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GI Flashcards

1
Q

Anterior 2/3 of tongue

a. Origin
b. Taste
c. Sensation
d. Motor

A

a. 1st arch
b. Facial nerve (7)
c. CN V3
d. CN XII (12)

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2
Q

Posterior 1/3

a. origin
b. taste
c. sensation
d. motor

A

a. 3rd and 4th arch
b. Glossopharyngeal (9)
c. CN 9
d. CN X11 (12)

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3
Q

Causes of Glossitis

A

B12, Niacin, Riboflavin deficiency

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4
Q

Oral hairy leukoplakia

A

white patch on tongue caused by EBV (in immunocompromised patients)

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5
Q

Oral thrush

A

White spot on buccal mucosa/tongue

Caused by candida albicans

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6
Q

Apthous ulcers causes

A

Canker sore

Citrus fruits, B12 deficiency

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7
Q

Parotid secretions

A

Serous secretions

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8
Q

Submandibular gland

A

Serous AND mucinous secretions

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9
Q

Sublingual gland

A

Mucinous secretions

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10
Q

Secretions in sympathetic vs. parasympathetic

A

Sympathetic - very thick secretion by superior cervical ganglion
Parasympathetic - serous secretion by CN 5 and 7

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11
Q

Xerostomia

A

Sjogrens
Antihistamines
Anticholinergic

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12
Q

Sialolithiasis

A

Stone in salivary gland duct that prevents release of saliva

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13
Q

Most common place of salivary gland

A

parotid

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14
Q

Most common tumor of salivary gland

A

Pleomorphic adenoma

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15
Q

2nd most common benign tumor of salivary gland

A

Warthin tumor

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16
Q

Most common malignant salivary tumor

A

Mucoepidermoid tumor

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17
Q

Sublingual gland - benign vs. malignant tumor

A

> 70% change it is malignant

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18
Q

a. foregut
b. midgut
c. hindgut

A

a. pharynx to duodenum (Celiac artery)
b. duodenum to proximal 2/3 of transverse colon (SMA)
c. distal 1/3 transverse colon to anal canal above pectinate line (IMA)

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19
Q

Developmental defects of anterior abdominal wall due to failure of:

a. rostral fold closure
b. lateral fold closure
c. caudal fold closure

A

a. sternal defecs
b. omphalocele, gastroschisis
c. bladder exstrophy

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20
Q

Extrusion of abdominal contents through abdominal folds, NOT covered by peritoneum

A

Gastroschisis

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21
Q

Persistence of herniation of abdominal contents into umbilical cord, SEALED by peritoneum

A

Omphalocele

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22
Q

Cause of duodenal atresia

A

Failure to recanalize (trisomy 21)

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23
Q

Cause of jejunal, ileal, colonic atresia

A

Due to vascular accident

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24
Q

Drooling, choking, vomiting with first feeding

A

Esophageal atresia with distal tracheoesophageal fistula

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25
Q

Gasless abdomen on CXR

A

Pure esophageal atresia

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26
Q

Palpable olive mass in epigastric region and NONbilious projectile vomiting in 2-6 week old infant. Cause? Result?

A

Pyloric stenosis from hypertrophy of pylorus

Results in hypokalemic, hypochloremic metabolic alkalosis

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27
Q

What tissues are they derived from?

a. Pancreas
b. Spleen

A

a. Endoderm (from hepatic diverticulum)

b. Mesoderm (still supplied by foregut)

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28
Q

a. Cause of annular pancreas

b. Cause of pancreas divusm

A

a. Abnormal migration; ventral pancreatic bud encircles 2nd part of duodenum –> bilious vomiting
b. Ventral and dorsal pancreatic parts fail to fuse; mostly asymptomatic –> may cause pancreatitis, abdominal pain

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29
Q

Retroperitoneal structures

A 
Suprarenal glands (adrenals)
Aorta and IVC
Duodenum (2nd through 4th parts)
Pancreas (except tail)
Ureters
Colon (ascending, descending)
Kidneys
Esophagus (thoracic portion)
Rectum
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30
Q

Contents of Hepatoduodenal ligament

A

Portal vein
Proper Hepatic artery
Common bile duct

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31
Q

Falciform ligament connects:

A

liver to anterior abdominal wall

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32
Q

Gastrohepatic ligament connects and contains what?

