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Gastroenterology > Peptic Ulcer disease > Flashcards

Peptic Ulcer disease Flashcards

1
Q

Symptom complex associated with PUD

A

Burning epigastric pain exacerbated by fasting and relieved by meals

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2
Q

Types of cyclooxygenases

A

COX 1: constitutive

COX 2: Inducible

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3
Q

Tissues expressing COX 1

A

stomach

platelets

kidneys

endothelial cells

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4
Q

basal acid production is highest at

A

night

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5
Q

prinicipal contributors of basal acid secretion

A

Cholinergic from vagus

Histaminergic from local gastric sources

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6
Q

Somatostatin is secreted by _______ cells

A

D

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7
Q

parietal cell receptor for gastrin

A

gastrin/CCKB

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8
Q

parietal cell receptor for histamine and Ach

A

histamine- H2

Ach-M3

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9
Q

Why H+ K+ ATPase is inactive in tubulovesicles?

A

tubulovesicles are impermeable to K+

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10
Q

pH required for pepsin activity

A

2

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11
Q

pH at which pepsin is irreversibly inactivated and denatured

A

>=7

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12
Q

Ulcers

A

breaks in the mucosal surface >5 mm in size, with depth to the submucosa

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13
Q

peak age of incidence of gastric ulcers

A

6th decade

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14
Q

Why gastric ulcers are less common than duodenal ulcers?

A

Higher likelihood of GUs being silent and presenting only after a complication develops

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15
Q

Site of duodenal ulcers

A

first part of duodenum(>95%)

90% located within 3 cm of the pylorus

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16
Q

Size of duodenal ulcers

A

<1 cm in diameter

ocassionally giant ulcers(3-6cm) are seen

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17
Q

Apperance of duodenal ulcers

A

margins sharply demarcated

depth at times reaches muscularis propria

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18
Q

Base of duodenal ulcer

A

zone of eosinophilic necrosis with surrounding fibrosis

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19
Q

Malignant DU

A

extremely rare

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20
Q

What is the next step on identifying a gastric ulcer?

A

Biopsy

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21
Q

Site of benign gastric ulcers

A

distal to junction between antrum and acid secreting mucosa

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22
Q

histology of benign GU

A

Similar to DU

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23
Q

Benign gastric ulcers are rare in which site?

A

Fundus

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24
Q

Benign GUs associated with H. pylori are also associated with

A

antral gastritis

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25
Q

Benign GU not accompanied by chronic active gastritis

A

NSAID induced

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26
Q

Chemical gastropathy

A

Foveolar hyperplasia

edema of lamina propria

epithelial regeneration in absence of H.Pylori

extension of smooth muscle fibres into upper portions of mucosa

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27
Q

gastric acid output in Duodenal and gastric ulcers

A

DU: average basal and nocturnal gastric acid secretion increased

GU:Gastric acid output (basal and stimulated) tends to be normal or decreased

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28
Q

Types of gastric ulcers based on location

A

Type 1: Body,low gastric acid production

Type 2: antrum,Low to normal gastric acid production

Type 3: within 3cm of pylorus,accompanied by DU,normal or high gastric acid production

Type 4:cardia,low gastric acid production

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29
Q

Characteristic of H.Pylori

A

gram negative,microaerophilic rod

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30
Q

Transmission of H.pylori

A

person to person

oral-oral or fecal oral route

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31
Q

Percentage of pts with gastric and duodenal ulcers with H.pylori infection

A

gastric: 30–60%
duodenal: 50–70%

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32
Q

Diseases caused by H.pylori

A

Gastritis

MALT lymphoma

PUD

gastric adenocarcinoma

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33
Q

Corpus predominant atrophic gastritis leads to

A

asymptomatic H.pylori infection

GU

gastric adenocarcinoma

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34
Q

non atrophic pangastritis is associated with

A

MALT

asymptomatic H.Pylori infection

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35
Q

Why NSAIDs are dangerous?

