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472 Cards in this Set

  • Front
  • Back
Baby vomits milk when fed and
has a gastric air bubble.
Blind esophagus with lower
segment of esophagus attached
to trachea.
After a stressful life event,
30-year-old man has diarrhea
and blood per rectum;
intestinal biopsy shows
transmural inflammation.l
Crohn’s disease.
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.
Penicillamine for Wilson’s
disease.
most common cause
20-year-old male presents with
idiopathic hyperbilirubinemia.
Gilbert’s disease.
55-year-old male with chronic
GERD presents with esophageal
cancer. what is the most common subtype
Adenocarcinoma.
Female presents with alternating
bouts of painful diarrhea and
constipation. Colonoscopy is
normal.
Irritable bowel syndrome.
derivations of
GI blood supply
Embryonic gut
region
Celiac = Foregut
SMA = Midgut
IMA = Hindgut
Structures supplied by
celiac artery
Stomach to proximal duodenum; liver, gallbladder, pancreas
Structures supplied by
SMA artery
Distal duodenum to proximal 2/3 of transverse colon
Structures supplied by
IMA artery
Distal 1/3 of transverse colon to upper portion of rectum
Branches of celiac trunk:
common hepatic, splenic, left gastric. These comprise the
main blood supply of the stomach.
Short gastrics have poor
anastomoses if ?
splenic artery
is blocked.`
If the abdominal aorta is blocked, these arterial anastomoses (with origin) compensate
name 4
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)
Portal-systemic
anastomoses
name 5
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
what verices are are commonly seen with
portal hypertension
Varices of gut, butt, and caput
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.
Myenteric
(Auerbach's)
Enteric nerve plexi.
Which one
Coordinates Motility along entire gut wall.?
Myenteric
(Auerbach's)
Enteric nerve plexi.
Which one
Contains cell bodies of some
parasympathetic terminal effector neurons?
Both
Myenteric
(Auerbach's)
and
Submucosal
(Meissner's)
Enteric nerve plexi.
Which one
Located between inner (circular) and
outer (longitudinal) layers of smooth muscle in GI tract wall.?
Myenteric
(Auerbach's)
Enteric nerve plexi.
Which one
Regulates local Secretions, blood flow, and absorption?
Submucosal
(Meissner's)
Enteric nerve plexi.
Located between mucosa and inner layer
of smooth muscle in GI tract wall?
Submucosal
(Meissner's)
layers in order that a knife wuold go through in the lateral abdomen
skin
superficial fascia
external oblique
internal oblique
tranversus abdominis
transversalias facia
extraperitoneal tissue
peritoneum
Secrete alkaline mucus to neutralize acid contents entering the duodenum from the
stomach. Located in duodenal submucosa?
Brunner’s glands
the only GI submucosal glands
Brunner’s glands
Brunner’s glands
what doe they secrete and why?
alkaline mucus to neutralize acid contents entering the duodenum from the
stomach.
Brunner’s glands
where are they?
Located in duodenal submucosa (the only GI submucosal glands)
Hypertrophy of Brunner’s glands is seen in?
peptic ulcer disease.
Hypertrophy of ?????? is seen in peptic ulcer disease
Brunner’s glands
Unencapsulated lymphoid tissue found in lamina
propria and submucosa of small intestine.
Contain specialized M cells that take up antigen
Peyer’s patches
Peyer’s patches
special cells
M cells
what do stimulated B cells that leave peyer's patches become and how does it work
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.
What to think about Peyer patch related antibodies
Think of IgA, the
Intra-gut Antibody. And
always say “secretory IgA.
what layer are peyer's patches in
lamina
propria and submucosa of small intestine.
what are spaces of Disse
perisinusoidal space in the liver
where is the Cystic duct
btw the gall bladder and the common bile duct
what joins to make the common bile duct
Cystic duct and
Common hepatic duct
lower Pectinate line
what forms it
Formed where hindgut meets ectoderm.
Formed where hindgut meets ectoderm.
Pectinate line
Name the ligament that connects the Liver to anterior abdominal
wall?
Falciform
Name the ligament that connects the Liver the the duodenum?
Hepatoduodenal
Name the ligament that connects the Liver to lesser curvature
of stomach?
Gastrohepatic
Name the ligament that connects the Greater curvature and
transverse colon?
Gastrocolic
Name the ligament that connects the Greater curvature and
spleen?
Gastrosplenic
Name the ligament that connects the Spleen to posterior
abdominal wall?
Splenorenal
What Structures are contained in the Falciform Ligament?
Ligamentum teres
What Structures are contained in the Hepatoduodenal Ligament?
Portal triad: hepatic artery,
portal vein, common
bile duct
What Structures are contained in the Gastrohepatic Ligament?
Gastric arteries
What Structures are contained in the Gastrocolic Ligament?
Gastroepiploic arteries
What Structures are contained in the Gastrosplenic Ligament?
No vessels
What Structures are contained in the Splenorenal Ligament?
Splenic artery and vein
Important GI ligaments
which one May be compressed
between thumb and
index finger placed in epiploic
foramen (of Winslow)
to control bleeding?
Hepatoduodenal
Important GI ligaments
which one Separates R greater and
lesser sacs
May be cut during surgery
to access lesser sac?
Gastrohepatic
Important GI ligaments
which one is part of greater omentum?
Gastrocolic
Important GI ligaments
which one Separates L greater and
lesser sacs?
Gastrosplenic
what is the clinical importance of the foramen of winslow
Portal triad can be compressed by thumb and index finger to conrtol bleeding
Layers of gut wall (inside to
outside):
mucosa
submucosa
muscularis externa
serosa/advetiia
Frequencies of basal electric
rhythm: in the stomach and small bowel.
Stomach––3 Hz
Duodenum––12 Hz
Ileum––8–9 Hz 
layers and functions of the gut wall mucosa
mucosa is the inner most layer and its layers are

epithelium (absorption),

lamina propria (support),

muscularis mucosa (motility)
internal hemorrhoids:
where are they?
Arterial supply?
Venous drainage?
nervous system?
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
external hemorrhoids:
where are they?
Arterial supply?
Venous drainage?
nervous system?
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
which hemorrhoids are painful
external hemorrhoids
cancer and hemorrhoids
External hemorrhoids/ squamous cell carcinoma. often mistaken of one another
Femoral triangle Contains
femoral nerve, artery, vein,
Femoral region organization
Lateral to medial: Nerve-(Artery-Vein-Empty space- Lymphatics)

N-(AVEL)
Femoral sheath
what and where?