A

Connects liver to lesser curvature of stomach; contains gastric arteries

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33
Q

Layers of gut wall (inside to outside)

A

Mucosa - epithelium, lamina propria, muscularis mucosa
Submucosa - Submucosal nerve plexus (Meissner); secrets fluid
Muscularis externa - includes Myenteric nerve plexus (Auerbach), motility
Serosa - (when intraperitoneal), Adventitia (when retroperitoneal)

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34
Q

Erosions affect which layers of gut wall?

Ulcers affect which layers of gut wall?

A

Erosions are MUCOSA ONLY

Ulcers extend into submucosa, inner or outer muscular layer

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35
Q

Digestive tract histology

a. Esophagus
b. Stomach
c. Duodenum
d. Jejunum
e. Ileum
f. Colon

A

a. Nonkeratinized stratified squamous epithelium
b. Gastric glands
c. Villi and microvilli increase absorptive surface; brunner glands (secrete bicarbonate) and crypts of Lieberkuhn
d. Plicae circulares and crypts of Lieberkuhn
e. Peyer patches, plicae circulares, crypsts of Lieberkuhn
f. Colon has crypts of Liberkuhn but no villi; abundant goblet cells

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36
Q

Branches of celiac trunk

A

Common hepatic artery
Splenic artery
Left gastric artery

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37
Q

Branches of common hepatic artery

A

Proper hepatic artery
Right gastric artery
Gastroduodenal artery

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38
Q

Branches of gastroduodenal artery

A

Anterior superior pancreaticoduodenal artery

Right gastro-omental (epiploic) artery

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39
Q

Anastomoses of celiac trunk

A

Right gastro-omental and left gastro-omental (epiploic)

Left and right gastrics

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40
Q

Portosystemic anastomoses (sign and vessels involved)

a. Esophagus
b. Umbilicus
c. Rectum

A

a. Esophageal varices; left gastric –> esophageal
b. Caput medusae; paraumbilical –> small epigastric veins of anterior abdominal wall
c. Anorectal varices; superior rectal –> middle and inferior rectal

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41
Q

What is Pectinate line?
Pathology above pectinate line?
Pathology below pectinate line?

A
  • Where endoderm (hindgut) meets ectoderm
  • Above the pectinate line –> internal hemorrhoids (NOT PAINFUL, visceral innervation), adenocarcinoma
  • Below pectinate line –> external hemorrhoids (PAINDUL, pudendal nerve innervation), squamous cell carcinoma
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42
Q

Arterial supply and venous drainage above pectinate line

Lymphatic drainage

A
  • arterial supply - Superior rectal artery from IMA
  • venous drainage - superior rectal vein –> inferior mesenteric vein –> portal system
  • lymphatic drainage - internal iliac lymph nodes
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43
Q

Arterial supply, venous drainage and lymphatic drainage below pectinate line

A
  • arterial supply: inferior rectal artery (branch of internal pudendal artery)
  • venous drainage: inferior rectal vein –> internal iliac vein –> common iliac vein –> IVC
  • lymphatic drainage: superficial inguinal nodes
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44
Q

Zones of liver and what they are susceptible to

A
  • Zone 1: periportal zone; affected first by viral hepatitis; ingested toxins
  • Zone 2: intermediate; yellow fever
  • Zone 3: pericentral vein zone; affected 1st by ischemia, contains p450 system, most sensitive to metabolic toxins, site of alcoholic hepatitis
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45
Q

a. Sliding hiatal hernia

b. Paraesophageal hernia

A

a. most common, gastroesophageal junction is displaced upward (hourglass stomach)
b. gastroesophageal junction is normal, funds protrudes into the thorax

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46
Q

Common location of diaphragmatic hernia

A

Left side due to relative protection of right hemidiaphragm by liver

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47
Q

Indirect vs. Direct inguinal hernia

a. site of protrusion
b. lower border
c. medial border
d. lateral border

A

a. indirect = deep inguinal ring, direct = Hesselbach triangle
b. BOTH = inguinal ligament
c. indirect = inferior epigastric vessels, direct = rectus abdominis muscle
d. indirect = XXX, direct = inferior epigastric vessels

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48
Q

Femoral hernia

A

Protrudes below inguinal ligament through femoral canal below and lateral to pubic tubercle; more common in females

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49
Q

Which kind of hernia most commonly becomes incarcerated and descends into scrotum?

