Clin - Nausea, Vomiting, Epigastric Pain Flashcards

1
Q

what is gastroparesis

A

slowing of gastric emptying

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2
Q

sx gastroparesis

A
  1. chronic or intermittent sx of postprandial fullness

2. nausea and vomiting

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3
Q

diagnostic test for gastroparesis

A

gastric scintigraphy (gastric emptying scan)

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4
Q

what is an abnormal result in a gastric scintigraphy

A

gastric retention of 60% after 2 hours or more than 10% after 4 hours

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5
Q

tx for acute exacerbations of gastroparesis

A

nasogastric suction and IV fluids

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6
Q

what is acute paralytic ileus

A

neurogenic failure or loss of peristalsis in the intestine in the absence of any mechanical obstruction

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7
Q

diagnostic test for acute paralytic ileus

A

plain abd radiography or CT scan

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8
Q

tx for acute paralytic ileus

A

treat the precipitating condition

- restrict oral intake w/ gradual liberalization of diet as bowel function returns

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9
Q

tx for severe or prolonged ileus

A

nasogastric suction and parenteral administration of fluids and electrolytes

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10
Q

sx acute small bowel obstruction

A
  • N/V
  • constipation
  • distention
  • high pitched bowel sounds
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11
Q

diagnostic test for acute small bowel obstruction

A
  • plain abd radiography or CT scan
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12
Q

tx for acute SBO

A

nasogastric tube to suction, surgery if this isn’t helpful

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13
Q

5 differential diagnoses for dyspepsia

A
  1. pyrosis/GERD
  2. food poisoning/viral gastroenteritis
  3. gastritis and/or PUD
  4. biliary tract dz (cholecystitis)
  5. pancreatitis
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14
Q

how do hiatal hernias cause indigestion

A

they promote acid flow into the esophagus

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15
Q

alarm features in GERD/heartburn/indigestion

A
  1. weight loss
  2. persistent vomiting
  3. constant/severe pain
  4. palpable mass or adenopathy
  5. hematemesis
  6. melena
  7. anemia
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16
Q

compare clinical features between duodenal and gastric ulcers

A

duodenal: burning gnawing epigastric pain 1-3 hours after meals, relieved by food
gastric: burning epigastric pain within 30 mins of eating, food aversion

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17
Q

pathophysiology of duodenal ulcers

A

inflammatory cells releasing cytokines –> stimulate antral G cells and diminished production of somatostatin by D cells –> gastric acid hypersecretion

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18
Q

tx for perforated viscus

A
  • NPO
  • IV antibiotics
  • preoperative labs
  • surgery consult
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19
Q

Cag A positive toxin

A

H. pylori

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20
Q

signet ring cells on histo

A

gastric adenocarcinoma

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21
Q

what are cholesterol and pigment gallstones made of

A

cholesterol: cholesterol monohydrate
pigment: calcium bilirubinate

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22
Q

sx of cholelithiasis

A

many are “silent” but sx include:

  • severe steady ache in RUQ or epigastrum 30-90 mins after meals that can radiate to right scapula or back
  • nausea/vomiting
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23
Q

diagnostic testing in cholelithiasis

A
  • labs: elevation in bilirubin

- imaging: US showing acoustic shadow

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24
Q

demographic most at risk for gallstones

A

american indians

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25
Q

sx of acute cholecystitis

A
  • attacks after fatty meals
  • RUQ tenderness w/ Murphy sign
  • muscle guarding and rebound tend.
  • sometimes palpable gallbladder
  • sometimes jaundice
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26
Q

compare acalculous and calculous cholecystitis

A

calculous: stone in cystic duct causing inflammation behind obstruction
acalculous: true cholecystitis from acute illness

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27
Q

lab results in cholecystitis

A
  1. leukocytosis
  2. bilirubinemia
  3. serum aminotransferase
  4. alkaline phosphatase
  5. serum amylase
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28
Q

