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Semestre 6: bloque 3 > Digestive System Pathophysiolgy > Flashcards

Digestive System Pathophysiolgy Flashcards

(113 cards)

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1
Q

Principal symptoms of GERD

A

Heartburn
Regurgitation
Dysphagia

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2
Q

Alarm signs of GERD (7)

A

Dysphagia
Odynophagia
Weight loss
Family history of GI cancers
Persistent nausea and emesis
Symptoms >10 years duration
Incomplete response to treatment

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3
Q

Main pathophysiologic mechanism of GERD

A

Transient inappropriate relaxation of lower esophageal sphincter (LES)

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4
Q

What is the lower esophageal sphincter and its function

A

Segment of smooth muscle in lower esophagus
Chronically contracted to maintain a pressure that is 15 mmHg above intragastric pressure

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5
Q

What are the two patterns of LES dysfunction

A

Hypotensive LES
Pathologic transient LES relaxations

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6
Q

Gastric factors that promote GERD

A

↑ gastric volume after meals
↑ gastric pressure due to obesity
Recumbency after meals
Delayed gastric emptying or gastroparesis

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7
Q

Medications that decrease LES pressure

A

B adrenergic agonists
A adrenergic antagonists
Anticholinergics
Calcium channel blockers

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8
Q

Foods that exacerbate GERD

A

Caffeine
Chocolate
Peppermint
Alcohol
Carbonated beverages

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9
Q

Lifestyle factors that exacerbate GERD

A

Weight gain
Smoking
Eating prior to recumbency

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10
Q

Duration of GERD symptoms to suspect pathology

A

Typical symptoms >2x week for >4-8 weeks

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11
Q

Respiratory pathology associated with GERD

A

Asthma

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12
Q

What happens in laryngopharengeal reflux

A

Regurgitated gastric contents reach upper aerodigestive tract
Ear, nose, throat symptoms

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13
Q

How is classic GERD diagnosis done

A

Thorough symptom history and confirmed by complete response to medical therapy

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14
Q

Which patients should have diagnostic testing done for GERD

A

Px who fail to respond to a trial of adequate medical therapy or px who have alarm symptoms

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15
Q

What should you do if a px with GERD has alarm symptoms or persistent symptoms despite therapeutic measures

A

EGD

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16
Q

Pharmacological therapy for GERD

A

PPIs

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17
Q

Function of radiologic studies for GERD

A

Rule out other conditions or assess for complications

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18
Q

Types of radiologic studies for GERD

A

Barium swallow and upper GI series

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19
Q

Function of upper endoscopy in GERD

A

Can exclude presence of other diseases and detect grade and severity of GERD esophagitis

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20
Q

Initial test of choice in evaluating complicated GERD px and symptoms refractory to medical therapy

A

Upper endoscopy

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21
Q

Who does de ACP recommend should have upper endoscopy in GERD

A

Reflux px with alarm symptoms
Persistent symptoms despite 4-8 weeks of 2x PPI therapy
Severe esophagitis
Recurrent dysphagia in setting of history of stricture

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22
Q

Who should have an esophageal biopsy for GERD

A

Px with eosinophilic esophagitis suspected

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23
Q

What is pH monitoring in GERD

A

Objective quantification of overall reflux burden and assessment of correlation between px-reported symptoms and reflux events

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24
Q

2 techniques to do pH monitoring in GERD

A

Probe that is passed transnasally to localize pH sensor 5 cm above manometrically determined LES
Endoscopically-placed pill-sized capsule (Bravo wireless capsule) attached to distal esophagus

