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Internal medicine > Peptic ulcer > Flashcards

Peptic ulcer Flashcards

1
Q

What is a peptic ulcer?

A

a mucosal break penetrating the muscularis mucosa

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2
Q

What is an erosion?

A

a lesion superficial to the muscularis mucosa

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3
Q

difference between peptic ulcer & erosion

A

peptic ulcer penetrates muscularis mucosa but erosion is superficial to it

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4
Q

which one is more common, duodenal or gastric ulcer?

how many times more common?

A

dudeonal ulcer

5x

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5
Q

lifetime risk of peptic ulcer

A

10%

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6
Q

where is “duodenal bulb”?

A

the portion of the duodenum closest to the stomach (first 5cm of duodenum)

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7
Q

over 95% of peptic ulcers are in ___ and ___

A

duodenal bulb and antrum

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8
Q

peptic ulcer more in male of female?

A

slightly more in male

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9
Q

common age of duodenal ulcers and gastric ulcers

A

DU: 30 - 55 yrs
GU: 55 - 75 yrs

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10
Q

H. pylori is associated more with ___ ulcers

Aspirin and NSAIDs are associated more with ___ ulcers

A

H. pylori - duodenal

Aspirin and NSAIDs - gastric

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11
Q

2 main factors in the pathophysiology of peptic ulcers:

A

H. pylori and NSAIDs

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12
Q

helicobacter pylori microbiology

A

spiral-shaped, flagellated, Gram-negative bacillus with urease activity

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13
Q

H. pylori is seen in __% of DUs and __% of GUs

A

DU - 90%

GU - 70%

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14
Q

Urease changes ____ to ____ .

function:

A

Urease changes urea to ammonia

ammonia is alkaline, it helps resist acid

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15
Q

how and when is H. pylori transmitted?

A

orally, mostly during childhood

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16
Q

H. pylori is mostly in the ___

A

antrum

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17
Q

If H. pylori is in the duodenum, it is associated with

A

metaplastic gastric epithelium

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18
Q

Ulcer disease develops in __% of infected people

A

10%

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19
Q

H pylori GU tends to occur at the junction of ___ and ___

A

body and antrum

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20
Q

risk of GU and DU in long term NSAID use

A

GU: 10 - 20 %
DU: 2 - 5%

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21
Q

There is greater risk of ulcer from NSAIDs in:

A 
first 3 months of therapy
>60 yrs
Hx of ulcer
NSAIDs + aspirin
steroids
anticoagulants
co-morbidities
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22
Q

Mucosal injury and, thus, peptic ulcer occur when the balance between the ____ factors and the ______ mechanisms is disrupted

A

aggressive defensive

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23
Q

Aggressive factors (factors that cause ulcers)

A 
NSAIDs
h. pylori
alcohol
bile salts
acid
pepsin
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24
Q

defensive mechanisms (protect against ulcers)

A 
tight intercellular junctions
mucus
bicarbonate
mucosal blood flow
cellular restitution
epithelial renewal
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25
Q

pathophysiolofy of H. pylori causing ulcers:

A

H pylori interact with G and D cells causing increased gastrin and hence acid production, mostly localized resulting in ulcer

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26
Q

In patients infected withH pylori,high levels of ___ and ____ and reduced levels of ____ have been measured

A

high: gastrin & pepsinogen
low: somatostatin

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27
Q

Virulence factors produced byH pylori:

A

urease
catalase
vacuolating cytotoxin
lipopolysaccharide

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28
Q

pathophysiology of H. Pylori causing duodenal ulcers:

A

increased gastric secretion + reduced duodenal bicarbonate secretion
= low pH
= gastric metaplasia
= duodenitis (predisposes to ulcers)

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29
Q

Non-selective NSAIDs inhibit __ synthesis

A

PG

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30
Q

Non-selective NSAIDs inhibit PG synthesis via _____ inhibition of ____

A

reversible

both cox1 and cox2

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31
Q

Aspirin causes _____ inhibition of __________

A

irreversible

cox1, cox2 and platelets aggregation

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32
Q

Coxibs are

A

selective cox2 inhibitors

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33
Q

the principal enzyme involved with cyto-protection in stomach and duodenum

A

Cox1

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34
Q

Coxibs reduce incidence of ___ by 75% compared with nsNSAIDs

A

ulcers

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35
Q

nsNSAIDS:

