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GI 2 Pathology--Chapt 16 and 17 > Chapter 17 part 6--Small Intestine counted > Flashcards

Chapter 17 part 6--Small Intestine counted Flashcards

1
Q

Celiac disease

A
  • also called gluten-sensitive enteropathy or celiac sure
  • immune-mediated diarrheal disorder triggered by ingestion of gluten-containing foods (e.g., derived from wheat, oat, rye, or barley) in genetically predisposed individuals
  • worldwide incidence=0.6% to 1%
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2
Q

Pathogenesis of Celiac Disease

A

-results from gluten-mediated delayed-type hypersensitivity–specifically to a 33 amino acid a-gliadin polypeptide resistant to digestive enzymes

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3
Q

What does gliadin do?

A
  • induces epithelial IL-15 expression with local activation and proliferation of CD8+ cytotoxic cells that can drive enterocyte apoptosis
  • Gliadin access to underlying tissue permits increased deamination by transglutaminase
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4
Q

Morphologic alterations in celiac disease

A
  • villous atrophy

- increased numbers of intraepithelial lymphocytes (IELs), and epithelial proliferations with crypt elongation

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5
Q

Pathogenesis of celiac disease

A

-Both innate (CD8+ intraepithelial T cells activated by IL-15) and adaptive (CD4+ T cells and B cells sensitization to gliadin) immune mechanisms are involved in the tissue responses to gliadin

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6
Q

NKG2D

A

-natural killer cell marker and receptor for MIC-A

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7
Q

Pathogenesis of Celiac disease–what happens after gliadin permits increased deamination by transglutaminase?

A
  • Deaminated peptide binds to specific MHC on Ag-presenting cells in susceptible individuals (expressing human leukocyte antigen [HLA}-DQ2 or HLA-DQ8)
  • leads to CD4+ T cell activation and cytokine mediated epithelial damage
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8
Q

Additional factors that influence Celiac disease susceptibility

A

-polymorphisms of genes that affect immune regulation and epithelial polarity

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9
Q

Morphology of celiac disease

A
  • Diffusely flattened (atrophic) villi and elongated regenerative crypts are associated with intraepithelial CD8+ T cells and exuberant lamina propria chronic inflammation
  • severity is greatest in the more proximal intestine
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10
Q

Clinical features of celiac disease

A
  • occurs in infants to middle age
  • S/S: diarrhea, flatulence, weight loss, effects of anemia
  • most sensitive tests look for presence of IgA Abs to tissue transglutaminase or IgA or IgG to dominated gliadin
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11
Q

Celiac disease associations with other diseases

A
  • associated with pruritic, blistering skin disorder dermatitis hepetiformis
  • Lymphocytic gastritis or colitis also more common
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12
Q

Celiac disease increases the risk for

A
  • iron and vitamin deficiencies

- ENTEROPATHY-ASSOCIATED T-CELL LYMPHOMA and small intestine adenocarcinoma

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13
Q

Celiac disease usually responds to?

A

-gluten withdrawl

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14
Q

Environmental Enteropathy

A
  • Also called tropical enteropathy or tropical sprue
  • malabsorption and malnutrition syndrome that occurs in areas with poor sanitation–affects 150 million children worldwide
  • histology similar to celiac disease
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15
Q

Etiology of Environmental Enteropathy

A

-Infectious etiology implicated with defective intestinal barrier function

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16
Q

Consequences of Environmental Enteropathy

A
  • in developing children there may be associated irreversible losses in physical development and cognition
  • Even with oral antibiotics and nutritional supplementation, the deficits may not be corrected
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17
Q

Autoimmune Enteropathy

A
  • X-linked disorder of children characterized by a persistent auto-immune driven diarrhea
  • A severe familial form (IPEX, immune dysregulation, polyendocrinopathy, enteropathy and X-linked) is due to gremlin mutations in the FOXP3 gene–TF responsible for differentiation of CD4+ regulatory T cells
  • AutoAbs to a variety of GI epithelial cell types may be present
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18
Q

Lactase (Disaccharide) Deficiency–what is lactase?

A

-an apical membrane disacchridase of surface absorptive cells

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19
Q

Lactase deficiency–what happens?

