2007 First Aid Ch 10 Gastrointestinal

Front 1

Baby vomits milk when fed and
has a gastric air bubble.

Back 1

Blind esophagus with lower
segment of esophagus attached
to trachea.

Front 2

After a stressful life event,
30-year-old man has diarrhea
and blood per rectum;
intestinal biopsy shows
transmural inflammation.l

Back 2

Crohn’s disease.

Front 3

treatment for a Young man presents with mental
deterioration and tremors. He
has brown pigmentation in a
ring around the periphery of his
cornea and altered LFTs.

Back 3

Penicillamine for Wilson’s
disease.

Front 4

most common cause
20-year-old male presents with
idiopathic hyperbilirubinemia.

Back 4

Gilbert’s disease.

Front 5

55-year-old male with chronic
GERD presents with esophageal
cancer. what is the most common subtype

Back 5

Adenocarcinoma.

Front 6

Female presents with alternating
bouts of painful diarrhea and
constipation. Colonoscopy is
normal.

Back 6

Irritable bowel syndrome.

Front 7

derivations of
GI blood supply

Back 7

Embryonic gut
region
Celiac = Foregut
SMA = Midgut
IMA = Hindgut

Front 8

Structures supplied by
celiac artery

Back 8

Stomach to proximal duodenum; liver, gallbladder, pancreas

Front 9

Structures supplied by
SMA artery

Back 9

Distal duodenum to proximal 2/3 of transverse colon

Front 10

Structures supplied by
IMA artery

Back 10

Distal 1/3 of transverse colon to upper portion of rectum

Front 11

Branches of celiac trunk:

Back 11

common hepatic, splenic, left gastric. These comprise the
main blood supply of the stomach.

Front 12

Short gastrics have poor
anastomoses if ?

Back 12

splenic artery
is blocked.`

Front 13

If the abdominal aorta is blocked, these arterial anastomoses (with origin) compensate
name 4

Back 13

Internal thoracic/mammary (subclavian) . Superior epigastric (internal thoracic) .Inferior epigastric
(external iliac)

Superior pancreaticoduodenal (celiac trunk) . Inferior pancreaticoduodenal (SMA)

Middle colic (SMA) . Left colic (IMA)

Superior rectal (IMA) . Middle rectal (internal iliac)

Front 14

Portal-systemic
anastomoses
name 5

Back 14

1. Left gastric ¨ azygous

(esophageal varices)

2. Superior ¨ inferior rectal
(external hemorrhoids)

3. Paraumbilical ¨ inferior
epigastric (caput
medusae at navel)

4. Retroperitoneal ¨ renal

5. Retroperitoneal ¨
paravertebral

Front 15

what verices are are commonly seen with
portal hypertension

Back 15

Varices of gut, butt, and caput

Front 16

Coordinates Motility along entire gut wall. Contains cell bodies of some
parasympathetic terminal effector neurons. Located between inner (circular)
outer (longitudinal) layers of smooth muscle in GI tract wall.

Back 16

Myenteric
(Auerbach's)

Front 17

Enteric nerve plexi.
Which one
Coordinates Motility along entire gut wall.?

Back 17

Myenteric
(Auerbach's)

Front 18

Enteric nerve plexi.
Which one
Contains cell bodies of some
parasympathetic terminal effector neurons?

Back 18

Both
Myenteric
(Auerbach's)
and
Submucosal
(Meissner's)

Front 19

Enteric nerve plexi.
Which one
Located between inner (circular) and
outer (longitudinal) layers of smooth muscle in GI tract wall.?

Back 19

Myenteric
(Auerbach's)

Front 20

Enteric nerve plexi.
Which one
Regulates local Secretions, blood flow, and absorption?

Back 20

Submucosal
(Meissner's)

Front 21

Enteric nerve plexi.
Located between mucosa and inner layer
of smooth muscle in GI tract wall?

Back 21

Submucosal
(Meissner's)

Front 22

layers in order that a knife wuold go through in the lateral abdomen

Back 22

skin
superficial fascia
external oblique
internal oblique
tranversus abdominis
transversalias facia
extraperitoneal tissue
peritoneum

Front 23

Secrete alkaline mucus to neutralize acid contents entering the duodenum from the
stomach. Located in duodenal submucosa?

Back 23

Brunner’s glands

Front 24

the only GI submucosal glands

Back 24

Brunner’s glands

Front 25

Brunner’s glands
what doe they secrete and why?

Back 25

alkaline mucus to neutralize acid contents entering the duodenum from the
stomach.

Front 26

Brunner’s glands
where are they?

Back 26

Located in duodenal submucosa (the only GI submucosal glands)

Front 27

Hypertrophy of Brunner’s glands is seen in?

Back 27

peptic ulcer disease.

Front 28

Hypertrophy of ?????? is seen in peptic ulcer disease

Back 28

Brunner’s glands

Front 29

Unencapsulated lymphoid tissue found in lamina
propria and submucosa of small intestine.
Contain specialized M cells that take up antigen

Back 29

Peyer’s patches

Front 30

Peyer’s patches
special cells

Back 30

M cells

Front 31

what do stimulated B cells that leave peyer's patches become and how does it work

Back 31

IgA secreting plasma cells in mesinteric lymphnodes. IgA receives
protective secretory component and is then
transported across epithelium to gut to deal
with intraluminal antigen.

Front 32

What to think about Peyer patch related antibodies

Back 32

Think of IgA, the
Intra-gut Antibody. And
always say “secretory IgA.

Front 33

what layer are peyer's patches in

Back 33

lamina
propria and submucosa of small intestine.

Front 34

what are spaces of Disse

Back 34

perisinusoidal space in the liver

Front 35

where is the Cystic duct

Back 35

btw the gall bladder and the common bile duct

Front 36

what joins to make the common bile duct

Back 36

Cystic duct and
Common hepatic duct

Front 37

lower Pectinate line
what forms it

Back 37

Formed where hindgut meets ectoderm.

Front 38

Formed where hindgut meets ectoderm.

Back 38

Pectinate line

Front 39

Name the ligament that connects the Liver to anterior abdominal
wall?

Back 39

Falciform

Front 40

Name the ligament that connects the Liver the the duodenum?

Back 40

Hepatoduodenal

Front 41

Name the ligament that connects the Liver to lesser curvature
of stomach?

Back 41

Gastrohepatic

Front 42

Name the ligament that connects the Greater curvature and
transverse colon?

Back 42

Gastrocolic

Front 43

Name the ligament that connects the Greater curvature and
spleen?

Back 43

Gastrosplenic

Front 44

Name the ligament that connects the Spleen to posterior
abdominal wall?

Back 44

Splenorenal

Front 45

What Structures are contained in the Falciform Ligament?

Back 45

Ligamentum teres

Front 46

What Structures are contained in the Hepatoduodenal Ligament?

Back 46

Portal triad: hepatic artery,
portal vein, common
bile duct

Front 47

What Structures are contained in the Gastrohepatic Ligament?

Back 47

Gastric arteries

Front 48

What Structures are contained in the Gastrocolic Ligament?

Back 48

Gastroepiploic arteries

Front 49

What Structures are contained in the Gastrosplenic Ligament?

Back 49

No vessels

Front 50

What Structures are contained in the Splenorenal Ligament?

Back 50

Splenic artery and vein

Front 51

Important GI ligaments
which one May be compressed
between thumb and
index finger placed in epiploic
foramen (of Winslow)
to control bleeding?

Back 51

Hepatoduodenal

Front 52

Important GI ligaments
which one Separates R greater and
lesser sacs
May be cut during surgery
to access lesser sac?

Back 52

Gastrohepatic

Front 53

Important GI ligaments
which one is part of greater omentum?

Back 53

Gastrocolic

Front 54

Important GI ligaments
which one Separates L greater and
lesser sacs?

Back 54

Gastrosplenic

Front 55

what is the clinical importance of the foramen of winslow

Back 55

Portal triad can be compressed by thumb and index finger to conrtol bleeding

Front 56

Layers of gut wall (inside to
outside):

Back 56

mucosa
submucosa
muscularis externa
serosa/advetiia

Front 57

Frequencies of basal electric
rhythm: in the stomach and small bowel.

Back 57

Stomach––3 Hz
Duodenum––12 Hz
Ileum––8–9 Hz 

Front 58

layers and functions of the gut wall mucosa

Back 58

mucosa is the inner most layer and its layers are

epithelium (absorption),

lamina propria (support),

muscularis mucosa (motility)

Front 59

internal hemorrhoids:
where are they?
Arterial supply?
Venous drainage?
nervous system?

Back 59

Above pectinate line.

Superioar rectal artery (from IMA).

rectal artery (branch of IMA).