A

non-selective non-steroidal anti-inflammatory drugs

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36
Q

Coxibs reduce incidence of endoscopicallay visible ulcers by __% compared with nsNSAIDs

A

75

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37
Q

Coxibs result in __% reduction in incidence of serious complications of petic ulcers (obstruction, bleeding, perforation)

A

50%

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38
Q

risk of CVS complications (MI, CVA) with Coxib vs placebo

A

2 fold higher with coxibs

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39
Q

the only nsNSAIDs that do not increase risk of CV events:

A

Aspirin & naproxen

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40
Q

even low dose aspirin can increease risk of bleeding by:

A

2 fold

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41
Q

Risk factors for GIB

A
  1. Hx of PU/GIB
  2. Combining aspirin and NSAIDs or coxibs (10 fold increased PU complications than each alone)
  3. H.pylori + low dose aspirin (3 fold increased complications)
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42
Q

Less than 5-10 % of ulcers are caused by other conditions:

A 
Acid hypersecretion/ZES
Systemic mastocytosis 
CMV/transplant patients 
Crohn disease 
Lymphoma
Medications/alendronates 
Chronic medical illness (cirrhosis, CKD…)
Rarely idiopathic
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43
Q

clinical features of peptic ulcer

A

asymptomatic (20%, present with complications) (60% of NSAID ulcers)
epigastric pain (80 - 90 %) - not severe, dull, gnawing, aching, hunger-like
dyspepsia

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44
Q

Alarm features that warrant prompt gastroenterology referralinclude:

A 
bleeding
anemia
early satiety
unexplained weight loss
progressive dysphagia or odynophagia
recurrent vomiting
FHx of GI cancer
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45
Q

Food aggravates or relieves pain?
stomach -
duodenum -

A

stomach - aggravates

duodenum - relieves

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46
Q

50% of peptic ulcers are relieved with food,

pain recurds in __ - __ hours

A

2 - 4 hours

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47
Q

_/3 of DUs and _/3 of GUs cause nocturnal pain that awakens the patient

A

2/3 of DUs 1/3 of GUs

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48
Q

nausea and anorexia may occur with GU/DU?

A

GU

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49
Q

is significant vomiting and weight loss normal for peptic ulcer?

A

no, it could be GOO or malignancy

50
Q

physical examination can show what in peptic ulcers?

A

deep epigastric tenderness

51
Q

lab investigation results in uncomplicated ulcers:

A

normal

52
Q

Lab. tests may be ordered to look for complications or other diagnoses like:

A

Anemia (blood loss)
Leukocytosis (penetration / perforation)
Raised amylase in severe epigastric pain (pancreatic penetration / perforation )

53
Q

what test do we do if we suspect ZES?

A

fasting gastrin level

54
Q

test of choice for peptic ulcers:

A

endoscopy

55
Q

risk of malignancy is DU

A

0

56
Q

when do u biopsy a gastric ulcer?

A

always

57
Q

if ulcer doesnt heal after how long will u be suspicious its malignant?

A

3 months

58
Q

CT for peptic ulcer can show what?

A

perforation
obstruction
penetration

59
Q

CLO stands for _________ and is also known as __________

A

Campylobacter-like organism

Rapid Urease Test

60
Q

explain how the CLO test is done:

A

Abiopsyof mucosa is taken from theantrumof thestomach, and is placed into a medium containing urea and an indicator such asphenol red.
The urease produced byH. pylorihydrolyzes urea to ammonia, which raises thepHof the medium, and changes the color of the specimen from yellow (NEGATIVE) to red (POSITIVE)

61
Q

during what is the CLO test done?

A

gastroscopy

62
Q

H pylori tests

A 
CLO test
histology
urea breath test
stool antigen
serum antibody
63
Q

what do u need to do before Urea breath and stool antigen test?

A

Stop PPI for 1-2 weeks and antibiotic for 2-4 weeks before

64
Q

DDx of peptic ulcer

A 
Dyspepsia 
Atypical GERD
Biliary disease
Chronic pancreatitis
Abdominal malignancy/gastric, pancreatic in particular 
Carbohydrate malabsorption
Chronic mesenteric ischemia
65
Q

DDx for acute severe pain (instead of perforated/penetrated PU)

A 
Acute pancreatitis
Acute cholecystitis
Choledaucholithiasis
Esophageal rupture
Gastric volvulus
Ruptured aortic aneurysm
66
Q

Treatment for PU involves doing what?

A

acid suppression
h pylori eradication
removing nsaid

67
Q

what do PPIs do?

