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GI Flashcards

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USMLE® Step 1 flashcards
1
Q

Pleomorphic adenoma (gland)

A

Mixed epithelial and stroma tumor usually in parotid; benign but has high rate of recurrence and is associated with radiation

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2
Q

Warthin’s tumor

A

Benign heterotopic salivary gland tissue trapped ina lymph node, surrounded by lymphatic tissue

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3
Q

Mucoepidermoid carcinoma

A

Most common malignant tumor of salivary glands; usually located in the sublingual gland (most parotid tumors are benign while most sublingual are malignant)

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4
Q

Zenker diverticulum

A

Above upper esophogeal sphincter; risk for adenocarcionma

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5
Q

Traction diverticulum

A

midpoint of esophagus; risk for adenocarcinoma

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6
Q

Epiphrenic diverticulum

A

immediately above lower esophageal sphincter

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7
Q

Acute gastritis histology

A

neutrophils above BM, loss of surface epithelium, fibrin-containing purulent exudate

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8
Q

Chronic gastritis histology

A

lymphoid cell aggregates in lamina proria, columnar absorptive cells, atrophy of glandular structures

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9
Q

Zollinger ellison syndrome histology

A

Thickening of gastric folds, elevated gastrin levels, glandular hyperplasia

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10
Q

Drugs promoting gastric motility

A

Cholinergic agonists (bethanechol), acetylcholinesterase inhibitor like neostigmine, Metoclopramide (5HT agonist and Dopamine antagonist - potential for seizures), Macrolides (stimulate smooth muscle receptors)

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11
Q

tubular adenomas

A

pedunculated and smaller; dysplastic colonic mucosal cells that form tubular-shaped glands

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12
Q

Villous adenomas

A

cauliflower or fingerlike projections; dysplastic epithelial cells forming villi-like projections; can cause bleeding, secretory diarrhea and partial intestinal obstruction. Are larger sessile and more severely dysplastic than tubular; high risk of progression to adenocarcinoma

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13
Q

Tubulovillous adenoma

A

mixture of villous and tubular histology

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14
Q

Hamartomatous polyp

A

can occur sporadically or as part of Peutz-Jeghers syndome and Juvenile polyps. Can cause bleeding and intussusception but not diarrhea.

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15
Q

Peutz-Jeghers syndrome

A

associated with multpiple hamartomatous polyps and black spots on skin and mucosa of young patients. Secretory diarrhea is not common in this condition. Rare compared to adenomatous polyps; increased risk of CRC

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16
Q

Signet ring cell carcinoma can be found here

A

stomach, breast, ovary, colorectal area.

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17
Q

Treatment for acute arsenic poisoning

A

Dimercaprol - displaces arsenic from sulfydryl groups

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18
Q

Treatment of choice for Mercury and lead poisoning

A

EDTA which complexes with mono-, di- and trivalent ions

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19
Q

Secretin

A

Duodenal S cells release secretin in response to H+; stimulates pancreatic cells to increase bicarb secretion; As pancreatic juice flow rates and secretin stimulation increase the bicarb concentration increases and Cl concentration decreases

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20
Q

Curling ulcer

A

ulcers arising in proximal duodenum assoc with severe trauma or burns.

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21
Q

Cushing ulcer

A

esophageal, stomach, or duodenal ulcers associated with high intracranial pressure. Due to to impaired oxygenation of tissues, induced by vagus stimulation from brain resulting in hypersecretion.

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22
Q

Two subtypes of gastric adenocarcinoma

A

Intestinal: intestinal glands similar to colonic adenocarcinoma; Diffuse: signet-ring cells. Gastritis, barrett esophagus, H pylori, nitrate consumption, diet lacking in fruit and vegetables, cigarette smoking are risk factors

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23
Q

Opioid side effects on GI system

A

Constriction of sphincter of Oddi which can cause increase in common bile duct pressure. Cause histamine release leading to vasodilation and itching. Cause constipation by slowing motility, decrease parietal cell acid secretion, can indirectly increase somatostain secretion.