Venous drainage is to superior rectal vein (inferior
mesenteric vein) (portal system)

Internal hemorrhoids receive
visceral innervation, and are
therefore NOT painful.n

Front 60

external hemorrhoids:
where are they?
Arterial supply?
Venous drainage?
nervous system?

Back 60

Below pectinate line

Arterial supply from inferior
rectal artery (branch of internal pudendal artery).

Venous drainageto inferior rectal vein (internal pudendal vein) (internal iliac vein)(IVC).

External hemorrhoids receive
somatic innervation and are
therefore painful.i

Front 61

which hemorrhoids are painful

Back 61

external hemorrhoids

Front 62

cancer and hemorrhoids

Back 62

External hemorrhoids/ squamous cell carcinoma. often mistaken of one another

Front 63

Femoral triangle Contains

Back 63

femoral nerve, artery, vein,

Front 64

Femoral region organization

Back 64

Lateral to medial: Nerve-(Artery-Vein-Empty space- Lymphatics)

N-(AVEL)

Front 65

Femoral sheath
what and where?

contents?

Back 65

Fascial tube 3–4 cm below inguinal ligament

Contains femoral vein, artery, and canal (deep inguinal lymph nodes),
but not femoral nervea

Front 66

A hernia is a

Back 66

protrusion of peritoneum through an opening, usually sites of weakness.

Front 67

Diaphragmatic
hernia

what is it

Back 67

Abdominal structures enter the thorax;

Front 68

Diaphragmatic
hernia

in infants

Back 68

may occur
in infants as a result of defective development of
pleuroperitoneal membrane.

Front 69

Diaphragmatic
hernia

most common type and desciption

Back 69

a hiatal hernia,

stomach herniates
upward through the esophageal hiatus of the
diaphragm.

Front 70

Paraesophageal Hernia

Back 70

GE junction is
normal.
Cardia moves into
the thorax.

Front 71

which hernia
Follows the path of the descent
of the testes. Covered by all
three layers of spermatic
fascia.

Back 71

Indirect inguinal
hernia

Front 72

Indirect inguinal
hernia.
Path?

Back 72

Goes through the INternal (deep) inguinal
ring, external (superficial) inguinal ring, and
INto the scrotum. Enters internal inguinal ring
lateral to inferior epigastric artery.

Front 73

Indirect inguinal
hernia.
Who?

Back 73

INfants owing to failure of processus vaginalis
to close.
Much more common in males

Front 74

Direct inguinal
hernia
Path?

Back 74

Protrudes through the inguinal (Hesselbach’s)
triangle. Bulges directly through abdominal
wall medial to inferior epigastric artery.
Goes through the external (superficial)
inguinal ring only. Covered by transversalis
fascia.

Front 75

Direct inguinal
hernia
Who?

Back 75

Usually in older men.

Front 76

Femoral hernia
path?

Back 76

Protrudes through femoral canal below and lateral Leading
to pubic tubercle.

Front 77

Femoral hernia
Who?

Back 77

More common in women.

Front 78

Leading cause of bowel
incarcerationo

Back 78

Femoral hernia

Front 79

Hiatal hernias:
Mech

Back 79

Sliding (most
common): GE junction is
displaced

Front 80

which hernia has
GE junction is
displaced

Back 80

Hiatal hernias:

Front 81

which hernia has
GE junction is
normal

Back 81

Paraesophageal:

Front 82

Inguinal hernia
mnemonic

Back 82

MDs don’t LIe:

Medial to inferior epigastric
artery = Direct hernia.

Lateral to inferior epigastric
artery = Indirect hernia.e

Front 83

Hesselbach’s triangle:
borders

Back 83

Inferior epigastric artery
Lateral border of rectus
abdominis
Inguinal ligament

Front 84

-Inferior epigastric artery
-Lateral border of rectus
abdominis
-Inguinal ligament

Back 84

Hesselbach’s triangle:
borders

Front 85

Salivary secretion glands and
Which glands are most serous vs Mucinous

Back 85

Parotid (most serous),

submandibular,submaxillary, and

sublingual (most mucinous)
glands.

Front 86

Function and contents of Saliva

Back 86

1. á-amylase (ptyalin) begins starch digestion;
inactivated by low pH on reaching stomach

2. Bicarbonate neutralizes oral bacterial acids,
maintains dental health

3. Mucins (glycoproteins) lubricate fooda

Front 87

saliva and autonomics
which nerves

Back 87

Salivary secretion is stimulated
by both
sympathetic (T1¨CT3
superior cervical ganglion)

and parasympathetic (facial,
glossopharyngeal nerve) activity.

Front 88

saliva tonicity changes

Back 88

Low flow rate leads to hypotonic.


High flow rate leads to closer to
isotonic

Front 89

GI secretory products
what cell and organ does Intrinsic
factor come from?

Back 89

Parietal cells
Stomach

Front 90

GI secretory products
what cell and organ does Gastric acid come from?

Back 90

Parietal cells
Stomach

Front 91

GI secretory products
what cell and organ does HCO3
– come from?

Back 91

Mucosal cells
Stomach
Duodenum

Front 92

GI secretory products
what cell and organ does Cholecysto-
kinin come from?

Back 92

I cells
Duodenum
Jejunum

Front 93

GI secretory products
what cell and organ does Pepsin come from?

Back 93

Chief cells
Stomach

Front 94

GI secretory products
what cell and organ does Gastrin come from?

Back 94

G cells
Antrum of
stomach

Front 95

GI secretory products
what cell and organ does Secretin come from?

Back 95

S cells
Duodenum

Front 96

GI secretory products
what cell and organ does Somatostatin come from?

Back 96

D cells
Pancreatic
islets
GI mucosa

Front 97

GI secretory products
what cell and organ does Gastric
inhibitory
peptide
(GIP) come from?

Back 97

K cells
Duodenum
Jejunum

Front 98

GI secretory products
what cell and organ does Vasoactive
intestinal
polypeptide
(VIP) come from?

Back 98

Parasympathetic
ganglia in
sphincters,
gall bladder,
small intestine

Front 99

GI secretory products
what cell and organ does Nitric oxide come from?

Back 99

Intrinsic
factor

Gastric acid

Front 100

GI secretory products What substances do Chief cells
Stomach produce?

Back 100

Pepsin

Front 101

GI secretory products What substances do Mucosal cells
Stomach
Duodenum produce?

Back 101

HCO3–

Front 102

GI secretory products What substances do G cells
Antrum of
stomach produce?

Back 102

Gastrin

Front 103

GI secretory products What substances do I cells
Duodenum
Jejunum produce?

Back 103

Cholecysto-
kinin

Front 104

GI secretory products What substances do S cells
Duodenum
produce?

Back 104

Secretin

Front 105

GI secretory products What substances do D cells
Pancreatic
islets
GI mucosa produce?

Back 105

Somatostatin

Front 106

GI secretory products What substances do K cells
Duodenum
Jejunum produce?

Back 106

Gastric
inhibitory
peptide
(GIP)r

Front 107

GI secretory products What substances do Parasympathetic
ganglia in
sphincters,
gall bladder,
small intestine produce?

Back 107

Vasoactive
intestinal
polypeptide
(VIP)

Front 108

GI secretory products
action of Intrinsic
factor?

Back 108

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

Front 109

GI secretory products
action of Gastric acid?

Back 109

lower stomach pH

Front 110

GI secretory products
action of Pepsin?

Back 110

Protein digestion

Front 111

GI secretory products
action of HCO3–?

Back 111

Neutralizes acid
Prevents
autodigestion

Front 112

GI secretory products regulation of Gastric acid?

Back 112

increased by histamine, ACh,
gastrin

decreased by somatostatin,
GIP, prostaglandin,
secretin

Front 113

GI secretory products regulation of pepsin?

Back 113

increased by vagal stimulation,
local acid?

Front 114

GI secretory products regulation of HCO3–?

Back 114

increased by secretin

Front 115

Autoimmune destruction
of parietal cells ¨leads to

Back 115

chronic gastritis and
pernicious anemia.

Front 116

Inactive pepsinogen
becomes pepsin by

Back 116

H+

Front 117

GI Hormones Action of Gastrin?

Back 117

Increases gastric H+ secretion
Increases growth of gastric
mucosa
Increases gastric motility

Front 118

GI Hormones Action of Cholecysto-
kinin?

Back 118

Increases pancreatic secretion
Increases gallbladder
contraction


decreasesgastric emptying

Front 119

GI Hormones Action of Secretin?

Back 119

↑ pancreatic HCO3
–
secretion
↓ gastric acid secretion

Front 120

GI Hormones Action of Somatostatin?

Back 120

↓ gastric acid and
pepsinogen secretion
↓ pancreatic and small
intestine fluid secretion
↓ gallbladder contraction
↓ insulin and glucagon
release

Front 121

GI Hormones Action of Gastric
inhibitory
peptide
(GIP)?