A

Indirect inguinal hernia

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50
Q

What do these cells secrete?

a. G cells
b. D cells
c. I cells
d. S cells
e. K cells

A

a. Gastrin
b. Somatostatin
c. CCK
d. Secretin
e. Glucose dependent insulinotropic peptide

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51
Q

a. Regulation of Gastrin

b. Actions of Gastrin

A

a. Increased by stomach distension/alkalinization/amino acids/vagal stimulation/peptides and decreased by pH

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52
Q

When would gastrin levels be increased?

A

In ZE, in chronic atrophic gastritis (H. pylori) and in chronic PPI use

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53
Q

a. Regulation of Somatostatin

b. Actions of Somatostatin

A

a. Increased by acid, decreased by vagal stimulation
b. It decreases gastric acid and pepsinogen secretion, decreases pancreatic and small intestine fluid secretion, decreases gallbladder contraction, decreases insulin and glucagon release and decreases splanchnic blood flow

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54
Q

Uses of Somatostatin analog (Octreotide)

A

Variceal bleeding
Acromegaly
Insulinoma
Carcinoid syndrome

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55
Q

a. Regulation of CCK

b. Actions of CCK

A

a. Increased by fatty acids and amino acids
b. Increases pancreatic secretion and gallbladder contraction, decreases gastric emptying and causes relaxation of Sphincter of Oddi

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56
Q

a. Regulation of Secretin

b. Actions of Secretin

A

a. Increased by acid and fatty acids in duodenum
b. Causes increased pancreatic bicarbonate secretion and increased bile secretion, causes decreased gastric acid secretion

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57
Q

a. Regulation of GIP

b. Actions of GIP

A

a. Increased by fatty acids, amino acids and ORAL glucose

b. Exocrine: decreased gastric H+ secretion, Endocrine: Increased insulin release

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58
Q

a. Regulation of Motilin

b. Actions of Motilin

A

a. Increased in fasting state
b. Produces migratory motor complexes (motilin receptor agonists are used to stimulate intestinal peristalsis - Erythromycin)

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59
Q

a. Regulation of VIP (vasoactive intestinal peptide)

b. Actions of VIP

A

a. Increased by distension and vagal stimulation, Decreased by adrenergic input
b. Increases intestinal water and electrolyte secretion, increases relaxation of intestinal smooth muscle and sphincters

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60
Q

VIPoma

A

Pancreatic tumor that secretes VIP

Causes copious watery diarrhea, hypokalemia and achlorhydria

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61
Q

Source and action of:

a. Intrinsic factor
b. Gastric acid
c. Pepsin
d. HCO3

A

a. Parietal cells –> binds Vitamin B12 for uptake in ileum
b. Parietal cells –> decrease stomach pH
c. Chief cells –> protein digestion
d. Mucosal cells and Brunner glands –> neutralizes acid

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62
Q

Regulation of:

a. Intrinsic factor
b. Gastric acid
c. Pepsin
d. HCO3

A

a. —-
b. Increased by histamine, Ach and gastrin; decreased by Somatostatin, GIP, prostaglandin and secretin
c. Increased by vagal stimulation and local acid
d. Increased by pancreatic and biliary secretion with secretin

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63
Q

How does Gastrin increase acid production?

