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GI Flashcards

1
Q

Why is a pancreatic pseudocyst called a “pseudo”cyst?

A

Lined by granulation tissue and fibrosis not epithelium. Filled with enzymes and inflammatory debris

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2
Q

pancrease lesion shows glycogen rich cuboidal epithelium

A

serous pancreatic neoplasm

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3
Q

pancreatic lesion with columnar mucinous epithelium

A

mucinous cystic neoplasm of pancreas

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4
Q

What causes fatty liver (mechanism) of alcoholics?

A 
Excess NADH (from alch dehydrogenase and aldehyde dehydrogense)
-->decrease in fatty acid oxidation
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5
Q

What do you see on histology of kaposi’s sarcoma? Macroscopically?

A
  1. Spindle shaped tumor cells with angiogenesis

2. red/violat flat lesions or hemorrhagic nodules

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6
Q

Histology of cryptosporidium

A

Basophilic clusters on surface of intestinal mucosal cells

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7
Q

tx: wilson’s dz

A

lactulose to treat the cirrhosis

penicillamine to remove the excess copper

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8
Q

tx: hemachromatosis

A

defuroxamine

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9
Q

Sequelae/complications of ulcerative colitis

A

toxic megacolon

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10
Q

Main clinical manifestation of crohn’s

A

abdominal pain

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11
Q

main clinical manifestation of UC

A

bloody diarrhea

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12
Q

Skip lesions

A

Crohns. terminal ileum usually but lesions ANYWHERE form mouth to anus.

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13
Q

Granulomas in intestine

A

Crohns

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14
Q

Rectum is always involved in which IBD

A

Ulcerative colitis

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15
Q

mesenteric adenitis in children with abd pain, fever, nausea

A

Yersinia enterocolitica

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16
Q

Describe the schilling test

A

Give oral labeled B12 and IM b12 and measure excretion in urine. If normal urinary excretion of radiolabeled B12, this means normal absorption

  • -Administer with intrinsic factor to see if pernicious anemia or malabsorption
  • -If celiac/diphyllobothrium, no correction with intrinsic factor
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17
Q

Drugs causing esophagitis

A

tetracycline
potassium chloride
bisphosphonates

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18
Q

What do patients on opioid NOT develop tolerance to?

A

constipation

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19
Q

histology findings in alcoholic hep

A

hepatocellular swelling/necrosis

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20
Q

Hist: Acetaminophen tox

A

centrilobular necrosis

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21
Q

His: reye’s syndrome

A

microvesicular steatosis of the liver

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22
Q

Hist: Primary biliary cirrhosis

A

granulomatous bile duct destruction with lots of lymphocytes “florid ducts”

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23
Q

What are the four types of non-neoplastic polyps?

A
  1. hyperplastic polyps: from mucosal gland/crypt cells
  2. hamartomatous polyps: from smooth muscle/CT. Seen in juvenile polyposis and peutz-jegers
  3. inflammatory polyps: UC and Crohns
  4. lymphoid polyps: children
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24
Q

What factors tell you malignant potential of polyps?

A
  1. degree of dysplasia, sessile (not pedunculated)
  2. villous vs tubular
  3. size: adenomas < 2 cm usually benign.
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25
Q

Secretin is produced by

A

duodenum.

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26
Q

Action of secretin

A

increased bicarbonate secretion from exocrine pancreas

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27
Q

What stimulates secretin release?

A

HCl in the duodenum

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28
Q

Sx: PBC

A

pruritis
fatigue
xanthomas, hepatosplenomegally leading to jaundice

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29
Q

Labs: PBC

A

Elevated alkaline phosphatase, elevated IgM

-anti-mitochondrial antibodies

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30
Q

PBC associated with

A 
Sjogren''s 
raynaud's
scleroderma
hypothyroid
celiacs
BASICALLY AUTOIMMUNITY
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31
Q

Budd chiari

A

thrombosis of hepatic veins/IVC
–Portal HTN
ascites
hepatosplenomegaly

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32
Q

OATP (organic anion transporting polypeptide)

A

Used to take up indirect (unconjugated bilirubin). Passive process

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33
Q

Organic anion transporter (MRP2)

A

energy dependent transporter for excreting conjugated bilirubin. Without this, will have elevated direct hemoglobin which is excreted in urine

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34
Q

PSC associated with

A

Ulcerative colitis. Will have a high Alk Phos

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35
Q

Cobblestone colonoscopy

A

Crohn’s

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36
Q

string sign

A

colonal stricture on barium swallow seen in Crohn’s

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37
Q

Cause of duodenal atresia:

A

failure of recanalization–congenital defect

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38
Q

Cause of jejunal, ileal, and colonic atresia in newborn:

A

Vascular ischemia causing necrosis. Gives “appeal peel” appearance.

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39
Q

sternal defects in baby=

A

problem with rostral abdominal fold closure

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40
Q

bladder exstrophy caused by

A

failure of caudal abdominal wall to fold

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41
Q

duodenal atresia caused by

A

failure to recanalize

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42
Q

when does the midgut herniate through the umbilical ring

A

6th week

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43
Q

When does the midgut return to the abdominal cavity and rotate around the SMA?

A

10th week

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44
Q

malrotation of gut, volvulus arise from

A

pathology of midgut herniation/rotation

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45
Q

What is gastroschisis

A

extrusion of abdominal contents through abdominal folds, not covered by peritonium

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46
Q

what is omphalocele

A

persistence of herniation of abdominal contents into umbilical cord, not covered by peritoneum

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47
Q

Most common type of tracheoesophageal anomaly

A

esophageal atresia with distal tracheoesophageal fistula.