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24
Q

Duodenal ulcer associateions

A

pain decreased with meals. Almost always H pylori. Some have increased gastric acid secretion as in ZE syndrome. Hypertrophy of Brunner’s glands. NOT assoc w risk of carcinoma (esophageal, gastric and colonic ulcers are)

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25
Q

Duodenal ulcer location

A

Most occur in duodenal bulb; when found in distal duodenum or other atypical locations Zollinger-Ellison syndrome is suspected. Multiple ulcers, ones refractory to therapy also.

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26
Q

Midgut embryology; timing and potential problems

A

6th week midgut herniates (allows for rapid growth of intestine and liver despite slower growth of abdominal cavity). 10th week 270degree turn counterclockwise around SMA. If this is abnormal, malrotation occurs and cecum is found in RUQ, fixed fibrous bands to second portion of duodenum. Obstruction occurs dt bands which compress duodenum which results with bilious vomiting. Twisting around SMA can also cause midgut volvulus with intestinal gangerene.

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27
Q

VIP

A

produced by pancreatc islet cells and neurons in GI mucosa. Relaxes smooth m, inhibits H+ secretion, stimulates pancreatic bicarb and chloride secretion.

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28
Q

CCK

A

increases secretion of Pancreatic enzymes and contraction of gall bladder, inhibits gastric emptying. Produced by I-cells of proximal small bowel mucosa in response to fatty acids and monoglycerides

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29
Q

Secretin

A

produced by S-cells in respnse to duodenal acidity and fatty acids. Increases pancreatic and biliary bicarb secretion and decreases gastric acid secretion

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30
Q

Gastrin

A

G-cells in stomach mucosa. Stimulates gastric acid production and growth of gastric mucosa, gastrinomas classically cause intractable peptic ulcer disease

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31
Q

Glucagonoma

A

pancreatic alpha-cell tumor that hypersecretes glucagon. Secondary diabetes mellitus and necrolytic migratory erythema of the skin

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32
Q

Ulcerative colitis associated carcinoma differs from sporadic how

A

affects younger patients; progresses from flat non-polypoid dysplasia; appears mucius or has signet ring morphology; early p53 but late APC gene mutation, opposite of sporadic; distributed within proximal colon; multifocal in nature.

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33
Q

Amatoxins (death cap mushroom toxins)

A

Bind to DNA-dependent RNA polymerase II and halt mRNA synthesis. Results in apoptosis of hepatic cells.

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34
Q

Modes of transmission of campylobacter versus shigella

A

Both are fecal-oral but campylobacter is carried by domestic animals where shigella is not. Campylobacter is mostly acquired from animals or undercooked poultry or unpasteurized milk.

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35
Q

Somatostatin

A

made in a bunch of different locations such as hypothalamus, stomach, intestine, and pancreas. It inhibits GH, TSH, and suppresses all other GI hormones

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36
Q

Why is shigella’s Infective dose so low?

A

it is resistiant to acid and bile, it also binds to intestinal mucosal M cells on peyer’s patches. Other organisms with small infective inoculum are Campylobacter, Entamoeba histolytica (it takes only 1), Giardia (only 1 needed)

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37
Q

GERDs typical cause

A

LES transient relaxation. Acidic gastric contents reflux back into esophagus and irritate mucosa leading to inflammation. Presents with nocturnal cough many times. Biopsy shows basal cell hyperplasia, elongation of lamina propria and inflammatory cells (eosiniphils, neutrophils, lymph)

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38
Q

Anal fissure

A

tear in the lining of anal canal distal to the dentate line that occurs most often on the posterior midline (this area is poorly perfused making it sensitive to trauma by hard fecal mass). Patients complain of severe tearing pain with passage of bowel movements. Assoc w low fiber and constipation.

