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Step 1 > GI > Flashcards

GI Flashcards

1
Q

Foregut

A

Pharynx → duodenum

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2
Q

Midgut

A

Duodenum → proximal 2/3 of transverse colon

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3
Q

Hindgut

A

Distal 1/3 of transverse colon to anal canal above pectinate line

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4
Q

Midgut development

A
  • 6th week → physiologic midgut herniates through umbilical ring
  • 10th week → returns to abdominal cavity + rotates around superior mesenteric artery (SMA), total 270 degree counterclockwise
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5
Q

Defect rostral fold closure

A

Sternal defects

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6
Q

Defect lateral fold closure

A

Omphalocele, gastroschisis

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7
Q

Defect caudal fold closure

A

Bladder exstrophy

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8
Q

Duodenal atresia

A
  • Failure to recanalize
  • Dilation of the stomach and proximal duodenum (“double bubble” on x-ray)
  • Associated with Down syndrome
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9
Q

Jejunal and ileal atresia

A
  • Disruption of mesenteric vessels
  • Ischemic necrosis
  • Segmental resorption (bowel discontinuity or “apple peel”)
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10
Q

Hypertrophic pyloric stenosis is associated with exposure to

A

Macrolides

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11
Q

Hypertrophic pyloric stenosis is associated with what type of alkalosis

A

Results in hypokalemic and hypochloremic metabolic alkalosis (secondary to vomiting of gastric acid and subsequent volume contraction)

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12
Q

Annular pancreas

A

Ventral pancreatic bud abnormally encircles 2nd part of the duodenum. Forms a ring of pancreatic tissue that may cause duodena narrowing and nonbilious vomiting.

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13
Q

Pancreas divisum

A

Ventral and dorsal parts fail to fuse at 8 weeks. Common anomaly, mostly asymptomatic but may cause chronic abdominal pain and/or pancreatitis

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14
Q

Embryology of spleen

A

Arises in mesentery of stomach (hence is mesodermal) but has foregut supply (celiac trunk → splenic artery)

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15
Q

Retroperitoneal structures

A

Include GI structures that lack a mesentery and non-GI structures. Injuries to retroperitoneal structures can cause blood or gas accumulation in the retroperitoneal space.

  • Suprarenal (adrenal) glands
  • Aorta and IVC
  • Duodenum (2nd through 4th parts)
  • Pancreas (except tail)
  • Ureters
  • Colon (descending and ascending)
  • Kidneys
  • Esophagus (thoracic portion)
  • Rectum (partially)

“SAD PUCKER”

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16
Q

Superior mesenteric artery syndrome

A

Characterized by intermittent intestinal obstruction symptoms (primarily postprandial pain) when transverse (3rd) portion of duodenum is compressed between the SMA and aorta. Typically occurs in conditions associated with diminished mesenteric fat (eg low body weight/malnutrition)

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17
Q

Branches of celiac trunk

A

Common hepatic, splenic, and left gastric

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18
Q

Kupffer cells

A

Specialized macrophages that form the lining of sinusoids

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19
Q

Hepatic stellate (Ito) cells

A

Located in space of Disse and store vitamin A when quiescent and produce extracellular matrix when activated.

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20
Q

Zone I

A
  • Periportal zone
  • Affected 1st by viral hepatitis
  • Ingested toxins (eg cocaine)
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21
Q

Zone II

A
  • Intermediate zone

- Yellow fever

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22
Q

Zone III

A
  • Pericentral vein (centrilobular) zone
  • Affected 1st by ischemia
  • Contains cytochrome P450 system
  • Most sensitive to metabolic toxins
  • Site of alcoholic hepatitis
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23
Q

Painless jaundice

A

Usually caused by tumors that arise in the head of pancreas (usually ductal adenocarcinoma) that can cause obstruction of the common bile duct