A

It causes increased acid secretion primarily through its effects on ECL cells leading to histamine release (rather than direct effect on parietal cells)

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64
Q

Intracellular signaling of: (all on parietal cells)

a. Ach acting on M3 receptor (vagus)
b. Gastrin acting on CCK receptor
c. Histamine acting on H2 receptor
d. Prostaglandins on parietal cell
e. Somatostatin on parietal cell

A

a. Gq –> IP3/Calcium –> activates H+/K+ ATPase (proton pump)
b. Gq –> IP3/Calcium –> activates proton pump (more importantly it activates ECL cells)
c. Gs –> increases cAMP –> activates proton pump
d. Gi –> decreases cAMP –> inhibits proton pump
e. Gi –> decreases cAMP –> inhibits proton pump

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65
Q

Carbohydrate absorption

A

ONLY monosaccharides are absorbed by enterocytes
Glucose and galactose taken up by SGLT1 (Na dependent)
Fructose taken up by facilitated diffusion by GLUT-5
All transported to blood but GLUT2 transporter

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66
Q

What is the D-xylose absorption test?

A

It distinguishes GI mucosal damage from other causes of malabsorption

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67
Q

Where are they absorbed?

a. Iron
b. Folate
c. Vitamin B12

A

a. As Fe 2+ in duodenum
b. In small bowel
c. In terminal ileum (requires intrinsic factor)

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68
Q

What are Peyer patches?

A

Unencapsulated lymphoid tissue found in lamina propria and submucosa of ileum; contain specialized M cells that sample and present antigens to immune cells

69
Q

Rate limiting step of bile synthesis

A

Cholesterol 7 alpha hydroxylase

70
Q

Excretion of bilirubin

A
  1. Conjugated bilirubin made into Urobilinogen by gut bacteria
  2. Urobilinogen excreted in feces as Stercobilin or enters Enterohepatic circulation and goes to liver OR kidney
  3. Urobilinogen that goes to Kidney is excreted in urine as Urobilin (yellow) 10%
  4. Urobilinogen that goes to Liver (90%) is used again
71
Q

a. Cause of Achalasia
b. Presentation
c. Imaging findings
d. Complications/Associations

A

a. LES fails to relax due to loss of myenteric Auerbach plexus –> high LES resting pressure and uncoordinated peristalsis (Secondary achalasia could be due to Chagas disease or malignancy)
b. Progressive dysphagia to solids AND liquids
c. Barium swallow shows bird’s beak (dilated esophagus with area of distal stenosis)
d. Increased risk of esophageal squamous cell carcinoma

72
Q

Boerhaave syndrome

A

Rupture of esophagus –> Transmural, usually distal esophageal with pneumomediastinum due to violent retching
Surgical EMERGENCY

73
Q

Infiltration of eosinophils in the esophagus in atopic patients

A

Eosinophilic esophagitis; causes dysphagia, heartburn, strictures

74
Q

Lye ingestion and acid reflux association

A

Esophageal stricture

75
Q

Associated with reflux, infection in immunocompromised or chemical ingestion

a. white pseudomembrane, hyphae
b. punched-out ulcers
c. Linear ulcers with clear perinuclear halo in cells

A

Esophagitis

a. Candida
b. HSV-1
c. CMV

76
Q

Dysphagia, Iron deficiency anemia, Esophageal webs, Glossitis –> increases risk of what?

A

Plummer Vinson syndrome

a. Increases risk of esophageal squamous cell carcinoma

77
Q

Esophagus association with CREST syndrome

A

Esophageal dysmotility from smooth muscle atrophy –> decreased LES pressure –> acid reflux and dysphagia

78
Q

Metaplasia seen in Barrett esophagus

Risk of what kind of cancer?

A

Replacement of nonkeratinized stratified squamous epithelium with intestinal epithelium (non-ciliated columnar with goblet cells)
Risk of esophageal adenocarcinoma

79
Q

Risk factors for

a. Esophageal Adenocarcinoma
b. Esophageal Squamous cell carcinoma
c. Both

A

a. Barrett esophagus, Obesity, GERD, Caucasian
b. Alcohol, Diverticula, Esophageal web, Hot liquids, African americans
c. Cigarettes

80
Q

Causes of acute gastritis

A
  1. NSAIDs –> decreased PGE2 –> decreased gastric mucosa protection
  2. Burns (Curling ulcer) –> decreased plasma volume –> sloughing of gastric mucosa
  3. Brain injury (Cushing ulcer) –> increased vagal stimulation –> increased Ach –> increased H+ production
81
Q

Chronic gastritis causes

A
  1. Type A (fundus/body) –> Autoimmune destruction with auto Abs to parietal cells –> pernicious anemia, Achlorhydria
  2. Type B (antrum) –> Most common type; caused by H. pylori infection
82
Q

Type B chronic gastritis increases risk of what?

