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Flashcards in Gastrointestinal Deck (302):
1

Retroperitoneal structures:

"SAD PUCKER"
-Suprarenal (adrenal) gland
-Aorta and IVC
-Duodenum (2nd, 3rd, and 4th parts)
-Pancreas (except tail)
-Ureters
-Colon (descending and ascending)
-Kidneys
-Esophagus (lower 2/3)
-Rectum (upper 2/3)

2

GI ligament that is a derivative of the fetal umbilical vein? what structure does it contain? what does it connect?

Falciform ligament
-contains the ligamentum teres
-derivative of the fetal umbilical vein
-connects liver to anterior abdominal wall

3

GI ligament that contains the portal triad (hepatic artery, portal vein, common bile duct)?

Hepatoduodenal ligament

4

Which GI ligament may be compressed to control bleeding by placing fingers in the omental foramen?

Hepatoduodenal ligamentf

5

Frequency of waves/peristalsis in stomach? duodenum? ileum?

stomach--> 3 waves/min
duodenum--> 12 waves/min
ileum--> 8-9 waves/min

6

Meissner's plexus:
-where's it located?
-other name?
-what's its function?

-located in Submucosa
-"submucosal plexus"
-controls secretory activity; secretes mucus (so is near the lumen...)

7

Auerbach's plexus:
-where's it located?
-other name?
-what's its function?

-located in Musculara externa (really, between muscularis externa inner circular and outer longitudinal layers)
-"Myenteric plexus"
-controls muscle contractions; coordinates motility along entire gut wall

8

Roles of the mucosa of the GI tract?

mucosa = innermost layer of gut wall
*has 3 parts, each with a role:
-epithelium--> absorption
-lamina propria--> support
-muscularis mucosa--> motility

9

cell type in esophagus?

stratified squamous epithelium

10

cell type in stomach?

gastric glands

11

where in GIT are Brunner's glands?

Duodenum
-->submucosal glands that produce alkaline-rich/bicarb secretion

12

Where in GIT are Crypts of Lieberkuhn?

Duodenum, Jejunum, Ileum, and Colon

13

Where in GIT are villi and microvilli?

Small intestine; not Colon (makes sense, b/c villi are there to increase absorptive surface)

14

Where in GIT are goblet cells?

Ileum--> has most goblet cells in the small intestine; but, also found in other parts of small intestine: as go along the small intestine, # of goblet cells increases

15

Where in GIT are Peyer's patches?

only in Ileum

16

Where does celiac trunk come off the abdominal aorta?

T12

17

Where does the SMA come off the abdominal aorta?

L1

18

Where do the renal arteries come off the abdominal aorta?

L1

19

Where does the inferior mesenteric artery come off the abdominal aorta?

L3

20

What level is the bifurcation of the abdominal aorta?

L4

21

Muscle types composing the Esophagus:

*upper 3rd--> striated muscle (voluntary)
*middle 3rd--> striated + smooth muscle
*lower 3rd--> smooth muscle (involuntary)

22

Artery that supplies the Foregut? Innervation of the foregut?

-Celiac artery
-Vagus nerve

23

Artery and Nerve that supply the Midgut?

-SMA
-Vagus nerve

24

Artery and Nerve that supply the hindgut?

-IMA
-Pelvic nerve

25

Watershed area of the GIT?

=> splenic flexure
-supplied by the terminal branches of the IMA and SMA, so most sensitive to hypoxia

26

What structures make up the foregut? midgut? hindgut?

*foregut: stomach to proximal duodenum; also: liver, gallbladder, pancreas, spleen

*midgut: Distal duodenum to proximal 2/3 of transverse colon

*hindgut: distal 1/3 or transverse colon to upper part of rectum; inludes splenic flexure (watershed area)

27

Portal triad:

-Hepatic artery
-Portal vein
-Common bile duct

28

Branches of celiac trunk?

*celiac trunk comes off abdominal aorta at T12
*branches:
-common hepatic artery
-splenic artery
-left gastric artery

--> these branches make up the main blood supply of the stomach!

29

Which arteries supply the lesser curvature of the stomach? greater curvature?

*lesser curvature --> L and R gastric arteries (L gastric comes off the Celiac trunk; the two gastrics anastamose)
*Greater curvature: L and R gastro-omental arteries (also anastomose with each other)

30

3 Portosystemic shunts (alleviate portal hypertension)

1) Esophageal varices --> anastomosis at the esophagus

2) Caput medusae --> anastomosis at the umbilicus

3) Internal hemorrhoids --> anastomosis at the rectum

31

type of hemorrhoids and cancers seen above and below the pectinate line:

*above pectinate line:
-internal hemorrhoids (not painful)
-adenocarcinoma

*below pectinate line:
-external hemorrhoids (painful)
-squamous cell carcinoma (main risk factor for squamous cell carcinoma here = HPV 16,18,31)

32

Pathway of bile: from production to secretion into duodenum:

Bile made in liver --> R and L hepatic ducts --> Common hepatic duct --> some into common bile duct, some into cystic duct --> from cystic duct, stored in gallbladder, then released back into cystic duct when needed, into common bile duct --> common bile duct meets pancreatic duct at Ampulla of Vater --> bile released via Sphincter of Oddi into Ampulla of Vater in duodenum!

33

Lodging of a gallstone where may lead to obstruction of both bile and pancreatic ducts?

if gallstone is lodged in Ampulla of Vater

34

What sort of tumor may obstruct the common bile duct?

Tumors of head of pancreas --> can compress ampulla, like a gallstone, thus obstructing common bile duct

35

Lateral to Medial organization of the Femoral Region:

Lateral: "NAVeL" :Medial
-Nerve
-Artery
-Vein
-Lymphatics

36

Femoral triangle:
-formed by?
-contains?

*formed by:
-inguinal ligament
-sartorius muscle
-adductor longus muscle

*contains:
-femoral nerve, artery, vein (lateral-->medial)

37

What does the femoral sheath contain?

-Contains femoral vein, artery, and lymphatics, but NOT femoral nerve

38

Sliding vs Paraesophageal Hiatal Hernias:

*Both are types of diaphragmatic hernias, which occur at the gastro-esophageal jxn; stomach herniates upward through the esophageal hiatus of the diaphragm.

-sliding hiatal hernia: GE jxn is displaced; have an "hourglass stomach"

-paraesophageal hernia: GE jxn is normal; cardia of stomach moves into the thorax

39

"hourglass stomach"

sliding hiatal hernia

40

What kind of inguinal hernia occurs in infants?