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24
Q

Layers of spermatic cord and their derivatives

A
  • Internal spermatic fascia (transversalis fascia)
  • Cremasteric muscle and fascia (internal oblique)
  • External spermatic fascia (external oblique)

“ICE tie”

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25
Q

Carbohydrate absorption

A
  • Only monosaccharides (glucose, galactose, fructose) are absorbed by enterocytes
  • Glucose and galactose are taken up by SGLT1 (Na+ dependent)
  • Fructose is taken up by facilitated diffusion by GLUT-5
  • All are transported to blood by GLUT-2
  • D-xylose absorption test: distinguishes GI mucosal damage from other causes of malabsorption
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26
Q

Where is iron absorbed

A

Duodenum

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27
Q

Where is folate absorbed

A

Small bowel, therefore clinically relevant in patients with small bowel disease or after resection.

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28
Q

Where is B12 absorbed

A

Terminal ileum along with bile salts, requires intrinsic factor

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29
Q

Pleomorphic adenoma

A
  • Salivary gland tumor
  • Benign mixed tumor
  • Most common salivary gland tumor
  • Composed of chondromyxoid stroma and epithelium and recurs if incompletely excise or ruptured intraoperatively
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30
Q

Mucoepidermoid carcinoma

A
  • Salivary gland tumor
  • Most common malignant tumor
  • Has mucinous and squamous components
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31
Q

Warthin tumor

A
  • Salivary gland tumor
  • Papillary cystadenoma lymphomatosum
  • Benign cystic tumor with germinal centers
32
Q

Sclerodermal esophageal dysmotility

A

Esophageal smooth muscle atrophy → ↓ LES pressure and dysmotility → acid reflux and dysphagia → stricture, Barret esophagus, and aspiration. Part of CREST syndrome.

33
Q

Eosinophilic esophagitis

A

Infiltration of eosinophils in the esophagus often in atopic patients. Food allergens → dysphagia, food impaction. Esophageal rings and linear furrows often seen on endoscopy. Unresponsive to GERD therapy.

34
Q

How do burns cause acute gastritis

A

Burns (Curling ulcers) → hypovolemia → mucosal ischemia

“Burned by the Curling iron”

35
Q

How does brain injury cause acute gastritis

A

Brain injury (Cushing injury) → ↑ vagal stimulation → ↑ ACh → ↑ H+ production

“Always Cushion the brain”

36
Q

Mentrier disease

A

Gastric hyperplasia of the mucosa → hypertrophied rugae (looking like brain gyri), excess mucus production with resultant protein loss and parietal cell atrophy with ↓ acid production. PRECANCEROUS.

37
Q

Complication of ulcers

A

Hemorrhage, obstruction, perforation

HEMORRHAGE: gastric, duodenal (posterior > anterior); most common complication; ruptured gastric ulcer on the lesser curvature of the stomach → bleeding from the LEFT GASTRIC ARTERY; an ulcer on the posterior wall of the duodenum → bleeding from the GASTRODUODENAL ARTERY

OBSTRUCTION: pyloric channel, duodenal

PERFORATION: duodenal (anterior > posterior); may see free air under diaphragm with referred pain to the shoulder via phrenic nerve

38
Q

Pathological findings of celiac disease

A
  • Villous atrophy (blunting)
  • Crypt hyperplasia
  • Intraepithelial lyphocytosis
39
Q

Pathological findings of lactose intolerance

A

Normal appearing villi except with secondary to injury at tips of villi (eg viral enteritis)

40
Q

Location of celiac disease vs tropical sprue

A

CELIAC DISEASE: ↓ mucosal absorption primarily affects distal duodenum and/or proximal jejunum

TROPICAL SPRUE: ↓ mucosal absorption affecting duodenum and jejunum but can involve ileum with time (associated withe megaloblastic anemia due to folate deficiency and later B12 deficiency)

