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USMLE Step 1 > Gastrointestinal - First Aid > Flashcards

Gastrointestinal - First Aid Flashcards

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USMLE® Step 1 flashcards
1
Q

Normal Gastrointestinal Embryology:

Foregut

A

esophagus to upper duodenum

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2
Q

Normal Gastrointestinal Embryology:

Midgut

A

lower duodenum to proximal 2/3 of transverse colon

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3
Q

Normal Gastrointestinal Embryology:

Hindgut

A

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

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4
Q

Normal Gastrointestinal Embryology:

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° counterclockwise
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5
Q

Ventral wall defects are developmental defects due to failure of _____.

A
  • rostral fold closure
    • sternal defects (ectopia cordis)
  • lateral fold closure
    • omphalocele
    • gastroschisis
  • caudal fold closure
    • bladder exstrophy
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6
Q

Ventral Wall Defects:

  • extrusion of abdominal contents through abdominal folds (typically right of umbilicus)
  • not covered by peritoneum or amnion
  • not associated with chromosome abnormalities
A

Gastroschisis

The abdominal contents are coming out of the G.

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7
Q

Ventral Wall Defects:

  • failure of lateral walls to migrate at umbilical ring → persistent midline herniation of abdominal contents into umbilical cord
  • surrounded by peritoneum (light gray shiny sac)
  • associated with congenital anomalies (eg.. trisomies 13 and 18, Beckwith-Wiedemann syndrome) and other structural abnormalities (eg. cardiac, GU, neural tube)
A

Omphalocele

The abdominal contents are sealed in the O.

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8
Q

_____ occurs with the failure of umbilical ring to close after physiologic herniation of the intestines. Small defects usually close spontaneously.

A

Congenital Umbilical Hernia

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9
Q

Tracheoesophageal Anomalies

A
  • Esophageal atresia (EA) with distal tracheoesophageal fistula (TEF) is the most common (85%) and often presents as polyhydramnios in utero (due to inability of fetus to swallow amniotic fluid).
  • Neonates drool, choke, and vomit with first feeding.
  • TEFs allow air to enter stomach (visible on CXR).
  • Cyanosis is 2° to laryngospasm (to avoid reflux-related aspiration).
  • Clinical Test: failure to pass nasogastric tube into stomach
  • In H-type, the fistula resembles the letter H.
  • In pure EA, CXR shows gasless abdomen.
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10
Q

_____ presents with bilious vomiting and abdominal distension within first 1–2 days of life.

A

Intestinal Atresia

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11
Q

Intestinal Atresia:

  • failure to recanalize
  • associated with “double bubble” (dilated stomach, proximal duodenum) on x-ray
  • associated with Down syndrome
A

Duodenal Atresia

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12
Q

Intestinal Atresia:

disruption of mesenteric vessels → ischemic necrosis → segmental resorption (bowel discontinuity or “apple peel”)

A

Jejunal and Ileal Atresia

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13
Q

GI Pathologies:

  • most common cause of gastric outlet obstruction in infants (1:600)
  • palpable olive-shaped mass in the epigastric region, visible peristaltic waves, and nonbilious projectile vomiting at ∼ 2–6 weeks old
  • more common in firstborn males; associated with exposure to macrolides
  • results in hypokalemic hypochloremic metabolic alkalosis (2° to vomiting of gastric acid and subsequent volume contraction)
  • ultrasound shows thickened and lengthened pylorus
  • treatment is surgical incision (pyloromyotomy)
A

Hypertrophic Pyloric Stenosis

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14
Q

Pancreas Embryology

A
  • derived from foregut
  • ventral pancreatic buds contribute to uncinate process and main pancreatic duct
  • the dorsal pancreatic bud alone becomes the body, tail, isthmus, and accessory pancreatic duct
  • both the ventral and dorsal buds contribute to pancreatic head
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15
Q

_____ occurs when abnormal rotation of the ventral pancreatic bud forms a ring of pancreatic tissue → encircles 2nd part of duodenum. May cause duodenal narrowing and vomiting.

A

Annular Pancreas

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16
Q

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

A

Pancreas Divisum

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17
Q

Spleen Embryology

A

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

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18
Q

Retroperitoneal Structures

A

SAD PUCKER:

  • 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)

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

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19
Q

Important Gastrointestinal Ligaments

A
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20
Q

Important Gastrointestinal Ligaments:

  • connects the liver to the anterior abdominal wall
  • contains the ligamentum teres hepatis (derivative of fetal umbilical vein) and patent paraumbilical veins
  • derivative of ventral mesentery
A

Falciform Ligament

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21
Q

Important Gastrointestinal Ligaments:

  • connects the liver to the duodenum
  • contains the Portal triad:
    • proper hepatic artery
    • portal vein
    • common bile duct
  • Pringle Maneuver
    • ligament may be compressed between the thumb and index finger placed in omental foramen to control bleeding
  • borders the omental foramen, which connects the greater and lesser sacs
  • part of the lesser omentum
A

Hepatoduodenal Ligament

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22
Q

Important Gastrointestinal Ligaments:

  • connects the liver to the lesser curvature of the stomach
  • contains the gastric vessels
  • separates greater and lesser sacs on the right
  • may be cut during surgery to access lesser sac
  • part of the lesser omentum
A

Gastrohepatic Ligament

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23
Q

Important Gastrointestinal Ligaments:

  • connects the greater curvature and the transverse colon
  • contains the gastroepiploic arteries
  • part of the greater omentum
A

Gastrocolic Ligament

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24
Q

Important Gastrointestinal Ligaments:

  • connects the greater curvature and the spleen
  • contains the short gastrics and left gastroepiploic vessels
  • separates the greater and lesser sacs on the left
  • part of greater omentum
A

Gastrosplenic Ligament

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25
Q

Important Gastrointestinal Ligaments:

  • connects the spleento the posterior abdominal wall
  • contains the splenic artery and vein and the tail of the pancreas
A

Splenorenal Ligament

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26
Q

Digestive Tract Anatomy

A

Layers of Gut Wall (inside to outside—MSMS):

  • Mucosa—epithelium, lamina propria, muscularis mucosa
  • Submucosa—includes Submucosal nerve plexus (MeiSsner), Secretes fluid
  • Muscularis Externa—includes Myenteric nerve plexus (Auerbach), Motility
  • Serosa (when intraperitoneal), Adventitia (when retroperitoneal)

Ulcers can extend into submucosa, inner or outer muscular layer. Erosions are in the mucosa only.

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27
Q

Frequencies of Basal Electric Rhythm

A

slow waves:

  • Stomach—3 waves/min
  • Duodenum—12 waves/min
  • Ileum—8–9 waves/min
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28
Q

Digestive Tract Histology:

nonkeratinized stratified squamous epithelium

A

Esophagus

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29
Q

Digestive Tract Histology:

gastric glands

A

Stomach

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30
Q

Digestive Tract Histology:

  • villi and microvilli ↑ absorptive surface
  • Brunner glands (HCO3−-secreting cells of submucosa) and crypts of Lieberkühn (contain stem cells that replace enterocytes/goblet cells and Paneth cells that secrete defensins, lysozyme, and TNF).
A

Duodenum

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31
Q

Digestive Tract Histology:

  • plicae circulares (also present in distal duodenum)
  • crypts of Lieberkühn
A

Jejunum

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32
Q

Digestive Tract Histology:

  • Peyer patches (lymphoid aggregates in lamina propria, submucosa)
  • plicae circulares (proximal ileum)
  • crypts of Lieberküh
  • largest number of goblet cells in the small intestine
A

Ileum

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33
Q

Digestive Tract Histology:

  • crypts of Lieberkühn but no villi
  • abundant goblet cells
A

Colon

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34
Q

Abdominal Aorta and Branches

A
  • Arteries supplying GI structures are single and branch anteriorly.
  • Arteries supplying non-GI structures are paired and branch laterally and posteriorly.
  • Two areas of the colon have dual blood supply from distal arterial branches (“watershed regions”) → susceptible in colonic ischemia:
    • Splenic Flexure—SMA and IMA
    • Rectosigmoid Junction—the last sigmoid arterial branch from the IMA and superior rectal artery
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35
Q

Gastrointestinal Blood Supply and Innervation:

Foregut—Artery

A

Celiac

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36
Q

Gastrointestinal Blood Supply and Innervation:

Foregut—Parasympathetic Innervation

A

Vagus

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37
Q

Gastrointestinal Blood Supply and Innervation:

Foregut—Vertebral Level

A

T12/L1

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38
Q

Gastrointestinal Blood Supply and Innervation:

  • Artery—Celiac
  • Parasympathetic Innervation—Vagus
  • Vertebral Level—T12/L1
  • pharynx (vagus nerve only) and lower esophagus
    (celiac artery only) to proximal duodenum;
    liver, gallbladder, pancreas, spleen (mesoderm)
A

Foregut

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39
Q

Gastrointestinal Blood Supply and Innervation:

Midgut—Artery

A

SMA

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40
Q

Gastrointestinal Blood Supply and Innervation:

Midgut—Parasympathetic Innervation

A

Vagus

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41
Q

Gastrointestinal Blood Supply and Innervation:

Midgut—Vertebral Level

A

L1

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42
Q

Gastrointestinal Blood Supply and Innervation:

  • Artery—SMA
  • Parasympathetic Innervation—Vagus
  • Vertebral Level—L1
  • distal duodenum to proximal 2/3 of transverse colon
A

Midgut

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43
Q

Gastrointestinal Blood Supply and Innervation:

Hindgut—Artery

A

IMA

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44
Q

Gastrointestinal Blood Supply and Innervation:

Hindgut—Parasympathetic Innervation

A

Pelvic

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45
Q

Gastrointestinal Blood Supply and Innervation:

Hindgut—Vertebral Level

A

L3

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46
Q

Gastrointestinal Blood Supply and Innervation:

  • Artery—IMA
  • Parasympathetic Innervation—Pelvic
  • Vertebral Level—L3
  • distal 1/3 of transverse colon to upper portion of rectum
A

Hindgut

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47
Q

Celiac Trunk

A
  • Branches:
    • common hepatic
    • splenic
    • left gastric
  • The branches constitute the main blood supply of the stomach.
  • Strong anastomoses exist between:
    • left and right gastroepiploics
    • left and right gastrics
  • Posterior duodenal ulcers penetrate gastroduodenal artery causing hemorrhage.
  • Anterior duodenal ulcers perforate into the anterior abdominal cavity, potentially leading to pneumoperitoneum.
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48
Q

Portosystemic Anastomoses

A

Sites of Anastamosis (Portal ↔ Systemic):

① Esophagus

  • esophageal varices
  • left gastric ↔ azygos

② Umbilicus

  • caput medusae
  • paraumbilical ↔ small epigastric veins of the anterior abdominal wall

③ Rectum

  • anorectal varices
  • superior rectal ↔ middle and inferior rectal

Varices of gut, butt, and caput (medusae) are commonly seen with portal hypertension.

