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GI Tract Flashcards

1
Q

What are aphtous ulcers?

A
  • painful superficial ulceration of oral mucosa

- stress induced, resolves spontaneously, often recurrs

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2
Q

How can one ID an aphtous ulcer

A

grayish base surrounded by erythema. the gray base represents granulation tissue

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3
Q

what is behcet’s syndrome?

A

recurrent aphtous/genital ulcers, uveitis

  • immune complex vasculitis : small vessels
  • can be seen after viral infxn
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4
Q

What do oral herpes look like?

A

shallow, painful, red ulcers

- HSV 1 associated

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5
Q

When is the primary oral herpes infxn usually?

A
  • childhood
    Virus stays dormant in ganglia of trigeminal nerve
  • stress/ sunlight cause reactivation of virus
  • vesicles often arise on lips (cold sores
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6
Q

What are the risk factors for SCC of mouth?

A

tobacco and EtOH

- floor of mouth is a common location

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7
Q

What are precursor lesions for SCC of mouth?

A

Leukoplakia or erythoplakia

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8
Q

What is leukoplakia?

A

white plaque

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9
Q

What is hairy leukoplakia due to?

A

EBV
hairy, shaggy on lateral tongue
- ICPs
only hyperplasia

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10
Q

What is erythroplakia

A

Red plaque due to angiogenesis

- more suggestive of squamous dysplasia

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11
Q

What is the primitive gut tube made up of?

A
  • incorporates yolk sac during development
  • endoderm: epithelial lining of mucosa
  • mesdoerm - all other layers
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12
Q

What are the divisions of the GI tract?

A
  1. foregut = pharynx to duodenum
  2. Midgut - duodenum to transverse colon
  3. Hindgut = distal transverse colon to rectum
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13
Q

What are some development defects of anterior abdominal wall due to failure of…

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

A

a) sternal defects
b) omphalocele, gastroschisis
c) bladder exstrophy

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14
Q

What is gastroschisis?

A

extrusion of abdominal contents through lateral abdominal folds; not covered by peritoneum. hernia is right to umbilicus

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15
Q

What is omphalocele?

A

persistence of herniation of abdominal contents into umbilical cord, covered by peritoneum and amnion of umbilical cord

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16
Q

What are other things than an omphalocele associated w/?

A

Beckwith Wiedemann syndrome
Chromosomal abnormaliity
congenital heart dz

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17
Q

What are jejunal, ileal, and colonic atresia due to?

A 
vascular accident (apple peel atresia)
- bilious vomiting
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18
Q

What is seen on x-ray for the small and large bowel atresias?

A
  1. distended bowl proximal to atresia

2. absence of air distal to atresia

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19
Q

What are the steps for midgut development?

A

6th wk = midgut herniates thru umbilical range

10th wk = returns to abdominal cavity and rotates around SMA

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20
Q

What is the most common esophagus anomaly?

A

esophageal atresia w/ distal tracheoesophageal fistula due to malformation of trachesophageal septum

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21
Q

What is the clinical presentation of trachesophageal fistula?

A

drooling, choking, and vomiting w/ first feeding

  • allows air to enter stomach (visible on CXR)
  • cyanosis is secondary to larngospasm (to avoid reflux related aspiration)
  • polyhydraminos b/c can’t digest amniotic fluid
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22
Q

What is the clinical test to dx trachesophageal fistula?

A

failure to pass NG tube into stomach

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23
Q

What is a H type esophagus anomaly?

A

fistula alone

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24
Q

What is seen on CXR of a pure esophageal atresia?

A

gasless abdomen

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25
Q

What is congenital pyloric stenosis?

A
  • hypertrophy of pylorus causes obstruction

- palpable olive mass in epigastric region and nonbilious projectile vomiting at 2 wks of age

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26
Q

What is Rx for congenital pyloric stenosis?

A

surgical incision

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27
Q

who is congenital pyloric stenosis common in?

A

first born males

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28
Q

What is the pancreas derived from?

A

foregut

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29
Q

What makes up the components of the pancreas?

A

Ventral pancreatic bud and dorsal pancreatic bud

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30
Q

What does the ventral pancreatic bud form?

A

pancreatic head and main pancreatic duct

uncinate process

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31
Q

What does the dorsal pancreatic bud form?

A

body, tail, isthmus, and accessory pancreatic bud

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32
Q

What is annular pancreas?

A

ventral pancreatic bud abnormally encircles 2nd part of duodenum
- forms a ring of pancreatic tissue that may causes duodenal narrowing
2/3 pts usually Asx

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33
Q

What is associated a/ infantile annular pancreas?

A

polyhrdraminos, Down’s, esophageal and duodenal atresia, imperforate anus, Meckel’s diverticulum

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34
Q

What is associated w/ adult annular pancreas?

A

ab pain, postprandial fullness, nausea, peptic ulceration, pancreatitis

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35
Q

What is pancreas divisum?

A

ventral and dorsal parts fail to fuse at 8 wks

  • MC pancreatic congenital anomaly
  • usually Asx
  • drainage is preserved via major/minor papillae
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36
Q

What are signs/symptoms of pancreas divisum?

A

occurs when orifice of minor papillae inadequately drains the accessory ducts
- recurrent pancreatitis

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37
Q

What does the spleen arise from?

A

arises in mesentery of stomach (mesodermal) but is supplied by foregut (celiac artery)

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38
Q

What are the retriperitoneal structures?

A 
- include GI structures that lack a mesentery and non GI structures.
SAD PUCKER
Suprarenal glands
Aorta and IVC
Duodenum (2nd and 3rd part)
Pancreas (except tail)
Ureters
Colon (descending and ascending)
Kidneys
Esophagus (lower 2/3)
Rectum (lower 2/3)
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39
Q

What is the parietal peritoneum innervated by?

A

intercostal, ilioinguinal, and iliohypogastric nerves

- sensitive and somatic pain = focal region of pain

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40
Q

What communicates w/ the lesser and greater sac in the GI tract?

A

omental foramen aka epiploic foramen of Winslow

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41
Q

What does the falciform ligament connect?

A

liver to anterior abdominal wall

- divides liver into 2 lobes

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42
Q

What is contained in the falciform ligament?

A

ligamentum teres hepatis (derivative of fetal umbilical vein)

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43
Q

What does the hepatoduodenal ligament connect?

A

liver to duodenum

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44
Q

What does the hepatoduodenal ligament contain?

A

portal triad thus ligament can be compressed b/w thumb and index finger to control bleeding.

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45
Q

What does the gastrohepatic ligament connect?

A

liver to lesser curvature of stomach

  • may be cut during surgery to access lesser sac
  • separates greater and less sac on the right
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46
Q

What does the gastrophepatic ligament contain?

A

gastric arteries

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47
Q

What does the gastrocolic ligament connect and contain?

A
  • greater curvature to transverse colon
  • gastroepiploic arteries
  • parter of greater omentum
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48
Q

What does the gastrosplenic ligament connect and contain?

A
  • greater curvature to spleen
  • contains short gastric, left gastroepiploic vessels
  • separates greater and lesser sac on left
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49
Q

What does the splenorenal ligament connect and contain?

A

spleen to posterior abdominal wall

- contains splenic artery and vein, tail of pancreas

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50
Q

What happens during the early development of the GI tract?

A
  1. dorsal embryonic mesentery - suspends all guts from dorsal body wall
  2. ventral embryonic mesentery - suspends foregut from ventral body wall
  3. visceral developement: spleen, pancreas, liver and biliary structures develop w/in mesentery
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51
Q

What are the layers of the digestive tract?

A

MSMS

  1. Mucosa
  2. Submucosa
  3. Muscularis externa
  4. Serosa
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52
Q

What makes up the mucosa of the GIT?

A 
epithelium (absorption)
lamina propria (support) - loose CT
muscularis mucosa (motility) - thin SM
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53
Q

What makes up the submucosa of the GIT?

A

submucosal nerve plexus (meissner’s) - loose CT, mucus secreting glands

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54
Q

What makes up the muscularis externa of the GIT?

A

includes myenteris nerve plexus (Auerbach”s) - peristalsis

- inner circular and outer longitudinal muscle layer

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55
Q

What makes up the serosa of the GIT?

A

when intraperitoneal called serosa

- when retroperitoneal called adventitia

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56
Q

How deep do ulcers extend? and erosions?

A

Ulcers- into submucosa, inner or outer muscular layer

Erosions - mucosa layer only

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57
Q

What are the frequencies of basal electric rhythm in the GIT?

A
  1. stomach - 3 waves/min
  2. Duodenum - 12 waves/ min
  3. Ileum - 8-9 waves/min
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58
Q

What is the histology of the esophagus?

A

nonkeratinzed stratified squamous epithelium and mucous glands

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59
Q

What is the histology of the stomach?

A

gastric glands and pits, mucous glands, chief, parietal, and EE cells

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60
Q

What is the histology of the duodenum?

A

villi and microvilli increase absorptive surface, Brunner’s glands in submucosa, crypts of Lierberkuhn, goblet, paneth and EE cells
- simple columnar epithelium

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61
Q

What is the histology of the jejunum?

A

villi, microvilli, goblet, paneth, and EE cells

  • plicae circularies and crypts of Lieberkuhn
  • simple columnar epithelium
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62
Q

What is the histology of the ileum?

A
  • M cells
  • Peyer’s patches (lamina propria, submucosa)
  • Plicae circulares (proximal ileum) and crypts of Lieberkuhn
  • largest number of goblet cells in the small intestine to secrete Bicarb
  • simple columnar epithelium
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63
Q

What is the histology of the colon?