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48
Q

sx of EA with distal TEF

A

chocking
Air in stomach,
failure to pass NG tube into stomach

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49
Q

H type TE anomaly

A

Normal except with a fistula only

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50
Q

Pure EA

A

atresia or stenosus of esophagus alone

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51
Q

CSR of pure esophageal atresia

A

No gas in abdomen

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52
Q

olive like mass in epigastric region with projectile vomiting (nonbilius) at 2 weeks

A

congenital pyloric stenosis

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53
Q

congenital pyloric stenosis occurs in

A

first born males.

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54
Q

Tx: cong pyloric stenosis

A

surgery

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55
Q

Annular pancreas causes narrowing of

A

duodenum

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56
Q

Ventral pancreatic bud makes

A

pancreatic head, main pancreatic duct and uncinate process

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57
Q

GI retroperitoneal structures. These can cause blood or gas accumulation in retroperitoneal space

A 
Suprarenal
Aorta and IVC
Duodenum (2nd and third parts)
Pancreas
Ureters
Colon (ascending, descending)
Kidneys
Esophagus (lower 2/3)
Rectum (lower 2/3)
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58
Q

falciform ligament connects

A

liver to anterior abdominal wall

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59
Q

falciform contains

A

ligamentum teres hepatis

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60
Q

hepatoduodenal ligament connects

A

liver to duodenum

–also connects greater and lesser sacs

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61
Q

hepatoduodenal ligament contains

A

portal triad: hep arter, portal vein, common bile

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62
Q

Gastrohepatic ligament connects

A

Liver to lesser curvature of stomach

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63
Q

gastrohepatic contains

A

gastric arteries

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64
Q

You need to cut this during surgery to access the lesser sac

A

gastrohepatic ligament

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65
Q

You can use the pringle maneuver to compress this ligament to control bleeding in the omental foramen

A

hepatoduodenal

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66
Q

gastrocolic connects

A

greater curvature to transverse colon

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67
Q

gastrocolic contains

A

gastroepiploic arteries

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68
Q

gastroplenic connects

A

greater curvature and spleen

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69
Q

structures inside gastrosplenic

A

short gastrics, left gastroepiploic vessles

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70
Q

separates greater and lesser sacs on the left

A

gastrosplenic

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71
Q

splenorenal lig contains

A

splenic artery+V, tail of pancreas

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72
Q

erosions of digestive tract only extend to

A

mucosa

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73
Q

submucosa contains

A

meissner’s plexus

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74
Q

muscularis externa contains

A

myenteric nerve plexus

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75
Q

How fast do stomach/duodenum/ileum contract?

A

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

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76
Q

where do you see crypts of liberkuhn

A

duodenum, jejunum, and ileum

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77
Q

where do you see peyer’s patches?

A

ileum

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78
Q

where do you see brunner’s glands

A

duodenum

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79
Q

where do you see the largest number of goblet cells in the small intestine?

A

ileum

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80
Q

what do you see in the colon?

A

no villi, numerous goblet cells

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81
Q

When the third part of the duodenum is entrapped between SMA and aorta, causing intestinal obstruction in females

A

Superior mesenteric artery syndrome

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82
Q

parasympathetic innervation of hindgut

A

pelvic (errything else is vagus)

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83
Q

celiac artery exits at

A

T12/L1

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84
Q

SMA artery exits at

A

L1

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85
Q

IMA artery exists at

A

L3

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86
Q

supplies distal duodenum to prox 2/3 or transverse colon

A

SMA

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87
Q

supplies stomach, prox duodenum, liver, gallbladder, pancreas, spleen (mesoderm)

A

Celiac artery

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88
Q

Branches of the celiac trunk

A

common hepatic
splenic
left gastric

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89
Q

Which arteries do not have good anastamoses?

A 
short gastrics (splenic artery blockage)
However, left and right gastrics and epiploics have good anastamoses
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90
Q

branches of the common hepatic

A

hepatic artery proper
–>right gastric
gastroduodenal
–>right gastroepiploic

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91
Q

branches of the splenic

A

L gastroepiploic

short gastric arteries

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92
Q

branches of the L gastric

A

esophageal branches

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93
Q

anastamoses between external iliac and internal thoracic

A

superior/inferior epigastric

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94
Q

anastamoses between celiac trunk and SMA

A

superior/inferior pancreaticoduodenal

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95
Q

anastamoses between SMA and IMA

A

middle/left colic

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96
Q

anastamoses between IMA and internal iliac

A

superior rectal/middle and inferior rectal

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97
Q

Name the three portosystemic shunt systems

A
  1. left gastric(portal)–>esophageal(systemic)
  2. paraumbilical–>epigastric veins (systemic)
  3. superior rectal (portal)–>middle and inferior rectal (systemic)
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98
Q

How do the three portosystemic shunt explain portal HTN findings?

A
  1. esophageal varices
  2. caput medusa
  3. internal hemorroids
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99
Q

rectal adenocarcinoma

A

above pectinate line

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100
Q

rectal squamous cell carcinoma

A

below pectinate

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101
Q

rectal internal hemorrhoids vs external

A

internal: above pectinate
external: below

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102
Q

blood supply above pectinate

A

superior rectal (IMA)

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103
Q

blood supply below pectinate

A

inferior rectal (internal pudendal)

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104
Q

venous drainage above pectinate line

A

superior rectal–>inferior mesenteric–>portal system

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105
Q

venous drainage below pectinate line

A

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

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106
Q

innervation below pectinate

A

painful external hemorrhoids

–inferior rectal branch of pudendal nerve

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107
Q

lymphatic drainage above pectinate line

A

deep nodes

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108
Q

lymphatic drainage below pectinate line

A

superficial inguinal nodes

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109
Q

which liver zone affected first by viral hepatitis?