US findings indicating acute cholecystitis

A

gallbladder wall thickening, pericholecystic fluid, sonographic murphy sign

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29
Q

what imaging will show you an obstructed cystic duct in cholecystitis

A

hepatic iminodiacetic acid (HIDA) scan

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30
Q

how does gangrene of the gallbladder occur

A

results fro ischemia due to splanchnic vasoconstriction and intravascular coagulation in acute cholecystitis

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31
Q

chronic inflammation of the gallbladder is almost always associated with _____

A

gallstones

32
Q

sx of chronic cholecystitis

A

may be asymptomatic for years, then:

- symptoms of acute cholecystitis (RUQ or epigastric pain and dyspepsia)

33
Q

lab results in chronic cholecystitis

A

usually normal

34
Q

US findings in chronic cholecystitis

A

gallstones within a contracted gabladder

35
Q

describe porcelain gallbladder

A

a complication of chronic cholecystitis causing calcified lesion on the gallbladder
–> increased risk for gallbladder cancer

36
Q

tx for chronic cholecystitis

A

surgery if pt is symptomatic or if porcelain gallbladder is seen

37
Q

pathophysiology of acute pancreatitis

A

1) cellular injury from protein kinases, inflammatory mediators, digestive enzymes (trypsinogen)
2) saponification

38
Q

describe saponification of the pancreas

A

activated lipase causes fat necrosis in triglycerides –> releases fatty acids from fat cells –> fatty acids combine with calcium –> form insoluble salts (saponification)

39
Q

major etiologies of acute pancreatitis

A

1) biliary tree gallstones
2) heavy alcohol use
3) hypertriglyceridemia
4) trauma

40
Q

sx of acute pancreatitis

A

1) epigastric abd pain boring straight through to the back

2) RUQ pain/dyspepsia

41
Q

diagnostic criteria for acute pancreatitis

A

at least 2 of the 3:

  • epigastric pain
  • lipase 3x upper limit of normal
  • CT changes consistent with pancreatitis
42
Q

common lab findings in acute pancreatitis

A

1) leukocytosis
2) hyperglycemia
3) hyperbilirubinemia
4) increased BUN and creatinine
5) increased alk phos and ALT
6) hypocalcemia
7) hypertriglyceridemia
8) elevated hematocrit

43
Q

“sentinel loop” findings on x-ray showing segment of air-filled small intestine most often in LUQ

A

acute pancreatitis

44
Q

“colon cutoff sign” showing gas filled segment of transverse colon abruptly ending at the area of pancreatic inflammation

A

acute pancreatitis

45
Q

when should you do a rapid-bolus IV contrast CT in a patient with acute pancretitis

A

following aggressive volume resuscitation after 3 days of severe acute pancreatitis to look for pancreatic necrosis

46
Q

when should you do a perfusion CT in a patient with acute pancreatitis and what do the results indicate

A

performed on day 3 looking for areas of ischemia to predict development of necrosis
- presence of fluid correlates w/ increased mortality rate

47
Q

ranson criteria is used predict prognosis in what disease process

A

acute pancreatitis

48
Q

what APACHE II score indicates higher mortality in acute pancreatitis patients

A

> 8

49
Q

describe BISAP (bedside index for severity in acute pancreatitis) scoring in acute pancreatitis

A

0-1: mortality M1%

5: mortality of 27%

50
Q

describe the HAPS (harmless acute pancreatitis score) scoring in acute pancreatitis

A

predicts a non-severe course of acute pancreatitis based on:

  • no abd tenderness or guarding
  • normal hematocrit
  • normal serum creatinine
51
Q

important treatment in mild acute pancreatitis

A

LOTS of fluid resuscitation

- 1/3 of total 72 hour fluid volume administered within 24 hours of presentation

52
Q

tx/management in severe acute pancreatitis

A

1) surgical consult
2) hemodynamic monitoring
3) give calcium gluconate IV for hypocalcemia w/ tetany
4) within 48 hours of admission start enteral feedings w/ FG tube