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25
How are acid reflux episodes defined with pH
Acid reflux episodes defined as esophageal pH below 4
26
AET values in GERD
AET >6% → conclusive evidence of GERD AET <4% → evidence against pathologic reflux AET 4-6% → borderline or inconclusive
27
What does the multichannel intraluminal impedance testing do
Detects changes in resistance of electrical current on a catheter placed within esophagus
28
Meaning of multichannel intraluminal impedance testing in GERD
Total reflux episodes <40: against GERD Total reflux episodes >80: adjunctive evidence for GERD
29
Conclusive evidence for GERD
LA grades C and D esophagitis Long segment Barretts Peptic esophageal stricture AET >6%
30
Adjunctive or supportive evidence for GERD
Reflux symptom association Reflux episodes >80 Low MNB1 or PSPWI Hiatus hernia
31
Evidence against GERD
AET <4% Reflux episodes <40
32
Main complications of GERD
Esophageal ulcers Peptic esophageal strictures Esophageal carcinoma
33
Medical treatment of GERD
Antacid and antisecretory agents
33
Cornerstone of treatment for GERD
Lifestyle modifications
34
How does antacids provide symptom relief in GERD
Increases esophageal pH and inactivates pepsin
35
How does PPIs provide symptom relief in GERD
By blocking hydrogen-potassium ATPase on apical surface of parietal cells
36
Complications of PPI usage in GERD
Higher rates of community acquired pneumonia, C difficile infection, hip fractures
37
Function of Baclofen in GERD
Effective in increasing basal LES tone and inhibiting LES relaxation
38
Mainstay of antireflux therapies and who should have it
Surgery For px who wish to discontinue medications or px who have failed medical therapy
39
Most used procedure for GERD
Nissen fundoplication: involves wrapping fundis around bottom of esophagus to enhance antireflux barrier
40
Surgery for obese px with GERD
Bariatric
41
Management of peptic esophageal strictures
Esophageal dilation and PPI
42
When can you withdraw medicines for GERD
Symptom relief should be sustained for 2-3 months
43
What is Barrett esophagus
Replacement of normal squamous epithelium of distal esophagus with specialized intestinal metaplasia
44
What is the criteria of high-grade dysplasia for Barrett
Should be confirmed by 2 expert GI pathologists
45
Risk factors of Barrett progression to adenocarcinoma
Dysplasia, long segment Barrett esophagus, mucosal abnormalities (nodules, ulcerations, strictures)
46
Cause of Barrett esophagus
Chronic GERD
47
Epidemiology of Barrett esophagus
Caucasian Middle-aged male Alcohol and smoking
48
Genes induced by acid and bile for progression to Barrett esophagus
Cdx
49
Gold standard diagnosis for Barrett esophagus
Upper endoscopy with biopsy of distal esophagus
50
What should be present in biopsy to dx Barrett
3 cm of columnar-lined distal esophagus with SIM
51
Who should have screening for Barrett esophagus
Px over 50 with chronic GERD symptoms
52
Best method of surveillance biopsies once GERD has been well controlled by therapy
Upper endoscopy with four-quadrant jumbo biopsies at 2 cm intervals
53
Where should biopsies be taken for surveillance of Barrett
Beginning at end of tubular esophagus (top gastric folds) and continuing proximally to SC
54
What is the recommendation for a px found Barrett incidentaly without dysplasia
A repeat esophagogastroduodenoscopy (EGD) be performed in 3-5 years
55
What are the recommendations for low-grade dysplasia in Barrett
Confirm pathology Endoscopic therapy preferred, annual surveillance
56
What are the recommendations for high-grade dysplasia in Barrett
Confirm pathology Endoscopic therapy preferred, otherwise 3 months surveillance
57
Clinical risk factors for progression to adenocarcinoma in Barrett
High BMI Male gender Older age Tobacco and alcohol
58
Endoscopic risk factors for progression to adenocarcinoma in Barrett
Long segment Barrett Nodularity Ulceration Strictures
59
Histologic risk factors for progression to adenocarcinoma in Barrett
High-grade dysplasia
60
Treatment for non dysplastic Barrett
Once daily PPI therapy indefinitely
61
Biopsy obtained adjacent to ulcer and numerous neutrophils infiltrate epithelium, grade of Barrett dysplasia?
Indefinite
62
Treatment of indefinite grade dysplasia in Barrett
Aggressive antisecretory therapy and repeat surveillance biopsies in 3 months
63
Management of low grade dysplasia in Barrett
A repeat EGD with surveillance biopsies should be performed within 3-6 months after low-grade dysplasia is detected
64
Treatment of high grade dysplasia in Barrett
Endoscopic therapy
65
Mucosal defects in stomach or small intestine
Peptic ulcers
66
Main causes of peptic ulcer disease
H pylori infection NSAIDS and aspirin
67
Size of peptic ulcers
>5 mm
68
Pathogenesis of peptic ulcer disease
Imbalance of protective and aggressive factors in gastric mucosa
69
Main complications of peptic ulcer disease
