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4/20/2015
ABIM GASTROENTEROLOGY
BOARD REVIEW
Mark F. Young, M.D.
ETSU Quillen College of Medicine
I,
Mark F. Young, M.D.,
DO NOT have a financial
interest/arrangement or affiliation
with one or more organizations that
could be perceived as a real or
apparent conflict of interest in the
context of the subject of this
presentation.
DISCLOSURE STATEMENT OF FINANCIAL INTEREST
WHAT DO I NEED TO KNOW?
1
4/20/2015
CASE 1
A
25 year old, white male with a history of Asthma
and Allergy Rhinitis presents to the Emergency
Department with a food impaction. He has had
solid food Dysphagia for two years. He takes over
the counter Omeprazole for intermittent GER
symptoms. Emergent Endoscopy in the ED reveals
the following Endoscopic and Histologic features:
2
4/20/2015
3
4/20/2015
?
A.
The condition is curable within 8 weeks.
B.
This condition is unlikely to occur in
patients with atopic predisposition.
C.
Esophageal Eosinophilia is usually greater
than 100 EOS per high power field.
D.
Summer is the most common seasonal
presentation.
E.
The condition occurs most often in males.
WHICH IS TRUE?
This condition is unlikely to
occur in patients with atopic
predisposition.
B.
Esophageal Eosinophilia is
usually greater than 100 EOS
per high power field.
C.
Summer is the most common
seasonal presentation.
D.
The condition occurs most
often in males.
E.
The condition is curable within
8 weeks.
0%
0%
0%
0%
Su
m
m
er
tio
ge
al
E
on
di
is c
Es
op
ha
Th
0%
n is un
lik
el
y .
os
.
in
op
h
is
ili
th
a i
Th
.. .
e m
e c
os
on
t c
di
o.
tio
..
n Th
oc
e c
cu
on
rs
m
di
tio
os
.. .
n is cu
ra
bl
e ...
A.
4
4/20/2015
EOSINOPHILIC ESOPHAGITIS
 Chronic
>
allergy / immune mediated
15 Eosinophils per high power field
 Eosinophilia
inhibitor trial
persists after proton pump
 Immunologic
triggers food antigen in
children and adults
EOSINOPHILIC ESOPHAGITIS
 Atopic
Predisposition
 Male
 Endoscopic
– Concentric mucosal rings / Linear
Furrowing / Stricture / White Exudates
 Most
common cause ED – Food Impaction
*Dellon E, Gonsalves N, Furuta et al
ACG Clinical Guidelines: Evidence based approach to the diagnosis and
management of esophageal eosinophilia and eosinophilic esophagitis
Am J Gastroenterol 2013 May; 108 (5): 679-692
CASE 2
A 50 year old, white male presents for
intermittent dysphagia to solids. He has
no reflux symptoms. He has no weight loss
or blood in the stool. Esophagram is
performed.
5
4/20/2015
THERAPY FOR THE ABOVE
PROBLEM WOULD INCLUDE ALL
OF THE FOLLOWING, EXCEPT:
Su
rg
ic a
l c
r r
e
c. .
.
0%
tio
n fo
...
re
s
su
pp
ila
wi
th
cid
f a
ge
al
d
ila
t io
n tia
t io
n o
In
i
Es
op
ha
0%
d
Repeated dilation for
recurrent symptoms
0%
n of
h
e.
..
D.
0%
ct
io
Surgical correction of hernia
or
re
C.
at
ed
Initiation of acid suppression
after dilation
pe
B.
Re
Esophageal dilation with
large diameter dilator
(50 French)
..
.
A.
LOWER ESOPHAGEAL RING:
 Intermittent
 Recurrent
dysphagia to solids.
therapy may be needed
 Some
studies indicate PPI’s may delay
reformation of ring
 “Steak
House Syndrome”
*Sleisenger, Feldman et al 2010
6
4/20/2015
 Long-term
acid suppressive therapy may
prevent the relapse of lower esophageal
(Schatzki's) rings: a prospective,
randomized, placebo-controlled study.
*Sgouros SN, Vlachogiannakos J, Karamanolis G, Vassiliadis K,
Stefanidis G, Bergele C, Papadopoulou E, Avgerinos A, Mantides
A, . - Am. J. Gastroenterol. - September 1, 2005; 100 (9); 1929-34
CASE 3
 An
80 year old male complains of a two
year history of regurgitation of
undigested food. His wife states halitosis
is a significant problem. He states he
maintains good oral hygiene. When
swallowing liquids, there is gurgling in the
back of throat. No anorexia, no weight
loss, no tobacco or alcohol use.
WHAT IS THE ETIOLOGY OF THE PROBLEM?
Esophageal Cancer
C.
Longstanding Reflux
D.
Gastric Inlet Pouch
E.
Restrictive Myopathy of the
Cricopharyngeus Muscle
0%
0%
0%
0%
0%
cc
id
en
t
ge
al
C
an
ce
sta
r
nd
in
g R
Ga
ef
st
Re
lu
r
x
st
ic ric
In
le
t iv
t P
e ou
M
yo
ch
pa
th
y o
f .
..
Cerebral Vascular Accident
B.
Ce
re
b
Lo
ng
Es
op
ha
ra
l V
as
cu
la
r A
A.
7
4/20/2015
HYPO PHARYNGEAL DIVERTICULUM
(ZENKERS)
 Most
common manifestation of Cricopharyngeal
Dysfunction
 Elderly
 Area
weakness posterior midline region
pharyngoesophageal wall
 Triangle
of Killian
 Definitive
treatment – Cricopharyngeal Myotamy
*Cook and Kahrilas 1999
TRIANGLE OF KILLIAN
ZENKERS
8
4/20/2015
CASE 4
A
healthy 60 year old man presents for
dysphagia to solids and liquids of a three
year duration. He has regurgitation of
food and fluid at night and halitosis. He
has non-exertional chest pain and
weight loss. Esophagram is performed.
THE NEXT APPROPRIATE DIAGNOSIS STUDY
WOULD BE:
er
E
Up
p
0%
al
0%
er
r
PI
0%
Re
f
st
C
he
ty
o
f
Sc
an
l M
ot
ili
CT
ge
a
Es
op
ha
0%
St
ud
y
0%
EN
T ENT Referral
sc
op
y
Empiric Trial BID PPI
E.
l B
ID
P
D.
nd
o
Upper Endoscopy
ria
Esophageal Motility Study
C.
c T
CT Scan of Chest
B.
Em
pi
ri
A.
9
4/20/2015
THE BEST THERAPEUTIC OPTION FOR THIS
PATIENT IS:
A.
Calcium Channel Blocker
B.
Endoscopic Injection
Botulinum
C.
Laparoscopic Myotomy
D.
Esophageal Dilation over
Guidewire with Bougie
E.
Large Diameter “BAG”
Dilatation
er
0%
0%
pa
r
je
ct
io
lo
ck
0%
La
ha
nn
el
B
c I
n
C
c iu
m
sc
op
i
Ca
l
En
do
0%
