IM GI 2 SEIDENSCHWARZ
Main
Where does the colonoscope go?
Terminal ileum
Obscure GI bleed is a GI bleeder where you cannot actually see
the source of the bleeding in endoscopy and colonoscopy.
Patient comes in with melena/hematochezia, no bleeding in
imaging. Most common cause is human error, maybe you just
have missed it. Most common location would be the small
intestine simply because it cannot be visualized.
Assuming you want to see the small intestine, what can we
order? Barium, capsule enteroscopy, CT scan
Most common source of LGIB in children is metals, and in
adults/as a whole is hemorrhoids.
One of the most important things is we bleed whole blood. How
is hematocrit done? You spin in centrifuge. So what is
hematocrit, what are you measuring? What does hematocrit
mean? The blood cell component, percentage of blood that is
solid. Since we bleed whole blood, if you lose both sides equally
(cells and plasma) of the ratio, the ratio does not change.
What comes back first? PLASMA comes back very fast.
(nay nanawag kay doc Seidenschwarz, oo, oo, oo, nag SOAP
siya over the phone)
Basically, you never expect the CBC to be accurate the first few
hours. It drops after 12 hours, because the plasma goes back
rapidly to preserve the blood pressure. RBC are replaced rather
slowly.
Melena implies that the GI bleed has happened for at least 14
hours, meaning acute rapid, brisk bleeding does not cause
melena.
If you have a massive rupture, tear or whatever and you are
hemorrhaging like crazy, you won’t have melena, why? Because
blood is a laxative, blood makes you really really really pass out
stool. Patient comes from the ER, massive amounts of
hematochezia, hypotensive, sweating – it is not a lower GI
bleed, it is an upper GI bleed. Any patient with hematochezia
and hypotension, the answer is ENDOSCOPY – because the
colon seldom bleeds to cause low blood pressure. It is usually
the upper GI tract.
Melena from a lower GI bleed IF they haven’t defecated long
enough.
Restrictive transfusion strategy
Aggressive transfusion basically increases mortality
How high is does your wedge pressure in order for the varices
to bleed? –
If we keep on transfusing blood, we keep on applying pressure
to the system, overtransfusing blood is dangerous, at the same
time, we don’t want to transfuse blood unless we have to.
The two main prokinetics are erythromycin and metoclopramide.
Do these 2 do anything for bleeding? No, not at all. Why do we
give them? To pass blood out.
For cirrhotics, it is a class 1 recommendation to always start an
antibiotic when you are bleeding. Why? Because the number 1
trigger for bleeding cirrhotics is an infection. You have a patient
with cirrhosis for 4-5 years, then he starts vomiting blood, odds
are something triggered him. Trigger can be anything, but most
common trigger is infection, SBP (spontaneous bacterial
peritonitis). SBP is when your ascitic fluid gets infected.
mechanism is bacterial translocation. DOC for SBP is
CETRIAXONE or QUINOLONES.
Ok anyway, basically, unknown bleeding
1. Capsule endoscopy
2. Enteroscopy
3. Mesenteric angiography – the gold standard for
mesenteric ischemia
4. RBC technicium scanning – inject the intestine with
radioactive dye and we take multiple photographs to
see blood leaking out.
Mesenteric angiography is also therapeutic because you can
embolise the bleeding vessel. The only problem is that it is
expensive and invasive.
Technicium scanning – more sensitive
RBC tag – most sensitive. The disadvantage is there is no
therapy
Use the RBC tag to find the oozing vessel, and use the
mesenteric angiography to embolize everything in that region.
ESOPHAGUS
Hernia
The most common esophageal hernia is hiatal hernia
Hernia is when one tissue pocket extends to another.
Hiatal hernia is when the stomach protrudes upward into the
beyond the diaphragm. Your diaphragm is one of the strongest
tissues which adds strength to the LES.
4 kinds of hernia
Most common is sliding hernia, where the entire upper part goes
thru the diaphragm.
V= If the cardiac region goes thru the diaphragm, that is your
sliding hernia.
If your fundus goes to the esophagus, that is your
paraesophageal hernia aka Type 2.
Type 3 is both. Type 4 is the WHOLE STOMACH,
EVERYTHING FROM THE BOTTOM HERNIATES
What is the number 1 cause or mechanism of GERD? Why
some have reflux disease and some have not?
- Transient lower esophageal sphincter relaxation
TLESR
GERD IS NOT A DISEASE OF HIGH ACIDITY. It is a disease
where acid is in a place where it doesn’t belong. Your esophagus
is not designed to handle stomach acid. When your lower
sphincter relaxes, acid can come back up.