A

Over 80% of patients with serious NSAID-related complications did not have preceding dyspepsia

no dose of NSAID is completely safe

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36
Q

Risk factors for NSAID induced disease

A

advanced age

h/o ulcer

concomitant use of anticoagulants,clopidogrel,glucocorticoids

high dose

multiple NSAIDs

multisystem disease

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37
Q

direct toxicity of NSAIDs to gastric mucosa is due to

A

ion trapping

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38
Q

Blood group associated with increased risk of PUD

A

O

Non secretor type

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39
Q

Why O blood group pts may be at high risk for PUD?

A

H.pylori binds preferentially to O group antigens

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40
Q

chronic diseases with strong association to PUD?

A

Systemic mastocytosis

alpha 1 antitrypsin deficiency

CKD

CLD

COPD

nephrolithiasis

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41
Q

Chronic disorders with possible association to PUD

A

hyperparathyroidism

CAD

polycythemia vera

chronic pancreatitis

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42
Q

Infectious causes of non-Hp and non-NSAID Ulcer disease

A

CMV

Herpes simplex virus

H.heilmannii

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43
Q

Drugs causing Non-Hp and Non-NSAID Ulcer Disease

A

Bisphosphonates

chemotherapy

glucocorticoids(along with NSAID)

Kcl

MMF

clopidogrel

crack cocaine

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44
Q

Miscellaneous causes of Non-Hp and Non-NSAID Ulcer Disease

A

Basophilia in myeloproliferative disease
Duodenal obstruction (e.g., annular pancreas)
Infiltrating disease
Ischemia
Radiation therapy
Sarcoidosis
Crohn’s disease
Idiopathic hypersecretory state

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45
Q

______ % of pts with NSAID-induced mucosal disease can present with a complication (bleeding, perforation, and obstruction) without antecedent symptoms

A

10

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46
Q

Most discriminating symptom of duodenal ulcer

A

Pain that awakes the patient from sleep (between midnight and 3 A.M.)

two-thirds of DU patients describing this complaint

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47
Q

Typical pain pattern in Duodenal ulcer

A

Occurs 90 minutes to 3 hours after a meal and is frequently relieved by antacids or food

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48
Q

Fraction of NUD pts presenting with nocturnal pain

A

1/3rd

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49
Q

Pain in gastric ulcer

A

discomfort may actually be precipitated by food

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50
Q

Nausea and weight loss are more common in..

DU or GU?

A

GU

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51
Q

Mechanisms for development of abdominal pain in ulcer patients

A

acid-induced activation of chemical receptors in the duodenum

enhanced duodenal sensitivity to bile acids and pepsin

altered gastroduodenal motility

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52
Q

Dyspepsia that becomes constant, is no longer relieved by food or antacids, or radiates to the back

A

indicate a penetrating ulcer (pancreas)

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53
Q

Sudden onset of severe, generalized abdominal pain in PUD

A

perforation

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54
Q

Jeopardy

indicate a penetrating ulcer (pancreas)

A

Dyspepsia that becomes constant, is no longer relieved by food or antacids, or radiates to the back