n Bo
os
t..
co
Es
.
pi
op
c M
ha
yo
ge
to
al
m
D
La
y
i
la
rg
tio
e Di
n ov
am
e.
et
.
.
er
“B
AG
” D
i..
.
0%
ACHALASIA MONOMETRIC TRIAD:
 Poorly
relaxing LES to swallow
 Hypertensive
LES
 Lack
of peristalsis in esophagus in
response to swallowing
ACHALASIA:
 Always
rule out secondary achalasia –
Esophageal Malignancy with Endoscopy
 Chagas
Disease South America
 Myotomy
better for young patients
 Botulinum
Temporizing
*Francis DL, Katzka DA, Achalasia; update on the disease and
it’s treatment; Gastroenterology 2010; 139 (2): 369-379
10
4/20/2015
TISSUE TAKEN FROM THIS PATIENT’S LOWER
ESOPHAGEAL SPHINCTER WOULD REVEAL A
LACK OF WHICH NEUROTRANSMITTER?
0%
e
e
0%
lin
na
dr
e
e
ch
ol
in
nc
e
0%
yl
Su
bs
ta
0%
Ac
et
P
0%
No
ra
Noradrenaline
n
Nitric Oxide
E.
xid
Motilin
D.
tri
c O
Acetylcholine
C.
Ni
Substance P
B.
M
ot
ili
A.
ACHALASIA:
 Cause
of primary achalasia unknown
 Postganglionic
 Tissue
 Also
denervation of smooth muscle
from these patients lack nitric oxide
decrease inhibitory neurotransmitter VIP
CASE 5
A
16 year old, white female presents for
acute onset of painful swallowing over
24 hours duration. She recently saw her
dermatologist and was prescribed
Doxycycline for acne. She is a diabetic.
Upper Endoscopy and esophagram are
performed.
11
4/20/2015
THE NEXT MOST APPROPRIATE STEP
WOULD BE:
A.
Nystatin swish and swallow
B.
Swallowed Fluticasone
C.
Discontinue Doxycycline
D.
High dose oral PPI
E.
Repeat Upper Endoscopy in
8 weeks
0%
0%
0%
Di
sc
ish
a
w
sw
in
Sw
all
o
Ny
st
at
0%
nd
sw
al
lo
w
ed
Fl
ut
on
ic a
t in
so
ue
ne
D
ox
yc
yc
Hi
lin
gh
Re
e
do
pe
se
at
o
U
ra
pp
l P
er
PI
E
nd
os
co
py
in
0%
PILL ESOPHAGITIS:
 Mid-Esophageal
 Tetracycline,
Quinidine
 DC
erosions
Iron, Bisphosphonates, NSAI, K+,
offending agent
 Topical
relief “GI Cocktail”
12
4/20/2015
 Esophageal
Disorders Caused by
Medications, Trauma, and Infection
*Sleisenger and Fordtran’s Gastrointestinal and Liver Disease,
Chapter 46, 763-772.e5
CASE 6:
47y M seen in the ER w/ 1 week of odynophagia associated
with abdominal pain, n/v, diarrhea and low-grade fever. He
has lost 10lbs during this time. Medications include prednisone,
tacrolimus, and mycophenolate mofetil taken for a kidney
transplant he received 6 months ago. He has no HIV risk factors
or other medical problems.
PE: 148/94 mmhg, 90/min, 100.8 F
EGD: 2.5 cm esophageal ulcer with raised borders, biopsy
shows inflammatory infiltrates with granulation tissue associated
with inclusion body cells, the remainder esophagus appears
normal
WHAT IS THE LIKELY DIAGNOSIS?
git
i
s
0%
so
ph
a
ag
i
tis
0%
ed
E
s
al
ov
i
git
i
so
ph
a
a e
om
eg
Cy
t
di
d
Ca
n
0%
ru
s 0%
nd
uc
Pill-induced Esophagitis
l‐i
HIV esophagitis
D.
P il
Cytomegalovirus
C.
so
ph
Candida esophagitis
B.
HI
V e
A.
13
4/20/2015
INFECTIOUS ESOPHAGITIS
 Common
in Immunsuppressed Pts. (HIV/AIDS,
chemo, systemic steroids, etc.)
 Immunocompetent
 Most
(Inhaled Corticosteroids)
Common Pathogens
 Candida
(2/3 will also have oral thrush)
 HSV/CMV
(less likely to have oral lesions)
INFECTIOUS ESOPHAGITIS
 See
thrush? Treat w/ fluconazole
 No
Thrush? EGD w/ brushing, biopsy, etc.
to establish definitive diagnosis
 NO
Barium Swallow (Nonspecific)
HSV ESOPHAGITIS
14
4/20/2015
CANDIDA ESOPHAGITIS
CMV INCLUSION BODY
CASE 7
A
45 year old, white male is evaluated for chest
pain which proves to be non cardiac. His internist
institutes a trial of Omeprazole 40mg twice a day
which was of no help. Upper Endoscopy reveals
a small hiatal hernia. Esophageal Manometry
reveals Nutcracker Esophagus.
15
4/20/2015
WHAT IS THE BEST APPROACH FOR
SYMPTOM RESOLUTION?
Nitrates
B.
Calcium Channel Blocker
C.
Benzodiazepine
D.
Continue PPI another twelve
weeks
E.
Serotonin-Norepinephrine
Reuptake Inhibitor
0%
0%
0%
0%
0%
Ca
l
c iu
m
C
Ni
tra
te
ha
s
nn
el
B
lo
c
ke
Be
Co
r n
nt
zo
in
di
ue
az
ep
P
PI
in
Se
a
e
no
ro
to
th
ni
e
r
n‐
t.
No
..
re
pi
ne
ph
r i.
.
A.
NON CARDIAC CHEST PAIN
 Visceral
Hypersensitivity
 Omeprazole
test essentially rules out
Esophagus as a cause
 Most
have nonspecific findings on
motility (except Achalasia)
NON CARDIAC CHEST PAIN
Treatment:
 Longer
 Little
therapy with PPI provide no benefit
data to support Nitrates
 Calcium
Channel Blockers only temporary
 Pain
modulators best option-SNRI, Tricyclics,
Trazodone, SSRI’s
*Herghcovice T, et al Aliment Pharmocol Ther 2012; 35: 5-14
16
4/20/2015
CASE 8
A
50 year old, white male with centripetal obesity
and GER for 15 years presents for evaluation. He
wants to be screened for Barretts. He has no
Dysphagia. Upper Endoscopy reveals the following:
SHOULD UPPER ENDOSCOPY HAVE BEEN
PERFORMED?
No
0%
0%
No
Yes
B.
Ye
s
A.
17
4/20/2015
HIS ANNUAL RISK OF
ADENOCARCINOMA IS:
20%
C.
2%
D.
.5%
0%
0%
20
%
5%
0%
0%
.5
%
5%
B.
2%
A.
HIGH GRADE DYSPLASIA IS REPORTED BY
THE PATHOLOGIST. THE NEXT STEP IS:
Repeat Endoscopy in one year
C.
Confirmation by expert
pathologist
D.
Repeat Endoscopy in six months
E.
Radio Frequency Ablation
0%
0%
0%
0%
0%
ge
nd
ct
os
om
co
y
py
in
on
at
io
e
.. .
n Re
by
pe
ex
at
E
pe
nd
rt
..
os
.
co
Ra
py
di
in
o Fr
si
eq
x.
..
ue
nc
y A
bl
at
io
n
Esophagectomy
B.
fi r
m
Co
n
Re
pe
at
E
Es
op
ha
A.
18
4/20/2015
BARRETTS ESOPHAGUS
 Columnar
 Male
?
Epithelium in the Tubular Esophagus
/ White / Centripetal Obesity / Chronic GER
Endoscopy in correct population
BARRETTS ESOPHAGUS