contents?
Fascial tube 3–4 cm below inguinal ligament

Contains femoral vein, artery, and canal (deep inguinal lymph nodes),
but not femoral nervea
A hernia is a
protrusion of peritoneum through an opening, usually sites of weakness.
Diaphragmatic
hernia

what is it
Abdominal structures enter the thorax;
Diaphragmatic
hernia

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

most common type and desciption
a hiatal hernia,

stomach herniates
upward through the esophageal hiatus of the
diaphragm.
Paraesophageal Hernia
GE junction is
normal.
Cardia moves into
the thorax.
which hernia
Follows the path of the descent
of the testes. Covered by all
three layers of spermatic
fascia.
Indirect inguinal
hernia
Indirect inguinal
hernia.
Path?
Goes through the INternal (deep) inguinal
ring, external (superficial) inguinal ring, and
INto the scrotum. Enters internal inguinal ring
lateral to inferior epigastric artery.
Indirect inguinal
hernia.
Who?
INfants owing to failure of processus vaginalis
to close.
Much more common in males
Direct inguinal
hernia
Path?
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.
Direct inguinal
hernia
Who?
Usually in older men.
Femoral hernia
path?
Protrudes through femoral canal below and lateral Leading
to pubic tubercle.
Femoral hernia
Who?
More common in women.
Leading cause of bowel
incarcerationo
Femoral hernia
Hiatal hernias:
Mech
Sliding (most
common): GE junction is
displaced
which hernia has
GE junction is
displaced
Hiatal hernias:
which hernia has
GE junction is
normal
Paraesophageal:
Inguinal hernia
mnemonic
MDs don’t LIe:

Medial to inferior epigastric
artery = Direct hernia.

Lateral to inferior epigastric
artery = Indirect hernia.e
Hesselbach’s triangle:
borders
Inferior epigastric artery
Lateral border of rectus
abdominis
Inguinal ligament
-Inferior epigastric artery
-Lateral border of rectus
abdominis
-Inguinal ligament
Hesselbach’s triangle:
borders
Salivary secretion glands and
Which glands are most serous vs Mucinous
Parotid (most serous),

submandibular,submaxillary, and

sublingual (most mucinous)
glands.
Function and contents of Saliva
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
saliva and autonomics
which nerves
Salivary secretion is stimulated
by both
sympathetic (T1¨CT3
superior cervical ganglion)

and parasympathetic (facial,
glossopharyngeal nerve) activity.
saliva tonicity changes
Low flow rate leads to hypotonic.


High flow rate leads to closer to
isotonic
GI secretory products
what cell and organ does Intrinsic
factor come from?
Parietal cells
Stomach
GI secretory products
what cell and organ does Gastric acid come from?
Parietal cells
Stomach
GI secretory products
what cell and organ does HCO3
– come from?
Mucosal cells
Stomach
Duodenum
GI secretory products
what cell and organ does Cholecysto-
kinin come from?
I cells
Duodenum
Jejunum
GI secretory products
what cell and organ does Pepsin come from?
Chief cells
Stomach
GI secretory products
what cell and organ does Gastrin come from?
G cells
Antrum of
stomach
GI secretory products
what cell and organ does Secretin come from?
S cells
Duodenum
GI secretory products
what cell and organ does Somatostatin come from?
D cells
Pancreatic
islets
GI mucosa
GI secretory products
what cell and organ does Gastric
inhibitory
peptide
(GIP) come from?
K cells
Duodenum
Jejunum
GI secretory products
what cell and organ does Vasoactive
intestinal
polypeptide
(VIP) come from?
Parasympathetic
ganglia in
sphincters,
gall bladder,
small intestine
GI secretory products
what cell and organ does Nitric oxide come from?
Intrinsic
factor

Gastric acid
GI secretory products What substances do Chief cells
Stomach produce?
Pepsin
GI secretory products What substances do Mucosal cells
Stomach
Duodenum produce?
HCO3–
GI secretory products What substances do G cells
Antrum of
stomach produce?
Gastrin
GI secretory products What substances do I cells
Duodenum
Jejunum produce?
Cholecysto-
kinin
GI secretory products What substances do S cells
Duodenum
produce?
Secretin
GI secretory products What substances do D cells
Pancreatic
islets
GI mucosa produce?
Somatostatin
GI secretory products What substances do K cells
Duodenum
Jejunum produce?
Gastric
inhibitory
peptide
(GIP)r
GI secretory products What substances do Parasympathetic
ganglia in
sphincters,
gall bladder,
small intestine produce?
Vasoactive
intestinal
polypeptide
(VIP)
GI secretory products
action of Intrinsic
factor?
Vitamin B12 binding
protein (required for
B12 uptake in terminal
ileum)
GI secretory products
action of Gastric acid?
lower stomach pH
GI secretory products
action of Pepsin?
Protein digestion
GI secretory products
action of HCO3–?
Neutralizes acid
Prevents
autodigestion
GI secretory products regulation of Gastric acid?
increased by histamine, ACh,
gastrin

decreased by somatostatin,
GIP, prostaglandin,
secretin
GI secretory products regulation of pepsin?
increased by vagal stimulation,
local acid?
GI secretory products regulation of HCO3–?
increased by secretin
Autoimmune destruction
of parietal cells ¨leads to
chronic gastritis and
pernicious anemia.
Inactive pepsinogen
becomes pepsin by
H+
GI Hormones Action of Gastrin?
Increases gastric H+ secretion
Increases growth of gastric
mucosa
Increases gastric motility
GI Hormones Action of Cholecysto-
kinin?
Increases pancreatic secretion
Increases gallbladder
contraction


decreasesgastric emptying
GI Hormones Action of Secretin?
↑ pancreatic HCO3

secretion
↓ gastric acid secretion
GI Hormones Action of Somatostatin?
↓ gastric acid and
pepsinogen secretion
↓ pancreatic and small
intestine fluid secretion
↓ gallbladder contraction
↓ insulin and glucagon
release
GI Hormones Action of Gastric
inhibitory
peptide
(GIP)?
Exocrine:
↓ gastric H+ secretion
Endocrine:
↑ insulin release
GI Hormones Action of Vasoactive
intestinal
polypeptide
(VIP)?
↑ intestinal water and
electrolyte secretion
↑ relaxation of intestinal
smooth muscle and
sphincters
GI Hormones Action of Nitric oxide?
↑ smooth muscle
relaxation, including
lower esophageal
sphincter
GI hormones regulation of Gastrin?
↑ by stomach
distention, amino
acids, peptides,
vagal stimulation