53
Q

how can acute pancreatitis cause prerenal azotemia

A

can cause leakage of fluids into pancreatic bed (3rd spacing) causing prerenal azotemia (decreased fluid to the kidney)

54
Q

complications of acute pancreatitis

A

1) prerenal azotemia
2) pleural effusion (from fluid collection)
3) pseudocysts
4) infections
5) ARDS

55
Q

diagnostic test for upper GI bleed

A

upper endoscopy within 24 hours of arriving in ED

56
Q

what anatomical landmark separates upper and lower GI bleed

A

ligament of treitz

57
Q

initial step is assessing a pt with GI bleed

A

assess hemodynamic status

58
Q

first step to stabilize pt with upper GI bleed

A

place two large bore 18 gauge or larger IV lines to give fluid (0.9% NaCl or lactated ringer)

59
Q

pharmacologic therapies for upper GI bleed

A

1) acid inhibition (IV or oral PPI)

2) Octreotide (reduces splanchnic blood flow to control bleeding)

60
Q

sx associated with upper GI bleed

A
  • hypotension, tachycardia
  • angina, syncope
  • weakness, confusion
  • possible hematemesis, melena, hematochezia
61
Q

what transfusions should you give pts with upper GI bleed and how much

A

1) PRBCs (packed red blood cells)
- 1 unit of PRBCs raises the HGB in adults by 1 g/dL

2) FFP (fresh frozen plasma)

3) platelets
- 6 units of platelets increases platelet count by 50,000

62
Q

sx of esophageal varices

A

1) acute GI hemorrhage (melena, hematochezia, hematemesis)

2) recent retching or dyspepsia

63
Q

red whale markings on endoscopy

A

esophageal varices

64
Q

tx/management of esophageal varices

A

1) rapid assessment and resuscitation with fluids or blood
2) IV vitamin K due to coagulopathy
3) emergent upper endoscopy w/ variceal banding

65
Q

tx for prevention of rebleed in esophageal varices patients

A

1) nonselective beta adrenergic blockers

2) long term band ligation

66
Q

etiology of hemorrhagic (erosive) gastropathy/gastritis

A

1) aspirin/NSAIDs
2) alcoholic (portal HTN gastropathy)
3) severe stress/critically ill

67
Q

most common clinical manifestation of erosive gastritis

A

upper GI bleed w/ hematemesis (coffee ground emesis) or bloody aspirate

68
Q

diagnostic test for erosive gastritis

A

upper endoscopy with biopsy

69
Q

tx for erosive gastritis

A

1) remove offending agnet: aspirin/NSAID/alcohol
2) beta blocker in portal HTN gastropathy
3) H2 blocker of PPI for prevention

70
Q

PUD that isn’t responsive to treatment and is severe, atypical, or recurrent

A

zollinger-ellison syndrome

71
Q

large mucosal folds on EGD

A

hypertrophic gastropathy (zollinger ellison or menetrier)

72
Q

diagnostic criteria for zollinger ellison

A

1) >1000 serum (fasting) gastrin
2) positive secretin stimulation test
3) large mucosal folds on EDG

73
Q

tx for zollinger ellison

A

PPI

74
Q

giant thickened gastric folds involving predominantly the body of the stomach

A

menetrier’s dz

75
Q

tx for mallory weiss tear

A

bleeding usually abates spontaneously

- locally injected epinephrine or cauterization therapy if needed

76
Q

tx boerhaave

A
  • NPO
  • parenteral antibiotics
  • surgery
  • endoscopic stenting
77
Q

compare billroth I and II gastroduodenostomy

A

1: excision of pylorus and antrum and partial closure of gastric end w/ end-to-end anastomosis of stomach and duodenum
2: removal or pylorus and first part of the duodenum, cut end of stomach is anastomosed to the jejunum