30 – 50 Fold increased risk of Adenocarcinoma

Annual incident of .5%

Overall survival comparable to age and gender matched
population

Repeat Endoscopy in one year thin there to five years

Low Grade Dysplasia – Confirmed – 6-12 months

High Grade Dysplasia – Confirmed – EMR/RFA/Surgery
*The Role of Endoscopy in Barretts Esophagus. Volume 7G, No. 6: 2012 Gastrointestinal Endoscopy
CASE 9
A
50 year old, white male presents for epigastric
pain of three weeks duration. The pain is relieved by
antacids. He takes Goody Powders for headache.
There is no blood in stool or weight loss.
19
4/20/2015
THE MOST APPROPRIATE WORKUP COULD
INCLUDE THE FOLLOWING EXCEPT:
St
oo
l A
0%
sio
ico
b.
..
n
0%
pp
re
s
te
r
er
E
ba
c
0%
Su
0%
Up
p
ico
H
el
or
og
y f
ro
l
Se
Di
sc
o
nt
in
ui
ng
Go
od
y P
o.
..
0%
Ac
id
Start Acid Suppression
St
ar
t Stool Antigen for Helicobacter
E.
sc
op
y
Upper Endoscopy
D.
fo
r H
el
Serology for Helicobacter
C.
nd
o
Discontinuing Goody Powder
B.
nt
ige
n
A.
CASE 10
 Stool
antigen for Helicobacter is positive.
The patient was treated for a sinusitis
several months ago with a macrolide
antibiotic.
YOU SHOULD TREAT THIS PATIENT WITH:
BID PPI/Clarithromycin/Amoxicillin
B.
BID PPI/Clarithromycin/Flagyl
C.
BID PPI/Bisthmyth/Metronidazole/
Tetracycline
D.
Levofloxacin/Amoxicillin/PPI
E.
Bismuth/PCN
0%
0%
0%
0%
0%
BI
D PP
I/C
la
r it
BI
hr
D om
PP
I/C
yc
in
la
r it
...
BI
h
ro
D PP
m
yc
I/B
in
ist
/F
Le
hm
. ..
vo
yt
flo
h/
xa
M
c in
et
r. .
/A
.
m
ox
ici
lli
n.
..
Bi
sm
ut
h/
PC
N
A.
20
4/20/2015
THE FOLLOWING ARE TRUE STATEMENTS
ABOUT HP EXCEPT:
ra
.. .
he
st
om
ac
h.
..
n t
on
E
uo
...
0%
p i
on
c
m
m
0%
ee
of
d
to
ch
i
n ns
hi
p
d i
ire
A co
at
io
el
Ac
qu
e r
In
ve
rs
0%
d
Lives deep in the stomach lining
0%
se
E.
0%
w
or
e GER may be wore on Eradication
au
D.
ay
b
e A common cause of duodenal
ulcer
L iv
es
Acquired in childhood
C.
GE
R m
B.
so
. ..
Inverse relationship to
socioeconomic status
ld
ho
od
A.
DYSPEPSIA:
 Discomfort
nausea
in mid abdomen with bloating and
 Functional-No
relief with Acid suppression
 PUD/GER/Malignancy/Biliary
Tract Disease
WARNING SIGNS:
 Dysphagia
 Odynophagia
 Fe
Deficiency Anemia
 Jaundice
 GI
Bleed
 Lymphadenopathy
 Family
history Cancer Proximal Tract
21
4/20/2015
WORK UP:
 NSAI
or GER – Stop Agent and TX PPI
<
55 No Alarms – Test and Treat – HP
>
55 or Alarm - EGD
HELICOBACTER
 Gram
 Strong
 Risk
negative Microaerophilic Rod
Urease producer
factor for Gastric Malignancy
 Old
Age/Inverse relationship Socioeconomic
status
TREATMENT AND TESTING
 You
should be aware of Macrolide Resistance!!!
 You
should be aware of limitations of testing!!!
22
4/20/2015
WHEN DO WE DOCUMENT ERADICATION?
 Complicated
 Personal
 Need
PUD (Bleeding or Perforation)
history of Gastric Cancer
for future NSAID
REFERENCES
 Chey
WD, Wong BC; Practice parameters
committee of the American College of
Gastroenterology. American College of
Gastroenterology guideline on the management
of Helicobacter Pylori Infection; AM J
Gastroenterol 2007; 102: 1808-1825
 Luther
J, Higgins PD, Schoenfeld PS, Moayyedi,
Vakil N, Chey WD, Empiric Quadruple vs Triple
Therapy for primary treatment of Helicobacter
Pylori Infection; AM J Gastroenterol. 2010 Jan 105
(1): 65-73
CASE 11
A
30 year old, white female presents for Chronic
Diarrhea. She is rather thin and states intentional
weight loss has been an issue and is using osmotic
laxatives. Stool leukocytes are negative.
23
4/20/2015
WHICH OF THE FOLLOWING VALUES WOULD
BE MOST CONSISTENT?
Fecal Na 50mmol/L, K+mmol/L,
Stool 290 Osmol
B.
Fecal Na 50mmol/L, K+ 30mmol/L,
Stool 230 Osmol
C.
Fecal Na 100mmol/L, K+ 30mmol/L,
Stool 290 Osmol
D.
Fecal Na 150mmol/L, K+ 75mmol/L,
Stool 480 Osmol
E.
Fecal Na 45mmol/L, K+ 60mmol/L,
Stool 290 Osmol
0%
0%
0%
50
m
al
N
a l N
a 0%
Fe
c
Fe
ca
0%
m
ol
/L
, K
+m
50
. ..
m
Fe
m
ol
ca
/L
l N
,
a K+
10
..
0m
.
Fe
ca
m
ol
l N
/L
a , K
15
+.
0m
Fe
..
ca
m
l N
ol
/L
a , K
45
+.
m
..
m
ol
/L
, K
+ .
..
A.
OSMOTIC DIARRHEA
 Calculate
 Normal
Gap
Gut Osmolality – 2 (Fecal Na + Fecal K+)
(290mosm/kg)
>
50 mosm/kg is Osmotic Diarrhea
 Osmotic
Laxatives / Carbohydrate Malabsorption
SECRETORY DIARRHEA