↓ by stomach
pH < 1.5
GI hormones regulation of Cholecysto-
kinin?
↓ by secretin and
stomach pH < 1.5
↑ by fatty acids,
amino acids
GI hormones regulation of Secretin?
↑ by acid, fatty acids
in lumen of
duodenum
GI hormones regulation of Somatostatin?
↑ by acid
↓ by vagal
stimulation
GI hormones regulation of Gastric
inhibitory
peptide
(GIP)?
↑ by fatty acids, amino
acids, oral glucose
GI hormones regulation of Vasoactive
intestinal
polypeptide
(VIP)?
↑ by distension and
vagal stimulation
↓ by adrenergic input
GI hormones regulation of Nitric oxide?
?
Gastrin
wrt when is it Very Very high
↑↑ in Zollinger-
Ellison syndrome.
what is ↑↑ in Zollinger-
Ellison syndrome.
gastrin
Gastrin What are Very potent stimulators
Phenylalanine and
tryptophan are
potent stimulators.
Phenylalanine and
tryptophan are
potent stimulators of what GI hormone
Gastrin
In cholelithiasis, pain
worsens after fatty
food ingestion due
to?
↑ CCK.
↑ HCO3
– neutralizes
gastric acid in
duodenum, allowing?
pancreatic enzymes
to function.
Used to treat VIPoma
and carcinoid
tumors.
Somatostatin
what hormone?
An oral glucose load
is used more rapidly
than the equivalent
given by IV.
Gastric
inhibitory
peptide
(GIP)
Gastric inhibitory peptide
(GIP)
wrt Oral Vs IV
An oral glucose load
is used more rapidly
than the equivalent
given by IV.
VIPoma:
what is it and what are the symps and Tx
VIPoma: non-α, non-ß
islet cell pancreatic
tumor that secretes
VIP. Copious
diarrhea.

Tx is Somatostatin
Loss of ?????
is implicated in ↑
lower esophageal
tone of achalasia.
NO secretion
Loss of NO secretion
is implicated in
↑lower esophageal
tone of achalasia.
Pancreatic
enzymes
Which are secreted in their active form
α-amylase––starch digestion, secreted in active form.
Pancreatic
enzymes name the carb ones
α-amylase––starch digestion, secreted in active form.
Pancreatic
enzymes name the Fat ones
Lipase, phospholipase A, colipase––fat digestion.
Pancreatic
enzymes name the protein ones
Proteases (trypsin, chymotrypsin, elastase, carboxypeptidases)––protein digestion,
secreted as proenzymes.
activation cascade for pancratic protein enzymes
Trypsinogen is converted to active enzyme trypsin by enterokinase, a duodenal brushborder
enzyme. Trypsin activates other proenzymes and more trypsinogen (positive
feedback loop).
Pancreatic
enzymes
Which are secreted in their in active form
Proteases (trypsin, chymotrypsin, elastase, carboxypeptidases)––protein digestion,
secreted as proenzymes.
Trypsinogen is converted to active enzyme trypsin by ?
enterokinase,
Carbohydrate digestion
name all the enzymes
Salivary amylase

Pancreatic amylase

Oligosaccharide
hydrolases
Carbohydrate digestion

Salivary amylase

where from and what it does?
Starts digestion, hydrolyzes α-1,4 linkages to yield disaccharides (maltose, maltotriose,
and α-limit dextrans).
Carbohydrate digestion

Salivary amylase

where from and what it does?
Highest concentration in duodenal lumen, hydrolyzes starch to oligosaccharides and
disaccharides.
Carbohydrate digestion

Salivary amylase

where from and what it does?
At brush border of intestine, the rate-limiting step in carbohydrate digestion, produce
monosaccharides from oligo- and disaccharides.
hydrolyzes α-1,4 linkages to yield disaccharides (maltose, maltotriose,
and α-limit dextrans).
Salivary amylase
Highest concentration in duodenal lumen, hydrolyzes starch to oligosaccharides and
disaccharides.
Pancreatic amylase
At brush border of intestine, the rate-limiting step in carbohydrate digestion, produce
monosaccharides from oligo- and disaccharides.
Oligosaccharide
hydrolases
the rate-limiting step in carbohydrate digestion,
Oligosaccharide
hydrolases
Carbohydrate
absorption
what is absorbed
Only monosaccharides (glucose, galactose, fructose) are absorbed by enterocytes.
Carbohydrate
absorption
mech for Glucose
into enterocytes
Glucose and galactose are taken up by SGLT1 (Na+ dependent).
Carbohydrate
absorption
mech for Galactose
into enterocytes
Glucose and galactose are taken up by SGLT1 (Na+ dependent).
Carbohydrate
absorption
mech for Fructose
into enterocytes
Fructose is taken up by
facilitated diffusion by GLUT-5.
Carbohydrate
absorption
mech for Glucose
from enterocytes into blood
All (Glucose, Galactose, Fructose) are transported to blood by GLUT-2.
Carbohydrate
absorption
mech for Galactose
from enterocytes into blood
All (Glucose, Galactose, Fructose) are transported to blood by GLUT-2.
Carbohydrate
absorption
mech for Fructose
from enterocytes into blood
All (Glucose, Galactose, Fructose) are transported to blood by GLUT-2.
Apical surface of hepatocytes face ???????
Basolateral surface face?????
bile canaliculi.

sinusoids.
Zones of the liver portal triads
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
Zones of the liver portal triads Which Zone is periportal zone?
I
Zones of the liver portal triads Which Zone is most sensitive to toxic injury?
III
Zones of the liver portal triads Which Zone is affected first by viral hepatitis?
I
Zones of the liver portal triads Which Zone is intermediate zone?
II
Zones of the liver portal triads Which Zone is pericentral vein zone?
III
Zones of the liver portal triads Which Zone is contains P-450 system?
III
Zones of the liver portal triads Which Zone is affected first by ischemia?
III
Zones of the liver portal triads Which Zone is alcoholic hepatitis?
III
Zones of the liver portal triads blood flow direction ?
1 to 3
Zones of the liver portal triads bile flow direction ?
3 to 1
Direct bilirubin is combined with what and why
conjugated with glucuronic acid; water soluble.
Direct bilirubin
aka
conjugated
Indirect bilirubin
aka
unconjugated
Jaundice (yellow skin, sclerae) results from
elevated bilirubin levels.
Bile is made of
Composed of bile salts (bile acids conjugated to glycine or taurine making them water
soluble), phospholipids, cholesterol, bilirubin, water, and ions.
The only significant
mechanism for cholesterol excretion.
Bile
one major importance of bile
The only significant
mechanism for cholesterol excretion.
A-chalasia =
absence of
relaxation.
“Bird beak” on barium swallow.
A-chalasia
2° achalasia may arise from
?
Chagas’ disease.
Achalasia and cancer
Associated with an ↑ risk of esophageal
carcinoma.
Achalasia mech
Failure of relaxation of lower esophageal sphincter
(LES) due to loss of myenteric (Auerbach’s)
plexus.
Achalasia and imaging
Barium swallow shows dilated
esophagus with an area of distal stenosis.
High LES opening pressure and
uncoordinated peristalsis leads to what wrt symptoms
to progressive
dysphagia.
Glandular metaplasia–– replacement of nonkeratinized
squamous epithelium with intestinal (columnar)
epithelium in the distal esophagus. Due to
chronic acid reflux.
Barrett’s esophagus
Barrett’s esophagus
hisologic mech
Glandular metaplasia–– replacement of nonkeratinized
squamous epithelium with intestinal (columnar)
epithelium in the distal esophagus.
Barrett’s esophagus
due to
Due to
chronic acid reflux.
Barrett’s esophagus
wrt cancer
BARRett’s = Becomes
Adenocarcinoma, Results
from Reflux.
Risk factors for esophageal cancer are:
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
Esophageal cancer
which types are most common
Worldwide, squamous cell is
most common.

