Gi Tract 2

Front 1

Congenital disorders of the small intestine

Back 1

duplication
malrotation
omphalocele
gastroschisis

Front 2

omphalocele

Back 2

abominal musculature fails to form -- birth of an infant with hernitaion of abdominal contents into a ventral membranous sac.

Front 3

gastroschisis

Back 3

a portion of the abdominal wall fails to form altogether, causing extrusion of the intestines.

Front 4

Atresia

Back 4

a COMPLETE occlusion of the intesitinal lumen.

stenosis: narrows, but doesn't occlude the lumen.

Front 5

Meckel diverticulum

Back 5

is a congenital sacculation on the antimesenteric border of the ileum caused by persistence of the VITELLINE DUCT.

TRUE diverticulum: possesses all the coats of the normal intestine = mucosa, submucosa, muscularis propria.

Front 6

meconium ileus

Back 6

earliest manifestation of cystic fibrosis = accumulation of tenacious meconium in the small intestine.

Front 7

Bacterial diarrhea

Back 7

the most significant factor in infectious diarrhea is increased intestinal secretion stimulaed by bacterial toxins and enteric hormones.

Front 8

toxigenic diarrhea

Back 8

refers to frequent, watery stools caused by infection with toxin-producing bacteria.

prototypic organisms: vibrio cholerae, and toxigenic strains of E. Coli

aka travelers' diarrhea (e.coli is most common pathogen)

Front 9

Toxigenic diarrhea characterized by 3 things:

Back 9

 Damage to the intestinal mucosa is minimal or absent.
 The organism remains on the mucosal surface, where it secretes its toxin.
 Fluid secreted into the small intestine causes watery diarrhea, which can lead to dehydration, particularly in the case of cholera.

Front 10

Diarrhea caused by invasive bacteria

Back 10

cause diarrhea by directly injuring the intestinal mucosa.

Shigella, salmonella, certain strains of E.coli

tend to infect the DISTAL ILEUM AND COLON.

Ulceration and hemorrhage may accompany diarrhea.

Front 11

Hirschsprung disease = congenital megacolon

Back 11

• An uncommon familiar disorder in which colonic dilatation results from defective innervation of the rectum.
• The lesion is a congenital absence of ganglion cells in the wall of the rectum.
• Rectum reveals a constricted and spastic segment that corresponds to the aganglionic zone. Bowel is dilated proximal to this zone.

Front 12

Secretory diarrhea

Back 12

Net intestinal fluid secretion leads to the output of more than 500 mL of fluid stool per day, which is isotonic with plasma and persists during fasting.

Front 13

Osmotic diarrhea

Back 13

Excessive osmotic forces exerted by luminal solutes lead to output of more than 500 mL of stool per day, which abates upon fasting. Stool exhibits an osmotic gap (stool osmolality exceeds plasma electrolyte concentration by ≥50 mOsm).

Front 14

exudative diseases

Back 14

Mucosal destruction leads to output of purulent, bloody stools that persist on fasting; stools are frequent but may be small or large volume.

Front 15

deranged motility

Back 15

Improper gut neuromuscular function may produce highly variable patterns of increased stool volume; other forms of diarrhea must be excluded.

Front 16

Describe malabsorption syndromes.

Back 16

Malabsorption is characterized by defective absorption of fats, fat-soluble and other vitamins, proteins, carbohydrates, electrolytes and minerals, and water.
The most common clinical presentation is chronic diarrhea, and the hallmark of malabsorption is steatorrhea (excessive fecal fat content).

Front 17

Celiac disease

Back 17

Celiac disease (also referred to as celiac sprue, gluten-sensitive enteropathy) is a chronic disease, in which there is a characteristic mucosal lesion of the small intestine and impaired nutrient absorption, which improves on withdrawal of wheat gliadins and related grain proteins from the diet.

Front 18

celiac disease is characterized by what 3 things?

Back 18

o Generalized malabsorption
o A typical, but nonspecific, small intestinal mucosal lesion
o A prompt clinical, but slower histologic, response to the withdrawal of gluten-containing foods from the diet.

Front 19

Hallmark of celiac disease

Back 19

• Hallmark: flat, small, intestinal mucosa with:
o Blunting or total disappearance of cilli
o Damaged epithelial cells on the mucosal surface
o Increased cellularity of the lamina propria but not of the deeper layers.

Front 20

Lactase Deficiency

Back 20

• Lactose is one of the most common disaccharides in the diet.
• Widespread disorder of carbohydrate absorption.
• Affects 2/3 of Asian and African adults
• Symptoms begin during adolescence.
• Patients complain of abdominal distention, flatulence (gas), diarrhea after ingestion of dairy products. Symptoms relieved by eliminated milk from the diet.

Front 21

appendicitis

Back 21

Inflammatory disease of vermiform appendix that may result in transmural necrosis and perforation.

Front 22

complications of appendicitis

Back 22

Periappendiceal abscesses; fistulous tracts; pylephebitis, abscesses, diffuse peritonitis and septicemia, wound infection

Front 23

carcinoid tumor

Back 23

arise from cells of the neuroendocrine system of the gut.

most commonly secreted hormone: serotonin

Malignant potential related to size > 1cm malignancy is at risk.