A

Zone 1 (periportal)

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110
Q

Which liver zone affected first by ischemia and alcoholic hepatitis?

A

Zone 3 (central vein)

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111
Q

which liver zone has the P450 system

A

Zone 3

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112
Q

Order of structures in femoral region

A

nerve, artery, vein, empty space, lymph (from lateral to medial)

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113
Q

femoral triangle

A

femoral vein, artery, nerve

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114
Q

femoral sheath

A

femoral vein, artery, and canal with deep inguinal nodes

NO NERVE

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115
Q

External spermatic cord

A

external oblique

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116
Q

cremaster muscle and fascia made of

A

internal oblique

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117
Q

internal spermatic fascia made of

A

transversalis fascia

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118
Q

Why doesn’t the spermatic cord have transversus abdominis muscle?

A

There’s a hole in the muscle where it passes through. The normal order is

  1. transversalis
  2. transversus abdominis
  3. internal oblique
  4. external oblique
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119
Q

GE junction is displaced upwards through diaphragm=hourglass stomach

A

sliding hiatal hernia

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120
Q

fundus of stomach protrudes into thorax, although GE junction is normal

A

paraesophageal hernia. bowel sounds in the lung fields

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121
Q

This type of hernia passes lateral to the inferior epigastric artery

A

indirect inguinal hernia

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122
Q

cause of indirect inguinal hernia

A

failure of processus vaginalis to close. Occurs in infants

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123
Q

this inguinal hernia passes medial to inferior epigastric

A

direct inguinal hernia. passes through hesselbach’s triangle

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124
Q

Indirect hernias are covered by

A

all three layers of spermatic fascia

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125
Q

direct hernias are covered by

A

only external spermatic fascia. usually happens in old men

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126
Q

which Amino acids are potent stimulators of gastrin

A

phenylalanine

tryptophan

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127
Q

what produces cholecystokinin?

A

I cells

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128
Q

Where are I cells found

A

duodenum/jejunum

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129
Q

Action: CCK

A 
pancreatic secretions
gallbladder contractions
sphincter of oddi relaxation
decreased gastric emptying
THINK: RELEASE OF PANCREATIC ENZYMES
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130
Q

stimulant: CCK

A

fatty acids/amino acids

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131
Q

where do you find S cells?

A

duodenum

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132
Q

action: secretin

A

pancreatic HCO3
decrease gastric acid
increase bile secretion
THINK: DECREASING ACIDITY

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133
Q

How is secretin regulated?

A

Increased by acid, fatty acids in lumen of duodenum

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134
Q

action: somatostatin

A

decreases gastric acid secretion
decreases pancreatic secretions
decreases gallbladder
decreases insulin/glucaton

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135
Q

regulation: somatostatin

A

Increased by acid

decreased by vagal stimulation

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136
Q

which cells release somatostatin?

A

D cells of pancreas, GI mucosa

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137
Q

glucose dependent insulinotropic peptide (GIP) effects

A

decrease gastric acid

Increase insulin release

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138
Q

which cells release GIP?

A

K cells of duodenum/jejunum

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139
Q

source: vasoactive intestinal polypeptide (VIP)

A

parasympathetic ganglia

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140
Q

Action: VIP

A

increase water/electrolyte secretion

relaxation of intestinal smooth muscle

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141
Q

Stimulation: VIP

A

vagal stimulation and distention

inhibited by adrenergics (duh)

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142
Q

copious watery diarrhea, hypokalemia, and achlorhydria (little to no stomach acid)

A

VIPoma

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143
Q

Nitric oxide’s role in GI

A

relaxes GEJ sphincter

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144
Q

motilin action

A

migrating motor complexes for peristalsis in small intestin

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145
Q

when is motilin high

A

fasting state

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146
Q

which drugs work as motilin agonists

A

erythromycin

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147
Q

How do you regulate gastric acid?

A

Increase: histamine, ACh, gastrin
Decrease: somatostatin, GIP, prostaglandin, secretin

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148
Q

which cells secrete pepsin

A

chief cells

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149
Q

what stimulates pepsin release

A

vagal stimulation, acid

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150
Q

What secretes HCO3

A

Mucosal cells and brunner’s glands

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151
Q

Stimulation: HCO3

A

increased pancreatic/biliary secretion

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152
Q

is saliva stimulated by sympathetic or parasympathetic activity?

A

Both. Note that it is hypotonic with low flow rates but isotonic at high flow rates

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153
Q

vagus nerve stimulates

A

Parietal cells and G cells

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154
Q

what happens in stomach when you give atropine?

A

Mild decrease in stomach acid.

  • vagus nerve releases ACh on parietal cells
  • vagus nerve releases GRP on G cells–>gastrin–>ECL cells–>histamine–>parietal cells

The pathway through GRP and histamine is much stronger stimulator

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155
Q

brunner gland hypertrophy

A

peptic ulcer disease. Because working overtime to secrete alkaline mucus

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156
Q

How else can gastrin release acid?