In US, squamous and
adenocarcinoma are equal in
incidence.
“olive”
Congenital pyloric
stenosis
Congenital pyloric
stenosis
presentation
Palpable “olive” mass in epigastric region
and nonbilious projectile vomiting at ≈ 2 weeks of age.
Congenital pyloric
stenosis
how common and Tx
Treatment is surgical incision.

Occurs in 1/600 live births, often in 1st-born males.
Malabsorption
syndromes
name 5
-Celiac sprue

-Tropical sprue

-Whipple’s disease

-Disaccharidase
deficiency

-Pancreatic
insufficiency
Celiac sprue
mech location and testing
Autoantibodies to gluten (gliadin) in wheat and other grains.
Proximal small bowel only.
Abnormal xylose test.
Malabsorption
syndromes
what symptoms
Can cause diarrhea, steatorrhea, weight loss, weakness.
Celiac sprue associated risks
Associated with ↑ risk of T cell lymphoma.
Malabsorption
syndromes Associated with ↑ risk of T cell lymphoma.
Celiac sprue
Tropical sprue
mech location and Tx
Probably infectious; responds to antibiotics. Can affect entire small bowel.
Whipple’s disease
mech and symptoms
Infection with Tropheryma whippelii; Arthralgias, cardiac, and neurologic symptoms are
common. Most often occurs in older men.
PAS-positive macrophages in intestinal lamina
propria, mesenteric nodes.
Whipple’s disease
Whipple’s disease
Histo
PAS-positive macrophages in intestinal lamina
propria, mesenteric nodes.
Disaccharidase
deficiency
most common and features
Most common is lactase deficiency → milk intolerance. Osmotic diarrhea.
Due to CF, chronic pancreatitis. Causes malabsorption of protein, fat, vitamins A, D,
E, K.
Pancreatic
insufficiency
Pancreatic
insufficiency
due to?
What it causes?
Due to CF, chronic pancreatitis.

Causes malabsorption of protein, fat, vitamins A, D,
E, K.
Autoimmune-mediated intolerance of gliadin (wheat) leading to steatorrhea.
Celiac sprue
Celiac sprue
who gets it
Associated
with people of northern European descent.
Celiac sprue
histo and lab findings
Findings include blunting of villi,
lymphocytes in the lamina propria,
and abnormal D-xylose test.
Celiac sprue what portion of bowel
Tends to affect
jejunum.
Celiac sprue associations
Associated with dermatitis herpetiformis. 10–15% lead to malignancy (most
often T-cell lymphoma).
Associated with dermatitis herpetiformis. 10–15% lead to malignancy (most
often T-cell lymphoma).
Celiac sprue associations
Gastritis
which is erosive and which
is non erosive
Acute gastritis
(erosive)

Chronic gastritis
(nonerosive)
Acute gastritis
mech
and causes
Disruption of mucosal barrier → inflammation.

Canbe caused by
stress,
NSAIDs,
alcohol,
uricemia,
burns (Curling’s ulcer),
and brain injury (Cushing’s
ulcer).
Curling’s ulcer which type and cause
acute gastritis/erosive

Burns
Cushings ulcer which type and cause
acute gastritis/erosive

Brain injury
Chronic gastritis
(nonerosive)
types and locations
Type A (fundus/
body)

Type B (antrum)
Chronic gastritis
(nonerosive)
Type A

mech and findings
Autoimmune disorder characterized by Autoantibodies to parietal cells leading to pernicious
Anemia, and Achlorhydria.
Chronic gastritis
(nonerosive)
Type B
mech and findings
Caused by H. pylori infection.
↑ risk of MALT lymphoma.
Gastritis
which has ↑ risk of MALT lymphoma.
Chronic gastritis
(nonerosive)
Type B
Chronic gastritis
(nonerosive)
mnemonic
AB pairing
Pernicious Anemia affects
gastric Body.
H. pylori Bacterium affects
Antrum.
Peptic ulcer disease
Gastric or Duodenal?
Pain Greater with meals––weight loss.
Gastric
Peptic ulcer disease
Gastric or Duodenal?
Often occurs in older patients.
Gastric
Peptic ulcer disease
Gastric or Duodenal?
H. pylori infection in 70%; chronic NSAID use also
Gastric
Peptic ulcer disease
Gastric or Duodenal?
Due to ↓ mucosal protection against gastric acid.
Gastric
Peptic ulcer disease
Gastric or Duodenal?
Pain Decreases with meals––weight gain.
Duodenal
Peptic ulcer disease
Gastric or Duodenal?
Almost 100% have H. pylori infection.
Duodenal
Peptic ulcer disease
Gastric or Duodenal?
Due to ↑ gastric acid secretion or ↓ mucosal protection.
Duodenal
Peptic ulcer disease
Gastric or Duodenal?
Hypertrophy of Brunner’s glands.
Duodenal
Peptic ulcer disease
Gastric or Duodenal?Tend to have clean, “punched-out” margins unlike the raised/irregular margins of
carcinoma.
Duodenal
Peptic ulcer disease
Gastric or Duodenal?
Potential complications include bleeding, penetration, perforation, and
obstruction
Duodenal
Peptic ulcer disease
Gastric or Duodenal?
not intrinsically precancerous
Duodenal
Potential complications Duodenal ulcer
bleeding,
penetration,
perforation,
obstruction
Stomach cancer
What type is it
Almost always adenocarcinoma.
Stomach cancer
spread patterns
Early aggressive
local spread and node/liver mets.

Virchow’s node––involvement
of supraclavicular node by
mets from stomach.
Stomach cancer
associated with
dietary nitrosamines, achlorhydria,
chronic
gastritis,
type A blood.
Stomach cancer
when diffusly infiltrative
Termed linitis plastica
when diffusely infiltrative (thickened, rigid
appearance
Stomach cancer
hiso apperance
signet ring cells
Krukenberg’s tumor
what
bilateral
mets to ovaries. Abundant
mucus, “signet-ring” cells. from Stomach cancer
bilateral
mets to ovaries. Abundant
mucus, “signet-ring” cells
Krukenberg’s tumor
involvement
of supraclavicular node by
mets from stomach.
Virchow’s node
Crohn’s disease
Vs
Ulcerative colitis
WRT
etiology
Crohn’s disease---
Post-infectious.