④Treatment with a transjugular intrahepatic portosystemic shunt (TIPS) between the portal vein and hepatic vein relieves portal hypertension by shunting blood to the systemic circulation, bypassing the liver. Can precipitate hepatic encephalopathy.

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49
Q

Pectinate (Dentate) Line

A
  • Formed where endoderm (hindgut) meets ectoderm.
  • Above
    • adenocarcinoma
    • internal hemorrhoids—receive visceral innervation and are therefore not painful
  • Below
    • anal fissures
    • squamous cell carcinoma
    • external hemorrhoids—receive somatic innervation (inferior rectal branch of pudendal nerve) and are therefore painful if thrombosed
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50
Q

_____ is a tear in the anal mucosa below the pectinate line. Pain while pooping; blood on toilet Paper. Located posteriorly becaus this area is poorly perfused. Associated with low-fiber diets and constipation.

A

Anal Fissure

  • ​Pectinate line
  • Pain while Pooping
  • blood on toilet Paper
  • Posterior
  • Poorly Perfused
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51
Q

Liver Tissue Architecture

A
  • The functional unit of the liver is made up of hexagonally arranged lobules surrounding the central vein with portal triads on the edges (consisting of a portal vein, hepatic artery, bile ducts, as well lymphatics).
  • Apical surface of hepatocytes faces bile canaliculi.
  • Basolateral surface faces sinusoids.
  • Kupffer cells, which are specialized macrophages, are located in the sinusoids.
  • Hepatic stellate (Ito) cells in space of Disse store vitamin A (when quiescent) and produce extracellular matrix (when activated). Responsible for hepatic fibrosis.
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52
Q

Liver Tissue Zones

A

Zone I—periportal zone:

  • affected 1st by viral hepatitis
  • ingested toxins (eg. cocaine)

Zone II—intermediate zone:

  • yellow fever

Zone III—pericentral vein (centrilobular) zone:

  • afected 1st by ischemia
  • high concentration of cytochrome P-450
  • most sensitive to metabolic toxins (eg. ethanol, CCl4, halothane, rifampin)
  • site of alcoholic hepatitis
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53
Q

Biliary Structures

A
  • Gallstones that reach the confluence of the common bile and pancreatic ducts at the ampulla of Vater can block both the common bile and pancreatic ducts (Double Duct sign), causing both cholangitis and pancreatitis, respectively.
  • Tumors that arise in head of pancreas (usually ductal adenocarcinoma) can cause obstruction of common bile duct → enlarged gallbladder with painless jaundice (Courvoisier sign).
  • Cholangiography shows filling defects in the gallbladder and cystic duct.
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54
Q

Femoral Region

A

You go from lateral to medial to find your NAVeL

  • Nerve
  • Artery
  • Vein
  • Lymphatics

Femoral Triangle

  • contains femoral nerve, artery, and vein

Femoral Sheath

  • fascial tube 3–4 cm below inguinal ligament
  • contains femoral vein, artery, and canal (deep inguinal lymph nodes) but not femoral nerve
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55
Q

Inguinal Canal

A
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56
Q

____ are protrusion of peritoneum through an opening, usually at a site of weakness. Contents may be at risk for incarceration (not reducible back into abdomen/pelvis) and strangulation (ischemia and necrosis). Complicated cases can present with tenderness, erythema, fever.

A

Hernias

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57
Q

Diaphragmatic Hernia

A
  • Abdominal structures enter the thorax.
  • May occur due to congenital defect of pleuroperitoneal membrane or from trauma.
  • Commonly occurs on left side due to relative protection of right hemidiaphragm by liver.
  • Most commonly a hiatal hernia, in which stomach herniates upward through the esophageal hiatus of the diaphragm.
  • Sliding Hiatal Hernia
    • gastroesophageal junction is displaced upward as gastric cardia slides into hiatus
    • “hourglass stomach”
    • most common type
  • Paraesophageal Hiatal Hernia
    • gastroesophageal junction is usually normal but gastric fundus protrudes into the thorax
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58
Q

Indirect Inguinal Hernia

A
  • Goes through the internal (deep) inguinal ring, external (superficial) inguinal ring, and into the scrotum.
  • Enters internal inguinal ring lateral to inferior epigastric vessels.
  • Caused by failure of processus vaginalis to close (can form hydrocele).
  • May be noticed in infants or discovered in adulthood.
  • Much more common in males.
  • An indirect inguinal hernia follows the path of descent of the testes.
  • Covered by all 3 layers of spermatic fascia.

MDs don’t LIe.

  • Medial to inferior epigastric vessels = Direct hernia
  • Lateral to inferior epigastric vessels = Indirect hernia
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59
Q

Direct Inguinal Hernia

A
  • Protrudes through the inguinal (Hesselbach) triangle.
  • Bulges directly through parietal peritoneum medial to the inferior epigastric vessels but lateral to the rectus abdominis.
  • Goes through the external (superficial) inguinal ring only.
  • Covered by external spermatic fascia.
  • Usually occurs in older men due to an acquired weakness in the transversalis fascia.

MDs don’t LIe.

  • Medial to inferior epigastric vessels = Direct hernia
  • Lateral to inferior epigastric vessels = Indirect hernia
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60
Q

Femoral Hernia

A
  • Protrudes below inguinal ligament through femoral canal below and lateral to pubic tubercle.
  • More common in females, but overall inguinal hernias are the most common.
  • More likely to present with incarceration or strangulation than inguinal hernias.
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61
Q

Inguinal (Hesselbach) Triangle:

A
  • Inferior Epigastric Vessels
  • Lateral Border of Rectus Abdominis
  • Inguinal Ligament
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62
Q

Gastrointestinal Regulatory Substances:

  • G cells (antrum of stomach, duodenum)
  • ↑ gastric H+ secretion
  • ↑ growth of gastric mucosa
  • ↑ gastric motility
  • ↑ by stomach distention/alkalinization, amino acids, peptides, vagal stimulation via gastrin-releasing peptide (GRP)
  • ↓ by pH < 1.5
  • ↑ by chronic PPI use
  • ↑ in chronic atrophic gastritis (eg. H. pylori)
  • ↑↑ in Zollinger-Ellison syndrome (gastrinoma)
A

Gastrin

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63
Q

Gastrointestinal Regulatory Substances:

  • D cells (pancreatic islets, GI mucosa)
  • ↓ gastric acid and pepsinogen secretion
  • ↓ pancreatic and small intestine fluid secretion
  • ↓ gallbladder contraction
  • ↓ insulin and glucagon release
  • ↑ by acid
  • ↓ by vagal stimulation
  • inhibits secretion of various hormones (encourages somato-stasis)
  • Octreotide is an analog used to treat acromegaly, carcinoid syndrome, and variceal bleeding.
A

Somatostatin

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64
Q

Gastrointestinal Regulatory Substances:

  • I cells (duodenum, jejunum)
  • ↑ pancreatic secretion
  • ↑ gallbladder contraction
  • ↓ gastric emptying
  • ↑ sphincter of Oddi relaxation
  • ↑ by fatty acids, amino acids
  • acts on neural muscarinic pathways to cause pancreatic secretion
A

Cholecystokinin

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65
Q

Gastrointestinal Regulatory Substances:

  • S cells (duodenum)
  • ↑ pancreatic HCO3– secretion
  • ↓ gastric acid secretion
  • ↑ bile secretion
  • ↑ by acid, fatty acids in lumen of duodenum
  • ↑ HCO3– neutralizes gastric acid in duodenum, allowing pancreatic enzymes to function
A

Secretin

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66
Q

Gastrointestinal Regulatory Substances:

  • K cells (duodenum, jejunum)
  • Exocrine: ↓ gastric H+ secretion
  • Endocrine: ↑ insulin release
  • ↑ by fatty acids, amino acids, and oral glucose
  • also known as Gastric Inhibitory Peptide (GIP)
  • oral glucose load leads to ↑ insulin compared to IV equivalent due to GIP secretion
A

Glucose-Dependent Insulinotropic Peptide

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67
Q

Gastrointestinal Regulatory Substances:

  • small intestine
  • produces migrating motor complexes (MMCs)
  • ↑ in fasting state
  • _____ receptor agonists (eg. erythromycin) are used to stimulate intestinal peristalsis
A

Motilin

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68
Q

Gastrointestinal Regulatory Substances:

  • parasympathetic ganglia in sphincters, gallbladder, and small intestine
  • ↑ intestinal water and electrolyte secretion
  • ↑ relaxation of intestinal smooth muscle and sphincters
  • ↑ by distention and vagal stimulation
  • ↓ by adrenergic input
A

Vasoactive Intestinal Polypeptide

VIPoma—non-α, non-β islet cell pancreatic tumor
that secretes VIP. Causes Watery Diarrhea, Hypokalemia, and Achlorhydria (WDHA syndrome).