41
Q

Microscopic morphology of Crohn disease vs ulcerative colitis

A

CROHN DISEASE: noncaseating granulomas and lymphoid aggregates

ULCERATIVE COLITIS: crypt abscesses and ulcers, bleeding, no granulomas

42
Q

Cause of Zenker diverticulum

A

Esophageal dysmotility causes herniation of the mucosal tissue at Killian triangle between the thyropharyngeal and cricopharyngeal parts of the interior pharyngeal constrictor

43
Q

Meckels diverticulum is a persistence of what

A

Vitelline duct

44
Q

Malrotation

A

Anomaly of midgut rotation during fetal development → IMPROPER POSITIONING OF BOWEL, formation of fibrous bands (Ladd bands). Can lead to volvulus, duodenal obstruction.

45
Q

Volvulus is the twisting of a portion of bowel around its

A

Mesentery.

46
Q

Acute mesenteric ischemia

A

Critical blockage of intestinal blood flow (often embolic occlusion of SMA) → small bowel necrosis → abdominal pain out of proportion to physical findings. May see red “currant jelly” stools.

47
Q

Chronic mesenteric ischemia

A

“Intestinal angina”: atherosclerosis of celiac artery, SMA or IMA → intestinal hypoperfusion → postprandial epigastric pain → food aversion and weight loss

48
Q

Angiodysplasia

A

Tortuous dilation of vessels → hematochezia. Most often found in cecum, terminal ileum, ascending colon. More common in older patients. Confirmed by angiography.

49
Q

Ileus

A

Intestinal hypomotility without obstruction → constipation and ↓ flatus; distended/tympanic abdomen with ↓ bowel sounds. Associated with abdominal surgeries, opiates, hypokalemia, sepsis. Treatment: bowel rest, electrolyte correction, cholinergic drugs (stimulate motility)

50
Q

Hyperplastic colonic polyp

A

Non-neoplastic. Generally smaller and majority located in rectosigmoid area.

51
Q

Hamartomatous colonic polyp

A

Generally non-neoplastic; solitary lesions do not have a significant risk of malignant transformation. Growths of normal colonic tissue with distorted architecture. Associated with Peutz-Jeghers syndrome and juvenile polyposis.

52
Q

Adenomatous colonic polyp

A

Neoplastic, via chromosomal instability pathway with mutations in APC and KRAS. Tubular histology has less malignant potential than villous; tubulovillous has intermediate malignant potential. Usually asymptomatic, may present with occult bleeding.

53
Q

Serrated colonic polyp

A

Premalignant, via CpG hypermethylatin phenotype pathway with microsatellite and mutations in BRAF. “Saw tooth” pattern of cysts on biopsy. Up to 20% of cases sporadic CRC.

54
Q

Familial adenomatous polyposis

A
  • AD mutation of APC tumor suppressor gene on chromosome 5q
  • 2-hit hypothesis
  • Thousands of polyps arise staring after puberty
  • Pancolonic
  • Always involves the rectum
  • Prophylactic colectomy or else 100% progress to CRC
55
Q

Gardner syndrome

A

FAP + osseous and soft tissue tumors, congenital hypertrophy of retinal pigment epithelium, impacted/supernumerary teeth.

56
Q

Turcot syndrome

A

FAP + malignant CNS tumor.

57
Q

Juvenile polyposis syndrome

A

AD syndrome in children (

58
Q

Peutz-Jeghers syndrome

A

AD syndrome featuring numerous hamartomas throughout GI tract, along with hyperpigmented mouth, lips, hands, genitalia. Associated with ↑ risk of breast and GI cancers (eg colorectal, stomach, small bowel, pancretic)

59
Q

Non-alcoholic fatty liver disease

A
  • Metabolic syndrome (insulin resistance)
  • Obesity → fatty infiltration of hepatocytes → cellular “ballooning” and eventual necrosis
  • May cause cirrhosis and HCC
  • Independent of alcohol use
  • ALT > AST
60
Q