INdirect inguinal hernia in INfants
-->goes through the INternal/deep inguinal ring, external/superficial inguinal ring, and into the scrotum (Basically, follows the path of the testes)

-->occurs in infants d/t failure of processus vaginalis to close

--> Covered by all 3 layers of spermatic fascia

41

What type of inguinal hernia passes through the inguinal/Hesselbach's triangle?

Direct inguinal hernia
--> only covered by external spermatic fascia (unlike indirect, which is covered by all 3 layers)
-->usually in older men

42

Hernia that's most common in women?

Femoral hernia

43

Hernia that's a leading cause of bowel incarceration/obstruction?

Femoral Hernia

44

Hesselbach's triangle:
-borders?
-what type of hernia goes through it?

*Borders:
-inguinal ligament
-inferior epigastric artery
-lateral border of rectus abdominis

*Direct inguinal hernias (older men) go through Hesselbach's triangle

45

G cells (antrum of stomach) secrete?

Gastrin ("pro-gastric")

46

I cells (duodenum, jejunum) secrete?

CCK ("pro-duodenum", "anti-gastric"--> CCK stimulates pancreatic secretions)

47

S cells (duodenum) secrete?

Secretin ("pro-HCO3", "nature's antacid")

48

D cells (pancreatic islets, GI mucosa) secrete?

Somatostatin (inhibits everything!)

49

Which hormone is increased in Zollinger-Ellison syndrome?

Gastrin
="gastrinoma"

50

Which GI hormone is stimulated by Phenylalanine and Tryptophan?

Gastrin

51

What AAs may stimulate gastrin release?

Phenylalanine and Tryptophan

52

What does CCK cause?

Stimulates pancreatic secretion, gallbladder contraction, and gastric emptying

53

What does Secretin do?

Stimulates pancreatic HCO3- secretion, decreased gastric acid secretion, increased bile secretion
--> it's "nature's antacid" --> neutralizes gastric acid in duodenum to allow pancreatic enzymes to function

54

Somatostatin:
-where is it secreted from?
-what does it do?

-secreted from D cells in pancreas (islets) and GI mucosa
-inhibits:
-->decreased gastric acid and pepsinogen secretion
-->decreased pancreatic and intestinal secretions
-->decreased gallbladder contraction (so, if lots of somatostatin, may get biliary stones)
-->decreases insulin and glucagon release

***so overall inhibits digestion and absorption of substances needed for growth...

55

What is used more rapidly: oral glucose load or equivalent given by IV?

oral glucose is used more rapidly, d/t GIP = Gastric Inhibitory Peptide = Glucose-dependent insulinotropic peptide

56

VIP = Vasoactive Intestinal Peptide:
-secreted from?
-actions?

*source: Parasympathetic ganglia in sphincters, gallbladder, small intestine

*actions:
-increases intestinal water and electrolytes secretion
-increases relaxation of intestinal smooth muscle and sphincters

57

VIPoma:
-origin
-symptoms?

non-alpha, non-beta pancreatic islet cell tumor
-may be associated with MEN I
-secretes VIP
-symptoms:
-->tons of watery diarrhea (b/c VIP stimulates intestinal water and electrolyte secretion) --> so, as a result also have: dehydration, hypokalemia, etc...

58

Endocrine tumor that leads to lots of watery diarrhea?

VIPoma (pancreatic tumor, secretes tons of VIP)

59

Action = binds vitamin B12 to allow uptake of B12 in terminal ileum?

Intrinsic Factor

60

Which substances are secreted by Parietal Cells of stomach?

-Intrinsic Factor
-Gastric Acid

61

Gastrinoma

gastrin-secreting tumor; get constant high levels of acid secretions and ulcers
-->=zollinger-ellison syndrome

62

Secreted by chief cells of stomach

Pepsin

63

Action of pepsin?

protein digestion

64

what activates pepsinogen-->pepsin?

Acid (H+)

65

Which cells secrete HCO3-?

-mucosal cells (in stomach, duodenum, salivary glands, pancreas)
-Brunner's glands (in submucosa of duodenum)

66

How do NSAIDs lead to acidic damage in stomach?

-Prostaglandins generate mucus that covers that covers the gastric epithelium
-->NSAIDs-->decrease PGs--> decrease mucus --> decrease HCO3- --> increased susceptibility to acidic damage in stomach

67

Which glands secrete saliva? What stimulates saliva secretion (PSNS, SNS?)? When is saliva hypotonic/isotonic?

-secreted from parotid, submandibular, sublingual glands
-stimulated by Sympathetic AND Parasympathetic activity
-Normally is hypotonic, but is more isotonic with higher flow rates, b/c less time for absorption

***Sympathetic stimulation--> thicker secretions
***Parasympathetic stimulation--> watery secretions

68

How does Gastrin stimulate acid secretion in stomach?

G cells in antrum of stomach are stimulated by vagus nerve (via GRP transmitter)--> release Gastrin into circulation --> Gastrin stimulates ECL (EnteroChromaffin-Like) cells to release Histamine --> Histamine induces Parietal cells to secrete HCl

69

Affects of atropine on GI secretions?

Atropine = anti-cholinergic
--> blocks vagal stimulation of parietal cells (use ACh as transmitter)
--> BUT, no effect on G cell stimulation by vagal cells, because G cells use a different transmitter, GRP (not ACh) --> so, Gastrin can still stimulate parietal cells to secrete Intrinsic Facor and (via enterochromaffin-like cells and histamine) to secrete HCl

70

How do prostaglandins protect the stomach?

-decrease acid secretion (Gi-->decreased cAMP-->decreased proton pumping)
-increase mucus and HCO3- production

71

3 factors that stimulate G-cells to make Gastrin?

-Hypercalcemia
-Phenylalanine
-Tryptophan

72

What may cause hypertrophy of Brunner's glands?

Peptic ulcer disease (b/c lots of acid to deal with)
-->Brunner's glands are located in duodenal submucosa; function = secrete alkaline mucus to neutralize acid contents entering duodenum from stomach

73

Trypsinogen:
-secreted by?
-converted to trypsin by?
-action?