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55
Q

Jeopardy

perforation

A

Sudden onset of severe, generalized abdominal pain in PUD

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56
Q

Pain worsening with meals, nausea, and vomiting of undigested food

A

GOO

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57
Q

Most frequent physical exam finding in GU/DU

A

Epigastric tenderness

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58
Q

Jeopardy

GOO

A

Pain worsening with meals, nausea, and vomiting of undigested food

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59
Q

Examination finding suggestive of GOO

A

Succussion splash

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60
Q

Tachycardia and orthostasis in PUD patient

A

dehydration secondary to vomiting or GI bleeding

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61
Q

PUD pain may be found to right of midline in ________ % of pts

A

20

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62
Q

Most common complication observed in PUD

A

GI bleeding

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63
Q

GI bleeding is more common in individuals more than _______ yrs of age

A

60

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64
Q

second most common ulcer-related complication

A

perforation

65
Q

A form of perforation in which the ulcer bed tunnels into an adjacent organ

A

penetration

66
Q

Jeopardy

penetration

A

A form of perforation in which the ulcer bed tunnels into an adjacent organ

67
Q

Types of penetration in PUD

A

DU: pancreas

GU: Left hepatic lobe

gastrocolic fistulas

68
Q

Least common ulcer-related complication

A

GOO

69
Q

Types of GOO

A

Relative: due to peripyloric inflammation and edema

Fixed: mechanical obstruction secondary to scar formation

70
Q

Rx of fixed mechanical GOO

A

Surgery

endoscopic dilatation

71
Q

Symptoms of GOO

A

New onset of early satiety, nausea, vomiting, increase of postprandial abdominal pain, and weight loss

72
Q

The most commonly encountered diagnosis among patients seen for upper abdominal discomfort is

A

NUD

73
Q

DD for ulcer like symptoms

A

proximal GI tumors

gastroesophageal reflux

vascular disease

pancreaticobiliary disease (biliary colic, chronic pancreatitis)

gastroduodenal Crohn’s disease

74
Q

In which individuals empirical therapy for PUD is enough?

A

<45 yrs of age

75
Q

Sensitivity of barium meals for detecting DU is decreased in

A

Small ulcers <0.5cm

presence of previous scarring

postoperative pts

76
Q

Invasive tests for detecting H.Pylori

A

Rapid urease

Histology

Culture

77
Q

Non invasive tests for detecting H.pylori

A

Serology

Urea breath test

Stool antigen

78
Q

Disadvantage of serological tests for detection of H.Pylori

A

Not useful for early followup

79
Q

Disadvantages of urea breath test

A

False negatives with recent therapy

Exposure to low-dose radiation with 14C test

80
Q

Test for H.pylori useful for early followup?

A

urea breath test

81
Q

Side effect of aluminium hydroxide

A

phosphate depletion

constipation

82
Q

Side effect of magnesium hydroxide

A

loose stools

83
Q

Side effects of Mg and Al containing antacids in CKD pts?