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69
Q

Gastrointestinal Regulatory Substances:

  • ↑ smooth muscle relaxation, including lower esophageal sphincter (LES)
  • loss of secretion is implicated in ↑ LES tone of achalasia
A

Nitric Oxide

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70
Q

Gastrointestinal Regulatory Substances:

  • stomach
  • ↑ appetite
  • ↑ in fasting state
  • ↓ by food
  • ↑ in Prader-Willi syndrome
  • ↓ after gastric bypass surgery
A

Ghrelin

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71
Q

Gastrointestinal Secretory Products:

  • parietal cells (stomach)
  • Vitamin B12–binding protein (required for B12 uptake in terminal ileum)
  • autoimmune destruction of parietal cells → chronic gastritis and pernicious anemia
A

Intrinsic Factor

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72
Q

Gastrointestinal Secretory Products:

  • parietal cells (stomach)
  • ↓ stomach pH
  • ↑ by histamine, vagal stimulation (ACh), and gastrin
  • ↓ by somatostatin, GIP, prostaglandin, and secretin
A

Gastric Acid

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73
Q

Gastrointestinal Secretory Products:

  • chief cells (stomach)
  • protein digestion
  • ↑ by vagal stimulation (ACh), and local acid
A

Pepsin

  • Pepsinogen (inactive) is converted to Pepsin (active) in the presence of H+.
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74
Q

Gastrointestinal Secretory Products:

  • mucosal cells (stomach, duodenum, salivary glands, pancreas) and Brunner glands (duodenum)
  • neutralizes acid
  • ↑ by pancreatic and biliary secretion with secretin
  • trapped in mucus that covers the gastric epithelium
A

Bicarbonate

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75
Q

Locations of Gastrointestinal Secretory Cells

A

Gastrin ↑ acid secretion primarily through its effects on enterochromaffin-like (ECL) cells (leading to histamine release) rather than through its direct effect on parietal cells.

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76
Q

Pancreatic secretions are _____.

A

Isotonic

  • low flow → high Cl−
  • high flow → high HCO3−
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77
Q

Pancreatic Secretions:

  • starch digestion
  • secreted in active form
A

α-amylase

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78
Q

Pancreatic Secretions:

fat digestion

A

Lipases

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79
Q

Pancreatic Secretions:

  • protein digestion
  • includes trypsin, chymotrypsin, elastase, and carboxypeptidases
  • secreted as proenzymes also known as zymogens
A

Proteases

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80
Q

Pancreatic Secretions:

  • converted to active enzyme trypsin → activation of other proenzymes and cleaving of additional trypsinogen molecules into active trypsin (positive feedback loop)
  • converted to trypsin by enterokinase/enteropeptidase, a brush-border enzyme on duodenal and jejunal mucosa
A

Trypsinogen

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81
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 via Facilitated diffusion by GLUT5.
  • All are transported to blood by GLUT2.
  • D-Xylose Absorption Test: distinguishes GI mucosal damage from other causes of malabsorption
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82
Q

Vitamin/Mineral Absorption:

absorbed as Fe2+ in the duodenum

A

Iron

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83
Q

Vitamin/Mineral Absorption:

absorbed in the small bowel

A

Folate

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84
Q

Vitamin/Mineral Absorption:

  • absorbed in the terminal ileum along with bile salts
  • requires intrinsic factor
A

Vitamin B12

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85
Q

GI Physioology:

  • unencapsulated lymphoid tissue found in the lamina propria and submucosa of ileum
  • contain specialized M cells that sample and present antigens to immune cells
  • B cells stimulated in germinal centers of _____ differentiate into IgA-secreting plasma cells, which ultimately reside in the lamina propria
  • IgA receives protective secretory component and is then transported across the epithelium to the gut to deal with intraluminal antigen
A

Peyer Patches

Intra-gut Antibody

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86
Q

Bile Composition

A
  • bile salts
    • bile acids conjugated to glycine or taurine, making them water soluble
  • phospholipids
  • cholesterol
  • bilirubin
  • water
  • ions
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87
Q

_____ catalyzes rate‑limiting step of bile acid synthesis.

A

Cholesterol 7α-Hydroxylase

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88
Q

Bile Functions

A
  • digestion and absorption of lipids and fat-soluble vitamins
  • cholesterol excretion (body’s 1° means of eliminating cholesterol)
  • antimicrobial activity (via membrane disruption)

↓ absorption of enteric bile salts at distal ileum (as in short bowel syndrome, Crohn disease) prevents normal fat absorption. Calcium, which normally binds oxalate, binds fat instead, so free oxalate is absorbed by gut → ↑ frequency of calcium oxalate kidney stones.

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89
Q

Bilirubin

A
  • Heme is metabolized by heme oxygenase to biliverdin, which is subsequently reduced to bilirubin.
  • Unconjugated bilirubin is removed from blood by liver, conjugated with glucuronate, and excreted in bile.
  • Direct Bilirubin
    • conjugated with glucuronic acid
    • water soluble
  • Indirect Bilirubin
    • unconjugated
    • water insoluble
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90
Q

GI Pathologies:

  • stone(s) in salivary gland duct
  • can occur in 3 major salivary glands (parotid, submandibular, sublingual)
  • single stones are more common in the submandibular gland (Wharton duct)
  • presents as recurrent pre-/periprandial pain and swelling in affected gland
  • caused by dehydration or trauma
  • treated conservatively with NSAIDs, gland massage, warm compresses, and sour candies (to promote salivary flow)
A

Sialolithiasis

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91
Q

GI Pathologies:

inflammation of salivary gland due to obstruction, infection, or immune-mediated mechanisms

A

Sialadenitis

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92
Q

GI Pathologies:

  • most commonly benign and in parotid gland
  • tumors in smaller glands more likely malignant
  • typically present as painless mass/swelling
  • facial pain or paralysis suggests malignant involvement of CN VII
A

Salivary Gland Tumors

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93
Q

Salivary Gland Tumors:

  • most common salivary gland tumor
  • composed of chondromyxoid stroma and epithelium and recurs if incompletely excised or ruptured intraoperatively
  • may undergo malignant transformation
A

Pleomorphic Adenoma

(Benign Mixed Tumor)

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94
Q

Salivary Gland Tumors:

  • most common malignant tumor
  • has mucinous and squamous components
A

Mucoepidermoid Carcinoma

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95
Q

Salivary Gland Tumors:

  • benign cystic tumor with germinal center
  • typically found in smokers
  • bilateral in 10%
  • multifocal in 10%
A

Warthin Tumor

(Papillary Cystadenoma Lymphomatosum)

Warriors from Germany love smoking.

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96
Q

GI Pathologies:

  • failure of the LES to relax due to loss of myenteric (Auerbach) plexus due to loss of postganglionic inhibitory neurons (which contain NO and VIP)
  • manometry findings include uncoordinated or absent peristalsis with high LES resting pressure → progressive dysphagia to solids and liquids (vs. obstruction—solids only)
  • barium swallow shows dilated esophagus with an area of distal stenosis (“bird’s beak”)
  • associated with ↑ risk of esophageal cancer
  • 2° _____ (pseudo_____) may arise from Chagas disease (T. cruzi infection) or extraesophageal malignancies (mass effect or paraneoplastic)
A

Achalasia

A-chalasia = absence of relaxation.

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97
Q

Esophageal Pathologies:

  • transmural
  • usually distal esophageal rupture with pneumomediastinum due to violent retching
  • subcutaneous emphysema may be due to dissecting air (crepitus may be felt in the neck region or chest wall)
  • surgical emergency
A

Boerhaave Syndrome

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98
Q

Esophageal Pathologies:

  • infiltration of eosinophils in the esophagus often in atopic patients
  • food allergens → dysphagia, food impaction
  • esophageal rings and linear furrows often seen on endoscopy
  • typically unresponsive to GERD therapy
A

Eosinophilic Esophagitis

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99
Q

Esophageal Pathologies:

associated with caustic ingestion and acid reflux

A

Esophageal Strictures

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100
Q

Esophageal Pathologies:

  • dilated submucosal veins in the lower 1 ⁄3 of esophagus 2° to portal hypertension
  • common in cirrhotics
  • may be source of life-threatening hematemesis
A

Esophageal Varices

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101
Q

Esophageal Pathologies:

associated with reflux, infection in immunocompromised (Candida: white pseudomembrane; HSV-1: punched-out ulcers; CMV: linear ulcers), caustic ingestion, or pill _____ (eg. bisphosphonates, tetracycline, NSAIDs, iron, and potassium chloride)

A

Esophagitis

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102
Q

Esophageal Pathologies:

  • commonly presents as heartburn, regurgitation, and dysphagia
  • may also present as chronic cough and hoarseness (laryngopharyngeal reflux)
  • associated with asthma
  • transient decreases in LES tone
A

Gastroesophageal Reflux Disease (GERD)

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103
Q

Esophageal Pathologies:

  • partial-thickness mucosal lacerations at gastroesophageal junction due to severe vomiting
  • often presents with hematemesis
  • usually found in alcoholics and bulimics
A

Mallory-Weiss Syndrome

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104
Q

Esophageal Pathologies:

  • triad of dysphagia, iron deficiency anemia, and esophageal webs
  • may be associated with glossitis
  • increased risk of esophageal squamous cell carcinoma
A

Plummer-Vinson Syndrome

Plumbers DIE.

  • Dysphagia
  • Iron deficiency anemia
  • Esophageal webs
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105
Q

Esophageal Pathologies:

  • esophageal smooth muscle atrophy → ↓ LES pressure and dysmotility → acid reflux and dysphagia → stricture, Barrett esophagus, and aspiration
  • part of CREST syndrome
A

Sclerodermal Esophageal Dysmotility

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106
Q

Esophageal Pathologies:

  • specialized intestinal metaplasia
  • replacement of nonkeratinized stratified squamous epithelium with intestinal epithelium (nonciliated columnar with goblet cells) in distal esophagus
  • due to chronic gastroesophageal reflux disease (GERD)
  • associated with ↑ risk of esophageal adenocarcinoma
A

Barrett Esophagus

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107
Q

Esophageal cancer typically presents with _____ and has poor prognosis.

A
  • progressive dysphagia (first solids, then liquids)
  • weight loss
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108
Q

Esophageal Cancer:

  • upper 2/3
  • alcohol, hot liquids, caustic strictures, smoking, achalasia
  • more common worldwide
A

Squamous Cell Carcinoma

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109
Q

Esophageal Cancer:

  • lower 1/3
  • chronic GERD, Barrett esophagus, obesity, smoking, achalasia
  • more common in America
A

Adenocarcinoma

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110
Q

Gastritis:

  • erosions can be caused by:
    • NSAIDs—↓ PGE2 → ↓ gastric mucosa protection
    • burns (Curling ulcer)—hypovolemia → mucosal ischemia
    • brain injury (Cushing ulcer)—↑ vagal stimulation → ↑ ACh → ↑ H+ production
  • common among alcoholics and patients taking daily NSAIDs (eg. patients with rheumatoid arthritis)
A

Acute Gastritis

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111
Q

Gastritis:

  • caused by burns
  • hypovolemia → mucosal ischemia
A

Curling Ulcer

Burned by the Curling iron.