Back 121

Exocrine:
↓ gastric H+ secretion
Endocrine:
↑ insulin release

Front 122

GI Hormones Action of Vasoactive
intestinal
polypeptide
(VIP)?

Back 122

↑ intestinal water and
electrolyte secretion
↑ relaxation of intestinal
smooth muscle and
sphincters

Front 123

GI Hormones Action of Nitric oxide?

Back 123

↑ smooth muscle
relaxation, including
lower esophageal
sphincter

Front 124

GI hormones regulation of Gastrin?

Back 124

↑ by stomach
distention, amino
acids, peptides,
vagal stimulation

↓ by stomach
pH < 1.5

Front 125

GI hormones regulation of Cholecysto-
kinin?

Back 125

↓ by secretin and
stomach pH < 1.5
↑ by fatty acids,
amino acids

Front 126

GI hormones regulation of Secretin?

Back 126

↑ by acid, fatty acids
in lumen of
duodenum

Front 127

GI hormones regulation of Somatostatin?

Back 127

↑ by acid
↓ by vagal
stimulation

Front 128

GI hormones regulation of Gastric
inhibitory
peptide
(GIP)?

Back 128

↑ by fatty acids, amino
acids, oral glucose

Front 129

GI hormones regulation of Vasoactive
intestinal
polypeptide
(VIP)?

Back 129

↑ by distension and
vagal stimulation
↓ by adrenergic input

Front 130

GI hormones regulation of Nitric oxide?

Back 130

?

Front 131

Gastrin
wrt when is it Very Very high

Back 131

↑↑ in Zollinger-
Ellison syndrome.

Front 132

what is ↑↑ in Zollinger-
Ellison syndrome.

Back 132

gastrin

Front 133

Gastrin What are Very potent stimulators

Back 133

Phenylalanine and
tryptophan are
potent stimulators.

Front 134

Phenylalanine and
tryptophan are
potent stimulators of what GI hormone

Back 134

Gastrin

Front 135

In cholelithiasis, pain
worsens after fatty
food ingestion due
to?

Back 135

↑ CCK.

Front 136

↑ HCO3
– neutralizes
gastric acid in
duodenum, allowing?

Back 136

pancreatic enzymes
to function.

Front 137

Used to treat VIPoma
and carcinoid
tumors.

Back 137

Somatostatin

Front 138

what hormone?
An oral glucose load
is used more rapidly
than the equivalent
given by IV.

Back 138

Gastric
inhibitory
peptide
(GIP)

Front 139

Gastric inhibitory peptide
(GIP)
wrt Oral Vs IV

Back 139

An oral glucose load
is used more rapidly
than the equivalent
given by IV.

Front 140

VIPoma:
what is it and what are the symps and Tx

Back 140

VIPoma: non-α, non-ß
islet cell pancreatic
tumor that secretes
VIP. Copious
diarrhea.

Tx is Somatostatin

Front 141

Loss of ?????
is implicated in ↑
lower esophageal
tone of achalasia.

Back 141

NO secretion

Front 142

Loss of NO secretion
is implicated in

Back 142

↑lower esophageal
tone of achalasia.

Front 143

Pancreatic
enzymes
Which are secreted in their active form

Back 143

α-amylase––starch digestion, secreted in active form.

Front 144

Pancreatic
enzymes name the carb ones

Back 144

α-amylase––starch digestion, secreted in active form.

Front 145

Pancreatic
enzymes name the Fat ones

Back 145

Lipase, phospholipase A, colipase––fat digestion.

Front 146

Pancreatic
enzymes name the protein ones

Back 146

Proteases (trypsin, chymotrypsin, elastase, carboxypeptidases)––protein digestion,
secreted as proenzymes.

Front 147

activation cascade for pancratic protein enzymes

Back 147

Trypsinogen is converted to active enzyme trypsin by enterokinase, a duodenal brushborder
enzyme. Trypsin activates other proenzymes and more trypsinogen (positive
feedback loop).

Front 148

Pancreatic
enzymes
Which are secreted in their in active form

Back 148

Proteases (trypsin, chymotrypsin, elastase, carboxypeptidases)––protein digestion,
secreted as proenzymes.

Front 149

Trypsinogen is converted to active enzyme trypsin by ?

Back 149

enterokinase,

Front 150

Carbohydrate digestion
name all the enzymes

Back 150

Salivary amylase

Pancreatic amylase

Oligosaccharide
hydrolases

Front 151

Carbohydrate digestion

Salivary amylase

where from and what it does?

Back 151

Starts digestion, hydrolyzes α-1,4 linkages to yield disaccharides (maltose, maltotriose,
and α-limit dextrans).

Front 152

Carbohydrate digestion

Salivary amylase

where from and what it does?

Back 152

Highest concentration in duodenal lumen, hydrolyzes starch to oligosaccharides and
disaccharides.

Front 153

Carbohydrate digestion

Salivary amylase

where from and what it does?

Back 153

At brush border of intestine, the rate-limiting step in carbohydrate digestion, produce
monosaccharides from oligo- and disaccharides.

Front 154

hydrolyzes α-1,4 linkages to yield disaccharides (maltose, maltotriose,
and α-limit dextrans).

Back 154

Salivary amylase

Front 155

Highest concentration in duodenal lumen, hydrolyzes starch to oligosaccharides and
disaccharides.

Back 155

Pancreatic amylase

Front 156

At brush border of intestine, the rate-limiting step in carbohydrate digestion, produce
monosaccharides from oligo- and disaccharides.

Back 156

Oligosaccharide
hydrolases

Front 157

the rate-limiting step in carbohydrate digestion,

Back 157

Oligosaccharide
hydrolases

Front 158

Carbohydrate
absorption
what is absorbed

Back 158

Only monosaccharides (glucose, galactose, fructose) are absorbed by enterocytes.

Front 159

Carbohydrate
absorption
mech for Glucose
into enterocytes

Back 159

Glucose and galactose are taken up by SGLT1 (Na+ dependent).

Front 160

Carbohydrate
absorption
mech for Galactose
into enterocytes

Back 160

Glucose and galactose are taken up by SGLT1 (Na+ dependent).

Front 161

Carbohydrate
absorption
mech for Fructose
into enterocytes

Back 161

Fructose is taken up by
facilitated diffusion by GLUT-5.

Front 162

Carbohydrate
absorption
mech for Glucose
from enterocytes into blood

Back 162

All (Glucose, Galactose, Fructose) are transported to blood by GLUT-2.

Front 163

Carbohydrate
absorption
mech for Galactose
from enterocytes into blood

Back 163

All (Glucose, Galactose, Fructose) are transported to blood by GLUT-2.

Front 164

Carbohydrate
absorption
mech for Fructose
from enterocytes into blood

Back 164

All (Glucose, Galactose, Fructose) are transported to blood by GLUT-2.

Front 165

Apical surface of hepatocytes face ???????
Basolateral surface face?????

Back 165

bile canaliculi.

sinusoids.

Front 166

Zones of the liver portal triads

Back 166

Zone I: periportal zone
–affected first by viral hepatitis

Zone II: intermediate zone

Zone III: pericentral vein zone
–most sensitive to toxic injury
–contains P-450 system
–affected first by ischemia
–alcoholic hepatitis

Front 167

Zones of the liver portal triads Which Zone is periportal zone?

Back 167

I

Front 168

Zones of the liver portal triads Which Zone is most sensitive to toxic injury?

Back 168

III

Front 169

Zones of the liver portal triads Which Zone is affected first by viral hepatitis?

Back 169

I

Front 170

Zones of the liver portal triads Which Zone is intermediate zone?

Back 170

II

Front 171

Zones of the liver portal triads Which Zone is pericentral vein zone?

Back 171

III

Front 172

Zones of the liver portal triads Which Zone is contains P-450 system?

Back 172

III

Front 173

Zones of the liver portal triads Which Zone is affected first by ischemia?

Back 173

III

Front 174

Zones of the liver portal triads Which Zone is alcoholic hepatitis?

Back 174

III

Front 175

Zones of the liver portal triads blood flow direction ?

Back 175

1 to 3

Front 176

Zones of the liver portal triads bile flow direction ?

Back 176

3 to 1

Front 177

Direct bilirubin is combined with what and why

Back 177

conjugated with glucuronic acid; water soluble.

Front 178

Direct bilirubin
aka

Back 178

conjugated

Front 179

Indirect bilirubin
aka

Back 179

unconjugated

Front 180

Jaundice (yellow skin, sclerae) results from

Back 180

elevated bilirubin levels.

Front 181

Bile is made of

Back 181

Composed of bile salts (bile acids conjugated to glycine or taurine making them water
soluble), phospholipids, cholesterol, bilirubin, water, and ions.

Front 182

The only significant
mechanism for cholesterol excretion.