A
  • undigested and unabsorbed lactose exerts an osmotic pull, causing diarrhea and malabsorption
  • bacterial fermentation of lactose can cause abdominal distention and flatus
  • histo: mucosa is unremarkable
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20
Q

Rare congenital autosomal recessive form of lactase deficiency is due to

A

-mutations in lactase gene

21
Q

Acquired form of lactase deficiency is caused by

A
  • downregulation of lactase gene expression

- common in Native American, African-American and Chinese populations

22
Q

Abetalipoproteinemia

A
  • rare autosomal recessive disease caused by inability of lipids to egress absorptive epithelial cells
  • underlying defect is a mutation in microsomal triglyceride transfer protein (MTP) responsible for transferring lipids to apolipoprotein B within the rough ER so the MTP impacts lipoprotein and fatty acid export from mucosal cells
23
Q

Symptoms of Abetalipoproteinemia in infants

A
  • failure to thrive
  • diarrhea
  • steatorrhea
  • absence of all lipoproteins containing apolipoprotein B (although apolipoprotein B gene is unaffected)
  • Failure to absorb essential fatty acids leads to deficiencies of fat-soluble vitamins as well as lipid membrane defects
24
Q

Consequences of Abetalipoproteinemia

A
  • Increased enterocyte triglyceride stores manifest as lipid vacuolation
  • Altered erythrocyte lipid membranes manifest as acanthocytes (burr cells)
25
Q

Symptoms of infectious enterocolitis

A

-range from urgency to diarrhea to incontinence and perianal discomfort to abdominal pain

26
Q

Outcomes of infectious enterocolitis

A
  • dehydration, malabsorption, or hemorrhage
  • half of all deaths worldwide before age 5 is due to infectious enterocolitis!!
  • In developing countries, 2000 children die daily from it–bacterial infections usually responsible but most common pathogen differ based on geography, age, nutrition and host immune status
27
Q

Pediatric infectious diarrhea is usually caused by

A

-Enteric viruses

28
Q

Cholera is caused by

A
  • Vibrio cholera, gram-negative bacteria typically transmitted by drinking contaminated water
  • humans, shellfish and plankton are the only reservoirs
29
Q

Cholera pathogenesis

A
  • Vibrio organisms are noninvasive, although flagellar proteins are important for epithelial attachment and efficient bacterial colonization
  • mucosal biopsies show normal histology
  • causes diarrhea by production of a cholera toxin that is internalized after binding enterocyte surface GM1 gangliosides
30
Q

Steps of Vibrio cholera toxin

A
  • Toxin A subunit processed in ER to a fragment and enters cytosol
  • Toxin A fragment interacts with (ADP) ribosylation factors to activate the G protein Gsa
  • Activated Gsa stimulates adenylate cyclase (AC)
  • Resulting surge cAMP opens cystic fibrosis conductance regulator, CFTR and releases chloride ions into lumen
  • Luminal chloride causes secretion of bicarb and sodium, with obligate water, leading to massive diarrhea
31
Q

Clinical features of cholera

A
  • Only minority develop severe diarrhea; in those that get it, unto 1L/hr of “rice-water”-like stool can be produced
  • Without Tx, the mortality is 50% due to dehydration, hypotension, and shock but most can be saved with timely rehydration
32
Q

Campylobacter Enterocolitis–Campylobacter jejuni

A
  • gram negative
  • most common bacterial enteric pathogen in developed countries and important cause of traveler’s diarrhea
  • Transmission is often though ingestion of poorly cooked chicken but water or milk contamination can also occur
33
Q

Pathogenesis of Campylobacter Enterocolitis

A

-major virulence factors=flagellar motility, adherence molecules to facilitate colonization, cytotoxins and a cholera toxin-like enterotoxin

34
Q

Campylobacter enterocolitis infection can also result in

A
  • extraintestinal complications like reactive arthritis, and erythema nodosum
  • 40% of Guillain-Barre syndrome are associated with Campylobacter infection in the preceding 1-2 weeks
35
Q

Clinical features of campylobacter enterocolitis

A
  • Dx is primarily through stool cultures
  • Biopsies show only nonspecific neutrophilic colitis with variable epithelial damage
  • Diarrhea is typically watery; dysentery, associated with invasive strains occurs in 15% of cases
  • Abx therapy is usually not required; patients can shed bacteria for a month after symptoms resolve
36
Q

