may eventually rupture
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8
Q

Acquired Megacolon

Etiologies

A
  • Chagas disease: Trypanosoma cruzi infection (protozoan transmitted by triatomids “kissing bugs”) ⇒ destruction of enteric plexus
  • Obstruction: tumor, stricture, adhesions
  • Toxic Megacolon: seen in ulcerative colitis
    • Inflammatory mediators ⇒ damage muscularis propria ⇒ disturb neuromuscular function
    • Results in colonic dilation and toxic megacolon, which can perforate
  • Functional psychosomatic disorder
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9
Q

Malabsorption

Overview

A
  • Definition: Suboptimal absorption of foodstuff
  • Signs and sx: abnormal stools (steatorrhea), weight loss, ↑ bowel sounds, vitamin deficiencies
  • Disorder in one of the following:
    • Intraluminal digestion
    • Terminal digestion
    • Transepithelial transport (sometimes due to epithelial injury)
    • Lymphatic transport
  • Etiologies: non-infectious and infectious
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10
Q

Malabsorption

Intraluminal Digestion Defects

A
  • Gastric disease: absence of normal acid output and intrinsic factor
  • Pancreatic disease: absence of pancreatic enzymes and hormones
  • Bacterial overgrowth in blind loop
  • Enterohepatic circulation problem: ↓ or absent bile salts due to liver, biliary tree or intestinal problem
  • Histology: small intestine biopsy w/ non-specific changes: mild villous blunting, chronic inflammation
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11
Q

Malabsorption

Terminal Digestion Defect

A

Lactose deficiency

  • Congenital (rare): AR mutation in lactase gene
  • Acquired: African-American > White; elderly > young
  • Defect: inability to break lactose → glucose and galactose
  • Results in osmotic diarrhea due to lactose
  • Diagnostic test: ↑ breath hydrogen (d/t ↑ bacterial fermentation in the gut)
  • Treatment: lactose free diet
  • Histology: non-specific
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12
Q

Malabsorption

Transepithelial Transport Defect

A

Caused by epithelial injury

  • Celiac Sprue
  • Tropical Sprue (uncertain etiology)
  • Whipple’s disease (infectious): actually due to defective lymphatic transport
  • Abetalipoproteinemia
  • Cystic Fibrosis
  • Inflammatory bowel disease
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13
Q

Celiac Sprue

Overview & Pathogenesis

A

“Gluten sensitive enteropathy, Non-tropical sprue”

  • Definition: Mucosal injury due to ingestion of gluten
    • Protein found in cereal grains (wheat, barley, rye, oats)
    • Luminal and brush-border enzymes digest gluten → amino acids and other peptides (α-gliadin) ⇒ resistant to protease degradation
  • Pathogenesis caused by Gliadin-derived peptides
    • Interact w/ HLA class II on cell surface ⇒ ⊕ T cells ⇒ mucosal injury
    • ⊕ Epithelial cells to express IL-15 ⇒ activation/proliferation of CD8+ lymphocytes
    • NKG2D ⊕ T-cells attack MIC-A ⊕ enterocytes
    • Damage ⇒ ↑ passage of other gliadin peptides into lamina propria
    • Deaminated by tissue transglutaminase
    • Interact w/ HLA-DQ2 or DQ8 on APCs ⇒ ⊕ CD4+ T cells ⇒ cytokines ⇒ tissue damage
  • Genetic susceptibility: Almost everyone w/ disease carries Class II HLA-DQ2 or HLA-DQ8 allele
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14
Q

Celiac Sprue

Appearance

A

Biopsy 2nd part of duodenum or jejunum

  • ↑ CD8+ T lymphocytes
  • ↑ plasma cells, mast cells and eosinophils
  • ↑ epithelial turnover
  • Villous atrophy
  • Crypt hyperplasia
  • Loss of mucosal and brush-border surface area
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15
Q

Celiac Sprue

Clinical Characteristics

A
  • Serology:
    • IgA anti-tissue transglutaminase Ab
    • IgA anti-endomysial Ab
  • Presentation: ± GI symptoms, ± Anemia
  • Associations: IDDM, Autoimmune Disease, Down’s syndrome, lymphocytic gastritis, IgA deficiency, Dermatitis herpetiformis
  • ↑ risk of many malignancies including:
    • T-cell lymphoma (10x)
    • Small intestine adenocarcinoma (otherwise uncommon)
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16
Q

Tropical Sprue

A

“Environmental Enteropathy”

  • Clinical: malabsorption, malnutrition, stunted growth, defective intestinal mucosal immune function
  • Proposed pathogenesis: defective intestinal barrier function, chronic exposure to fecal pathogens, diarrhea during first 2-3 years of life
    • No one organism definitively linked
  • Histology: villous atrophy, crypt hyperplasia
  • High Incidence areas: Sub-Saharan Africa, Caribbean, Far East, India
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17
Q

Whipple Disease

A
  • Defective lymphatic transport
  • Infectious disease w/ ongoing injury in susceptible host
  • Pathogen: Tropheryma whippelii (gram ⊕ actinomycete)
  • Epidemiology: Caucasians; 4-5th decade; M:F 10:1
  • Symptoms: diarrhea, weight loss, arthralgia; ± polyarthritis, neuropsychiatric sx, lymphadenopathy
  • Pathology:
    • MΦ containing PASD ⊕ granules
    • Lysosomes stuffed w/ partly digested bacteria
    • MΦ can accumulate in many sites
    • Mucosal plaques ⇒ represents lymphatic dilatation and mucosal lipid deposition
  • Differential diagnosis:
    • Whipple disease (AFB ⊖)
    • Other fungal infection (e.g., Histoplasmosis)
    • Macroglobulinemia (deposition of IgM in mucosa in pts w/ hematopoietic dyscrasia)
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18
Q

Mycobacterium Avium Intracellulare (MAI)

Infectious disease

A
  • Atypical Mycobacteria
  • Most commonly occurring in AIDS pts
  • Pathology: MΦ containing rod shaped organisms, ⊕ PASD, ⊕ acid-fast stain
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19
Q