A 
crypts but NO villi
numerous goblet cells
absorptive cells, EE cells, lymphoid follicles
- Na/H20 reabsorption
K/ Bicarb secretion
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64
Q

What is the function of the GIT immune function?

A
  • produce Vit K
  • Assists digestion
  • protect against overgrowth of pathogenic bacteria
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65
Q

What is the location of the esophagus?

A

mediastinum
behind trachea and left atrium
- enters abdominal cavity through esophageal hiatus of diaphragm at T10 level

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66
Q

What are the 4 narrow points of the esophagus?

A
  1. at origin - pharynx
  2. arch of aorta
  3. left primary bronchiole
  4. esophageal hiatus
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67
Q

Compare the muscles found in the esophagus?

A

upper 1/3 - skeletal muscle
lower 1/3 - smooth muscle
- middle 1/3 = mixed

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68
Q

What is the blood supply of the esophagus?

A
  1. upper 1/3 = inferior thyroid artery branches
  2. middle 1/3 = bronchial artery and aorta
  3. lower 1/3 = inferior phrenic and left gastric artery branches
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69
Q

What is the venous drainage of the esophagus?

A
  1. upper 1/3 = inferior thyroid veins
  2. middle 1/3 = bronchial, azygos, and hemiazygos
  3. portal venous system
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70
Q

What are the abdominal aorta branches?

A
  1. Celia artery at T 12
  2. Left inferior phrenic artery
  3. SMA at L1
  4. left middle suprarenral artery
  5. renal arteries at L1
  6. Gonadal arteries
  7. IMA at L 3
  8. Bifurcation of abdominal aorta at L4
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71
Q

What is SMA syndrome?

A

when transverse portion of duodenum is entrapped b/w SMA and aorta causing intestinal obstruction

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72
Q

What does the celiac artery supply?

A

foregut –> stomach to proximal duodenum, liver, gallbladder, pancreas, spleen (mesoderm)

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73
Q

What does the SMA supply?

A

midgut –> distal duodenum to proximal 2/3 of transverse colon

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74
Q

What does the IMA supply?

A

hindgut –> distal 1/3 of transverse colon to upper portion of rectum (above pectinate line)

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75
Q

How is the GIT innervated?

A
  1. foregut - vagus and T12/L1 vertebral level
  2. midgut - vagus and L1 vertebral level
  3. hindgut - pelvic and L3 vertebral level
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76
Q

What is the referred pain for the GIT?

A

1 foregut - epigastric

  1. midgut - umbilical
  2. hindgut - hypogastric
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77
Q

What is the role of Paneth cells?

A

produce lysozymes/defensins to protect from pathogenic microorganisms, found at the base of crypts

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78
Q

What are the branches of celiac trunk?

A

common hepatic, splenic, left gastric

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79
Q

What are the branches of the common hepatic artery?

A
  1. right gastric artery
  2. hepatic artery proper
  3. gastroduodenal artery ==> anterior superior pancreaticoduodenal and right gastroepiploic artery
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80
Q

What are some collateral circulations in the GIT?

A
  1. superior epigastric (internal thoracic/mammary) and inferior epigastric (external iliac)
  2. superior pancreaticoduodenal (celiac trunk) and inferior (SMA)
  3. middle colic (SMA) and left colic (IMA)
  4. superior rectal (IMA) and middle/inferior rectal (internal iliac)
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81
Q

What are the sites for the portosystemic anastomoses?

A
  1. esophagus - esophageal varices
  2. umbilicus - caput medusae
  3. Rectum - internal hemorrhoids
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82
Q

What makes up the liver’s dual blood supply?

A
  1. 75% due to portal vein

2. 25% due to hepatic arteryy

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83
Q

What veins are involved in esophageal varices?

A

left gastric and esophageal veins

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84
Q

What veins are involved in caput medusae?

A
  1. paraumbilical and superficial/inferior epigastric below the umbilicus
  2. paraumbilical and superior epigastric/lateral thoracic above the umbilicus
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85
Q

What veins are involved in internal hemorrhoids?

A

superior rectal and middle/inferior rectal

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86
Q

What is TIPS ( transjugular intrahepatic portosystemic shunt)?

A

shunt exists b/w portal vein and hepatic vein percutaneously relieves portal HTN by shunting blood to systemic circulation

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87
Q

How does the liver develop?

A
  • it’s an outgrowth of foregut endoderm

- hepatic diverticulum enters vental mesentery

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88
Q

What does the embryonic liver differentiate into?

A
  1. distally into liver and gall bladder

2. proximally into biliary duct system

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89
Q

What are hepatocytes?

A
  • functionally polarized liver cells
  • has multiple apical/basal surfaces
    1. Apical surface is faces bile canaliculi
    2. Basal surface is next to sinusoids
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90
Q

What is the space of Disse?

A

b/w capillary endothelial cells and hepatocytes

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91
Q

What is a kuffer cell?

A

specialized monocytes

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92
Q

What is an Ito cell (stellate cell)?

A

mesenchymal cells - store fat soluble vitamins

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93
Q

What are the different zones in the liver anatomy?

A

Zone 1 - periportal zone
Zone 2 - intermediate zone
Zone 3 - pericentral vein (centrilobular)

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94
Q

What zone in the liver is affected by viral hepatitis?

A

zone 1

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95
Q

What is the function of zone 1 in the liver?

A

oxidative functions and synthesis of proteins/cholesterol

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96
Q

What zone in the liver plays a role in glycolysis, lipogenesis, alcohol detoxification?

A

zone 3

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97
Q

What zone is affected 1st by ischemia?

A

zone 3

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98
Q

What zone is the site of alcoholic injury?

A

zone 3

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99
Q

what zone is most sensitive to toxic injury

A

zone 3

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100
Q

what zone contains the P450 system?

A

zone 3

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101
Q

What is a portal lobule in the liver?

A
  • triangular structure
    central vein at each corner
    portal tract in center
    bile flows from periphery to center
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102
Q

How do blood and bile flow in the liver?

A
  1. blood flows from portal triad to central vein

2. bile flows from central vein to portal triad

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103
Q

What makes up the portal triad?

A
  1. biel ductule
  2. hepatic artery
  3. portal vein
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104
Q

What is the function of the gall bladder?

A
  • stores bile
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105
Q

What artery supplies the gall bladder?

A

cystic artery (branch of right hepatic artery)

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106
Q

What are the different parts of the pancreas bordered by?

A
  1. uccinate process - crossed by SMA
  2. neck - anterior to hepatic portal vein
  3. body = left and anteriorly to aorta
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107
Q

What makes up the biliary tree?

A
  1. The left and right hepatic duct connect to form the common hepatic duct
  2. Common hepatic duct combines w/ the cystic duct to form the common bile duct
  3. Common bile duct combines w/ main pancreatic duct to expel their contents at the ampulla of vater
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108
Q

What can cause obstruction of the common bile duct

A

gallstones at ampulla of Vater and in the common bile duct

- tumors that arise in head of pancreas

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109
Q

What does the femoral triangle contain?

A

femoral vein, artery, and nerve

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110
Q

what is the order of contents in the femoral region?

A

NAVEL from lateral to medial

- Nerve, artery, vein, empty, lymphatics

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111
Q

What is the femoral sheath?

A

fascial tube 3/4 cm below the inguinal ligament

- contains the femoral vein, artery, and canal (deep inguinal lymph nodes) but NOT femoral nerve

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112
Q

What are the border of the femoral triangle?

A
  1. superior - inguinal ligament
  2. laterally - sartorius muscle
  3. medially - adductor longus muscle
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113
Q

What does the inguinal canal contain?

A
  1. in women = found ligament of uterus

2. men = spermatic cord and contents

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114
Q

What is a diaphragmatic hernia?

A

abdominal structures enters the thorax

  • may often occur in infants as a result of defective development of pleuroperitoneal membrane; complicated by lung hypoplasia
  • most commonly a hiatal hernia
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115
Q

What is a hiatal hernia?

A
  • stomach herniates upward through the esophageal hiatus of the diaphragm
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116
Q

What is a sliding hiatal hernia?

A

GE junction is displaced upward

- hourglass stomach

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117
Q

What is paraesophageal hernia?

A
  • GE junction is normal

- fundus protrudes into the thorax

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118
Q

What is indirect inguinal hernia?

A
  • goes thru the interal (deep) inguinal ring, external (superficial) inguinal ring, and into the scrotum
  • enters internal inguinal ring lateral to inferior epigastric artery
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119
Q

What does an indirect inguinal hernia take place in infants?

A
  • due to failure of processus vaginalis to close ( can form hydrocele); much more in common in males
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120
Q

What does an indirect inguinal hernia follow?

A

the path of descent of testes

- covered by all 3 layers of the spermatic fascia

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121
Q

What is a direct inguinal hernia?

A
  • goes thru Hesselbach’s triangle
  • bulges directly through the abdominal wall medial to inferior epigastric artery
  • goes thru external inguinal ring only
  • covered by external spermatic fascia
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122
Q

Who does a direct inguinal hernia occur in?

A

older men

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123
Q

How to remember the indirect and direct inguinal hernias?

A

MD’s dont LIe:
Meidal to inferior epigastric artery = Direct
Lateral to inferior epigastric artery = Indirect

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124
Q

What is a femoral hernia?

A
  • protrudes below inguinal ligament thru the femoral canal below and lateral to pubic tubercle
  • more common in women
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125
Q

What is the leading cause of bowel incarceration?

A

femoral hernia

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126
Q

What is in the Hesselbach’s triangle?

A

=inferior epigastric vessels

  • lateral border of rectum abdominis
  • inguinal ligament
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127
Q

Where is gastrin made?

A

G cells in antrum of stomach

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128
Q

What is the role of gastrin?