A

binds to CCK receptor and upregulates H/K ATPase

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157
Q

intracellular signaling of H2 receptor:

A

cAMP increases–>H/KATPase

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158
Q

intracelular signalling of Ach and Gastrin

A

Gq

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159
Q

intracellular signaling of somatostatin

A

Gi

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160
Q

Describe the flow of pancreatic secretions

A

low flow=high Cl-

high flow=high HCO3-

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161
Q

Pancreatic acid secretions

A

alpha-amylase
Lipases (phospholipase A, colipase)
Proteases (trypsin, chymotrypsin, elastase)
trypsinogen

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162
Q

salivary amylase hydrolyzes

A

alpha 1,4 linkages–>disaccharides

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163
Q

glucose/galactose transporter

A

SGLT1 (sodium dependent)

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164
Q

fructose transporter

A

GLUT-5 (facilitate difusion)

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165
Q

GLUT2

A

transports monosaccharides to gut

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166
Q

iron absorbed in

A

duodenum

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167
Q

folate absorbed in

A

jejunum

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168
Q

D xylose tells you

A

integrity of gastric mucosa in absorption.

D xylose requires NO breakdown! If problem is with breakdown (i.e. no secretions) then D xylose should be normal

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169
Q

Maltose is made of

A

glucose+glucose

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170
Q

lactose is made of

A

glucose+galactose

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171
Q

where are lipids digested/absorbed?

A

digested in duodenum, absorbed in jejunum

172
Q

special cells in peyer’s patches that take up antigen

A

M cells

173
Q

what happens when B cells in peyer’s patches are stimulated?

A

differentiate into IgA secreting plasma cells

174
Q

difference between bile acids vs salts?

A

bile acids are conjugated to glycine/taurine

175
Q

rate limiting step of bile acid secretion

A

cholesterol 7a-hydroxylase

176
Q

What carries bilirubin in blood?

A

albumin

177
Q

urobilinogen

A

conjugated bilirubin that has been processed by the gut bacteria

178
Q

how much of urobilinogen is reabsorbed?

A

20%. Of that, 10% is excreted in urine and 90% goes back to liver

179
Q

painless mobile mass in neck made of cartilage and epithelium and recurs frequently. A salivary tumor

A

pleomorphic adenoma. Most common!

180
Q

salivary tumor: A benign cystic tumor in germinal centers

A

warthin’s tumor

181
Q

salivary gland: mucinous and squamous components. presents as a PAINFUL mass

A

mucoepidermoid carcinoma

182
Q

achalasia=increased risk for

A

esophageal squamous cell carcinoma

183
Q

secondary achalasia

A

chagas, CREST

184
Q

pts with achalasia have problems swallowing

A

BOTH solids in liquids!

If obstructive mass, liquids are fine

185
Q

Can also present as nocturnal cough/dyspnea or adult onset asthma

A

GERD

186
Q

causes of esophagitis

A

reflux
infections (like candida etc)
chemical ingestion

187
Q

punched out ulcers in esophagus

A

HSV-1

188
Q

linear ulcers in the esophagus

A

CMV

189
Q

mucosal lacerations at the GEJ from severe vomiting

A

mallory weiss syndrome

190
Q

who is at risk of mallory weiss?

A

alcoholics/bulimics

191
Q

transmural esophageal rupture from violent retching

A

boerhaave syndrome. May have crackling beneath skin from air in mediastinum

192
Q

esophageal strictures associated with

A

lye ingestion and acid reflux

193
Q

Plummer vinson syndrome

A

dysphagia
glossitis
iron deficiency anemia

194
Q

barrett’s esophagus predisposes to what cancer

A

esophageal ADENOcarcinoma (not squamous)

195
Q

which esophageal cancer is most common worldwide?

A

squamous

196
Q

alcohol=type of esophageal cancer?

A

squamous

197
Q

cigarettes=type of esophageal cancer?

A

both

198
Q

diverticula=type of esophageal cancer?

A

squamous

199
Q

esophagela web=type of esophageal cancer?

A

squamous

200
Q

fat=type of esophageal cancer?

A

adeno

201
Q

GERD=type of esophageal cancer?

A

adeno

202
Q

hot liquids=type of esophageal cancer?

A

squamous

203
Q

How to treat tropical sprue?

A

antibiotics. We don’t understand the cause! but it looks similar to celiac’s
- -AFFECTS JEJUNUM AND ILEUM not duodenum

204
Q

PAS positive foamy macrophages in intestine and mesenteric nodes

A

Whipple’s disease

205
Q

Presentation: Whipple’s disease

A

cardiac symptoms
arthralgias
neuro sx
–>usually presents in older men

206
Q

Which part of the intestine is affected in celiac’s

A

distal duodenum

  • -LESS so jejunum/ileum
  • -hyperplasia of crypts seen
207
Q

histology of lactose intolerant peeps

A

normal villi!!!!

208
Q

lactose tolerance test

A
  1. symptomatic

2. glucose rises t absorbing that milk!)

209
Q

child presents with malabsorption and neuro deficits, biopsy shows fat accumulation within enterocytes. Also no VLDL or LDL

A

abetalipoproteinemia. Missing B48 and B100

210
Q

Three causes of pancreatic insufficiency

A
  1. cystic fibrosis
  2. cancer
  3. chronic pancreatitis
211
Q

Celiac HLA predisposition

A

HLA-DQ2, HLA-DQ8

212
Q

Antibodies in celiac sprue?

A

anti-TTG
anti-endomysial
anti-gliadin

213
Q

histology findings in celiacs

A

blunting of villi

lymphocytes in lamina propria

214
Q

skin condition associated with celiac’s

A

dermatitis herpetiformis

215
Q

celiac malignancy

A

T cell lymphoma. Think about refractory celiacs that has been well controlled

216
Q

Gastric ulcer in burn victim

A

curling’s ulcer. Happens cuz low plasma volume allows sloughing of mucosa

217
Q

gastric ulcer in pt with TBI

A

cushing’s ulcer

–>increased vagal sitmulation increases acid production

218
Q

Type A chronic gastritis

A

pernicious anemia

219
Q

pernicious anemia affects which part of the stomach?

