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NON-NEOPLASTIC ILEUM and COLON PATHOLOGY - Coggle Diagram
NON-NEOPLASTIC ILEUM and COLON PATHOLOGY
normal anatomy and histology of the small intestine
it includes duodenum, jejunum and ileum
it is about 7m long
most common finding: malabsorption (rarely, neoplastic pathologies)
layers: lamina propria, muscularis mucosae, submucosa, tunica muscularis and serosa
histological hallmark: VILLI, covering the entire small intestine mucosa (7x surface area; velvety texture)
VILLI
villi range from 10 to 40 per mm2 in density and from 0.5 to 1.0 mm in height, allowing digestion and absorption of nutrients
morphology varies throughout the small intestine
proximal duodenum: broad ridges with a leaf-like shape
distal duodenum and proximal jejunum: tall and foliate
distal jejunum and ileum: shorted and with a finger-like shape
due to different functions along the tract
in the proximal duodenum the absorption task predominates, thus villi are longer and broader and then progressively shrink in size
structure
inflammatory and immune cells (lymphocytes and plasma cells) in the villus core to modulate the immune defense
lymphatic vessels in the villus core
blood vessels in the core
enterocytes on the villus surface, with brush border to increase the available surface for absorption
(PAS+++ --> calciform cells rich in mucin)
muciparous goblet cells among enterocytes
at their base --> Lieberkun crypts
enteroendocrine cells: possible origin of carcinoids
paneth cells: antimicrobial defense
stem cells: relevant during neoplastic transformation
DUODENUM
villi have a leaf-like shape
Brunner's glands are found in the submucosa and they are tubuloacinar mucous glands producing an alkaline secretion
Brunner's glands' ducts drain into the Lieberkun crypts
both the pancreatic and the common bile ducts drain through the ampulla of Vater into the duodenum
DISTAL DUODENUM and
PROXIMAL JEJUNUM
villi have a finger-like shape
plicae circulares are well-developed
no glands in the submucosa
DISTAL JEJUNUM
and ILEUM
villi are shorter
M cells (APCs) are present
histological hallmark: Peyer patches (large follicles formed by lymphoid aggregates spanning lamina propria and submucosa)
APPENDIX
lymphoid follicles here receive continuous stimulation
--> secondary immune organ
lymphatic tissue can also stimulate growth of some types of beneficial gut bacteria
small intestine pathology
OBSTRUCTION
functional causes
e.g. paralytic ileus
the motor activity of the bowel is impaired, secondary to neuromuscular failure involving the myenteric (Auerbach’s) and submucosal (Meissner’s) plexus
reflectory ileus: after abdominal/retroperitoneal surgery (spinal surgery) or induced by intra-abdominal/retroperitoneal lesions (tumor, hemorrhage, infection)
drug-induced ileus: opioids or neuroleptic drugs
metabolic ileus: hypokalemia or DM
vascular ileus: bowel hypoperfusion
mechanical causes
in the duodenum
quite rare
caused by
congenital anomalies, e.g. atresia associated with Down syndrome
malrotation: duodenojejunal flexure is turned to the right and Ladd's band obstructs it
in jejunum and ileum
external compression (tumor, inflammation, infection)
coprostasis
intussisception (common in children <3y)
adhesions (after abdominal surgery)
volvulus (the intestine twists on its axis)
stricture (e.g. due to Crohn's disease)
meconium ileus (early manifestation of cystic fibrosis)
inguinal hernia (displacement of the bowel from the peritoneal cavity)
Meckel's diverticulum (congenital saccular ajection arising on the antimesenteric border of the distal ileum and causing bleeding and ulceration)
BLEEDING
heterotopies
the main sign is bleeding (dark staining of the feces because of the presence of digested blood)
they manifest with multiple small nodules
the sample is obtained by endoscopy
the pathologist is asked to determine whether it is gastric or pancreatic
gastric: glands are well visible in the ectopic mucosa; manifesting as duodenal polyps and as a consequence of various types of gastrites
pancreatic: acini typical of pancreatic tissue; ectopic pancreas is a congenital abnormality
complication:
bleeding
stricture
ulceration
pancreatitis
pseudocyst
malignant transformation
duodenal ulcer
the main symptom is nocturnal pain
at microscopy, a necrotic layer, inflammatory granulation tissue and fibrosis can be seen
mesenteric ischemia
it can cause massive bleeding
ischemic symptoms (post-prandial pain, fear of eating, weight loss) are not so common
much more common in the colon, where anastomosing arcades are less numerous
OCCLUSIVE MI
arterial embolism:
in the mid-to-distal end of the superior mesenteric artery
caused by thrombosis due to AF, cardiac dysarrhythmias or bacterial endocarditis
arterial thrombosis
(intestinal angina):
