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pathoma unit 6 > gastrointestinal > Flashcards

gastrointestinal Flashcards

1
Q

tracheoesophageal fistula

A

congenital defect resulting in a connection between the esophagus and trachea.

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2
Q

most common variant of tracheoesophageal fistula

A

proximal esophageal atresia with the distal esophagus arising from the trachea. presents with vomiting, polyhydraminos, abdominal distention, and aspiration.

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3
Q

esophageal web characteristics

A

thin protrusion of the esophageal muscosa. most often in the upper esophagus. presents with dysphagia for poorly chewed food.

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4
Q

what is esophageal web increase the risk for?

A

squamous cell carcinoma.

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5
Q

plummer-vinson syndrome

A

esophageal web, iron anemia deficiency and a beefy-red tongue due to atrophic glossitis. increased risk for squamous cell.

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6
Q

zenker diverticula

A

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

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7
Q

how does zenker diverticula present

A

with dysphagia, obstruction and halitosis.

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8
Q

mallory-weiss syndrome

A

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

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9
Q

boerhave syndrome

A

rupture of esophagus leading to air in the mediastinum and subcutaneous emphysema/

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10
Q

esophageal varices

A

dilated mucosal veins in the lower esophagus, arise secondary to portal hypertension. this is usually asymptomatic /but there is a risk for rupture.

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11
Q

what is the most common cause of death cirrhosis

A

rupture of esophageal varices from portal hypertension.

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12
Q

achalasia

A

inability to relax the lower esophageal sphincter due to damaged ganglion cells in the myenteric plexus

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13
Q

what is a common cause of ganglion cell damage in the esophagus?

A

infection by t. cruzi

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14
Q

clinical symptoms of achalasia

A

dysphagia for solids and liquids, putrid breath, high LES pressure, bird beak sign on barium swallow studies. increased for esophageal squamous cell carcinoma

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15
Q

GERD

A

reflux of stomach acid due to loss of LES tone.

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16
Q

risks for GERD

A

alcohol, obesity, fat-rich diet, caffiene, and hiatal hernia;

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17
Q

how does GERD manifest

A

heart burn, asthma and cough, damage to the enamel of the teeth

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18
Q

what are the late complications of GERD

A

esophageal stricture, barretts esophagus

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19
Q

barrets esophagus

A

metaplasia of the lower esophageal mucosa from stratified squamous epithelium to nonciliated columnar epithelium with goblet cells.

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20
Q

how frequently is Barrets E seen?

A

10% of GERD patients

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21
Q

what can GERD progress to?

A

dysplasia and adenocarcinoma

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22
Q

esophageal carcinoma subclassifications

A

adenocarcinoma or squamous cell

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23
Q

adenoma carcinoma of the esophagus

A

most commmon in the west. arises from preexisting barrels usually involves the lower 1/3

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24
Q

squamous cell carcinoma of the esophagus

A

most common worldwide. usually in the upper or middle esophagus.

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25
Q

major risk factors for squamous cell carcinoma of the esophagus

A

alcohol and tobacco, very hot tea, achalasia, esophageal web, esophageal injury,

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26
Q

how does esophageal cancer present?

A

late, with a poor prognosis. progressive dysphagia, weight loss, pain, hemoptysis.

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27
Q

squamous cell additional presentations

A

hoarse voice, cough,

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28
Q

where does the upper 1/3n of esophageal cancer spread too?

A

cervical lymph nodes,

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29
Q

where does the middle 1/3 spread

A

mediastinal or tracheal bronchial tubes

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30
Q

where does the lower 1/3 spread

A

celiac and gastric nodes

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31
Q

gastroschisis

A

congenital malformation of the anterior abdominal wall leading got exposure of the abdominal contents.

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32
Q

ophalocele

A

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.

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33
Q

pyloric stenosis

A

congenital hypertrophy of the pyloric sm that is more common in males. classically presents two weeks after birth

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34
Q

how does pyloric stenosis present

A

projectile vomiting that is nonbilious, visible peristalsis, olive-like mass in the abdomen

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35
Q

treatment for pyloric stenosis

A

myotomy

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36
Q

acute gastritis

A

acidic damage to the stomach mucosa, caused by an imbalance to the stomachs defenses and the acidic environment.