Ulcerative colitis---
Autoimmune.
Crohn’s disease
Vs
Ulcerative colitis
WRT
Location
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.
Crohn’s disease
Vs
Ulcerative colitis
WRT
Gross morphology
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.
Crohn’s disease
Vs
Ulcerative colitis
WRT
Microscopic
morphology
Crohn’s disease---
Noncaseating granulomas and lymphoid
aggregates.

Ulcerative colitis---
Crypt abscesses and ulcers,
bleeding, no granulomas.
Crohn’s disease
Vs
Ulcerative colitis
WRT
Complications
Crohn’s disease---
Strictures, fistulas, perianal disease, malabsorption,
nutritional depletion.

Ulcerative colitis---
Severe stenosis, toxic
megacolon, colorectal
carcinoma.
Crohn’s disease
Vs
Ulcerative colitis
WRT
Extraintestinal
manifestations
Crohn’s disease---
Migratory polyarthritis, erythema nodosum,
ankylosing spondylitis, uveitis, immunologic
disorders.

Ulcerative colitis---
Pyoderma gangrenosum, 1°
sclerosing cholangitis.
Crohn’s disease
mnemonic
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).
Crohn’s disease
Or
Ulcerative colitis
Transmural inflammation.
Crohn’s disease
Crohn’s disease
Or
Ulcerative colitis
Crohn’s disease
Crohn’s disease
Or
Ulcerative colitis
Post-infectious.
Crohn’s disease
Crohn’s disease
Or
Ulcerative colitis
Strictures, fistulas, perianal disease, malabsorption,
nutritional depletion
Crohn’s disease
Crohn’s disease
Or
Ulcerative colitis
ankylosing spondylitis, uveitis, immunologic
disorders.
Crohn’s disease
Crohn’s disease
Or
Ulcerative colitis
Pyoderma gangrenosum, 1°
sclerosing cholangitis.
UC
Crohn’s disease
Or
Ulcerative colitis
Crypt abscesses and ulcers,
bleeding, no granulomas.
UC
Crohn’s disease
Or
Ulcerative colitis
Severe stenosis, toxic
megacolon, colorectal
carcinoma.
UC
Appendicitis
who?
All age groups; most common indication for emergent abdominal surgery in children.
most common indication for emergent abdominal surgery in children.
Appendicitis
Appendicitis
presentation?
Initial diffuse periumbilical pain →localized pain at McBurney’s point. Nausea, fever;
may perforate →peritonitis.
pain at McBurney’s point
Appendicitis
presentation
Appendicitis
differential Dx
Differential: diverticulitis (elderly),
ectopic pregnancy (use β-hCG to rule out).
Diverticulum
true Vs False
“True” diverticulum––all 3 gut
wall layers outpouch.

“False” diverticulum or
pseudodiverticulum––only
mucosa and submucosa
outpouch. Occur especially
Diverticulum
where are most
Sigmoid colon
false Diverticulum occur most at what types of locations
Occur especially
where vasa recta perforate
muscularis externa.
Diverticulum
true Vs False
whcih is more common
false
Diverticulosis
what is it and who gets it
Many diverticula. Common (in ~50% of people > 60
years).
Diverticulosis associations
Associated with
low-fiber diets.
Diverticulosis mech
Caused by ↑ intraluminal pressure and
focal weakness in colonic wall.
Diverticulosis location
Most often in sigmoid colon.
Diverticulosis symps
Often asymptomatic or associated
with vague discomfort and/or
rectal bleeding.
Diverticulitis what is it and symps
Inflammation of diverticula classically causing LLQ
pain, fever, May cause bright red rectal bleeding.
Diverticulitis
wrt labs
leukocytosis
Diverticulitis complications
May →perforation,
peritonitis,
abscess formation,
or bowel stenosis
Meckel’s
diverticulum
mnemonic
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).
Meckel’s
diverticulum
derivation
Persistence of the vitelline duct or yolk stalk.
Meckel’s
diverticulum
contents
May contain ectopic acid–secreting gastric mucosa
and/or pancreatic tissue.
Meckel’s
diverticulum
how common
2%
and/or pancreatic tissue. Most common congenital
anomaly of the GI tract.
Meckel’s
diverticulum
complications
Can cause bleeding,
intussusception, volvulus, or obstruction near the
terminal ileum.
Meckel’s
diverticulum
and something else to contrast it with
Contrast with omphalomesenteric
cyst = cystic dilatation of vitelline duct.
Most common congenital
anomaly of the GI tract.
Meckel’s
diverticulum
omphalomesenteric
cyst
what
cystic dilatation of vitelline duct.
cystic dilatation of vitelline duct.
aka
omphalomesenteric
cyst
Zenker’s diverticulum
what is it and presentation
False diverticulum. Herniation of mucosal tissue at junction of pharynx and esophagus.

Presenting symptoms: halitosis, dysphagia, obstruction.
False diverticulum. Herniation of mucosal tissue at junction of pharynx and esophagus.
Zenker’s diverticulum
Intussusception
what
complications
and cause
Intussusception––“telescoping” of 1 bowel segment into distal segment;

can compromise
blood supply (see Color Image 34).

Often due to intraluminal mass.
Volvulus
what
complications
where does it occur
––twisting of portion of bowel around its mesentery;

can lead to obstruction and
infection.

