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Clin Med III Exam 1 > PUD and Gastric CA > Flashcards

PUD and Gastric CA Flashcards

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1
Q

PUD definition

A

defect in gastric or duodenal mucosa that extends through the muscularis mucosa into deeper layers of the wall

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2
Q

Layers of stomach wall

A

mucosa, submucosa, muscularis

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3
Q

Etiology of PUD

A
  1. H. pylori *
  2. NSAIDs *
  3. Other
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4
Q

Most common cause of PUD

A

H. pylori; incidence increases w/ age

may predispose to gastric CA

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5
Q

Inhibit gastrin release

A

low pH
prostaglandins
SS

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6
Q

Increase gastrin release

A

stomach distention

presence of peptides/AA

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7
Q

Gastrin role

A

increase gastric motility

stimulate parietal cells to secrete HCl and pepsinogen

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8
Q

Secretin role

A

inhibit stomach motility
decrease bile secretion
increase bicarb secretion from pancrea

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9
Q

1 cause of GI bleed

A

PUD

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10
Q

H. pylori description

A

gram (-) rod
Motile flagella (attaches to gastric mucosa)
oral-oral or fecal-oral route
disrupts protective properties by decreasing gastric mucus and mucosal bicarb secretion
raises pH

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11
Q

Increase risk of PUD w/ NSAIDs

A
  • prior hx of PUD/ulcer complications
  • H. pylori infection
  • > 75 YO
  • increased dose, time, duration of use
  • concomitant use of steroid, other NSAID, anticoag, low dose ASA, SSRI, alendronate
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12
Q

H. pylori virulence factors

A
  1. flagella- attach, move
  2. urease - hydrolyze gastric urea to form ammonia, that helps neutralize gastric acid, enabling it to penetrate gastric mucosa
  3. Adhesins: adhere to epithelial cells
  4. Cause inflammation: causes G cells in antrum to secrete gastrin and therefore HCl increases

(ulcers are immediately friable)

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13
Q

Concomitant drugs that worsen PUD from NSAID

A 
steroid
other NSAID
anticoagulants
ASA
SSRI
alendronate
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14
Q

NSAIDs

A

ibuprofen
ASA
naproxen
toradol

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15
Q

MOA of PUD w/ NSAIDs

A

NSAIDs block COX, therefore preventing prostaglandin synthesis (PGE2) – prostaglandins inhibit gastrin secretion and increase mucous secretion, and promote epithelial cell proliferation

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16
Q

Prostaglandin role in stomach health

A
  • inhibit gastrin secretion
  • increase mucous secretion
  • promote epithelial cell proliferation
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17
Q

Presentation of PUD

A

asymptomatic (70%)
Abdominal pain/discomfort

dyspepsia (belching, bloating, distention)
Nausea, early satiety, comiting

Complications: hematemesis, melena, fatigue, dyspnea

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18
Q

Gastric vs. duodenal ulcers

A

gastric: worse after meal (30min-1hr), vomiting, more likely to hemorrhage/hematemesis; weight loss/anorexia
duodenal: relieved by meals! (worse 2-3 hrs post meal), vomiting uncommon), less likely to hemorrhage (melena), weight gain