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37
Q

what are the stomachs defenses against acid

A

mucin layer (produced by foveolar cells, bicarbonate secretion by surface epithelium, normal blood supply.

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38
Q

risk factors for acute gastritis

A

severe burns lead to lack of blood supply, NSAIDs, heavy alcohol consumption, chemotherapy, increased intracranial pressure, increased stimulation of the vagas nerve, shock.

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39
Q

what can be seen in ICU patients due to shock?

A

multiple stress ulcers.

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40
Q

what does acid damage do to the mucosa

A

superficial inflammation, erosion, ulcer.

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41
Q

chronic gastritis

A

chronic inflammaiton of the stomach mucosa.

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42
Q

what are the two causes of chronic gastritis

A

chronic autoimmune or chronic h pylori

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43
Q

what is the cause of chronic autoimmune gastritis

A

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

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44
Q

clinical features of chronic gastritis

A

atrophy of mucosa with intestinal metaplasia, achlorhydria with increased gastrin levels and astral g-cell hyperplasia, megaloblastic anemia, increased risk for gastric adenocarcinoma

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45
Q

chronic inflammation with h pylori

A

this is the most common form of gastritis 90%. he creases and proteases weaken the mechanisms of defense antrum is the most common site.

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46
Q

how does h pylori present

A

epigastric abdominal pain, increased risk for ulceration, adenocarcinoma, MALT lymphoma.

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47
Q

how do we treat h pylori

A

triple therapy.

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48
Q

prognosis of h pylori post treat

A

reverses gastritis and intestinal metaplasia, negative urea breath test and lack of stool antigen confirms eradication.

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49
Q

peptic ulcer disease

A

most prevalent in the stomach or duodenum (90%), almost always caused by h pylori, rarely ZE.

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50
Q

how does peptic ulcer present

A

epigastric pain that improves with meals.

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51
Q

what does endoscope show for peptic ulcer disease

A

ulcer with hypertrophy of brunner glands.

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52
Q

where odes the ulcer usually occur?

A

in the anterior duodenum.

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53
Q

what are the risks of ulcer in the posterior duodenum

A

bleeding from artery or acute pancreatitis

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54
Q

gastric ulcer

A

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.

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55
Q

is duodenal carcinoma rare?

A

yes. extremely.

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56
Q

gastric carcinoma

A

malignant surface epithelial cells. subcalssified into diffuse and intestinal types.

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57
Q

which type of gastric carcinoma is more common, diffuse or intestinal

A

intestinal

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58
Q

how does intestinal gastric carcinoma present

A

large irregular ulcer with heaped up margins and most commonly involves the lesser curvature of the antrum of the stomach.

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59
Q

what characterizes the diffuse type?

A

signet ring cells that diffusely infiltrate the gastric wall. desmoplasia results in thickening of the stomach wall.

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60
Q

what is linitus plastica

A

thickening of the stomach wall

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61
Q

what is the diffuse type not associated with>

A

h pylori, nitrosamines, intestinal metaplasia

62
Q

how does gastric carcinoma present?

A

late with weight loss, abdominal pain, anemia, early satiety,

63
Q

how can it gastric carcinoma present rarely

A

acanthosis nigricans, leser trelat sign.

64
Q

what lymph nodes can be involved in gastric carcinoma

A

the supra;navicular nodes. virchow nodes.

65
Q

where does gastric carcinoma usually metastasize

A

to the liver, periumbical region, bilateral ovaries

66
Q

sister mary joseph nodule

A

gastric cancer mets to the periumbilical region

67
Q

krukenburg tumor

A

gastric cancer mets to bilateral ovaries.

68
Q

duodenal atresia

A

congenital failure of the duodenum to canalize associated with down syndrome

69
Q

clinical feature of duodenal atresia

A

polyhydraminos, distention of the stomach and blind loop of the duodenum (double-bubble sign), bilious vomiting.

70
Q

meckel diverticula

A

outpouching of all three layers of the bowel wall. failure of the vitelline duct to involute. rule of 2’s

71
Q

what is the rule of 2’s for meckel diverticula

A

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.

72
Q

volvulus

A

twisting of the bowel along its mesentery. results in obstruction and disruption of blood supply with infarction.