A
  • increase gastric acid secretion
  • increases growth of gastric mucosa
  • increases gastric motility
  • increases pepsinogen secretion
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129
Q

How is gastrin regulated?

A
  1. increased by stomach distention/alkalinization, amino acids, peptides, vagal stimulation
  2. decreased by stomach pH < 1.5
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130
Q

What AA are potent stimulators of gastrin?

A

Phe and Trp

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131
Q

Where is CCK made?

A

I cells in duodenum and jejunum

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132
Q

What is the role of CCK?

A
  1. increase pancreatic secretion
  2. Increases gallbladder contraction
  3. decrease gastric emptying
  4. increase sphinter of Oddi relaxation
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133
Q

How is CCK regulated?

A

increased by fatty acids and amino acids

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134
Q

What does CCK act on to play it’s role in the GIT?

A

muscarinic pathways to cause pancreatic secretion

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135
Q

Where is secretin made?

A

S cells of duodenum

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136
Q

What is the role of secretin?

A
  1. increase pancreatic bicarb secretion
  2. decrease gastric acid secretion
  3. increase bile secretion
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137
Q

How is secretin regulated?

A
  1. increased by acid, fatty acids in lumen of duodenum
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138
Q

Where is somatostatin made?

A

D cells of pancreatic islets and GI mucosa

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139
Q

What is the role of somatostatin?

A
  1. decrease gastric acid and pepsinogen secretion
  2. decrease pancreatic and small intestine fluid secretion
  3. decrease gall bladder contraction
  4. decreased insulin and glucagon release
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140
Q

How is somatostatin regulated?

A
  • increased by acid entering duodenum

- decreased by vagal stimulation

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141
Q

Where is glucose-dependent insulinotropic peptide made? GIP

A

K cells of duodenum and jejunum

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142
Q

What is the role of GIP?

A

Exocrine - decrease gastric H secretion

Endocrine - increase insulin release

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143
Q

How is GIP regulated?

A

increased by fatty acids, amino acids, and oral glucose

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144
Q

Where is vasoactive intestinal peptide made (VIP)?

A

parasympathetic ganglia in sphincters, gall bladders, small intestine

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145
Q

What is the role of VIP?

A
  1. increase intestinal water and electrolyte secretion

2. increase relaxation of intestinal smooth muscle and sphincters

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146
Q

How is VIP regulated?

A
  • increased by distention and vagal stimulation

- decreased by adrenergic input

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147
Q

What is a VIPoma?

A

non-alpha, non-beta islet cell pancreatic tumor that secretes VIP

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148
Q

What are the symptoms of VIPoma?

A
  • copious watery diarrhea
  • hypokalemia
  • achlorhydria
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149
Q

What is the role of NO?

A

increase SM relaxation, including LES

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150
Q

What is the role of motilin?

A

produces migrating motor complexes by initiating myenteric motor complexes

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151
Q

Where is intrinsic factor made?

A

parietal cells in stomach

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152
Q

What is the role of intrinsic factor?

A

vitamin B12 binding protein (required for B12 uptake in terminal ileum)

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153
Q

What happens w/ autoimmune destruction of parietal cells?

A

chronic gastritis and pernicious anemia

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154
Q

Where is gastric acid made?

A

parietal cells in stomach

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155
Q

What is the role of gastric acid?

A
  1. decreases stomach pH
  2. protects against bacteria
  3. activates pepsinogen
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156
Q

How is gastric acid regulated?

A
  1. increased by histamine, Ach, and gastrin

2. decreased by somatostatin, GIP, low pH, PGs, secretin

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157
Q

Where is pepsin made?

A

chief cells in stomach for protein digestion

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158
Q

How is pepsin regulated?

A
  • increased by vagal stimulation, local acid, and gastrin
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159
Q

Where is bicarb made in the GIT?

A
  • mucosal cells in stomach, duodenum, salivary glands, pancreas, and Brunner glands in duodenum
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160
Q

How is bicarb regulated?

A
  • increased by pancreatic and biliary secretion w/ secretin and by vagal stimulation
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161
Q

How is saliva production regulated?

A

by both SNS and PNS in the salivary glands

  1. parotid gland - 25% of saliva volume; serous
  2. submandibular - 70% of volume; mucinous and serous
  3. sublinguinal - 5% of volume; mixed as well
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162
Q

What are the contents of saliva?

A
  • amylase - digests starch
  • bicard - neutralized bacterial acids
  • mucins - lubricate fod
  • lipase, lysozyme, defensins, lactoferrin, IgA, growth factors
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163
Q

What is the concentration of saliva normally?

A

hypotonic b/c of absorption of Na and Cl at low flow rates

- isotonic w/ higher flow rates

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164
Q

Where is the parotid gland located?

A
  • surface of masseter muscle
  • anterior to external auditory meatus
  • cranial nerve 7 runs thru it but is innervated by V3
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165
Q

What is the content of gastric secretions?

A
  • high in H, K and Cl, low in Na
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166
Q

How does vagal stimulation activate gastric acid release from parietal cells?

A
  1. GRP stimulates G cells to release gastrin

2. acts on M3 receptor of parietal cell for Gq to increase Ca and activate HKATPase –> This can be blocked by Atropine

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167
Q

How does gastrin activate gastric acid release from parietal cells?

A
  1. binds to CCKB receptor on and Gq to increase Ca and activated HKATPase
  2. activates histamine release from ECL cells
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168
Q

How does histamine activate gastric acid release from parietal cells?

A

released from ECL cells and bind to H2 receptors via Gs to increase cAMP to activate HKATPase

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169
Q

How do PGs, misoprostol, and somatostatin inhibit release of gastric acid from parietal cells?

A
  • they activate Gi and decrease cAMP levels
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170
Q

What is the main enzyme needed to set up the H and Cl secretion from parietal cell?

A
  • Carbonic anhydrase
    exchanged Bicarb fro Cl and causes alkaline tide in venous blood
  • H is secreted by HKATPase
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171
Q

What happens to Brunner glands in PUD?

A

hypertrophy

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172
Q

What is the tonicity of pancreatic secretions?

A

isotonic

  1. low flow - high in Cl
  2. high flow - high in Bicarb
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173
Q

What pancreatic enzyme is going to do the following digestions?

  1. starch
  2. fat
  3. protein
A
  1. alpha-amylase
  2. lipase, PLA2, colipase
  3. proteases - trypsin, chymotrypsin, elastase, carboxypeptidases. secreted as proenzymes
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174
Q

What does trypsinogen do?

A
  • converted to active trypsin and then activates teh other zymogens and creates more trypsinogen (positive feedback loop)
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175
Q

How is trypsinogen activated?

A

by enterokinase/enteropeptidase

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176
Q

What enzymes are involved in carbohydrate digestion?

A
  1. salivary amylase
  2. pancreatic amylase
  3. oligosaccharide hydrolases
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177
Q

What is the role of salivary amylase?

A

hydrolyzes alpha 1,4 linkages to yield disaccharides (maltose and alpha-limit dextrins)

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178
Q

What is the role of pancreatic amylase

A

hydrolyzes starch to oligosaccharides and disaccharides. highest concentration in duodenal lumen

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179
Q

What is the role of oligosaccharides hydrolases?

A
  • at brush border
  • rate limiting step in carb digestion
  • producces monosaccharides from olio/disaccharides
  • lactases, sucrases, alpha-dextrinases, etc
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180
Q

How are carbs absorbed in the GIT?

A
  1. only monosaccharides are absorbed by enterocytes (glu, gal, fru)
  2. glucose and galactose taken up by SGLT1 (Na dependent)
  3. Fructose taken up by facilitated diffusion by GLUT-5
    - all transported to blood by GLUT-2
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181
Q

Where is Fe absorbed in the GIT?

A
  • as Fe2+ in duodenum via ATPases
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182
Q

Where is folate absorbed in GIT?

A
  • jejunum
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183
Q

Where is B12 absorbed in GIT?

A
  • terminal ileum along w/ bile acids, requires IF
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184
Q

Where are TGs absorbed in GIT?

A
  • small intestine as CM via pancreatic lipase then goes thru lacteals
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185
Q

Where does the net absorption of water take place in the GIT?

A

jejenum

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186
Q

What are Peyer’s patches?

A
  • unencapsulated lymphoid tissue found in lamina propria and submucosa of ileum
  • contain specialized M cells that take up Ag
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187
Q

What happens to B cells stimulated in germinal centers of Peyer’s patches?

A
  • differentiate into IgA secreting plasma cells, which ultimately reside in lamina propria
  • IgA receives protective secretory component and is then transported across the epithelium to the gut to deal w/ intraluminal Ag
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188
Q

What is bile made up of?

A

bile salt (bile acids conjugated to glycine or taurine, making them water soluble); phospholipids, cholesterol, bilirubin, water, and ions

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189
Q

What is the E involved in the rate limiting step to make bile?

A

Cholesterol 7 alpha hydroxylase

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190
Q

What is the function of bile?

A
  1. digestion/absorption of lipids and fat soluble vitamins
  2. cholesterol excretion (body’s only means of eliminating cholesterol)
  3. antimicrobial activity via membrane disruption
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191
Q

What is the product of heme metabolism?

A

bilirubin - removed from blood by liver and conjugated w/ glucornate and excreted in bile

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192
Q

What are the steps of heme metabolism?

A
  1. heme degraded to unconjugated bilirubin ( water insolube)
  2. UCB binds to albumin and goes to liver
  3. UDP glucuronosyltransferase conjugates the UCB so now water soluble
  4. CB travels to gut and processed by bacteria to become urobilinogen
  5. 80% of urobilinogen excreted in feces as stercobilin
  6. 20% of urobilinogen undergoes enterohepatic cirulation and some excreted in urine as urobilin
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193
Q

What is the most common salivary gland tumor?