Treatment of choice: PPI
Your PPIs do nothing for your transient lower esophageal
relaxations, but they reduce acid so that you can heal.
Lifestyle changes to reduce GERD:
1. WEIGHT LOSS – the m ore you weigh, the more
pressure it is on your stomach, the more pressure it is
on your stomach, the more likely your sphincter is
going to loosen
2. No meals before bed – eat 3 hours before bed
 3. Avoid foods that weaken the LES (e.g. spicy food)
When we have GERD, we also have the problem that the LES
is also beyond repair, beyond medical management. In this
case, we don’t operate all hernias, but intractable GERD
symptoms – FUNDOPLICATION (last resort for GERD
management)
How long do you give PPIs in GERD patients? – 8 WEEKS
ACHALASIA
- When the lower sphincter does not relax
- Why it happens? – ganglion cells fail to migrate at the
LES, LES is tight forever
Primary achalasia
Secondary achalasia
- Chagas disease – nerves destroyed by the parasite
BIRD’S BEAK APPEARANCE
Problem with achalasia is that there is no proper treatment. We
have 2 main approaches. 1 is medical, 2 is surgical.
Medical treatment: CCB (reduce muscular contraction), Nitrates,
botox. Try each of this first before you do surgery
Surgical: Myotomy + Fundoplication – cutting the muscle
Per Orem Esophageal Myometry - noninvasive, thru the
endoscope
MALLORY-WEISS SYNDROME
- Tearing of LES where you have retching, vomiting
- Very common after binge drinking
- Pancreatitis
- Treatment is supportive – painkillers, PPIs,
dehydration
- If mag burst: BOERHAAVE SYNDROME
BARRET’S ESOPHAGUS
- Metaplastic disease
- Normal mucosa of the esophagus: nonkeratinized
stratified squamous
- Metaplasia: columnar epithelium
- Cancer cells can appear
- Columnar epithelium is not good in withstanding sheer
pressure because it is not designed for it. You are more
prone to tear and cuts
- The stomach and the esophagus now look the same
- Adenocarcinoma
- No cure. Once Barret’s esophagus forms, it will be
Barret’s forever
- Treatment: Lifetime of PPIs
- Surgery: routine endoscopy, if you biopsy dysplastic
tissue or adenocarcinoma forming, then you operate.
If not, PPIs with regular monitoring
Gold standard of GERD diagnosis – HISTORY AND PE
Majority of GERD patients are non-erosive (normal ang
endoscopy, adjunct lang siya, only do these adjunct tests if
medication does not work properly.
When do you tell the patient he needs endoscopy?
- Everybody with new onset abdominal pain over the age
of 50
- Below 50 is anybody not responding therapy or having
warning signs (bleeding, dysphagia, weight loss etc)
LIVER
Liver disease gold standard is Liver biopsy
Liver has a dual blood supply
Portal vein – drainage in the liver
- Accumulation of all GI blood supply
- 80% of the blood to the liver
- Deoxygenated blood
Main oxygen supply of the liver is from the hepatic artery
Hepatic vein – merges with inferior vena cava
Liver can’t feel pain.
Pain in the upper right quadrant – pain from the liver by
stretching the Glisson’s capsule (e.g. dengue)
If the liver is hurting - INFECTION
Itching – mosyt common problem of liver patients
- This is due to bilirubin in the skin
- Use anti-histamines to address itchiness
- Lifetime
Jaundice
- Obstruction
o Correctible
- Cholestatic disease
o Primary pathology is the parenchyma
o No cure because the liver is damage
- Hallmark sign
- 2.5 mg/dL – cause jaundice
- Where is jaundice most obvious? Check first
o Sclera
o Under the tongue
o Palms of your hand
- Urine often darkens first – conjugated bilirubin
IM GI 3 SEIDENSCHWARZ
Abuse – drink so much something bad happens (e.g. damage
your car)
Dependent – you need a drink every day
CAGE questionnaire – 1 positive can be sensitive for
dependency/risk factor
Alcoholic Liver Cirrhosis
Feminism – bigger boobs, losing hair
Decompensated Liver Disease – Liver Cirrhosis
- Hepatic encephalopathy something is wrong
- 4 stages of hepatic encephalopathy
o Stage 1 – irritability or insomnia
o Stage 2 -
o Stage 3 and 4 – seizures, coma
o Always ask if patient is agitated, difficulty
sleeping, fighting with people
- Ammonia is excessive in blood in hepatic
encephalopathy
o Excess of nitrogen in the body, converted into
ammonia
o When the body is stressed out – body can no
longer keep up the ammonia
- Lactulose is the DOC for hepatic encephalopathy
 Albumin maintains oncotic pressure
- It is just big, cannot diffuse; Cannot transfer from one
chamber to another
- Albumin is only made in the liver
- If the liver fails, no albumin, no albumin, water seeps
the blood stream
Cholangitis, obstruction – ERCP
MRCP – moderately high bilirupin, ALkPhos
Ultrasound – SCREENING, mass lesions
Transient

