Clin - Nausea, Vomiting, Epigastric Pain Flashcards
what is gastroparesis
slowing of gastric emptying
sx gastroparesis
- chronic or intermittent sx of postprandial fullness
2. nausea and vomiting
diagnostic test for gastroparesis
gastric scintigraphy (gastric emptying scan)
what is an abnormal result in a gastric scintigraphy
gastric retention of 60% after 2 hours or more than 10% after 4 hours
tx for acute exacerbations of gastroparesis
nasogastric suction and IV fluids
what is acute paralytic ileus
neurogenic failure or loss of peristalsis in the intestine in the absence of any mechanical obstruction
diagnostic test for acute paralytic ileus
plain abd radiography or CT scan
tx for acute paralytic ileus
treat the precipitating condition
- restrict oral intake w/ gradual liberalization of diet as bowel function returns
tx for severe or prolonged ileus
nasogastric suction and parenteral administration of fluids and electrolytes
sx acute small bowel obstruction
- N/V
- constipation
- distention
- high pitched bowel sounds
diagnostic test for acute small bowel obstruction
- plain abd radiography or CT scan
tx for acute SBO
nasogastric tube to suction, surgery if this isn’t helpful
5 differential diagnoses for dyspepsia
- pyrosis/GERD
- food poisoning/viral gastroenteritis
- gastritis and/or PUD
- biliary tract dz (cholecystitis)
- pancreatitis
how do hiatal hernias cause indigestion
they promote acid flow into the esophagus
alarm features in GERD/heartburn/indigestion
- weight loss
- persistent vomiting
- constant/severe pain
- palpable mass or adenopathy
- hematemesis
- melena
- anemia
compare clinical features between duodenal and gastric ulcers
duodenal: burning gnawing epigastric pain 1-3 hours after meals, relieved by food
gastric: burning epigastric pain within 30 mins of eating, food aversion
pathophysiology of duodenal ulcers
inflammatory cells releasing cytokines –> stimulate antral G cells and diminished production of somatostatin by D cells –> gastric acid hypersecretion
tx for perforated viscus
- NPO
- IV antibiotics
- preoperative labs
- surgery consult
Cag A positive toxin
H. pylori
signet ring cells on histo
gastric adenocarcinoma
what are cholesterol and pigment gallstones made of
cholesterol: cholesterol monohydrate
pigment: calcium bilirubinate
sx of cholelithiasis
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
diagnostic testing in cholelithiasis
- labs: elevation in bilirubin
- imaging: US showing acoustic shadow
demographic most at risk for gallstones
american indians
sx of acute cholecystitis
- attacks after fatty meals
- RUQ tenderness w/ Murphy sign
- muscle guarding and rebound tend.
- sometimes palpable gallbladder
- sometimes jaundice
compare acalculous and calculous cholecystitis
calculous: stone in cystic duct causing inflammation behind obstruction
acalculous: true cholecystitis from acute illness
lab results in cholecystitis
- leukocytosis
- bilirubinemia
- serum aminotransferase
- alkaline phosphatase
- serum amylase
US findings indicating acute cholecystitis
gallbladder wall thickening, pericholecystic fluid, sonographic murphy sign
what imaging will show you an obstructed cystic duct in cholecystitis
hepatic iminodiacetic acid (HIDA) scan
how does gangrene of the gallbladder occur
results fro ischemia due to splanchnic vasoconstriction and intravascular coagulation in acute cholecystitis
chronic inflammation of the gallbladder is almost always associated with _____
gallstones
sx of chronic cholecystitis
may be asymptomatic for years, then:
- symptoms of acute cholecystitis (RUQ or epigastric pain and dyspepsia)
lab results in chronic cholecystitis
usually normal
US findings in chronic cholecystitis
gallstones within a contracted gabladder
describe porcelain gallbladder
a complication of chronic cholecystitis causing calcified lesion on the gallbladder
–> increased risk for gallbladder cancer
tx for chronic cholecystitis
surgery if pt is symptomatic or if porcelain gallbladder is seen
pathophysiology of acute pancreatitis
1) cellular injury from protein kinases, inflammatory mediators, digestive enzymes (trypsinogen)
2) saponification
describe saponification of the pancreas
activated lipase causes fat necrosis in triglycerides –> releases fatty acids from fat cells –> fatty acids combine with calcium –> form insoluble salts (saponification)
major etiologies of acute pancreatitis
1) biliary tree gallstones
2) heavy alcohol use
3) hypertriglyceridemia
4) trauma
sx of acute pancreatitis
1) epigastric abd pain boring straight through to the back
2) RUQ pain/dyspepsia
diagnostic criteria for acute pancreatitis
