gastrointestinal Flashcards
tracheoesophageal fistula
congenital defect resulting in a connection between the esophagus and trachea.
most common variant of tracheoesophageal fistula
proximal esophageal atresia with the distal esophagus arising from the trachea. presents with vomiting, polyhydraminos, abdominal distention, and aspiration.
esophageal web characteristics
thin protrusion of the esophageal muscosa. most often in the upper esophagus. presents with dysphagia for poorly chewed food.
what is esophageal web increase the risk for?
squamous cell carcinoma.
plummer-vinson syndrome
esophageal web, iron anemia deficiency and a beefy-red tongue due to atrophic glossitis. increased risk for squamous cell.
zenker diverticula
out pouching of pharyngeal muscosa through acquired defect in the muscular wall arises above the upper esophageal sphincter at the junction of the esophagus and pharynx
how does zenker diverticula present
with dysphagia, obstruction and halitosis.
mallory-weiss syndrome
longitudinal laceration of the mucosa at the GE junction. caused by vomiting due to alcoholism or bulimia. presents with painful hematemesis risk of boerhave syndrome
boerhave syndrome
rupture of esophagus leading to air in the mediastinum and subcutaneous emphysema/
esophageal varices
dilated mucosal veins in the lower esophagus, arise secondary to portal hypertension. this is usually asymptomatic /but there is a risk for rupture.
what is the most common cause of death cirrhosis
rupture of esophageal varices from portal hypertension.
achalasia
inability to relax the lower esophageal sphincter due to damaged ganglion cells in the myenteric plexus
what is a common cause of ganglion cell damage in the esophagus?
infection by t. cruzi
clinical symptoms of achalasia
dysphagia for solids and liquids, putrid breath, high LES pressure, bird beak sign on barium swallow studies. increased for esophageal squamous cell carcinoma
GERD
reflux of stomach acid due to loss of LES tone.
risks for GERD
alcohol, obesity, fat-rich diet, caffiene, and hiatal hernia;
how does GERD manifest
heart burn, asthma and cough, damage to the enamel of the teeth
what are the late complications of GERD
esophageal stricture, barretts esophagus
barrets esophagus
metaplasia of the lower esophageal mucosa from stratified squamous epithelium to nonciliated columnar epithelium with goblet cells.
how frequently is Barrets E seen?
10% of GERD patients
what can GERD progress to?
dysplasia and adenocarcinoma
esophageal carcinoma subclassifications
adenocarcinoma or squamous cell
adenoma carcinoma of the esophagus
most commmon in the west. arises from preexisting barrels usually involves the lower 1/3
squamous cell carcinoma of the esophagus
most common worldwide. usually in the upper or middle esophagus.
major risk factors for squamous cell carcinoma of the esophagus
alcohol and tobacco, very hot tea, achalasia, esophageal web, esophageal injury,
how does esophageal cancer present?
late, with a poor prognosis. progressive dysphagia, weight loss, pain, hemoptysis.
squamous cell additional presentations
hoarse voice, cough,
where does the upper 1/3n of esophageal cancer spread too?
cervical lymph nodes,
where does the middle 1/3 spread
mediastinal or tracheal bronchial tubes
where does the lower 1/3 spread
celiac and gastric nodes
gastroschisis
congenital malformation of the anterior abdominal wall leading got exposure of the abdominal contents.
ophalocele
persistant herniation of the bowel into the umbilical cord this is due to failure of the intestines to return to the body cavity during development. contents are covered by the peritoneum and amnion of the umbilical cord.
pyloric stenosis
congenital hypertrophy of the pyloric sm that is more common in males. classically presents two weeks after birth
how does pyloric stenosis present
projectile vomiting that is nonbilious, visible peristalsis, olive-like mass in the abdomen
treatment for pyloric stenosis
myotomy
acute gastritis
acidic damage to the stomach mucosa, caused by an imbalance to the stomachs defenses and the acidic environment.
what are the stomachs defenses against acid
mucin layer (produced by foveolar cells, bicarbonate secretion by surface epithelium, normal blood supply.
risk factors for acute gastritis
severe burns lead to lack of blood supply, NSAIDs, heavy alcohol consumption, chemotherapy, increased intracranial pressure, increased stimulation of the vagas nerve, shock.
what can be seen in ICU patients due to shock?
multiple stress ulcers.