Abetalipoproteinemia

A
  • Malabsorption d/t transepithelial transport defect
    • Autosomal recessive
  • Pathogenesis: Inability to synthesize apoprotein B
    • Protein needed to form chylomicrons for effective fat transport from epithelial cells
    • Lipids (triglycerides) accumulate intracellularly
    • Absence of circulating apoprotein B containing lipoproteins: chylomicrons, VLDL, LDL
  • Burr cells (acanthocytic erythrocytes) on blood smear
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20
Q

Cystic Fibrosis

A

Malabsorption d/t transepithelial transport defect

  • Absent or reduced amount of epithelial Cystic Fibrosis Transmembrane Conductance Regulator (CFTR)
    • Defect in intestinal chloride ion secretion
    • Interferes w/ bicarb, sodium and water secretion ⇒ ↓ water in luminal secretions
  • Leads to duct obstruction in pancreas ⇒ injury, inflammation, and fibrosis ⇒ exocrine pancreatic insufficiency
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21
Q

Malabsorption

Mechanical Causes

A
  • Gastrectomy (complete or partial)
  • Intestinal surgery:
    • Bypass w/ blind loop and bacterial overgrowth
    • Loss of critical mass
    • Loss of critical functional area
  • Lymphatic or luminal obstruction due to tumors, adhesions, fistula
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22
Q

Infectious Gastroenteritis

Overview

A
  • Bacterial, viral, mycobacterial, fungal, parasitic, protozoa etiologies
  • Some organisms can be visualized and identified based on morphologic and staining characteristics
  • Histology varies: no visible disease, non-specific changes, granulomatous disease, ulceration
  • Diagnosis (multimodal approach):
    • Serology
    • Stool exam for ova and parasites
    • Biopsy
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23
Q

Bacterial Enterocolitis

A
  • Organisms:
    • Vibrio cholera, Shigella, Campylobacter jejuni, Yersinia, Salmonella, E. coli
    • Clostridium difficile
  • Mechanisms of disease:
    • Ingestion
      • Preformed toxin
      • Toxin producing organism
    • Adherence to epithelium w/ interference of function
    • Invasion and destruction of epithelium and mucosal integrity
    • Spread elsewhere in the body w/ extraintestinal manifestations and/or carrier state
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24
Q

Pseudomembranous Colitis

A

“Antibiotic-Associated Colitis”

  • Acute colitis w/ adherent yellow-green fibrinopurulent exudate
  • Organism: Clostridium difficile
    • Normal gut commensal
    • Setting of abx use due to overgrowth
    • Exotoxins (A and B)
      • Disaggregation of actin microfilaments
      • Intestinal secretion and acute inflammation
    • C. difficile is prevalent in hospitals
    • Up to 30% of hospitalized pts colonized w/ C. difficile but most don’t have disease
  • Other causes: any form of severe mucosal injury
  • Diarrhea can be very severe
  • Can lead to dehydration, hypoalbuminemia, even death
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25
Q

Giardia Lamblia

A
  • Most common pathogenic parasitic infection
  • Transmission: fecal contaminated water or food
    • Present in unfiltered public water supplies, rural streams
    • Worse in immunocompromised
  • Pear shape trophozoite on duodenal biopsy
  • No obvious invasion ⇒ nl intestinal morphology by LM
  • Mechanism: organisms adhere to surface, ↓ expression of brush-border enzymes (including lactase) and damage microvilli
  • Clinical: acute or chronic diarrhea, malabsorption, and wt loss
    • Dx infection by finding cysts in stool samples
    • Oral abx effective but recurrence is common
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26
Q

Entamoeba histolytica

A
  • Parasitic causes of enterocolitis
  • Etiologic agent of amebiasis
  • Transmission: Fecal-oral
    • Cyst form:
      • Infectious form
      • Form identified in colon and feces
  • Pathogenesis:
    • Penetrates mucosa
    • ± Deep ulceration
    • ± Portal system spread w/ systemic dissemination and formation of liver, lung, and brain abscesses
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27
Q

Non-infectious Enterocolitis

Etiologies

A
  • Drug Induced
  • Treatment related: chemotherapy, radiation
  • Neutropenic colitis (typhlitis)
  • Obstruction related
  • Diversion colitis
  • Diverticular disease related
  • Graft vs Host disease
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28
Q

Mechanical Bowel Obstruction

Etiologies

A
  • Hernia
  • Adhesions
  • Intussusception
  • Volvulus
  • Tumors and strictures (some due to Crohn Disease)
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29
Q

Hernia

A

Protrusion of a portion of the peritoneal sac through a defect in the wall of the peritoneal cavity

  • # 1 cause of intestinal obstruction world-wide; #3 cause US
  • Incarcerated: Hernia contains entrapped bowel
  • Strangulated: Infarction of trapped bowel due to compromise of blood flow
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30
Q

Adhesions

A

Fibrosis between bowel loops or bowel to other structure

  • #1 cause of intestinal obstruction in US
  • Etiology: surgery, inflammatory bowel disease, endometriosis, peritonitis (common denominator)
  • Complication: ‘internal herniation’, obstruction, infarction
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31
Q

Intussusception

A

Segment of small intestine becomes ‘telescoped’ into the more distal intestine, peristalsis propels the segment distally

Children: w/ or without lesion

Adult: w/ lesion (intraluminal mass as ‘lead point’)

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32
Q

Volvulus

A

Twisting of a loop of bowel about its mesenteric base of attachment

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33
Q

Ischemic Bowel Disease

Overview

A
  • ↓ Blood supply ⇒ hypoxia, accumulation of metabolic byproducts, bacterial overgrowth ⇒ necrosis
  • Extent:
    • Mucosal: mucosa only
    • Mural: mucosa and submucosa (may be due to non-occlusive flow problem)
    • Transmural: necrosis of all layers (vessel is often mechanically obstructed)
      • Sharply defined border w/ normal
      • Infarcted bowel intensely congested (dusky to purple red)
      • Wall edema w/ coagulative necrosis of muscularis propria 1-4 days after onset
  • Chronic ischemic colitis may mimic Idiopathic IBD
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34
Q

