pom from jennifer--Jaundice, GI bleeding Flashcards
(29 cards)
vomiting of red blood, or coffee grounds material
hematemesis
black, tarry, foul smelling stool
melena
passage of bright red or maroon blood from rectum
hematochezia
absence of overt bleeding; occurs in conjunction with iron deficiency or (+) fecal occult blood test
occult
What is the fifth way that patients could present?
With symptoms of blood loss or anemia (light headed, syncope, angina, dyspnea).
Upper GI bleeding
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)
• Hematemesis:
Upper GI source (above the ligament of Treitz; before the jejunum)
• Melena:
Blood present in GI tract for at least 12-14 hrs (and as long as 3-5days)
• Hematochezia
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).
Elevated BUN can mean upper GI bleed
• 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
PeptIc Ulcer Bleed
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
Medical Therapy of Peptic Ulcer Bleed:
- Proton Pump Inhibitors (PPI);
- Helicobacter pylori eradication;
- 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.
clean based ulcers
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
Flat spot or pigmentation risk of rebleed is
low
Adherent clot or visible vessel risk of re-bleed is
HIGH (1/2)…you have to treat it
Take out clot …need Endoscopy and control the bleed during endscopy
How PPIs work
•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
Lower GI Bleeds present as
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
Colonic sources of bleeding in hemodynamically stable
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
Colonic sources of bleeding in hemodynamically UNstable
Diverticular bleed > AVM> IBD
if they are passing drops of blood w. stools then they DO NOT get admitted
Diverticular bleed
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
Jaundice
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
Bilirubin Metabolism
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
Biochemistry of
• 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
UCG-Biirubin should not be in urine.
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