what does acid damage do to the mucosa
superficial inflammation, erosion, ulcer.
chronic gastritis
chronic inflammaiton of the stomach mucosa.
what are the two causes of chronic gastritis
chronic autoimmune or chronic h pylori
what is the cause of chronic autoimmune gastritis
autoimmune of parietal cells located in the body and funds. this is associated with antibodies against parietal cells or intrinsic factor. the destruction seems to be mediated by t cells however. type 4 sensitivity
clinical features of chronic gastritis
atrophy of mucosa with intestinal metaplasia, achlorhydria with increased gastrin levels and astral g-cell hyperplasia, megaloblastic anemia, increased risk for gastric adenocarcinoma
chronic inflammation with h pylori
this is the most common form of gastritis 90%. he creases and proteases weaken the mechanisms of defense antrum is the most common site.
how does h pylori present
epigastric abdominal pain, increased risk for ulceration, adenocarcinoma, MALT lymphoma.
how do we treat h pylori
triple therapy.
prognosis of h pylori post treat
reverses gastritis and intestinal metaplasia, negative urea breath test and lack of stool antigen confirms eradication.
peptic ulcer disease
most prevalent in the stomach or duodenum (90%), almost always caused by h pylori, rarely ZE.
how does peptic ulcer present
epigastric pain that improves with meals.
what does endoscope show for peptic ulcer disease
ulcer with hypertrophy of brunner glands.
where odes the ulcer usually occur?
in the anterior duodenum.
what are the risks of ulcer in the posterior duodenum
bleeding from artery or acute pancreatitis
gastric ulcer
due to h pylori in 75% NSAIDs are another as well as bile reflux. presents with epigastric pain that gets worse with meals. ulcer is usually in the lesser curvature of the antrum. rupture carries risk of bleeding from the left gastric artery.
is duodenal carcinoma rare?
yes. extremely.
gastric carcinoma
malignant surface epithelial cells. subcalssified into diffuse and intestinal types.
which type of gastric carcinoma is more common, diffuse or intestinal
intestinal
how does intestinal gastric carcinoma present
large irregular ulcer with heaped up margins and most commonly involves the lesser curvature of the antrum of the stomach.
what characterizes the diffuse type?
signet ring cells that diffusely infiltrate the gastric wall. desmoplasia results in thickening of the stomach wall.
what is linitus plastica
thickening of the stomach wall
what is the diffuse type not associated with>
h pylori, nitrosamines, intestinal metaplasia
how does gastric carcinoma present?
late with weight loss, abdominal pain, anemia, early satiety,
how can it gastric carcinoma present rarely
acanthosis nigricans, leser trelat sign.
what lymph nodes can be involved in gastric carcinoma
the supra;navicular nodes. virchow nodes.
where does gastric carcinoma usually metastasize
to the liver, periumbical region, bilateral ovaries
sister mary joseph nodule
gastric cancer mets to the periumbilical region
krukenburg tumor
gastric cancer mets to bilateral ovaries.
duodenal atresia
congenital failure of the duodenum to canalize associated with down syndrome
clinical feature of duodenal atresia
polyhydraminos, distention of the stomach and blind loop of the duodenum (double-bubble sign), bilious vomiting.
meckel diverticula
outpouching of all three layers of the bowel wall. failure of the vitelline duct to involute. rule of 2’s
what is the rule of 2’s for meckel diverticula
2% of population, 2 inches long, seen within 2 feet of the ileocecal valve. present within the first 2 years of life with bleeding. due to heterotrophic gastric mucosa. volvulus, intussusception or obstruction. most cases are asymptomatic.
volvulus
twisting of the bowel along its mesentery. results in obstruction and disruption of blood supply with infarction.
what are most common locations of volvulus for elderly
sigmoid colon
what are the most common locations of volvulus for young adults
cecum
intussusception
telescoping of the proximal segment of the bowel into the distal. the telescoped segment is pulled forward due to peristalsis resulting in obstruction and disruption of blood supply with infarction. associated with a leading edge, focus of traction.
what is the most common cause of intussusception in children
lymphoid hyperplasia. due to rotavirus. usually arises in the terminal ileum leading to intus. into the cecum.
what is the most common cause of intussusception in adults
tumor.
small bowel infarction
the small bowel is highly susceptible to infarct. transmural occurs with thrombosis/embolism, of SMA or thrombosis of the mesenteric vein.
when can mucosal infarction occur?