A

Mg: hypermagnesemia

Al: Neurotoxicity

84
Q

Adverse effect of longterm use of calcium carbonate

A

Milk alkali syndrome

85
Q

Milk alkali syndrome

A

Hypercalcemia

Hyperphosphatemia

renal calcinosis

Renal insufficiency

86
Q

Side effect of sodium bicarbonate

A

systemic alkalosis

87
Q

H2 receptor antagonists

A

Cimetidine

Famotidine

Ranitidine

nizatidine

88
Q

Side effects of cimetidine

A

reversible gynacomastia

impotence

weak antiandrogenic effect

89
Q

Drug interaction of cimetidine

A

Inhibits CYT P450

Phenytoin

theophylline

warfarin

90
Q

Rare adverse effects due to cimetidine

A

confusion

elevation of transaminases,creatinine,prolactin

91
Q

Dosing of H2 receptor blockers

A

Cimetidine 300mg qid

Ranitidine 300mg hs

nizatidine 300mg hs

famotidine 40mg hs

92
Q

H2 receptor antagonists that donot bind to CYT P450

A

famotidine

nizatidine

93
Q

Rare,reversible systemic side effects due to H2 receptor blockers

A

pancytopenia

94
Q

MOA of PPI

A

Covalently bind and irreversibly inhibit H+ K+ ATPase

95
Q

PPIs admnistered as enteric coated granules in sustained release capsules

A

omeprazole

lansoprazole

pantoprazole

rabeprazole

96
Q

pharmacokinetics of omeprazole and lansoprazole

A

acid labile

dissolves in small intestine at a pH of 6

97
Q

PPI that can be given in dysphagia pts

A

Lansoprazole available as a orally disintegerating tablet

Can be taken with or without water

98
Q

Omeprazole-soda bicarb combination

A

protect the omeprazole from acid degradation

promote rapid gastric alkalinization and subsequent proton pump activation

99
Q

PPIs should be administered

A

Before a meal

100
Q

Onset of maximum acid inhibitory effect of PPIs

A

2-6 hours

101
Q

Duration of action of PPI

A

72-96 hrs

102
Q

PPIs inhibit basal and secretagogue-stimulated acid production by >95% after

A

1 week of therapy

103
Q

Gastric acid secretion returns to normal levels _______ days after discontinuation of PPIs

A

2 and 5 days

104
Q

PPIs and gastrin levels

A

Mild to moderate hypergastrinemia

No risk for development of carcinoid tumors

105
Q

Adverse effect of stopping PPI

A

Rebound gastric acid hypersecretion

worsening of dyspepsia or GERD

106
Q

Rebound gastric acid hypersecretion

A

occurs after short duration use(2 months) and lasts for upto 2 months after discontinuation of drug

occurs in H.pylori negative individuals

107
Q

How to prevent rebound gastric acid hypersecretion?

A

Taper PPI dose

Add H2 receptor blockers

108
Q

IF production with PPI use

A

decreased

but Vit B12 deficiency doesnot develop as stores are adequate

109
Q

PPIs interfere with absorption of

A

digoxin

ketoconazole

ampicillin

iron

110
Q

PPIs that inhibit CYT P450 system

A

omeprazole

lasoprazole

111
Q

Adverse effect of longterm administration of PPIs

A

Community acquired pneumonia

clostridium difficle infection

hip fractures in elderly women

112
Q

Mechanism of negative effect of PPI on antiplatelet action of clopidogrel

A

Bind to same cytochrome p450 (CYP2C19)

113
Q

PPI that has advantage over other PPIs in interaction with clopidogrel

A

pantoprazole

114
Q

How to circumvent PPI,clopidogrel drug interaction

A

give the drugs 12 hrs apart

PPI before breakfast,clopidogrel at bedtime

115
Q

New PPI with longer half life

A

Tenatoprazole

116
Q

Relevance of inhibition of nocturnal acid secretion

A

GERD

117
Q

New class of H+ K+ ATPase inhibitors

A

potassium-competitive acid pump antagonists (P-CABs)

118
Q

Most common adverse effect of sucralfate

A

constipation

119
Q

MOA of sucralfate

A

Insoluble in water,forms a viscous paste and bind to active sites of ulceration

Physicochemical barrier

binds to trophic factors

enhances prostaglandin synthesis

stimulates mucus and bicarbonate secretion

120
Q

Sucralfate is avoided in

A

CRF pts

To prevent aluminium toxicity

121
Q

Rare adverse effect of sucralfate

A

gastric bezoar formation

hypophosphatemia

122
Q

standard dosing of sucralfate

A

1g qid

123
Q

Most widely used bismuth containing compounds

A

CBS(colloidal bismuth subcitrate)

BSS-pepto bismol(bismuth subsalicylate)

124
Q

adverse effects of bismuth

A

black stools

constipation

darkening of tongue

neurotoxicity

125
Q

why the new interest in bismuth containing compounds

A

anti H.pylori activity

126
Q

most common toxicity of prostaglandin analogues

A

diarrhoea

uterine bleeding

uterine contractions

127
Q

standard dose of misoprostol

A

200µg qid

128
Q

__________ % of patients with gastric MALT lymphoma experience complete remission of the tumor in response to H. pylori eradication