73
Q

what are most common locations of volvulus for elderly

A

sigmoid colon

74
Q

what are the most common locations of volvulus for young adults

A

cecum

75
Q

intussusception

A

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.

76
Q

what is the most common cause of intussusception in children

A

lymphoid hyperplasia. due to rotavirus. usually arises in the terminal ileum leading to intus. into the cecum.

77
Q

what is the most common cause of intussusception in adults

A

tumor.

78
Q

small bowel infarction

A

the small bowel is highly susceptible to infarct. transmural occurs with thrombosis/embolism, of SMA or thrombosis of the mesenteric vein.

79
Q

when can mucosal infarction occur?

A

with marked hypotension.

80
Q

clinical features of infarction of the GI

A

abdominal pain, bloody diarrhea, decreased bowel sounds.

81
Q

lactose intolerance

A

decreased function of the lactase enzyme found on the brush border of intestinal cells. breaks down lactose into galactose and glucose.

82
Q

how does lactose intolerance present

A

abdominal distension, diarrhea upon consumption of milk product. undigested lactose is osmotically active.

83
Q

celiac disease

A

immun mediated damage to small intestinal villi due to gluten exposure.

84
Q

what HLA is celiac

A

HLA-DQ2 and DQ8

85
Q

where does gluten come from?

A

wheat and grain.

86
Q

what is the most pathogenic component of gluten

A

gliadin.

87
Q

what is the pathogenesis of gluten allergy

A

gliadin is broken down by transglutaminase, presented by APC via MHC class II. helper t cells mediate tissue damage.

88
Q

clinical presentation of gluten allergy in children

A

children: abdominal distension, diarrhea, failure to thrive.

89
Q

presentation of gluten allergy in adults

A

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.

90
Q

what are the labs for gluten allergy

A

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.

91
Q

what are late presenting refractory diseases for gluten allergy

A

small bowel carcinoma and t cell lymphoma. even despite good dietary control

92
Q

tropical sprue

A

damage to small bowel villi by unknown organism resulting in malabsorption

93
Q

what are the differences between celiac and tropical sprue

A

occurs in tropical regions, arises after infectious diarrhea and responds to antibiotics. damage is most prominent in the jejunum and ileum.

94
Q

what are secondary symptoms of tropical sprue

A

b12 and folate deficiency

95
Q

whipple disease

A

systemic damage characterized by macrophages loaded with whippelii organisms partially destroyed are present in the lysosomes.

96
Q

what is the classic site of whipple disease damage

A

small bowel lamina propia. macrophage compress lacteals. chylomicrons cannot be transferred from enterocytes to lymphatics. there is fat malabsorption and steatorrhea.

97
Q

what are other common sites of whipple disease involvement

A

heart, synovium of joints. lymph nodes and CNS

98
Q

abetalipoproteinemia

A

autosomal recessive deficiency in apolipoprotein b-48 and b-100

99
Q

clinical features of abeatlipoproteinemia

A

malabsorption and absent plasma VLDL and LDL.

100
Q

carcinoid tumor.

A

malignant prol of neuroendocrine cells, low grade malignancy.

101
Q

what will carcinoid tumor cells stain positive for?

A

chromogranin

102
Q

what is the most common site for carcinoid tumor

A

small bowel. but can arise anywhere. grows as a submucosal polyp like nodule

103
Q

what does the carcinoid tumor often secrete

A

serotonin

104
Q

what is elevated in the urine with a carcinoid tumor

A

5-HIAA. serotonin into the blood stream gets taken to the river where it is broken down to 5-HIAA

105
Q

how can carcinoid tumors bypass the livers metabolism?

A

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.

106
Q

characteristics of carcinoid syndrome

A

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.

107
Q

what is carcinoid heart disease

A

right sided valvular fibrosis leading to tricuspid regurgitation and pulmonary valve stenosis

108
Q

why are left-sided valvular lesions not seen in carcinoid tumors

A

because there is monoamine oxidase in the lung.

109
Q

acute appendicitis

A

acute inflammation of the appendix. most common cause of acute abdomen. related to obstruction by lymphoid hyperplasia in children or fecalith in adults.

110
Q

clinical features of appendicitis

A

periumbilical pain, fever, nausea. pain eventually will locate to the right lower quadrant.