often occuring in the proximal half of the mesenteric artery
usually caused by atherosclerosis
because of the development of collateral vessels, the pt can tolerate major visceral artery occlusion before symptoms of ischemia show up
75% of patients have pre-existing chronic mesenteric ischaemia
NON-OCCLUSIVE MI
diagnosed with chronic or remittent splanchnic hypoperfusion
during low-flow states, splanchnic vasoconstriction is an early and profound phenomenon (threshold: 50%)
causes
increased age
increased BMI
heart failure
hemorrhage
pre-existing vascular disease
arterial hypotension
elevated sympathomimetic activity, tobacco, strenuous exercise, severe psychological stress
hypovolemia, sepsis, use of vasopressors
intra-aortic balloon pump
effects
MUCOSAL
in the first stages, the damage is limited to the mucosa
at the microscope, the tips of villi are completely hemorrhagic; epithelium and enterocyes are lost
changes are rversible and not extended to the outer layers
BEST PROGNOSIS, COMPLETE REMISSION
MURAL
it affects mucosa, submucosa and smooth muscle layers
specific pathological changes: edema, erosion, hemorrhage and necrosis
if the neural plexuses are involved, impaired motor function and loss of peristalsis are determined
fibrotic stricture of the bowel eventually forms as the late outcome, if perfusion restores
TRANSMURAL
the whole wall is affected
WORST PROGNOSIS
pts are usually old
diagnosis is usually delayed (when the damage is already irreversible)
DIARRHEIC DISEASES
causes
infectious
non-infectious (drugs, toxic, amyloidosis)
malabsorption
motility alterations
inflammation
infectious ileitis
Salmonella Typhi
transmission occurs through the fecal-oral route
followed by an incubation period of 7-14 days
adhesion to the mucosa and the invasion of epithelial cells
pathogenesis
once in the submucosa, it encounters dendritic cells, enterocytes and macrophages, enters in the PEyer's patches and reaches mesenteric LNs and spread through the reticuloendothelial system (liver, spleen and bone marrow)
in 14 days, bacteria appear in the bloodstream, facilitating secondary metastatic foci
in some pts, gallbladder infection leads to long-term carriage of S. typhi or paratyphi in bile and secretion in the stools
microscopically, three stages are recognized
stage I: Peyer’s patches hyperplasia due to the presence of the pathogen
stage II: patches hyperplasia can impair the circulation and blood supply, causing necrosis and eschar
stage III: ulcer
Whipple disease
quite rare cause of infectious ileitis
aka intestinal lipodystrophy
more frequent in middle-aged males
etiology: Tropheryma Whippelii (gram+)
increased serous and mucosal thickness with mesenteric and satellite lymphadenopathy
sometimes, heart valves and lungs are affected
treated with antimicrobials
pathognomonic sign at microscopy:
MACROPHAGES CONTANING PAS+ BACTERIA
parasites
Giardia, Schistosoma, Tapeworm ascaris, Ancylostoma, Strongyloides
peripheral blood sign: HYPEREOSINOPHILIA
APPENDICITIS
ACUTE
unknown cause, probably multifactorial (intraluminal obstruction, dietary and familial factors)
obstruction of the appendix by feces can cause bacterial infections
obstruction of the appendiceal orifice leads to an increase in intraluminal and intramural pressure, resulting in small vessel occlusion and lymphatic stasis
bacterial infection then occurs in the appendix
aerobic organisms predominate in early appendicitis and mized aerobes and anaerobes later during the course
E. coli, Peptostreptococcus, Bacteroides, Pseudomonas
if left untreated, mural necrosis and perdoration, with local abscess formation and peritonitis may occur
the wall of the appendix becomes ischemic and necrotic
microscopically, neutrophilic infiltration is seen at early stages along with crypt abscess formation
the exudate can become transmural and fistulize with the peritoneum, causing acute peritonitis
RECURRENT and CHRONIC
far less frequent
no need for surgical appendix excision
long-standing inflammation or fibrosis of the appendix, manifesting as RLQ pain of >48h or intermittent RLQ pain
the tissue is completely atrophic and fibrotic
the tip of the appendix must always be studied (it is the site where the carcinoids may arise)
MALABSORPTION
defective intraluminal digestion
fat and proteins digestion (pancreatic insufficiency, cystic fibrosis or Zollinger-Ellison syndrome)
solubilization of fat due to defective bile secretion (ileal dysfunction or resection with decreased bile salts uptake, cessation of bile flow)
nutrients reabsorption or modification by bacterial overgrowth
primary mucosal cell abnormalities
defective terminal digestion (disaccharididase deficiency or bacterial overgrowth)
defective epithelial transport (abetalipoproteinemia, primary bile acid malabsorption)