A

MALT lymphoma

83
Q

Gastric hyperplasia of mucosa?

What does it cause?

A 
Menetrier disease (protein losing gastroenteropathy)
Hypertrophied rugae, excess mucus production with resultant loss of protein and parietal cell atrophy with decreased acid production
84
Q

Acanthosis nigricans, weight loss, early satiety

A

Gastric adenocarcinoma

85
Q

Types of gastric adenocarcinoma

A
  1. Intestinal - associated with H. pylori, dietary nitrosamines, tobacco, achlorhydria, chronic gastritis
    2 Diffuse - NOT associated with H. pylori; Signet ring cells seen; stomach all is grossly thickened and leathery (linitis plastica)
86
Q

Linitis plastica

A

Seen in diffuse gastric adenocarcinoma

Stomach wall looks leathery and thickened

87
Q

Signet ring cells

A

Munin-Filled cells with peripheral nuclei - seen in diffuse gastric adenocarcinoma

88
Q

Involvement of left supraclavicular node by metastasis from stomach

A

Virchow node

89
Q

Bilateral gastric adenocarcinoma metastases to ovaries

A

Krukenberg tumor

90
Q

Subcutaneous periumbilical metastasis of gastric adenocarcinoma

A

Sister Mary Joseph nodule

91
Q

Compare:

a. Gastric ulcer
b. Peptic ulcer

A

a. Pain greater with meals (weight loss), H. pylori in 70%, from decreased mucosal protection against gastric acid, also caused by NSAIDs, increased risk of carcinoma
b. Pain decreases with meals (weight gain), H. pylori in 100%, from decreased mucosal production or increased gastric acid secretion, associated with ZE, generally benign

92
Q

H. pylori treatment

A

PPI + Clarithromycin + Amoxicillin

PPI + Bismuth + Metronidazole + Tetracycline

93
Q

Complications of ulcers

A
  1. Hemorrhage - generally posterior;

2. Perforation - generally anterior; may see free air under diaphragm with referred pain to shoulder via phrenic nerve

94
Q

Blunting of villi, Lymphocytes in lamina propria

A

Celiac disease

95
Q

Risk of malignancy in Celiac disease?

A

Increased risk of T cell lymphoma

96
Q

Histology in Lactase deficiency

A

Normal appearing villi

97
Q

Cause of self limiting lactase deficiency

A

Viral enteritis (lactase is at tips of intestinal villi)

98
Q

Causes of pancreatic insufficiency

Results of pancreatic insufficiency

A

CF, Obstructing cancer, Chronic pancreatitis

Malabsorption of fat (steatorrhea) and fat soluble vitamins (A, D, E, K)

99
Q

CF effects on pancreas

A

Decreases secretion of fluid into pancreatic ducts in CF –> enzymes accumulate in ducts and can digest pancreas –> cause pancreatic insufficiency

100
Q

Difference between tropical sprue and Celiac disease?

A

Tropical sprue has similar findings to Celiac but it RESPONDS to antibiotics; seen in residents or visitors of Tropics

101
Q

PAS + foamy macrophages in lamina propria

Symptoms?