-secreted by pancreas
-enterokinase/enteropeptidase converts trypsinogen-->trypsin
-converts other proenzymes/zymogens and more trypsinogen to active form
-trypsin (and other zymogens)--> involved in protein digestion

74

alpha-amylase

secreted by pancreas
-digests starch
***also have amylase in saliva, which digests starch in saliva

75

Lipase

secreted by pancreas
-digests fat

76

salivary amylase vs pancreatic amylase:

*both digest starch
-salivary: hydrolyzes alpha-1,4-linkages to form disaccharides
-pancreatic: hydrolyzes starch to oligosaccharides and disaccharides

77

D-Xylose absorption test

Test to distinguish GI mucosal damage from other causes of malabsorption
-->D-xylose is normally easily absorbed by intestines; if problem with intestinal absorption, get low levels of D-xylose in urine and blood

78

SGTL1 = Sodium-Glucose-Co-Transporter:

Na-dependent transporter; absorbs Glucose and Galactose in enterocytes

79

GLUT-5

absorbs Fructose (by facilitated diffusion) into enterocytes

80

GLUT-2

Transports all monosaccharides (Glucose, Galactose, Lactose) from intestines into blood

81

Where in GIT is Iron absorbed?

Duodenum

82

Where in GIT is folate absorbed?

Jejunum

83

Where in GIT is Vitamin B12 absorbed?

Terminal ileum, along with bile acids; requires intrinsic factor (from parietal cells)!

84

Peyer's patches:
-where?
-function?

-located in ileum
-Peyer's patches = lymphoid tissue in lamina propria and submucosa of small intestine
-function:
-->contain M-cells that take up antigen
-->B-cells stimulated in germinal centers of Peyer's patches differentiate into IgA-secreting plasma cells. IgA ultimately resides in lamina propria. IgA protects gut from pathogens!

85

Lymphoid tissue of the GIT?

Peyer's patches
-located in ileum
-B-cells in germinal centers of Peyer's patches differentiate into IgA-secreting plasma cells --> IgA lives in lamina propria and protects gut from pathogens!

86

specialized M-cells that take up antigen in GIT?

-in Peyer's patches --> the lymphoid tissue of GIT!

87

IgA in GIT comes from?

Peyer's patches: have B-cells in germinal centers of Peyer's patches (lymphoid tissue) that differentiate into IgA-secreting plasma cells
-->IgA protects the gut from pathogens!

88

Only way body can excrete cholesterol?

Bile

89

How is copper excreted from the body?

Bile; can't excrete it in Wilson's disease though...

90

3 functions of Bile:

1) Digest and absorb lipids and fat-soluble vitamins
2) Excrete cholesterol
3) Anti-microbial activity (by disrupting membranes)

91

Pale/Clay-colored stools?

-problem processing bilirubin

92

Cholestyramine

-Bile Acid Resin --> a lipid-lowering agent
-->interferes with ability to reabsorb Urobilinogen--> so, more is excreted in stool or kidney; the liver then must use cholesterol to make more...

93

Colestipol

Bile-acid resin (like Cholestyramine; lipid-lowering agent)

94

Colesevelam

-Bile-acid resin (like cholestyramine; lipid-lowering agent)

95

Urobilin

breakdown product of bilirubin, excreted in urine; gives urine it's color

96

Stercobilin

breakdown product of bilirubin, excreted in feces; gives color of stool (without it, have pale/clay-colored stool)

97

Urobilinogen

-breakdown product of conjugated/direct bilirubin, after gut bacteria alter it in the gut; has 3 possible fates:
1) excreted in feces as Stercobilin (about 80% of it)
2) excreted in urine as Urobilin (very little of it --> about 2%)
3) reabsorbed by liver via enterohepatic circulation (about 18% of it)

98

Biggest risk factor for a malignant salivary gland tumor?

Smoking

99

most common location of benign salivary gland tumor?

Parotid gland

100

Pleomorphic salivary gland adenoma:

-most common salivary gland tumor
-painless, movable mass, benign, recurs

101

Warthin's tumor

-benign salivary gland tumor; trapped in a lymph node, surrounded by lymph tissue

102

Mucooepidermoid carcinoma

-most common malignant salivary gland tumor

103

loss of Myenteric/Auerbach's plexus?

Achalasia
-->can't relax Lower Esophageal Sphincter
-->get esophageal aperistalsis
-->progressive dysphagia of solids and liquids (vs obstruction, which is dysphagia to solids only)
-->increased risk of esophageal carcinoma

104

Bird's beak on barium swallow

Achalasia (esophageal aperistalsis; can't relax LES d/t loss of Myenteric/Auerbach's plexus)

105

2 conditions that may lead to secondary achalasia?

-Chaga's disease (mega-esophagus)
-CREST scleroderma (Esophageal dysmotility)

106

increased risk of what cancer with Achalasia?

--> esophageal carcinoma

107

progressive dysphagia of solids AND liquids, vs just solids vs progressive dysphagia first of solids THEN of liquids?

*solids + liquids--> Achalasia
*only solids--> obstruction
*solids, then liquids--> esophageal cancer

108

Painless bleeding in lower 1/3rd of esophagus?

Esophageal varices
-->associated with portal HTN

109

Dysphagia + Glossitis (swollen, smooth tongue) + Iron-deficiency anemia

Plummer-Vinson syndrome
-->Dysphagia is d/t esophageal webs = thin membrane-like protrusion into esophagus
-->associated with increased risk of Squamous Cell Carcinoma of Esophagus

110

Boerhaave syndrome:

-TRANSMURAL esophageal rupture d/t violent vomiting
--> vs Mallory-Weiss which is just lacerations at the G-E jxn

111

Esophageal pathology associated with lye ingestion and acid reflux?

Esophageal strictures

112

Barrett's esophagus: what sort of metaplasia occurs? increased risk of what kind of cancer?

Glandular metaplasia: squamous epithelium of distal esophagus is replaced with columnar/intestinal epithelium
-d/t chronic GERD
-assoc w/increased risk of Adenocarcinoma of esophagus
-also associated with esophagitis and esophageal ulcers

113

What type of esophageal cancer is most common worlwide? in US?

-worlwide: Squamous cell > Adenocarcinoma
-US: Adenocarcinoma > Squamous Cell

114

*What part of esophagus is affected in each of these cancers?
-What risk factors cause Squamous Cell Carcinoma?
-What risk factors associated with Adenocarcinoma?

*Squamous Cell: upper 2/3
-smoking
-alcohol
-achalasia
-esophageal webs (ie Plummer-Vinson syndrome)

*Adenocarcinoma: lower 1/3
-Barret's esophagus
-Esophagitis
-Diverticula (like Zenker's)

115

Whipple's disease:

-Tropheryma whippelii infection (gram +)
-PAS + foamy macrophages in intestinal lamina propria
-mostly older men
-CAN:
-->cardiac symptoms
-->Arthralgias
-->Neurologic symptoms
***Also, classic malabsorption symptoms: diarrhea, steatorrhea, weight loss, weakness
-treat with antibiotics!