Hepatic encephalopathy

A
  • Cirrhosis → portosystemic shunts → ↓ NH3 metabolism → neuropsychiatric dysfunction
  • Spectrum from disorientation/asterixis (mild) to difficult arousal or coma (severe
  • Triggers include ↑ NH3 production and absorption (due to dietary protein, GI bleed, constipation, infection) or ↓ NH3 removal (due to renal failure, diuretics, bypassed hepatic blood flow post-TIPS)
  • TREATMENT: lactulose (↑ NH4+ generation) and rifamixin or neomycin (↓ NH4+ producing gut bacteria)
61
Q

Pathology of primary sclerosing cholangitis

A

Unknown cause of concentric “onion skin” bile duct fibrosis → alternating strictures and dilation with “beading” of intra and extra hepatic bile ducts on ERCP, magnetic resonance cholangiopancreatography.

62
Q

Pathology of primary biliary cirrhosis

A

Autoimmune reaction → lymphocytic infiltrate + granulomas → destruction of intralobular bile ducts

63
Q

Pathology of secondary biliary cirrhosis

A

Extrahepatic biliary obstruction → ↑ pressure in intrahepatic ducts → injury/fibrosis and bile stasis

64
Q

Cholesterol stones are associated with

A
  • Obestity
  • Crohn disease
  • Advanced age
  • Estrogen therapy
  • Multiparity
  • Rapid weight loss
  • Native American origin
65
Q

Pigment stones are associated with

A
  • Crohn disease
  • Chronic hemolysis
  • Alcoholic cirrhosis
  • Advanced age
  • Biliary infections
  • Total parenteral nutrition (TPN)
66
Q

Cholecystitis via primary infection occurs by which organism

A

CMV

67
Q

Causes of acute pancreatitis

A
  • Idiopathic
  • Gallstones
  • Ethanol
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune disease
  • Scorpion sting
  • Hypercalcemia/Hypertriglyceridemia

“I GET SMASHED”

68
Q

Complications of acute pancreatitis

A
  • Pseudocyst (lined by granulation tissue, not epithelium)
  • Necrosis
  • Hemorrhage
  • Infection
  • Organ failure (ARDS, shock, renal failure)
  • Hypocalcemia (precipitation of Ca2+ soaps)
69
Q

What is Courvoisier’s sign

A

Obstructive jaundice with palpable, nontender gallbladder. Associated with pancreatic adenocarcinoma.

70
Q

Pancreatic adenocarcinoma is associated with what tumor marker

A

CA 19-9 but also CEA (less specific)

71
Q

Conditions developed above and below pectinate/dentate line

A

Above pectinate line → internal hemorrhoids, adenocarcinoma

Below pectinate line → external hemorrhoids, anal fissures, squamous cell carcinoma

72
Q

Compare the arterial supply above and below the pectinate line

A

Above the pectinate line → superior rectal artery (branch of IMA)

Below the pectinate line → inferior rectal artery (branch of inferior pudendal artery)

73
Q

Compare the venous supply above and below the pectinate line

A

Above the pectinate line: superior rectal vein → inferior mesenteric vein → portal system

Below the pectinate line: inferior rectal vein → internal pudendal vein → inferior iliac vein → common iliac vein → IVC

74
Q

Compare lymphatic drainage above and below the pectinate line

A

Above the pectinate line → internal iliac lymph nodes

Below the pectinate line → superficial inguinal nodes

75
Q

Internal hemorrhoids

A

Receive visceral innervation and are therefore not painful

76
Q

External hemorrhoids

A

Receive somatic innervation (inferior rectal branch of pudendal nerve) and are therefore painful if thrombosed

77
Q

Anal fissure

A
  • Tear in the anal mucosa below the Pectinate line
  • Pain while Pooping
  • Blood on the toilet Paper
  • Located Posteriorly because this area is Poorly Perfused
  • Associated with low fiber diets and constipation

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