A

fundus/body

220
Q

Type B chronic gastritis

A

H pylori.

221
Q

H pylori affects which part of stomach?

A

antrum

222
Q

Gastric hypertrophy with protein loss, parietal cell atrophy and lots of mucous cells. Rugae look like brain gyri

A

Menetrier’s disease

223
Q

what are you worried about with menetrier’s?

A

gastric cancer

224
Q

skin findings in stomach cancer

A

acanthosis nigracans

LOTS of seborrheic keratoses (leser-Trelat sign)

225
Q

possible nodal spread of stomach cancer

A
  1. virchow’s node
  2. krukenberg’s tumor: bilateral metastases to ovaries
  3. sister mary joseph’s nodule: periumbilical metastasis
226
Q

histology findings of krukenberg tumor

A

mucus and signet ring cells

227
Q

Intestinal stomach cancer associated with

A 
H pylori
nitrosamines (smoked food)
achlorhydria
chronic gastritis
TYPE A BLOOD?! weird!
228
Q

what does intestinal stomach cancer look like?

A

ulcer with raised margins

229
Q

Appearance of diffuse stomach cancer

A

thick and leathery stomach (linitis plastica)

230
Q

histology of diffuse stomach cancer

A

signet cell rings

231
Q

which type of ulcer has more pain with meals? less pain with meals?

A

gastric: more pain
duodenal: less pain

232
Q

which ulcer is more associated with H pylori?

A

duodenal ulcers almost always H pylori

gastric ulcer 70%

233
Q

zollinger ellison causes which type of ulcer

A

duodenal. caused by increased acid secretion

Note that increased acid secretion does not cause gastric ulcers! The stomach is prepared to handle acidity. usually caused by a problem with mucosal barrier.

234
Q

Which type of ulcer is associated with carcinomas?

A

gastric ulcer.

–>duodenal ulcers are more benign

235
Q

Which type of ulcer can hemorrhage?

A

Both!

236
Q

You find a duodenal ulcer that is hemorrhaging. is it more likely to bleed from the posterior or anterior wall?

A

posterior–from gastroduodenal artery

237
Q

You find a duodenal ulcer that is perforated. Is it more likely to perforate on the posterior or anterior wall?

A

anterior

238
Q

etiology of crohn’s disease

A

disordered response to intestinal bacteria

239
Q

which IBD is Th1 mediated? Th2?

A

Th1=crohn’s

Th2=UC

240
Q

IBD: pyoderma gangrenosum

A

UC

241
Q

IBD: erythema nodosum

A

Crohn’s

242
Q

IBD: primary sclerosing cholangitis

A

UC

243
Q

IBD: migratory polyarthritis and calcium oxalate stones

A

Crohn’s

244
Q

IBD: histology shows crypt abscesses and ulcers

A

UC

245
Q

IBD: “lead pipe appearance” on imaging

A

UC

–from loss of haustra in the colon

246
Q

IBD: creeping fat (fat growing out closer to serosa)

A

Crohn’s

247
Q

IBD: friable mucosal pseudopolyps with freely hanging mesentary

A

UC

248
Q

IBD treatment: steroidx, TNF-alpha inhibitors, azathioprine, methotrexate

A

crohn’s

249
Q

IBD tx: sulfazalazine, 6MP, TNF-alpha inhibitors, colectomy

A

UC

250
Q

Sx of IBS

A
  1. pain improves with defecation
  2. change in stool frequency
  3. change in appearance of stool
251
Q

Causes of appendicitis in kids

A

fecalith in adults

lymphoid hyperplasia in kids

252
Q

false diverticula are missing

A

muscularis externa. Only mucosa and submucosa

253
Q

diverticulosis

A

many false diverticulae in elderly from weakness of colonic walls

254
Q

diverticulosis associated with

A

low fiber diets

255
Q

sx of diverticulosis

A

hematochezia

256
Q

LLQ pain, fever, leukocytosis

A

diverticulitis

257
Q

complication of diverticulitis

A

fistula with bladder forms.

–pneumaturia: gas or air in the urine

258
Q

Zencker’s occurs btw which muscles

A

thyropharyngeal and cricopharyngeal portions of the inferior pharyngeal constrictor

259
Q

Meckel’s diverticulum caused by

A

persistence of vitelline (omphalomesenteric) duct

260
Q

The five 2’s of meck

A

2 inches long, 2 feet from ileocecal valve, 2% of population, presents in first 2 years of life

261
Q

Dx: meckel’s

A

pertechnetate study for ectopic uptake (gastric/pancreatic mucosa)

262
Q

complications of meckel’s

A

intussusception
volvulus
obstruction

263
Q

currant jelly stools

A

intussusception

264
Q

Volvulus usually occurs in what age group

A

Elderly.

265
Q

which section of colon susceptible to volvulus?

A

cecum/sigmoid colon

266
Q

vitelline sinus vs vitelline cyst etiology

A

Same as meckels, only varying degrees of malformation.

vitelline sinus–just a small string of mesentery connecting to umbilicus.

vitelline cyst has a small area of dilation outside of intestine

267
Q

chronic constipation early in life with a congenital megacolon

A

hirschsprung

268
Q

Dx: hirschsprung’s

A

rectal suction biopsy. treat with resection

269
Q

who is at risk for hirschsprungs

A

down’s syndrome

270
Q

bilious vomiting

A

duodenal atresia

271
Q

double bubble on X ray

A

duodenal atresia

–proximal stomach distention

272
Q

meconium ileus common in

A

cystic fibrosis

–meconium plug blocks intestine

273
Q

neonate with necrosis of intestinal mucosa

A

necrotizing enterocolitis

274
Q

extreme pain after eating and weight loss but normal abdominal exam in an elderly patient

A

ischemic colitis

275
Q

which areas of colon most susceptible to ischemic colitis?