112
Q

Gastritis:

  • caused by brain injury
  • ↑ vagal stimulation → ↑ ACh → ↑ H+ production
A

Cushing Ulcer

Always Cushion the brain.

113
Q

Gastritis:

  • mucosal inflammation
  • often leading to atrophy (hypochlorhydria → hypergastrinemia) and intestinal metaplasia (↑ risk of gastric cancers)
A

Chronic Gastritis

114
Q

Chronic Gastritis:

  • most common
  • ↑ risk of peptic ulcer disease and MALT lymphoma
  • affects antrum first and spreads to body of stomach
A

H. pylori

115
Q

Chronic Gastritis:

  • autoantibodies to parietal cells and intrinsic factor
  • ↑ risk of pernicious anemia
  • affects body/fundus of stomach
A

Autoimmune

116
Q

GI Pathologies:

  • hyperplasia of gastric mucosa → hypertrophied rugae (look like brain gyri)
  • causes excess mucus production with resultant protein loss and parietal cell atrophy with ↓ acid production
  • precancerous
  • presents with epigastric pain, anorexia, weight loss, vomiting, and edema (due to protein loss)
A

Ménétrier Disease

117
Q

GI Pathologies:

  • most commonly adenocarcinoma; lymphoma, GI stromal tumor, carcinoid (rare)
  • early aggressive local spread with node/liver metastases
  • often presents late, with weight loss, abdominal pain, early satiety, and in some cases acanthosis nigricans or Leser-Trélat sign
  • associated with blood type A
A

Gastric Cancer

118
Q

Gastric Cancer:

  • associated with H. pylori, dietary nitrosamines (smoked foods), tobacco smoking, achlorhydria, and chronic gastritis
  • commonly on lesser curvature
  • looks like ulcer with raised margins
A

Intestinal

119
Q

Gastric Cancer:

  • not associated with H. pylori
  • signet ring cells—mucin-filled cells with peripheral nuclei
  • stomach wall grossly thickened and leathery (linitis plastica)
A

Diffuse

120
Q

Gastric Cancer:

involvement of left supraclavicular node by metastasis from stomach

A

Virchow Node

121
Q

Gastric Cancer:

  • bilateral metastases to ovaries
  • bundant mucin-secreting, signet ring cells
A

Krukenberg Tumor

122
Q

Gastric Cancer:

subcutaneous periumbilical metastasis

A

Sister Mary Joseph Nodule

123
Q

Peptic Ulcer Disease:

  • pain can be greater with meals—weight loss
  • H. pylori in ~ 70%
  • ↓ mucosal protection against gastric acid
  • caused by NSAIDs
  • ↑ risk for carcinoma
  • biopsy margins to rule out malignancy
A

Gastric Ulcer

124
Q

Peptic Ulcer Disease:

  • pain decreases with meals—weight gain
  • H. pylori in ~ 90%
  • ↓ mucosal protection against gastric acid or ↑ gastric acid secretion
  • caused by Zollinger-Ellison syndrome
  • generally benign
  • hypertrophy of Brunner glands
A

Duodenal Ulcer

125
Q

Ulcer Complications:

  • gastric, duodenal (posterior > anterior)
  • most common complication
  • ruptured gastric ulcer on the lesser curvature of stomach → bleeding from left gastric artery
  • ulcer on the posterior wall of duodenum → bleeding from gastroduodenal artery
A

Hemorrhage

126
Q

Ulcer Complications:

  • pyloric channel
  • duodenal
A

Obstruction

127
Q

Ulcer Complications:

  • duodenal (anterior > posterior)
  • may see free air under diaphragm with referred pain to the shoulder via irritation of phrenic nerve
A

Perforation

128
Q

Malabsorption syndromes can cause _____.

A
  • diarrhea
  • steatorrhea
  • weight loss
  • weakness
  • vitamin and mineral deficiencies
129
Q

Malabsorption syndromes are screened with _____.

A

fecal fat (eg. Sudan stain)

130
Q

Malabsorption Syndromes

A
  • Celiac Disease
  • Lactose Intolerance
  • Pancreatic Insufficiency
  • Tropical Sprue
  • Whipple Disease
131
Q

Malabsorption Syndromes:

  • gluten-sensitive enteropathy, celiac sprue
  • autoimmune-mediated intolerance of gliadin (gluten protein found in wheat) → malabsorption and steatorrhea
  • associated with HLA-DQ2, HLA-DQ8, northern European descent, dermatitis herpetiformis, ↓ bone density
A

Celiac Disease

132
Q

Malabsorption Syndromes:

  • IgA anti-tissue transglutaminase (IgA tTG), anti-endomysial, anti-deamidated gliadin peptide antibodies
  • villous atrophy, crypt hyperplasia, and intraepithelial lymphocytosis
  • moderately ↑ risk of malignancy (eg. T-cell lymphoma)
  • ↓ mucosal absorption primarily affects distal duodenum and/or proximal jejunum
A

Celiac Disease

133
Q

Malabsorption Syndromes:

  • passively absorbed in proximal small intestine
  • blood and urine levels ↓ with mucosa defects or bacterial overgrowth
  • normal in pancreatic insufficiency
A

D-Xylose Test

134
Q

Malabsorption Syndromes:

Celiac Disease Treatment

A

gluten-free diet

135
Q

Malabsorption Syndromes:

  • lactase deficiency
  • normal-appearing villi, except when 2° to injury at tips of villi (eg. viral enteritis)
  • osmotic diarrhea with ↓ stool pH (colonic bacteria ferment lactose)
  • Lactose Hydrogen Breath Test: ⊕ for lactose malabsorption if post-lactose breath hydrogen value rises > 20 ppm compared with baseline
A

Lactose Intolerance

136
Q

Malabsorption Syndromes:

  • due to chronic pancreatitis, cystic fibrosis, or obstructing cancer
  • causes malabsorption of fat and fat-soluble vitamins (A, D, E, K) as well as vitamin B12
  • ↓ duodenal pH (bicarbonate) and fecal elastase
A

Pancreatic Insufficiency

137
Q

Malabsorption Syndromes:

  • similar findings as celiac sprue (affects small bowel), but responds to antibiotics
  • cause is unknown, but seen in residents of or recent visitors to tropics
  • ↓ mucosal absorption affecting duodenum and jejunum but can involve ileum with time
  • associated with megaloblastic anemia due to folate deficiency and, later, B12 deficiency
A

Tropical Sprue

138
Q

Malabsorption Syndromes:

  • infection with Tropheryma whipplei (intracellular gram ⊕)
  • PAS ⊕ foamy macrophages in intestinal lamina propria and mesenteric nodes
  • cardiac symptoms, arthralgias, and neurologic symptoms are common
  • diarrhea/steatorrhea occur later in disease course
  • most common in older men
A

Whipple Disease

Foamy Whipped cream in a CAN:

  • Cardiac symptoms
  • Arthralgias
  • Neurologic symptoms
139
Q

Inflammatory Bowel Disease

A
  • Crohn Disease
  • Ulcerative Colitis
140
Q

Crohn Disease:

Location

A
  • any portion of the GI tract
  • usually the terminal ileum and colon
  • skip lesions
  • rectal sparing
141
Q

Crohn Disease:

Gross Morphology

A
  • transmural inflammation → fistulas
  • cobblestone mucosa
  • creeping fat
  • bowel wall thickening (“string sign” on barium swallow x-ray)
  • linear ulcers
  • fissures
142
Q

Crohn Disease:

Microscopic Morphology

A
143
Q

Crohn Disease:

Complications

A
  • malabsorption/malnutrition
  • colorectal cancer (↑ risk with pancolitis)
  • fistulas (eg. enterovesical fistulae, which can cause recurrent UTI and pneumaturia)
  • phlegmon/abscess
  • strictures (causing obstruction)
  • perianal disease
144
Q

Crohn Disease:

Intestinal Manifestation

A

diarrhea that may or may not be bloody

145
Q

Crohn Disease:

Extraintestinal Manifestations

A
  • rash (pyoderma gangrenosum, erythema nodosum)
  • eye inflammation (episcleritis, uveitis)
  • oral ulcerations (aphthous stomatitis)
  • arthritis (peripheral, spondylitis)
  • kidney stones (usually calcium oxalate)
  • gallstones
  • may be ⊕ for anti-Saccharomyces cerevisiae antibodies (ASCA)
146
Q

Crohn Disease:

Treatment

A
  • Corticosteroids
  • Azathioprine
  • Antibiotics (eg. Ciprofloxacin, Metronidazole)
  • Infliximab
  • Adalimumab
147
Q

Crohn Disease:

Findings

A

A fat granny and an old crone (Chron) skip down a cobblestone road away from the wreck.