May occur at sigmoid colon, where there is redundant mesentery.
Hirschsprung’s
disease
what is it
Congenital megacolon characterized by lack of
enteric nervous plexus in segment (Auerbach’s and
Meissner’s plexuses) on intestinal biopsy.
Hirschsprung’s
disease
mech
failure of neural crest cell migration. leads to lack of
enteric nervous plexus in segment (Auerbach’s and
Meissner’s plexuses)
Hirschsprung’s
disease
presentation
Presents as
chronic constipation early in life.
Hirschsprung’s
disease
who gets it
Risk ↑ with Down syndrome.
Hirschsprung’s
disease
what is the transition zone
Dilated portion
of the colon proximal to the aganglionic segment,
resulting in a “transition zone.”
Hirschsprung’s
disease
mnemonic
Think of a giant spring that
has sprung in the colon.
Colonic polyps
most are
90% are benign hyperplastic hamartomas, not neoplasms.
Colonic polyps
locations
Often rectosigmoid. Saw-tooth
appearance.
Colonic polyps
what affects prognosis
The more villous the polyp, the more likely it is to be malignant.
Colorectal cancer
(CRC)
cause
. Most are sporadic, due to chromosomal instability (85%) or
microsatellite instability (15%).
Colorectal cancer
(CRC)
risk factors
Risk factors: colorectal villous adenomas, chronic IBD (especially ulcerative colitis, ↑ age),
FAP, HNPCC, past medical or family history;
Colorectal cancer
screenin guidlines
screen patients >50 years with stool
occult blood test and colonoscopy.
Colorectal cancer
marker
CEA
Colorectal cancer
wrt imaging
“Apple core” lesion seen on barium swallow x-xay.
Familial
adenomatous
polyposis (FAP)
genetics
Autosomal dominant mutation of APC gene on chromosome 5q. Two-hit hypothesis.
Autosomal dominant mutation of APC gene on chromosome 5q. Two-hit hypothesis.
Familial
adenomatous
polyposis (FAP)
genetics
Familial
adenomatous
polyposis (FAP)
Features
Thousands of polyps; pancolonic; always involving the rectum.
Gardner’s syndrome
FAP with osseous and soft tissue tumors, retinal hyperplasia.
FAP with osseous and soft tissue tumors, retinal hyperplasia.
Gardner’s syndrome
FAP with possible brain involvement (glioblastoma).
Turcot’s syndrome
Turcot’s syndrome
FAP with possible brain involvement (glioblastoma).
HNPCC
aka
Lynch syndrome
Lynch syndrome
aka
HNPCC
HNPCC
mech and features
Mutations of DNA repair genes. ~80% progress to CRC. Proximal colon always involved.
Peutz-Jeghers
what and risks
polyposis syndrome, associated with ↑ risk of CRC.
↑ risk of other
visceral malignancies (breast, stomach, ovary).
Peutz-Jeghers
findings
hamartomatous polyps of colon and small intestine; hyperpigmented mouth,
lips, hands, genitalia.
polyposis syndrome, associated with ↑ risk of CRC.
↑ risk of other
visceral malignancies (breast, stomach, ovary).
Peutz-Jeghers
Cirrho (Greek) =
tawny yellow.
Cirrhosis
Micronodular features and causes
Micronodular––nodules < 3 mm,
uniform size. Due to
metabolic insult (e.g., alcohol,
hemochromatosis, Wilson’s
disease).
Cirrhosis
Macronodular features and causes
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.
Cirrhosis
which type has
↑ risk of
hepatocellular carcinoma.
Macronodular
procedure to relieve protal hypertension
Portacaval shunt between
splenic vein and left renal
vein
11 effects of liver falure
• 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
Fetor hepaticus
(breath
smells like a freshly
opened corpse)
Liver "flap"
aka
asterixis
asterixis
aka
Liver "flap"
Effects of
portal hypertension
what leads to melena
Esophageal varices
and
Peptic
ulcer
Enzyme markers
of GI pathology
name 6 enzymes
-Aminotransferases (AST and ALT)
-GGT (γ-glutamyl transpeptidase)
-Alkaline phosphatase
-Amylase
-Lipase
-Ceruloplasmin (↓)
Enzyme markers
of GI pathology
Aminotransferases (AST and ALT)
Major diagnostic use?
Viral hepatitis
Alcoholic hepatitis
Myocardial infarction (AST)
Enzyme markers
of GI pathology
GGT (γ-glutamyl transpeptidase)
Major diagnostic use?
Various liver diseases
Enzyme markers
of GI pathology
Alkaline phosphatase
Major diagnostic use?
Obstructive liver disease
(hepatocellular carcinoma),
bone disease
Enzyme markers
of GI pathology
Amylase
Major diagnostic use?
Acute pancreatitis, mumps
Enzyme markers
of GI pathology
Lipase
Major diagnostic use?
Acute pancreatitis
Enzyme markers
of GI pathology
Ceruloplasmin (↓)
Major diagnostic use?
Wilson’s disease (see Color
Image 51)
Which GI enzyme gives info on Viral hepatitis,
Alcoholic hepatitis,
Myocardial infarction
Aminotransferases (AST and ALT)

Myocardial infarction (AST)
Which GI enzyme gives info on Obstructive liver disease
(hepatocellular carcinoma),
bone disease
Alkaline phosphatase
Which GI enzyme gives info on Acute pancreatitis
Amylase, lipase
Which GI enzyme gives info on mumps
Amylase
Which GI enzyme gives info on Wilson’s disease
Ceruloplasmin (↓)
Alcoholic hepatitis
histo
Swollen and necrotic hepatocytes, neutrophil
infiltration, Mallory bodies (intracytoplasmic
eosinophilic inclusions), fatty change, and
sclerosis around central vein (Zone III).
Mallory bodies
(intracytoplasmic
eosinophilic inclusions) seen in alcoholic hepatitis
(intracytoplasmic
eosinophilic inclusions) seen in alcoholic hepatitis
Mallory bodies
Alcoholic hepatitis
mnemonic with liver enzymes
You've sGOT toASTed with alcoholic
hepatitis. (sGOT)AST > ALT(SGPT)

ALT > AST in viraL hepatitis.
SGOT (AST) to SGPT (ALT) ratio is
usually
> 1.5.
Budd-Chiari
syndrome
what is it and complications
Occlusion of IVC or hepatic veins with centrilobular congestion and necrosis, leading to
congestive liver disease (hepatomegaly, ascites, abdominal pain, and eventual liver
failure).
Budd-Chiari
syndrome
causes
Associated with polycythemia vera, pregnancy, hepatocellular carcinoma.
Wilson’s disease
mech
Inadequate hepatic copper excretion and failure of
copper to enter circulation as ceruloplasmin.
Leads to copper accumulation,
Wilson’s disease
Tx
Treat with penicillamine.
Wilson’s disease
inheritance.
Autosomal-recessive
inheritance.
Wilson’s disease is characterized by:
ABDC
Asterixis
Basal ganglia degeneration (parkinsonian
symptoms)
Ceruloplasmin ↓, Cirrhosis, Corneal deposits
(Kayser-Fleischer rings), Copper accumulation,
Carcinoma (hepatocellular), Choreiform
movements
Dementia
What is the C
in the ABCD
of
Wilson’s disease
Ceruloplasmin ↓,
Cirrhosis,
Corneal deposits
(Kayser-Fleischer rings), Copper accumulation,
Carcinoma (hepatocellular), Choreiform movements
Hemochromatosis
mech
Hemosiderosis is the deposition of hemosiderin
(iron); hemochromatosis is the disease caused by
this iron deposition.
Hemochromatosis
presentation
Classic triad of
micronodular
cirrhosis,
pancreatic fibrosis,
and skin
pigmentation → “bronze” diabetes.
Classic triad of
micronodular
cirrhosis,
pancreatic fibrosis,
and skin
pigmentation → “bronze” diabetes.
Hemochromatosis
Hemochromatosis
results in
CHF and ↑ risk of hepatocellular carcinoma.
Hemochromatosis
ways to have it
Disease may be 1° (autosomal recessive) or 2° to
chronic transfusion therapy.
Hemochromatosis
lab values
↑ ferritin, ↑ iron,
↓ TIBC →↑transferrin saturation
Associated with HLA A3.
Hemochromatosis
Hemochromatosis
associated with what marker
HLA A3
Hemochromatosis
cool thing!
Total body iron may reach 50 g,
enough to set off metal
detectors at airports.
Hemochromatosis
Tx
-repeated phlebotomy,

