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Pathophysiology - Gastrointestinal > Pathology of the Small Intestine > Flashcards

Pathology of the Small Intestine Flashcards

1
Q

What parts of the small bowel are intraperitoneal vs retroperitoneal? What marks the beginning of the jejunum?

A

The duodenum is entirely intraperitoneal except for its proximal part, then is retroperitoneal.

After the ligament of Treitz, the small intestine becomes the jejunum, which is intraperitoneal like the ileum

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2
Q

What is the blood supply of the small intestine?

A

Gastroduodenal artery supplies the first part of the duodenum (off of Celiac trunk), then SMA supplies the rest

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3
Q

What are the circumferential submucosal folds in the small intestine? What is their function?

A

Plicae circularis

These serve to increase the surface area of the small intestine along with the mucosal folds (villi)

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4
Q

What is serosa vs adventitia?

A

Serosa - discrete layer of mesothelial cells on outside of a peritoneal structure

Adventitia - made of loose connective tissue with no descrete mesothelial covering

Both would be the outer layers of a given structure depending on if it’s intra or retroperitoneal

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5
Q

What are microvilli made of?

A

Actin which is cross-linked to the cell membrane by myosin and anchored down by the terminal web

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6
Q

What explains the post-viral diarrhea that occurs after the infection has been cleared?

A

Younger stem cells in the crypts of Lieberkuhn are involved in secretion of Na/Cl/H20 -> when new cell populations are being repopulated, these cells predominate and increase excretion

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7
Q

What are Paneth cells?

A

Cells unique to the small intestine which secrete antibacterial substances like lysozyme to regulate the normal flora

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8
Q

What is the luminal phase of digestion?

A

Digestion by pancreatic enzymes and emulsification of fat by bile acids
-> occurs via substances exogenous to the native GI tract lumen

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9
Q

What is the mucosal phase of digestion?

A

Digestion via brush border enzymes, i.e. disaccharidases, lipases, and peptidases which are tethered to the brush border. These facilitate the final step of digestion before absorption

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10
Q

What is absorbed maximally in the duodenum vs jejunum vs ileum?

A

Duodenum - water soluble vitamins, iron, and calcium

Jejunum - most nutrient absorption of macromolecules (maximal here), vitamin B9

Ileum - bile salts, vitamin B12

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11
Q

Who tends to get hypertrophic pyloric stenosis, and what are the common presenting signs and symptoms?

A

Firstborn Caucasian males

  1. Olive-shaped mass in epigastric region
  2. Visible peristaltic waves after eating (hypertrophy)
  3. Nonbilious projecting vomiting starting after feedings about 3-4 weeks after birth (takes a while for food to build in stomach)
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12
Q

What is the treatment for hypertrophic pyloric stenosis?

A

Pyloromyotomy - make an incision in pylorus (don’t penetrate mucosa), which is just enough to relieve the pressure and allow normal expansion of sphincter

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13
Q

What is the most common place for intestinal atresia to occur and what is thought to cause it?

A

Duodenum - failure to recanalize due to loss of blood supply during development

Associated with Down’s syndrome

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14
Q

What happens in normal rotation of the gut and what will happen if this is done incorrectly?

A

Normally, the gut rotates 270 degrees around the superior mesenteric artery via a counterclockwise rotation from the frontal view. This allows the colon which was pointing downwards to sit on your right side on your posterior abdomen, anterior to the duodenum

If this is done incorrectly -> malrotation occurs

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15
Q

How does omphalocele occur and is its prognosis better or worse than gastroschisis?

A

Ompalocele - failure of physiologic hernation (which occurs during growth rotation of gut during development) to return from umbilical cord back into abdomen. Will be covered by peritoneum and amnion.

Prognosis is worse than gastroschisis even though it looks less ugly, because more genetic abnormalities are associated with it

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16
Q

What is gastroschisis? Where does it typically happen?

A

Extrusion of abdominal contents through abdominal wall, not covered by peritoneum or amnion -> typically due to an abdominal wall defect on the right side

Can be repaired surgically

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17
Q

What type of diverticulum is a Meckel diverticulum and what causes it?

A

A true diverticulum - all layers of the abdominal wall

Caused by a failure of the regression of the vitelline duct, which normally communicates with the yolk sac during development

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18
Q

What are the rules of 2’s for Meckel’s?

A

2 inches long, 2 feet from ileocecal valve, in 2% of the population, occurring in first two years of life

Most common congenital anomaly of the GI tract

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19
Q

Why do Meckel’s diverticula sometimes cause problems?

A
  1. Often contains heterotopic gastric mucosa which secretes acid, causing bleeding
  2. Volvulus, intussusception, or obstruction can occur
  3. Can present as a fistula which drains into umbilicus
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20
Q

How is are mucoid cells of the ectopic gastric mucosa in a Meckl’s detected?