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39
Q

Typical signs of lead poisoning

A

Colicky abdominal pain “lead colic”, constipation, headaches, impaired short-term memory, blue pigmentation at gum-tooth line “lead lines”; wrist drow or foot drop due to peripheral neuropathy; microcytic hypochromic anemia and basophilic stippling

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40
Q

CEA

A

serum carcinoembryonic antigen, marker for colon cancer. It is a glycoprotein involved in cell adhesion. Produced in the embryonic pancreas.

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41
Q

Leptin action

A

produced in adipocytes; decreases food intake by decreasing production of neuropeptide Y (an appetite stimulant in arcuate nucleus); stimulates POMC in arcuate nucleas which is cleaved to MSH which inhibits food intake.

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42
Q

Erosions versus ulcers

A

erosive gastritis: caused by NSAID use, trauma, burns, alcohol or tobacco, stress, bacteria. Defined as mucosal defects that don’t penetrate the muscularis mucosa. Ulcers extend into submucosal inner muscular and outer muscular layers.

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43
Q

hyperplastic polyp

A

well-differentiated mucosal cells that form glands and crypts

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44
Q

Hamartomatous polyp

A

mucosal glands, smooth muscle and CT. May be sporadic or in Peutz-Jeghers or juvenile polyposis.

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45
Q

Inflammatory polyps

A

seen in IBD. Composed of regenerating intestinal mucosa

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46
Q

Lymphoid polyps

A

found in children and consist of intestinal mucosa infiltrated with lymphocytes

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47
Q

Malignant potential of adenomatous polyps (adenomatous polyps are the ones that contain dysplastic cells that can transform into carcinoma)

A

Degree of dysplasia, villous histology, size >1cm

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48
Q

Imperforate anus

A

abnormal development of anorectal structures; most often associated with urorectal, urovesical, or urovaginal fistulas. When a fistula is present, meconium may discharge from the urethra or the vagina. Associated findings are renal agenesis, hypospadias, epispadias, and bladder extrophy.

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49
Q

Intestinal atresia

A

occurs due to vascular accidents in utero. If the SMA is obstructed the “apple-peel” atresia occurs. It manifests as blind-ending proximal jejunum with absence of a long length of small bowel and dorsal mesentery. The terminal ileum distal to the atresia assumes a spiral configuration around an ileocolic vessel.

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50
Q

Crohn’s disease molecular pathogenesis

A

NF-kB is responsible for the cytokine production seen. NOD2 gene (expressed in epithelial cells and leukocytes) appears to act as microbial receptor that triggers NF-kB. NF-kB induces cytokines in response to infectious pathogens. The NOD2 mutation increases NF-kB allowing intracellular microbes persisting and inducing chronic inflammation within GI tract

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51
Q

Fibrosis of islets of pancreas

A

DM type I

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52
Q

pacnreatic ducts filled with mucus plugs

A

Cystic fibrosis

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53
Q

Lymphocytic infiltration of islets of langerhans

A

DM type 1

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54
Q

Lipid digestion

A

occurs in duodenum and is ABSORBED in the Jejunum.

55
Q

Complications of Ulcerative colitis

A

Sclerosing cholangitis, CRC, Toxic Megacolon (presents with bloody diarrhea, fever, signs of shock; perforation is a life-threatening complication of megacolon, do not do any barium or contrast studies for fear of perforation)

56
Q

Complications of Crohn’s

A

Strictures, fistulas, perianal disease, CRC

57
Q

Esophageal squamous carcinoma risk factors

A

alcohol, tobacco smoking, nitroso containing foods; asian and african descent

58
Q

Esophageal adenocarcinoma risk factors

A

Barrett esophagus, obesity, GERD, tobacco use

59
Q

Vitelline duct abnormalities

A

Persistent vitelline duc, meckel diverticulum, viteline sinus, and vitelline duct cyst. This normally obliterates during week 7. Also called omphalomesenteric duct

60
Q

esophageal varices

A

shunt involving Left gastric vein and esophageal vein

61
Q

Caput medusae

A

Paraumbilical veins to superficial and inferior epigastric

62
Q

Hemorrhoids in ascites

A

Superior rectal veins to middle and inferior rectal veins which drain into interna linguinal vein

63
Q

acute interstitial pancreatitis pathyphys

A

stasis of secretions leads to lipase autodigestion and calcium doposition onto free FA’s. Pancreas looks edematous with focal fat necrosis and calcium. If the inflammatory process continues it can lead to necrosis.