GI bleeding, perforation, and gastric outlet obstruction
70
Role of cigarrette smoking in peptic ulcer disease
Promotes development of ulcers and may interact with H pylori or NSAIDs to increase mucosal injury Impairs ulcer healing and increases ulcer recurrence
71
72
Spiral gram (-) urease-producing bacteria
H pylori
73
Factors that enable H pylori to survive in acid stomach environment
Ability to produce urease, helps alkalize surrounding pH
74
Risk factors for H pylori
Low socioeconomic status, household crowding, country of origin
75
Main transmission mechanism of H pylori
Intra familial
76
Malignancies associated with H pylori
Gastric adenocarcinoma and MALT lymphoma
77
Carcinogen classification of H pylori
Group 1 carcinogen
78
79
Virulence factors that facilitate attachment of bacteria to gastric epithelium
BabA and OipA
80
Which IL does CagA induce in H pylori
IL-8
81
Virulence function of CagA in H pylori infection
Cag pathogenicity island encodes components of type IV secretion island that translocated CagA in host cells and affects cell growth and cytokine production
82
How are NSAIDS risk factors for peptic ulcers
Inhibition of COX1 impairs mucosal protection (no prostaglandins) and leads to ulcers
83
Classic symptom of peptic ulcers
Epigastric pain
84
Pain associated with duodenal ulcer
Relieved with ingestion of milk/food/antacids but recurs 2-4 hrs after eating
85
Pain associated with gastric ulcer
Eating exacerbates pain; relief when fasting, nausea, avoidance of food/anorexia
86
Alarm symptoms of peptic ulcers (suggest GI bleeding)
Melena, hematemesis, guaiac-positive stools, unexplained anemia
87
Alarm symptoms of possible obstruction in peptic ulcers
Persistent vomiting
88
Alarm symptoms that suggest ulcer perforation
Tachycardia and orthostasis
89
Age onset of gastric and duodenal peptic ulcers
Gastric: 55-70 years Duodenal: 30-50 years
90
Definitive diagnosis for peptic ulcers
Upper endoscopy
91
Which ulcers are more probable to become malignant
Ulcers >3 cm in size and those associated with a mass
92
When should you consider evaluation for Zollinger-Eddison syndrome
Px who have multiple ulcers, refractory ulcers or ulcers in unusual locations, or who have diarrhea and weight loss
93
Characteristics for barium studies for peptic ulcers
Safer and cheaper than endoscopy but have limited accuracy, does not permit biopsy
94
Non invasive tests for H pylori infection
Serologic testing Urea breath test Stool antigen test
95
Why shouldn´t serologic testing be used to assess success of tx for H pylor
Antibody titers can persist for years and do not always become negative
96
Characteristics of urea breath test and stool antigen test
Urea breath test → detect H pylori-derived urease activity in stomach Stool antigen test → uses polyclonal anti-H pylori capture antibody adsorbed in microwells
97
How long should you wait to confirm cure success in H pylori treatment
At least 4 weeks after completing eradication therapy to confirm successful cure
98
99
What is found in biopsies that suggest H pylori infection
Presence of polymorphonuclear leukocytes in inflamed gastric tissue
100
All ulcer px should be tested and tx for H pylori. True or false?
True
101
Recommendations for px with aspirin therapy with peptic ulcers
Aspirin should be restarted as soon as risk for cardiovascular events outweighs risk for recurrent ulcer complications → 1-7 days after bleeding stops
102
Main therapy for H pylori
Quadruple bismuth therapy
103
Quadruple bismuth therapy
PPI 2x daily Tetracycline 4x daily Metronidazole 3x daily Bismuth 4x daily
104
When shouldn´t clarithromycin, metronidazole or levofloxacin be used for H pylori tx
When resistant rate in that area is >15%
105
H pylori 1st line therapy in areas with low primary resistance to clarithromycin
Concomitant therapy non bismuth quadruple therapy
106
Concomitant therapy non bismuth quadruple therapy
PPI 2x daily Amoxicillin 2x daily Metronidazole/Tinidazole 2x daily Clarithromycin 2x daily
107
What should you do if px fails 1st line tx of H pylori
Avoid reusing antibiotics in failed regimen, especially clarithromycin or levofloxacin
108
What should you do if px fails 1st and 2nd line tx of H pylori
Consider culture with susceptibility testing
109
Main characteristic of H pylori that promotes gastric adenocarcinoma
Chronic inflammation
110
Role of IL-1B in H pylori progression to adenocarcinoma
IL-1B increased in H pylori infection, and this is an important proinflammatory cytokine with powerful inhibition of acid secretion
111
What is produced by macrophages in H pylori that has important role in promoting survival and proliferation of neoplastic B cells
APRIL: proliferation-inducing ligand
112
Eradication of H pylori leads to complete remission of lymphoma. True or false?
True

Semestre 6: bloque 3 (2 decks)

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