111
Q

what happens if the appendix ruptures

A

peritonitis that presents with guarding and rebound tenderness.

112
Q

what is a common complication of appendicitis

A

periappendiceal abscess

113
Q

inflammatory bowel disease

A

chronic relapsing inflammation of the bowel. possibly due to abnormal immune response to enteric flora.

114
Q

how does inflammatory bowel disease presetn

A

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.

115
Q

how is inflammatory bowek disease classified

A

as either ulcerative colitis or crohn’s disease.

116
Q

hirsprungs disease

A

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

117
Q

what are the clinical features of hirsprung

A

failure to pass meconium empty rectal vault on digital rectal exam. massive dilation of the bowel proximal to obstruction with risk of rupture.

118
Q

colonic diverticula

A

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.

119
Q

where do colonic diverticula arisew

A

where the vasa recta transverse the muscular propria. sigmoids colon is the most common location

120
Q

what are the clinical manifestations of colonic diverticula

A

usually asymptomatic. there can be bleeding, diverticulitis, fistula.

121
Q

diverticulitis

A

inflammation of a diverticula due to obstructing fecal material. presents with appendicitis-like symptoms in the left lower quadrant.

122
Q

fistula

A

inflamed diverticula ruptures and attaches to local structure

123
Q

colovesicular fistula

A

presents with air or stool in urine

124
Q

angiodysplasia

A

acquired malformation of mucosal and submucosal capillary beds. usually in cecum and right colon due to high wall tension.

125
Q

what does angiodysplasia rupture present as

A

older adult with hematochezia.

126
Q

hereditary hemorrhagic telangiectasia

A

AD resulting in thin-walled blood vessels especially in the mouth and GI tract. rupture presents as bleeding.

127
Q

ischemic colitis

A

ischemic damage to the colon. usually in the splenic flexure. atherosclerosis of the SMA is the most common cause.

128
Q

how does ischemic colitis present

A

as postprandial pain and weight loss. infarction results in pain and bloody stool.

129
Q

irritable bowel syndrome

A

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.

130
Q

colonic polyps

A

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.

131
Q

hyperplastic polyps

A

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.

132
Q

adenomatous polyps

A

due to neoplastic proliferation of glands. 2nd most common type. benign, but premalignant. may progress to adenocarcinoma via the carcinoma sequence.

133
Q

adenoma-carcinoma sequence

A

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

134
Q

what impedes the progression from adenoma to carcinoma

A

aspirin

135
Q

goal of endoscopy?

A

to remove adenomatous polyps before they progress.

136
Q

what is greatest risk of progression from adenomatous to carcinoma

A

size >2 cm sessile growth and villous histology

137
Q

familial adenomatous polyposis FAP

A

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.

138
Q

what is the treatment for FAP

A

prophylactic removal of the colon and rectum otherwise almost all patients develop carcinoma y 40

139
Q

gardner sydnrome

A

FAP with fibromatosis and osteomas

140
Q

turcot syndrome

A

FAP with CNS tumors

141
Q

juvenile polyp

A

sporadic. hamartomas that arises in children. presents as solitary rectal polyp that prolapses and bleeds.

142
Q

juvenile polyposis

A

multiple juvenile polyps that arise in the stomach and the colon large # increases the risk for carcinoma.

143
Q

peutz-jeghers syndrome

A

hamartomas throughout GI and mucotaneous hyper pigmentation on the lips oral mucosa and genital skin. AD disorder.

144
Q

what risks are associated with peutz-jeghers syndrome

A

increased risk of breast, colorectal and gynecological cancers

145
Q

colorectal carcinoma

A

3rd most common site of cancers. arises from the colonic or rectal. usually arises from the sequence, but can arise from microsatelite instability

146
Q

when does screening for colorectal begin

A

age 50

147
Q

where does carcinoma develop

A

anywhere along the entire length

148
Q

napkin-ring lesion

A

left-sided colon cancer. presents with decreased stool caliber, left lower quadrant pain, and blood streaked stool.

149
Q

right sided carcinoma

A

raised lesion, presents with iron deficiency anemia and vague pain,

150
Q

older adult with iron deficiency anemia

A

has colon cancer until proven otherwise

151
Q

what is colon cancer associated with

A

streptococcus bovis endocarditis

pathoma unit 6 (3 decks)

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