pom from jennifer--Jaundice, GI bleeding

Question 1

vomiting of red blood, or coffee grounds material

Answer 1

hematemesis

Question 2

black, tarry, foul smelling stool

Answer 2

melena

Question 3

passage of bright red or maroon blood from rectum

Answer 3

hematochezia

Question 4

absence of overt bleeding; occurs in conjunction with iron deficiency or (+) fecal occult blood test

Answer 4

occult

Question 5

What is the fifth way that patients could present?

Answer 5

With symptoms of blood loss or anemia (light headed, syncope, angina, dyspnea).

Question 6

Upper GI bleeding

Answer 6

Ulcers> Varices> Erosions (w. NSAID use)
The following are the common sources of bleed in upper GI bleeding: ulcers, varices, gastroduodenal erosions, Mallory-Weiss tears, erosive esophagitis, neoplasm and vascular ectasia.
Peptic ulcer bleed is the most common cause of UGI bleed. Suspect in pts on NSAIDs and check for H. pylori.
Mallory-Weiss Tears – classic Hx is vomiting, retching, or coughing preceeding hematemesis (esp in alcoholics)
Esophageal varicies, suspect in patients with cirrhosis; poorest outcome among all cases of UGI bleed
Hemorrhagic & Erosive Gastropathy/Gastritis – mucosal lesions (thus don’t cause major bleeding); associated
with NSAIDs, alcohol use and stress (serious trauma, burns, surgery, or sever illness)

Question 7

• Hematemesis:

Answer 7

Upper GI source (above the ligament of Treitz; before the jejunum)

Question 8

• Melena:

Answer 8

Blood present in GI tract for at least 12-14 hrs (and as long as 3-5days)

Question 9

• Hematochezia

Answer 9

Usually from lower GI source, sometimes from a brisk Upper GI source in patients with hemodynamic instability (might start with an upper endoscopy to rule out a brisk bleed).

Question 10

Elevated BUN can mean upper GI bleed

Answer 10

• Small intestinal source: melena or hematochezia; most common causes in adults are vascular ectasias, tumors and NSAID induced erosions and ulcers.
• Elevated BUN in UGIB: blood proteins absorbed in small bowel;
could also be due to volume depletion (also possible in LGIB
start w. upper endoscopy

Question 11

PeptIc Ulcer Bleed

Answer 11

check for H. pylori and suspect in patients who have NSAIDs
Mallory Weiss Tear
Varices–
Hemorrhagic & Erosive Gastropathy/Gastritis
–seen in pts. w NSAIDs, Stress (trauma, burns, ICU–major illness) or alcohol

Question 12

Medical Therapy of Peptic Ulcer Bleed:

Answer 12

1. Proton Pump Inhibitors (PPI);
2. Helicobacter pylori eradication;
3. Avoidance of NSAIDs;
   [Use PPI with NSAIDs, if NSAIDs clinically indicated]
   Consider endoscopic therapy also if the ulcer has an adherent clot, visible vessel or active bleeding. (combo of PPI and endoscopic therapy for high risk lesions is more effective for monotherapy alone.
   •Endoscopic therapy can be accomplished with: Thermal electrocoagulation, injection of Epi or Mechanical clips or bands.

Question 13

clean based ulcers

Answer 13

Clean based ulcers or ones with flat spots/pigmentation are less likely to rebleed

Don’t need endoscopy therapy. Make sure that they are not abusing NSAIDs

Give them NSAIDs

Question 14

Flat spot or pigmentation risk of rebleed is

Answer 14

low

Question 15

Adherent clot or visible vessel risk of re-bleed is

Answer 15

HIGH (1/2)…you have to treat it

Take out clot …need Endoscopy and control the bleed during endscopy

Question 16

How PPIs work

Answer 16

•Platelet aggregation and fibrin formation requires pH>6.8 (Pepsin, which digests blood clots) is inactivated at pH >4. Only PPIs can keep gastric pH >6.8 over 24hrs, and a constant infusion ensures its continuous presence to inhibit any newly activated proton pumps.