116

Which part of intestine is affected in Celiac sprue?

-Proximal small bowel, mostly

117

What part of intestine is affected in lactase deficiency?

only tips of intestinal villi (b/c that's where lactase is located)
-->so, get normal look villi

118

fat accumulation in enterocytes + malabsorption in childhood + neurologic manifestations?

Abeta-lipoproteinemia
-->have decreased synthesis of apo-B --> can't generate chylomicrons --> decreased secretion of cholesterol and VLDL into bloodstream --> so, fat accumulates in enterocytes
***this is a malabsorption syndrome
-treat with vitamin E supplementation (helps body produce some apoproteins)

119

Causes of pancreatic insufficiency? What must be supplemented?

Causes:
-cystic fibrosis
-obstructing cancer
-chronic pancreatitis

*get malabsorption of fat and fat-soluble vitamins (A, D, E, K)
*get increased fat in stool
*treat by pancreatic enzyme replacement, limit fat intake, and supplement A, D, E, K.

120

List the Malabsorption syndromes:

"These Will Cause Devastating Absorption Problems"
-Tropical sprue
-Whipple's disease
-Celiac sprue
-Disaccharidase deficiency (like lactose intolerance)
-Abetalipoproteinemia
-Pancreatic insufficiency

121

Blunting of villi + Crypt hyperplasia in small intestines?

Celiac sprue

122

Curling's ulcer

Burning of the esophagus --> can lead to sloughing of gasric mucosa and Acute Erosive Gastritis

123

Cushing's ulcer

Brain injury that can lead to Acute Erosive Gastritis:
brain injury--> increased vagal stimulation --> increased ACh --> increased H+ production --> Gastritis

124

Main causes of Acute Erosive Gastritis:

*Acute Erosive Gastritis = disrupton of mucosal barrier --> inflammation

*Main causes:
-Alcoholics
-Pts taking daily NSAIDs (ie Rheumatoid Arthritis pts)
-Curling's ulcer = burning esophagus
-Cushing's ulcer = brain injury resulting in increased vagal stimulation
-Stress

125

Autoimmune disorder with:
-autoantibodies to parietal cells
-pernicious anemia (b/c no parietal cells, so no IF, so no B12)
-Achlorydia (b/c no acid from parietal cells)

Chronic/Non-erosive gastritis of the Fundus/Body = Type A

126

Cause of chronic/non-erosive gastritis to the fundus/body of the stomach

Autoimmune disorder with:
-autoantibodies to parietal cells
-pernicious anemia
-achlorydia

127

Cause of chronic/non-erosive gastritis affecting the antrum of the stomach?

H. pylori
-this is the most common type of chronic gastritis
-increased risk of MALT lymphoma

128

What part of the stomach does H. pylori affect?

Antrum

129

Disease in which rugae of stomach look like brain gyrae?

Menetrier's disease
-->gastric hypertrophy
-protein loss
-parietal cell atrophy
-increased mucous cells
-precancerous
-->rugae are so hypertrophied that look like brain gyri!

130

Main type of stomach cancer?

Adenocarcinoma (almost always)

131

Acanthosis nigricans

seen in hyperinsulinemia and in visceral malignancies; often seen in gastric adenocarcinoma

132

Virchow's node:

metastasis from stomach to left supraclavicular node

133

Krukenberg's tumor:

bilateral metastasis from stomach to ovaries
-->see lots of mucus and signet ring cells in ovaries

134

Sister Mary Joseph's nodule:

metastasis from stomach adenocarcinoma to subcutaneous periumbilical area

135

signet ring cells

cells seen in diffuse stomach cancer
-->filled with mucin; nucleus is pushed to periphery
-->see in stomach; also see if metastasis from stomach to ovaries (Krukenber's tumor)

136

Linitis Plastica

Stomach adenocarcinoma; stomach looks like a leather bottle --> thickened and leathery

137

Pain is increased with eating? decreased with eating?

*Increased with eating --> gastric peptic ulcer
*Decreased with eating --> duodenal peptic ulcer (b/c have bicarb secretion, which soothes ulcer)

138

Role of H. pylori in gastric and duodenal peptic ulcers?

*gastric ulcers--> H. pylori in 70% of cases
*duodenal ulcers--> H. pylori in about 100% of cases

139

Is there an increased risk of cancer with Peptic Ulcer disease?

Trick question:
*If gastric ulcer --> increased risk of carcinoma
*If duodenal ulcer --> NO increased risk of carcinoma

140

Recurrent ulcers despite treatment?

Check gastrin levels; may be Zollinger-Ellison syndrome

141

Part of Intestines affected in Crohn's?

Any part of GIT can be affected; but, usually involves terminal ileum and colon; have skip lesions
-->rectal sparing!

142

Part of intestines affected in ulcerative colitis?

-always the rectum
-then, have continuous colonic lesions up from there

143

How much of intestinal wall is affected in Crohn's? in Ulcerative colitis?

Crohn's--> transmural
Ulcerative Colitis--> only mucosal and submucosal

144

Creeping fat

Crohn's

145

Cobblestone mucosa

Crohn's

146

"string sign" on barium swallow

Crohn's

147

"lead pipe" appearance of intestines on imaging?

Ulcerative Colitis (d/t loss of haustra)

148

IBD with: Noncaseating granulomas and Th1 mediated lymphoid aggegates on microscopy:

Crohn's disease
(no granulomas in UC; also UC is Th2-mediated)

149

IBD that has a higher association with colorectal cancer?

Ulcerative Colitis
(Crohn's also is associated with it; but higher risk with UC)

150

Treatment for Crohn's?

-Corticosteroids
-Infliximab

151

Treatment for Ulcerative Colitis?

-Aminosalicylic Acid preparations (like Sulfasalazine)
-6-MP
-Infliximab
-Colectomy

152

STD that is commonly mistaken for IBD?

L1,L2, L3 subtypes of Chlamydia --> cause Lymphogranuloma venereum

153

Dx criteria for IBS?

Recurrent abdominal pain + at least 2 of:
-pain improves with defecation
-change in stool frequency
-change in appearance of stool

154

McBurney's point:

1/3 distance from ASIS to umbilicus (or 2/3 distance from umbilicus to ASIS!)
-->pain is localized here in appendicitis

155

Risk/Complication of appendicitis?