A 
Whipple disease (Tropheryma whipplei, gram positive)
Cardiac symptoms, Arthralgias, Neurologic symptoms, Hyperpigmentation, Weight loss, Lymphadenopathy
102
Q

Crohn’s

a. Location
b. Gross morphology
c. Histology
d. Complications
e. Intestinal manifestation
f. Extraintestinal manifestatin
g. Treatment

A

a. Any portion of GI tract, usually the terminal ileum and colon; skip lesions and rectal sparing
b. Transmural inflammation –> fistulas; cobblestone mucosa, creeping fat, bowel wall thickening, linear ulcers, fissures (String sign on barium swallow)
c. Non-caseating granulomas and lymphoid aggregates (TH1)
d. Strictures (obstruction), fistulas, perianal disease, malabsorption, nutritional depletion, colorectal cancer, gallstones
e. Diarrhea (may or may not be bloody)
f. Migratory polyarthritis, erythema nodosum, ankylosing spondylitis, pyoderma gangrenosum, apthous ulcers, uveitis, kidney stones
g. Corticosteroids, Azathioprine, ABx, Infliximab, Adalimumab

103
Q

Ulcerative colitis

a. Location
b. Gross morphology
c. Histology
d. Complications
e. Intestinal manifestation
f. Extra-intestinal manifestation
g. Treatment

A

a. Colon inflammation, continuous, always with rectal involvement
b. Mucosal and submucosal inflammation ONLY, friable musocal pseudopolyps; loss of haustra (lead pipe appearance)
c. Crypt abscesses and ulcers; bleeding, no granulomas (TH2)
d. Malnutrition, sclerosing cholangitis, toxic megacolon, colorectal carcinoma
e. Bloody diarrhea
f. Pyoderma gangrenosum, erythema nodosum, sclerosing cholangitis, ankylosing spondylitis, aphthous ulcers, uveitis
g. 5-aminosalicylic preparations, 6 mercaptopurine, Infliximab, Colectomy

104
Q

Ulcerative colitis (ULCCCERS)

A 
Ulcers
Large intestine
Continous, Colorectal carcinoma, Crypt abscesses
Extends proximally
Red diarrhea
Sclerosing cholangitis
105
Q

Irritable bowel syndrome

A

Recurrent abdominal pain associated with at least 2 of the following

  1. pain improves with defecation
  2. change in stool frequency
  3. change in appearance of stool
106
Q

True vs. False Diverticula

A 
True = all 3 gut layers out pouch
False = only mucosa and submucosa out pouch (occur especially where vasa recta perforate muscular externa)
107
Q

Most common location of diverticula

A

Sigmoid colon

108
Q

Diverticulosis

  • Cause
  • Symptoms
  • Associations
A

Many false diverticula of colon (sigmoid usually)

  • Increased intraluminal pressure and focal weakness in colonic wall
  • Vague discomfort, Hematochezia
  • Low fiber diets, Diverticulitis, fistulas
109
Q

Diverticulitis

-Complications

A

Inflammation of diverticular causing LLQ pain, fever, leukocytosis
-May perforate –> peritonitis, abscess formation, bowel stenosis or cause colovesical fistula

110
Q

Caused by CF and Hirschsprung

A

Meconium ileus

111
Q

Common in post op

A

Intestinal ileus

112
Q

Currant jelly stools

A

Intussuception

113
Q

Virus associated with intussuception

A

Adenovirus

114
Q

Cause of Hirschsprung disease

A

Failure of neural crest cell migration; associated with mutations in RET gene

115
Q

Pain out of proportion to physical findings

A

Acute mesenteric ischemia, ischemic colitis

116
Q

Tortuous dilation of vessels causing hematochezia

A

Angiodysplasia; seen more in elderly; most often in cecum, terminal ileum and ascending colon

117
Q

Double bubble on X ray

A

Duodenal atresia (proximal stomach distension)

118
Q

Intestinal hypomotility WITHOUT obstruction

Associations

A

Ileus

Associated with abdominal surgeries, opiates, hypokalemia, sepsis

119
Q

Necrotizing enterocolitis

A

Seen in premature, formula-fed infants with immature immune system –> causes necrosis of intestinal mucosa with possible perforation

120
Q

Characteristics of polyps:

a. Hyperplastic
b. Hamartomatous
c. Adenomatous
d. Serrated

A

a. NON neoplastic; smaller and majority in rectosigmoid
b. NON neoplastic; solitary lesions do not have significant risk of malignant transformation; NORMAL colonic tissue with distorted architecture (Peutz Jeghers and juvenile polyposis)
c. Neoplastic; mutations in APC or KRAS via chromosomal instability pathway - Tubular histology has LESS malignant potential than villous
d. Premalignant; via CpG hypermethylation phenotype pathway with micro satellite instability and mutations in BRAF (Saw tooth pattern)

