Clinical Approach to the GI Patient: Upper GI Bleeding Flashcards

1
Q

How is an acute upper GI bleed defined?

A

the source is proximal to the ligament of Treitz

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2
Q

what is the most common cause of an upper GI bleed?

A

PUD

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3
Q

what might the history be in a patient with an UGIB?

A

hematemesis (vomit bright red blood or coffee grounds); melena, and hematochezia (bright red blood per rectum) in massive UGIB

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4
Q

what are the severe symptoms of an acute upper GI bleed and what do they indicate?

A

indicate: anemia/ hypovolemia; orthostatic dizziness, confusion, angina, tachycardia, syncope, weakness, SOB

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5
Q

what are some co-morbid conditions that a patient with an acute upper GI bleed could have?

A

aortic stenosis, renal disease, smoking, liver disease, EtOH abuse, H. pylori, NSAIDs

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6
Q

how could a history of aortic stenosis and renal disease lead to an acute upper GI bleed?

A

the patient could have AVM, telangiectasias, and angiodysplasia

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7
Q

what medications could cause an acute upper GI bleed?

A

salicylates (aspirin), glucocorticoids, NSAIDs, and anticoagulants

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8
Q

what are the signs of hypovolemia?

A

resting tachycardia, orthostatic hypotension, supine hypotension

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9
Q

what might the abdominal exam be in a patient with an acute upper GI bleed?

A

severe abdominal pain, rebound tenderness and involuntary guarding, raises concern for perforation–> rule out perforation prior to endoscopy

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10
Q

what are the diagnostic tools used when dealing with an acute upper GI bleed?

A

x-ray/CT/MRI if suspect complication; EGD with biopsy (diagnostic and therapeutic)

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11
Q

what is the treatment/management of a patient with an acute upper GI bleed?

A

identify and stabilize unstable patients; 2 large bore IVs (18 gauge or larger); IV fluid bolus if signs of shock

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12
Q

what should you consider in patients with varices who are presenting with an acute upper GI bleed?

A

possibly octreotide–> it inhibits the secretion of gastric acid, reduces blood flow to the gastroduodenal mucosa, and causes splanchnic vasoconstriction; antibiotics if a variceal bleed

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13
Q

what are 8 things that could cause an upper GI bleed?

A

PUD, stress ulcers, esophageal varices, hemorrhagic gastritis, zollinger-ellison syndrome, mallory-weiss tear/ boerhaave syndrome, dieulafoy lesion, and GAVE syndrome

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14
Q

what is the etiology of stress ulcers (aka stress related mucosal disease)?

A

burns, CNS damage, and severe surgical or medical illness (stress)

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15
Q

how do you diagnose a stress ulcer?

A

EGD (diagnostic and therapeutic)

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16
Q

how do treat/manage a patient with a stress ulcer?

A

PPI; prevention of stress ulcers in critically ill patients (ICU)–> use of H2 blocker or PPI to reduce the incidence; the use of enteral nutrition reduces the risk of stress-related bleeding

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17
Q

where are curling ulcer’s typically found?

A

in the duodenum

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18
Q

what are esophageal varices and what causes them?

A

they are dilated submucosal veins in the esophagus; most commonly develop secondary to portal hypertension (cirrhosis)

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19
Q

what is the presentation of esophageal varices?

A

they are asymptomatic unless they are complicated by bleeding

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20
Q

when do esophageal varices bleed?

A

occurs after recent retching; 1/3 of patients with varices end up having an upper GI bleed

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21
Q

how do you diagnose esophageal varices?

A

EGD with biopsy (diagnostic and therapeutic)

22
Q

when is a person at increased risk of bleeding from esophageal varices?

A

when the size of the varices is larger than 5 mm; the presence at endoscopy of red wale markings; the severity of liver diseases; active alcohol abuse

23
Q

what is the treatment/management for esophageal varices?

A

acute resuscitation in ICU; IV fluids or blood products are essential; correct coagulopathy (underlying cirrhosis); emergent upper endoscopy with variceal banding

24
Q

how can you prevent esophageal varices?

A

nonselective beta-adrenergic blocker (propranolol, nadolol)- reduce the risk of rebleeding: common side effects: fatigue and hypotension; long term treatment with band ligation reduces the incidence of rebleeding to about 30%

25
Q

what is the cause of hemorrhagic erosive gastritis?