Perforation--> get peritonitis

156

"true" vs "false" diverticulum?

true: all 3 gut wall layers involved (ie Meckel's)
false: only mucosa and submucosa outpouch

157

Most common site of diverticula?

Sigmoid colon

158

Most common cause of severe left lower quadrant pain?

Diverticulitis (inflammation of diverticula)

159

Treatment for diverticulitis?

Antibiotics

160

left lower quadrant pain + bright red rectal bleeding?

Diverticulitis

161

stinky breath (halitosis) + dysphagia + esophageal obstruction?

Zenker's diverticulum = "false" diverticulum at junction of pharynx and esophagus
-->have stinky breath d/t trapped food!

162

Cause of Meckel's diverticulum?

Persistent vitelline duct or yolk sac

163

Most common congenital anomaly of GI tract?

Meckel's diverticulum

164

Pertechnetate study

Dx for Meckel's diverticulum

165

The five 2's of Meckel's diverticulum?

-2 inches long
-2 ft from ileocecal valve
-2% of popl
-usually presents during first 2 years of life
-may have 2 types of epithelia (gastric/pancreatic)

166

currant jelly stools?

Intussusception

167

Where does intussusception commonly occur?

commonly at ileocecal junction

168

What age group does volvolus usually affect? Where does volvulus usually occur?

-usually in elderly
-may occur at cecum and sigmoid colon (b/c have redundant mesentery)

169

Congenital megacolon d/t failure of neural crest migration?

Hirschsprung's disease
-lack of ganglion cells/enteric nervous plexuses (Auerbach's and Messner's) in segment of intestines

170

What part of GIT is usually affected in Hirschsprung's?

Involves rectum

171

Failure to pass meconium?

-Hirschsprung's
-Cystic Fibrosis

172

Increased risk of Hirschsprung in people with what other syndrome?

Down syndrome

173

4 GI conditions associated with Down syndrome:

-Hirschsprung
-Celiac
-Duodenal atresia
-Annular pancreas

174

Bilous vomiting in baby + "double bubble" (proximal stomach distention)

Duodenal atresia = blind duodenum
-->associated with Down syndrome

175

Necrotizing enterocolitis: most common in what pt popl?

-preemie infants (b/c decreased immunity)

176

Pain after eating in elderly + weight loss (but, not a gastric ulcer...)

ischemic colitis
-->usually occurs at splenic flexure (watershed area) and distal colon

177

Sawtooth appearance of masses in gut lumen?

Colonic polyps

178

Area often involved in colonic polyps?

-Rectosigmoid

179

90% of colonic polyps are not malignant; which types are most likely to be malignant?

-Adenomatous, villous polyps (more villous the polyp, more likely to be malignant)

180

multiple non-malignant hamartomas throughout GIT + hyperpigmented mouth, lips, hands, genitalia (so, hyperpigmented mucosal surfaces) + increased risk of Colorectal cancer?

Peutz-Jeghers syndrome
-->autosomal dominant

181

autosomal dominant mutation of APC gene on chromosome 5q?

FAP = Familial Adenomatous Polyposis
-->100% of pts progress to colorectal cancer

182

Lynch syndrome/HNPCC (Hereditary NonPolyposis Colorectal Cancer)

-->autosomal dominant mutation of DNA mismatch repair genes
--> 80% of pts progress to Colorectal Cancer
--> always involves proximal colon

183

FAP + osseous and soft tissue tumors + retinal hypertrophy?

Gardner's syndrome

184

FAP + malignant CNS tumor?

Turcot's syndrome

185

"apple core" lesion on barium enema?

colorectal cancer

186

CEA tumor marker

colorectal cancer

187

Iron deficiency anemia in older males or post-menopausal females?

Suspect colorectal cancer

188

Most common sites of carcinoid tumors?

-appendix
-rectum
-ileum

189

Bronchospasm + Flushing + Diarrhea + Right-sided heart lesion

Serotonin Syndrome (carcinoid tumor that secretes serotonin)

190

Why is carcinoid syndrome only a "syndrome" once it metastasizes out of GI system?

--> b/c just tumor alone = carcinoid tumor, not syndrome
--> if tumor is in the GI, it may secrete serotonin, but don't see any of the symptoms, b/c the liver metabolizes serotonin
-->once it metastasizes, usually to liver, then start seen symptoms associated with serotonin secretion; then it becomes "syndrome"

191

form of bilirubin in bloodstream?

unconjugated bilirubin-albumin complex = indirect (water-insoluble) bilirubin

192

form of bilirubin in liver?

conjugated/direct (water-soluble) bilirubin

193

form of bilirubin in stool?

stercobilin

194

form of bilirubin in urine?

urobilin

195

uridine glucuronyl transferase = UDP glucuronyl transferase

enzyme, converts indirect bilirubin to direct bilirubin in liver

196

Effects of Portal Hypertension

-Esophageal varices --> Hematemesis
-Melena
-Splenomegaly
-Caput medusae, ascites
-Hemorrhoids
-Portal hypertensive gastropathy

197

Effects of liver cell failure:

-Coma--> hepatic encephalopathy; from release of ammonia and other toxic metabolites from liver
-Scleral icterus
-musty smelling breath
-gynecomastia
-jaundice
-testicular atrophy
-asterixis (hand flap)
-bleeding tendency (from decreased prothrombin and clotting factors)
-anemia
-ankle edema

198

liver enzymes (AST, ALT) in alcoholic vs viral hepatitis?

alcoholic hepatitis: AST>ALT
viral hepatitis: ALT>AST

199

Lactulose

-Osmotic laxative
-Also: Treatment for hepatic encephalopathy (in liver failure) --> b/c gut bacteria break it down, promoting nitrogen excretion as NH4+

200

GGT (gamma-glutamyl transpeptidase)

serum marker for liver disease; elevated with heavy alcohol consumption

201

decreased ceruloplasmin?

Wilson's disease

202

elevated amylase?

-acute pancreatitis
-also elevated in MUMPS!

203

elevated lipase?

acute pancreatitis

204

elevated Alkaline Phosphatase?

*non-specific:
-obstructive liver disease (hepatocellular carcinoma)
-bone disease
-bile duct disease

*if elevated ALP, can then check GGT. If elevated GGT, then know it's d/t liver disease

205

What is Reye's syndrome? What are the signs/symptoms?

=Childhood Hepatoencephalopathy:
-->mitochondrial abnormalities
-->fatty liver (microvesicular fatty change)
-->hypoglycemia
-->vomiting
-->hepatomegaly
-->coma

Mechanism: aspirin metabolites decrease Beta-oxidation by reversible inhibition of mitochondrial enzymes

206

One disease when children should be treated with aspirin?