PPIs suppress acid production and keep the pH neutral so that pepsin will not come and eat away the clots

Question 17

Lower GI Bleeds present as

Answer 17

melena or hematochezia

Most common causes in adults are vascular ectasias, tumors, and NSAID-induced erosions and ulcers

Kids–>Meckel’s diverticulum is the most common cause of significant lower GIB (LGIB) in children, decreasing in frequency as a cause of bleeding with age

Question 18

Colonic sources of bleeding in hemodynamically stable

Answer 18

Hemorrhoids: probably the most common cause of LGIB, followed by anal fissures
Most common causes of significant LGIB in adults are diverticula, vascular ectasias, neoplasms (primarily adenocarcinoma), and colitis (infectious, inflammatory bowel disease, ischemic or radiation-induced)

***more common today because they are treated w. PPIs so successfully

Question 19

Colonic sources of bleeding in hemodynamically UNstable

Answer 19

Diverticular bleed > AVM> IBD

if they are passing drops of blood w. stools then they DO NOT get admitted

Question 20

Diverticular bleed

Answer 20

Abrupt onset, painless, massive LGIB ( in contrast to bleeding from colonic vascular ectasias which tends to be chronic, and only occasionally hemodynamically significant)
Minor and occult bleeding is not characteristic
Stops spontaneously in ∼80% of patients and rebleed in about 20–25% of patients

Question 21

Jaundice

Answer 21

Jaundice, or icterus, is a yellowish discoloration of tissue resulting from the deposition of bilirubin
Sign of either liver dysfunction or, less often, a hemolytic disorder
Presence of scleral icterus indicates a serum bilirubin of at least 3 mg/dL
Always examine the sclera and under the tongue, under natural light

Question 22

Bilirubin Metabolism

Answer 22

Metabolite of heme
Provides color to bile, stool and urine
Accumulation potentially toxic, leads to kernicterus, jaundice.
Means to excrete unwanted heme derived from hemoglobin (80%), myoglobin, P450 enzymes

Question 23

Biochemistry of

Answer 23

• Heme → biliverdin → Bilirubin. The Unconjugated bilirubin gets bound to albumin and is taken up by the hepatocyte (usually passively); In the hepatocyte, it’s conjugated/glucuronylated and its transferred to the bile canaliculous to be excreted into the bile. It remains unabsorbed until it reaches the large intestines where bacteria chew away at the conjugation moiteties. Then, the UroB gets recycled and gives urine and feces its color

Question 24

UCG-Biirubin should not be in urine.

Answer 24

bilirubin in urine is conjugated bilirubin and suggests liver bilirubin in urine dysfunction. If you see UCG–BILI in urine person may have renal dysfunction

Question 25

• Prehepatic; Disorders of bilirubin metabolism:

Answer 25

Normal LFTs except serum bilirubin
• Increased production (hemolysis, ineffective erythropoiesis, massive blood transfusion)
• Decreased hepatocellular uptake (drugs such as rifampin)
• Decreased conjugation (Gilbert’s syndrome, Crigler-Najjar type I & II, physiologic jaundice of the newborn, breast milk jaundice, HIV protease inhibitors)
• CONJUGATED HYPERBILIRUBINEMIA: Dubin-Johnson syndrome, Rotor’s syndrome

Question 26

Intrahepatic (liver dysfunction)

Answer 26

• 1. Autoimmune –> Primary Biliary Cirrhosis , 2. Ischemic, 3. Viral or Alcoholic hepatitis
• 4. Toxins (Acetominophen, jamacia bush tea, amanita phalloides mushrooms…)
• 5. Cholestatic conditions (pregnancy, infection, sepsis)
• 6. Infiltrative disorders (TB, lymphoma, amyloid

Question 27

Bile Duct Obstruction

Answer 27

Choledocholithiasis 
Diseases of the bile ducts (sclerosing cholangitis, AIDS cholangiopathy, hepatic arterial chemotherapy, postsurgical strictures,parasitic disease such as ascariasis cholangiocarcinoma) 
Extrinsic compression (pancreatic carcinoma, metastatic lymphadenopathy, hepatoma, pancreatitis, aneurysm, cavernous transformation of portal vein)

Question 28

High AST/ALT

Answer 28

pre, intrahepatic or post-hepatic

then get imaging and do biopsy if necessary

Question 29

High Alk Phos w. high transaminases w. jaundice

Answer 29

bile duct obstruction

—can go to US, CT or ERCP