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19
Q

Melena

A

duodenal ulcer

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20
Q

hematemesis

A

gastric ulcer

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21
Q

Worse w/ meals

A

Gastric ulcer

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22
Q

vomiting uncommon

A

duodenal ulcer

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23
Q

weight gain

A

duodenal ulcer

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24
Q

PUD alarm sx

A 
bleeding
unexplained IDA
early satiety
unintentional weight loss
progressive dysphagia/odynophagia
acute onset of upper ab pain
persistent vomiting
family hx of UGI CA
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25
Complications of PUD
bleeding (most common) perforation penetration gastric outlet obstruction (rare)
26
Hemorrhage in PUD
hematemesis, melena or hematochezia
27
Dx/Tx of hemorrhage in PUD
stabilize with IV fluids or PRBCs start IV PPI perform EGD!!
28
Dark tarry store (melena)
UGI
29
Hematemesis
UGI (gastric)
30
Hematochezia
bad sign! hemorrhaging fast and can't digest the blood
31
Tx of bleeding
thermal coagulation hemoclip placement injection tx
32
Perforation presentation
``` severe, diffuse, abdominal pain tachycardia weak pulse N/V may progress to "board-like abdominal rigidity" ```
33
Dx of perforation
hx/PE UPRIGHT CHEST AND ABDOMINAL X-RAY possible CT to localize
34
Tx of perforation
``` IV fluid NG tube NG suction for gastric decompression IV PPI broad spectrum abx SURGERY!!! ```
35
Contraindicated with perforation
UGI with barium (use gastrografin)
36
Dx of hemorrhage
EGD
37
Dx of perforation
Upright chest/ab X-ray
38
Penetration definition
penetration of ulcer through bowel wall w/o free perforation and leakage of luminal contents into peritoneal cavity; goes into some other structure -- pancreas!
39
Presentation of penetration
sx due to affected structure sx like pancreatitis pain w/o meal association, more intense pain, pain referral to back
40
Gastric outlet obstruction cause
scarring/fibrosis or inflammation/edema in pyloric channel; blockage of contents leaving stomach into duodenum
41
Presentation of gastric outlet obstruction
``` vomiting early satiety bloating epigastric pain weight loss anorexia ```
42
Dx of gastric obstruction
imaging- dilated stomach
43
Tx of gastric obstruction
IV fluid NG tube- gastric decompression IV PPI EGD w/ endoscopic balloon dilation or surger -- if fail w/ medical tx
44
PE for PUD
ab exam: epigastric tender, RUQ tender, peritoneal signs (perforation), succussion splash Vitals: hypotension, tachy (complications) Rectal exam: melena, hemoccult positive, bright red blood
45
Succussion splash
place stethoscope over upper abdomen and rock the pt back and forth at hips; retained gastric material >3 hours after meal will generate splash sound and indicate presence of hollow viscus filled w/ both fluid a gas
46
Succussion splash suggests
gastric outlet obstruction
47
Dx of PUD
EGD - gold standard UGI H. pylori: - urea breath test - fecal antigen test - serology - bx during EGD (most specific and sensitive!!!)
48
Urea breath test
identifies active H. pylori infection - discontinue PPI 2 weeks prior and bsimuth/abx 4 weeks prior - drink urea, urease converts to CO2 and NH3, test measures radioactive CO2
49
Fecal antigen test
antigen in feces discontinue PPI 2 weeks prior discontinue bismuth/abx 4 weeks prior
50
Serology
identifies IgG antibody to H. pylori HIGH FALSE POSITIVE; AND FALSE NEGATIVE * not recommended *
51
Tx of PUD
1. eradicate H. pylori and confirm eradication in 4 weeks after treatment 2. PPI if h. pylori absent or sx after eradication 3. if sx persist, treat 8-12 weeks with TCA! 4. if sx persist, treat 4 weeks w/ PROKINETIC 5. if sx persist, perform EGD (discontinue NSAID, ASA, alcohol, tobacco)
52
H. pylori treatment
Bismuth quadruple therapy x 14 days: - PPI BID - Bismuth 524 mg QID - Tetracycline 500 mg QID - metronidazole 250 mg QID
53
Zollinger-Ellison Syndrome (ZES): what is if?
gastrinoma (dudoenum or pancreas) hypersecretes gastrin - increased HCl - increased gastric motility (absorption issues) more common in men
54
Etiology of ZES
sporadic (80%) | MEN1 (20%) - also in pituitary tumors, pancreas, parathyroid
55
Presentation of ZES
recurrent PUD - often distal to duodenal bulb* (multiple on EGD***) abdominal pain diarrhea (steatorrhea)
56
Dx of ZES
fasting serum gastrin >1000 pg/mL (10x) gastric pH <2 Secretin stimulation test (gastrin should dec but it doesn't) CT abdomen to localize tumor
57
Tx of ZES
PPI* | or H2 blocker
58
Gastric CA risk factors
``` gastric ulcers*** adenomatous polyps intestinal metaplasia dietary (nitroso compounds, high-salt diet w/ few veggies) ETOH/tobacco use Chronic H.pylori infection ```
59
Sx of gastric CA
``` early: asymptomatic weight loss persistent ab pain early satiety nausea, anorexia, dysphagia Gastric ulcer hx (25%) Occult GI bleed Late: palpable stomach mass, succussion splash, paraneoplastic syndromes ```
60
Dx of gastric CA
EGD* - gastric vs esophageal CA UGI- 2nd line Staging (TNM) determine nodal involvement, distant lesions, invasion of vasculature, depth of tumor
61
Most common type of gastric CA
adenocarcinomas (95%)
62
Gastric CA on EGD
subtle polypoid protrusion, superficial plaque, mucosal discoloration, depression or ulcer
63
Signs of metastatic disease
Virchow's node (most specific) sister Mary Joseph's node/nodule Left axillary node (irish node)
64
Virchow's node
left supraclavicular lymph node (most common); most specific for gastric cancer
65
Sister Mary Josephs nodule
periumbilical nodule
66
irish node
left axillary node (nonspecific)
67
Tx of Gastric CA
early (rare)- endoscopic mucosal resection advanced- total or partial gastrectomy if resection possible unresectable - chemo vs chemoradiotherapy
68
Workup for dyspepsia
>60 YO: EGD!!! - PUD- treat - no organic cause, either function of H. pylori <60 YO: EGD if any of the following: - weight loss - overt GI bleed (visible) - > 1 alarm feature - Rapidly progressive alarm features if no EGD- test for H. pylori
69
Alarm features
``` unintentional weight loss progressive dysphagia odynophagia unexplaind IDA persistent vomiting palpable mass or LAD family hx of UGI CA ```

Clin Med III Exam 1 (5 decks)

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