A

Pertechnetate scan (Actively uptaken and secreted by mucosal epithelial cells of gastric tissue)

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21
Q

How can malabsorptive syndromes cause anemia?

A

Failure to absorb B12 in ileum
Failure to absorb iron in duodenum
Failure to absorb vitamin K due to steatorrhea -> bleeding

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22
Q

What happens to exocrine pancreas in cystic fibrosis? What will this do to vitamin absorption?

A

Mucous plugs form in ducts due to increased water reabsorption (Cl- can’t leave)

  • > duct dilatation and cystic change, leading to acinar atrophy and fibrosis because of inappropriate enzyme activation
  • > decreases fat and fat-soluble vitamin absorption
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23
Q

What is one complication of CF only seen in infants?

A

Meconium ileus -> thick secretions obstruct the bowel. Only seen when small bowel is small enough for this to still happen (infancy)

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24
Q

What happens rarely to the liver and often to the vas deferens in CF?

A

Liver - secondary biliary cirrhosis due to mucosal plugs blocking bile secretion

Vas deferens - congenital bilateral absence causing obstructive azoospermia. CFTR is thought to be required for development of vas deferens

25
Q

What is seen pathologically in lactose intolerance and what happens?

A

Absolutely nothing

Lack of lactase in brush border enzymes -> osmotic diarrhea

26
Q

What is the pathogenesis of Celiac disease?

A

Gliadin is a soluble portion of grains, is absorbed into GI tract and deaminated by tissue transglutaminase (tTG)

Deaminated gliadin is presented by MHC class II and activates CD4 T cells -> T cell mediated damage of intestinal mucosa

27
Q

Who is susceptible to Celiac disease?

A

Caucasians with HLA-DQ2 and HLA-DQ8 -> MHC Class II which can present the deaminated gliadin on their APCs

28
Q

What is seen on anatomic pathology of Celiac disease? Where is the damage worst?

A

Villous atrophy / blunting with crypt hyperplasia for regeneration, and chronic inflammation surrounding

Worst in proximal small intestine

29
Q

What antibodies are detected by serology in Celiac disease?

A

IgA antibodies:

  1. Anti-tissue transglutaminase
  2. Anti-deaminated gliadin
  3. Anti-endomysial antibodies - connective tissue which ensheaths muscle fibers, thought to be cross-reactive to a tissue transglutaminase
30
Q

What skin condition is associated with Celiac disease?

A

Dermatitis herpetiformis

  • > intensely itchy, grouped vesicles on extensor surfaces of extremities and back
  • > thought to be caused by IgA antibodies and microabscesses within the papillary dermis
31
Q

What malignancies is Celiac disease associated with?

A

T-cell lymphoma - due to lymph hyperplasia / inflammation

Small intestinal adenocarcinoma (rare, associated with the crypt hyperplasia)

32
Q

What is Tropical sprue and what is the treatment?

A

Infectious disease within unknown cause which is responsive to antibiotics, seen in tropics.

Pathologic and clinical findings are identical to Celiac disease

33
Q

What is abetalipoproteinemia and what are the clinical presenting symptoms?

A

Autosomal recessive disorder of apoplipoprotein B synthesis -> failure to make chylomicrons, VLDL, and LDL

Presenting symptoms are of malabsorption and failure to thrive

34
Q

What is seen pathologically and on peripheral smear of abetalipoproteinemia?

A

Pathologically - vacuolization of enterocytes due to accumulation of fats which cannot be packaged into chylomicrons

Peripheral smear - acanthocytes (spur cells) - spiky RBCs due to abnormal lipoproteins in their membrane

35
Q

What causes Whipple disease and who tends to get it? How is it treated?

A

Typically found in older men, it is a systemic bacterial infection caused by Tropheryma whipplei

-> intracellular gram + bacteria normally cleared by immune system, but some people are unable to

It is responsive to antibiotics

36
Q

How is Whipple disease detected pathologically?

A

Numerous, distended foamy macrophages in lamina propria as well as mesenteric lymph nodes which stain PAS+. They can only be seen by EM since they are so small

37
Q

What are the symptoms of Whipple disease?

A

Foamy Whipped cream in a CAN

Foamy - macrophages
Whipped - Whipple disease
CAN:
Cardiac symptoms - invade heart valves
Arthralgias - also live in joint synovial membranes
Neurologic symptoms - invade brain, cause psychiatric complaints

38
Q

What are the viral causes of acute gastroenteritis, and what does the intestinal pathology look alot like acutely?

A

Rotavirus, Norovirus, adenovirus, astrovirus

Looks alot like Celiac disease -> loss of brush border with compensatory hyperplasia of crypts and shortening of villi with lymph infiltration

39
Q

What intolerance is characteristic of postenteritis syndrome?

A

Diary intolerance - loss of brush border due to intestinal damage depletes lactase and causes a secondary lactose intolerance until cells heal

40
Q

What are the etiologies of transmural infarcts of the bowel due to low oxygen (ischemic bowel disease)?