A

50

129
Q

In whom should H.pylori be eradicated

A

documented PUD

130
Q

Duration of therapy for H.Pylori eradication

A

14 days

131
Q

Most feared complication with amoxycillin

A

pseudomembranous colitis

132
Q

Adverse effects of amoxycillin

A

antibiotic associated diarrhoea

nausea

vomiting

skin rash

allergic reaction

133
Q

adverse effects of tetracycline

A

rashes

hepatotoxicity

anaphylaxis

134
Q

H.pylori strains are least resistant to which drugs

A

amoxycillin

tetracycline

135
Q

Quadruple therapy

A

Omeprazole (lansoprazole) 20 mg (30 mg) daily
Bismuth subsalicylate 2 tablets qid
Metronidazole 250 mg qid
Tetracycline 500 mg qid

136
Q

BSS based triple therapy

A

Bismuth subsalicylate 2 tablets qid
Metronidazole 250 mg qid
Tetracycline 500 mg qid

137
Q

Bismuth citrate based regimen

A

Ranitidine bismuth citrate 400 mg bid
Tetracycline 500 mg bid
Clarithromycin or metronidazole 500 mg bid

138
Q

PPI based triple therapy

A

Omeprazole (lansoprazole) 20 mg bid (30 mg bid)
Clarithromycin 250 or 500 mg bid
Metronidazole 500 mg bid or
Amoxicillin 1 g bid

139
Q

Treatment of failure of H. pylori eradication with triple therapy

A

Quadruple therapy , where clarithromycin is substituted for metronidazole (or vice versa)

pantoprazole, amoxicillin, and rifabutin for 10 days

levofloxacin, amoxicillin, PPI for 10 days

furazolidone, amoxicillin, PPI for 14 days

140
Q

Next step in pts who have failed two courses of antibiotics against H.pylori

A

culture and sensitivity

141
Q

Sequential therapy against H.pylori

A

5 days of amoxicillin and a PPI, followed by an additional 5 days of PPI plus tinidazole and clarithromycin

142
Q

recurrent H.pylori infection occuring within the first 6 months after completing therapy

A

recrudescence as opposed to reinfection

143
Q

Treatment of NSAID induced ulcer after discontinuation of NSAID

A

H2 receptor antagonist or PPI

144
Q

Treatment of NSAID induced ulcer with NSAID continued

A

PPI

145
Q

prophylactic therapy for NSAID induced ulcer

A

Misoprostal

PPI

selective COX 2 inhibitor

146
Q

NSAIDs with lower likelihood of GI toxicity

A

diclofenac

aceclofenac

brufen

147
Q

Any patient who needs treatment longterm with traditional NSAID therapy should be considered for

A

H. pylori testing and treatment if positive

148
Q

Test of choice for documenting eradication

A

UBT

urea breath test

149
Q

Rx of PU with H.pylori present

A

triple therapy for 14 days followed by continued acid-suppressing drugs (H2 receptor antagonist or PPIs) for a total of 4–6 weeks

150
Q

Definition of H.pylori eradication

A

organisms gone at least 4 weeks after completing antibiotics

151
Q

preparation before performing UBT

A

patient must be off antisecretory agents

152
Q

Why serologic testing is not useful for demonstrating eradication?

A

titres fall slowly or donot become undetectable

153
Q

Repeat endoscopy in gastric ulcers

A

After 8-12 weeks to document healing and biopsy

154
Q

Refractory ulcer

A

A GU that fails to heal after 12 weeks and DU after 8 weeks

155
Q

Stepwise approach to refractory ulcers

A
  1. poor compliance,H.pylori resistance
  2. NSAID use,cigarette smoking
  3. GU-malignant ulcer
  4. ZES
156
Q

Treatment of refractory ulcers

A

More than 90% of refractory ulcers (either DUs or GUs) heal after 8 weeks of treatment with higher doses of PPI (omeprazole, 40 mg/d; lansoprazole 30–60 mg/d)

157
Q

Causes of refractory ulcers

A

Ischemia

crohn

amyloidosis

sarcoidosis

lymphoma

eosinophilic gastroenteritis

158
Q

Infectious causes of refractory ulcers

A

CMV

TB

syphilis

159
Q
A

Gastroenterology (3 decks)

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