-deferoxamine.
Jaundice type
Hepatocellular
wrt
-Hyperbilirubinemia ?
-Urine bilirubin ?
-Urine urobilinogen?
Conjugated/unconjugated



Normal/↓
Jaundice type
Obstructive
wrt
-Hyperbilirubinemia ?
-Urine bilirubin ?
-Urine urobilinogen?
Conjugated



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

Absent (acholuria)

Hereditary hyperbilirubinemias
name them
Gilbert’s syndrome

Crigler-Najjar
syndrome, type I and II

Dubin-Johnson
syndrome

Rotor's syndrome
Gilbert’s syndrome
mech
symptoms
Mildly ↓ UDP-glucuronyl transferase. Asymptomatic.
Elevated unconjugated bilirubin without
overt hemolysis.
Associated with stress.
Crigler-Najjar
syndrome, type I
mech and outcomes
Absent UDP-glucuronyl transferase.
Presents early
in life; patients die within a few years.
Crigler-Najjar
syndrome, type I
findings
Findings: jaundice, kernicterus (bilirubin deposition
in brain), ↑ unconjugated bilirubin.
Crigler-Najjar
syndrome,
Tx
Type 1 - Treatment: plasmapheresis and phototherapy.

Type II --phenobarbital,
Crigler-Najjar
syndrome, type II
severity and Tx mech
Type II is less severe and
responds to phenobarbital,
which ↑ liver enzyme
synthesis.
Dubin-Johnson
syndrome
mech and findings
Conjugated hyperbilirubinemia due to defective
liver excretion. Grossly black liver. Benign.
Rotor’s syndrome
like Dubin-Johnson (conjugated hyperbilirubinemia)
syndrome but milder and no black liver
Dubin-Johnson
syndrome
complications
Grossly black liver. Benign.
Charcot’s triad wrt GI:
Charcot’s triad of cholangitis:
1. Jaundice
2. Fever
3. RUQ pain
1. Jaundice
2. Fever
3. RUQ pain
Charcot’s triad of cholangitis:
can indicate Primary sclerosing
cholangitis
Primary sclerosing
cholangitis
what and where
Inflammation and fibrosis
of bile ducts →alternating strictures and dilation.

Both intra- and extrahepatic.
Primary sclerosing
cholangitis
appearance
alternating strictures and dilation
with “beading” on ERCP.
Primary sclerosing
cholangitis
associations
Associated with
ulcerative colitis.
Primary sclerosing
cholangitis complications
Can lead to 2° biliary cirrhosis.
Primary sclerosing
cholangitis
findings
Charcot’s triad of cholangitis:
1. Jaundice
2. Fever
3. RUQ pain
Primary Biliary cirrhosis
location, mechanism, symps, and findings
Intrahepatic,

autoimmune disorder;

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

↑ alkaline phosphatase, ↑ serum mitochondrial
antibodies.
↑ alkaline phosphatase, ↑ serum mitochondrial
antibodies.
Primary Biliary cirrhosis
secondary Biliary cirrhosis
mech?
Due to extrahepatic biliary obstruction. ↑ in pressure in intrahepatic ducts → injury/
fibrosis.
Primary Biliary cirrhosis associatoins
Associated with scleroderma, CREST syndrome.
what is the common lab value in scleroderma/CREST and primary biliary sclerosis
↑ serum mitochondrial
antibodies.
secondary Biliary cirrhosis
complications and histo/lab findings
Often complicated by ascending cholangitis (bacterial infection),

bile stasis,
and “bile lakes.”

↑ alkaline phosphatase, ↑ conjugated bilirubin.
Most common 1° malignant tumor of the liver in
adults.
hepatocellular carcinoma
↑ incidence of hepatocellular carcinoma
is associated with
-hepatitis B and C,
-Wilson’s disease, -hemochromatosis, -α1-antitrypsin
deficiency,
-alcoholic cirrhosis,
-carcinogens
(e.g., aflatoxin B1).
Hepatocellular
carcinoma
spread mech
Commonly spread by
hematogenous
dissemination.
Hepatocellular
carcinoma
presentation
Can present with tender
hepatomegaly, ascites, polycythemia, and
hypoglycemia.
Hepatocellular
carcinoma
marker
Elevated α-fetoprotein.
Reye’s syndrome
findings
fatty liver (microvesicular
fatty change),
hypoglycemia,
coma.
Reye’s syndrome
cause
fatty change), hypoglycemia, Associated with viral infection (especially VZV
and influenza B) treated with salicylates
what to give a kid to lower fever
acetaminophen, not aspirin
Rare, often fatal childhood hepatoencephalopathy.
aka
Reye’s syndrome
Gallstones Form when
solubilizing bile acids and lecithin are
overwhelmed by ↑ cholesterol and/or bilirubin.
Gallstones
mnemonic
Risk factors (4 F’s):
1. Female
2. Fat
3. Fertile
4. Forty
Gallstones
which are radiolucent
Cholesterol stones (80-90% of them)

and

Mixed stones
Gallstones
which are radioopaque
Pigment stones
Gallstones
Cholesterol stones
associations
9 of them
-obesity,
-Crohn’s disease,
-cystic fibrosis,
-advanced age,
-clofibrate,
-estrogens,
-multiparity,
-rapid weight loss,
-Native American origin.
gallstones Mixed stones what are they made of
cholesterol and pigment components.
Gallstones
most common type
Mixed stones
Gallstones
pigment stones
associations
4 of them
seen in patients
with:
-chronic RBC hemolysis, -alcoholic cirrhosis,
-advanced age,
-and biliary infection.
Gallstones
can lead to
Can cause ascending cholangitis, acute pancreatitis,
bile stasis, cholecystitis.
Gallstones
Dx and Tx
Diagnose with ultrasound.
Treat with cholecystectomy.
Acute pancreatitis
causes
I GET SMASHeD.
Idiopathic, Gallstones, Ethanol, Trauma, Steroids,
Mumps, Autoimmune disease, Scorpion sting,
Hypercalcemia/Hyperlipidemia, Drugs (e.g.,
sulfa drugs).
Acute pancreatitis
presentation
Clinical presentation: epigastric abdominal pain
radiating to back; anorexia, nausea.
Acute pancreatitis
labs
Labs: elevated amylase, lipase (higher specificity).
Acute pancreatitis
leads to
Can lead to DIC, ARDS, diffuse fat necrosis,
hypocalcemia, pseudocyst formation, hemorrhage,
and infection.
Chronic calcifying pancreatitis
associations
Chronic calcifying pancreatitis is strongly associated
with alcoholism
Chronic obstructive pancreatitis associations
Chronic obstructive pancreatitis is strongly associated
with gallstones.
Pancreatic
adenocarcinoma
prognosis
Prognosis averages 6 months or less; very aggressive; usually already metastasized at
presentation;
Pancreatic
adenocarcinoma
location and findings
tumors more common in pancreatic head (obstructive jaundice).
Pancreatic
adenocarcinoma
who adn risk factors
↑ risk in Jewish and African-American males.