reduced small intestine surface area
gluten sensitive enteropathy, Crohn's disease
infection
acute infectious enteritis, parasitic infestation, tropical sprue, Whipple disease
lymphatic obstruction
lymphoma, TBC and tuberculous lymphadenitis
iatrogenic
subtotal or total gastrectomy, short-gut syndrome after extensive surgical resection, distal ileal resection or bypass
specific examples
AMYLOIDOSIS
cause of duodenal malabsorption due to amyloid deposition
it may also be lethal
impaired nutrients absorption
continuous diarrhea
imporribility to treat myeloma
forms
primary
associated with multiple myeloma due to monoclonal immunoglobulin light chain deposition
secondary
associated with chronic inflammation due to deposition of serum amyloid protein A
pathological diagnosis
congo red staining: amyloids appear orange; green-apple birefringence under polarized light
IHC with anti-amyloid antibodies
CELIAC DISEASE
phenotypes
TYPICAL: early onset, diarrhea and stunting
ATYPICAL: late onset, with intestinal and extraintestinal symptoms
SILENT: absence of striking symptoms, very frequent
POTENTIAL: ositive serological tests, but normal intestinal biopsy
aka "celiac sprue", "gluten enteropathy"
--> increased sensitivity to products with gluten
pathogenesis
genetic predisposition to hypersensitivity to gliadin
gluten is partially digested by human proteases, crosses the intestinal wall and is eventually deamidated by TG2
once deamidated, gluten peptides can bind to HLA DQ2/8 on APCs
gluten-specific CD4+ T-cells are activated and secrete proinflammatory cytokines, stimulating B-cell response and activation of Intraepithelial Lymphocytes
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complications
increased risk of lymphoma
diagnosis
intestinal biopsy
NECESSARY in the adult only
at least 4 biopsies must be taken
the specimen must beproperly oriented and sectioned
VILLI APPEAR COMPLETELY ATROPHIC
genetic
pediatric: no need for intestinal biopsy
adult: in doubtful cases only
identification of 1st degree family members at risk
specific protocol for children and adolescents without duodenal biopsy
+++ for anti-tTG IgA antibodies 10x greater than the cutoff
confirmation by positivity for anti-endomysium IgA
the presence of compatibl genetic profile (HLA-DQ2 and/or DQ8)
histological diagnostic criteria
IHC staining with anti-CD3 antibodies
Marsh system
based on the length of the villi and the extent of lymphocytic infiltration and identifies Type 1, 2 and 3
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used in the past
Corazza and Villanaci
grade A
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grade B1
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grade B2
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COLLAGENOUS SPRUE
peculiar type of celiac disease which is refractory to a gluten-free diet
paraneoplastic causes?
symptoms: persistent diarrhea, weight loss and severe malabsorption
microscopically
subepithelial collagen deposits, completely impairing absorption
normal anatomy and histology of the large intestine
mucosa of the colon
single layer of absorptive columnar cells and goblet cells
water and electrolytes absorption
formation and transport of feces
chemical digestion by gut microbes
specific innervation
Meissner submucosal plexus and Auerbach myenteric lìplexus
taenia coli are useful for the insertion of the peritoneum
glands of the colon are homogeneously covered by mucous cells that produce mucin
mucosa of rectum and anus
the mucosa gradually transitions from the typical intestinal columnar type to stratified squamous epithelium from the rectum into the anal canal
the stratified squamous epithelium transitions from a non-keratinized to a keratinized type
large intestine pathology
HEMORRHOIDS
sinusoids in the mucosa (neither arterial nor venous)
causes: increase in pressure at the anus due to
straining during bowel movements, chronic diarrhea, constipation
cirrhosis: hemorrhoidal plexus is a possible site of porto-systemic venous anastomosis
pregnancy
complications
thrombosis
severe
pain
possible surgical intervention
(hemorrhoidectomy)
CONGENITAL
MALFORMATIONS
dolicocolon
colon longer than normal
long segment congenital
(Hirschprung disease)
frequent in the pediatric population
permanent spasm affecting the anorectal tract
upstream dilation and hypertrophy of the muscle layer
caused by a frank reduction in the number of ganglion cells in the two plexuses
loss of intrinsic excitatory and inhibitory innervation
net effect: spastic contraction of the aganglionic segment, including the internal anal sphincter, with impaired peristalsis and defecation
nerve fiber hypertrophy
generally, surgical resection of aganglionic bowel is recommended
DIVERTICULAR DISEASE
very frequent
among the causes, low-slag diet