A

splenic flexure and distal colon. USUALLY ATHEROSCLEROSIS OF SMA.

276
Q

most common cause of small bowel obstruction

A

adhesion

277
Q

tortuous dilation of vessels and hematochezia in an older adult located in CECUM terminal ileum, and ascending colon (right side)

A

angiodysplazia

278
Q

malignancy risk in adenomatous polyp

A

size > 1cm
villous
epithelial dysplasia

279
Q

most common type of non-neoplastic polyp?

A

hyperplastic

280
Q

juvenil polyps occur in

A

rectum

281
Q

a 4 yr old child presents with a single juvenile polyp. Does he have increased cancer risk?

A

No. However, if he has juvenile polyposis syndrome, he IS at increased risk of adenocarcinoma

282
Q

inheritance of peutz-Jeghers

A

autosomal dominant

283
Q

associated sx of peutz-jeghers

A

hyperpigmented mouth, lips, hands, genitalia

284
Q

pts with peutz jegers SYNDROME (not single polyp) are at risk for

A

CRC and other visceral malignancies

285
Q

Third most common cancer in US and third most deadly

A

CRC

286
Q

APC gene chromosome #

A

5q

287
Q

FAP+osseous and soft tissue tumors AND congenital hypertrophy of retinal pigment epithelium

A

Gardner’s syndrome

288
Q

FAP + malignant CNS tumor

A

Turcot’s syndrome

289
Q

CRC caused by DNA mismatch repair genes

A

HNPCC (aka lynch)

–Causes microsatellite instability

290
Q

inheritance of HNPCC

A

Autosomal dominant

291
Q

HNPCC usually involves which part of colon?

A

proximal. Also at risk for ovarian and endometrial carcinoma.

292
Q

FAP usually involves which part of colon?

A

rectum and the entire colon

293
Q

CRC usually affects which parts of colon?

A

rectosigmoid>ascending>descending

294
Q

CRC with exophytic mass, iron deficiency anemia, weight loss

A

ascending colon. Usually with HNPCC

295
Q

CRC with infiltrating mass, partial obstruction, hematochezia.

napkin ring lesion with decreased stool caliber

A

descending colon

296
Q

apple core lesion on barium enema

A

THINK CRC!!

297
Q

amrker for CRC

A

CEA

298
Q

APC gene codes for

A

beta catenin which is important for chromosomal stability

299
Q

Progression of CRC mutations

A
  1. APC=formation of polyp
  2. Kras=growth of polyp
  3. p53 and DCC=adenoma and carcinoma
300
Q

most common malignancy in the small intestine

A

carcinoid tumors

301
Q

pt presents with wheezing, diarrhea, flushing and right sided heart murmurs.

A

carcinoid syndrome

302
Q

dense core bodies on EM of small intestine

A

carcinoid

303
Q

pt has 5-HIAA in urine

A

Dx: carcinoid tumor!

304
Q

pt has 5-HIAA in urine but no carcinoid sx. What does this tell you?

A

The tumor is confined to the GI. All of the serotonin product is brought through portal vein to the liver, which breaks down serotonin

305
Q

Tx: carcinoid tumor

A

resection
octreotide
somatostatin

306
Q

breath smells musty and asterixis

A

liver failure

307
Q

uncommon causes of liver failure

A

hemachromatosis and biliary disease

308
Q

LFTs with viral hepatitis

A

ALT>AST

309
Q

Alkaline phosphatase tells you presence of:

A
  1. obstructive liver disease
  2. bone disease
  3. bile duct disease
310
Q

Alkaline phosphatase is elevated. What other test do you need to make sure caused by hepatic system and not by bone disease?

A

Get a gamma-glutamyl transpeptidase (GGT)

–will not be elevated in bone disease

311
Q

elevated amylase

A

pancreatitis

mumps

312
Q

decreased ceruloplasmin

A

wilson’s disease

313
Q

Hist: reye’s syndrome

A

microvesicular fatty change

314
Q

Sx: reye’s

A

hypoglycemia
vomiting
hepatomegaly
coma

315
Q

Mech: reye’s

A

aspirin inhibits enzyme causing beta oxidation of fat in mitochondria

316
Q

Hist: alcoholic hepatitis

A

swollen and necrotic hepatocytes with neutrophilic infiltration
-mallory bodies

317
Q

Hist: alcoholic cirrhosis

A

sclerosis around central vein (zone III)

318
Q

uncommon causes of HCC

A

wilson’s
hemachromatosis
a1-AT deficiency
aflatoxin exposure from aspergillus

319
Q

which marker is elevated in hepatocellular carcinoma?

A

alpha-fetoprotein

320
Q

common benign liver tumor in peeps age 30-50.

A

cavernous hemangioma

321
Q

what is contraindicated in cavernous hemangioma?