Front 24

clinical features of carcinoid syndrome

Back 24

Vasomotor distubances
Cutaneous flushes and apparent cyanosis (most patients)
Intestinal hypermotility
Diarrhea,Cramps, nausea, vomiting (most patients)
Asthmatic bronchoconstrictive attacksCouth, wheezing, dyspnea (about one third of patients)
Hepatomegaly
Nodular liver owing to hepatic metastases (some patients)
Systemic fibrosis (some patients)
Cardiac involvement
Pulmonic and tricuspid valve thickening and stenosis
Endocardial fibrosis, principally in the right ventricle (Bronchial carcinoids affect the left side)
Retroperitoneal and pelvic fibrosis
Collagenous pleural and intimal aortic plaques

Front 25

mediterranean lymphoma

Back 25

1) poor countries;
2) young men;
3) proliferative disorder of intestinal B cells that secrete IgA;
4)Leads plasma cell infiltrates that produce mucosal atrophy and malabsorption.

Front 26

western type lymphoma

Back 26

1) Older adults and children;
2) fungating mass that projects into the ileum;
3) plaque-like nodules;
4) diffuse thickening or elevated ulcerated lesions;
5)occult bleeding is common;
6) Microscopically all varieties of lymphoma;
7) 5-year survival rate is <10%.

Front 27

adenocarcinoma (SI)

Back 27

Located in duodenum and jejunum. Risk for Chron’s patient is ~100%, Occult bleeding is prominent may lead to iron deficiency anemia. 5-year survival <20%.

Front 28

primary lymphoma (SI)

Back 28

15% of bowel cancers. Risk is increased in patients with immunodeficiency or those treated with immunosuppressive drugs.

Front 29

colorectal carcinogenesis

Back 29

see slides

Front 30

Inherited Adenomatous Polyposis Syndromes

Back 30

Gardner Syndrome:
o An autosomal dominant, familial disorder characterized by
1. Gastrointestinal polyposis, principally in the colon but commonly in the stomach and the vicinity of the ampulla of Vater
2. Osteomas of the skull, mandible, and long bones
3. Soft-tissue tumors of the skin
o Garner syndrome ultimately progresses to cancer of the colon.

Front 31

Peutz-Jeghers Syndrome

Back 31

An autosomal dominant, hereditary disorder characterized by intestinal polyps and mucocutaneous melanin pigmentation, which is particularly evident on the face, buccal mucosa, hands, feet, and perianal region, as well as genital areas.

Polyps are NOT true neoplasms but are hamartomas.

2-3% of patients develop adenocarcinoma.

Front 32

Familial Adenomatous Polyposis

Back 32

FAP is the archetype of the adenomatous polyposis syndromes. It is caused by mutations of the adenomatous polyposis coli (APC) gene on chromosome 5q21.

Classified as classic FAP, attenuated FAP, Gardner syndrome, and Turcot syndrome.

Front 33

Adenomatous polyps are segregated into three subtypes on the basis of the epithelial architecture:

Back 33

Tubular adenomas: tubular glands
Villous adenomas: villous projections
Tubulovillous adenoma: a mixture of the above.

Front 34

intussusception

Back 34

• A form of intraluminal small bowel obstruction in which a segment of bowel (intussusceptum) protrudes distally into a surrounding outer portion (intrussuscipiens), much in the same way that a segment of a telescope inserts into the adjacent one.
• Usually a disorder of infants/children = unknown cause.
• Adults – leading cause is commonly a lesion in the bowel wall, such as a Meckel diverticulum or polypoid tumor.
• Peristalsis drives the intussusceptum forward.

Front 35

volvulus

Back 35

• A cause of an acute abdomen and an example of an intestinal obstruction in which a segment of gut twists on its mesentery, thereby kinking the bowel and usually interrupting the blood supply.

Front 36

adhesions

Back 36

• Fibrous scars from previous surgery or peritonitis may cause obstruction by bending/angulating the bowel or by directly compressing the lumen.

Front 37

hernias

Back 37

incarceration of a loop of bowel in an inguinal or femoral hernia.

Front 38

predisposing conditions for ischemia

Back 38

arterial thrombosis
arterial embolism
venous thrombosis
non-occlusive ischemia
Miscellaneous: radiation injury, volvulus, stricture, amyloidosis, diabetes mellitus, and internal or external herniation.

Front 39

diverticular disease

Back 39

see slides

Front 40

Non-neoplastic (Benign) Polyps

Back 40

Hyperplastic polyps
Hamartomatous polyps
Juvenile polyps
Peutz-Jeghers polyps
Inflammatory polyps
Lymphoid polyps

Front 41

Neoplastic Epithelial Lesions

Back 41

Benign 
Adenoma*
Malignant: 
Adenocarcinoma*
Carcinoid tumor
Anal zone carcinoma

Front 42

Mesenchymal Lesions

Back 42

Gastrointestinal stromal tumor (GIST)
-Neuroma
-Lipoma
-Angioma
-Kaposi sarcoma

Front 43

The malignant risk with an adenomatous polyp

Back 43

Correlated with three interdependent features:
polyp size,
histologic architecture,
severity of epithelial dysplasia.
Cancer is rare in tubular adenomas smaller than 1 cm in diameter.
The risk of cancer is high (approaching 40%) in sessile villous adenomas more than 4 cm in diameter.
Severe dysplasia, when present, is often found in villous areas.

Front 44

consequences of malabsorption

Back 44

see slide