121
Q

a. AD mutation of APC tumor suppressor gene on chromosome 5q
b. FAP + malignant CNS tumor
c. FAP + osseous and soft tissue tumor, congenital hypertrophy of retinal pigment epithelium, impacted teeth, lipomas
d. AD syndrome featuring hamartomas throughout GI tract, hyper pigmented mouth/lips/hands/genitalia; associated with increased risk of small bowel, colorectal, stomach, breast and pancreatic cancers
e. AD syndrome in children featuring numerous hamartomatous polyps in the colon, stomach, small bowel; associated with increased risk of CRC

A

a. Familial adenomatous polyposis
b. Turcot syndrome
c. Gardner syndrome
d. Peutz Jeghers syndrome
e. Juvenile polyposis syndrome

122
Q

AD mutation in DNA mismatch repair genes with subsequent micro satellite instability –> 80% progress to CRC. Proximal colon always involved. Associated with enodmetrial, ovarian and skin cancers

A

Lynch syndrome

123
Q

Risk factors for colorectal cancer

A

Adenomatous and serrated polyps, familial cancer syndromes, IBD, tobacco use, diet of processes meat with low fiber

124
Q

Presentation of colorectal cancer (depending on location)

A

Ascending: exophytic mass, iron deficiency anemia, weight loss
Descending: infiltrating mass, partial obstruction, colicky pain, hematochezia

125
Q

Bacteria associated with colorectal cancer

A

Streptococcus bovis (Group D Strep - growth in bile, NOT in NaCl)

126
Q

Apple core lesion on barium enema x-ray

A

Colorectal cancer

127
Q

CEA tumor marker

A

Good for monitoring recurrence of colorectal cancer

NOT good for screening

128
Q

2 molecular pathways that lead to colorectal cancer

A
  1. Microsatellite instability pathway (15%): DNA mismatch repair gene mutations –> Lynch syndrome
  2. APC/B-catenin (chromosomal instability) (85%) –> sporadic cancer
129
Q

Relationship of aspirin and colon adenocarcinoma

A

Increased COX2 is linked to colon adenocarcinoma

Aspirin may decreased adematous polyp formation

130
Q

Histology of liver cirrhosis

A

Diffuse bridging fibrosis and nodular regeneration via stellate cells

131
Q

AST > ALT

A

Alcoholic hepatitis

132
Q

ALT > AST

A

Viral hepatitis

133
Q

gamma glutamyl transpeptidase

A

Increased in various liver and biliary diseases (NOT elevated in bone disease like ALP)

134
Q

Most specific marker for acute pancreatitis

A

Lipase

135
Q

Findings in Reye syndrome

A 
Mitochondrial abnormalities
Fatty liver (microvesciular fatty change)
Hypoglycemia
Vomiting
Hepatomegaly
Coma
136
Q

Associations with Reye syndrome

A

Viral infection that was treated with Aspirin- especially VZV and influenza B

137
Q

Mechanism of Reye syndrome

A

Aspirin metabolites decrease Beta oxidation by reversible inhibition of mitochondrial enzymes

138
Q

Macrovesicular fatty liver change

A 
Hepatic steatosis
(Microvesicular = Reye syndrome)
139
Q

Swollen and necrotic hepatocytes with neutrophilic infiltration

A

Alcoholic hepatitis

140
Q

Intracytoplasmic eosinophilic inclusions of damaged keratin filaments

A

Mallory bodies - seen in alcoholic hepatitis

141
Q

Micro nodular irregularly shrunken liver with hobnail appearance; sclerosis around central vein (zone III)

A

Alcoholic cirrhosis

142
Q

Fatty infiltration of hepatocytes –> cellular ballooning and eventual necrosis

A

Non-alcoholic fatty liver disease

143
Q

Cause of hepatic encephalopathy

A

Cirrhosis –> portosystemic shunts –> decreased NH3 metabolism –> neuropsych dysfunction