Shigellosis–shigella

A
  • nonencapsulated, gram negative bacilli
  • facultative anaerobes and one of the most common causes of bloody diarrhea
  • Humans are the only reservoir
  • fecal-oral transmission is accomplished with as few as several hundred microbes
  • Most infections and deaths occur in children under age 5
  • in endemic areas, Shigella causes 10% of pediatric diarrhea, 75% of diarrhea related deaths
37
Q

Pathogenesis of shigellosis

A
  • Organisms are highly resistant to gastric acidity
  • taken up by intestinal M cells, escape into lamina propria, and ingested by macrophages which then undergo apoptosis
  • Subsequent inflammation and release of Shiga toxin causes epithelial damage that facilitates even greater bacterial access
38
Q

Cholera toxin transport and signaling

A
  • After retrograde toxin transport to the ER, the A subunit is released by the action of protein disulfide isomerase (PDI) and is then able to access the epithelial cell cytoplasm
  • In concert with an ADP-ribosylation factor (ARF), the A subunit then APD-ribosylates Gsa which locks it in in the active, GTP-bound state
  • leads to AC activation, and the cAMP produced opens CFTR to drive chloride secretion and diarrhea
39
Q

Morphology of shigellosis

A

-Mucosa is hemorrhagic and ulcerated, often with pseudomembranes

40
Q

Clinical features of Shigella

A
  • typically a self-limited diarrhea of approximately 6 days
  • Initially watery diarrhea becomes dysenteric in half of patients
  • Fever and abdominal pain persists after diarrhea stops
  • Dx requires stool cultures
  • Antibiotics can shorten the clinical course and reduce the duration of bacterial shedding
41
Q

Salmonella

A
  • gram-negative bacillus
  • Salmonella typhi and Salmonella paratyphi cause typhoid fever whereas non typhoid Salmonella is usually due to S. enteritides
  • Transmission is through contaminated food; children and the elderly are most commonly affected
42
Q

Pathogenesis of Salmonella

A
  • Virulence factors include type III secretion system that transfers bacterial proteins into M cells and enterocytes and facilitates bacterial uptake and growth in phagosomes
  • some strains also express a virulence factor that prevents TLR4 activation
  • Mucosal Th17 responses limit infection to colon but can cause secondary injury
43
Q

Clinical features of Salmonella

A
  • Symptoms and pathologic appearances are similar to other enteric pathogens
  • Dx requires stool cultures
  • Most infections are self limited (exceptions are immunocompromised hosts) and last approximately a week
  • Antibiotics not recommended bc they prolong the carrier state and do not shorten the duration of diarrhea
44
Q

Typhoid fever

A
  • In endemic areas, children and adolescents mostly affected
  • infxn associated with travel in India, Mexico and Philippines and less-developed countries
  • Humans= only reservoir and transmission= contaminated food and water
  • Gallbladder colonization associated with gallstones and chronic carrier state
45
Q

Pathogenesis of Typhoid fever

A
  • Organisms resistant to gastric acid–invade M cells and are subsequently engulfed by mononuclear cells in the mucosal lymphoid tissues
  • Bacteria then disseminate widely via lymphatics and blood vessels causing systemic macrophage and lymph node hyperplasia
46
Q

Morphology of Typhoid fever

A
  • marked expansion of Peyer patches and draining nodes
  • Acute and chronic inflammatory cell recruitment to lamina propria associated with necrotic debris and overlying mucosal ulceration
  • Liver shows focal hepatocyte necrosis with macrophage aggregates called typhoid nodules
47
Q

Clinical features of typhoid fever

A

-initial dysentery followed by bacteremia (90% of patients), fever and abdominal pain that persists for 2 weeks without antibiotic treatment (typhoid fever)

48
Q

Systemic dissemination of typhoid fever causes

A
  • extraintestinal complications including encephalopathy, meningitis, endocarditis, myocarditis, pneumonia and cholecystitis
  • Patients with sickle cell disease are prone to osteomyelitis

GI 2 Pathology--Chapt 16 and 17 (14 decks)

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