Back 182

Bile

Front 183

one major importance of bile

Back 183

The only significant
mechanism for cholesterol excretion.

Front 184

A-chalasia =

Back 184

absence of
relaxation.

Front 185

“Bird beak” on barium swallow.

Back 185

A-chalasia

Front 186

2° achalasia may arise from
?

Back 186

Chagas’ disease.

Front 187

Achalasia and cancer

Back 187

Associated with an ↑ risk of esophageal
carcinoma.

Front 188

Achalasia mech

Back 188

Failure of relaxation of lower esophageal sphincter
(LES) due to loss of myenteric (Auerbach’s)
plexus.

Front 189

Achalasia and imaging

Back 189

Barium swallow shows dilated
esophagus with an area of distal stenosis.

Front 190

High LES opening pressure and
uncoordinated peristalsis leads to what wrt symptoms

Back 190

to progressive
dysphagia.

Front 191

Glandular metaplasia–– replacement of nonkeratinized
squamous epithelium with intestinal (columnar)
epithelium in the distal esophagus. Due to
chronic acid reflux.

Back 191

Barrett’s esophagus

Front 192

Barrett’s esophagus
hisologic mech

Back 192

Glandular metaplasia–– replacement of nonkeratinized
squamous epithelium with intestinal (columnar)
epithelium in the distal esophagus.

Front 193

Barrett’s esophagus
due to

Back 193

Due to
chronic acid reflux.

Front 194

Barrett’s esophagus
wrt cancer

Back 194

BARRett’s = Becomes
Adenocarcinoma, Results
from Reflux.

Front 195

Risk factors for esophageal cancer are:

Back 195

ABCDE
-Alcohol
-Barrett’s esophagus
-Cigarettes
--Diverticuli (e.g., Zenker’s diverticulum)
-Esophageal web (e.g., Plummer-Vinson)/
-Esophagitis (due to reflux, irritants,
infection)
-Familial

Front 196

Esophageal cancer
which types are most common

Back 196

Worldwide, squamous cell is
most common.

In US, squamous and
adenocarcinoma are equal in
incidence.

Front 197

“olive”

Back 197

Congenital pyloric
stenosis

Front 198

Congenital pyloric
stenosis
presentation

Back 198

Palpable “olive” mass in epigastric region
and nonbilious projectile vomiting at ≈ 2 weeks of age.

Front 199

Congenital pyloric
stenosis
how common and Tx

Back 199

Treatment is surgical incision.

Occurs in 1/600 live births, often in 1st-born males.

Front 200

Malabsorption
syndromes
name 5

Back 200

-Celiac sprue

-Tropical sprue

-Whipple’s disease

-Disaccharidase
deficiency

-Pancreatic
insufficiency

Front 201

Celiac sprue
mech location and testing

Back 201

Autoantibodies to gluten (gliadin) in wheat and other grains.
Proximal small bowel only.
Abnormal xylose test.

Front 202

Malabsorption
syndromes
what symptoms

Back 202

Can cause diarrhea, steatorrhea, weight loss, weakness.

Front 203

Celiac sprue associated risks

Back 203

Associated with ↑ risk of T cell lymphoma.

Front 204

Malabsorption
syndromes Associated with ↑ risk of T cell lymphoma.

Back 204

Celiac sprue

Front 205

Tropical sprue
mech location and Tx

Back 205

Probably infectious; responds to antibiotics. Can affect entire small bowel.

Front 206

Whipple’s disease
mech and symptoms

Back 206

Infection with Tropheryma whippelii; Arthralgias, cardiac, and neurologic symptoms are
common. Most often occurs in older men.

Front 207

PAS-positive macrophages in intestinal lamina
propria, mesenteric nodes.

Back 207

Whipple’s disease

Front 208

Whipple’s disease
Histo

Back 208

PAS-positive macrophages in intestinal lamina
propria, mesenteric nodes.

Front 209

Disaccharidase
deficiency
most common and features

Back 209

Most common is lactase deficiency → milk intolerance. Osmotic diarrhea.

Front 210

Due to CF, chronic pancreatitis. Causes malabsorption of protein, fat, vitamins A, D,
E, K.

Back 210

Pancreatic
insufficiency

Front 211

Pancreatic
insufficiency
due to?
What it causes?

Back 211

Due to CF, chronic pancreatitis.

Causes malabsorption of protein, fat, vitamins A, D,
E, K.

Front 212

Autoimmune-mediated intolerance of gliadin (wheat) leading to steatorrhea.

Back 212

Celiac sprue

Front 213

Celiac sprue
who gets it

Back 213

Associated
with people of northern European descent.

Front 214

Celiac sprue
histo and lab findings

Back 214

Findings include blunting of villi,
lymphocytes in the lamina propria,
and abnormal D-xylose test.

Front 215

Celiac sprue what portion of bowel

Back 215

Tends to affect
jejunum.

Front 216

Celiac sprue associations

Back 216

Associated with dermatitis herpetiformis. 10–15% lead to malignancy (most
often T-cell lymphoma).

Front 217

Associated with dermatitis herpetiformis. 10–15% lead to malignancy (most
often T-cell lymphoma).

Back 217

Celiac sprue associations

Front 218

Gastritis
which is erosive and which
is non erosive

Back 218

Acute gastritis
(erosive)

Chronic gastritis
(nonerosive)

Front 219

Acute gastritis
mech
and causes

Back 219

Disruption of mucosal barrier → inflammation.

Canbe caused by
stress,
NSAIDs,
alcohol,
uricemia,
burns (Curling’s ulcer),
and brain injury (Cushing’s
ulcer).

Front 220

Curling’s ulcer which type and cause

Back 220

acute gastritis/erosive

Burns

Front 221

Cushings ulcer which type and cause

Back 221

acute gastritis/erosive

Brain injury

Front 222

Chronic gastritis
(nonerosive)
types and locations

Back 222

Type A (fundus/
body)

Type B (antrum)

Front 223

Chronic gastritis
(nonerosive)
Type A

mech and findings

Back 223

Autoimmune disorder characterized by Autoantibodies to parietal cells leading to pernicious
Anemia, and Achlorhydria.

Front 224

Chronic gastritis
(nonerosive)
Type B
mech and findings

Back 224

Caused by H. pylori infection.
↑ risk of MALT lymphoma.

Front 225

Gastritis
which has ↑ risk of MALT lymphoma.

Back 225

Chronic gastritis
(nonerosive)
Type B

Front 226

Chronic gastritis
(nonerosive)
mnemonic

Back 226

AB pairing
Pernicious Anemia affects
gastric Body.
H. pylori Bacterium affects
Antrum.

Front 227

Peptic ulcer disease
Gastric or Duodenal?
Pain Greater with meals––weight loss.

Back 227

Gastric

Front 228

Peptic ulcer disease
Gastric or Duodenal?
Often occurs in older patients.

Back 228

Gastric

Front 229

Peptic ulcer disease
Gastric or Duodenal?
H. pylori infection in 70%; chronic NSAID use also

Back 229

Gastric

Front 230

Peptic ulcer disease
Gastric or Duodenal?
Due to ↓ mucosal protection against gastric acid.

Back 230

Gastric

Front 231

Peptic ulcer disease
Gastric or Duodenal?
Pain Decreases with meals––weight gain.

Back 231

Duodenal

Front 232

Peptic ulcer disease
Gastric or Duodenal?
Almost 100% have H. pylori infection.

Back 232

Duodenal

Front 233

Peptic ulcer disease
Gastric or Duodenal?
Due to ↑ gastric acid secretion or ↓ mucosal protection.

Back 233

Duodenal

Front 234

Peptic ulcer disease
Gastric or Duodenal?
Hypertrophy of Brunner’s glands.

Back 234

Duodenal

Front 235

Peptic ulcer disease
Gastric or Duodenal?Tend to have clean, “punched-out” margins unlike the raised/irregular margins of
carcinoma.

Back 235

Duodenal

Front 236

Peptic ulcer disease
Gastric or Duodenal?
Potential complications include bleeding, penetration, perforation, and
obstruction

Back 236

Duodenal

Front 237

Peptic ulcer disease
Gastric or Duodenal?
not intrinsically precancerous

Back 237

Duodenal

Front 238

Potential complications Duodenal ulcer

Back 238

bleeding,
penetration,
perforation,
obstruction

Front 239

Stomach cancer
What type is it

Back 239

Almost always adenocarcinoma.

Front 240

Stomach cancer
spread patterns

Back 240

Early aggressive
local spread and node/liver mets.

Virchow’s node––involvement
of supraclavicular node by
mets from stomach.

Front 241

Stomach cancer
associated with

Back 241

dietary nitrosamines, achlorhydria,
chronic
gastritis,
type A blood.