  • creeping fat
  • noncaseating granulomas
  • skip leasions
  • cobblestone mucosa
  • rectal sparing
148
Q

Ulcerative Colitis:

Location

A
  • colitis = colon inflammation
  • continuous colonic lesions
  • always with rectal involvement
149
Q

Ulcerative Colitis:

Gross Morphology

A
  • mucosal and submucosal inflammation only
  • friable mucosa with superficial and/or deep ulcerations
  • loss of haustra → “lead pipe” appearance on imaging
150
Q

Ulcerative Colitis:

Microscopic Morphology

A
  • crypt abscesses and ulcers
  • bleeding
  • no granulomas
  • Th2 mediated
151
Q

Ulcerative Colitis:

Complications

A
  • malabsorption/malnutrition
  • colorectal cancer (↑ risk with pancolitis)
  • fulminant colitis
  • toxic megacolon
  • perforation
152
Q

Ulcerative Colitis:

Intestinal Manifestation

A

bloody diarrhea

153
Q

Ulcerative Colitis:

Extraintestinal Manifestations

A
  • rash (pyoderma gangrenosum, erythema nodosum)
  • eye inflammation (episcleritis, uveitis)
  • oral ulcerations (aphthous stomatitis)
  • arthritis (peripheral, spondylitis)
  • 1° sclerosing cholangitis
  • associated with p-ANCA
154
Q

Ulcerative Colitis:

Treatment

A
  • 5-Aminosalicylic preparations (eg. Mesalamine)
  • 6-Mercaptopurine
  • Infliximab
  • Colectomy
155
Q

Ulcerative Colitis:

Findings

A

ULCCCERS:

  • Ulcers
  • Large intestine
  • Continuous, Colorectal carcinoma, Crypt abscesses
  • Extends proximally
  • Red diarrhea
  • Sclerosing cholangitis
156
Q

GI Pathologies:

  • recurrent abdominal pain associated with ≥ 2 of the following:
    • related to defecation
    • change in stool frequency
    • change in form (consistency) of stool
  • no structural abnormalities
  • most common in middle-aged women
  • chronic symptoms may be diarrhea-predominant, constipation-predominant, or mixed
  • pathophysiology is multifaceted
  • first-line treatment is lifestyle modification and dietary changes
A

Irritable Bowel Syndrome

157
Q

GI Pathologies:

  • acute inflammation of the appendix, can be due to obstruction by fecalith (in adults) or lymphoid hyperplasia (in children)
  • initial diffuse periumbilical pain migrates to McBurney point (1 ⁄3 the distance from right anterior superior iliac spine to umbilicus)
  • nausea, fever
  • may perforate → peritonitis
  • may elicit psoas, obturator, and Rovsing signs, guarding and rebound tenderness on exam.
  • Differentials:
    • diverticulitis (elderly)
    • ectopic pregnancy (use β-hCG to rule out)
    • pseudoappendicitis
A

Appendicitis

158
Q

Diverticula of the GI Tract:

  • blind pouch protruding from the alimentary tract that communicates with the lumen of the gut
  • most diverticula (esophagus, stomach, duodenum, colon) are acquired and are termed “false diverticula”
A

Diverticulum

159
Q

Diverticula of the GI Tract:

all gut wall layers outpouch (eg. Meckel)

A

“True” Diverticulum

160
Q

Diverticula of the GI Tract:

  • only mucosa and submucosa outpouch
  • occur especially where vasa recta perforate muscularis externa
A

“False” Diverticulum or Pseudodiverticulum

161
Q

Diverticula of the GI Tract:

  • many false diverticula of the colon, commonly sigmoid
  • common (in ~ 50% of people > 60 years)
  • caused by ↑ intraluminal pressure and focal weakness in colonic wall
  • associated with obesity and diets low in fiber, high in total fat/red meat
  • often asymptomatic or associated with vague discomfort
  • Complications include diverticular bleeding
  • (painless hematochezia), diverticulitis.
A

Diverticulosis

162
Q

Diverticula of the GI Tract:

  • inflammation of diverticula with wall thickening classically causing LLQ pain, fever, and leukocytosis
  • treat with antibiotics
  • Complications:
    • abscess
    • fistula (colovesical fistula → pneumaturia), obstruction (inflammatory stenosis), perforation (→ peritonitis)
A

Diverticulitis

163
Q

Diverticula of the GI Tract:

  • pharyngoesophageal false diverticulum
  • esophageal dysmotility causes herniation of mucosal tissue at Killian triangle between the thyropharyngeal and cricopharyngeal parts of the inferior pharyngeal constrictor
  • Presenting Symptoms:
    • dysphagia
    • obstruction
    • gurgling
    • aspiration
    • foul breath
    • neck mass
  • most common in elderly males
A

Zenker Diverticulum

Elder MIKE has bad breath.

  • Elderly
  • Males
  • Inferior pharyngeal constrictor
  • Killian triangle
  • Esophageal dysmotility
  • Halitosis
164
Q

Diverticula of the GI Tract:

  • true diverticulum
  • persistence of the vitelline (omphalomesenteric) duct
  • may contain ectopic acid–secreting gastric mucosa and/or pancreatic tissue
  • most common congenital anomaly of GI tract
  • can cause hematochezia/melena (less commonly), RLQ pain, intussusception, volvulus, or obstruction near terminal ileum
  • contrast with omphalomesenteric cyst = cystic dilation of vitelline duct
  • Diagnosis: pertechnetate study for uptake by heterotopic gastric mucosa
A

Meckel Diverticulum

The rule of 2’s:

  • 2 times as likely in males
  • 2 inches long
  • 2 feet from the ileocecal valve
  • 2% of population
  • commonly presents in first 2 years of life
  • may have 2 types of epithelia (gastric/pancreatic)
165
Q

GI Pathologies:

  • congenital megacolon characterized by lack of ganglion cells/enteric nervous plexuses (Auerbach and Meissner plexuses) in distal segment of colon
  • due to failure of neural crest cell migration
  • associated with mutations in RET
  • presents with bilious emesis, abdominal distention, and failure to pass meconium within 48 hours → chronic constipation
  • normal portion of the colon proximal to the aganglionic segment is dilated, resulting in a “transition zone”
  • risk ↑ with Down syndrome
  • explosive expulsion of feces (squirt sign) → empty rectum on digital exam
  • diagnosed by absence of ganglionic cells on rectal suction biopsy
A

Hirschsprung disease

166
Q

GI Pathologies:

  • anomaly of midgut rotation during fetal development → improper positioning of bowel (small bowel clumped on the right side)
  • formation of fibrous bands (Ladd bands)
  • can lead to volvulus, duodenal obstruction
A

Malrotation

167
Q

GI Pathologies:

  • twisting of portion of bowel around its mesentery
  • can lead to obstruction and infarction
  • can occur throughout the GI tract
  • midgut volvulus more common in infants and children
  • sigmoid volvulus (coffee bean sign on x-ray)
  • more common in elderly
A

Volvulus

168
Q

GI Pathologies:

  • telescoping of proximal bowel segment into a distal segment, commonly at ileocecal junction
  • compromised blood supply → intermittent abdominal pain often with “currant jelly” stools
  • patient may draw legs to chest to ease pain
  • exam may reveal sausageshaped mass
  • utrasound shows “target sign”
  • often due to a lead point, but can be idiopathic
  • most common pathologic lead point is a Meckel diverticulum (children) or intraluminal mass/tumor (adults)
  • majority of cases occur in children; unusual in adults
  • may be associated with rotavirus vaccine, Henoch-Schönlein purpura, and recent viral infection (eg. adenovirus; Peyer patch hypertrophy creates lead point)
A

Intussusception

169
Q

GI Pathologies:

  • 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
A

Acute Mesenteric Ischemia

170
Q

GI Pathologies:

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

Chronic Mesenteric Ischemia

171
Q

GI Pathologies:

  • reduction in intestinal blood flow causes ischemia
  • crampy abdominal pain followed by hematochezia
  • commonly occurs at watershed areas (splenic flexure, distal colon)
  • typically affects elderly
  • thumbprint sign on imaging due to mucosal edema/hemorrhage
A

Colonic Ischemia

172
Q

GI Pathologies:

  • tortuous dilation of vessels → hematochezia
  • most often found in the right-sided colon
  • more common in older patients
  • confirmed by angiography
  • associated with aortic stenosis and von Willebrand disease
A

Angiodysplasia

173
Q

GI Pathologies:

  • fibrous band of scar tissue
  • commonly forms after surgery
  • most common cause of small bowel obstruction, demonstrated by multiple dilated small bowel loops on x-ray
A

Adhesion

174
Q

GI Pathologies:

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

Ileus

175
Q

GI Pathologies:

in cystic fibrosis, meconium plug obstructs intestine, preventing stool passage at birth

A

Meconium Ileus

176
Q

GI Pathologies:

  • seen in premature, formula-fed infants with immature immune system
  • necrosis of intestinal mucosa (primarily colonic) with possible perforation, which can lead to pneumatosis intestinalis, free air in abdomen, and portal venous gas
A

Necrotizing Enterocolitis

177
Q

GI Pathologies:

  • growths of tissue within the colon
  • may be neoplastic or non-neoplastic
  • grossly characterized as flat, sessile, or pedunculated (on a stalk) on the basis of protrusion into colonic lumen
  • generally classified by histologic type
A

Colonic Polyps

178
Q

Colonic Polyps:

Non-Neoplastic

A
  • Hamartomatous Polyps
  • Mucosal Polyps
  • Inflammatory Pseudopolyps
  • Submucosal Polyps
  • Hyperplastic Polyps
179
Q

Colonic Polyps:

  • non-neoplastic
  • solitary lesions do not have significant risk of transformation
  • growths of normal colonic tissue with distorted architecture
  • associated with Peutz-Jeghers syndrome and juvenile polyposis
A

Hamartomatous Polyps

180
Q

Colonic Polyps:

  • non-neoplastic
  • small, usually < 5 mm
  • look similar to normal mucosa
  • clinically insignificant
A

Mucosal Polyps

181
Q

Colonic Polyps:

  • non-neoplastic
  • due to mucosal erosion in inflammatory bowel disease
A

Inflammatory Pseudopolyps

182
Q

Colonic Polyps:

  • non-neoplastic
  • may include lipomas, leiomyomas, fibromas, and other lesions
A

Submucosal Polyps

183
Q

Colonic Polyps:

  • non-neoplastic
  • most common
  • generally smaller and predominantly located in rectosigmoid region
  • occasionally evolves into serrated polyps and more advanced lesions
A

Hyperplastic Polyps

184
Q

Colonic Polyps:

Malignant Potential

A
  • Adenomatous Polyps
  • Serrated Polyps
185
Q

Colonic Polyps:

  • malignant potential
  • neoplastic via chromosomal instability pathway with mutations in APC and KRAS
  • tubular histology has less malignant potential than villous (“villous histology is villainous”)
  • tubulovillous has intermediate malignant potential
  • usually asymptomatic
  • may present with occult bleeding
A

Adenomatous Polyps

186
Q

Colonic Polyps:

  • malignant potential
  • premalignant
  • characterized by CpG island methylator phenotype (CIMP; cytosine base followed by guanine, linked by a phosphodiester bond)
  • defect may silence MMR gene (DNA mismatch repair) expression
  • mutations lead to microsatellite instability and mutations in BRAF
  • “sawtooth” pattern of crypts on biopsy
  • up to 20% of cases of sporadic CRC
A