Associated with cigarettes,
but not ETOH.
Pancreatic
adenocarcinoma
Often presents with:
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)
Courvoisier’s sign
Obstructive painless jaundice with palpable gallbladder

often means cancer in pancreatic head
Trousseau’s syndrome
Migratory thrombophlebitis

often means adenoarcinoma of the pancreas or lung
Obstructive painless jaundice with palpable gallbladder
Courvoisier’s sign
Migratory thrombophlebitis

often means adenoarcinoma of the pancreas or lung
Trousseau’s syndrome
Tumor of endocrine cells. Comprise 50% of small bowel tumors.
Carcinoid
Carcinoid
what type of tumor
and
how common
Tumor of endocrine cells. Comprise 50% of small bowel tumors.
Carcinoid
most common site and
visualization
Most common site is
appendix. “Dense core bodies” seen on EM.
Carcinoid
what they produce
5-HT / Serotonin
Carcinoid
classic symps
wheezing,
right-sided heart lesions, diarrhea,
flushing.
H2 blockers
Names
-idine
H2 blockers
mech
Reversible block of histamine H2 receptors →↓H+ secretion by parietal cells.
H2 blockers
clinical use
Peptic ulcer, gastritis, mild esophageal reflux.
H2 blockers
toxicity wrt hormones
Cimetidine has antiandrogenic effects (prolactin
release, gynecomastia, impotence, ↓ libido in males);
H2 blockers
toxicity wrt CNS
cimetidine can cross BBB (confusion,
dizziness, headaches) and placenta.
H2 blockers
toxicity wrt renal
Both cimetidine and ranitidine ↓ renal excretion
of creatinine.
H2 blockers
toxicity which ones
Cimetidine (many)

ranitidine(only renal)

others much much less
H2 blockers
toxicity WRT Liver
Cimetidine is a potent inhibitor of P-450;
Proton pump
inhibitors
names
omeprazole
lansoprazole

-prazole
Proton pump
inhibitors
mech
Irreversibly inhibit H+/K+ ATPase in stomach parietal cells.
Proton pump
inhibitors
clinical use
Peptic ulcer, gastritis, esophageal reflux, Zollinger-Ellison syndrome.
Bismuth, sucralfate
mech
Bind to ulcer base, providing physical protection,
and allow HCO3
– secretion to reestablish pH
gradient in the mucus layer.
Bismuth, sucralfate
clinical use
↑ ulcer healing,
traveler’s diarrhea.
Triple/quad therapy of H. pylori ulcers
MAke Tummy Better

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

can also Add PPI
please MAke Tummy Better
Misoprostol
mech
A PGE1 analog. ↑ production and secretion of gastric mucous barrier, ↓ acid
production.
Misoprostol
clinical use
-Prevention of NSAID-induced peptic ulcers;
-maintenance of a patent ductus arteriosus.
-Also used to induce labor.
Misoprostol
toxicity
-Diarrhea.

-Contraindicated in women of childbearing potential (abortifacient).
-Prevention of NSAID-induced peptic ulcers;
-maintenance of a patent ductus arteriosus.
-Also used to induce labor.
Misoprostol
GI Muscarinic antagonists
name
Pirenzepine, propantheline.
GI Muscarinic antagonists
mech
Block M1 receptors on ECL cells (↓ histamine secretion) and M3 receptors on
parietal cells (↓ H+ secretion).
GI Muscarinic antagonists
clinical use
Peptic ulcer.
GI Muscarinic antagonists
Toxicity
Tachycardia, dry mouth, difficulty focusing eyes.
Antacid overuse
wrt other drugs
Can affect absorption, bioavailability, or urinary
excretion of other drugs by altering gastric and
urinary pH or by delaying gastric emptying.
Aluminum hydroxide
toxicity
constipation and
hypophosphatemia; proximal muscle
weakness, osteodystrophy, seizures
Magnesium hydroxide
––diarrhea, hyporeflexia,
hypotension, cardiac arrest.
Calcium carbonate
hypercalcemia,
rebound acid ↑
all antacids can cause
hypokalemia.
Infliximab
mech
A monoclonal antibody to TNF-α, proinflammatory cytokine.

Infliximab Inflix Pain on TNF-α
Infliximab
Clinical use
Crohn’s disease, rheumatoid arthritis.
Infliximab
Toxicity
Respiratory infection, fever, hypotension.
A monoclonal antibody to TNF-α, proinflammatory cytokine.
Infliximab
Sulfasalazine
Mech
A combination of sulfapyridine (antibacterial) and mesalamine (anti-inflammatory).
Activated by colonic bacteria.
Sulfasalazine
Clinical use
Ulcerative colitis, Crohn’s disease.
Sulfasalazine
Toxicity
Malaise, nausea, sulfonamide toxicity, reversible oligospermia.
drug used in both Ulcerative colitis, Crohn’s disease.
Sulfasalazine
Ondansetron
Mech
5-HT3 antagonist. Powerful central-acting antiemetic.
Ondansetron
Clinical use
Control vomiting postoperatively and in patients
undergoing cancer chemotherapy.

You will not vomit with
ONDANSetron, so you can
go ON DANCing.
Ondansetron
Tocicity
Headache, constipation.
Pro-kinetic agents
names
Cisapride

Metoclopramide
Cisapride
mech and uses
Acts through serotonin receptors to ↑ ACh release at the myenteric plexus. ↑ esophageal
tone; ↑ gastric and duodenal contractility, improving transit time (including through
the colon).
Cisapride
Toxicity
No longer used. Serious interactions (torsades des pointes) with erythromycin,
ketoconazole, nefazodone, fluconazole.
No longer used. Serious interactions (torsades des pointes) with erythromycin,
ketoconazole, nefazodone, fluconazole.
Cisapride
Metoclopramide
mech
D2 receptor antagonist. ↑ resting tone, contractility, LES tone, motility. Does not
↑ transit time through colon.
Metoclopramide
Clinical use
Diabetic and post-surgery gastroparesis.
Metoclopramide
Toxicity
↑ parkinsonian effects. Restlessness, drowsiness, fatigue, depression, nausea,
constipation. Drug interaction with digoxin and diabetic agents.
Metoclopramide contraindications
patients with small bowel obstruction.
drug Contraindicated in
patients with small bowel obstruction.
Metoclopramide