A

pleomorphic adenoma (benign mixed tumor)

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194
Q

How does a pleomorphic adenoma usually present?

A
  • painless, mobile mass, circumscribed, recurs frequently b/c of irregular margins
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195
Q

What is a pleomorphic adenoma composed of?

A

cartilage and epithelium

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196
Q

What is a Warthin’s tumor?

A

papillary cystadenoma lymphomatosum

  • benign cystic tumor w/ germinal centers.
  • 2nd MC tumor in salivary gland
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197
Q

What is the MC malignant tumor of salivary glands?

A
  • mucoepidermoid carcinoma
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198
Q

What are the components of mucoepidermoid carcinoma?

A
  • mucinous and squamous components
199
Q

How does mucoepidermoid carcinoma present?

A

as a painful mass b/c of common involvement of the facial nerve

200
Q

What is achalasia?

A

failure of relaxation of LES due to loss of myenteric plexus

- HIgh LES opening pressure and uncoordinated peristalsis –> progressive dysphagia to solids and liquids

201
Q

How can one Dx achalasia?

A
  • barium swallow shows dilated esophagus w/ an area of distal stenosis
    Bird’s beak
202
Q

When are some causes of secondary achalasia?

A

Chagas dz, Scelroderma (CREST syndrome)

203
Q

What else is achalasia associated w/?

A

increased risk of esophageal SCC

204
Q

What are risk factors for GERD?

A

EtOH, tobacco, obesity, fat rich diet, caffeine, hiatal hernia,

205
Q

What are the common clinical findings of GERD?

A

heartburn and regurgitation due to decrease in LES tone upon lying down
- may also present w/ nocturnal cough and dyspnea, adult onset asthma,

206
Q

What is esophageal varices?

A

painless bleeding of dilated submucosal veins in lower 1/3 of esophagus secondary to portal HTn
- MCC of death in cirrhois

207
Q

What is esophagitis?

A
  • associated w/ reflux, infxn, or chemical ingestion
208
Q

What are the infxn related to esophagitis?

A
  1. Candida - white psuedomembrane
  2. HSV 1- punched out ulcers
  3. CMV - linear ulcers
209
Q

What is Mallory Weiss syndrome?

A
  • mucosal lacerations at GEJ due to severe vomiting
  • leads to painful hematemesis
  • usually found in alcoholics and bulimics
210
Q

What is BoerHaave Syndrome?

A

transmural esophageal rupture due to violent retching

- related to pneumothorax

211
Q

What is esophageal strictures?

A

associated w/ lye ingestion and acid reflux

212
Q

What is Plummer-Vinson syndrome?

A
  1. Dysphagia due to esophageal webs
  2. glossitis
  3. Iron deficiency anemia
213
Q

What are esophageal webs?

A
  • thin protrusion of esophageal mucosa often in upper esophagus
  • increase risk of SCC
214
Q

What infxn is known to infame parotid gland?

A
  • Mumps ; also causes orchitis, pancreatitis, aseptic meningitis, serum amylase increased
215
Q

What are causes of sialadenitis?

A

MCC is obstructing stone leading to S. Aureus and Strep Viridans infxn
- usually unilateral

216
Q

What is Barrett’s esophagus?

A
  • Glandular metaplasia: replacement of nonkeratinized stratified squamous epithelium w/ intestinal epithelium in the distal esophagus
  • due to chronic GERD
217
Q

what can Barrett’s esophagus be associated w?

A

esophagitis, esophageal ulcers, and increased risk of esophageal adenocarcinoma

218
Q

What cancers arise in the esophagus?

A
  1. upper 2/3 = squamous

2. lower 1/3 = adenocarcinoma

219
Q

What are the risk factors for esophageal SCC?

A

achalasia, alcohol, tobacco, Zenker’s diverticula, esophageal webs, hot liquids (china and iran)

220
Q

What are the risk factors for adenocarcinoma SCC?

A

Barrett’s esophagus, tobacco, fat (obesity), GERD

221
Q

What is the lymph node drainage of the esophagus?

A
  1. upper 1/3 = cervical
  2. middle 1/3 = mediastinal or tracheobroncial
  3. lower 1/3 = celiac and gastric
222
Q

What are the symptoms of malabsorption syndromes?

A
  • diarrhea, steatorrhea, wt loss, weakness, vitamin and mineral deficiencies
223
Q

What is tropical sprue?

A
  • unknown cause but responds to antibiotics
  • can affect entire small bowel
  • arises after infectious diseases
224
Q

What is Whipple’s Disease?

A
  • infxn w/ Tropheryma whipplei (gram posiitve) - PAS stain
225
Q

What are the symptoms of Whipple’s Dz?

A
  • cardiac symptoms
  • arthralgias
  • neurologic symptoms are common
226
Q

What is the histology of Whipple’s Dz?

A

PAS positive foamy macrophages in intestinal lamina propria

227
Q

What is the treatment for Whipple’s Dz?

A
  • IV Abx for 1 day

TMP-SMX for 1 year

228
Q

What Abs are found in Celiac dz?

A

AutoAbs to gliadin, endomysial, transglutaminase

229
Q

What is the histology of Celiac dz?

A
  • blunting of villi
  • lymphocytes in lamina propria (intraepithelially)
  • crypt hyperplasia
230
Q

What area of the GIT is commonly affected in Celiac dz?

A

distal duodenum

231
Q

What are the HLA associations of Celiac dz?

A

DQ2 and DQ8

232
Q

What is associated w/ Celiac sprue?

A
  1. Dermatits Herpetiforms - due to IgA deposition at tip of dermal papillae
    - resolves w/ gluten free diet
  2. moderately increased risk of malignancy - T cell lymphoma
233
Q

What is the pathogenesis of celiac dz?

A
  • deamidated gliadin is presented by APCs via MHC II

- helped T cells mediate tissue damage

234
Q

What is the most common disaccharidase deficiency?

A

lactase deficiency –> milk intolerance

  • osmotic diarrhea
  • abdominal distention
235
Q

What does acquired disaccharidase deficiency arise from?

A

aging and GI infxn

236
Q

How do you dx lactose tolerance test?

A

positive for lactase deficiency if

  1. admin of lactose produces symptoms
  2. glucose rises < 20 mg/dl
237
Q

Histology of disaccharidase deficiency?

A
  • normal appearing villi
238
Q

What is abetalipoproteinemia?

A
  • decreased synthesis of apolipoprotein B –> inability to generate CM –> decreased secretions of cholesterol, VLDL into bloodstream –> fat accumulation in enterocytes
239
Q

When does abetalipoproteinemia present?

A

in childhood w/ malabsorption and neurologic manifestations

240
Q

What are causes of pancreatic insufficiency?

A
  • CF, obstructing cancer, chronic pancreatitis
241
Q

What are malabsorption syndromes?

A
  1. tropical sprue
  2. Whipple’s Dz
  3. Celiac sprue
  4. Disaccharidase deficiency
  5. Abetalipoproteinemia
  6. Pancreatic insufficiency
242
Q

What cancer is found above the pectinate line? below?

A

above- adenocarcinoma

below - SCC

243
Q

What type of hemorrhoids are found above the pectinate line? below?

A

above - internal

below - external

244
Q

What is the arterial supply above the pectinate line? below?

A

above - superior rectal artery (branch of IMA)

below- inferior rectal artery (branch of internal pudendal artery)

245
Q

What is the venous drainage above the pectinate line? below?

A

above - superior rectal vein –> IM vein –> portal system

below - inferior rectal vein –> internal pudendal vein –> internal iliac vein –> IVC

246
Q

What is the embryologic germ layer above the pectinate line? below?

A

above - mesoderm

below - ectoderm

247
Q

Why are internal hemorrhoids not painful?

A

b/c of visceral innervation and are therefore not painful

248
Q

Why are external hemorrhoid painful?

A

b/c of somatic innervation from the inferior rectal branch of pudendal nerve

249
Q

What is the lymphatic drainage above and below the pectinate line?

A
  • above - deep nodes

below - superficial inguinal nodes

250
Q

What are common causes of acute gastritis (erosive)?

A
  • NSAIDS (decrease PGE1 = decreased gastric mucosa protection)
  • Alcohol
  • Uremia
  • Burns (Curling’s ulcer - decreased plasma volume –> sloughing of gastric mucosa)
  • brain injury due to increased intracranial pressure (Cushing’s Ulcer –> increased vagal stimulation –> increased Ach –> increased H production)
251
Q

What are causes of chronic gastritis?

A
  1. Type A - autoimmune mediated (10%)

2. Type B - H. Pylori meidated (90%)

252
Q

Where is type A and type B chronic gastritis found in the GIT?

A
  1. Type A = fundus/body

2. Type B = antrum

253
Q

What is the MCC of vitamin B12 deficiency?

A

Type A chronic gastritis due to autoAbs to parietal cells - lack of IF

254
Q

What findings are associated w/ Abs to parietal cells?

A
  • Pernicious anemia and Achlorhydria
255
Q

What is the consequence of achlorhydria in pernicious anemia?

A
  • low acid production leads to increased gastrin levels and antral G cell hyperplasia
256
Q

How does H. pylori cause chronic gastritis?

A
  • urease and proteases weaken mucosal defenses b/c of virulence factors that penetrate through mucus layer and cause damage
257
Q

What cancer is at increased risk due to H. pylori?

A

MALT lymphoma and gastric adenocarcinoma

258
Q

What dz is associated w/ gastric hypertrophy w/ protein loss, parietal cell atrophy, and increased mucus cells?