Ischemic Bowel Disease

Etiologies

A
  • Arterial occlusion (30-50%)
    • Thrombus: Usually proximal and w/ plaque
    • Embolus: Cardiac vegetations, procedures, aortic plaque
    • Dissecting aortic aneurysm
    • Other: iatrogenic, vasculitis, hypercoagulable states
  • Nonocclusive Ischemia (30-50%)
    • Splanchnic vasoconstriction: associated w/ myocardial infarction, congestive failure, shock, trauma, hypovolemia, drugs
  • Mesenteric venous thrombosis (10-15%)
    • Hypercoagulable states: oral contraceptives, invasive neoplasms
    • Cirrhosis
    • Sepsis
  • Miscellaneous
    • Radiation injury
    • Mechanical causes of obstruction
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35
Q

Ischemic Bowel Disease

Pathogenesis

A
  • Intestinal response to ischemia has 2 phases:
    • Hypoxic injury
      • At onset of vascular compromise
      • Epithelial cells are relatively resistant to transient hypoxia
    • Reperfusion injury
      • More damaging
      • May trigger multiorgan failure
      • May be due to leakage of gut lumen bacterial products into systemic circulation, free radical production, neutrophil infiltration
  • Variables:
    • Severity of vascular compromise
    • Time frame of development
    • Vessels affected
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36
Q

GI Malignant Lymphoma

Overview

A
  • GI tract = most common site of extranodal lymphoma
  • 1-4% of GI malignancies
  • > 95% are B cell type
  • Sites: stomach (55-60%) > small intestine (25-30%) > colon (10-15%)
  • Prognosis is dependent on: stage, lymphoma type
    • If disease limited to mucosa or submucosa, 10 yr survival ~ 85%
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37
Q

Primary GI Malignant Lymphomas

Types

A
  • B Cell
    • MALT (Mucosal Associated Lymphoid Tissue) type
      • Low grade and High grade
    • Mediterranean Lymphoma
      • Pts have underlying chronic diffuse mucosal plasmacytosis
      • Cells make abnormal IgA, often preceded by malabsorption
    • Mantle Cell Lymphoma
    • Burkitt and Burkitt-like Lymphoma
    • EBV-Associated Lymphoproliferative Disease
    • Other types as seen in lymph nodes
  • T Cell
    • EATL (Enteropathy Associated T-cell Lymphoma)
    • Other
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38
Q

Primary GI Malignant Lymphomas

Risk Factors

A
  • Helicobacter gastritis
  • Natives of Mediterranean region
  • Immunodeficiencies
    • Congenital
    • HIV
    • Immunosuppressed
    • EBV related
  • Celiac sprue
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39
Q

Chronic Colitis

Overview

A
  • Etiology unknown
  • Must exclude known causes first
  • Idiopathic inflammatory bowel disease (IIBD)
    • Ulcerative Colitis (UC)
    • Crohn Disease (CD)
    • Indeterminate Colitis (~10% of IBD pts)
  • Microscopic colitis
    • Collagenous colitis
    • Lymphocytic colitis
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40
Q

Inflammatory Bowel Disease

Overview

A
  • Initially individuals may have a dx of chronic colitis, etiology unknown
  • Idiopathic inflammatory bowel disease (IIBD)
    • Ulcerative Colitis (UC)
    • Crohn Disease (CD)
    • Indeterminate Colitis
      • ~10% of IBD pts
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41
Q

Inflammatory Bowel Disease

Differential Diagnosis

A
  • Consider other possibilities when pts present w/ 1st episode suspicious for IBD
  • Must r/o other causes:
    • Parasitic disease
    • Bacterial pathogens (C. difficile, Salmonella, Shigella, E. coli, Campylobacter)
    • Diverticulitis
    • Ischemia and other potential causes for bleeding, diarrhea, fever, and/or abd pain
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42
Q

Inflammatory Bowel Disease

Epidemiology

A
  • ↑ Worldwide incidence
    • Areas adopting a more “Western” lifestyle
  • More common in Jewish individuals
  • Less common in African-Americans
  • Anyone can develop IBD regardless of race/ethnicity
  • M=F incidence
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43
Q

Inflammatory Bowel Disease

Risk Factors

A
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44
Q

Inflammatory Bowel Disease

Etiology and Pathogenesis

A
  • Genetics / Fhx
    • ~10-15% of lBD pts have an affected 1° family member
    • MZ twins: CD ~60% concordance, UC concordance ~15%
  • Pathogenesis
    • Genetic susceptibility, environmental factors, and immune response
    • “Trigger” in susceptible host ⇒ abnormal immune response ⇒ inflammation ⇒ tissue injury
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45
Q

NOD 2/Card 15

Gene

A

Susceptibility locus for IBD

  • NOD2 activates down-stream inflammatory cell signaling
  • Ass. w/: aggressive disease, fibrostenotic disease, and recurrence post-op
  • Common in Caucasian population
  • Up to 20% carry one mutation, 1% carry two
  • Chance of NOD-2 homozygotes developing CD no greater than 4%
46
Q

Inflammatory Bowel Disease

Serologic Markers

A
47
Q

IBD

Clinical Comparison

A
48
Q

Crohn’s Disease

Clinical Characteristics

A
  • Location:
    • Limited to the ileum (ileitis) (~40%)
    • Terminal ileum and colon (ileocolitis) (~40%)
    • Only the colon (20%)
  • Predominant sx: crampy pain, diarrhea, fever, weight loss
  • Physical exam findings vary w/ location and severity of disease
    • ± Aphthous mouth ulcers
    • ± TTP over involved bowel (usu. RLQ TTP & thickening)
    • ± Perianal disease (fistulas or tender induration)
  • ± Anemia from chronic disease or blood loss
  • CRP or ESR may be used to monitor inflammation
49
Q