A

Only severe infarcts

  1. Arterial thrombosis - i.e. atherosclerosis, polyarteritis nodosa
  2. Arterial embolism - i.e. mural thrombi or plaque rupture
  3. Venous thrombosis - due to hypercoagulability
  4. Vascular compression
41
Q

What are some causes of vascular compression in ischemic bowel disease?

A

Extrinsic mechanical factors - herniation, volvulus, intussusception

Intrinsic vascular disease - amyloidosis

42
Q

What is the typical etiology of a mucosal infarction in ischemic bowel?

A

Marked hypotension, i.e. cardiogenic or septic shock

43
Q

What causes the majority of the injury in ischemic bowel, and what area is particularly susceptible?

A

Secondary reperfusion injury -> due to oxygen-derived free radicals

Splenic flexure is most vulnerable - watershed area between SMA / IMA

44
Q

How does acute ischemic bowel appear grossly and microscopically?

A

Grossly - purplish-red region with intraluminal hemorrhage, wall may be edematous or thin and attenuated, about to burst

Microscopic - coagulative necrosis with hemorrhage (red infarct) with some acute inflammation

45
Q

What is the clinical presentation of ischemic bowel disease?

A

Abdominal pain (especially postprandial) with some bloody diarrhea

-> often suspected as a diagnosis of exclusion in older adults

46
Q

Why does necrotizing enterocolitis happen?

A

Happens usually in premature infants due to intestinal ischemia during neonatal RDS, followed by presence of oral bacteria from oral feedings, and increased workload of gut
-> immature mucosa with increased permeability leads to infection and increased ROS damage

47
Q

What is seen in anatomic pathology of necrotizing enterocolitis?

A

Hemorrhagic infarct of small and/or large intestines with possible perforation

Air can also seep into the wall -> “pneumatosis intestinalis”

48
Q

Where does gastrointestinal carcinoid tumor tend to appear and how does it appear grossly / microscopically?

A

Ileum (remember this is the only common primary malignancy of small bowel, per pathoma), appendix, rectum

Grossly - yellow-to-white mass with variable degree of wall inflammation and fibrosis which may lead to kinking

Microscopic - Small round cells with salt and pepper chromatin and high vascularization

49
Q

How are carcinoid tumor cells identified cytochemically?

A

Dense-core secretory granules due to presence of chromogranins

50
Q

What are the differences in presentation between the locations of carcinoid tumors of the GI tract?

A

Small bowel - may cause obstruction due to prominent desmoplasia, and can metastasis

Appendix / rectal - Usually found incidentally, almost never metastasize

51
Q

When will you actually get the symptoms of carcinoid syndrome with carcinoid tumor? Why?

A

Tumor must metastasize to liver first -> all portal blood going to the liver will metabolize the serotonin to inactive 5-hydroxyindoleacetic acid (5-HIAA)

52
Q

What are the symptoms of carcinoid syndrome?

A

Bronchospasm, diarrhea, wheezing, flushing worsened by emotional stress which stimulate serotonin release from the tumor

Damage includes: right-sided valvular fibrosis, tricuspid regurg, and pulmonary valve stenosis. Left-sided valves not affected due to MAO in the lung.

53
Q

What is the most common kind of lymphoma of the GI tract in terms of cell type? Most common subtype?

A

B cell lymphomas

MALT lymphoma - marginal zone lymphoma associated with chronic gastritis due to H. pylori

54
Q

What is Mediterranean lymphoma and what is the treatment?

A

Immunoproliferative small-intestinal disease

  • > a B cell lymphoma of children and young adults, preceded by malabsorption
  • > may be due to infection because it is treatable with antibiotics
55
Q

What aggressive B cell lymphoma is often found in the abdomen or pelvis and is often not associated with EBV?

A

Burkitt lymphoma - sporadic form seen here in the U.S.

t(8;14) which happens independent of EBV

56
Q

Who gets Intestinal T-cell lymphoma?

A

Enteropathy-associated

-> associated with long-standing malabsorption, i.e. Celiac disease

57
Q

How do all Primary GI lymphomas appear grossly?

A

Start as superficial plaques and then can assume any form -> need biopsy to distinguish from adenocarcinoma

58
Q

What is a leiomyosarcoma?

A

A malignancy of smooth muscle cells, most commonly found in muscularis propria of small intestine

59
Q

What neoplasm is derived from the interstitial cells of Cajal and what mutation is commonly associated with it? What tumor does it look similar to and what is the treatment?

A

Gastrointestinal stromal tumor
- tyrosine kinase mutations, specifically c-KIT -> treated well with imatinib

  • looks very similar to leiomyosarcoma (grows outward and will not cause symptoms unless obstructing lumen)

Pathophysiology - Gastrointestinal (24 decks)

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