Small Osmotic Gap

Stool Osmolality Physiologically 290 mosm/kg

*Contaminated Stool with water/Osmolaliy <290

*Contaminated with urine Stool Osmolality >290

High Volume

Persists with fasting
*Sleisenger and Fordtran Gastrointestinal and Liver Disease 2010 p211-232
24
4/20/2015
CASE 12
A
22 year old, white female presents for 16
months of watery diarrhea and bloating.
Bloating improves after bowel movement. No
travel. No family history of GI Disease. No weight
loss, anemia, melena, or floating stools. Physical
exam is normal. Her friend was recently
diagnosed with Celiac Disease and she is
concerned.
WHAT IS THE BEST INITIAL TEST TO EVALUATE
FOR CELIAC?
C.
D-xylose Absorption Test
D.
IgA Tissue Transglutaminase
Antibody
E.
HLA Genotyping
0%
0%
0%
0%
0%
G
lia
di
n An
t ib
m
id
od
at
ie
ed
s
D‐
G
xy
lu
lo
te
se
n .
Ab
Ig
..
A T
so
rp
iss
t io
ue
n T
T
ra
es
ns
t
gl
ut
am
in
HL
a.
.
A G
en
ot
yp
in
g
IgG Deamidated Gluten
Peptides
Ig
A
IgA Gliadin Antibodies
B.
Ig
G De
a
A.
IS UPPER ENDOSCOPY TRULY NECESSARY TO
CONFIRM A DIAGNOSIS OF CELIAC DISEASE?
No
0%
0%
No
Yes
B.
Ye
s
A.
25
4/20/2015
 She
goes on a Gluten Free Diet after
Consultation with the Dietician. She does
extremely well until two years later when
diarrhea begins again.
THE MOST LIKELY CAUSE OF
HER SYMPTOMS IS:
De
v
ge
s..
.
S
in
pr
u
ge
n
te
n
g I
B
0%
e
0%
ou
s S
Co
...
ic 0%
la
icr
M
ia
te
d
0%
As
so
c
el
op
m
en
t o
f L
os
co
p
ym
ph
om
a
0%
nt
G
lu
Inadvertent Gluten ingestion
dv
er
te
Collagenous Sprue
E.
In
a
Overriding IBS
D.
r id
in
Associated Microscopic Colitis
C.
Ov
er
Development of Lymphoma
B.
Co
l
A.
CELIAC DISEASE
 Small
intestine malabsorption of nutrients after
ingestion of wheat, gluten or related proteins
from rye or barley
 HLA-DQ2
or HLA-DQ8 Haplotype
 Remember
diarrhea and iron deficiency!!!
26
4/20/2015
CELIAC ASSOCIATION
 Autoimmune
 Type
Thyroid Disease
1 Diabetes – 10%
 Unexplained
 Premature
 Increase
Transaminase Elevation
Osteoporosis
Lymphoma Risk
CELIAC DIAGNOSIS
 IgA
test
Tissue Transglutaminase Antibody preferred
 >95%
sensitivity and specificity
 Small
Bowel biopsy necessary to confirm
 *IgA
Gliadin Antibodies No Role*
 If
low IgA Level, use IgG Testing or HLA
Genotyping
CELIAC
 Noncompliance
with diet most likely cause of
refractory symptoms
 D-Xylose
low – Mucosal Disease
 D-Xylose
normal – Suspect Pancreatic Disease
 Be
on the look out for Dermatitis Herpetiformis
*Rubio-Tapia A, Hill IO, Kelly CP et al ACG Guidelines: Diagnosis and
Management of Celiac Disease AM J Gastroenterol 2013; 108 (5) 656-676
27
4/20/2015
DERMATITIS HERPETIFORMIS
CASE 13
A
40 year old, white male had twenty
centimeters of small intestine resected after a
motor vehicle accident. He now has diarrhea.
28
4/20/2015
THE MOST LIKELY CAUSE IS:
Crohns Disease
C.
Bile Salt Malabsorption
D.
Steatorrhea
E.
IBS
0%
0%
0%
0%
Cr
o
Ce
li
0%
IB
S
Celiac Disease
B.
ac
D
ise
as
e
hn
Bi
s D
le
Sa
ise
lt as
M
e
al
ab
so
rp
tio
n
St
ea
to
rr
he
a
A.
ILEAL RESECTION
<
100cm TI – Loss of Bile Salt Absorption –
Hepatic Overproduction – Questran
 >100cm
TI Resection – Bile Salt DeficiencySteatorrhea
CASE 14
A
29 year old, white male presents with bloody
diarrhea of two weeks duration. He has had
associated Arthralgia with weight loss. He also
has experienced Pneumaturia. Physical exam
reveals no abnormalities except mild guarding in
the right lower quadrant. Labs reveal iron
deficiency anemia. Stool studies are negative.
He is FIT positive and ASCA positive and ANCA
negative. Barium x-ray is performed.
29
4/20/2015
COLONOSCOPY AND BIOPSY WOULD
LIKELY REVEAL?
D.
Arteriovenous Malformation
E.
Mucosal Disease Only
0%
0%
0%
0%
ul
o
Co
l
e er
t ic
n th
In
vo
l
Di
v
as
” i
M
or
e re
A
kip
“S
0%
sis
en
r io
t i
n ve
“W
no
...
us
M
alf
M
or
uc
m
os
a.
al
..
D
ise
as
e On
ly
More Involvement in
“Watershed” areas
Ar
te
Diverticulosis
C.
on
“Skip Areas” in the Colon
B.
ve
m
A.
COLONOSCOPY IS PERFORMED AND REVEALS
CROHNS DISEASE WITH A FISTULA TO THE
URINARY BLADDER.
TREATMENT WOULD CONSIST OF:
Infliximab
B.
Mesalamine
C.
Cyclosporine
D.
Steroid Enemas
E.
Masalamine Suppositories
0%
0%
0%
0%
0%
In
fli
xim
ab
M
es
al
am
in
e
Cy
c lo
sp
or
in
St
e
M
er
as
oid
al
En
am
em
in
e S
as
up
po
sit
or
ie
s
A.
30
4/20/2015
CROHNS DISEASE
 Trans
 Skip
mural Inflammation
Lesions
 *Stricture/Fistula/Abscess
 ASCA
Positive 50 % Crohns Patients
 Increase
CRP
CROHNS DISEASE - TREATMENT
 Fistula
– Infliximab/Adalimumab/Certolizumab
 Small
Bowel Disease –
MTX/6MP/Azathioprine/Biologics/Budesonide/Steroids
 Colon
- Mesalamine
ULCERATIVE COLITIS
 Bloody
Diarrhea/Tenesmus
 Weight
Loss
 pANCA
Positive 77%
 Mucosal/Disease
Limited to Colon
31
4/20/2015
ULCERATIVE COLITIS- TREATMENT
 Mesalomine
– First Line
 Prednisone/Immune
 Colectomy
Modulators/Biologics
Curative!!!
IBD - KNOW THE FOLLOWING
 Begin
screening after 10 years Colonic involvement
 Confirmed
low grade Dysplasia equals Colectomy
 Antiperistaltics
in U.C. can precipitate Toxic Mega
Colon which equals surgery
 Surgery
Crohns
is curative in Ulcerative Colitis and avoided in
AZOTHIOPRINE / 6MP
 Pancreatitis
 Leukopenia
 Hepatosplenic
 Latent
T Cell Lymphoma
TB (Screen Prior to Starting)
 Reactivation
of Hepatitis B
32
4/20/2015
IBD – KNOW THE FOLLOWING
Improvement with
Disease Control:
Do Not Improve with
Disease Control:
• Pyoderma Gangrenosum
• Sacroileitis
• Erythema Nodosum
• PSC – Increased AP
• Peripheral Arthritis
• Ankylosing Spondylitis
• Uveitis
*Urogenital Complications of Crohns
Disease. AM J Gastroenterol 2006; 101:
S640-S643
*Sandborn WJ Infliximab for induction and
maintenance therapy for Ulcerative Colitis
N Engl J Med 2005; 353: 2462-76
PYODERMA GANGRENOSUM
33
4/20/2015
ERYTHEMA NODOSUM
UVEITIS
CASE 15

A 50 year old, white male presents for Colon Cancer
Screening. He would like to know options offered by
the U.S. Preventative Task Force.
34
4/20/2015
THEY INCLUDE ALL OF THE FOLLOWING
EXCEPT:
D.
Stool Guaiac Testing
0%
0%
. ..
gm
oid
nn
ua
l
T A
ve
ry
1
0 ye
0%
Fle
xi
bl
e
Si
py
e
St
oo
l F
I
on
os
co
Co
l
0%
es
t in
g
Flexible Sigmoidoscopy every
5 years
...
C.
T
Colonoscopy every 10 years
and continue until age 75
St
oo
l G
ua
iac
B.
os
co
py
e
Stool FIT Annually
ly
A.
COLONOSCOPY IS PERFORMED AND REVEALS
TWO TUBULAR ADENOMAS (<1CM) REPEAT
COLONOSCOPY SHOULD BE PERFORMED IN:
6 Months
1 Ye
a
r
0%
0%
0%
0%
hs
10 Years
D.
6 M
on
t
5 Years
C.
rs
B.
10
Y
ea
1 Year
5 Ye
ar
s
A.
POLYP FOLLOW UP RECOMMENDATIONS:

< 3 Tubular Adenomas < than 1cm No FH  Colon 5 Years

Multiple Adenomas/Large Adenoma > 1cm/Villous
Histology/High Grade Dysplasia or Positive Family History
Repeat 3 Years

*Hyperplastic* routine CRC 10 Years

SSA – Increased risk of missed Right Colon Cancers
*U.S. Multi-Society Task Force on Colorectal Cancer
35
4/20/2015
STOOL FIT

Detects human globin

More specific for human blood

No false negative with vitamin C

Preferred cancer detection test

No randomized trial where outcome is CRC

Questionable better adherence
*Morekowa T, Kato S, Yamaji, Et al A Comparison of
Immunochemical Fecal Occult Blood Test and Total
Colonoscopy in Asymptomatic Population Gastroenterology
2005; 129 422-4285
SCREENING/SURVEILLANCE
RECOMMENDATIONS FOR FAP PATIENTS
APC gene
mutation +
At-risk
individuals
Annual FS starting at age 12
APC gene
mutation Genotype not
available
FS at age 25
Age 12:
annual FS
Age 25:
FS every
2 years
Age 35:
FS every
3 years
Age 50: follow
screening for
average-risk
patients
Retained rectum: FS every 6 months
Affected
individuals
Retained J-pouch: FS every 1-2 years
Annual physical exam
and routine blood tests
Upper GI surveillance every 3-4
years; annually if polyps found
Adapted from Cruz-Correa M, et al. Gastroenterol Clin N Am. 2002;31:537.
EXTRACOLONIC FEATURES OF FAP AND HNPCC
Other lesions
Extracolonic Cancers in FAP

Duodenal (5%-11%)

Pancreatic (2%)

Thyroid (2%)

Brain (medulloblastoma) < 1%

Hepatoblastoma (0.7% of children
years old)
Extracolonic Cancers in HNPCC
<5

Congenital hypertrophy of the retinal pigment
epithelium (CHRPE)

Nasopharyngeal angiofibroma

Osteomas

Radiopaque jaw lesions

Supernumerary teeth

Lipomas, fibromas, epidermoid cysts
Desmoid tumors

Endometrial (39-60%


Stomach (12-19%)

Gastric adenomas/fundic gland polyps

Ovarian (9%)

Duodenal, jejunal, ileal adenomas

Ureter and renal pelvis (4-10%)

Café au lait spots

Biliary tract (2-18%)

Sebaceous gland adenomas, carcinomas

Brain (glioblastoma) (4%)

Keratoacanthomas

Small bowel (1-4%)

Endometrial (39-60%)
Adapted from Cruz-Correa M, et al. Gastroenterol Clin N Am. 2002;31:537.
36
4/20/2015
CASE 16

A 42 year old, female is admitted with epigastric pain,
nausea and emesis. On exam, she is Afebrile with a
heart rate of 150 beats per minute. Her abdomen is
diffusely tender. WBC count is 15,000 with a left shift.
HCT 47, BUN 28mg/dl, Serum Cr 1.0 with normal Liver
Function Tests. Amylase 5200, Lipase 2800. A
diagnosis of Acute Pancreatitis is made.
ALL OF THE FOLLOWING PREDICTS SEVERITY
EXCEPT:
A.
Ranson’s Scoring System
takes 48 hours to complete
B.
Marked elevation of Amylase
and Lipase predict severity
C.
Apache-0 is useful in severity
assessment
D.
SIRS identifies patient with
increased mortality
E.
Initial and subsequent BUN
levels can predict severity
0%
0%
0%
0%
co
r
el
e
ke
d Ap
ac
M
ar
Ra
ns
on
’s S
va
t
in
g S
ys
te
m
...
io
n o
he
f A
‐0
is
m
y
us
...
SI
ef
RS
ul
id
in
en
se
t if
ve
ie
In
. ..
s
p
iti
at
al
ie
a
nt
nd
w
su
i
..
bs
eq
ue
nt
B
..
0%
PANCREATITIS
 Ranson/Glasgow
 Apache
take 48 hours to complete
II accurate at 24 hours
 Apache-0
added BMI
 Admission
BUN >25mg/dl and BUN increase of
5mg/dl in first 24 hours – Increased Mortality!!!
 Amylase
and Lipase levels do not predict severity
*WUBU et al Early changes in blood urea nitrogen predict mortality in Acute
Pancreatitis
Gastroenterology 2009; 137: 129-36
37
4/20/2015
CASE 17

A 65 year old man is admitted with severe abdominal
pain, fever, nausea and vomiting. On examination
he is febrile, with stable vital signs. The upper
abdomen is diffusely tender, with rebound and
absent bowel sounds. Left flank ecchymosis is
present. Serum amylase and lipase are elevated.
After aggressive fluid resuscitation, a contrast CT scan
on day 2 of illness demonstrates an edematous
pancreas with non enhancement of about 30% of
the gland and multiple peri-pancreatic fluid
collections.
IN TERMS OF MANAGEMENT, WHICH OF THE
FOLLOWING STATEMENTS ABOUT NUTRITION
IS CORRECT?
p
ar
ta
l
.
sis
co
nt
r..
n.
..
p.
..
e 0%
ec
ro
t io
ut
ri
0%
n is th
t io
is ut
ri
or
t l n
ra
up
p
l s
To
en
te
t io
na
ta
l p
ar
To
Nu
tri
0%
re
at
ic n
Pancreatic necrosis contraindicates
enteral feeding
0%
l n
E.
0%
ra
Enteral nutrition is the preferred route
for nutritional support in patients with
severe acute pancreatitis
iti
o
D.
l n
ut
r
Total parenteral nutrition is associated
with mortality reduction in acute
pancreatitis
En
te
ra
C.
Pa
nc
Nutritional support is indicated in
patients with mild pancreatitis to
reduce complications
...
B.
in
d.
..
Total parenteral nutrition and enteral
nutrition result in similar metabolic
complications
en
te
A.
PANCREATITIS/FEEDING

Mild Pancreatitis - Hydration Alone

Initial Feeding with low fat diet is Safe

Enteral Feeding is Safe and Tolerated in Acute
Pancreatitis

Enteral Feeding may preserve barrier function

Improved outcomes with Enteral Feeding compared
to Parenteral Feeding with less infectious
complications reduce cost and better Glycemic
control
*Petrov MS, van Santvoort HC, Besselink MS, et al Enteral nutrition and the risk of
mortality and infectious complications in patients with severe acute pancreatitis:
a meta-analysis of randomized trials. Arch Surg 2008; 143: 1111-17
38
4/20/2015
CASE 18