Crohn’s Disease

Gross Pathology

A
  • Disease is regional ⇒ skip lesions
  • Earliest lesion is the aphthous ulcer
  • Multiple lesions can coalesce into linear ulcers
  • Some mucosa is spared ⇒ cobblestone appearance
  • Diseased tissue is depressed
  • Can develop fissures between mucosal folds
  • These can extend transmurally to become fistula tract or perforation site
  • Bowel wall thickens ⇒ fibrotic
  • Mesenteric fat can extend to cover the serositis ⇒ ‘creeping fat’
50
Q

Crohn’s Disease

Histology

A
  • Active Crohn’s disease:
    • Cryptitis
      • Neutrophils infiltrate ⇒ damage crypt epithelium
    • Crypt abscess
      • Cluster of neutrophils w/in a crypt
    • Often associated w/ crypt destruction
    • Ulceration
  • Repeated cycles of crypt destruction and regeneration lead to:
    • Distortion of mucosal architecture
      • Crypts w/ bizarre branching shapes and unusual orientations to one another
    • Epithelial metaplasia w/ gastric antral-appearing glands (Pseudo-pyloric metaplasia)
    • Paneth cell metaplasia
    • Mucosal atrophy w/ loss of crypts
    • Noncaseating granulomas (~35%)
      • Any layer of intestinal wall or in mesenteric lymph nodes
51
Q

Crohn’s Disease and Neoplasia

A

6x ↑risk of carcinoma

↑ Risk of EBV-Associated Lymphoma related to therapy

52
Q

Ulcerative Colitis

Clinical Characteristics

A
  • Location:
    • May involve rectum only (ulcerative proctitis)
    • Varying degrees of sigmoid and descending colon (left sided colitis)
    • Disease proximal to the splenic flexure (pancolitis)
  • Dominant feature of UC is bloody diarrhea
  • Bowel urgency, rectal discomfort, and abdominal cramping
  • ± Systemic complications (ex. fever and weight loss)
    • Depends on the extent of colonic involvement
  • Episodic > continuous disease
  • Abdominal TTP common (often over left colon)
  • Labs:
    • Anemia from blood loss
    • ↑ WBC
    • ↑ ESR or CRP
53
Q

Ulcerative Colitis

Gross Pathology

A
  • Continuous involvement
  • Friable surface w/ easy bleeding
  • Broad-based ulceration
  • Pseudopolyps
  • Isolated islands of regenerating mucosa
    • Can fuse to create ‘mucosal bridges’
  • Leather strap appearance
  • Mucosal atrophy
    • Smooth surface w/o folds
  • Backwash ileitis (10%)
    • Mild mucosal inflammation of the distal ileum in severe cases w/ pancolitis
  • Inflammation may disturb neuromuscular function ⇒ colonic dilation and toxic megacolon ⇒ ± perforation
54
Q

Ulcerative Colitis

Histology

A
  • Active UC (similar to Crohn’s)
    • Inflammatory infiltrates
    • Crypt abscesses
    • Architectural crypt distortion
    • Epithelial metaplasia
    • But inflammatory process is diffuse & limited to mucosa and superficial submucosa
  • Healed disease:
    • Submucosal fibrosis
    • Mucosal atrophy
    • Distorted mucosal architecture
    • May also revert to near normal after prolonged remission
  • Granulomas are not present in UC
55
Q

UC Association w/ Dysplasia/Carcinoma

A
  • 20-30x ↑ risk for neoplastic transformation of colonic mucosa
  • Highest risk of dysplasia:
    • Disease >10 years duration
    • Pancolitis
  • Inactive disease is not protective
  • Absolute risk of 35% at 30 yrs of disease
56
Q

Crohn’s Disease vs Ulcerative Colitis

Path Features

A
57
Q

Inflammatory Bowel Disease

Extra-intestinal Manifestations

A
  • Aphthous ulcers in the mouth
  • Sclerosing cholangitis in UC
    • Does not improve w/ tx of the UC
  • Ankylosing spondylitis
    • Is not influenced by tx
  • Migrating large joint arthritis
    • Usually asymmetric
    • May precede the onset of IBD
    • Usually responds to IBD treatment
  • Pyoderma gangrenosum
    • Ulcerating and undermining skin lesion
    • May respond to aggressive IBD therapy
  • Erythema nodosum
    • Painful and hyperemic nodules on the anterior leg
    • Usually responds well to IBD therapy
  • Ocular complications include episcleritis, scleritis, and uveitis
58
Q

Inflammatory Bowel Disease

Complications

A
  • Fibrostenosis ⇒ Stricture
  • Stricture ⇒ proximal dilation and pressure ⇒ abscess and fistula
  • Penetrating Disease ⇒ Fistula
    • Fistulas can form between: Entero-Enteric, Entero-Colonic, Entero-Vesicular, Entero-Vaginal, Entero-Cutaneous
  • Perianal Disease w/ abscess
  • Superinfection
    • C. difficile is a common offender
  • Toxic Megacolon
    • Leads to intestinal perforation
  • Short Bowel Syndrome
    • Severe malabsorption due to loss of small bowel surface area
  • Colorectal Neoplasm
    • ↑ Colon cancer risk w/ duration of illness and extent of disease
    • Guidelines for screening vary on the location / extent of disease
  • Pts w/ primary sclerosis cholangitis at risk for cholangiocarcinoma
59
Q

Inflammatory Bowel Disease

Treatment

A
  • Potential pharm IBD treatments:
    • Mesalamine
    • Steroids
    • Immunomodulators
    • Antibiotics
    • Anti-TNF agents
  • Surgical:
    • Severe and unresponsive UC may require a colectomy
    • Surgery for CD is usually for obstruction and/or abscess in the small bowel and for chronicity in large bowel disease
    • Resections performed w/ aim of preserving as much small bowel as possible
    • Newer treatment options ⇒ ↓ need for surgery in IBD
60
Q