Serrated Polyps

187
Q

Polyposis Syndromes

A
  • Familial Adenomatous Polyposis
  • Gardner Syndrome
  • Turcot Syndrome
  • Peutz-Jeghers Syndrome
  • Juvenile Polyposis Syndrome
188
Q

Polyposis Syndromes:

  • autosomal dominant mutation of APC tumor suppressor gene on chromosome 5q21
  • 2-hit hypothesis
  • thousands of polyps arise starting after puberty
  • pancolonic, always involves rectum
  • prophylactic colectomy or else 100% progress to CRC
A

Familial Adenomatous Polyposis

189
Q

Polyposis Syndromes:

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

Gardner Syndrome

190
Q

Polyposis Syndromes:

FAP/Lynch syndrome + malignant CNS tumor (eg. medulloblastoma, glioma)

A

Turcot Syndrome

191
Q

Polyposis Syndromes:

  • autosomal dominant 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, pancreatic)
A

Peutz-Jeghers Syndrome

192
Q

Polyposis Syndromes:

  • autosomal dominant syndrome in children (typically < 5 years old) featuring numerous hamartomatous polyps in the colon, stomach, small bowel
  • associated with ↑ risk of CRC
A

Juvenile Polyposis Syndrome

193
Q

GI Pathologies:

  • previously known as hereditary nonpolyposis colorectal cancer (HNPCC)
  • autosomal dominant mutation of DNA mismatch repair genes with subsequent microsatellite instability
  • ∼ 80% progress to CRC
  • proximal colon is always involved
  • associated with endometrial, ovarian, and skin cancers
A

Lynch Syndrome

194
Q

Colorectal Cancer

A
  • Most patients are > 50 years old.
  • ~ 25% have a family history.
  • Risk Factors:
    • adenomatous and serrated polyps
    • familial cancer syndromes
    • IBD
    • tobacco use
    • diet of processed meat with low fiber
  • Rectosigmoid > Ascending > Descending Colon
  • Ascending
    • exophytic mass, iron deficiency anemia, weight loss
  • Descending
    • infiltrating mass, partial obstruction, colicky pain, hematochezia.
  • Rarely, presents with S. bovis (gallolyticus) bacteremia.
  • Right side bleeds, left side obstructs (narrower lumen).
195
Q

Colorectal Cancer Diagnosis

A
  • Iron deficiency anemia in males (especially > 50 years old) and postmenopausal females raises suspicion.
  • Screen low-risk patients starting at age 50 with colonoscopy; alternatives include flexible sigmoidoscopy, fecal occult blood testing (FOBT), fecal immunochemical testing (FIT), and CT colonography.
  • Patients with a first-degree relative who has colon cancer should be screened via colonoscopy at age 40, or starting 10 years prior to their relative’s presentation.
  • Patients with IBD have a distinct screening protocol.
  • “Apple core” lesion seen on barium enema x-ray.
  • CEA tumor marker: good for monitoring recurrence, should not be used for screening
196
Q

Molecular Pathogenesis of Colorectal Cancer

A
  • Chromosomal Instability Pathway: mutations in APC cause FAP and most sporadic CRC (via adenoma-carcinoma sequence); (firing order of events is AK-53).
  • Microsatellite Instability Pathway: mutations or methylation of mismatch repair genes (eg. MLH1) cause Lynch syndrome and some sporadic CRC (via serrated polyp pathway).
  • Overexpression of COX-2 has been linked to colorectal cancer, NSAIDs may be chemopreventive.
197
Q

Cirrhosis and Portal Hypertension

A

Cirrhosis

  • diffuse bridging fibrosis (via stellate cells) and regenerative nodules disrupt normal architecture of live
  • ↑ risk for hepatocellular carcinoma (HCC)
  • etiologies include alcohol, nonalcoholic steatohepatitis, chronic viral hepatitis, autoimmune hepatitis, biliary disease, and genetic/metabolic disorders

Portal Hypertension

  • ↑ pressure in portal venous system
  • etiologies include cirrhosis (most common cause in Western countries), vascular obstruction (eg. portal vein thrombosis, Budd-Chiari syndrome), and schistosomiasis
198
Q

GI Pathologies:

  • common and potentially fatal bacterial infection in patients with cirrhosis and ascites
  • often asymptomatic, but can cause fevers, chills, abdominal pain, ileus, or worsening encephalopathy
  • commonly caused by aerobic gram ⊝ organisms (eg. E. coli, Klebsiella) or less commonly gram ⊕ Streptococcus
  • Diagnosis:
    • paracentesis with ascitic fluid absolute neutrophil count (ANC) > 250 cells/mm3
  • empiric first-line treatment is 3rd generation cephalosporin (eg. Cefotaxime)
A

Spontaneous Bacterial Peritonitis

199
Q

Serum Markers of Liver Pathology:

Enzymes Released in Liver Damage

A
  • Aspartate Aminotransferase
  • Alanine Aminotransferase
  • Alkaline Phosphatase
  • γ-Glutamyl Transpeptidase
200
Q

Serum Markers of Liver Pathology:

  • released in liver damage
  • ↑ in most liver disease
  • ↑ in alcoholic liver disease
A

Aspartate Aminotransferase
Alanine Aminotransferase

  • ↑ in most liver disease: ALT > AST
  • ↑ in alcoholic liver disease: AST > ALT
  • AST > ALT in nonalcoholic liver disease suggests progression to advanced fibrosis or cirrhosis
201
Q

Serum Markers of Liver Pathology:

  • released in liver damage
  • ↑ in cholestasis (eg. biliary obstruction), infiltrative disorders, and bone disease
A

Alkaline Phosphatase

202
Q

Serum Markers of Liver Pathology:

  • released in liver damage
  • ↑ in various liver and biliary diseases (just as ALP can), but not in bone disease
  • associated with alcohol use
A

γ-Glutamyl Transpeptidase

203
Q

Serum Markers of Liver Pathology:

Functional Liver Markers

A
  • Bilirubin
  • Albumin
  • Prothrombin Time
  • Platelets
204
Q

Serum Markers of Liver Pathology:

  • functional liver marker
  • ↑ in various liver diseases (eg. biliary obstruction, alcoholic or viral hepatitis, cirrhosis) and hemolysis
A

Bilirubin

205
Q

Serum Markers of Liver Pathology:

  • functional liver marker
  • ↓ in advanced liver disease (marker of liver’s biosynthetic function)
A

Albumin

206
Q

Serum Markers of Liver Pathology:

  • functional liver marker
  • ↑ in advanced liver disease (↓ production of clotting factors, thereby measuring the liver’s biosynthetic function)
A

Prothrombin Time

207
Q

Serum Markers of Liver Pathology:

  • functional liver marker
  • ↓ in advanced liver disease (↓ thrombopoietin, liver sequestration) and portal hypertension (splenomegaly/splenic sequestration)
A

Platelets

208
Q

GI Pathologies:

  • rare, often fatal childhood hepatic encephalopathy
  • Findings:
    • mitochondrial abnormalities
    • fatty liver (microvesicular fatty change)
    • hypoglycemia
    • vomiting
    • hepatomegaly
    • coma
  • associated with viral infection (especially VZV and influenza) that has been treated with aspirin
  • Mechanism:
    • aspirin metabolites ↓ β-oxidation by reversible inhibition of mitochondrial enzymes
  • avoid aspirin in children, except in those with Kawasaki disease
A

Reye Syndrome

Reye of sunSHINE:

  • Steatosis of liver/hepatocytes
  • Hypoglycemia/Hepatomegaly
  • Infection (VZV, influenza)
  • Not awake (coma)
  • Encephalopathy
209
Q

Alcoholic Liver Disease:

macrovesicular fatty change that may be reversible with alcohol cessation

A

Hepatic Steatosis

210
Q

Alcoholic Liver Disease:

  • requires sustained, long-term consumption
  • swollen and necrotic hepatocytes with neutrophilic infiltration
  • Mallory Bodies (intracytoplasmic eosinophilic inclusions of damaged keratin filaments)
  • AST > ALT (ratio usually > 2:1)
A

Alcoholic Hepatitis

Make a toAST with alcohol.

211
Q

Alcoholic Liver Disease:

  • final and usually irreversible form
  • sclerosis around central vein may be seen in early disease
  • regenerative nodules surrounded by fibrous bands in response to chronic liver injury → portal hypertension and end-stage liver disease
A

Alcoholic Cirrhosis

212
Q

GI Pathologies:

  • 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
A

Nonalcoholic Fatty Liver Disease

ALT > AST (Lipids)

213
Q

Hepatic Encephalopathy

A
  • cirrhosis → portosystemic shunts → ↓ NH3 metabolism → neuropsychiatric dysfunction
  • reversible neuropsychiatric dysfunction ranging from disorientation/asterixis (mild) to difficult arousal or coma (severe)
  • Triggers:
    • ↑ NH3 production and absorption (due to dietary protein, GI bleed, constipation, infection)
    • ↓ NH3 removal (due to renal failure, diuretics, bypassed hepatic blood flow post-TIPS)
  • Treatment:
    • Lactulose (↑ NH4 + generation)
    • Rifaximin or Neomycin (↓ NH3 producing gut bacteria)
214
Q

GI Pathologies:

  • most common 1° malignant tumor of liver in adults
  • associated with HBV (+/− cirrhosis) and all other causes of cirrhosis (including HCV, alcoholic and nonalcoholic fatty liver disease, autoimmune disease, hemochromatosis, and α1-antitrypsin deficiency) and specific carcinogens (eg. aflatoxin from Aspergillus)
  • may lead to Budd-Chiari syndrome
  • Findings:
    • jaundice
    • tender hepatomegaly
    • ascites
    • polycythemia
    • anorexia
  • spreads hematogenously
  • Diagnosis:
    • ↑ α-fetoprotein
    • ultrasound or contrast CT/MRI
    • biopsy
A

Hepatocellular Carcinoma/Hepatoma

215
Q

GI Pathologies:

  • most common benign liver tumor
  • typically occurs at age 30–50 years
  • biopsy contraindicated because of risk of hemorrhage
A