Front 242

Stomach cancer
when diffusly infiltrative

Back 242

Termed linitis plastica
when diffusely infiltrative (thickened, rigid
appearance

Front 243

Stomach cancer
hiso apperance

Back 243

signet ring cells

Front 244

Krukenberg’s tumor
what

Back 244

bilateral
mets to ovaries. Abundant
mucus, “signet-ring” cells. from Stomach cancer

Front 245

bilateral
mets to ovaries. Abundant
mucus, “signet-ring” cells

Back 245

Krukenberg’s tumor

Front 246

involvement
of supraclavicular node by
mets from stomach.

Back 246

Virchow’s node

Front 247

Crohn’s disease
Vs
Ulcerative colitis
WRT
etiology

Back 247

Crohn’s disease---
Post-infectious.

Ulcerative colitis---
Autoimmune.

Front 248

Crohn’s disease
Vs
Ulcerative colitis
WRT
Location

Back 248

Crohn’s disease---
Any portion of the GI tract, usually the terminal
ileum and colon. Skip lesions, rectal sparing.

Ulcerative colitis---
Colitis = colon inflammation.
Continuous lesions, always
with rectal involvement.

Front 249

Crohn’s disease
Vs
Ulcerative colitis
WRT
Gross morphology

Back 249

Crohn’s disease---
Transmural inflammation. Cobblestone mucosa,
creeping fat, bowel wall thickening (“string sign”
on barium swallow x-ray), linear ulcers, fissures,
fistulas.

Ulcerative colitis---
Mucosal and submucosal
inflammation only. Friable
mucosal pseudopolyps with
freely hanging mesentery.

Front 250

Crohn’s disease
Vs
Ulcerative colitis
WRT
Microscopic
morphology

Back 250

Crohn’s disease---
Noncaseating granulomas and lymphoid
aggregates.

Ulcerative colitis---
Crypt abscesses and ulcers,
bleeding, no granulomas.

Front 251

Crohn’s disease
Vs
Ulcerative colitis
WRT
Complications

Back 251

Crohn’s disease---
Strictures, fistulas, perianal disease, malabsorption,
nutritional depletion.

Ulcerative colitis---
Severe stenosis, toxic
megacolon, colorectal
carcinoma.

Front 252

Crohn’s disease
Vs
Ulcerative colitis
WRT
Extraintestinal
manifestations

Back 252

Crohn’s disease---
Migratory polyarthritis, erythema nodosum,
ankylosing spondylitis, uveitis, immunologic
disorders.

Ulcerative colitis---
Pyoderma gangrenosum, 1°
sclerosing cholangitis.

Front 253

Crohn’s disease
mnemonic

Back 253

For Crohn’s, think of a fat granny and an old crone skipping down a cobblestone road
away from the wreck (rectal sparing) (see Images 114, 115).

Front 254

Crohn’s disease
Or
Ulcerative colitis
Transmural inflammation.

Back 254

Crohn’s disease

Front 255

Crohn’s disease
Or
Ulcerative colitis

Back 255

Crohn’s disease

Front 256

Crohn’s disease
Or
Ulcerative colitis
Post-infectious.

Back 256

Crohn’s disease

Front 257

Crohn’s disease
Or
Ulcerative colitis
Strictures, fistulas, perianal disease, malabsorption,
nutritional depletion

Back 257

Crohn’s disease

Front 258

Crohn’s disease
Or
Ulcerative colitis
ankylosing spondylitis, uveitis, immunologic
disorders.

Back 258

Crohn’s disease

Front 259

Crohn’s disease
Or
Ulcerative colitis
Pyoderma gangrenosum, 1°
sclerosing cholangitis.

Back 259

UC

Front 260

Crohn’s disease
Or
Ulcerative colitis
Crypt abscesses and ulcers,
bleeding, no granulomas.

Back 260

UC

Front 261

Crohn’s disease
Or
Ulcerative colitis
Severe stenosis, toxic
megacolon, colorectal
carcinoma.

Back 261

UC

Front 262

Appendicitis
who?

Back 262

All age groups; most common indication for emergent abdominal surgery in children.

Front 263

most common indication for emergent abdominal surgery in children.

Back 263

Appendicitis

Front 264

Appendicitis
presentation?

Back 264

Initial diffuse periumbilical pain →localized pain at McBurney’s point. Nausea, fever;
may perforate →peritonitis.

Front 265

pain at McBurney’s point

Back 265

Appendicitis
presentation

Front 266

Appendicitis
differential Dx

Back 266

Differential: diverticulitis (elderly),
ectopic pregnancy (use β-hCG to rule out).

Front 267

Diverticulum
true Vs False

Back 267

“True” diverticulum––all 3 gut
wall layers outpouch.

“False” diverticulum or
pseudodiverticulum––only
mucosa and submucosa
outpouch. Occur especially

Front 268

Diverticulum
where are most

Back 268

Sigmoid colon

Front 269

false Diverticulum occur most at what types of locations

Back 269

Occur especially
where vasa recta perforate
muscularis externa.

Front 270

Diverticulum
true Vs False
whcih is more common

Back 270

false

Front 271

Diverticulosis
what is it and who gets it

Back 271

Many diverticula. Common (in ~50% of people > 60
years).

Front 272

Diverticulosis associations

Back 272

Associated with
low-fiber diets.

Front 273

Diverticulosis mech

Back 273

Caused by ↑ intraluminal pressure and
focal weakness in colonic wall.

Front 274

Diverticulosis location

Back 274

Most often in sigmoid colon.

Front 275

Diverticulosis symps

Back 275

Often asymptomatic or associated
with vague discomfort and/or
rectal bleeding.

Front 276

Diverticulitis what is it and symps

Back 276

Inflammation of diverticula classically causing LLQ
pain, fever, May cause bright red rectal bleeding.

Front 277

Diverticulitis
wrt labs

Back 277

leukocytosis

Front 278

Diverticulitis complications

Back 278

May →perforation,
peritonitis,
abscess formation,
or bowel stenosis

Front 279

Meckel’s
diverticulum
mnemonic

Back 279

The five 2’s:

-2 inches long.
-2 feet from the ileocecal valve.
-2% of population.
-Commonly presents in first 2
years of life.
-May have 2 types of
epithelia (gastric/
pancreatic).

Front 280

Meckel’s
diverticulum
derivation

Back 280

Persistence of the vitelline duct or yolk stalk.

Front 281

Meckel’s
diverticulum
contents

Back 281

May contain ectopic acid–secreting gastric mucosa
and/or pancreatic tissue.

Front 282

Meckel’s
diverticulum
how common

Back 282

2%
and/or pancreatic tissue. Most common congenital
anomaly of the GI tract.

Front 283

Meckel’s
diverticulum
complications

Back 283

Can cause bleeding,
intussusception, volvulus, or obstruction near the
terminal ileum.

Front 284

Meckel’s
diverticulum
and something else to contrast it with

Back 284

Contrast with omphalomesenteric
cyst = cystic dilatation of vitelline duct.

Front 285

Most common congenital
anomaly of the GI tract.

Back 285

Meckel’s
diverticulum

Front 286

omphalomesenteric
cyst
what

Back 286

cystic dilatation of vitelline duct.

Front 287

cystic dilatation of vitelline duct.
aka

Back 287

omphalomesenteric
cyst

Front 288

Zenker’s diverticulum
what is it and presentation

Back 288

False diverticulum. Herniation of mucosal tissue at junction of pharynx and esophagus.

Presenting symptoms: halitosis, dysphagia, obstruction.

Front 289

False diverticulum. Herniation of mucosal tissue at junction of pharynx and esophagus.

Back 289

Zenker’s diverticulum

Front 290

Intussusception
what
complications
and cause

Back 290

Intussusception––“telescoping” of 1 bowel segment into distal segment;

can compromise
blood supply (see Color Image 34).

Often due to intraluminal mass.

Front 291

Volvulus
what
complications
where does it occur

Back 291

––twisting of portion of bowel around its mesentery;

can lead to obstruction and
infection.

May occur at sigmoid colon, where there is redundant mesentery.

Front 292

Hirschsprung’s
disease
what is it

Back 292

Congenital megacolon characterized by lack of
enteric nervous plexus in segment (Auerbach’s and
Meissner’s plexuses) on intestinal biopsy.

Front 293

Hirschsprung’s
disease
mech

Back 293

failure of neural crest cell migration. leads to lack of
enteric nervous plexus in segment (Auerbach’s and
Meissner’s plexuses)

Front 294

Hirschsprung’s
disease
presentation

Back 294

Presents as
chronic constipation early in life.

Front 295

Hirschsprung’s
disease
who gets it

Back 295

Risk ↑ with Down syndrome.

Front 296

Hirschsprung’s
disease
what is the transition zone

Back 296

Dilated portion
of the colon proximal to the aganglionic segment,
resulting in a “transition zone.”

Front 297

Hirschsprung’s
disease
mnemonic

Back 297

Think of a giant spring that
has sprung in the colon.