64
Q

Acute Necrotic pancreatitis

A

If inflammation from acute interstitial pancreatitis continues the edema cuts off blood supply rendering ischemic damage to acinar cells leading to inappropriate trypsin activation. The trpsin ten activates other proteoltic enmes and initiates autodigestion. The areas of white chaly fat necrosis can spread onto mesentery, omentum etc.

65
Q

Chronic Gastritis Types A and B

A

Type A is Autoimmune etiology and is found in the body (pernicious anemia); Type B is bacterial in nature (h pylori) and is found in the Antrum

66
Q

adenocarcinoma biopsy and colonoscopy findings

A

protuberant mass on scope; mucosal cells with gland formation on biopsy

67
Q

colonic CMV scope and biopsy

A

ulcers and mucosal erosions on scope; Inclusion bodies on micro

68
Q

Colonic cryptosporidium scope and microscopy

A

scope shows generalized inflammation; basophilic clusters are seen on surface of intestinal mucosal cells

69
Q

Entamoeba histolytica scope and microscopy

A

scope shows flask shatped ulcers; trophozoites have red blood cells

70
Q

Kaposi’s sarcoma scope and microscopy

A

Reddish violet flat maculopapular lesions or hemorrhagic nodules; the microscopy shows spindle-shaped tumor cells with small-vessel proliferation

71
Q

MSH2 gene

A

mutated in HNPCC and is responsible for DNA mismatch repair

72
Q

APC gene

A

located on Chromosome 5 responsible for regulation of growth and cell adhesion

73
Q

Systemic mastocytosis

A

abnormal proliferation of mast cells and increased histamine secretion. This causes many systemic effects mediated by histamine. In the GI system it leads to increased secretion of Gastric acid

74
Q

Histamine action on parietal cells

A

H2 receptor stimulates cAMP and PKA

75
Q

Acetylcholine action on parietal cells

A

M3 receptors leads to increased calcium via IP3

76
Q

Gastrin action on parietal cells

A

increase of intracellular calcium. It stimulates histamine synthesis and release by enterochromaffin-like cells which is most potent mechanism

77
Q

Risk factor for gallstone ileus

A

usually in patients with long history of gallstones, a long standing stone creates a fistula between gallbladder and adjoining gut tissue which allows passage into small bowel. This allows for gas to be let into the gallbladder. The gallstone blocks the ileocecal valve and you can see air in the biliary tree

78
Q

CREST

A

Calcinosis, Raynaud, Esophageal dysmotility, Sclerodactyly, Telangiectasia

79
Q

Factors recucing gastric secretion after a meal

A

peptide YY to block histamine release, Somatostatin, and prostaglandins

80
Q

Vitamins deficient after gastrojejunostomy

A

B12, Iron, folate, and fat-soluble vitamins

81
Q

Most common locations of colonic masses

A

rectosigmoid colon > Ascending colon > Left sided tumors (infiltrate wall of colon and narrow lumen)

82
Q

Causes of acute pancreatitis

A

Gallstones and alcohol are most common; less common are ERCP procedure, drugs, infection, hypertriglyceridemia, structural abnormalities, surgery, hypercalcemia

83
Q

Spcific antibodies for celiacs

A

anti-tissue transglutaminase; IgA endomysial antibody

84
Q

Gastric adenocarcinoma, two types

A

Signet-ring carcinoma: cells don’t form glands, diffuse involvement of stomach wall, have plaque appearance, infiltrate large areas of stomach creating leather-bottle stomach (linitis plastica). Intestinal-type adenocarcinoma: resmbles colon cancer, grows nodular polypoid and well-demarcated masses. Most important prognostic factors is depth of invasion and regional lymph. Nitrosamines, achlorhydria, chronic gastritis are risk factors so is type A blood