Kawasaki's (to prevent coronary artery thrombosis)

207

Best indicators of Liver function and progrnosis?

Prothrombin time and Serum albumin (albumin is made in liver, as are clotting factors)
*hypoalbuminemia + elevated PT = POOR prognosis.

208

3 stages of alcoholic liver injury:
-Reversible?

1) Hepatic steatosis
--> Macrovesicular steatosis/fatty change associated with moderate alcohol intake
-->REVERSIBLE with alcohol cessation

2) Alcoholic hepatitis:
-->from sustained, long-term alcohol intake
-->swollen and necrotic hepatocytes; neutrophil infiltration
-->Mallory bodies (intracytoplasmic eosinophilic inclusions)

3) Alcoholic cirrhosis:
-->shrunken liver with "hobnail" appearance
-->sclerosis around central vein
-->looks like chronic liver disease: hypoalbuminemia, jaundice...
-->IRREVERSIBLE

209

Hepatic steatosis:

-macrovesicular fatty change of liver; see hepatocytes filled with lipid droplets
-Reversible effect of moderate alcohol intake; can reverse by stopping to drink alcohol
***can also get fatty liver from certain HIV drugs; metabolic syndrome; etc...

210

Mallory bodies

intracytoplasmic eosinophilic inclusions within hepatocytes; see in alcoholic hepatitis

211

7 diseases associated with increased risk of hepatocellular carcinoma:

-Hepatitis B
-Hepatitis C
-Hemochromatosis
-Carcinogens (specifically Alfatoxin from Aspergillus)
-Alcoholic cirrhosis
-alpha-1-antitrypsin deficiency
-Wilson's disease

212

cancer associatd with elevated alpha-fetoprotein?

Hepatocellular carcinoma

213

Common benign liver tumor in 30-50 year olds?

-Cavernous Hemangioma
-->DON'T biopsy it! b/c may lead to hemorrhage

214

Nutmeg liver

Backup of blood into liver; d/t right heart failure and Budd-Chiari syndrome
-->if it persists, may result in cardiac cirrhosis

215

Condition that looks similar to Right Heart Failure (Hepatomegaly, etc) BUT, absence of jugular venous distension:

Budd-Chiari syndrome

216

Budd-Chiari syndrome:

-Occlusion of IVC or hepatic veins --> leads to congestive liver disease (hepatomegaly, ascites, abdominal pain, eventually liver failure)
-->may have varices and visible abdominal/back veins
-->Looks kind of similar to Right heart failure, BUT absence of JVD
-->Associated with:
-hepatocellular carcinoma
-pregnancy
-polycythemia vera
-hypercoagulable state

217

Liver cirrhosis + Panacinar Emphysema?

alpha-1-antitrypsin deficiency
-->this is a CODOMINANT trait

218

PAS-positive globules in liver?

alpha-1-antitrypsin deficiency

219

Cause of physiologic jaundice in neonates? Treatment?

Immature UDP-glucuronyl transferase at birth (physiologic): can't convert unconjugated bilirubin to conjugated in liver --> get unconjugated/indirect hyperbilirubinemia --> Jaundice

*Treat with phototherapy: converts unconjugated bilirubin to a water-soluble form, so it can be renally excreted! COOL!

220

What is jaundice? What are the 3 causes/types of pathologic jaundice (not counting physiologic neonatal jaundice)?

Jaundice = yellowing of skin and/or sclerae d/t elevated bilirubin
*Causes:
-Hepatocellular injury
-Obstruction to bile flow
-Hemolysis

221

Jaundice, elevated bilirubin in response to fasting, stress, exercise?

--> Gilbert's syndrome
--> have mildly decreased UDP-glucuronyl transferase (so decreased conversion of indirect to direct bilirubin) or decreased bilirubin intake
-->mild disease; quite common, but most pts don't even know they have it
-->when flares: have indirect hyperbilirubinemia

222

pathologic jaundice early in life + kernicterus (bilirubin deposition in brain) + elevated unconjugated bilirubin

Crigler-Najjar Syndrome Type 1
-->absent UDP-glucuronyl transferase (so can't convert indirect to direct bilirubin) --> get elevated indirect/unconjugated bilirubin

223

Treatment for Crigler-Najjar syndrome type 1?

-phototherapy (makes Unconjugated bilirubin water-soluble, so can excrete in urine)
-Plasmapheresis (get rid of excess unconjugated bilirubin)

-->Crigler Najjar type 1 is fatal within a few years

224

Crigler-Najjar type 2:
-what is it?
-treatment?

milder form of Crigler-Najjar type 1; have decreased amount of UDP-glucuronyl transferase (not absent, as in type 1)
-->can treat with phenobarbital (increases synthesis of liver enzymes, including UDP glucuronyl transferase)

225

Phenobarbital

Treatment for Crigler-Najjar type 2 (and can be used for symptomatic Gilbert's)
-->increases synthesis of liver enzymes --> so, increases synthesis of UDP-glucuronyl transferase

226

Conjugated Hyperbilirubinemia + Black liver on gross examination
-->otherwise benign

=Dubin-Johnson syndrome
-->defective liver excretion of bilirubin; so get elevated conjugated bilirubin in blood

227

Rotor's syndrome:

mild disorder, similar to Dubin-Johnson syndrome (but less severe); have defective liver excretion of bilirubin, so mildly elevated conjugated bilirubin in blood; unlike Dubin-Johnson syndrome, does not cause black liver

228

Disease d/t problem with bilirubin uptake into liver?

-Gilbert's
-->elevated unconjugated bilirubinemia

229

Diseases d/t problem with bilirubin conjugation

-Gilbert's
-Crigler-Najjar types 1 and 2
-physiologic neonatal jaundice

-->elevated unconjugated bilirubinemia

230

Diseases d/t problem with bilirubin excretion from liver?

-Dubin-Johnson
-Rotor's

-->elevated direct/conjugated bilirubinemia

231

Penicillamine

Treatment for Wilson's disease

232

Kayser-Fleischer ring

yellow-green-golden brown corneal ring seen in Wilson's disease

233

decreased levels of ceruloplasmin?

seen in Wilson's disease
-->ceruloplasmin=major copper-carrying protein in blood

234

Signs/symptoms of Wilson's disease: "CCCCCopper is Hella BADDD"

-decreased Ceruloplasmin
-Corneal deposits = Kayser-Fleischer rings
-Cirrhosis
-Copper accumulation (in liver, brain, cornea, kidneys, joints, etc)
-hepatocellular Carcinoma (increased risk)
-Hemolytic anemia
-Basal ganglia degeneration (specifically, degeneration of PUTAMEN); get parkinsonian symptoms
-Asterixis
-Dementia
-Dyskinesia
-Dysarthria

***Treat with Penicillamine

235

What part of brain is degenerated in Wilson's disease?