Microscopic Colitis

A
  • Unknown Etiology
  • No gross abnormality seen
  • Chronic watery diarrhea
  • Two forms:
    • Collagenous Colitis
    • Lymphocytic Colitis
61
Q

Collagenous Colitis

A
  • Type of microscopic colitis
  • Women 40-70 y/o
  • Focal thickening of subepithelial collagen
  • ↑ intraepithelial lymphocytes
  • ↑ mixed inflammatory cells in lamina propria
62
Q

Lymphocytic Colitis

A
  • Type of microscopic colitis
  • F=M
  • Marked ↑ intraepithelial lymphocytes
  • Associations: Celiac sprue, other autoimmune diseases
63
Q

Diverticular Disease

Overview

A
  • 1° in sigmoid colon (> 95%)
  • Pseudodiverticulum: mucosa and submucosa herniate through wall in area of muscle interruption
  • Epidemiology:
    • Affects 50% of those > 60 y/o in US
    • Rare under age 30
    • 80% are clinically silent
  • Pathogenesis:
    • Colonic structure issue
      • Weak areas in muscularis propria where the nerves, arterial vasa recta, and connective tissue sheaths penetrate inner circular muscle coat
      • Colonic external longitudinal layer of muscularis propria gathered into 3 bands (taeniae coli)
      • ↑ Intraluminal pressure from exaggerated peristaltic contractions, w/ spasmodic sequestration of bowel segments
      • Inner layers prolapse through muscle gaps (pseudodiverticula)
      • Enhanced by diets low in fiber (↓ stool bulk)
64
Q

Diverticulosis

A
  • Clinician dx: presence of diverticula
  • Pathological dx: presence of uninflamed diverticula
  • Pt may experience crampy discomfort, constipation, diarrhea, but most have no sx
65
Q

Diverticulitis

A
  • Diverticulum becomes obstructed ⇒ inflammation ⇒ diverticulitis
  • Clinical sx: fever, ↑ WBC count, peritoneal signs
  • Pathologist sees inflamed diverticula
  • If perforation occurs ⇒ pericolonic abscesses, sinus tracts, peritonitis
  • Pt can present w/ acute abdomen
  • Even without perforation, can be left w/ chronic issues ⇒ fibrosis, stricture, etc.
66
Q

Diverticula Complications

A
  • Bleeding
  • Abscess
  • Fistula
  • Stenosis
  • Rupture
  • Impaction
67
Q

Hemorrhoids

A
  • Variceal dilations of anal and perianal venous plexus due to ↑ venous pressure
  • Affects 5% of population
  • Risks include:
    • Straining at stool
    • Pregnant woman
    • Portal HTN
  • Complications:
    • Thrombosis
    • Infarction
    • Fissure
    • Ulceration
68
Q

Angiodysplasia

A
  • Malformed mucosal and submucosal vessels
  • Most often in cecum and right colon, usu. after age 60
  • Pathogenesis: interference w/ submucosal venous drainage ⇒ retrograde distension, ? loss of vascular integrity
  • Seen in 1% of adults but accounts for 20% of significant lower GI bleeding
    • Chronic, intermittent
    • Acute, massive
69
Q

Appendix

A
  • Worm-like structure: 7 cm length, 1 cm diameter
  • Lined by colonic type mucosa, rich in lymphoid follicles
  • Fibrous obliteration w/ ↑ age
  • Function unknown
  • Disorders:
    • Acute appendicitis
    • Mucocele
    • Tumors (Carcinoid is most common)
70
Q

Acute Appendicitis

A
  • Clinical features:
    • Relatively common
      • Lifetime risk is 7%, M>F
    • Primarily young adults
    • RLQ/periumbilical pain, N/V, fever
  • Pathogenesis:
    • Luminal obstruction by fecalith or other object (worms, gallstone, tumor, etc) seen in 50-80% of cases
    • Compromises venous outflow
    • Tissue undergoes ischemic injury
    • Stasis of lumen contents ⇒ bacterial proliferation ⇒ inflammatory response (edema, PMN infiltration)
    • Can result in perforation and peritonitis if not detected and removed
71
Q

Appendiceal Tumors

A
  • Most common is carcinoid
  • May also see adenomas or non-mucin-producing adenocarcinomas
  • Mucocele
    • Dilated appendix filled w/ mucin
    • Multiple etiologies:
      • Obstructed appendix filled w/ mucin
      • Mucinous cystadenoma
      • Mucinous cystadenocarcinoma
        • May result in pseudomyxoma peritonei: implantation of mucinous carcinoma cells on peritoneum
          • Can do repeated debulking’s but is usu. fatal
72
Q

Neuroendocrine (Carcinoid) Tumor

Overview

A
  • Arise from neuroendocrine cell of GIT
    • Neuroendocrine cell differentiates from gut stem cell
  • Endocrine and paracrine functions
  • Can also arise in the lung
  • Peaks in 6th decade
  • Location:
    • Appendix > small intestine > rectum > stomach > colon
  • May present w/ syndrome related to hormone production
  • Prognosis of GI carcinoids determined by location
    • Foregut carcinoids: rare metz, includes stomach
    • Midgut carcinoids: often aggressive, in jejunum and ileum, can invade and metastasize
    • Hindgut carcinoids: in appendix and colorectum, usually discovered incidentally, worse behavior in prox. colon than in rectum, rarely metastasize
  • For individual tumors, also consider:
    • Depth of penetration
    • Size
      • < 1 cm rarely metastasize
      • > 2 cm usually have metz
  • Overall survival: 90% exclusive of appendiceal
73
Q

Neuroendocrine (Carcinoid) Tumor

Appearance

A
  • Intramural or submucosal lesion w/ overlying mucosa that can ulcerate
  • Tumors are yellow or tan, and firm
  • Histology
    • Islands or strands of tumor cells w/ ‘salt and pepper’ chromatin
    • Stain for NE markers: chromogranin, synaptophysin, NE granules on EM
  • Histologic examination cannot distinguish benign from malignant tumors
74
Q