A 80 year old male is admitted with sever epigastric
pain, radiating to the back with nausea and
vomiting. He is febrile with a blood pressure of 120/80
an a pulse of 110. WBC 20,000, AST 300, ALT 400,
ALK FOS 245 and Total BILI 5, Lipase 5,000. Ultrasound
reveals multiple gallstones in the Gallbladder and a
Common Bile Duct size of 14mm. Antibiotics and IV
fluids have begun.
WHAT IS THE NEXT STEP?
Serial Amylase and Lipase
Levels
E.
Emergent ERCP
0%
on
su
l
f A
bd
om
y C
o
Sc
an
Su
rg
er
CT
0%
0%
0%
0%
En
l..
.
te
ra
ria
l N
l A
ut
m
rit
yl
as
io
n
e an
d L
ip
as
.
Em
..
er
ge
nt
E
RC
P
Enteral Nutrition
D.
Se
C.
nd
. ..
Surgery Consult for
Cholecystectomy
r C
ho
B.
en
a
CT Scan of Abdomen and
Pelvis
t f
o
A.
GALLSTONE PANCREATITIS
 Early
Biliary Sphincterotomy is beneficial in
SEVERE Acute Biliary Pancreatitis
 Early
ERCP not beneficial with mild Biliary
Pancreatitis and absence of Biliary Obstruction
 With
clinical deterioration, suggestive of
Ascending Cholangitis – ERCP recommended
*Petrov MS, van Santvoor HC, Besselink MG, et al. Early endoscopic
retrograde cholangiopancreatography versus conservative management in
acute biliary pancreatitis? A meta-analysis of randomized trials.
Ann Surg 2008;247:250-57
39
4/20/2015
CASE 19

A 65 year old male with a mechanical aortic valve
repair for aortic stenosis presents to the emergency
room with painless hematochezia. He is on
Coumadin, and takes Aspirin 81mg daily. He is
volume resuscitated with at least 6 units of packed
RBCs, and stabilized. An urgent Colonoscopy is
performed which demonstrates no fresh blood in the
terminal Ileum or Colon. There are a few small,
scattered diverticuli.
WHAT WOULD YOU DO NEXT?
nd
o
0%
0%
0%
y
Sc
an
0%
d R
BC
er
E
Up
p
Ta
gg
e
sc
op
y
0%
Su
rg
er
Surgery
g
Angiography
E.
ap
hy
Nothing
D.
og
r
Tagged RBC Scan
C.
An
gi
Upper Endoscopy
B.
No
th
in
A.
GI BLEEDING
 Up
to 18% of cases of significant Hematochezia
are presentations of Upper GI Bleeding.
 “Silent
Ulcer” – Aspirin, greater than age 60
40
4/20/2015
HEMATOCHEZIA ? EGD FIRST ?
 Significant
 High
Hemodynamic Compromise
Volume Requirements for Resuscitation
 Large
Magnitude of Decrement in Hematocrit
 Clinical
Risk Factors for Peptic Ulceration or Portal
Hypertension
*Rockall TA, Logan RF, Devlin HB, et al.
Risk management after acute upper gastrointestinal hemorrhage.
Gut 1996; 38:316-21
TOXICITY OF PROTON PUMP INHIBITORS
 Hip
Fracture – Retrospective Study
 Hypomagnesaemia
 Increased
Serum Gastrin Levels
 Increased
Risk of C-Diff Infection if Hospitalized
 Short
Term Use – Pneumonia
CASE 20

A 60 year old female presents for evaluation of
increasing abdominal girth. She states that she has
two glasses of wine per week. She is not overweight.
She states that she had “yellow jaundice” as a child.
Ultrasound of her abdomen reveals significant
Ascites. Echo reveals an ejection fraction of 75%.
Paracentesis is performed. Serum Albumin is 4.0gr/dL.
Ascitic Albumin is 3.1gr/dL. No evidence of SBP. The
fluid is sent for Cytology.
41
4/20/2015
HER MOST LIKELY DIAGNOSIS IS:
0%
0%
e H
Ov
ea
ar
ia
rt
n F a
Ca
ilu
nc
re
er
w
ith
M
...
ec
0%
ar
y C
irr
...
Pr
im
ar
ho
sis
S
Ci
rr
0%
ho
s is
0%
tiv
Ovarian Cancer with METS
Omentum
y B
ili
Congestive Heart Failure
E.
ge
s
Primary Biliary Cirrhosis
D.
Co
n
C.
NA
FL
D
Cirrhosis Secondary to
Alcoholism
y t
o A
NAFLD
B.
on
da
r
A.
KNOW THE SERUM – ALBUMIN GRADIENT
 Serum
Albumin – Ascitic Albumin
 1.1gm/dl
or Greater – Portal Hypertension or CHF
 Total
Ascites Protein Greater than 2.5gm/dl Heart Failure or Constrictive Pericarditis
 SAAG
Less than 1.1gm/dl – Malignancy, Infection
*Runyon, BA; AASLD Practice Guidelines Committee. Management of adult
patients with Ascites due to Cirrhosis: an update.
Hepatology, 2009; 49(6): 2087-2107.
CASE 21

A 50 year old male with diabetes presents with
elevated liver enzymes. His physical activity level has
recently decreased due to increasing pain in joints
including arthritis in his hands. AST 84 IU/L, ALT 60 IU/L,
ALP 120 IU/L, T bili 0.9 mg/dl. ANA 1:20, smooth muscle
ab neg, IgG quant 1503. HBsAg neg, HBsAb positive,
HCV ab negative, Iron is 143 ug/dL, Transferrin
saturation 62%, Ferritin 803 ug/L. A liver biopsy is
performed.
42
4/20/2015
WHICH OF THE FOLLOWING
COMPLICATIONS OF THIS DISORDER IS MOST
LIKELY REVERSIBLE WITH TREATMENT?
Cirrhosis
E.
Risk of HHC in the setting of
Cirrhosis
0%
0%
0%
0%
0%
Ci
rr
ho
sis
se
tti
ng
. .
Cardiac Dysfunction
D.
t h
e Hypogonadism
C.
Ri
sk
of
H
HC
in
Arthropathy
B.
Ar
th
ro
pa
th
Hy
y
po
go
Ca
na
rd
di
sm
iac
D
ys
fu
nc
tio
n
A.
HEMOCHROMATOSIS




Diagnosis
 Transferrin saturation > 50%
 Liver biopsy to assess hepatic iron level
(Hepatic iron index)
 Genetic testing for HFE
Treatment
 Phlebotomy to reduce iron content of the
body
 If iron stores normalize before fibrosis of liver
then normal life expectancy
Once cirrhosis develops then high risk of
hepatoma
SCREEN ALL FIRST DEGRE RELATIVES!!!
43
4/20/2015
HEMOCHROMATOSIS-COMPLICATIONS
Reversable:
Nonreversible:
• Cardiac Dysfunction
• Cirrhosis
• Glucose Intolerance
• Risk of HCC after Cirrhosis
• Hepatomegaly
• Arthropathy
• Skin Pigmentation
• Hypogonadism
• Early Fibrosis
*Bacon BR, Adams PC, Kowdley KV, Powell LW, Tavill AS. Diagnosis
and management of hemochromatosis: 2011 practice guideline
by the American Association for the Study of Liver Diseases.
Hepatology. 2011;54(1):328
CASE 22
You are asked to see a 65 year old man admitted 36
hours prior due to worsening Dyspnea, Palpitations and
feeling faint. On admission, his HR is 165 and blood
pressure is 70/40. The patient has a known history of
ASCVD with prior right ventricular infarction 6 months
ago, and atrial fibrillation for which he was recently
started on amiodarone. You are consulted for
evaluation of elevated liver tests: ALT 4,600 U/L, AST
6,900 U/L, Alkaline Phosphatase 180 U/L, Total Bilirubin
0.9 mg/dL, Albumin 3.2 g/dL, INR 2.3. The patient’s
history is also positive for Diabetes and Dyslipidemia.
Echocardiogram done on admission shows PAP 79/43,
dilated RV, and dilated LV with EF of 35%.
THE MOST LIKELY CAUSE OF
THE ABNORMAL LFT’S IS:
Acute Viral Hepatitis
E.
Acute Biliary Obstruction
0%
0%
0%
0%
0%
ba
l U
se
m
ic H
ep
at
e H
it i
ep
s
at
ot
Ac
ox
ut
ici
e V
ty
Ac
ira
ut
l H
e B
ep
ili
at
ar
iti
y O
s
bs
tr
uc
t io
n
D.
ro
n
Amiodarone
Hepatotoxicity
us
H
er
Ischemic Hepatitis
C.
Isc
he
B.
Am
io
da
Surreptitious Herbal Use
ep
t it
io
A.
Su
rr