at least 2 of the 3:
- epigastric pain
- lipase 3x upper limit of normal
- CT changes consistent with pancreatitis
common lab findings in acute pancreatitis
1) leukocytosis
2) hyperglycemia
3) hyperbilirubinemia
4) increased BUN and creatinine
5) increased alk phos and ALT
6) hypocalcemia
7) hypertriglyceridemia
8) elevated hematocrit
“sentinel loop” findings on x-ray showing segment of air-filled small intestine most often in LUQ
acute pancreatitis
“colon cutoff sign” showing gas filled segment of transverse colon abruptly ending at the area of pancreatic inflammation
acute pancreatitis
when should you do a rapid-bolus IV contrast CT in a patient with acute pancretitis
following aggressive volume resuscitation after 3 days of severe acute pancreatitis to look for pancreatic necrosis
when should you do a perfusion CT in a patient with acute pancreatitis and what do the results indicate
performed on day 3 looking for areas of ischemia to predict development of necrosis
- presence of fluid correlates w/ increased mortality rate
ranson criteria is used predict prognosis in what disease process
acute pancreatitis
what APACHE II score indicates higher mortality in acute pancreatitis patients
> 8
describe BISAP (bedside index for severity in acute pancreatitis) scoring in acute pancreatitis
0-1: mortality M1%
5: mortality of 27%
describe the HAPS (harmless acute pancreatitis score) scoring in acute pancreatitis
predicts a non-severe course of acute pancreatitis based on:
- no abd tenderness or guarding
- normal hematocrit
- normal serum creatinine
important treatment in mild acute pancreatitis
LOTS of fluid resuscitation
- 1/3 of total 72 hour fluid volume administered within 24 hours of presentation
tx/management in severe acute pancreatitis
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
how can acute pancreatitis cause prerenal azotemia
can cause leakage of fluids into pancreatic bed (3rd spacing) causing prerenal azotemia (decreased fluid to the kidney)
complications of acute pancreatitis
1) prerenal azotemia
2) pleural effusion (from fluid collection)
3) pseudocysts
4) infections
5) ARDS
diagnostic test for upper GI bleed
upper endoscopy within 24 hours of arriving in ED
what anatomical landmark separates upper and lower GI bleed
ligament of treitz
initial step is assessing a pt with GI bleed
assess hemodynamic status
first step to stabilize pt with upper GI bleed
place two large bore 18 gauge or larger IV lines to give fluid (0.9% NaCl or lactated ringer)
pharmacologic therapies for upper GI bleed
1) acid inhibition (IV or oral PPI)
2) Octreotide (reduces splanchnic blood flow to control bleeding)
sx associated with upper GI bleed
- hypotension, tachycardia
- angina, syncope
- weakness, confusion
- possible hematemesis, melena, hematochezia
what transfusions should you give pts with upper GI bleed and how much
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
sx of esophageal varices
1) acute GI hemorrhage (melena, hematochezia, hematemesis)
2) recent retching or dyspepsia
red whale markings on endoscopy
esophageal varices
tx/management of esophageal varices
1) rapid assessment and resuscitation with fluids or blood
2) IV vitamin K due to coagulopathy
3) emergent upper endoscopy w/ variceal banding
tx for prevention of rebleed in esophageal varices patients
1) nonselective beta adrenergic blockers
2) long term band ligation
etiology of hemorrhagic (erosive) gastropathy/gastritis
1) aspirin/NSAIDs
2) alcoholic (portal HTN gastropathy)
3) severe stress/critically ill
most common clinical manifestation of erosive gastritis
upper GI bleed w/ hematemesis (coffee ground emesis) or bloody aspirate
diagnostic test for erosive gastritis
upper endoscopy with biopsy
tx for erosive gastritis
1) remove offending agnet: aspirin/NSAID/alcohol
2) beta blocker in portal HTN gastropathy
3) H2 blocker of PPI for prevention
PUD that isn’t responsive to treatment and is severe, atypical, or recurrent
zollinger-ellison syndrome
large mucosal folds on EGD
hypertrophic gastropathy (zollinger ellison or menetrier)
diagnostic criteria for zollinger ellison
1) >1000 serum (fasting) gastrin
2) positive secretin stimulation test
3) large mucosal folds on EDG
tx for zollinger ellison
PPI
giant thickened gastric folds involving predominantly the body of the stomach
menetrier’s dz
tx for mallory weiss tear
bleeding usually abates spontaneously
- locally injected epinephrine or cauterization therapy if needed
tx boerhaave
- NPO
- parenteral antibiotics
- surgery
- endoscopic stenting
compare billroth I and II gastroduodenostomy
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