Carcinoid Syndrome

A
  • Due to excessive serotonin
  • Can test blood and urine for:
    • 5-hydroxy-tryptamine [5HT]
    • 5-HIAA (5-hydroxyindoleacetic acid)
  • Occurs in 1% of carcinoid pts and in 20% of those w/ metastases
  • Requires bypass of portal circulation
    • Metastases w/ GI tumors
    • Lung tumors, ovary tumors
  • Clinical features:
    • Vasomotor disturbances: cutaneous flushing, cyanosis
    • Intestinal hypermotility: diarrhea, cramps, nausea and vomiting
    • Asthmatic bronchoconstrictive attacks: cough, wheezing, dyspnea
    • Hepatomegaly: nodular liver
    • Systemic fibrosis: endocardial, valvular, retroperitoneal, pelvic
75
Q

Polyps

Overview

A
  • Most common in the colon, can see elsewhere
  • Begin as small mucosal elevations
    • Sessile: grow directly from surface w/o stalk
    • Pedunculated: have a stalk
76
Q

Polyp

Types

A
  • Non-neoplastic polyps
    • Hyperplastic polyps
    • Inflammatory polyps
    • Hamartomatous polyps (sporadic/syndromatic)
      • Juvenile polyps
      • Peutz Jegher polyps
  • Neoplastic polyps
    • Adenoma (see dysplasia)
77
Q

Hyperplastic Polyps

A
  • Non-neoplastic polyp
    • Due to delayed shedding of surface epithelial cells
  • Most common in rectosigmoid
  • Typically small (< 0.5 cm)
  • Usually seen in pts in 50s-60s
  • No known neoplastic potential
78
Q

Inflammatory Polyps

A

Ex. solitary rectal ulcer syndrome

  • Presents w/ rectal bleeding, mucus discharge, inflammatory lesion of anterior rectal wall
  • Due to impaired relaxation of anorectal sphincter
  • Creates sharp angle @ anterior rectal shelf ⇒ recurrent abrasions ⇒ ulceration of rectal mucosa ⇒ polyp & ± mucosal prolapse
79
Q

Hamartomatous Polyps

A

Examples:

  • Juvenile Polyps
  • Peutz Jeghers Syndrome
  • Cowden Syndrome and Bannayan-Ruvalcaba-Riley Syndrome
  • Cronkhite-Canada Syndrome
80
Q

Juvenile Polyps

A
  • Majority present as sporadic lesion in rectum
  • Most common in children < 5 yrs
  • In adults, sporadic lesion can be present ⇒ retention polyp
    • Pedunculated, dilated glands filled w/ mucin and inflammatory debris
81
Q

Juvenile Polyposis Syndrome

A
  • Autosomal dominant
  • 3-100 polyps throughout GI tract, most in colorectum
  • Can hemorrhage when ulcerated
  • Dysplasia in up to 20% of these polyps ⇒ ↑ risk of colon CA
  • Associated congenital defects: pulmonary AVMs
82
Q

Peutz Jegher Syndrome

A
  • Genetic defect: LOF mutation in LKB1/STK11 in 50% w/ familial syndrome
    • Encodes a kinase regulating cell growth and metabolism
    • Autosomal dominant
  • Presents near age 11
  • Clinical characteristics:
    • Melanotic mucosal and cutaneous pigmentation
      • Lips, buccal mucosa, genitalia, palmar surfaces
    • Hamartomatous polyps throughout GI tract
      • Most common in small intestine
  • Associations:
    • ↑ Risk of carcinoma
      • Colon, pancreas, breast, lung, ovary, uterus, testes
    • In women: ovarian sex cord tumor w/ annular tubules
83
Q

Cowden Syndrome and Bannayan-Ruvalcaba-Riley (BRR)

Syndromes

A
  • Hamartomatous polyp syndromes
  • LOF mutation in PTEN
    • Tumor suppressor gene
    • Autosomal dominant
  • Cowden
    • Microcephaly, hamartomatous polyps in intestine, benign skin tumors, subcutaneous hemangiomas
    • ↑ Risk of breast, follicular thyroid and endometrial CA
  • BRR
    • Also mental deficiency, developmental delay
    • Less neoplasia than Cowden
84
Q

Cowden Syndrome (CS)

Pathognomonic Mucocutaneous Features

A

a. Trichilemmomas on the nape of the neck
b. Palmar keratoses
c. Perioral papillomatous papules and nasal polyposis
d. Gastric hamartomas

85
Q

Cronkhite-Canada Syndrome

A
  • Not hereditary
  • Usually seen over age 50
  • Clinical:
    • Diarrhea, wt loss, abd pain, weakness, nail atrophy and splitting, hair loss, skin hyperpigmentation/hypopigmentation
    • Hamartomatous polyps in stomach, small intestine and colorectum
  • Resemble juvenile polyps but non-polyp mucosa shows similar changes
  • Cause unknown, no specific therapy, 50% fatal
86
Q

Colonic Dysplasia

Overview

A
  • Neoplastic epithelium that remains confined w/in the basement membrane
  • Can develop in flat areas that look normal
  • Nuclear hyperchromasia (dark nuclei), elongation, and stratification
  • ± Large nucleoli and fewer goblet cells
  • Epithelial cells fail to mature as they move toward surface
  • Show genetic characteristics of neoplastic transformation
  • Colonoscopic appearance of dysplasia:
  • Flat mucosa w/ appearance of colitis/normal (sessile)
  • DALM: Dysplasia associated lesion or mass
  • Adenoma-like: polypoid projection w/ stalk (peduculated)
    • Graded as: Low grade, High grade
    • Precursor lesion to adenocarcinoma
87
Q

Dysplasia

Gross Appearances

A
88
Q

Adenomas

Overview

A
  • Benign pedunculated or sessile polypoid lesion composed of dysplastic tissue
  • Incidence is age related
  • 50% of adults in West have by age 50
  • Precursor lesion to adenocarcinoma
    • Recommend surveillance exam by age 50
    • Earlier for those w/ family hx
      • 10 yrs before youngest affected relative was dx
      • 4x risk for family members
  • Most adenomas won’t progress to adenocarcinoma, but don’t know which ones
  • No gender predominance
  • Often asymptomatic, can cause bleeding
89
Q