with marked hypotension.
clinical features of infarction of the GI
abdominal pain, bloody diarrhea, decreased bowel sounds.
lactose intolerance
decreased function of the lactase enzyme found on the brush border of intestinal cells. breaks down lactose into galactose and glucose.
how does lactose intolerance present
abdominal distension, diarrhea upon consumption of milk product. undigested lactose is osmotically active.
celiac disease
immun mediated damage to small intestinal villi due to gluten exposure.
what HLA is celiac
HLA-DQ2 and DQ8
where does gluten come from?
wheat and grain.
what is the most pathogenic component of gluten
gliadin.
what is the pathogenesis of gluten allergy
gliadin is broken down by transglutaminase, presented by APC via MHC class II. helper t cells mediate tissue damage.
clinical presentation of gluten allergy in children
children: abdominal distension, diarrhea, failure to thrive.
presentation of gluten allergy in adults
chronic diarrhea and bloating. small herpes like lesions may arise on the skin. due to IgA deposition at the tips of dermal papillae resolves with gluten free diet.
what are the labs for gluten allergy
IgA antibodies against endomysium, tTG, or gliadin, IgG are also present and helpful in diagnosing IgA deficiency. duodenal biopsy will show flattened villi hyperplasia of crypts and increased intraepithelial lymphocytes. damage is most pertinent in the duodenum. J and I are less involved.
what are late presenting refractory diseases for gluten allergy
small bowel carcinoma and t cell lymphoma. even despite good dietary control
tropical sprue
damage to small bowel villi by unknown organism resulting in malabsorption
what are the differences between celiac and tropical sprue
occurs in tropical regions, arises after infectious diarrhea and responds to antibiotics. damage is most prominent in the jejunum and ileum.
what are secondary symptoms of tropical sprue
b12 and folate deficiency
whipple disease
systemic damage characterized by macrophages loaded with whippelii organisms partially destroyed are present in the lysosomes.
what is the classic site of whipple disease damage
small bowel lamina propia. macrophage compress lacteals. chylomicrons cannot be transferred from enterocytes to lymphatics. there is fat malabsorption and steatorrhea.
what are other common sites of whipple disease involvement
heart, synovium of joints. lymph nodes and CNS
abetalipoproteinemia
autosomal recessive deficiency in apolipoprotein b-48 and b-100
clinical features of abeatlipoproteinemia
malabsorption and absent plasma VLDL and LDL.
carcinoid tumor.
malignant prol of neuroendocrine cells, low grade malignancy.
what will carcinoid tumor cells stain positive for?
chromogranin
what is the most common site for carcinoid tumor
small bowel. but can arise anywhere. grows as a submucosal polyp like nodule
what does the carcinoid tumor often secrete
serotonin
what is elevated in the urine with a carcinoid tumor
5-HIAA. serotonin into the blood stream gets taken to the river where it is broken down to 5-HIAA
how can carcinoid tumors bypass the livers metabolism?
is they mets to the liver. this is the underlying principle of carcinoid syndrome. the serotonin is leaked into the hepatic vein and systemic circulation via hepatosystemic shunts.
characteristics of carcinoid syndrome
bronchospasm diarrhea and flushing of the skin. symptoms can be triggered by alcohol or emotional stress which can stimulate release of serotonin from the tumor.
what is carcinoid heart disease
right sided valvular fibrosis leading to tricuspid regurgitation and pulmonary valve stenosis
why are left-sided valvular lesions not seen in carcinoid tumors
because there is monoamine oxidase in the lung.
acute appendicitis
acute inflammation of the appendix. most common cause of acute abdomen. related to obstruction by lymphoid hyperplasia in children or fecalith in adults.
clinical features of appendicitis
periumbilical pain, fever, nausea. pain eventually will locate to the right lower quadrant.
what happens if the appendix ruptures
peritonitis that presents with guarding and rebound tenderness.
what is a common complication of appendicitis
periappendiceal abscess
inflammatory bowel disease
chronic relapsing inflammation of the bowel. possibly due to abnormal immune response to enteric flora.
how does inflammatory bowel disease presetn
classically in young women as recurrent bouts of bloody diarrhea and abdominal pain. more prevalent in the west and particularly in caucasians and eastern european jews. this is a diagnosis of exclusion symptoms mimic other causes of bowel inflammation.