A

Menetrier’s dz - precancerous. Rugae of stomach are so hypertrophied that they look like brain gyri

259
Q

What is the most common stomach cancer?

A

adenocarcinoma - early aggressive local spread and node/liver mets. often presents w/ acanthosis nigricans

260
Q

What is intestinal adenocarcinoma causative agents?

A
  • H pylori
  • dietary nitrosamines (smoked foods)
  • achlorhydria
  • chronic gastritis
  • type A blood
261
Q

What is the location of intestinal adenocarcinoma on the stomach?

A

lesser curvature, looks like an ulcer w/ heaped up margins and non-radiating rugal folds

262
Q

What is diffuse type stomach cancer?

A
  • not assoicated w/ H pylori
  • signet ring cells
  • stomach wall grossly thickened and leathery (linitis plastica)
263
Q

What are the lymph nodes mets associated w/ stomach cancer?

A
  • Virhchow’s node

- Sister Mary Joseph’s nodule

264
Q

What is Virchow’s node?

A
  • left supraclavicular node by metastasis from stomach
265
Q

What is Sister Mary Joseph’s nodule?

A
  • subcutaneous periumbilical metastasis
266
Q

Name this finding: bilateral metastases to ovaries w/ abundant mucus and signet ring cells?

A

Krukenberg’s tumor

267
Q

Where are ulcers seen in PUD?

A
  1. gastric - 10%, distal

2. Duodenal - 90%

268
Q

What are the characteristics of gastric ulcers?

A
  1. pain greater w/ meals= wt loss
  2. 70% due to H pylori infxn
  3. caused by decreased mucosal protection against gastric acid and NSAIDS
  4. increased risk of carcinoma
  5. often occurs in older pts
269
Q

What are the characteristics of duodenal ulcers?

A
  1. pain decreases w/ meal = wt gain
  2. 100% due to H pylori
  3. caused by decreased mucosal protection or increased gastric acid secretion (ZE syndrome)
  4. generally benign and no increase in cancer
  5. Hypertrophy of brunner glands
270
Q

What are the characteristics of a benign ulcer?

A
  • small, punched out, flar margins
271
Q

What are the characteristics of a malignant ulcer?

A
  • irregular, larger, piling up of mucosa
272
Q

What are complications of PUD?

A
  1. Hemorrhage - gastric, duodenal (posterior > anterior): on lesser curvature bleeding from left gastric. Posterior bleeding from gastroduodenal artery
  2. perforation - duodenal (anterior> posterior)
273
Q

What is the classic presentation of IBD?

A

young female w/ recurrent bloody diarrhea and ab pain

- more prevalent in west especially whites and E. european jews

274
Q

What is the location of Crohn’s dz in the GIT?

A
  • any portion of the GIT usually the terminal ileum and colon. Skips lesions and rectal sparring
275
Q

What is the location of ulcerative colitis in the GIT?

A
  • colon inflammation that starts at rectum and is continuous so no skip lesions
276
Q

What is the gross morphology of Crohn’s Dz?

A
  • transmural inflammation
    Cobblestone mucosa, creeping fat, bowel wall thickening (string sign on barium swallow x-ray), linear ulcers, fissures, fistulas
277
Q

What is the gross morphology of ulcerative colitis?

A

mucosal and submucosal inflammation only.

  • friable mucosal pseudopolps w/ freely hanging mesentery
  • loss of haustra - lead pipe appearance
278
Q

What is the microscopic morphology of Crohn’s dz?

A
  • noncaseating granuloma

- lymphoid aggregates (Th1 mediated)

279
Q

What is the microscopic morphology of ulcerative colitis?

A
  • crypt abscesses and ulcers, bleeding, no granulomas (Th2 mediated)
280
Q

What are complications of Crohn’s dz?

A
  • strictures, fistulas, perianal dz, malabsorption, nutritional depletion, CRC, oxalate stones
281
Q

What are complications of Ulcerative colitis?

A
  • malnutrition, sclerosing cholagnitis, toxic megacolon, CRC (wrose w/ right sided colitis and pancolitis)
282
Q

What are the intestinal manifestations of Crohn’s and ulcerative colitis?

A
  • Crohn’s: diarrhea that may/may not be bloody

- UC: bloody diarrhea

283
Q

What are the extraintestinal manifestations of Crohn’s dz?

A
  • migratory polyarthritis, erythema nodosum, ankylosing spondylitis, uveitis, kidney stones
284
Q

What are the extraintestinal manifestations of Ulcerative colitis?

A
  • pyoderma gangrenosum, primary sclerosing cholangitis, ankylosing spondylitis, uveitis, P-ANCA
285
Q

What is the treatment for Crohn’s dz?

A

Steroids, azathioprine, MTX, infliximab, adalimumab, S-ASA agents for mild dz

286
Q

What is the treatment for ulcerative colitis?

A

ASA preparations (sulfasalazine) , 6MP, infliximab, colectomy can be curative

287
Q

What are the smoking associations of Crohn’s and UC?

A
  • Crohn’s: smoking increases risk

- UC: smoking is protective

288
Q

What are the symptoms of Irritable bowel syndrome?

A
  • recurrent abdominal pain associated w/ at least 2 of the following symptoms
    1. pain improves w/ defecation
    2. change in stool frequency
    3. change in appearance of stool
    4. bloating, flatulence, and change in bowel habits
    5. diarrhea, constipation or alternating symptoms.
289
Q

How do you dx irritable bowel syndrome?

A
  • dx of exclusion: check TSH, CBC, ESR, stool leukocytes

- everything will be normal: no structural abnormality, chronic symptoms

290
Q

What is the goal of Rx w/ irritable bowel syndrome?

A

treat symptoms

291
Q

What is the cause of appendicitis?

A
  • acute inflammation of appendix due to obstruction by fecalith (in adults) or lymphoid hyperplasia in kids
292
Q

What are the findings for appendicitis?

A
  • initial diffuse periumbilical pain that migrates to McBurney’s point.
  • Nausea, fever, may perforate and cause peritonitis
  • guarding and rebound tenderness
293
Q

What is the location of McBurney’s point?

A

1/2 the distance from anterior superior iliac spine to umbilicus

294
Q

What is a diverticulum?

A

a blind pouch protruding from the alimentary tract that communicates w/ lumen of the gut
- most are acquired and false in taht they lack or have an attenuated muscularis externa.

295
Q

What is the MC location of diverticulum?

A

sigmoid colon

296
Q

What is the difference btw and true and a false diverticulum?

A

True - all 3 gut layers outpouch

False - only mucosa and submucosa outpouch, occur especially where vasa recta perforate muscularis externa

297
Q

What age group is diverticulosis common in?

A
  • 60 yo and older
298
Q

What is a diverticulosis caused by?

A

increased intraluminal pressure and focal weakness in colonic wall. Associated w/ low fiber diets.
- they are many false diverticula

299
Q

What are the symptoms of diverticulosis?

A
  • often asx or associated w/ vague discomfort
  • common cause of hematochezia
  • complications include diverticulitis and fistulas
300
Q

What is diverticulitis?

A
  • inflammation of diverticular classically causing LLQ pain, fever, leukocytosis
  • may perforate to cause peritonitis, abscess formation, or bowel stenosis
  • Give Abx
301
Q

What has diverticulitis also been called?

A

left sided appendicitis due to overlapping clinical presentation

302
Q

What is the treatment for diverticulitis?

A
  • metronidazole, TMP-SMX, ciprofloxacin
303
Q

What is Zenker’s diverticulum?

A
  • False diverticulum above the UES
  • herniation of mucosal tissue at Killian’s triangle b/w the thyropharyngeal and cricopharyngeal parts of the inferior pharyngeal constrictor
304
Q

What are the presenting symptoms of Zenker’s diverticulum?

A
  • halitosis (due to trapped food particles), dysphagia, and obstruction
305
Q

What is a traction diverticulum?

A

false outpouching near midpoint of esophagus

306
Q

What is epiphrenic diverticulum?

A

false outpouching immediately above the LES

307
Q

What is a Meckel’s diverticulum?

A
  • failure of vitelline duct to obliterate wk 5-6 of embryogenesis
  • connection of gut lumen and umbilicius
  • meconium drainage from umbilicus
308
Q

What is associated w/ Meckels diverticulum?

A
  • ectopic acid-secreting gastric mucosa and/or pancreatic tissue
  • Melena, RLQ pain, intussuception, volvulus, or obstruction near the terminal ileum
309
Q

What is the most common congential anomaly of the GIT?

A
  • Meckel’s diverticulum
310
Q

How can you dx Meckel’s diverticulum?

A
  • pertechnetate study
311
Q

What are the five 2’s of Meckel’s diverticulum?

A
  • 2 inches long
  • 2 ft from ileocecal valve
  • 2% of population
  • commonly presents in first 2 yrs of life
  • many have 2 type of epithelia (gastric and pancreatic)
312
Q

What causes telescoping of 1 bowel segment into distal segment commonly at the ileocecal junction?

A
  • intussusception
313
Q

What is seen w/ intussusception?

A
  • currant jelly stools
    compromise blood supply
  • unusual in adults (associated w/ intraluminal mass or tumor)
  • majority of cases w/ kids usually idiopathic, may be viral adenovirus
314
Q

What is volvulus?

A
  • twisting portion of bowel around its mesentery
  • can lead to obstruction and infarction
  • may occur at cecum - young adults
  • at sigmoid - elderly
  • USUALLY in elderly so think SIGMOID
315
Q

What is a transmural small bowel infarction do to?

A
  • embolism/thrombosis of SMA of thrombosis of mesenteric vein
  • can be due to polycythemia vera, Atrial fibrillation, or vasculitis
316
Q

What is a mucosal small bowel infarction do to?

