GI bleeding Flashcards
1
Q
Diff b/t upper and lower GI bleeds?
A
- ligament of trietz (LoT) is at duodenojejunal jxn
- upper GI bleed is from a source above the LoT
- lower GI bleed from a source below the LoT
2
Q
Presentation of an upper GI bleed?
A
- hematemesis
- blood or coffee grounds (blood oxidized in acid)detected during nasogastric lavage
- melena
- BUN to serum creatinine ratio greater than 30
3
Q
Presentation of lower GI bleed?
A
- blood clots in the stool
- red blood that is mixed with solid brown stool
- dripping of blood into toilet after a BM
4
Q
How may hematemesis present?
A
- red or brown flakes like coffee grounds
5
Q
When does melena occur?
A
- may occur with just 50-100 mL of blood loss in upper GI tract
6
Q
What is hematochezia, source?
A
- red or maroon colored stool
- generally from lower GI source but can occur with loss of more than 1000 ml of blood in the upper GI tract
7
Q
What causes coffee-ground emesis?
A
- blood sitting in stomach acid causes iron to oxidize resulting in appearance of coffee ground like flakes
8
Q
All the main characteristics of an upper GI bleed?
A
- 2/3 of cases of GIB
- severity: more likely to have sig bleeding (may present with shock if sig blood loss)
- site: above LoT
- presentation: hematemesis, melena, hematochezia if massive UGI of more than 1000 ml
- NG lavage: blood
- bowel sounds: hyperactive
- BUN:creat ratio: greater than 30:1
9
Q
All the maincharacteristics of a lower GI bleed?
A
- severity: less likely to present with shock or reqr transfusion
- site: below the LoT
- present: hematochezia
- NG lavage: clear fluid
- bowel sounds: normal
- BUN:Creat: normal (could be diff with renal failure)
10
Q
Where does BUN come from?
A
- when protein is used for energy the carbon is cleaved from the aa and leaves behind a N, the N takes up 3 H+ to form NH3+ which is ammonia
- the ammonia is then processed through the liver to become urea, when urea enters the blood stream it is called blood urea nitrogen, this is then excreted by the kidney
11
Q
WHen does BUN increase?
A
- when protein is broken down and more ammonia is formed
- burns
- tetracyclines
- fever
- steroids
- catabolic state
- upper GI bleeding (breakdown of hemoglobin protein by stomach acid and enzymes)
12
Q
Epidemiology of upper GI bleeds?
A
- 250,000 hosp. a year in US for acute UGI
- mortality rate of 4-10%
- more than half of pts are older than 60
13
Q
Most common etiologies of upper GI bleeds?
A
- PUD 50% - hx should screen for RFs (h pylori, NSAIDs, ZES, smokers)
- portal HTN 20% - most common cause is cirrhosis, results in formation of esophageal, gastric and duodenal varices that can rupture (clotting enzymes also effected in liver)
- M-W tears 10%: laceration of gastroesophageal jxn, often report a hx of retching which may be due to heavy drinking
seizure, childbirth, straining, defectation, wt lifting - vascular anomalies 7%: angiodysplasia: small AV malformations (leaky), telangectasis: assoc with CT disease like CREST or HHT
- gastric neoplasm
- erosive gastritis: susually superficial bleeding that doesn’t lead to acute sig blood loss
- erosive esophagitis: secondary to chronic reflux
14
Q
Other causes of UGI bleeds?
A
- aortoenteric fistula: complication post AAA (initial presentation or post graft placement)
- hepatic tumor
- angioma
- penetrating trauma
- pancreatic malignancy
15
Q
Etiology of LGI bleeding depending on age?
A
- age younger than 50: infectious colitis anorectal disease IBD - older than 50: diverticulitis agioectasis malignancy ischemia
- LGI: more common bleed in pts older than 50