44
4/20/2015
ISCHEMIC HEPATITIS

Clinical picture for right heart failure

Hepatocellular enzymes in the thousands

Can also be seen in ICU post code

Also consider in patients found unresponsive outside
the hospital
*Taylor RM, Tujios S, Jinjuvadia K, et al. Short and long-term outcomes in
patients with acute liver failure due to ischemic hepatitis.
Dig Dis Sci 2012;57(3):777-85
CASE 23

A 26 year old woman presents with altered mental
status and jaundice. Her parents state that she has no
history of depression, but has had trouble with
academics and difficulty concentrating in school. Her
parents believe she may have ADHD. Oral
contraceptives are her only medication and she has
not taken any new medications recently. Alk Phos 72
IU/L, T Bili 15.1 mg/dL, D bili 6.0 mg/dL, INR 2.3,
AST 605 IU/L, ALT 351 IU/L, Hgb 9 g/dL, ceruloplasmin 24,
IgG 1703. Color Doppler US of liver is normal.
WHICH LABORATORY STUDY IS MOST LIKELY
TO CONFIRM THE DIAGNOSIS?
Serum Acetaminophen
Level
D.
Anti-nuclear Antibody
E.
Hypercoagulable Workup
0%
0%
0%
0%
0%
U
rin
ar
y Co
ru
pp
m
er
A
ru
lc o
m
A
ho
ce
l L
ta
ev
m
el
in
op
An
he
t i‐
n nu
L..
.
c
l
Hy
ea
r A
pe
rc
nt
oa
ib
od
gu
la
y
bl
e W
or
ku
p
Serum Alcohol Level
C.
Se
B.
24
hr
24hr Urinary Copper
Se
A.
45
4/20/2015
WILSON’S DISEASE

Decreased serum ceruloplasmin level


Increased urinary copper level
Excessive hepatic copper level

KAYSER FLEISCHER RING (copper deposit in cornea)

Treatment


D-penicillamine or trientine
Fulminant hepatitis requires liver transplant

Liver transplant corrects metabolic defect
WILSON’S DISEASE

Ceruloplasmin may be normal

Behavioral changes

Coombs negative hemolytic anemia
*Bewer GJ, Yuzbasiyan-Gurkan V. Wilson disease. Medicine (Baltimore)
1992; 71(3):139
KAYSER FLEISCHER RING
46
4/20/2015
CASE 24
A 25 year old woman presents with acute mental status
changes and jaundice. She has a history of anorexia
and depression. No other past medical history is
available. On examination she is lethargic and alert to
only person. Kayser-Fleisher rings are not seen on
ophthalmologic examination. No stigmata of chronic
liver disease are noted on physical exam. Labs: AST
945 IU/L, ALT 765 IU/L, Alk Phos 100 IU/L, T bili 16.8
mg/dL, D. bili 6.4 mg/dL, Hgb 10.4 g/dL, INR 5.2.
Ceruloplasmin 17, Acetaminophen level negative.
ANA 1:20. Hepatitis A Ab Neg, HCV Ab Neg, 24 hour
urine copper 119 mcg. HBV studies are pending. US
negative.

WHAT IS THE MOST APPROPRIATE NEXT STEP?
ER
CP
io
ps
y
B
...
0%
an
t
at
io
0%
L iv
er
D‐
pe
ni
ci
0%
n Re
f
nd
z
in
c
0%
L iv
er
0%
ni
so
ne
ERCP
e a
Liver Biopsy
E.
ra
ns
pl
Liver Transplantation Referral
D.
T
D-penicillamine and zinc
C.
Pr
ed
Prednisone
B.
lla
m
in
A.
ACUTE FULMINANT WILSON’S DISEASE

Young Age

Hemolytic Anemia


Psychiatric/Behavioral History
Elevated Transaminases with Normal or Low Alkaline
Phosphatase
Low Ceruloplasmin

POOR PROGNOSIS WITHOUT URGENT TRANSPLANT!!!

*Ala A, Walker AP, Ashkan K, et al. Wilson’s disease.
Lancet 2007 Feb 3;369(9559):397-408
47
4/20/2015
CASE 25
A 28 year old man presents with altered mental status
and jaundice. AST 186 IU/L, ALT 92 IU/L, ALP 240 IU/L,
total bilirubin 7.2 mg/dL, PT 32.2 sec, INR 3.3. Alcohol
was positive in blood and urine.

WHICH VALUE IS INCORPORATED INTO
MADDREY’S DISCRIMINANT FUNCTION?
Pr
ot
hr
0%
re
0%
Sc
o
om
a w
h
l P
in
in
r ia
Cr
ea
t
Ar
te
0%
C
0%
a
0%
m
e
Glascow Coma Score
Ti
Prothromin Time
E.
om
in
Ammonia
D.
Gl
as
co
Arterial Ph
C.
Am
m
on
i
Creatinine
B.
e
A.
MADDREY’S DISCRIMINANT FUNCTION

Discriminant Function = 4.6 x (Pt’s PT – Control PT) + TBili

Value >32 – Treat with Prednisalone 40mg Q Day for 6
Weeks

If Renal Failure, Sepsis, or GI Bleed – Treat with
Pentoxifilin 300mg BID

30 Day Mortality – 50% Without Treatment
*O’Shea RS, Dasarathy S, McCullough AJ, Alcoholic liver disease.
Hepatology 2010;51(1):307-28
48
4/20/2015
CASE 26

A 52 year old woman presents with pruritus and
fatigue. She complains of a painful skin lesion. On
examination, she is obese with a BMI of 35. Labs: AST
68 IU/L, ALT 73 IU/L. ALP 406 IU/L, T Bili 4.2 mg/dL, INR 1.1,
Cr 0.8 mg/dL, Glucose 187, total cholesterol 290 mg/dL,
AMA negative. Liver biopsy is performed.
49
4/20/2015
WHICH MEDICATION HAS BEEN SHOWN TO
IMPROVE SURVIVAL?
od
i
ol
0%
0%
s. .
.
0%
m
pr
ov
e
0%
on
at
e
No
M
ed
ic a
tio
n I
0%
Ur
s
No Medication Improves
Survival in this Condition
L ip
it o
r
Ursodiol
E.
en
dr
Alendronate
D.
Al
Lipitor
C.
ni
so
ne
Prednisone
B.
Pr
ed
A.
PRIMARY BILIARY CIRRHOSIS

AMA Hallmark but maybe Negative 5-10% of the time

Histology – Granuloma, Destruction of Biliary Ductule

Complications – Osteopenia, Hyperlipidemia, Pruritus,
Fat Soluble Vitamin Deficiency


Ursodiol improves transplant free survival
Increased risk of Death from Atherosclerosis

No Role for Prednisone
*Lindor K. Ursodeoxycholic acid for the treatment of primary biliary cirrhosis.
N Engl J Med 2007 Oct 11;357(15):1524-29
CASE 27