A
  • marked hypotension b/c furthest away from blood supply
317
Q

What are clinical features of small bowel infarction?

A

ab pain, bloody diarrhea, deceased bowel sounds

318
Q

What causes Hirschsprung’s dz?

A
  • congenital megacolon due to lack of ganglino cells/enteric nervous plexuses
  • due to failure of neural crest cell migration
319
Q

How does Hirschsprung’s dz present?

A
  • chronic constipation early in life
  • dilated portion of colon proximal to the aganglionic segment (megacolon) resulting in transition zone
  • involves rectum
  • usually failure to pass meconium
  • associated w/ Down’s
320
Q

What is ileus?

A

high pitched bowel sounds

321
Q

What are symptoms of duodenal atresia?

A
  • early bilious vomiting w/ proximal stomach distention
  • shows up as double bubble on X-ray b/c of failure of recanalization of small bowel
  • associated w/ Down’s
322
Q

What is meconium ileus found in?

A
  • CF b/c meconium plug obstructs intestine preventing stool passage at birth
  • Hirschsprung’s dz
323
Q

What is necrotizing enterocolitis?

A
  • necrosis of intestinal mucosa and possible perforation

- colon is usually involved but can involved entire GI tract

324
Q

In whom is necrotizing enterocolitis more common in?

A

preemies due to decreased immunity

325
Q

What is ischemic colitis?

A
  • reduction in intestinal blood flow causes ischemia
  • Pain out of proportion w/ physical findings
  • pain after eating = wt loss
  • commonly seen as splenic flexure and distal colon
  • typically affect elderly
326
Q

What is the MCC cause of small bowel obstruction?

A

Adhesions - fibrous band of scar tissue; commonly forms after surgery

327
Q

What is angiodysplasia?

A
  • tortuous dilation of vessels causing hematochezia
  • most often found in cecum, terminal ileum and ascending colon
  • more common in old people
328
Q

What are colonic polyps?

A

masses protruding into gut lumen

  • 90% are non-neoplastic
  • often found in rectosigmoid
  • can be tubular or villous
329
Q

What are precancerous colon polyps?

A
  • adenomatous especially sessile and villous
330
Q

Malignant risk of colon polyps are associated w/ what?

A
  • increased size, villous histology, increased epithelial dysplasia
331
Q

What are colon polyp symtpoms?

A

often Asx, lower GI bleed, partial obstruction, secretory diarrhea

332
Q

What are hyperplastic colon polyps?

A
  • MC non-neoplastic polyp

- serrated/stellate appearance

333
Q

What are juvenile colon polyps?

A
  • mostly sporadic lesions in kids less than 5
  • 80% in rectum
  • if single then no malignant potential
  • when multiple then increased risk of adenocarcinoma
334
Q

What is Peutz-Jegher syndrome?

A
  • AD syndrome featuring multiple nonmalignant hamartomas thru-out GIT along w/ hyperpigmented mouth, lips, hands, gentalia
  • associated w/ increased risk of CRC and other visceral malignancies such as breast, GYN, and other GI
  • single polyps are not malignant
335
Q

What mutation is Familial adenomatous polyposis associated w/?

A
  • AD mutation of APC gene on chromosome 5q

- 2 hit hypothesis and 100% progress to CRC

336
Q

Where are the polyps in FAP?

A

always involves rectum, thousands of polyps, pancolonic

337
Q

What condition is known as FAP + osseous and soft tissue tumors, congenital hypertrophy of retinal pigment epithelium?

A

Gardner’s syndrome

338
Q

What condition is known as FAP + malignant CNS tumor?

A

Turcot syndrome

339
Q

What CRC is associated w/ AD mutation of DNA mismatch repair genes?

A
  • Hereditary nonpolyposis colorectal cancer (HNPCC/Lynch syndrome)
  • 80% progress to CRC and proximal colon is always involved
340
Q

What other cancers are associated w/ HNPCC and Lynch syndrome?

A
  • increased risk of ovarian and endometrial cancer
341
Q

What are additional risk factor besides the genetics for CRC?

A
  • IBD, tobacco use, large villous adenomas, juvenile polyposis syndrome, Peutz-Jeghers syndrome
342
Q

What area of the colon is affected w/ CRC?

A
  • rectosigmoid > ascending > descending
343
Q

What type of lesion are seen w/ CRC in the ascending colon?

A
  • Raised lesions usually = exophytic masses that cause Fe deficiency anemia and wt loss - usually a vague pain
344
Q

What type of lesion are seen w/ CRC in the descending colon?

A
  • Napkin-Ring lesion = infiltrating mass, partial obstruction, colicky pain, hematochezia
345
Q

What bacteremia is associated w/ CRC?

A

Strep bovis

346
Q

How can one Dx CRC?

A
  1. Fe deficiency anemia in males (> 50) and postmenopausal females raises suspicion
  2. Screen pts > 50 w/ colonscopy or stool occult blood test
  3. Apple core lesions on barium enema x-ray
  4. CEA tumor marker, good for monitoring recurrence, not useful for screening
347
Q

What are the 2 molecular pathways that lead to CRC?

A
  1. Microsatellite instability pathway (15%)

2. APC/Beta Catenin pathway (85%)

348
Q

What is involved in the microsatellite instability pathway for CRC?

A
  • DNA mismatch repair gene mutations –> sporadic and HNPCC symptoms.
  • mutations accumulate but no defined morphologic correlates
349
Q

What is involved in the adenoma- carcinoma sequence of CRC?

A
  1. Normal colon initially but then a loss of APC gene = decreased intercellular adhesion and increased proliferation
  2. Colon at risk then get KRAS mutation = unregulated intracellular signal transduction
  3. Adenomas forms then acquires loss of P53 = increased tumorigenesis
350
Q

What is the most common small bowel tumor?

A
  • carcinoid tumor of neuroendocrine cells
351
Q

What is the immunostain for carcinoid tumors?

A
  • synaptophysin and chromogranin
352
Q

What are the most common sites for carcinoid tumors?

A
  • appendix, ileum, and rectum
353
Q

What is seen on EM for carcinoid tumor?

A

dense core bodies on EM

354
Q

What leads to carcinoid syndrome?

A

When the cancer has metastasized to the liver where it can no longer efficiently metabolize the 5HT w/ MAO.
- there are high levels of 5HT

355
Q

What are the symptoms for carcinoid syndrome?

A
  1. flushing
  2. right side heart valve disease
  3. wheezing due to bronchospasm
  4. diarrhea
356
Q

What is the treatment for carcinoid tumor?

A
  1. resection
  2. octreotide
  3. somatostatin
357
Q

What are the clinical effects of portal HTN?

A
  1. esophageal varices
  2. hematemesis
  3. peptic ulcers
  4. melena
  5. splenomegaly
  6. caput medusae, ascites
  7. portal hypertensive gastropathy
  8. hemorrhoids
358
Q

What are the effects of liver cell failure?

A
  1. coma, scleral icterus, fetor hepaticus (musty breath)
  2. spider nevi
  3. gynecomastia, jaundice, testicular atrophy
  4. liver flap = asterixis (coarse hand tremor)
  5. bleeding tendency (decreased clotting factors and increased PT time)
  6. anemia and ankle edema
359
Q

What is cirrhosis?

A

diffuse fibrosis and nodular regeneration destroys normal architecture of liver
- increased risk for HCC

360
Q

what are the common causes of liver cirrhosis?

A
  1. viral hepatitis
  2. alcohol
  3. biliary dz
  4. hemochromatosis
361
Q

What type of heart disease is associated w/ carcinoid tumor?

A
  • right sided valvular fibrosis

- tricupsid regurg and pulmonary valve stenosis

362
Q

What are the serum markers of liver pathology?

A
  1. ALT and AST
  2. ALP
  3. GGT
363
Q

What conditions are associated w/ increased ALT and AST?

A
  1. Viral hepatitis - ALT > AST

2. Alcoholic hepatitis AST > ALT

364
Q

What conditions are associated w/ increased ALP?

A
  • obstructive liver disease (HCC), bone disease, and bile duct disease
365
Q

What conditions are associated w/ increased GGT?

A
  • increased in various liver and biliary dz like ALP but not in bone disease
366
Q

What are serum markers for the pancreas?

A
  • amlyase : increased in acute pancreatitis and mumps

- lipase : increased in acute pancreatitis

367
Q

What is Reye’s syndrome?

A
  • rare, often fatal childhood hepatoencephalopathy

- due to giving kids ASA after a viral infxn

368
Q

When is the only time to give ASA to kids?

A

Kawasaki’s disease

369
Q

What are the pathologic findings for Reye’s syndrome?

A
  1. mitochondrial abnormalities
  2. fatty liver w/ microvesicular fatty change
  3. hypoglycemia
  4. vomiting
  5. hepatomegaly
  6. coma
370
Q

What is the mechanism of damage for Reye’s syndrome?

A
  • aspirin metabolits decrease beta- oxidation by reversible inhibition of mitochondrial enzyme
371
Q

What are initial signs of alcoholic liver disease?

A

hepatic steatosis - short term change w/ moderate alcohol intake
- macrovesicular fatty changes that may be reversible w/ alcohol cessation

372
Q

What happens w/ sustained, long term consumption of alcoholic liver dz?

A
  • alcoholic hepatitis - swollen and necrotic hepatocytes w/ neutrophilic infiltration
  • mallory bodies (intracytoplasmic eosinophilic inclusions) are present
373
Q

What is the irreversible form of alcoholic liver dz?

A
  • alcoholic cirrhosis
374
Q

What is seen w/ alcoholic cirrhosis?