Front 298

Colonic polyps
most are

Back 298

90% are benign hyperplastic hamartomas, not neoplasms.

Front 299

Colonic polyps
locations

Back 299

Often rectosigmoid. Saw-tooth
appearance.

Front 300

Colonic polyps
what affects prognosis

Back 300

The more villous the polyp, the more likely it is to be malignant.

Front 301

Colorectal cancer
(CRC)
cause

Back 301

. Most are sporadic, due to chromosomal instability (85%) or
microsatellite instability (15%).

Front 302

Colorectal cancer
(CRC)
risk factors

Back 302

Risk factors: colorectal villous adenomas, chronic IBD (especially ulcerative colitis, ↑ age),
FAP, HNPCC, past medical or family history;

Front 303

Colorectal cancer
screenin guidlines

Back 303

screen patients >50 years with stool
occult blood test and colonoscopy.

Front 304

Colorectal cancer
marker

Back 304

CEA

Front 305

Colorectal cancer
wrt imaging

Back 305

“Apple core” lesion seen on barium swallow x-xay.

Front 306

Familial
adenomatous
polyposis (FAP)
genetics

Back 306

Autosomal dominant mutation of APC gene on chromosome 5q. Two-hit hypothesis.

Front 307

Autosomal dominant mutation of APC gene on chromosome 5q. Two-hit hypothesis.

Back 307

Familial
adenomatous
polyposis (FAP)
genetics

Front 308

Familial
adenomatous
polyposis (FAP)
Features

Back 308

Thousands of polyps; pancolonic; always involving the rectum.

Front 309

Gardner’s syndrome

Back 309

FAP with osseous and soft tissue tumors, retinal hyperplasia.

Front 310

FAP with osseous and soft tissue tumors, retinal hyperplasia.

Back 310

Gardner’s syndrome

Front 311

FAP with possible brain involvement (glioblastoma).

Back 311

Turcot’s syndrome

Front 312

Turcot’s syndrome

Back 312

FAP with possible brain involvement (glioblastoma).

Front 313

HNPCC
aka

Back 313

Lynch syndrome

Front 314

Lynch syndrome
aka

Back 314

HNPCC

Front 315

HNPCC
mech and features

Back 315

Mutations of DNA repair genes. ~80% progress to CRC. Proximal colon always involved.

Front 316

Peutz-Jeghers
what and risks

Back 316

polyposis syndrome, associated with ↑ risk of CRC.
↑ risk of other
visceral malignancies (breast, stomach, ovary).

Front 317

Peutz-Jeghers
findings

Back 317

hamartomatous polyps of colon and small intestine; hyperpigmented mouth,
lips, hands, genitalia.

Front 318

polyposis syndrome, associated with ↑ risk of CRC.
↑ risk of other
visceral malignancies (breast, stomach, ovary).

Back 318

Peutz-Jeghers

Front 319

Cirrho (Greek) =

Back 319

tawny yellow.

Front 320

Cirrhosis
Micronodular features and causes

Back 320

Micronodular––nodules < 3 mm,
uniform size. Due to
metabolic insult (e.g., alcohol,
hemochromatosis, Wilson’s
disease).

Front 321

Cirrhosis
Macronodular features and causes

Back 321

Macronodular––nodules >
3 mm, varied size. Usually
due to significant liver injury
leading to hepatic necrosis
(e.g., postinfectious or druginduced
hepatitis). ↑ risk of
hepatocellular carcinoma.

Front 322

Cirrhosis
which type has
↑ risk of
hepatocellular carcinoma.

Back 322

Macronodular

Front 323

procedure to relieve protal hypertension

Back 323

Portacaval shunt between
splenic vein and left renal
vein

Front 324

11 effects of liver falure

Back 324

• Coma
• Scleral icterus
• Fetor hepaticus (breath
smells like a freshly
opened corpse)
• Spider nevi
• Gynecomastia
• Jaundice
• Loss of sexual hair
• Liver "flap" = asterixis
(coarse hand tremor)
• Bleeding tendency
(decreased prothrombin
and clotting factors)
• Anemia
• Ankle edema

Front 325

Fetor hepaticus

Back 325

(breath
smells like a freshly
opened corpse)

Front 326

Liver "flap"
aka

Back 326

asterixis

Front 327

asterixis
aka

Back 327

Liver "flap"

Front 328

Effects of
portal hypertension
what leads to melena

Back 328

Esophageal varices
and
Peptic
ulcer

Front 329

Enzyme markers
of GI pathology
name 6 enzymes

Back 329

-Aminotransferases (AST and ALT)
-GGT (γ-glutamyl transpeptidase)
-Alkaline phosphatase
-Amylase
-Lipase
-Ceruloplasmin (↓)

Front 330

Enzyme markers
of GI pathology
Aminotransferases (AST and ALT)
Major diagnostic use?

Back 330

Viral hepatitis
Alcoholic hepatitis
Myocardial infarction (AST)

Front 331

Enzyme markers
of GI pathology
GGT (γ-glutamyl transpeptidase)
Major diagnostic use?

Back 331

Various liver diseases

Front 332

Enzyme markers
of GI pathology
Alkaline phosphatase
Major diagnostic use?

Back 332

Obstructive liver disease
(hepatocellular carcinoma),
bone disease

Front 333

Enzyme markers
of GI pathology
Amylase
Major diagnostic use?

Back 333

Acute pancreatitis, mumps

Front 334

Enzyme markers
of GI pathology
Lipase
Major diagnostic use?

Back 334

Acute pancreatitis

Front 335

Enzyme markers
of GI pathology
Ceruloplasmin (↓)
Major diagnostic use?

Back 335

Wilson’s disease (see Color
Image 51)

Front 336

Which GI enzyme gives info on Viral hepatitis,
Alcoholic hepatitis,
Myocardial infarction

Back 336

Aminotransferases (AST and ALT)

Myocardial infarction (AST)

Front 337

Which GI enzyme gives info on Obstructive liver disease
(hepatocellular carcinoma),
bone disease

Back 337

Alkaline phosphatase

Front 338

Which GI enzyme gives info on Acute pancreatitis

Back 338

Amylase, lipase

Front 339

Which GI enzyme gives info on mumps

Back 339

Amylase

Front 340

Which GI enzyme gives info on Wilson’s disease

Back 340

Ceruloplasmin (↓)

Front 341

Alcoholic hepatitis
histo

Back 341

Swollen and necrotic hepatocytes, neutrophil
infiltration, Mallory bodies (intracytoplasmic
eosinophilic inclusions), fatty change, and
sclerosis around central vein (Zone III).

Front 342

Mallory bodies

Back 342

(intracytoplasmic
eosinophilic inclusions) seen in alcoholic hepatitis

Front 343

(intracytoplasmic
eosinophilic inclusions) seen in alcoholic hepatitis

Back 343

Mallory bodies

Front 344

Alcoholic hepatitis
mnemonic with liver enzymes

Back 344

You've sGOT toASTed with alcoholic
hepatitis. (sGOT)AST > ALT(SGPT)

ALT > AST in viraL hepatitis.

Front 345

SGOT (AST) to SGPT (ALT) ratio is
usually

Back 345

> 1.5.

Front 346

Budd-Chiari
syndrome
what is it and complications

Back 346

Occlusion of IVC or hepatic veins with centrilobular congestion and necrosis, leading to
congestive liver disease (hepatomegaly, ascites, abdominal pain, and eventual liver
failure).

Front 347

Budd-Chiari
syndrome
causes

Back 347

Associated with polycythemia vera, pregnancy, hepatocellular carcinoma.

Front 348

Wilson’s disease
mech

Back 348

Inadequate hepatic copper excretion and failure of
copper to enter circulation as ceruloplasmin.
Leads to copper accumulation,

Front 349

Wilson’s disease
Tx

Back 349

Treat with penicillamine.

Front 350

Wilson’s disease
inheritance.

Back 350

Autosomal-recessive
inheritance.

Front 351

Wilson’s disease is characterized by:

Back 351

ABDC
Asterixis
Basal ganglia degeneration (parkinsonian
symptoms)
Ceruloplasmin ↓, Cirrhosis, Corneal deposits
(Kayser-Fleischer rings), Copper accumulation,
Carcinoma (hepatocellular), Choreiform
movements
Dementia

Front 352

What is the C
in the ABCD
of
Wilson’s disease

Back 352

Ceruloplasmin ↓,
Cirrhosis,
Corneal deposits
(Kayser-Fleischer rings), Copper accumulation,
Carcinoma (hepatocellular), Choreiform movements

Front 353

Hemochromatosis
mech

Back 353

Hemosiderosis is the deposition of hemosiderin
(iron); hemochromatosis is the disease caused by
this iron deposition.