A

biopsy–hemorrhage risk

322
Q

liver tumor: malignant tumor of endothelial origin

A

angiosarcoma

323
Q

benign liver tumor associated with oral contraceptive use

A

hepatic adenoma

324
Q

associated with arsenic and polyvinylchloride

A

angiosarcoma

325
Q

Pt with signs of liver failure (ascites, hepatomegaly) with prominent abdominal and back veins and an absent JVD

A

Budd chiari syndrome. Caused by occlusion of IVC or hepatic veins

326
Q

Cause of budd chiari

A

hypercoagulable state
polycythemia vera
pregnancy
HCC

327
Q

PAS positive globules in liver with cirrhosis

A

alpha-1AT

328
Q

inheritance of a1AT

A

codominant

329
Q

Urine bilirubin is increased:

A

Heptaocellular and obstructive jaundice (none in hemolytic)

330
Q

urine urobilinogen is decreased

A

obstructive jaundice

331
Q

urine urobilinogen is increased

A

hemolytic jaundice

332
Q

labs: hepatocellular jaundice

A

direct/indirect bilirubin increased
increased urine bilirubin
normal or decrease urobilinogen (may not be secreting enough to GI tract)

333
Q

Pathophysiology of neonatal jaundice

A

immature UDP glucuronyltransferase

–>causes unconjugated hyperbilirubinemia

334
Q

Tx of neonatal jaundice

A

phototherapy

–converts unconjugated bilirubin to a soluble form

335
Q

Asymptomatic patient with high unconjugated bilirubin but not hemolysis. Labs are higher when pt is fasting or stressed

A

gilbert’s (mild decrease in UDP glucuronyltransferase)

336
Q

Tx: gilbert’s

A

none!

337
Q

Baby has jaundice. Labs show high levels of unconjugated bilirubin. Despite phototherapy, she still dies. Autopsy finds kernicterus.

Dx? how should she have been treated?

A

Crigler Najjer TYPE I. pts die in a few days. CANNOT conjugate ANY bilirubin!!

Tx: plasmapheresis and phototherapy

338
Q

Type II crigler-Najjar tx?

A

Less severe form

Tx: phenobarbital, which increases liver enzyme synthesis

339
Q

Asymptomatic patient presents with elevated direct bilirubin and jaundice. gross examination of liver biopsy shows a black liver

A

Dubin Johnson

340
Q

Tx: dubin johnson?

A

nothing. it’s benign.

341
Q

Rotor’s vs dubin johnson?

A

Rotor’s syndrome is milder and does not have a back liver

342
Q

inheritance of wilson’s disease

A

autosomal recessive

343
Q

chromosome wilson’s

A

13

344
Q

gene wilson’s

A

ATP7B

345
Q

Presentation of wilson’s

A 
Cirrhosis
hemolytic anemia
basal ganglia--parkinsonian sx
asterixis
dementia, dyskinesia, dysarthria
346
Q

pt has cirrhosis, diabetes, and bronze skin

A

hemochromatosis

347
Q

hemochromatosis mutation

A

C282Y
H63D
–>ON HFE gene

348
Q

HLA association hemochrom

A

HLA-A3

349
Q

Tx of hemochrom

A
  1. phlebotomy

defersirox/defuroxamine

350
Q

hemochromatosis risk:

A

CHF, HCC, testicular atrophy

351
Q

cause of 2ndary hemochromatosis

A

chronic transfusions (beta-thalassemia major)

352
Q

Labs: biliary cirrhosis

A

Increased conjugated bili
Increased cholesterol
Increased alkaline phosphatase

353
Q

Pathophys: Primary biliary cirrhosis

A

autoimmune rxn

354
Q

Hist: PBC

A

lymphocytic infiltrate and granulomas of the biliary tree

355
Q

Pathophys: primary sclerosing cholangitis

A

Unknown

356
Q

histology: PSC

A

onion skin bile duct fibrosis

  • -“beading” of bile ducts on ERCP
  • -alternate stricture and dilation
357
Q

antibodies in PBC

A

mitochondrial antibodies and IgM

358
Q

PBC associated with

A

Other autoimmune conditions (Crest, RA etc)

359
Q

PSC antibodies

A

hypergaammaglobulinemia IgM

360
Q

PSC associated with

A

UC

361
Q

Radiolucent gallstones

A

cholesterol. 80% of stones

362
Q

cholesterol stones associated with

A 
Crohn's
CF
rapid weight loss, clofibrate (Fat)
Age (forties)
Native Americans
estrogens (female)
multiparity (fertile)
363
Q

air in biliary tree

A

gallstone fistula with small intestine

364
Q

gallstone ileus: presentation

A

elderly female with a history of gallstone disease presents with recurrent bowel obstructions. Usually examination of nidus will show cholesterol

365
Q

Dx of gallstone

A

ultrasound, radionuclide biliary scan (HIDA scan). HIDA is definitive

366
Q

pigment stone: causes

A 
chronic hemolysis (black)
alcoholic cirrhosis
biliary infection (brown)
367
Q

Causes of acute pancreatitis

A

GET SMASHED

  1. gallstone
  2. ethanol
  3. trauma
  4. steroids
  5. mumps
  6. autoimmune
  7. scorpion sting
  8. hypercalcemia/hypertriglyceridemia
  9. ERCP
  10. Drugs (sulfa)
368
Q

Complications of acute pancreatitis

A 
DIC
ARDS
fat necrosis
hypocalcemia
pseudocyst
multiorgan failure
369
Q

why r u worried about a pancreatic pseudocyst?

A

Can rupture=hemorrhage

370
Q

do gallstones cause chronic pancreatitis?

A

NO!

371
Q

major causes of chronic pancreatitis

A

alcohol and idiopathic

372
Q

Marker for pancreatic carcinoma

A

CA-19-9

373
Q

most common site of pancreatic adenocarcinoma

A

pancreatic head–usually in ducts

374
Q

risk factors for pancreatic adenocarcinoma

A

tobacco
chronic pancreatitis
age>50
Jewish and AA males

375
Q

Sx of pancreatic cancer

A

weightloss
abdominal pain–>back
redness and tenderness on palpitation of extremities (migratory thrombophlebitis)
obstructive jaundice with NONTENDER gallbladder

376
Q

which h2 blocker inhibits CytoP450?

