Gastric Disorders 1 Flashcards

(40 cards)

1
Q

GERD patho

A

LES barrier is breached and reflux of caustic gastric acid interacted with unprotected esophagus

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2
Q

mechanisms that can cause reflux

A
  1. loss of LES tone
  2. increased frequency of relaxation
  3. loss of secondary peristalsis after relaxation
  4. increased stomach volume/pressure
  5. increased acid production
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3
Q

risk factors for GERD development

A

impaired LES tone (abnormal location, extrinsic compression)

extrinsic, increased pressure on intra abdominal organs

decreased acid cleaned

delayed gastric emptying/duodenalgastric reflux

hypersecreiton of acid

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4
Q

hiatal hernia and GERD

A

causes deficient LES bc removes added constriction to diaphragmatic cura

more acid reflux, slow acid clearance, inflammation

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5
Q

typical s/signs of GERD (5)

A

heartburn (after meals, received with antacid)

bitter regurgitation

increased salivation

chest and epigastric pain

dysphagia

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6
Q

atypical symptoms

A

chronic cough, asthma, hoarseness, sore throat

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7
Q

what exacerbated GERD symptoms

A

meals, bending or reclining/lying supine

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8
Q

factors that worsen GERD

increase acid

A

fatty food
spicy food
acidic food/drink
bananas

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9
Q

factors that worsen GERD

slow gastric emptying

A

TCA
anticholinergics
opioids

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10
Q

factors that worsen GERD

lower LES pressure

A
nitroglycerine 
CCB
progesterone
benzos
alchol
opiods
chocolate 
coffee
pepperment
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11
Q

diagnostic workup of GERD

A

presumptive diagnosis on clinical ground

six week trial of PPI or H2

endoscopy

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12
Q

when do we preform endoscopy in GERD

A
  1. doubt of diagnosis (alarm symptoms, persistent, erosive espohagitis)
  2. men > 50 with chronic GERD (increased risk of esophageal cancer)
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13
Q

complications of GERD

A
  1. esophageal stricture
  2. Barrett’s esophagus
  3. esophageal ulcers
  4. hemorrhage/perforation
  5. fistula formation
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14
Q

barrett’s esophagus

A

replacement of normal squamous epithelium with columnar epithelium

precursor of esophageal adenoma

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15
Q

dyspepsia

A

EPIGASTRIC pain/burning
early salty
fullness after meal

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16
Q

gastritis

A

inflammation associated with mucosal injury

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17
Q

gastropathy

A

non inflammatory mucosal injury

18
Q

gastritis mc causes

A

nonspecific inflammation of mucosal surfaces

  1. H. pylori
  2. NSAIDs
  3. stress related changes

can also be alcohol or atrophic

19
Q

h. pylori

A

gram negative rod found in gastric epithelium

60% of gastric,80% of duodenal ulcers

fecal orla

MC in low SES

20
Q

h. pylori pathophys

A

imbeds into mucosal layer and colonizes causing acute and chronic inflammation of gastric mucosa

produces large amounts of urease to break down acidic environment

increased risk of gastric adenocarcinoma and MALT lymphoma

21
Q

h. pylori urease

A

breaks down urea to alkaline ammonia and carbon dioxide

allows the immediate and surrounding areas to have a more neutral pH

22
Q

h. pylori gastritis

A

acute gastritis in antrum and then extends to entire mucosa (acute –> chronic)

may cause ulceration

23
Q

when is h. pylori detection performed

A

active PUD
early gastric CA/MALT lymphoma

CAN do IgG but unable to distinguish past or present infection

24
Q

h. pylori detection tests

A
  1. urea breath test
  2. stool antigen test
  3. stomach biopsy
25
urea breath test
pt drinks radioactive urea h. pylori urease will split the urea and detectable CO2 will be exhaled
26
wat can give false negative on urea breath test?
PPI Abx bismouth UGIB
27
stool antigen test
examine stool to look for h. pylori can document successful tx and presence NOT impacted by UGIB
28
stomach biopsy
lining of stomach/small intestine taken during EGD and rapid urease test done false neg: PPI, ABX, bismuth, UGIB
29
h. pylori triple therapy
10-14 days 1. proton pump inhibitor 2. Amoxicillin 3. Clarithromycin
30
quadruple therapy h. pylori
10-14 days 1. PPI 2. Bismuth 3. Metronidazole 4. Tetracycline
31
who gets quadruple h. pylori tx
resistance to clarithromycin or metronidazole | previous/recent metronidazole exposure
32
NSAID gastritis
loss of prostaglandin/COX 1 to stimulate new mucosal formation AND loss of blood supply to mucosal wall (decreased vasodilation)
33
risk factor of NSAID gastritis
duration of NSAID therapy increasing age, high NSAID dose, prior NSAID complication, concurrent steroid/anticoagulant/clopidigrel use
34
how do NSAIDS cause gastritis?
DIRECT toxic effect (topical injury) INDIRECT effect (hepatic metabolite damage, decreased production of mucosal prostaglandin)
35
prevention of NSAID gastritis
PPI/misoprostol can prevent BOTH gastric and duodenal ulcers H2 blockers can prevent duodenal ulcers
36
alarm dyspepsia features
``` weight loss without cause, anorexia vomiting dysphagia anemia GI bleed abdominal mass FH of GI CA previous malignancy ```
37
PUD
defect in GI mucosa of stomach or duodenum MC cause h. pylori infection and NSAIDS
38
PUD s/s
Ulcer or acid dyspepsia (gnawing/burning pain, relieved with food) food provoked dyspepsia/indigestion (aggravated by food) reflux dyspepsia
39
PUD diagnostic studies
empically tx with H2 blockers if mild >45, alarm symptoms = EGD + biopsy
40
complications of PUD
GI bleed tachycardia/pallor outlet obstruction perforation