Basal ganglia, specifically Putamen, degeneration
-->get Parkinsonian symptoms

236

micronodular Cirrhosis + Diabetes + skin pigmentation?

Hemochromatosis = "Bronze" diabetes

237

Deferoxamine

Treatment for hereditary Hemochromatosis
-->also do repeated phlebotomy

238

Causes of hemochromatosis?

-herditary (autosomal recessive)
-secondary to repeated blood transfusions (ie in Beta-thalassemia major)

239

lab findings in Hemochromatosis: ferritin, iron, TIBC, transferring?

-elevated ferritin (stores iron within cells)
-elevated iron
-decreased TIBC (indirect measure of transferrin, which transports iron in blood)
-elevated transferritin saturation (serum Fe/TIBC)

240

Which HLA is associated with hemochromatosis?

HLA-A3

241

Complications/Results of Hemochromatosis:

-CHF
-Testicular atrophy in males
-increased risk of hepatocellular carcinoma

242

Cause of primary biliary cirrhosis?

-->Autoimmune reaction: get lymphocytic infiltrate and granulomas
-->mostly seen in middle-aged women
-->anti-mitochondrial antibodies

243

Elevated anti-mitochondrial antibodies?

Primary biliary cirrhosis

244

Causes and pathophysiology of Secondary Biliary Cirrhosis?

-->Extrahepatic biliary obstruction (like a gallstone, biliary stricture, carcinoma of head of pancreas, chronic pancreatitis) --> so, get increased pressure in intrahepatic ducts --> injury and fibrosis --> bile stasis

245

"onion skin" bile duct fibrosis?

Primary Sclerosing Cholangitis (a biliary tract disease)

246

Presentation and Labs in Biliary Tract Diseases (Primary and Secondary Biliary Cirrhosis, Primary Sclerosing Cholangitis):

Presentation:
-Pruritis
-Jaundice
-Dark urine (b/c elevated urobilinogen in urine)
-Pale stools (b/c bile not making it into stools)
-Hepatosplenomegaly

Labs:
-Conjugated/Direct Hyperbilirubinemia
-elevated cholesterol
-elevated ALP

247

Pruritus in a middle-aged woman + elevated conjugated bilirubinemia?

-->Consider primary biliary cirrhosis
-->may also consider primary sclerosing cholangitis

248

Complication of Secondary Biliary Cirrhosis?

Ascending cholangitis = infection of biliary tree (makes sense, b/c have an obstruction of bile flow; bile stasis; etc...)

249

What condition is Primary Sclerosing Cholangitis associated with?

Ulcerative Cholitis
-primary sclerosing cholangitis can also lead to secondary biliary cirrhosis

250

Biliary tract disease with Hypergammaglobulinemia (IgM)?

-->Primary sclerosing cholangitis

251

5 main risk factors for gallstones/cholelithiasis:

5 F's:
-Female
-Forty
-Fat
-Fertile (multiparity)
-Feathers (Native Americans)

252

Charcot's triad of cholangitis (infection of biliary tree/common bile duct):

1) Jaundice
2) Fever
3) RUQ pain

253

Murphy's sign

-->positive in cholecystitis; good way to dx pain in the RUQ
-->positive: when deeply palpate, pt has inspiratory arrest b/c such deep pain

254

Pain on deep palpation, causing inspiratory arrest

Positive Murphy's sign
--> positive in cholecystitis; way to dx RUQ pain

255

3 causes of gallstones:

-elevated cholesterol and/or bilirubin
-decreased bile salts
-gallbladder stasis

-->all of these can cause stones

256

Most common cause of cholecystitis (inflammation of gallbladder)?

Gallstones
-->have positive Murphy's sign!

257

Ascending cholangitis =

inflammation of bile duct; usually d/t obstruction of duct by gallstones

258

What is acute pancreatitis?

=autoingestion of pancreas by pancreatic enzymes. ouch.

259

Causes of Acute Pancreatitis:

"GET SMASHED"
-->Gallstones and Ethanol = Most common causese
-Gallstones
-Ethanol
-Trauma
-Steroids
-Mumps
-Autoimmune disease
-Scorpion sting
-Hypercalcemia/Hypertriglyceridemia
-ERCP (Endoscopic Retrograde Cholangiopancreatography = endoscopic technique to dx/treat problems of pancreatic or biliary ducts; but, main risk of it = acute pancreatitis)
-Drugs (ie sultas, HIV drugs...)

260

#1 cause of chronic pancreatitis?
-other main cause?

#1 = alcoholism
other main cause = smoking

261

labs in acute pancreatitis:

-elevated amylase and lipase (lipase = more specific)

262

steatorrhea, fat-soluble vitamin deficiency, diabetes

pancreatic insufficiency; may be a result of chronic pancreatitis (which is usually d/t alcoholism or smoking)

263

CA-19-9

specific tumor marker for Pancreatic adenocarcinoma

264

CEA

less specific tumor marker for pancreatic adenocarcinoma

265

painless jaundice in male >50 years old?

consider Pancreatic adenocarcinoma

266

#1 risk factor for Pancreatic Adenocarcinoma?
-other risk factors?

#1 = Smoking (but, not alcoholism)
*other risk factors:
-chronic pancreatitis (which is usually caused by alcoholism or smoking... kind of contradicts the not alcoholism thing...)
-Jewish and African American males
- >50 years old
-Diabetes
-Genetics

267

Courvoiseier's sign:

-obstructive jaundice with palpable gallbladder
-->pruritus, dark urine, pale stools (all signs of obstructive jaundice...)
-->see with pancreatic adenocarcinoma

268

Trousseau's syndrome:

-migratory thrombophlebitis--> redness and tenderness on palpation of extremities
-->see with pancreatic adenocarcinoma

269

Presentation of pancreatic adenocarcinoma:

-abdominal pain that radiates to back
-weight loss
-redness and tenderness on palpation of extremities (migratory thromboephlebitis = Trousseau's sign)
-Obstructive jaundice and palpable gallbladder --> pruritus, dark urine, pale stools (=Courvoiseier's sign)

270

Asterixis:

See in:
-liver cell failure
-Wilson's disease
-Uremia (increased BUN and Creatinine, like in renal failure)

271

Drugs that end in "-dine"

H2 blockers: Cimetadine, Ranitidine, Famotidine, Nizatidine
--> take H2 blockers before you "dine"

272

Ranitidine

H2 blocker

273

Cimetidine

H2 blocker
-->inhibits cytochrome P450!
-->also:
-gynecomastia, impotence, decreased libido in males (anti-androgen effects)
-can cross BBB (headaches, dizziness, confusion)
-can cross placenta

274

Famotidine

H2 blocker

275

Nizatidine

H2 blocker

276

Drugs that can cause gynecomastia? (random, not necessarily GI)

"Some Drugs Create Awesome Knockers"
-Spirinolactone
-Digitalis
-Cimetidine
-Alcohol
-Ketoconazole

277

Mechanism of H2 blockers?