Front 354

Hemochromatosis
presentation

Back 354

Classic triad of
micronodular
cirrhosis,
pancreatic fibrosis,
and skin
pigmentation → “bronze” diabetes.

Front 355

Classic triad of
micronodular
cirrhosis,
pancreatic fibrosis,
and skin
pigmentation → “bronze” diabetes.

Back 355

Hemochromatosis

Front 356

Hemochromatosis
results in

Back 356

CHF and ↑ risk of hepatocellular carcinoma.

Front 357

Hemochromatosis
ways to have it

Back 357

Disease may be 1° (autosomal recessive) or 2° to
chronic transfusion therapy.

Front 358

Hemochromatosis
lab values

Back 358

↑ ferritin, ↑ iron,
↓ TIBC →↑transferrin saturation

Front 359

Associated with HLA A3.

Back 359

Hemochromatosis

Front 360

Hemochromatosis
associated with what marker

Back 360

HLA A3

Front 361

Hemochromatosis
cool thing!

Back 361

Total body iron may reach 50 g,
enough to set off metal
detectors at airports.

Front 362

Hemochromatosis
Tx

Back 362

-repeated phlebotomy,

-deferoxamine.

Front 363

Jaundice type
Hepatocellular
wrt
-Hyperbilirubinemia ?
-Urine bilirubin ?
-Urine urobilinogen?

Back 363

Conjugated/unconjugated

↑

Normal/↓

Front 364

Jaundice type
Obstructive
wrt
-Hyperbilirubinemia ?
-Urine bilirubin ?
-Urine urobilinogen?

Back 364

Conjugated

↑

↓

Front 365

Jaundice type
Hemolytic
wrt
-Hyperbilirubinemia ?
-Urine bilirubin ?
-Urine urobilinogen?

Back 365

Unconjugated

Absent (acholuria)

↑

Front 366

Hereditary hyperbilirubinemias
name them

Back 366

Gilbert’s syndrome

Crigler-Najjar
syndrome, type I and II

Dubin-Johnson
syndrome

Rotor's syndrome

Front 367

Gilbert’s syndrome
mech
symptoms

Back 367

Mildly ↓ UDP-glucuronyl transferase. Asymptomatic.
Elevated unconjugated bilirubin without
overt hemolysis.
Associated with stress.

Front 368

Crigler-Najjar
syndrome, type I
mech and outcomes

Back 368

Absent UDP-glucuronyl transferase.
Presents early
in life; patients die within a few years.

Front 369

Crigler-Najjar
syndrome, type I
findings

Back 369

Findings: jaundice, kernicterus (bilirubin deposition
in brain), ↑ unconjugated bilirubin.

Front 370

Crigler-Najjar
syndrome,
Tx

Back 370

Type 1 - Treatment: plasmapheresis and phototherapy.

Type II --phenobarbital,

Front 371

Crigler-Najjar
syndrome, type II
severity and Tx mech

Back 371

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

Front 372

Dubin-Johnson
syndrome
mech and findings

Back 372

Conjugated hyperbilirubinemia due to defective
liver excretion. Grossly black liver. Benign.

Front 373

Rotor’s syndrome

Back 373

like Dubin-Johnson (conjugated hyperbilirubinemia)
syndrome but milder and no black liver

Front 374

Dubin-Johnson
syndrome
complications

Back 374

Grossly black liver. Benign.

Front 375

Charcot’s triad wrt GI:

Back 375

Charcot’s triad of cholangitis:
1. Jaundice
2. Fever
3. RUQ pain

Front 376

1. Jaundice
2. Fever
3. RUQ pain

Back 376

Charcot’s triad of cholangitis:
can indicate Primary sclerosing
cholangitis

Front 377

Primary sclerosing
cholangitis
what and where

Back 377

Inflammation and fibrosis
of bile ducts →alternating strictures and dilation.

Both intra- and extrahepatic.

Front 378

Primary sclerosing
cholangitis
appearance

Back 378

alternating strictures and dilation
with “beading” on ERCP.

Front 379

Primary sclerosing
cholangitis
associations

Back 379

Associated with
ulcerative colitis.

Front 380

Primary sclerosing
cholangitis complications

Back 380

Can lead to 2° biliary cirrhosis.

Front 381

Primary sclerosing
cholangitis
findings

Back 381

Charcot’s triad of cholangitis:
1. Jaundice
2. Fever
3. RUQ pain

Front 382

Primary Biliary cirrhosis
location, mechanism, symps, and findings

Back 382

Intrahepatic,

autoimmune disorder;

severe obstructive jaundice, steatorrhea, pruritus,
hypercholesterolemia (xanthoma).

↑ alkaline phosphatase, ↑ serum mitochondrial
antibodies.

Front 383

↑ alkaline phosphatase, ↑ serum mitochondrial
antibodies.

Back 383

Primary Biliary cirrhosis

Front 384

secondary Biliary cirrhosis
mech?

Back 384

Due to extrahepatic biliary obstruction. ↑ in pressure in intrahepatic ducts → injury/
fibrosis.

Front 385

Primary Biliary cirrhosis associatoins

Back 385

Associated with scleroderma, CREST syndrome.

Front 386

what is the common lab value in scleroderma/CREST and primary biliary sclerosis

Back 386

↑ serum mitochondrial
antibodies.

Front 387

secondary Biliary cirrhosis
complications and histo/lab findings

Back 387

Often complicated by ascending cholangitis (bacterial infection),

bile stasis,
and “bile lakes.”

↑ alkaline phosphatase, ↑ conjugated bilirubin.

Front 388

Most common 1° malignant tumor of the liver in
adults.

Back 388

hepatocellular carcinoma

Front 389

↑ incidence of hepatocellular carcinoma
is associated with

Back 389

-hepatitis B and C,
-Wilson’s disease, -hemochromatosis, -α1-antitrypsin
deficiency,
-alcoholic cirrhosis,
-carcinogens
(e.g., aflatoxin B1).

Front 390

Hepatocellular
carcinoma
spread mech

Back 390

Commonly spread by
hematogenous
dissemination.

Front 391

Hepatocellular
carcinoma
presentation

Back 391

Can present with tender
hepatomegaly, ascites, polycythemia, and
hypoglycemia.

Front 392

Hepatocellular
carcinoma
marker

Back 392

Elevated α-fetoprotein.

Front 393

Reye’s syndrome
findings

Back 393

fatty liver (microvesicular
fatty change),
hypoglycemia,
coma.

Front 394

Reye’s syndrome
cause

Back 394

fatty change), hypoglycemia, Associated with viral infection (especially VZV
and influenza B) treated with salicylates

Front 395

what to give a kid to lower fever

Back 395

acetaminophen, not aspirin

Front 396

Rare, often fatal childhood hepatoencephalopathy.
aka

Back 396

Reye’s syndrome

Front 397

Gallstones Form when

Back 397

solubilizing bile acids and lecithin are
overwhelmed by ↑ cholesterol and/or bilirubin.

Front 398

Gallstones
mnemonic

Back 398

Risk factors (4 F’s):
1. Female
2. Fat
3. Fertile
4. Forty

Front 399

Gallstones
which are radiolucent

Back 399

Cholesterol stones (80-90% of them)

and

Mixed stones

Front 400

Gallstones
which are radioopaque

Back 400

Pigment stones

Front 401

Gallstones
Cholesterol stones
associations

Back 401

9 of them
-obesity,
-Crohn’s disease,
-cystic fibrosis,
-advanced age,
-clofibrate,
-estrogens,
-multiparity,
-rapid weight loss,
-Native American origin.

Front 402

gallstones Mixed stones what are they made of

Back 402

cholesterol and pigment components.

Front 403

Gallstones
most common type

Back 403

Mixed stones

Front 404

Gallstones
pigment stones
associations

Back 404

4 of them
seen in patients
with:
-chronic RBC hemolysis, -alcoholic cirrhosis,
-advanced age,
-and biliary infection.

Front 405

Gallstones
can lead to

Back 405

Can cause ascending cholangitis, acute pancreatitis,
bile stasis, cholecystitis.

Front 406

Gallstones
Dx and Tx

Back 406

Diagnose with ultrasound.
Treat with cholecystectomy.

Front 407

Acute pancreatitis
causes

Back 407

I GET SMASHeD.
Idiopathic, Gallstones, Ethanol, Trauma, Steroids,
Mumps, Autoimmune disease, Scorpion sting,
Hypercalcemia/Hyperlipidemia, Drugs (e.g.,
sulfa drugs).

Front 408

Acute pancreatitis
presentation

Back 408

Clinical presentation: epigastric abdominal pain
radiating to back; anorexia, nausea.

Front 409

Acute pancreatitis
labs

Back 409

Labs: elevated amylase, lipase (higher specificity).