85
Q

Retroperitoneal Structures

A

Abdominal Aorta, Pancreas, Descending and ascending colon, Spleen, Ureters, Suprarenal gland, kidney, IVC, deodenum (2nd 3rd and 4th parts), esophagus, rectum

86
Q

Falciform ligament

A

Attaches liver to anterior abdominal wall

87
Q

Hepatoduodenal ligament

A

Contains portal triad. Connects greater and lesser sacs

88
Q

Gastrohepatic ligament

A

Lesser curvature to liver. Contains R and L gastric artery, separates greater and lesser sacs.

89
Q

Gastrocolic ligament

A

Contains gastroepiploic arteries, part of greater omentum. Attaches to greater curvature.

90
Q

Gastrosplenic ligament

A

contains short gastric arteries, separates left greater and lesser sac

91
Q

Splenorenal ligament

A

Connects spleen to posteriosterior abdominal wall, holds splenic artery and vein

92
Q

Normal epithelium of esophagus

A

stratified squamous nonkeratinized

93
Q

Stomach epithelium

A

gastric glands

94
Q

Duodenal histology

A

Villi and microvilli. Brunner’s glands, Crypts of Leiberkuhn

95
Q

Jejunum histology

A

plicae circulares and crypts of lieberkuhn

96
Q

Ileum histology

A

Peyer’s patches, plicae circulares, crypts. Largest number of goblet cells (goblet cells increase density as you mover farther down the ileum)

97
Q

Colon Histology

A

Crypts but NO villi

98
Q

Layers of digestive tract anatomy

A

Epithelium (columnar), lamina propria, muscularis mucosa, submucosa with glands and meissner’s plexus, Muscularis externa with auerbach’s plexus then serosa

99
Q

Name branches and location of branches of abdominal aorta descending order

A

Inferior phrenic aa., Celiac trunk (T12), SMA (L1), L suprarenal a. (L1), R and L renal aa. (L1-L2), R and L testicular (ovarian) aa. (L2/3), IMA (L3), Bifurcation of aorta L4.

100
Q

Branches of the celiac trunk

A

L gastric, Spleenic, Common hepatic.

101
Q

Rectum above pectinate line, pathology and venous drainage

A

Adenocarcinoma, supplied from Superior rectal artery (IMA). Drains to Superior rectal vein and to IMA, then to portal system

102
Q

Rectum below pectinate line

A

Somatic innervation so hemorrhoids are painful. Drains to inferior rectal vein to internal pudendal then internal iliac to IVC. Squamous cell carcinoma and supplied arterially from Internal pudendal.

103
Q

Indirect Inguinal hernia

A

More common in males, happens in infants owing to failure of processus vaginalis to close (can form hydrocele). Covered by all 3 layers of spermatic fascia

104
Q

Direct inguinal hernia

A

Through hesselbach’s triangle (inferior epigastric, lateral rectus abdominis, inguinal ligament). Goes through superficial inguinal ring only covered by external spermatic fascia and is seen in older men.

105
Q

Femoral hernia

A

Protrudes below inguinal ligament, is a common cause of bowel strangulation. Through the femoral canal below and lateral to pubic tubercle. More common in women

106
Q

Gastrin

A

G cells (antrum); gastric mucosa growth, motility, H+; stomach distention or pH increase, amino acids, peptides, vagal.

107
Q

CCK

A

I cells (duodenum jejunum) stimulated by FA’s and Protein, increases pancreas secretion (via stimulation of parasympathetics), gallbladder contraction, increased sphincter of oddi relaxation, decrease emptying

108
Q

Secretin

A

S cells (duodenum) increases HCO3 from pancreas, decreases gastric acid secretion, increased by acid and fatty acids.

109
Q

Somatostatin

A

D cells (pancreas, GI mucosa); decreases all GI hormones, inhibits release of GH and TSH. Increased by acid and decreased by vagal stimulation.