1/3 subjects> 60 years
FALSE diverticula
flank shape with narrow collar
the outpouches get filled by agents causing inflammation and diverticulitis
inflammation can lead to
ulcerations of the diverticular mucosa
fistulae
possible complications
abscess: fever, pain and peritonitis
fistulae: either with another tract of the intestine, the bladder or the vertebrae (osteitis)
external fistulae: enterocutaneous
stenosis: infection and subsequent scarring
ISCHEMIC COLITIS
more frequent than ischemia of the small bowel due to the lower number of anastomosing arcades
more common in pts in their 6th-7th decades (especially, those with CV risk factors, DM, hypertension, hemodialysis, hypoalbuminemia, heart failure, digoxin/aspirin)
pts present with acute-onset abdominal pain with bloody stools
1/5 of cases require surgery
high mortality and morbidity
phases
ACUTE
small hemorrhages, ulceration and necrosis
REPAIR
larger hemorrhagic areas
hemosiderin-laden
macrophages
LATE
fibrosis
pathology
absence of mucosal epithelium, ulceration, fibrin deposition on the surface and inflammation; sometimes, glands vanishing can be appreciated with the presence of histiocytes
INFECTIOUS DISEASES
shigellosis (rectum-sigma)
salmonellosis
HP
amoeba
viruses
cryptosporidium
schistosoma
PSEUDOMEMBRANOUS COLITIS
possibly due to C. difficile, linked to antibiotic use, yellowish membranes adhering to the surface
IBD
CROHN'S DISEASE
full thickness inflammatory disease of the intestinal wall
mainly located in the terminal ileum, but possibly extenting to the whole GIT (mouth-colon; rectum is usually spared)
extra-GI manifestations are possibly found
endoscopy
aphthous lesions: erosions of the mucosa
single or multiple strictures
ulcerations: from small aphthae to serpiginous and discontinuous ulcers
"pavement" aspect of the mucosa due to extensive ulcerations
these lesions may eventually lead to
deep cracks
thickening of the wall
changes in the serosa
fistulae
microscopy
skip lesions (different from RUH, where lesions are continuous)
aphthous ulcer (progressing as serpentine ulcers along the axis of the bowel)
transmural inflammation
thickening of the submucosa (fibrosis and edema)
sarcoid-like granulomas (non-necrotizing)
razor-sharp cracks
fistulae
RECTOCOLITIS ULCERO-HEMORRHAGIC
primary location in the rectum (proctitis)
possible progression towards the colon (left-sided colitis) and towards the small intestine (pancolitis)
extra-intestinal manifestations
eyes: episcleritis, uveitis
mouth: stomatitis, aphtous ulcers
kidneys: stones. hydronephrosis, fistulae, UTIs
liver: steatosis
biliary tract: gallstones, sclerosing cholangitis
joints: spondylitis, sacroiliitis, peripheral arthritis
skin: erythema nodosum, pyoderma gangrenosum
circulatory system: phlebitis
one of the first manifestations may be cold-intolerance at the periphery and poor refill, followed by diarrhea
endoscopy
the colonic mucosa appears spongy, because it is friable, congested and focally ulcerated
although the disease appears segmental at the macroscopic examination, the inflammation is widespread and always affects the rectum
microscopy
absence of goblet cells: well-highlighted by stainig (much more blue than white)
crypts distortion
ulceration of the mucosa (creating little fibrosis)
abscess within the crypts
infiltration of plasma cells at the base of the crypts
ulcerations may lead to the formation of pseudopolyps, which are protruding areas of intact mucosa surrounded by the ulcerated one
in advanced stages of pancolitis
the rectum may be found in remission and show atrophic and sclerotic mucosa, gland distortion and chronic inflammatory infiltrate
abscesses
plasma cell infiltrate at the
base of the crypts
complications
toxic megacolon (fulminant): involvement of the transverse colon, which dilates acutely and becomes thinner, allowing full thickness ulceration, rupture and eventually peritonitis
hemorrhage
suprinfection
cancerization: related to the extension and duration of colitis, with the carcinoma being frequently multifocal, flat, infiltrating and poorly differentiated
if there is a high-grade dysplasia on a flat mucosa, a colectomy is proposed
stages of remission
crypts are atrophic and chronic inflammatory infiltrate is rich
unifying factors
epidemiology
relapsing chronic inflammatory diseases
F>M
frequent in Italy
racial factors (Jews+)
sometimes microscopic mixed apsects
extra-GIT locations
etiology and
pathology
genetic predisposition: HLA DR1/DQw5, HLA DR2
infections: viruses, Chlamydia, atypical bacteria, mycobacteria (probable measles and mycobacterium paratuberculosis)
abnormal host immune response: mucosal immunity is stimulated and fails to shrink
inflammation: non-specific tissue damage from inflammatory process
hypereosinophilic variant
DD: parasitic infection