A
  • micronodular, irregularly shrunken liver w/ hobnail appearance.
  • sclerosis around central vein (zone III)
  • has manifestations of chronic liver disease (jaundice and hypoalbuminemia)
375
Q

What is the fibrosis in liver cirrhosis mediated by?

A
  • stellate cells via TGF-beta

- stellate cells are beneath endothelial cells that line the sinusoids

376
Q

What are the symptoms of alcoholic cirrhosis?

A
  1. portal HTN
  2. decreased detoxification of metabolites - mental states changes, asterixis, coma all due to increased ammonia
  3. decreased protein synthesis - monitor w/ PT
377
Q

What are the symptoms of Acute viral hepatitis?

A
  • jaundice (mixed CB and UCB) w/ dark urine, fever, malaise, and nausea
378
Q

What happens to liver enzymes during acute viral hepatitis?

A
  • ALT&raquo_space; AST
379
Q

What is seen in microscopic pathology of acute viral hepatitis?

A
  • inflammation w/in portal tracts and w/in lobules of liver
380
Q

What is the most common primary tumor of the liver?

381
Q

What are risk factors for HCC?

A
  1. Hep B and C
  2. Wislon’s dz
  3. hemochromatosis
  4. alpha1 antitrypsin deficiency
  5. alcoholic cirrhosis
  6. carcinogens such as aflatoxin from Aspergillus
382
Q

What are the clinical findings for HCC?

A
  1. jaundice
  2. hepatomegaly
  3. ascites
  4. polycythemia
  5. hypoglycemia
383
Q

How does HCC commonly spread?

A
  • hematogenous dissemination
384
Q

What are some other liver tumors?

A
  1. carvenous hemangioma
  2. hepatic adenoma
  3. angiosarcoma
385
Q

What tumor is most common for the liver?

A

mets from stomach, pancreas, lung, colon, and breast

- they are multiple nodules in liver. Detected as hepatomegaly w/ nodules on free edge of liver

386
Q

What is cavernous hemangioma?

A
  • common, benign liver tumor
  • typically occurs 30-50 yrs of age
  • biopsy is contraindicated b/c of risk of hemorrhage
387
Q

What is a hepatic adenoma?

A
  • benign liver tumor associated w/ OCPS or steroid use
  • can regress spontaneously
  • there is a risk of rupture and intraperitoneal hemorrhage especially during pregnancy
388
Q

What is an angiosarcoma?

A
  • malignant tumor of endothelial origin; associated w/ exposure to arsenic and PVC
389
Q

What happens to the liver when there is passive congestion of blood due to right sided heart failure and Budd- Chiari syndrome?

A

Nutmeg liver

390
Q

What happens if a nutmeg liver’s conditions persists?

A
  • centrilobular congestion and necrosis can result in cardiac cirrhosis
391
Q

What is Budd- Chiara syndrome?

A
  • occlusion of IVC or hepatic vein w/ centrilobular congestion and necrosis, leading to congestive liver dz (hepatomegaly, ascites, abdominal pain, and eventual liver failure)
392
Q

What is Budd- Chiari syndrome associated w/?

A
  • hypercoaguable state, polycythemia vera, pregnancy, and HCC
393
Q

What can develop w/ Budd-Chiari syndrome?

A
  • varices and visible abdomina/back veins

- absence of JVD

394
Q

What happens to the liver w/ alpha1 antitrypsin deficiency?

A
  • misfolded gene products aggregate in hepatocellular ER leading to cirrhosis w/ PAS positive globules in liver
395
Q

What happens to the lungs w/ alpha 1 antitrpsin deficiency?

A
  • lack of functioning enzyme = decreased elastic tissue = panacinar emphysema
396
Q

What is the basic cause of jaundice?

A
  • yellow skin and/or sclera due to elevated bilirubin caused by direct hepatocellular injury, obstruction of bile flow, and hemolysis (extravascular) or ineffective erythopoiesis
397
Q

What is associated w/ obstructed bile flow?

A
  • gallstones, pancreatic carcinoma, cholangiocarcinoma, parasites
  • HLD, xanthomas, steatorrhea w/ malabsorption
398
Q

What kind of bilirubin is elevated w/ hepatocellular damaged type jaundice?

A
  • direct and indirect elevated
  • increased urine bilirubin
  • normal/decreased urine urobilinogen
399
Q

What kind of of bilirubin is elevated w/ obstructive type of jaundice?

A
  • direct
  • increased urine bilirubin = dark urine
  • decreased urine urobilinogen
400
Q

What kind of bilirubin is elevated w/ hemolytic type of jaundice?

A
  • indirect
  • no urine bilirubin
  • increased urine urobilinogen = dark urine b/c the UCB is converted to urobilinogen
401
Q

What is the pathogenesis of physiologic neonatal jaundice?

A
  • at birth, there are immature UDP-glucuronyl transferase –> UCB –> jaundice/kernicterus
402
Q

Why does kernicterus happen w/ physiologic neonatal jaundice?

A
  • b/c UCB is fat soluble and can deposit in teh basal ganglia leading to neurologic deficits and even death
403
Q

What are the hereditary hyperbilirubinemia disorders?

A
  1. Gilbert- UCB
  2. Crigler Najjar - UCB
  3. Dubin- Johnson - CB
    - all are AR
404
Q

What is Gilbert’s syndrome?

A
  • mildly decreased UDP-glucuronyl transferase or decreased bilirubin uptake
  • elevated UCB w/ overt hemolysis, fasting, and stress
  • Asx
405
Q

What is Crigler-Najjar syndrome type I?

A
  • absent UDP-glucuronyl transferase

- presents early in life and pts die w/in a few years

406
Q

What are the findings of Crigler-Najjar syndrome type I?

A
  • jaundice, kerniterus, increased UCB
407
Q

What are the findings of Crigler-Najjar syndrome type II?

A
  • less severe and responds to phenobarbital which increases liver enzyme synthesis
408
Q

What is the treatment for Crigler-Najjar syndrome type I?

A

plasmaphereis and phototheraphy

409
Q

What is Dubin-Jonhnson syndrome?

A
  • CB b/c of defective liver excretion = grossly black liver

- benign

410
Q

What is Rotor’s syndrome?

A
  • similiar to Dubin-JOhnson but even milder and does not cause black liver
411
Q

What is the pathogenesis of Wilson’s dz?

A

inadequate hepatic copper excretion and failure of copper to enter circulation as ceruloplasmis

  • due to defect in copper transporting ATPase (ATP7B gene)
  • AR (Ch13)
412
Q

Where do copper accumulate in Wilson’s dz?

A
  • liver, brain, cornea, kidneys, and joints
413
Q

What is Wilson’s disease characterized by?

A
  1. decreased ceruloplasmin, cirrhosis, corneal deposits leading to Kayser-Fleischer rings
  2. HCC
  3. hemolytic anemia
  4. Basal ganglia degenerations (Parkinsonian symptoms)
  5. Asterixis
  6. Dementia, Dyskinesia, Dysarthria
414
Q

What is the treament for Wilson’s dz?

A
  • pencillamine chelate coppers
415
Q

What is the classic triad of hemochromatosis?

A
  1. micronodular cirrhosis
  2. DM - brittle
  3. Skin pigmentation - bronzed
416
Q

What is the pathogenesis of hemochromatosis?

A
  • deposition of hemosidern (Fe)
  • excess Fe deposition due to C282Y gene or H63D mutation on HFE gene
  • associated a/ HLA-A3
417
Q

What are other associations of hemochromatosis?

A
  • CHF

testicular atrophy in males and increased risk of HCC

418
Q

What are the primary and secondary causes of hemochromatosis?

A

Primary - AR - loss of HFE gene; loss of enterocyte mediated Fe absorption dependent on body demand
Secondary - chronic transfusion therapy

419
Q

What are the lab findings for hemochromatosis?

A

increased ferritin, Fe, and increased saturation

- decreased TIBC

420
Q

What is the treatment for hemochromatosis?

A
  • phlebotomy, deferasirox, and deferoxamine
421
Q

What is the pathogenesis for Primary biliary cirrhosis?

A
  • autoimmune destruction of intraheptaic bile ducts ,lymphocytic infiltrate and granulomas
  • think WOMEN aged 40
422
Q

What is the pathogenesis of primary scleosing cholangitis?

A
  • unknown cause of concentric onion skin bile duct fibrosis –> alternating strictures and dilations w/ beading of intra and extra hepatic bile ducts on ERCP
  • think MEN
423
Q

What is the patogenesis of secondary biliary cirrhosis?

A
  • extrahepatic biliary obstruction (gallstones, biliary stricture, chronic pancreatitis, carcinoma of pancreatic head) –> increased pressure in intrahepatic ducts –> injury/fibrosis and bile stassis
424
Q

What presents as pruritus, jaundice, dark urine, light stools, hepatosplenomegaly?

A

Secondary biliary cirrhosis
Primary biliary cirrhosis
Primary scleorsing cholangitis

425
Q

What are the labs associated w/ PBC and PSC?

A
  • increased CB
  • increased cholesterol
  • increased ALP
426
Q

What antibodies is associated w/ Primary biliary cirrhosis?

A
  • increased serum mitochondrial Abs including IgM

- associated w/ other autoimmune conditions (eg CREST, RA, and Celiac dz)

427
Q

What is associated w/ Primary sclerosing cholangitis?

A
  • Hypergammaglobulinemia (IgM)
  • Associated w/ ulcerative colitis
  • can lead to secondary biliary cirrhosis
  • P-ANCA can be positive and there is an increased risk of cholangiocarcinoma
428
Q

What is biliary atresia?

A
  • failure to form extrahepatic biliary tree lumen
  • leads to biliary obstruction w/in 1st months of life
  • presents w/ Jaundice and progresses to cirrhosis due to CB
  • icterus, clay colored stools, dark colored urine
429
Q

What is ascending cholangitis?