Characteristic LIVER BIOPSY – GOLD STANDARD

- Orthopnea/Bradypnea
- Orthoaxia – unique to liver disease; they have to lie Child Pugh scoring
down to keep breathing well - Protime
- Bilirubin
Hepatitis A - Albumin
- The most common cause of jaundice in the Philippines - Ascites
- Food and water - Hepatic encephalopathy
- SGPT is extremely high (hundreds/thousands) - Remember the lowest score is 5
- You have jaundice, high SGPT but everything else is - Child Pugh A – pwede surgery but not transplant
extremely normal - Child Pugh B is 7, medical clearance before surgery
- Problem with SGPT it goes up for everything - Child Pugh C is palliative, too morbid, beyond help
- But when we talk about SGPT hundred times UNL – 3 - You need transplant in Class B
diseases come into mind - Predictor for survival
o Hepatitis
o Drugs How do we diagnosis cirrhosis?
o Heart failure - Low albumin and low protime
- Get the IgM, not the IgG - Albumin – weeks
- The only Hepatitis that doesn’t cause cirrhosis
What are the Vit K dependent factors?
Hepatitis B - Extrinsic pathway
- Acute – adult - If your liver fails, protime is low kay di na siya ka recycle
- Chronic – child sa mga factors
- Number 1 determinant for chronic hep B is age
- Treatment of choice for acute Hep B – SUPPORTIVE, How to normalize protime in cirrhotic patients for surgery?
you wait for it to go away - Coagulation factors
- Treatment for chronic Hep B – interferon, tenofovir - Fresh frozen plasma
- Transfuse from another person
Hepatitis C
- Screened by anti-HCV What is the most common cause of normocytic normochromic
- If you trigger, may Hep C na ba? anemia worldwide?
- The truth is you don’t know - Kidney failure
- Antibodies are for life - Enough iron, and bone marrow is working properly
- Absolutely requires TREATMENT if you have detected In cirrhotics
HCV RNA - Microcytic – chronically losing blood, varices can burst
- Interferon and ribavirin – traditional - Macrocytic – alcoholism
- Now – direct acting antivirals - DNA is impaired due to lack of folate – macrocytic

Hepatitis D Most common cause is cirrhosis in the Philippines is Hepatitis B

- Suspect if patient does not respond to HEP B treatment
You don’t test LMK1 to everybody
Only test if SGPT is too high, then negative on hepatitis tests,
normal tests results
Hepatitis C has a more potent chance to cause cirrhosis, but
incidents are low
15 grams paracetamol can cause liver shutdown
Safe levels of paracetamol 4 gms, 2 gms if cirrhotic

Non-alcoholic liver disease or fatty liver disease
- Imaging diagnosis
- Number 1 cause: diabetes, high blood glucose
- Treatment of choice – diet and exercise
CT SCAN – Hepatocellular cancer
Ferritin tests for hemochromatosis
Iron overload – hemochromatosis
Only way to get rid of too much iron is to drain blood
ANA for PBC
Alpha 1 antitrypsin can also destroy the liver

TRIPHASIC CT SCAN for liver Treatment is transplant

ERCP and MRCP – test of choice for the biliary tree All alcoholic cirrhotic patients – stop them drinking, most
important measure, prolong life
Why is the UTZ not good for the biliary tree?
- Because it is covered by the duodenum Alcoholic hepatitis
- Mallory pink bodies
ERCP – invasive - Biopsy is the end all
MRCP – picture
 - Tx: abstinence, thiamine and folic acid, proper diet with
proper protein
- Target is 7, no need to overtransfuse
- Does have a medical cure thru
prednisolone/prednisone or penoxifolen
- If the patient cannot tolerate steroids – give the 2nd drug
(naa sa Harrisons)

Bilirubin, INR, Creatinine – get the MELDS score

Melds score – 20
If 20 – start prednisolone, but not for everybody
SGPT is not a prognostic indicator
But SGPT on cirrhotic is low, completely useless in cirrhotics
because it is always going to be low because the liver is dead,
like getting a pulse on a corpse.

If a patient has Hep B and cirrhosis – normal SGPT

Primary Biliary Cirrhosis

- Autoimmune disease where immune cells destroy the
intrahepatic ducts
- The patient resembles an obstructive feature without
obstruction (everything is high but utz is clean)
- MRCP
- Consider PBC if MRCP is still negative
- AMA positive – no need biopsy
- All autoimmune disease – primarily in females
- DOC: ursa deoxycholic acid – maintenance for the rest
of your life
- Bright yellow skin

Liver transplant
- Option for Child Pugh score of B
- There is a limit for who can have transplant
- Unstable – can’t do a transplant
- Most important: if you’re drinking, you’re not allowed to
have a transplant

Portal Hypertension
- More than 5 mmHg
-