144
Q

Triggers of hepatic encephalopathy

A
  1. Increased NH3 production and absorption (dietary protein, GI bleed, constipation, infection)
  2. Decreased NH3 removal (renal failure, diuretics)
145
Q

Balloon degeneration (hepatocyte swelling), mononuclear cell infiltration, councilman bodies

A

Viral hepatitis

146
Q

Aflatoxin from Aspergillus

A

Hepatocellular carcinoma

147
Q

Tumor marker of Hepatocellular carcinoma

A

Increased alpha fetoprotein

148
Q

Benign liver tumor (collection of dilated blood vessels) that occurs at age 30-50; biopsy is C/I because of risk of hemorrhage

A

Cavernous hemangioma

149
Q

Rare, benign liver tumor related to oral contraceptive or anabolic steroid use

A

Hepatic adenoma (resect if > 5 cm)

150
Q

Malignant liver tumor of endothelial origin

Associations

A

Angiosarcoma

Associated with arsenic, vinyl chloride

151
Q

Nutmeg liver with absence of JVD

A

Budd Chiari syndrome (thrombosis or compression of hepatic veins)

152
Q

Budd Chiari associations

A

Hyper coagulable states
Polycythemia vera
Postpartum state
HCC

153
Q

PAS+ globules in liver, Autosomal Recessive inheritance

A

Alpha 1 antitrypsin deficiency

154
Q

Grossly black liver

Conjugated hyperbilirubinemia

A

Dubin Johnson syndrome - caused by defective liver excretion

155
Q

Wilson disease characteristics

A 
Decreased Ceruloplasmin
Cirrhosis
Corneal deposits (Kayser Fleischer rings)
Copper accumulation
Carcinoma
Hemolytic anemia
Basal ganglia degeneration (Parkinson symptoms)
Asterixis
Dementia, Dyskinesia, Dysarthria
156
Q

Wilson disease defect

A

Autosomal recessive (chr 13); defect in hepatocyte copper transporting ATPase (ATP7B gene)

157
Q

Defect causing primary Hematochromatosis

A

C282Y or H63D mutation on HFE gene

Associated with HLA-A3

158
Q

Biliary tract disease –> lymphocytic infiltrate + granulomas –> destruction of intralobular bile ducts

A

Primary Biliary Cirrhosis

159
Q

Features of Primary Biliary Cirrhosis

A

Anti-mitochondrial antibody

Other autoimmune conditions (CREST, Sjogren, RA, Celiac)

160
Q

Onion skin bile duct fibrosis –> beading of intra and extra hepatic bile ducts on ERCP

A

Primary sclerosing cholangitis

161
Q

Features of Primary Sclerosing Cholangitis

A

Hypergammaglobulinemia (IgM)
p-ANCA
Ulcerative colitis

162
Q

Associations of cholesterol stones

A

Obesity, Crohn disease, advanced age, clofibrate, estrogen therapy, multiparty, rapid weight loss, Native American origin

163
Q

Imaging of:

a. Cholesterol stones
b. Pigment stones

A

a. Radiolucent with 10-20% opaque because of calcifications

b. Black = adiopaque, Calcium bilirubinate, hemolysis; Brown = radiolucent, infection

164
Q

Associations of pigment stones

A

Patients with chronic hemolysis, alcoholic cirrhosis, advanced age, biliary infections, total parenteral nutrition

165
Q

Triad of Cholangitis

A

Fever
RUQ pain
Jaundice
(Pentad = plus hypotension and altered mental status)

166
Q

Porcelain gallbladder

A

Calcified gallbladder due to chronic cholecystitis; usually found incidentally on imaging

167
Q

CA 19-9 Tumor marker

A

Pancreatic adenocarcinoma

168
Q

Risk factors for pancreatic adenocarcinoma

A 
Tobacco use
Chronic pancreatitis
Diabetes
Age > 50
Jewish and African-Americal males
169
Q

Trousseau syndrome

A 
Migratory thrombophlebitis (redness and tenderness on palpation of extremities)
Seen with pancreatic adenocarcinoma

Step 1 AB (29 decks)

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