Cavernous Hemangioma

216
Q

GI Pathologies:

  • rare, benign liver tumor, often related to oral contraceptive or anabolic steroid use
  • may regress spontaneously or rupture (abdominal pain and shock)
A

Hepatic Adenoma

217
Q

GI Pathologies:

  • malignant tumor of endothelial origin
  • associated with exposure to arsenic and vinyl chloride
A

Angiosarcoma

218
Q

GI Pathologies:

  • most common overall liver tumor
  • from GI malignancies, breast and lung cancer
  • rarely solitary
A

Metastases

219
Q

GI Pathologies:

  • thrombosis or compression of hepatic veins with centrilobular congestion and necrosis → congestive liver disease (hepatomegaly, ascites, varices, abdominal pain, liver failure)
  • absence of JVD
  • associated with hypercoagulable states, polycythemia vera, postpartum state, HCC
  • may cause nutmeg liver (mottled appearance)
A

Budd-Chiari Syndrome

220
Q

GI Pathologies:

  • misfolded gene product protein aggregates in hepatocellular ER → cirrhosis with PAS ⊕ globules in liver
  • codominant trait
  • often presents in young patients with liver damage and dyspnea without a history of smoking
  • in the lungs, ↓ α1-antitrypsin → uninhibited elastase in alveoli → ↓ elastic tissue → panacinar emphysema
A

α1-Antitrypsin Deficiency

221
Q

_____ is the abnormal yellowing of the skin and/or sclera due to bilirubin deposition. Hyperbilirubinemia 2° to ↑ production or ↓ disposition (impaired hepatic uptake, conjugation, excretion).

A

Jaundice

222
Q

Common causes of ↑ bilirubin levels include _____.

A

HOT Liver:

  • Hemolysis
  • Obstruction
  • Tumor
  • Liver disease
223
Q

Hyperbilirubinemia:

Unconjugated (Indirect) Hyperbilirubinemia

A
  • Hemolytic,
  • Physiologic (newborns)
  • Crigler-Najjar Syndrome
  • Gilbert Syndrome
224
Q

Hyperbilirubinemia:

Conjugated (Direct) Hyperbilirubinemia

A
  • Biliary Tract Obstruction:
    • gallstones
    • cholangiocarcinoma
    • pancreatic or liver cancer
    • liver fluke
  • Biliary Tract Disease:
    • 1° sclerosing cholangitis
    • 1° biliary cholangitis
  • Excretion Defect:
    • Dubin-Johnson Syndrome
    • Rotor Syndrome
225
Q

Hyperbilirubinemia:

Mixed (Direct and Indirect) Hyperbilirubinemia

A
  • Hepatitis
  • Cirrhosis
226
Q

Physiologic Neonatal Jaundice

A
  • At birth, immature UDP-glucuronosyltransferase → unconjugated hyperbilirubinemia → jaundice/kernicterus (deposition of unconjugated, lipid-soluble bilirubin in the brain, particularly basal ganglia).
  • Occurs after first 24 hours of life and usually resolves without treatment in 1–2 weeks.
  • Treated with phototherapy (non-UV) which isomerizes unconjugated bilirubin to water-soluble form.
227
Q

Hereditary Hyperbilirubinemias are all _____.

A

Autosomal Recessive

228
Q

Hereditary Hyperbilirubinemias:

  • autosomal recessive
  • mildly ↓ UDP-glucuronosyltransferase conjugation and impaired bilirubin uptake
  • asymptomatic or mild jaundice usually with stress, illness, or fasting
  • ↑ unconjugated bilirubin without overt hemolysis
  • relatively common, benign condition
A

Gilbert Syndrome ①

Go! (asymptomatic/benign)

229
Q

Hereditary Hyperbilirubinemias:

  • autosomal recessive
  • absent UDP-glucuronosyltransferase
  • presents early in life
  • patients die within a few years
  • Findings:
    • jaundice
    • kernicterus (bilirubin deposition in brain)
    • ↑ unconjugated bilirubin
  • Treatment:
    • plasmapheresis
    • phototherapy
  • liver transplant is curative
A

Crigler-Najjar Syndrome, Type I ②

No-go! (symptomatic)

*Type II is less severe and responds to Phenobarbital, which ↑ liver enzyme synthesis.

230
Q

Hereditary Hyperbilirubinemias:

  • autosomal recessive
  • conjugated hyperbilirubinemia due to defective liver excretion
  • grossly black liver
  • benign
A

Dubin-Johnson Syndrome ③

Dark liver

231
Q

Hereditary Hyperbilirubinemias:

  • autosomal recessive
  • is similar to Dubin-Johnson syndrome, but milder in presentation without black liver
  • due to impaired hepatic uptake and excretion
A

Rotor syndrome

Regular liver

232
Q

GI Pathologies:

  • autosomal recessive mutations in hepatocyte copper-transporting ATPase (ATP7B gene; chromosome 13) → ↓ copper incorporation into apoceruloplasmin and excretion into bile → ↓ serum ceruloplasmin
  • copper accumulates, especially in liver, brain, cornea, kidneys
  • ↑ urine copper
  • presents before age 40 with liver disease (eg. hepatitis, acute liver failure, cirrhosis), neurologic disease (eg. dysarthria, dystonia, tremor, parkinsonism), psychiatric disease, Kayser-Fleischer rings (deposits in Descemet membrane of cornea), hemolytic anemia, and renal disease (eg. Fanconi syndrome)
  • Treatment:
    • chelation with penicillamine or trientine
    • oral zinc
A

Wilson Disease (Hepatolenticular Degeneration)

233
Q

GI Pathologies:

  • autosomal recessive
  • C282Y mutation > H63D mutation on HFE gene, located on chromosome 6
  • associated with HLA-A3
  • leads to abnormal iron sensing and ↑ intestinal absorption (↑ ferritin, ↑ iron, ↓ TIBC → ↑ transferrin saturation)
  • iron overload can also be 2° to chronic transfusion therapy (eg. β-thalassemia major)
  • iron accumulates, especially in liver, pancreas, skin, heart, pituitary, joints
  • Hemosiderin (iron) can be identified on liver MRI or biopsy with Prussian blue stain
A

Hemochromatosis

234
Q

GI Pathologies:

  • presents after age 40 when total body iron > 20 g
  • iron loss through menstruation slows progression in women
  • classic triad of cirrhosis, diabetes mellitus, and skin pigmentation (“bronze diabetes”)
  • also causes restrictive cardiomyopathy (classic) or dilated cardiomyopathy (reversible), hypogonadism, arthropathy (calcium pyrophosphate deposition; especially metacarpophalangeal joints)
  • HCC is the common cause of death
A

Hemochromatosis

235
Q

Hemochromatosis is treated with _____.

A
  • Repeated Phlebotomy
  • Dhelation
    • Deferasirox
    • Deferoxamine
    • Oral Deferiprone
236
Q

GI Pathologies:

  • may present with pruritus, jaundice, dark urine, light-colored stool, and hepatosplenomegaly
  • typically with cholestatic pattern of LFTs (↑ conjugated bilirubin, ↑ cholesterol, ↑ ALP)
A

Biliary Tract Disease

237
Q

Biliary Tract Disease:

  • unknown cause of concentric “onion skin” bile duct fibrosis → alternating strictures and dilation with “beading” of intra- and extrahepatic bile ducts on ERCP and magnetic resonance cholangiopancreatography (MRCP)
  • classically in middle-aged men with IBD
  • associated with ulcerative colitis
  • p-ANCA ⊕
  • ↑ IgM
  • can lead to 2° biliary cholangitis
  • ↑ risk of cholangiocarcinoma and gallbladder cancer
A

Primary Sclerosing Cholangitis

238
Q

Biliary Tract Disease:

  • autoimmune reaction → lymphocytic infiltrate + granulomas → destruction of lobular bile ducts
  • classically in middle-aged women
  • anti-mitochondrial antibody ⊕,
  • ↑ IgM
  • associated with other autoimmune conditions (eg. Sjögren syndrome, Hashimoto thyroiditis, CREST, rheumatoid arthritis, celiac disease)
A

Primary Biliary Cholangitis

239
Q

Biliary Tract Disease:

  • extrahepatic biliary obstruction → ↑ pressure in intrahepatic ducts ↑ injury/ fibrosis and bile stasis
  • patients with known obstructive lesions (gallstones, biliary strictures, pancreatic carcinoma)
  • may be complicated by ascending cholangitis
A

Secondary Biliary Cholangitis

240
Q

GI Pathologies:

  • caused by ↑ cholesterol and/or bilirubin, ↓ bile salts, and gallbladder stasis
  • ↑ risk in females, obese, multipara and ≥ 40 y.o.
  • most common complication is cholecystitis
  • can also cause acute pancreatitis and ascending cholangitis
  • diagnose with ultrasound
  • treat with elective cholecystectomy if symptomatic
A

Gallstones (Cholelithiasis)

Risk Factors (4 F’s):

  • Female
  • Fat
  • Fertile (multiparity)
  • Forty
241
Q

Gallstones (Cholelithiasis):

  • associated with nausea/vomiting and dull RUQ pain
  • neurohormonal activation (eg. by CCK after a fatty meal) triggers contraction of gallbladder, forcing stone into cystic duct
  • labs are normal
  • ultrasound shows cholelithiasis
A

Biliary Colic

242
Q

Gallstones (Cholelithiasis):

  • presence of gallstone(s) in common bile duct
  • leads to elevated ALP, GGT, direct bilirubin, and/or AST/ALT
A

Choledocholithiasis

243
Q

Gallstones (Cholelithiasis):

acute or chronic inflammation of gallbladder

A

Cholecystitis

244
Q

Cholecystitis:

  • most common type
  • due to gallstone impaction in the cystic duct resulting in inflammation and gallbladder wall thickening
  • can produce 2° infection
A

Calculous Cholecystitis

245
Q

Cholecystitis:

  • due to gallbladder stasis, hypoperfusion, or infection (CMV)
  • seen in critically ill patients
  • Murphy Sign:
    • inspiratory arrest on RUQ palpation due to pain
    • pain may radiate to right shoulder (due to irritation of phrenic nerve)
    • ↑ ALP if bile duct becomes involved (eg. ascending cholangitis)
  • diagnose with ultrasound or cholescintigraphy (HIDA scan)
  • failure to visualize gallbladder on HIDA scan suggests obstruction
A