A 59 year old man is currently listed for liver
transplantation for PSC. He had two episodes of
cholangitis in last six months requiring IV antibiotics. His
MELD score has increased from 15 to 25. His bilirubin
has increased from 2.5 to 12.0 mg/dL. He denies any
fevers, abdominal pain or vomiting, His cholangiogram
reveals a dominant stricture of the common bile duct.
50
4/20/2015
WHAT IS THE NEXT MOST APPROPRIATE STEP?
ERCP with Brushings and
Biopsy of Bile Ducts and
Stenting
C.
Percutaneous Trans hepatic
Cholangiography
D.
Observation
E.
Treat for Cholangitis with
Antibiotics
0%
0%
0%
0%
0%
ER
CP
L iv
w
er
it h
B
io
B
ps
ru
y
sh
rc
ut
in
gs
an
an
eo
us
d.
..
T
ra
ns
h
ep
at
Tr
..
ea
Ob
t f
se
or
rv
C
at
ho
i
on
la
ng
it i
s w
it.
..
Liver Biopsy
B.
Pe
A.
PRIMARY SCLEROSING CHOLANGITIS (PSC)

Men Greater than Women

Strictures throughout the Biliary Tree


“Trees in the Winter”
“Beads on a String”

No Therapy Available

Follow for Liver Transplantation and Development of
Cholangiocarcinoma in a Dominant Stricture
*Chapman R, Fevery J, Kalloo A, Nagorney D et al. Diagnosis and Management
of Primary Sclerosing Cholangitis. Hepatology 2010;51(2):660-6780
51
4/20/2015
CASE 28

A 70 year old man presents to the emergency room
with hematemesis. He describes early satiety and
intermittent nausea. He has lost 10 pounds in the past 4
weeks. He has a history of rheumatoid arthritis. He
denies any alcohol, drug use, or tattoos. On
examination, he is deeply jaundiced and frail
appearing, with no abdominal pain. AST 26 IU/L,
ALT 21 IU/L, ALP 253 IU/L, INR 0.7, T Bili 3.1 mg/dL, D Bili
1.9 mg/dL, albumin 3.5 g/dL. ANA positive, AMA
negative. Patient undergoes an EGD which reveals
non-bleeding fundal gastric varices. No esophageal
varices.
WHAT IS THE MOST APPROPRIATE NEXT STEP?
ER
CP
0%
0%
bd
om
en
0%
CT
A
0%
ro
GD
lo
f o
gy
r B
an
di
ng
..
B
io
ps
y
0%
Se
CT Abdomen
its
ERCP
E.
at
E
D.
L iv
er
Repeat EGD for Banding of
Gastric Varices
l H
ep
at
Viral Hepatits Serology
C.
Vi
ra
B.
pe
Liver Biopsy
Re
A.
52
4/20/2015
GASTRIC VARICES

Painless Jaundice/Unintentional Weigh loss  Pancreatic Cancer

Hematemesis with Gastric Varices/Evaluate for Pancreatic Cancer
with Splenic Vein involvement

Banding of Varices – Poor Results

Check CT for Splenic Vein Thrombosis and if Positive, Splenectomy
*DeLeve LD, Valla DC, Garcia-Tsao G. Vascular disorders of the liver.
Hepatology 2009’49(5):1729-64
CASE 29

A 54 year old male presents for follow up in the office
of Cirrhosis with Portal Hypertension. He has had no
alcohol intake in 3 years and has been very compliant
in follow up and has a strong family support system. He
asks “Doc, how’s my liver working and am I ready for a
transplant?”
0%
0%
AS
T
0%
in
in
0%
at
AST
Cr
e
Creatinine
D.
IN
R
INR
C.
in
Bilirubin
B.
Bi
lir
ub
A.
e
ALL OF THE FOLLOWING SEROLOGY WOULD
BE HELPFUL IN ANSWERING HIS QUESTION
EXCEPT:
53
4/20/2015
MELD

Model for End-Stage Liver Disease

Based on Logarithmic Calculation of Bilirubin, PT, Creatinine

Multiple Calculators available via the Web

Consider Liver Transplant consult when MELD is in the mid
teens

Transplant usually when MELD is in the mid twenties
HEPATORENAL SYNDROME
 Development
of acute renal failure in a patient
with cirrhosis or fulminant hepatic failure
 End
stage of a sequence of events that
reduces perfusion of kidneys
 Clinical
presentation
 Oliguiria
 Low
urine sodium (often undetectable)
 Bland
urine sediment
 Systemic
hypotension
 Absence
of another cause of renal failure
HEPATORENAL SYNDROME

Type I


50% reduction of plasma creatinine clearance to
a level below 20ml/min or doubling of serum
creatinine in less than 2 weeks. Rapidly fatal.
Type II

Less severe than type I, more indolent and
primarily characterized by diuretic refractory
ascities.
54
4/20/2015
HEPATORENAL SYNDROME

Treatment options

Liver transplant. Renal dysfunction improves after
transplant.

Midodrine (alpha-1 agonist) and Octreotide
(somatostatin analog)

Midodrine promotes systemic vasoconstriction,
octreotide inhibits vasodilitaion of splanchnic
vasculature. End result is improved perfusion of
kidneys.

Norepinephrine

Vasopressin analogs

TIPS (controversial)

Dialysis (only as a bridge to transplant)
HEPATORENAL SYNDROME

Prevention is key in certain clinical situations

SBP – administration of albumin

Primary prophylaxis for SBP in patients
with low albumin also reduces HRS
HEPATOCELLULAR CARCINOMA
 5th
most common
cancer worldwide

nearly 1,000,000 new
cases annually as of 2007

increasing incidence
 HBV
single most
important etiologic
factor worldwide

Risk increased without
cirrhosis
 HCV
and ETOH main risk
factors in West
55
4/20/2015
HEPATOCELLULAR CARCINOMA

Diagnosis possible without biopsy

AFP not sensitive or specific, levels over 200ng/dL
highly suspicious for HCC

Characteristic appearance with contrasted
imaging

HCC has arterial blood supply that
demonstrates uptake during early arterial
phase and contrast washout in the delayed
venous phase

Biopsy is warranted in a liver mass larger than
2 cm without typical radiographic findings
and no elevation in AFP
HEPATOCELLULAR CARCINOMA
 Early

Arterial Phase CT
heterogeneously
enhancing mass 4-5 cm
 Portal

Venous Phase CT
Decreased
enhancement, isoenhancing with liver
FINAL THOUGHTS ON THE LIVER

Always give your patients with Cirrhosis and
Gastrointestinal Bleeding Antibiotics because they
improve outcomes

Serum Ammonia Levels have no role in managing
patients with Hepatic Encephalopathy – Clinical
Diagnosis

Always remember precipitating causes of
Encephalopathy including Gastrointestinal Bleeding,
Sedating Drugs, Infection, and Medical NonCompliance
56
4/20/2015
FINAL THOUGHTS ON THE LIVER

Remember Risk Factors for Hepatitis C including IV
Drug Use, Nasal Cocaine Use, Blood Transfusion prior
to 1990

Poor Transmission of Hepatitis C by Sexual Intercourse

Doubt Treatment will be asked but Oral Anti
Replicase Agents have taken the place of older
therapies

Remember Hepatitis B can be Reactivated by
Chemo Therapy or Immunosuppression for
Inflammatory Bowel Disease
FINAL THOUGHTS ON THE LIVER

Remember there is no Chronic form of Hepatitis A
but you can get a relapsing Cholestatic Hepatitis

Remember the majority of Hepatitis B infections are
self limited where as the majority of Hepatitis C
infections are Chronic

Remember the risk of Cirrhosis from Hepatitis C is
approximately 20% after 20 years duration. Alcohol
can accelerate this process
GOOD LUCK ON THE EXAM!!!

Please feel free to contact me with any questions
prior to the Exam.
57