110
Q

GIP

A

K cells (duodenum jejunum) increases insulin release and decreases H+ secretion. Stimulated by oral glucose (more rapid than glucose given IV)

111
Q

VIP

A

Parasympathetic ganglia increases secretions and relaxes intestinal smooth m. adecreased by adrenergic input

112
Q

Motilin

A

Small intestine Produces migrating motor complexes, increased in fasting state

113
Q

Glucose and galactose absorption

A

SGLT1 (Na dependent)

114
Q

GLUT-5

A

Fructose transporter in intestine

115
Q

D-xylose test

A

distinguishes GI mucosal damage from other causes of malabsorption

116
Q

Peyer’s patches

A

Small intestin lamina propria and submucosa. M cells take up antigen. B cells stimulate germinal centers and IgA-secreting plasma cells are created. IgA receives protective secretory component and is then transported across epithelium to gut to deal with antigen.

117
Q

nocturnal couph and dyspnea

A

GERD or Barrett’s

118
Q

Diffuse esophageal spasm (DES)

A

esophageal motility disorder presenting with severe non-cardiac chest pain due to uncoordinated contractions of esophageal body, mimics angina

119
Q

Symptoms of whipple’s disease

A

cardiac, arthralgias, and neurological

120
Q

Celiac sprue antibodies and genetic association

A

HLA-B8, occurs primarily in jejunum, Anti-gliadin, anti-endomyseal, anti-reticulin,anti-transglutaminase

121
Q

Acute gastritis etiology

A

decreased protection of mucosa, dt stress, NSAIDS, alcohol, uremia, burns (curling), head trauma (cushings),

122
Q

Menetrier’s disease

A

gastric hypertrophy with protein loss, parietal cell atrophy, and increased mucous cells. Precancerous. Rugae of stomach look like brain gyri

123
Q

Virchow’s node

A

supraclavicular node on left side (drains lower GI) and is a place of mets from stomach

124
Q

Sister Mary Joseph’s nodule

A

Perimbilical gastric metastasis

125
Q

Familial adenomatous Polyposis (FAP)

A

AD; APC gene on chromosome 5q. Thousands of polyps.

126
Q

Gardner’s syndrome

A

FAP + osseous tumors and retinal hyperplasia with other soft tissue

127
Q

Turcot’s syndrome

A

FAP + CNS tumors

128
Q

HNPCC

A

MSH2 gene mutaiton in DNA mismatch repair. Proximal colon is most common location (R-sided)

129
Q

Carcinoid and B3 deficiency

A

Makes Serotonin which is synthsized by tryptophan so it can cause a secondary tryptophan deficiency leading to niacin deficiency

130
Q

Alcoholic hepatitis

A

destruction via acetaldehyde which stimulates cells that used to store vitamin A to change and make collagen and fibrous tissue instead. There is a neutrophilic infiltration. Formation of mallory bodies which are ubiquinated keratin microfilaments.

131
Q

Hepatocellular carcinoma risk factors

A

HBV HCV, alcohol, wilson’s disease, hemachromatosis, alpha-1-AT, carcinogens, Aspergillus toxins.

132
Q

Cavernous hemangioma

A

biopsy contraindicated due to risk of bleeding. Congenital malformations that enlarge by ectasia not hyperplasia. Common benign liver tumor; typically occurs at age 40.

133
Q

primary sclerosing cholangitis

A

associated with ulcerative colitis. Etiology unknown. It looks like a beaded structure with onion skin lesions. Mostly occurs in men, pANCA, risk for cholangiocarcinoma. Hyper IgM.

134
Q

Primary biliary sclerosis

A

autoimmune disease, histologically is granulomatous inflammation of INTRAhepatic bile ducts. Starts off variably throughout liver progresses to a diffuse green stained liver that is uniformly micronodular. + anti-mitochondrial antibodies. Associated with other autoimmune diseases especially women

USMLE (14 decks)

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