A

cimetidine

377
Q

side effects cimetidine

A

anti-androgenic effects

Dizziness (crosses BBB)

378
Q

Pt comes in with GERD. doc prescribes an H2 blocker. Follow up shows an increased creatinine level, pt has never had an history of renal disease. Which drug did the doc prescribe?

A

cimetidine or ranitidine

379
Q

Mechanism PPI

A

irreversibly inhibit H/K ATPase

380
Q

Tox: PPI

A

C. diff
pneumonia
hip fracture
decreased Mg2+

381
Q

mech: bismuth/sucralfate

A

bind to ulcer base, protects

382
Q

misoprostol mech

A

PGE1 analog. Increases production and secretion of gastric mucous. Decreases acid production

383
Q

Indications misoprostol

A
  1. prevention of NSAID INDUCED ulcers
  2. maintenance of patent ductus
  3. Induce labor
384
Q

tox: misoprostol

A

diarrhea

women who are trying to conceive!! (abortion)

385
Q

Mechanism: octreotide

A

Long-acting somatostatin analog

386
Q

Indications: octreotide

A

somatostatin analog

387
Q

Indications for octreotide

A
  1. VIPoma/carcinoid tumors
  2. acute variceal bleeds
  3. acromegaly
388
Q

Tox of antacids

A

hypokalemia

389
Q

Tox aluminum hydroxide

A

constipation (aluminimum amount of feces)
hypophosphatemia
osteodystrophy
muscle weakness

390
Q

Tox: mg OH

A

diarrhea (Mg must go to the bathroom)
cardiac arrest
hyporeflexia/hypotension

391
Q

Tox: Calcium carbonate

A

Hypercalcemia
Rebound acidemia
Can decrease effectiveness of other drugs like Tetracycline

392
Q

Osmotic laxatives

A

magnesium hydroxide, magnesium citrate

393
Q

which laxative can treat hepatic encephalopathy (ammonia in the brain)?

A

lactulose. Lactic acid promotes nitrogen excretion

394
Q

Tox of infliximab

A

TB reactivation, fever, hypotension

395
Q

Infliximab indications

A

Crohns

UC

396
Q

Sulfasalazine indications

A

UC

Crohns

397
Q

Tox: sulfasalazine

A

sulfonamide
oligospermia
malaise/nausea

398
Q

Ondansetron mechanism

A

5-HT3 antagonist. good for chemo pts

399
Q

mech: metoclopramide:

A

D2 antagonist
Increases gastric resting tone/motility/contractility
LES tone

400
Q

Indications for metoclopramide

A

Diabetic and post surgical gastroparesis

401
Q

Tox: metoclopramide

A

Parkinsons (Duh duz it’s a D2 antagonist!)

Interacts with digoxin and diabetic agents

402
Q

Metoclopramide is contraindicated in

A

pts with small bowel obstruction/parkinson’s

403
Q

Recurrent aphthous ulcer, genital ulcers, and uveitis

A

behcet syndrome. Aphthous is grey.

404
Q

Oral SCC risk factors

A

tobacco and alcohol

405
Q

hairy leukoplakis caused by

A

EBV in immunocompomised. NO dysplasia, only squamous hyperplasia.

Occurs on side of tongue!

406
Q

what virus can cause pancreatitis?

A

mumps

407
Q

which gland affected by pleomorphic adenoma?

A

parotid. high rate of recurrence. irregular margins.

408
Q

how do you know if pleomorphic adenoma has become cancerous?

A

facial nerve damage (pain)

409
Q

warthin tumor histology

A

lymphocytes and germinal centers in parotid

410
Q

where does esophagus spread (lymph nodes?)

A

upper 1/3: cervical
middle 1/3: mediastinal
lower 1/3: celiac/gastric nodes

411
Q

how do you make sure H pylori is gone?

A

urea breath test and stool antigen

412
Q

duodenal ulcer histology

A

hypertorphy of brunner’s glands

413
Q

intestinal gastric adeno distant metastases

A

periumbilical

414
Q

diffuse gastric adeno distant metastases

A

krukenberg

415
Q

Double bubble sign

A

duodenal atresia (bubble on either side of the atresed area)

416
Q

elderly volvulus vs teenage volulus

A

elderly=sigmoid

teen=cecum

417
Q

cause of intussusception in an adult

A

tumor

418
Q

transmural vs mucosal infarction

A

mucosa: hypotension
transmural: thrombosis

419
Q

Cause of dermatitis herpetiformis

A

deposition of IgA at dermal papillae. SHould resolve with a gluten free diet

420
Q

why test for IgG antibodies as well in celiacs?

A

Because many celiac patients also have IgA deficiency.

421
Q

carcinoid tumors stain positive with

A

chromogranin. Most common site is in the small bowel!! This is the only carcinoma in the small bowel.

422
Q

why does carinoid tumor only cause right sided valvular fibrosis?

A

lung also has monoamine oxidase to break down serotonin

423
Q

p-ANCA positive IBD

A

Ulcerative colitis

424
Q

smoking is protective against what type of IBD

A

UC

425
Q

Crohn’s disease in terminal ileum–risk for CRC?

A

NO-only if inflammation occurs in colon

426
Q

most common type of polyp

A

hyperplastic polyp. Serrated apperance.

427
Q

Enzymes that shut down trypsin

A

SPINK1
Trypsin also cleaves itself
–>without these, recurrent pancreatitis

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