Adenomas

Subtypes

A
  • Tubular: > 75% pit architecture
    • Most common adenoma (90%)
    • Usually small, pedunculated
  • Tubulovillous: 25-50% villous architecture
    • 5-10% of adenomas
  • Villous: > 50% villous
    • 1% of adenomas
    • Usually large and sessile
  • Sessile serrated:
    • Looks like hyperplastic polyps but are premalignant
  • Carcinoma risk
    • Consider size of adenoma, tubular vs villous, pedunculated vs sessile, and amount of dysplasia
    • ~40% risk of CA in sessile polyps > 4 cm
90
Q

Adenoma → Carcinoma

Transformation

A
  • Dysplastic epithelial cells breach BM → lamina propria or muscularis mucosa
  • Adenoma → intramucosal carcinoma
    • Does not metastasize
  • Polypectomy is adequate therapy unless:
    • Cannot be performed d/t location and/or size
    • Lesion on tissue margin
    • Intramucosal carcinoma poorly differentiated
    • Angiolymphatic invasion present
  • Next step would be invasion beyond muscularis mucosa
    • Now invasive adenoCA ⇒ can spread
91
Q

Adenoma → Carcinoma

Colonoscopic Change

A
92
Q

Colorectal Cancer

Overview

A
  • Most common GI cancer
  • Preventable cancer
    • High impact disease (incidence and death)
    • At-risk population (family hx, genetics, elderly etc.)
    • Precursor lesions (polyps or adenomas)
    • Tests to detect precursor lesions (colonoscopy ⇒ highly sensitive)
93
Q

Colorectal cancer

Epidemiology

A
  • USA
    • Most common GI malignancy, peak age 60-70
    • 2nd most common cause of CA death after lung
    • 130k new cases/yr; 55k deaths/yr
  • Worldwide
    • 30x difference in incidence rate in developed countries vs India, South America, Africa
    • Migration changes risk status
      • Lifestyle and diet changes
      • Low fiber, high carbs and fats associated w/ ↑ risk
      • NSAIDs may have protective effect
        • ⊗ COX -2
        • Highly expressed in colon CA
94
Q

Colorectal Cancer

Risk Factors

A
  • ⊕ Risk Factors
    • Age
      • ≥ 50 y/o
    • Hereditary syndromes
      • Present as early as 10-15 y/o
      • FAP (APC Pathway)
      • HNPCC (Microsatellite instability)
    • Family Hx ⇒ even w/o genetic syndromes
    • Diet
      • Low dietary fiber, High animal fat, High sugar
    • Red meat and smoking
      • Nitrosamines and heterocyclic amines
      • ? APC mutations
      • ? K-ras mutation
    • Alcohol
      • Acetaldehyde-DNA damage
    • Obesity
      • Insulin Resistance and high Insulin growth factors
    • Smoking
    • IBD
      • Crohn’s colitis
      • Ulcerative Colitis
  • ⊖ Risk Factors
    • Vegetables
      • Antioxidants ⇒ ↓ DNA damage
      • Folate ⇒ ↑ DNA integrity
      • ↓ Growth stimulus
      • ↓ Transit time
    • Physical activity/low body mass
95
Q

Colorectal Carcinoma

Pathogenesis

A

Typical progression up to 10 yrs

Multifactorial etiology:

  • Hereditary susceptibility
  • Diet & environmental factors
  • Somatic genetic change
    • Two distinct genetic pathways
      • Both involve stepwise accumulation of multiple mutations
      • Epigenetic events, e.g. methylation-induced gene silencing, may enhance progression along both
  • Genetic syndromes ⇒ can accelerate progression to < 3 yrs
96
Q

Colorectal Carcinoma

Genetic Pathways

A
  • Adenomatous Polyposis Coli (APC) / B-catenin Pathway
    • 80% of sporadic colon CA
    • Associated w/ WNT and classic adenoma-carcinoma sequence
    • Mutation in KRAS, p53, SMAD 2 and 4 play a role
  • Microsatellite Instability Pathway
    • Associated w/ defects in DNA mismatch repair
    • Mutation in MSH2, MLH1, and BRAF play a role
    • Common in SSA, mucinous CA, right colon site
97
Q

Colorectal Carcinoma

Specific Genetic Mutations

A
98
Q

Colorectal Cancer

Syndromes

A
  • FAP and variants (mutation in APC gene)
    • Familial adenomatous polyposis (FAP)
    • Attenuated FAP
      • Delay in polyps, < 100, delayed colon CA
    • Gardner syndrome
      • Soft tissue and bone tumors, epidermal cysts, dental issues
    • Turcot syndrome (CNS tumors)
      • ⅔ have APC gene mutation ⇒ medulloblastomas
      • ⅓ have DNA repair gene mutation ⇒ glioblastomas
  • Hereditary nonpolyposis colorectal cancer (HNPCC, Lynch syndrome)
99
Q

Familial Adenomatous Polyposis (FAP)

Pathogenesis

A
  • Autosomal dominant
  • Germline genetic defect:
    • Chromosome 5q21
    • Adenomatous polyposis coli (APC) gene
  • APC function:
    • Regulation of ß catenin induced signaling
    • Regulation of cell adhesion via ß-catenin and E-cadherin
    • Regulation of cell migration via microtubule interaction
    • Cell cycle block ⇒ ? inhibits cell cycle components
100
Q

Familial Adenomatous Polyposis (FAP)

Clinical Characteristics

A
  • Multiple adenomas
    • In colorectum: min 100, max > 2k
      • Look like sporadic ones
      • Flat or depressed adenomas and microscopic ones
    • In upper GI tract, most commonly around ampulla
    • In stomach, may develop adenomas, more commonly see fundic gland polyp
  • Extra-intestinal signs and symptoms
    • Congenital hypertrophy of retinal pigment epithelium
      • Can detect at birth
  • Virtually all pts develop colorectal carcinoma
    • Usually before age 30
  • Treatment:
    • Colectomy
      • Still need to monitor other GI sites
101
Q