Front 410

Acute pancreatitis
leads to

Back 410

Can lead to DIC, ARDS, diffuse fat necrosis,
hypocalcemia, pseudocyst formation, hemorrhage,
and infection.

Front 411

Chronic calcifying pancreatitis
associations

Back 411

Chronic calcifying pancreatitis is strongly associated
with alcoholism

Front 412

Chronic obstructive pancreatitis associations

Back 412

Chronic obstructive pancreatitis is strongly associated
with gallstones.

Front 413

Pancreatic
adenocarcinoma
prognosis

Back 413

Prognosis averages 6 months or less; very aggressive; usually already metastasized at
presentation;

Front 414

Pancreatic
adenocarcinoma
location and findings

Back 414

tumors more common in pancreatic head (obstructive jaundice).

Front 415

Pancreatic
adenocarcinoma
who adn risk factors

Back 415

↑ risk in Jewish and African-American males.

Associated with cigarettes,
but not ETOH.

Front 416

Pancreatic
adenocarcinoma
Often presents with:

Back 416

1. Abdominal pain radiating to back

2. Weight loss (due to malabsorption and anorexia)

3. Migratory thrombophlebitis (Trousseau’s syndrome)

4. Obstructive painless jaundice with palpable gallbladder (Courvoisier’s sign)

Front 417

Courvoisier’s sign

Back 417

Obstructive painless jaundice with palpable gallbladder

often means cancer in pancreatic head

Front 418

Trousseau’s syndrome

Back 418

Migratory thrombophlebitis

often means adenoarcinoma of the pancreas or lung

Front 419

Obstructive painless jaundice with palpable gallbladder

Back 419

Courvoisier’s sign

Front 420

Migratory thrombophlebitis

often means adenoarcinoma of the pancreas or lung

Back 420

Trousseau’s syndrome

Front 421

Tumor of endocrine cells. Comprise 50% of small bowel tumors.

Back 421

Carcinoid

Front 422

Carcinoid
what type of tumor
and
how common

Back 422

Tumor of endocrine cells. Comprise 50% of small bowel tumors.

Front 423

Carcinoid
most common site and
visualization

Back 423

Most common site is
appendix. “Dense core bodies” seen on EM.

Front 424

Carcinoid
what they produce

Back 424

5-HT / Serotonin

Front 425

Carcinoid
classic symps

Back 425

wheezing,
right-sided heart lesions, diarrhea,
flushing.

Front 426

H2 blockers
Names

Back 426

-idine

Front 427

H2 blockers
mech

Back 427

Reversible block of histamine H2 receptors →↓H+ secretion by parietal cells.

Front 428

H2 blockers
clinical use

Back 428

Peptic ulcer, gastritis, mild esophageal reflux.

Front 429

H2 blockers
toxicity wrt hormones

Back 429

Cimetidine has antiandrogenic effects (prolactin
release, gynecomastia, impotence, ↓ libido in males);

Front 430

H2 blockers
toxicity wrt CNS

Back 430

cimetidine can cross BBB (confusion,
dizziness, headaches) and placenta.

Front 431

H2 blockers
toxicity wrt renal

Back 431

Both cimetidine and ranitidine ↓ renal excretion
of creatinine.

Front 432

H2 blockers
toxicity which ones

Back 432

Cimetidine (many)

ranitidine(only renal)

others much much less

Front 433

H2 blockers
toxicity WRT Liver

Back 433

Cimetidine is a potent inhibitor of P-450;

Front 434

Proton pump
inhibitors
names

Back 434

omeprazole
lansoprazole

-prazole

Front 435

Proton pump
inhibitors
mech

Back 435

Irreversibly inhibit H+/K+ ATPase in stomach parietal cells.

Front 436

Proton pump
inhibitors
clinical use

Back 436

Peptic ulcer, gastritis, esophageal reflux, Zollinger-Ellison syndrome.

Front 437

Bismuth, sucralfate
mech

Back 437

Bind to ulcer base, providing physical protection,
and allow HCO3
– secretion to reestablish pH
gradient in the mucus layer.

Front 438

Bismuth, sucralfate
clinical use

Back 438

↑ ulcer healing,
traveler’s diarrhea.

Front 439

Triple/quad therapy of H. pylori ulcers

Back 439

MAke Tummy Better

-Metronidazole,
-Amoxicillin (or
-Tetracycline).
-Bismuth,

can also Add PPI
please MAke Tummy Better

Front 440

Misoprostol
mech

Back 440

A PGE1 analog. ↑ production and secretion of gastric mucous barrier, ↓ acid
production.

Front 441

Misoprostol
clinical use

Back 441

-Prevention of NSAID-induced peptic ulcers;
-maintenance of a patent ductus arteriosus.
-Also used to induce labor.

Front 442

Misoprostol
toxicity

Back 442

-Diarrhea.

-Contraindicated in women of childbearing potential (abortifacient).

Front 443

-Prevention of NSAID-induced peptic ulcers;
-maintenance of a patent ductus arteriosus.
-Also used to induce labor.

Back 443

Misoprostol

Front 444

GI Muscarinic antagonists
name

Back 444

Pirenzepine, propantheline.

Front 445

GI Muscarinic antagonists
mech

Back 445

Block M1 receptors on ECL cells (↓ histamine secretion) and M3 receptors on
parietal cells (↓ H+ secretion).

Front 446

GI Muscarinic antagonists
clinical use

Back 446

Peptic ulcer.

Front 447

GI Muscarinic antagonists
Toxicity

Back 447

Tachycardia, dry mouth, difficulty focusing eyes.

Front 448

Antacid overuse
wrt other drugs

Back 448

Can affect absorption, bioavailability, or urinary
excretion of other drugs by altering gastric and
urinary pH or by delaying gastric emptying.

Front 449

Aluminum hydroxide
toxicity

Back 449

constipation and
hypophosphatemia; proximal muscle
weakness, osteodystrophy, seizures

Front 450

Magnesium hydroxide

Back 450

––diarrhea, hyporeflexia,
hypotension, cardiac arrest.

Front 451

Calcium carbonate

Back 451

hypercalcemia,
rebound acid ↑

Front 452

all antacids can cause

Back 452

hypokalemia.

Front 453

Infliximab
mech

Back 453

A monoclonal antibody to TNF-α, proinflammatory cytokine.

Infliximab Inflix Pain on TNF-α

Front 454

Infliximab
Clinical use

Back 454

Crohn’s disease, rheumatoid arthritis.

Front 455

Infliximab
Toxicity

Back 455

Respiratory infection, fever, hypotension.

Front 456

A monoclonal antibody to TNF-α, proinflammatory cytokine.

Back 456

Infliximab

Front 457

Sulfasalazine
Mech

Back 457

A combination of sulfapyridine (antibacterial) and mesalamine (anti-inflammatory).
Activated by colonic bacteria.

Front 458

Sulfasalazine
Clinical use

Back 458

Ulcerative colitis, Crohn’s disease.

Front 459

Sulfasalazine
Toxicity

Back 459

Malaise, nausea, sulfonamide toxicity, reversible oligospermia.

Front 460

drug used in both Ulcerative colitis, Crohn’s disease.

Back 460

Sulfasalazine

Front 461

Ondansetron
Mech

Back 461

5-HT3 antagonist. Powerful central-acting antiemetic.

Front 462

Ondansetron
Clinical use

Back 462

Control vomiting postoperatively and in patients
undergoing cancer chemotherapy.

You will not vomit with
ONDANSetron, so you can
go ON DANCing.

Front 463

Ondansetron
Tocicity

Back 463

Headache, constipation.

Front 464

Pro-kinetic agents
names

Back 464

Cisapride

Metoclopramide

Front 465

Cisapride
mech and uses

Back 465

Acts through serotonin receptors to ↑ ACh release at the myenteric plexus. ↑ esophageal
tone; ↑ gastric and duodenal contractility, improving transit time (including through
the colon).

Front 466

Cisapride
Toxicity

Back 466

No longer used. Serious interactions (torsades des pointes) with erythromycin,
ketoconazole, nefazodone, fluconazole.

Front 467

No longer used. Serious interactions (torsades des pointes) with erythromycin,
ketoconazole, nefazodone, fluconazole.

Back 467

Cisapride

Front 468

Metoclopramide
mech

Back 468

D2 receptor antagonist. ↑ resting tone, contractility, LES tone, motility. Does not
↑ transit time through colon.

Front 469

Metoclopramide
Clinical use

Back 469

Diabetic and post-surgery gastroparesis.

Front 470

Metoclopramide
Toxicity

Back 470

↑ parkinsonian effects. Restlessness, drowsiness, fatigue, depression, nausea,
constipation. Drug interaction with digoxin and diabetic agents.

Front 471

Metoclopramide contraindications

Back 471

patients with small bowel obstruction.

Front 472

drug Contraindicated in
patients with small bowel obstruction.

Back 472

Metoclopramide