how is inflammatory bowek disease classified
as either ulcerative colitis or crohn’s disease.
hirsprungs disease
defective relaxation and peristalsis of the rectum and the sigmoid colon. associated with down syndrome. due to a congenital failure of ganglion cells to descend into the myenteric and submucosal plexi
what are the clinical features of hirsprung
failure to pass meconium empty rectal vault on digital rectal exam. massive dilation of the bowel proximal to obstruction with risk of rupture.
colonic diverticula
outpouchings of the mucosa and submnucosa through muscularis propria. related to wall stress. assocaited with constipation straining and low fiber diet. commonly seen in older adults.
where do colonic diverticula arisew
where the vasa recta transverse the muscular propria. sigmoids colon is the most common location
what are the clinical manifestations of colonic diverticula
usually asymptomatic. there can be bleeding, diverticulitis, fistula.
diverticulitis
inflammation of a diverticula due to obstructing fecal material. presents with appendicitis-like symptoms in the left lower quadrant.
fistula
inflamed diverticula ruptures and attaches to local structure
colovesicular fistula
presents with air or stool in urine
angiodysplasia
acquired malformation of mucosal and submucosal capillary beds. usually in cecum and right colon due to high wall tension.
what does angiodysplasia rupture present as
older adult with hematochezia.
hereditary hemorrhagic telangiectasia
AD resulting in thin-walled blood vessels especially in the mouth and GI tract. rupture presents as bleeding.
ischemic colitis
ischemic damage to the colon. usually in the splenic flexure. atherosclerosis of the SMA is the most common cause.
how does ischemic colitis present
as postprandial pain and weight loss. infarction results in pain and bloody stool.
irritable bowel syndrome
relapsing abdominal pain, bloating, flatulence and changes in bowel habits (diarrhea or constipation) that improves with defecation. classically seen in middle aged females. related to disturbed intestinal motility no identifiable pathological changes. increased dietary fiber might reverse symptoms.
colonic polyps
raised protrusions of the colonic mucosa most common are hyper plastic and adenomatous. testing/screening is performed by endoscopy or by occult blood. they can beed.
hyperplastic polyps
due to hyperplasia of the glands, show a serrated appearance on micro. most common type of polyp usually arise in the left colon (rectosigmoid). they are benign with no malignant potential.
adenomatous polyps
due to neoplastic proliferation of glands. 2nd most common type. benign, but premalignant. may progress to adenocarcinoma via the carcinoma sequence.
adenoma-carcinoma sequence
describes the molecular progression from normal mucosa to malignant adenomatous. APC mutations increase the risk. K-ras lead to the formation of the polyp. p53 and increased COX leads to the progression to carcinoma
what impedes the progression from adenoma to carcinoma
aspirin
goal of endoscopy?
to remove adenomatous polyps before they progress.
what is greatest risk of progression from adenomatous to carcinoma
size >2 cm sessile growth and villous histology
familial adenomatous polyposis FAP
AD leads to 100-1000 of adenomatous colonic polyps. due to APC gene mutation on chromosome 5. increases the propensity to develop the polyps throughout the colon and rectum.
what is the treatment for FAP
prophylactic removal of the colon and rectum otherwise almost all patients develop carcinoma y 40
gardner sydnrome
FAP with fibromatosis and osteomas
turcot syndrome
FAP with CNS tumors
juvenile polyp
sporadic. hamartomas that arises in children. presents as solitary rectal polyp that prolapses and bleeds.
juvenile polyposis
multiple juvenile polyps that arise in the stomach and the colon large # increases the risk for carcinoma.
peutz-jeghers syndrome
hamartomas throughout GI and mucotaneous hyper pigmentation on the lips oral mucosa and genital skin. AD disorder.
what risks are associated with peutz-jeghers syndrome
increased risk of breast, colorectal and gynecological cancers
colorectal carcinoma
3rd most common site of cancers. arises from the colonic or rectal. usually arises from the sequence, but can arise from microsatelite instability
when does screening for colorectal begin
age 50
where does carcinoma develop
anywhere along the entire length
napkin-ring lesion
left-sided colon cancer. presents with decreased stool caliber, left lower quadrant pain, and blood streaked stool.
right sided carcinoma
raised lesion, presents with iron deficiency anemia and vague pain,
older adult with iron deficiency anemia
has colon cancer until proven otherwise
what is colon cancer associated with
streptococcus bovis endocarditis
