GI - 4 Stomach pt 2 Flashcards

1
Q

List 3 risk factors/ causes of peptic ulcers

A

Smoking
NSAIDS (mainly aspirin)
H. Pylori

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2
Q

Where do Gastric Ulcers develop? What is it associated with?

A

In btwn body and antrum

Associated with decreased acid production (gastritis overwhelms mucosal defense mechanisms)

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3
Q

What do NSAIDs increase the risk of?

A

GU (40x), Complications with ulcers (bleeding, perforation, death)

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4
Q

Epigastric pain (hallmark) 80%
20% with complications (ie bleeding) are asymptomatic
Pain is a “gnawing, dull ache, hunger like”
50% report relief with food (esp DU) and recurrence 2-4hrs after

A

PUD

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5
Q

What is the main symptom of PUD?

A

Epigastric pain

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6
Q

Epigastric pain relieved by eating food is a sign of:

A

PUD (DU)

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7
Q

____ is procedure of choice for an Ulcer.

Also do what?

A

Endoscopy

Also Bx for H. Pylori

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8
Q

What is the treatment for DU? GU?

A

PPI
GU 4 weeks
DU 8 weeks

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9
Q

What are 3 Meds to eradicate H. pylori?

A

PPI 2 x day, Clarithromycin 500mg bid, Amoxicillin 1g BID

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10
Q

List 4 complications of PUD

A

GI hemorrhage
Ulcer perforation
Ulcer penetration
Gastric outlet obstruction

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11
Q

Melena, hematemesis, hematochezia

Nasogastric lavage shows “coffee grounds” or red blood

A

GI hemorrhage

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12
Q

Sudden, severe abdominal pain

Appear ill, rigid abd, no bowel sounds, rebound tenderness

A

Ulcer perforation

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13
Q

What is the treatment for Ulcer perforation?

A

40% seal on own
Surgery
H. pylori tx, fluids, IV PPI, abx

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14
Q

Located along posterior wall of duodenum or stomach may penetrate into pancreas, liver or biliary tree
Change in pattern/intensity of their pain
Severe constant pain, radiates to back, unresponsive to antacids, food
increased amylase. How is it diagnosed? Treated?

A

Ulcer Penetration
Endoscopy and barium studies confirm it’s an ulcer, but don’t show penetration
Treat: IV PPI (no surgical tx)

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15
Q

Edema or narrowing of pylorus or duodenal bulb
Most with known history of ulcers
Fullness and heaviness with meals progresses to early satiety, vomiting, wt loss
Chronic obstruction: dilated atonic stomach, severe wt loss, malnutrition
Dehydration, metabolic alkalosis, hypokalemia.
What is it? What’s the treatment?

A
Gastric Outlet Obstruction
Tx: Correct fluid and electrolytes
IV PPI
Nasogastric decompression of stomach
Endoscopy in 24-72 hrs to define nature of obstruction, R/o gastric cancer, and Dilatation of obstruction
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16
Q

Name 3 ways Gastric Outlet Obstruction is identified

A

Physical: Succussion splash may be heard in epigastrum
Nasogastric aspiration: >200cc foul smelling fluid is diagnostic
More subtle obstructions are diagnosed with a saline load test or nuclear gastric emptying study

17
Q

80% of gastrinomas arise:

A

within gastrinoma triangle: porta hepatis, neck of pancreas, and 3rd portion of duodenum

18
Q

PUD with similar symptoms
Ulcers are usually solitary in duodenum, may be multiple
GERD common
Diarrhea in 1/3, steatorrhea (presence of excess fat in feces), wt loss

A

Zollinger-Ellison Syndrome

19
Q

Laboratory findings in ____
Fasting gastrin > 150 pg/ml
Median level is 500-700 pg/ml, 60%> 1000pg/ml
Gastrin>1000 and acid hypersecretion is diagnostic
For others can do a secretin stimulation test

A

Zollinger-Ellison Syndrome

20
Q

What is a more common cause of Hypergastrinemia than Gastrinoma? What must you do to check?

A

Hypochlorhydria
must measure gastric pH in pt with hypergastrinemia
if pH>3 implies hypochlorhydia

21
Q

Imaging in Z-E Syndrome

A

Somatostatin Receptor Scintigraphy with SPECT scan >80% sensitive