Acalculous Cholecystitis

246
Q

Cholecystitis:

  • fistula between gallbladder and GI tract → stone enters GI lumen → obstructs at ileocecal valve (narrowest point)
  • can see air in biliary tree (pneumobilia)
A

Gallstone Ileus

247
Q

Gallstones (Cholelithiasis):

  • calcified gallbladder due to chronic cholecystitis
  • usually found incidentally on imaging
  • treated with prophylactic cholecystectomy due to high rates of gallbladder cancer (mostly adenocarcinoma)
A

Porcelain Gallbladder

248
Q

Gallstones (Cholelithiasis):

  • infection of biliary tree usually due to obstruction that leads to stasis/bacterial overgrowth
  • Charcot Triad:
    • jaundice
    • fever
    • RUQ pain
  • Reynolds Pentad:
    • Charcot Triad
    • altered mental status
    • shock (hypotension)
A

Ascending Cholangitis

249
Q

GI Pathologies:

  • autodigestion of pancreas by pancreatic enzymes
  • Diagnosis by 2 of 3 Criteria:
    • acute epigastric pain often radiating to the back
    • ↑ serum amylase or lipase (more specific) to 3× upper limit of normal
    • characteristic imaging findings
  • Complications:
    • pseudocyst (lined by granulation tissue, not epithelium)
    • abscess, necrosis
    • hemorrhage
    • infection
    • organ failure (ARDS, shock, renal failure)
    • hypocalcemia (precipitation of Ca2+ soaps)
A

Acute Pancreatitis

250
Q

Causes of Acute Pancreatitis

A

I GET SMASHED:

  • Idiopathic
  • Gallstones
  • Ethanol
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune disease
  • Scorpion sting
  • Hypercalcemia/Hypertriglyceridemia (> 1000 mg/dL)
  • ERCP
  • Drugs (eg. sulfa drugs, NRTIs, protease inhibitors)
251
Q

GI Pathologies:

  • chronic inflammation, atrophy, calcification of the pancreas
  • major causes include alcohol abuse and genetic predisposition (ie. cystic fibrosis)
  • can be idiopathic
  • complications include pancreatic insufficiency and pseudocysts
  • pancreatic insufficiency (typically when <10% pancreatic function) may manifest with steatorrhea, fat-soluble vitamin deficiency, and diabetes mellitus
  • amylase and lipase may or may not be elevated (almost always elevated in acute pancreatitis)
A

Chronic Pancreatitis

252
Q

GI Pathologies:

  • very aggressive tumor arising from pancreatic ducts (disorganized glandular structure with cellular infiltration)
  • often metastatic at presentation, with average survival ~ 1 year after diagnosis
  • tumors more common in pancreatic head (obstructive jaundice)
  • associated with CA 19-9 tumor marker (also CEA, less specific)
  • ↑ risk with tobacco use, chronic pancreatitis (especially > 20 years), diabetes, > 50 y.o., Jewish and African-American males
  • Findings:
    • abdominal pain radiating to back
    • weight loss (due to malabsorption and anorexia)
    • Migratory Thrombophlebitis—redness and tenderness on palpation of extremities (Trousseau Syndrome)
    • obstructive jaundice with palpable, nontender gallbladder (Courvoisier Sign)
  • Treatment:
    • Whipple procedure
    • chemotherapy
    • radiation therapy
A

Pancreatic Adenocarcinoma

253
Q

Acid Suppression Therapy

A
254
Q

Acid Suppression Therapy:

Histamine-2 Blockers

A

Dine on a table for 2:

  • Cimetidine
  • Ranitidine
  • Famotidine
  • Nizatidine
255
Q

Acid Suppression Therapy:

  • reversible block of histamine H2-receptors → ↓H+ secretion by parietal cells
  • used for peptic ulcer, gastritis, and mild esophageal reflux
A

Histamine-2 Blockers

256
Q

Acid Suppression Therapy:

  • histamine-2 blocker
  • potent inhibitor of cytochrome P-450 (multiple drug interactions)
  • also has antiandrogenic effects (prolactin release, gynecomastia, impotence, ↓ libido in males)
  • can cross blood-brain barrier (confusion, dizziness, headaches) and placenta
  • ↓ renal excretion of creatinine
A

Cimetidine

257
Q

Acid Suppression Therapy:

  • histamine-2 blocker
  • ↓ renal excretion of creatinine
A
  • Cimetidine
  • Ranitidine
258
Q

Acid Suppression Therapy:

Proton Pump Inhibitors

A
  • Omeprazole
  • Lansoprazole
  • Esomeprazole
  • Pantoprazole
  • Dexlansoprazole
259
Q

Acid Suppression Therapy:

  • irreversibly inhibit H+/K+ ATPase in stomach parietal cells
  • used for peptic ulcer, gastritis, esophageal reflux, Zollinger-Ellison syndrome, component of therapy for H. pylori, and stress ulcer prophylaxis
  • ↑ risk of C. difficile infection, pneumonia, and acute interstitial nephritis
  • ↓ serum Mg2+ with long-term use
  • ↓ serum Mg2+ and ↓ Ca2+ absorption (potentially leading to increased fracture risk in elderly)
A

Proton Pump Inhibitors

260
Q

Acid Suppression Therapy:

  • can affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying
  • all can cause hypokalemia
  • overuse can also cause the following problems
A

Antacids

261
Q

Antacids:

  • constipation and hypophosphatemia
  • proximal muscle weakness
  • osteodystrophy
  • seizures
A

Aluminum Hydroxide

Aluminimum amount of feces.

262
Q

Antacids:

  • hypercalcemia (milk-alkali syndrome)
  • rebound acid ↑
  • can chelate and ↓ effectiveness of other drugs (eg. tetracycline)
A

Calcium Carbonate

263
Q

Antacids:

  • diarrhea
  • hyporeflexia
  • hypotension
  • cardiac arrest
A

Magnesium Hydroxide

Mg2+ = must go to the bathroom

264
Q

Acid Suppression Therapy:

  • bind to ulcer base, providing physical protection and allowing HCO3– secretion to reestablish pH gradient in the mucous layer
  • require acidic environment
  • usually not given with PPIs/H2 blockers
  • ↑ ulcer healing
  • used for travelers’ diarrhea
A
  • Bismuth
  • Sucralfate
265
Q

Acid Suppression Therapy:

  • PGE1 analog
  • ↑ production and secretion of gastric mucous barrier
  • ↓ acid production
  • prevention of NSAID-induced peptic ulcers (NSAIDs block PGE1 production)
  • also used off-label for induction of labor (ripens cervix)
  • causes diarrhea
  • contraindicated in women of childbearing potential (abortifacient)
A

Misoprostol

266
Q

GI Drugs:

  • long-acting somatostatin analog
  • inhibits secretion of various splanchnic vasodilatory hormones
  • used for acute variceal bleeds, acromegaly, VIPoma, and carcinoid tumors
  • causes nausea, cramps, and steatorrhea
  • ↑ risk of cholelithiasis due to CCK inhibition
A

Octreotide

267
Q

GI Drugs:

  • a combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory)
  • activated by colonic bacteria
  • used for ulcerative colitis and Crohn disease (colitis component)
  • causes malaise, nausea, sulfonamide toxicity, and reversible oligospermia
A

Sulfasalazine

268
Q

GI Drugs:

  • agonist at μ-opioid receptors
  • slows gut motility
  • poor CNS penetration (low addictive potential)
  • used for diarrhea
  • causes constipation and nausea
A

Loperamide

269
Q

GI Drugs:

  • 5-HT3 antagonist
  • ↓ vagal stimulation
  • powerful central-acting antiemetic
  • control vomiting postoperatively and in patients undergoing cancer chemotherapy
  • causes headache, constipation, QT interval prolongation, and serotonin syndrome
A

Ondansetron

270
Q

GI Drugs:

  • D2 receptor antagonist
  • ↑ resting tone, contractility, LES tone, motility, promotes gastric emptying
  • does not influence colon transport time
  • used in diabetic and postsurgery gastroparesis, antiemetic therapy, and persistent GERD
  • causes ↑ parkinsonian effects, tardive dyskinesia, restlessness, drowsiness, fatigue, depression, and diarrhea
  • drug interaction with digoxin and diabetic agents
  • contraindicated in patients with small bowel obstruction or Parkinson disease (due to D2-receptor blockade)
A

Metoclopramide

271
Q

GI Drugs:

  • inhibits gastric and pancreatic lipase → ↓ breakdown and absorption of dietary fats
  • used for eight loss
  • causes abdominal pain, flatulence, and bowel urgency/frequent bowel movements
  • ↓ absorption of fat-soluble vitamins
A

Orlistat

272
Q

GI Drugs:

indicated for constipation or patients on opiates requiring a bowel regimen

A

Laxatives

273
Q

Laxatives:

  • soluble fibers draw water into gut lumen, forming a viscous liquid that promotes peristalsis
  • causes bloating
A

Bulk-Forming Laxatives:

  • Psyllium
  • Methylcellulose
274
Q

Laxatives:

  • provides osmotic load to draw water into GI lumen
  • causes diarrhea and dehydration
  • may be abused by bulimics
A

Osmotic Laxatives

  • Magnesium Hydroxide
  • Magnesium Citrate
  • Polyethylene Glycol
  • Lactulose
    • treats hepatic encephalopathy
    • gut flora degrade lactulose into metabolites (lactic acid, acetic acid) that promote nitrogen excretion as NH4+
275
Q

Laxatives:

  • enteric nerve stimulation
  • → colonic contraction
  • causes diarrhea and melanosis coli
A

Stimulants

  • Senna
276
Q

Laxatives:

  • promotes incorporation of water and fat into stool
  • causes diarrhea
A

Emollients

  • Docusate
277
Q

GI Drugs:

  • substance P antagonist
  • blocks NK1 (neurokinin-1) receptors in brain
  • used as an antiemetic for chemotherapy-induced nausea and vomiting
A

Aprepitant

USMLE Step 1 (18 decks)

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