Hereditary Nonpolyposis Colon Cancer (HNPCC) Syndrome

Overview

A

“Lynch Syndrome”

  • Most common type of familial colorectal CA syndrome
  • Accounts for 1-5% of cases of colorectal cancer
  • Do not see extensive polyposis but polyps present
  • Difficult to distinguish from “sporadic” cases
  • Early onset of colon CA (usually right colon)
  • And other cancers
    • Esp. those in endometrium, urinary tract, stomach and biliary system
102
Q

HNPCC

Genetic Defect

A
  • Germline mutation in a DNA mismatch-repair gene
    • MSH2, MLH1, PMS1, PMS2, MSH6
  • Encode proteins that repair mismatches of nucleotides
    • Occur when DNA polymerase inserts the wrong bases in newly made DNA
  • W/o repair, mistakes persist as unstable tandemly repeated DNA sequences ⇒ microsatellite instability
  • Also seen in 15% of sporadic cancers
103
Q

HNPCC

Diagnostic Criteria

A
  • Molecular testing
    • Demonstrate tumor has microsatellite instability
    • Test for germline mutation in DNA mismatch repair gene
  • Amsterdam Criteria
    • ≥ 3 members in at least 2 successive generations must have colorectal CA
    • At least one case dx before age of 50 yrs
    • One of the affected members should be a first degree relative of the other two
  • Bethesda Criteria
    • Amsterdam criteria individuals
    • Individuals w/ two HNPCC- related cancers
    • Individuals w/ colorectal CA and 1st degree relative w/ ≥ 1 of the following:
      • Colorectal CA dx’d under 45 yrs
      • HNPCC-related CA dx’ed under 45 yrs
      • Adenoma dx’ed under 40 yrs
    • Individuals < 45 yrs w/ colorectal or endometrial CA
    • Individuals w/ proximal cancer of undifferentiated type
    • Individuals < 45 yrs w/ signet-ring CA
    • Individuals < 40 yrs w/ adenomas
104
Q

Colon Cancer

Screening

A
  • Screen everyone between 50-75 y/o
    • FHx, genetic syndromes start at lower age
  • 76-85 y/o ⇒ screen if not done before and if relatively healthy
  • > 85 y/o ⇒ do not screen
105
Q

Colorectal Carcinoma

Clinical Characteristics

A
  • Precursor lesions (polyps) ⇒ many asymptomatic
    • Remains silent for years
  • Invasive component elicits a strong desmoplastic response ⇒ firm consistency
  • Clinical presentation: Symptoms insidious
    • Right colon (38%)
      • Fatigue, weakness, iron deficiency anemia (d/t occult blood loss)
      • Exophytic, polypoid lesions
        • Protrudes into lumen
    • Transverse colon (18%)
    • Descending (left) colon (8%)
      • Occult bleeding, change in bowel habit, LLQ discomfort
      • Annular, encircling lesions
        • Constricting, ‘napkin ring’ prone to obstruction
        • Colonic obstruction ⇒ abd pain, vomiting, inability to eat
    • Sigmoid colon (35%)
      • In the rectum, sigmoid colon, villous adenoma ⇒ diarrhea
    • Multiple sites 1%
    • Advanced stages
      • Grossly visible rectal bleeding
  • Spread:
    • Direct extension
    • Metastasizes through blood vessels and lymphatics
      • Preferred sites ⇒ LN, liver, lungs, bones
      • When cancer metastatic ⇒ weight loss
  • Prognosis: most influenced by depth of invasion and whether LN’s are positive
106
Q

Colon Cancer

Staging

A
  • T staging:
    • Rectal CA: Endoscopic US (EUS) and MRI are equivocal
    • Colon CA: EUS can be used, but usu. not needed
  • N staging:
    • Rectal CA: EUS has the best sensitivity, can biopsy, CT
    • Colon CA: CT, often better-established post-op (histology)
  • M staging:
    • CT, esp. combo w/ PET
    • Brain ⇒ MRI
    • Liver ⇒ Dynamic MRI/CT
107
Q

Colon CA

Grading

A
108
Q

Colon Cancer

Treatment

A
  • For carcinoma in situ (Tis), intramucosal carcinoma, or high-grade dysplasia
    • Polypectomy or endoscopic mucosal resection via colonoscopy
  • For all other stages
    • Tx options depend on disease specifics
      • Ex. depth of tumor invasion in the colon and presence of metastasis
    • Includes:
      • Surgery
      • Chemotherapy
      • Radiation therapy
109
Q

Anal Canal

Histology

A
  • Upper ⅓: lined by columnar rectal epithelium
  • Middle ⅓: transition to stratified squamous
  • Lower ⅓: stratified squamous
110
Q

Anal Carcinoma

Overview

A
  • 1.5% of digestive system CA
  • In US: 3,400 new cases per year
  • Can be glandular, squamous, or basaloid (cloacogenic CA)
  • Pure squamous cell CA often ass. w/ HPV infection
    • Also causes precursor lesions: Anal Intraepithelial Neoplasia (AIN), condyloma
111
Q

Anal Carcinoma

Clinical Features

A
  • Rectal bleeding: 45%
    • May be mistaken as hemorrhoid
  • Pain/rectal mass sensation: 30%
  • No rectal symptoms: 20%
  • Size of tumor most important prognosticator
    • ≤ 2cm: cure 80%
    • ≥ 5cm: cure < 50%
112
Q

Anal Carcinoma

Risk Factors

A
  • Strong evidence
    • HPV infection
    • Receptive anal intercourse
    • STI
    • > 10 sexual partners
    • Hx of cervical, vulvar or vaginal CA
    • Immunosuppression after solid organ transplantation
  • Moderately strong evidence
    • HIV infection
    • Long-term use of corticosteroids
    • Cigarette smoking

6. HDS GI Repro (30 decks)

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