A
  • bacterial infxn of bile ducts
  • usually due to ascending infxn w/ enteric gram negative bacteria
  • presents as sepsis, jaundice, and abdominal pain
  • increased incidence of choledocholithiasis
430
Q

What are causes of gallstones?

A
  • increased cholesterol and/or bilirubin
  • decreased bile salts
  • gall bladder stasis
431
Q

What are the types of stones?

A
  1. cholesterol - radiolucent w/ some califications

2. Pigment - radiopaque. Black = hemolysis. Brown = infxn

432
Q

What diseases are associated w/ cholesterol stones?

A
  • obesity, Crohn’s, CF, advance age, cirrhosis, clofibrate, estrogens, multiparity, rapid wt loss, and Native American origin
433
Q

What diseases are associated w/ pigment stones?

A
  • chronic hemolysis, alcoholic cirrhosis, advanced age, and biliary infxn
434
Q

What is biliary colic?

A
  • neurohormonal activation triggers contraction of gallbladder, forcing a stone into cystic duct. may present w/out pain= waxing and waning RUQ pain
435
Q

What are complications of gallstones?

A
  • fistulas btw gallbladder and small intestine leading to air in the biliary tree
  • can obstruct ileocecal valve
436
Q

How do you dx gallstones?

A
  • USG, radiouclide biliary scan (HIDA), cholescystectomy
437
Q

What are the risk factors for gallstones?

A
  1. Female
  2. Forty
  3. Fertile (pregnancy)
  4. Fat
438
Q

What is Charcot’s traid of cholangitis?

A
  • jaundice
  • fever
  • RUQ pain
439
Q

What is a positive Murphy’s sign?

A
  • inspiratory arrest on deep RUQ palpation due to pain
440
Q

What is cholecystitis?

A
  • inflammation of gall bladder
  • usually from gallstones, rarely ischemia of infxns (CMV)
  • increased ALP if bile duct becomes involved
441
Q

What is acute cholecystitis?

A
  • RUQ pain that radiates to right scapula
  • Fever w/ increased WBC, N/V
  • risk of rupture if left untreated
442
Q

What is chronic cholecystitis?

A
  • due to chemical irriation from longstanding cholethiasis
  • porcelain gallbladder = late complication
  • dystrophic calcifications
  • Rokitansky Aschoff sinus formation
443
Q

What is the pathogenesis of acute pancreatitis?

A
  • autodigestion of pancreas by pancreatic enzymes
444
Q

What are causes of acute pancreatitis?

A
  • gall stones, EtOH = main causes

- trauma, steroids, mumps, autoimmune dz, scorpion sting, hypercalcemia, Hyper TGs (>1000), ERCP, drugs

445
Q

What are the labs for acute pancreatitis?

A
  • elevated amylase, lipase

- hypocalcemia due to fat saponification

446
Q

What are complications of acute pancreatitis?

A
  • DIC, ARDS
  • diffuse fat necrosis
  • pseudocyst formation
  • hemorrhage
  • infxn
  • multiorgan failure
447
Q

What is the pathology of chronic pancreatitis?

A
  • chronic inflammation, atrophy, calcification of pancreas, fibrosis of pancreas parenchyma
  • islet damage
448
Q

What are causes of chronic pancreatitis?

A
  • Alcohol abuse and idiopathic

CF in kids

449
Q

What can chronic pancreatitis lead to?

A
  • pancreatic insufficiency –> steartorrhea, fat soluble vitamin deficiency, DM and increased risk of pancreatic adenocarcinoma
450
Q

What are risk factors for pancreatic adenocarcinoma?

A
  • tobacco use
  • chronic pancreatitis
    age >50
  • Jewish and African American males
451
Q

Tell me about pancreatic adenocarcinoma?

A
  • prognosis averages 6 months of less
  • very aggressive tumor arising from pancreatic duct
  • usually already metastasized at presentation
  • tumors are common in pancreatic head
  • associated w/ CA19-9 and CEA
452
Q

What does pancreatic adenocarcinoma usually present w/?

A
  • abdominal pain radiating to back
  • wt loss (due to malabsorption and anorexia)
  • migratory thrombophlebitis - redness and tenderness on palpation of extremities (Trousseau’s syndrome)
  • obstructive jaundice w/ palpable, nontender gallbladder (courvoisier’s sign)
453
Q

What is the treatment for pancreatic adenocarcinoma?

A

Whipple procedure, chemotherapy, radiation therapy

454
Q

What are the H2 blockers?

A

cimetidine, ranitidine, famotidine, nizatidine

455
Q

what is the mechanism of the H2 blockers?

A
  • reversible block of histamine H2 receptors –> decreased H secretion by parietal cells
456
Q

What is the clinical use of H2 blockers?

A
  • peptic ulcer, gastritis, mild esophageal reflux
457
Q

What is the toxicity of H2 blockers?

A
  1. Cimetidine - potent inhibitor of CYP450, decreases renal excretion of Creatinine, antiandrogenic effects (prolactin release, gynecomastia, impotence, decreased libido in males, can cross BBB (confusion, dizziness, headaches) and placenta
  2. Ranitidine - decreases renal excretion of creatinine
458
Q

What are the proton pump inhibitors?

A

Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole

459
Q

MOA of PPIs?

A

irreversibly inhibits HKATPase in stomah parietal cells

460
Q

Clinical use of PPIs

A
  • peptic ulcer, gastritis, esophageal reflux, ZE syndrome
461
Q

ADE of PPIs

A
  • increased risk of C difficile infxns, pneumonia, hip fractures, decreased serum Mg w/ long term use
462
Q

MOA of bismuth and sucralfate

A
  • binds to ulcer base, providing physical protection and allowing Bicarb secretion to reestablish pH gradient in the mucous layer
  • sucralfate needs acidic pH to function
463
Q

clinical use of bismuth and sucralfate

A

increases ulcer healing, traveler’s diarrhea

464
Q

MOA of MIsoprostol

A
  • PGE analog, increased production and secretion of gastric mucous barrier, decreased acid production
465
Q

Clinical use of misoprostol

A
  • prevention of NSAID induced peptic ulcers; maintenance of a patent ductus arteriosus
  • also used to induce labor (ripens cervix)
466
Q

ADE of Misoprostol

A
  • diarrhea

- contraindicated in women of childbearing potential (abortifacient)

467
Q

MOA of octreotide

A
  • long acting somatostatin analog
468
Q

clinical use of octreotide

A
  • acute variceal bleeding, acromegaly, VIPoma, carcinoid tumor
469
Q

ADE of octreotide

A
  • nausea, cramps, steatorrhea
470
Q

What are antacids used for?

A
  • can affect absortion, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying
  • all cause hypokalemia
471
Q

What are the antacids?

A
  • Al OH
  • MgOH
  • Ca carbonate
472
Q

ADE of AlOH

A
  • constipation and hypophosphatemia, proximal muscle weakness, osteodystrophy, seizures
473
Q

ADE of MgOH

A
  • diarrhea, hyporeflexia, hypotension, cardiac arrest
474
Q

ADE of Ca carbonate

A
  • hypercalcemia, rebound acid increase

- can chelate and decrease effectiveness of other drugs

475
Q

What are some osmotic laxative?

A
  • MgOH
  • Mg citrate
  • PEG
  • lactulose
476
Q

MOA of osmotic laxatives

A
  • provide osmotic load to draw water out
477
Q

what is the cinical use for osmotic laxatives

A
  • constipation
478
Q

clinical use for lactulose

A
  • treats hepatic encephalopathy since gut flora degrade it into metabolites (lactic acid and acetic acid) that promote nitrogen excretions as Nh4
479
Q

ADE of osmotic laxatives

A
  • diarrhea, dehyrdation, may be abused by bulimics
480
Q

MOA Infliximab

A
  • TNF alpha mab
481
Q

Clinical use for infliximab

A
  • Crohn’s disease, ulcerative colitis, RA
482
Q

ADE infliximab

A
  • infection (including reactivation of latent TB)
  • fever
  • hypotension
483
Q

MOA of sulfasalazine

A
  • combo of sulfapyridine (antibacterial) and 5 aminosalicylic acid (anti-inflammatory)
    activated by colonic bacteria
484
Q

clinical use of sulfazalazine

A
  • ulcerative colitis and Crohns
485
Q

ADE of sulfasalazine

A
  • malaise, nausea, sulfonamide toxicity, reversible oligospermia
486
Q

MOA of ondansetron

A

5HT antagonist, powerful centralacting antiemetic

487
Q

Clinical use of ondansetron

A
  • control vomiting postoperatively and in pts undergoing cancer chemotherapy
488
Q

ADE of ONdansetron

A

headache, constipation

489
Q

MOA of Metoclopramide

A
  • D2 receptor antagonist, increase resting tone, contractility, LES tone, motilits
  • does not influence colon transport time
490
Q

clinical use of metoclopramide

A
  • diabetic and post-surgery gastroparesis, antiemetic
491
Q

ADE of metoclopramide

A
  1. increase parkinsonian effect
  2. restlessness, drowsiness, fatigue, depression, nausea, diarrhea
  3. drug interaction w/ Digoxin and diabetic agents
  4. contraindicated in pts w/ small bowel obstruction of Parkinson’s disease
492
Q

MOA of prokinetic agents of GIT

A
  • increase Ach, increase 5HT, decrease D2
493
Q

What are prokinetic agents?

A
  1. Cholinergic agonists
  2. AchE inhibitors
  3. Domperidone - inhibits D2
  4. Cisapride = 5HT agonist
  5. Macrolide = stimulate 5HT motilin receptors

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