A

aspirin and NSAIDs, alcoholic (portal HTN gastropathy); severe stress/ critically ill

26
Q

how might the physical exam look in a patient with hemorrhagic erosive gastritis?

A

because erosive gastritis is superficial, hemodynamically significant bleeding is rare; vital signs will be normal; liver disease stigmata acutely distressed

27
Q

how do you diagnose a hemorrhagic erosive gastritis?

A

upper endoscopy with biopsy

28
Q

what does the biopsy show in a patient with a hemorrhagic erosive gastritis?

A

there is usually no significant inflammation on histologic examination

29
Q

how do you treat/manage a patient with a hemorrhagic erosive gastritis?

A

remove the offending agent: aspirin/ NSAID/ alcohol; if the patient has portal HTN gastropathy: beta-blocker (propanolol or nadolol)

30
Q

what is the etiology of zollinger-ellison syndrome?

A

primary gastrinoma- non-beta islet cell- gastrin secreting tumor (usually in the proximal duodenum)

31
Q

25% of primary gastrinomas are associated with what?

A

autosomal dominant familial syndrome MEN 1 (multiple endocrine neoplasia type 1)

32
Q

what are the symptoms associated with MEN 1?

A

pancreatic gastrinoma, hyperparathyroidism (increased calcium), and pituitary neoplasm (gigantism)

33
Q

what might the history/ presentation be in a patient with zollinger-ellison syndrome?

A

they have a PUD that isn’t responding to treatment, is severe, atypical, and recurrent

34
Q

how do you diagnose zollinger-ellison syndrome?

A

EGD, serum (fasting) gastrin

35
Q

what test is done first to diagnose zollinger-ellison syndrome? and is this confirmatory?

A

serum (fasting) gastrin: initial test done–> if it is >1000 pg/mL, then it can be confirmatory

36
Q

when is an EGD suggestive of zollinger-ellison syndrome?

A

when you see large mucosal folds (hypertrophic gastric mucosa)

37
Q

what is the confirmatory test if the serum (fasting) gastrin levels is less than 1000?

A

secretin stimulation test

38
Q

why would you use endoscopic US, CT and MRI scans in a patient you thing may have zollinger-ellison syndrome?

A

to look for large hepatic metastases and primary lesions

39
Q

in all patients with zollinger-ellison syndrome, what should you do?

A

draw levels of serum PTH-iPTH, prolactin, LH-FSH, and GH–> to exclude MEN 1

40
Q

what is the treatment/management for zollinger-ellison syndrome?

A

PPI; surgical resection; in patients with MEN 1: treat hyperparathyroidism first

41
Q

what is dieulafoy syndrome?

A

rare, potentially life threatening, an aberrant large-caliber submucosal artery; it runs a tortuous course within the submucosa and typically the lesion protrudes through a small mucosal defect

42
Q

where is the most common site for a dieulafoy lesion?

A

the stomach (proximal stomach causes recurrent intermittent bleeding)

43
Q

what might the history/presentation be like in a patient with dieulafoy lesion?

A

fatigue, hematemesis, occult GI bleed, pallor, elderly, male> female, often already hospitalized, no previous history

44
Q

how do you diagnose a dieulafoy lesion?

A

awareness/ clinical suspicion; careful upper EGD

45
Q

how do you treat a dieulafoy lesion?

A

transfusion if needed; endoscopic therapy; angiographic interventions for inaccessible lesions

46
Q

what is gastric antral vascular ectasias (GAVE) syndrome?

A

rare, multiple superficial telangiectasias in the gastric antrum

47
Q

when can GAVE syndrome be seen?/ what is it associated with?

A

in diffuse scleroderma and cirrhosis; more common in elderly

48
Q

what might the history/physical exam look like in a patient with GAVE syndrome?

A

fatigue, non descript abdominal pain, occult GI bleed, pallor

49
Q

how do you diagnose GAVE syndrome?

A

upper EGD

50
Q

what can GAVAE syndrome be confused with on an EGD?

A

portal hypertension gastropathy

51
Q

what is the difference between portal hypertension gastropathy and GAVE syndrome?

A

PHG has changes in the fundus more than the antrum

52
Q

how do you treat someone with GAVE syndrome?

A

transfusion if needed; endoscopic band ligation, sclerotherapy, heater probe, and argon plasma coagulation