-reversibly block Histamine (released from ECL cells, after stimulation by Gastrin) from binding to the H2 receptor on gastric parietal cells
-->get decreased cAMP, meaning no stimulation of the ATP-ase --> decreased H+ secretion from parietal cells into gastric lumen

278

What are more potent drugs: H2 blockers or PPIs?

PPIs are more potent than H2 blockers; so, use H2 blockers for less severe cases; PPIs for more severe

*note: H2 blockers are reversible; PPIs are irreversible

279

drugs ending in "-prazole"

PPIs (proton pump inhibitors)
-Omeprazole
-Lansoprazole
-Pantroprazole
-Esomeprazole

280

Omeprazole

PPI

281

Lansoprazole

PPI

282

1st line treatment for Zollinger-Ellison syndrome?

Proton Pump Inhibitors

283

Mechanism of PPIs?

Irreversibly inhibit Proton Pump (H/K-ATPase) in parietal cells (so, can't excrete H+ into gastric lumen from parietal cells)

284

Bismuth

-treatment of ulcers and traveler's diarrhea
-mechanism: binds to ulcer base, providing physical protection; thus allowing HCO3- secretion to reestablish pH gradient in mucus layer

285

Sucralfate

Same mechanism as bismuth; treatment of ulcers and traveler's diarrhea
-->bind to ulcers, providing physical protection; allows HCO3- secretion to reestablish pH gradient in mucus layer
-Requires an acidic environment to polymerize; WONT WORK IF TAKING ANTACIDS CONCURRENTLY!

286

Misoprostol:
-mechanism
-clinical uses
-side effect
-contraindications

*Prostaglandin analog
*Mechanism: binds receptor on parietal cell --> stimulates Gi --> decreased cAMP --> decreased stimulation of Proton Pump --> decreased acid production/secretion into gastric lumen

*Clinical uses:
-Prevent NSAID-induced peptic ulcers (b/c NSAIDs decrease prostaglandins)
-Treatment of PDA
-Induce labor

*Side effect:
-Diarrhea

*Conraindication:
-Pregnant women/women of child-bearing age (b/c induces labor)

287

Octreotide:
-mechanism
-clinical uses

Somatostatin analog
*Somatostatin/Octreotide --> Gi --> blocks/decrease cAMP --> blocks Proton Pump --> decreased acid secretion into gastric lumen

*Uses:
-secretory diarrhea
-acute variceal bleeds
-acromegaly (inhibits GH)
-VIPoma (pancreatic islet cell tumor that secretes lots of Vasoactive Intestinal Polypeptide, causing lots of diarrhea)
-Carcinoid tumors

288

Treatment of VIPoma?

Octreotide

289

Treatment of Carcinoid Syndrome?

Octreotide

290

Diphenoxylate

opiate-anti-diarrheal drug;
-->binds to Mu opiate receptors in GI tract and slows motility

291

Side effects of Antacids?

-all can cause hypokalemia (b/c block H/K-ATPase)
-Can chelate and decrease effectiveness of other drugs

292

Side effects of Aluminum Hydroxide (antacid) overuse?

-"aluMINIMUM of feces"= constipation
-hypokalemia and decrease efficacy of other drugs (all antacids)
-others

293

Side effects of Magnesium Hydroxide (antacid) overuse:

"Must Go to the bathroom" = diarrhea
-hypokalemia and decrease efficacy of other drugs (all antacids)
-others

294

Side effects of Calcium carbonate (antacid = TUMS!)

-Hypercalcemia
-may cause rebound increase in acid!
-hypokalemia and decrease efficacy of other drugs (all antacids)

295

Magnesium hydroxide

-osmotic laxative
-also an antacid (with side effect of diarrhea!)

296

Magnesium citrate

-osmotic laxative

297

Polyethylene glycol

Osmotic laxative

298

Infliximab clinical uses?

-monoclonal anti-TNF antibody
*Uses:
-Crohn's disease
-Rheaumatoid arthritis

299

Sulfasalazine:
-mechanism?
-clinical uses?

=combo of Sulfapyridine (antibacterial) + 5-ASA (aminosalicylic acid = anti-inflammatory)
-->activated by colonic bacteria (so, only effective in distal ileum and colon)

*clinical uses:
-Ulcerative Colitis (always)
-Crohn's (but, only acts in distal ileum and colon; so, only if disease is localized to those areas, which it often is)

300

Odansetron:
-mechanism
-clinical uses
-side effects

=anti-serotonin and anti-emetic
*Clinical uses:
-pts undergoing chemo, to combat nausea/vominiting
-pregnant women with morning sickness

*side effects:
-headache (think opposite of triptans, which are serotonin-agonists; relieve headaches)
-constipation (think opposite serotonin/carcinoid syndrome, which causes diarrhea)

301

Metoclopramide:
-mechanism
-uses
-toxicity/side-effects
-contraindications

=D2-receptor antagonist (Dopamine-blocker)

*uses:
-diabetic and post-surgery gastroparesis (delayed gastric emptying)

*Toxicities/Side effects:
-may lower seizure threshold
-parkinsonian symptoms (b/c block dopamine)
-diarrhea, etc...

*Contraindications:
-Parkinson's disease (duh)
-small bowel obstruction (duh)

302

4 Drugs that may lower seizure threshold? (random, not specific to GI)

1) Metoclopramide (treats gastroparesis)

2) Buproprion (anti-depressant w/out sexual side effects; increased seizures, especially pts with bulemia or anorexia)

3) Tramadol (used to treat chronic pain; weak opiod-agonist; inhibits serotonin and NE reuptake, but not used to treat depression)

4) Enflurane (inhaled anesthetic)