A

permenantly inhibit proton pump

68
Q

after PPI, restoration of acid require new pump with half life of __ hours

A

18

69
Q

PPIs have a half life of __ hours

A

60 min

24 hrs

70
Q

24 hr acid secretion inhibition

PPI: %
H2R antagonists: %

A

PPI >90%

H2R antagonists <65%

71
Q

with PPI, >90% of PUs heal within
GU:
DU:

A

GU: 8 weeks
DU: 4 weeks

72
Q

when in the day are PPIs taken?

A

30 min before breakfast / long fasting

73
Q

In 3% of patients on long term PPI ____ level increase considerably but normalizes in 2 weeks after stopping

A

gastrin

74
Q

which ones better. H2R antagonists or PPIs?

A

PPIs

75
Q

All H2R antagonists can inhibit nocturnal acid but not _____ acid

A

post prandial

76
Q

when in the day are H2R antagonists given?

A

once at bedtime

they suppress nocturnal acid, not post prandial like PPIs so not given before meals

77
Q

with H2R antagonists,85 - 90% of PUs heal within
GU:
DU:

A

GU: 8 weeks
DU: 6 weeks

78
Q

Agents enhancing mucosal defenses:

A

Bismuth
misoprostol
antacids

79
Q

general regimen for H pylori eradication is ___ + ___

A

PPI + antibiotics (1 or more)

80
Q

how does misoprostol work? (in the context of PUs)

A

Misoprostolis a synthetic prostaglandin E1 analog that stimulates prostaglandin E1 receptors on parietal cells in the stomach to reduce gastric acid secretion

81
Q

duration of H pylori eradicatio is

A

1 - 2 weeks

82
Q

Confirm h pylori eradication _ weeks after stopping antibiotics and _ weeks after stopping PPI

A

4

2

83
Q

UBT:

A

urea breath test

84
Q

explain the UBT

A
  • urea capsule is swallowed
  • h pylori urease breaks down the later to produce ammonia and CO2
  • CO2 is detected in breath
85
Q

re infection rate of h. pylori after eradication:

A

1 - 2 % per year

86
Q

when an ulcer recurs, we should exclude

A

NSAIDs and hypoer-secretory states

87
Q

if patient has ulcer but u cant stop NSAIDs

concomitant PPI once daily results in ulcer healing in __% in _ weeks

A

80% 8

88
Q

All NSAID-associated ulcers should be tested for

A

H pylori

89
Q

how to reduce NSAID induced ulcers

A 
1- outweigh benefit against risks
2- lowest effective dose
3- shortest period
4- less irritant agent
5- avoid combination with steroids and anticoagulants unless necessary
90
Q

All patients who require aspirin and anticoagulants should be given a

A

PPI

91
Q

what percentage of ulcers don’t heal by 8 weeks of 1 PPI / day?
2 PPI / day?

A

< 5%

almost all heal with 2

92
Q

most common cause of refractory ulcers:

A

non compliance

93
Q

causes of refractory ulcers

A 
noncompliance
NSAIDs, aspirin, iron, biphosphonates
H pylori
ZES
malignancy (adenocarcinoma or lymphoma)
Crohn
infection (CMV, HSV, mucormycosis, TB, syphilis, candida)
ischemia
94
Q

50% of UGIB are cuz of

A

peptic ulcers

95
Q

UGIB from PU is significant in __%

A

10

96
Q

what percent of PU bleeding stops spontaneously?

A

80%

97
Q

mortality rate of bleeding PU

A

7%

98
Q

mortality from bleeding PU is higher in:

A 
elderly
comorbidities
hospital associated
persistent HPO
bright red blood in vomit / NGT
severe coagulopathy
99
Q

H2RA for bleeding peptic ulcer

A

useless

100
Q

Recurrent PU bleeding occur in _/3 within _ years if no specific treatment is given

A

1/3 in 3 yrs

101
Q

if there is recurrent bleeding from PU and everything else failed, we do

A

surgical treatment endoscopically (<5%)

102
Q

surgical mortality for bleeding PU is 6% but higher if:

A

> 60 years
Comorbidities
Renal failure
Requiring >10 pints of blood

103
Q

alternative surgical treatment to endoscopy in bleeding PU is

A

angiographic embolization

104
Q

perforated peptic ulcer is usually in the

A

anterior wall of stomach and duodenum

105
Q

in perforated PU, sudden severe abdominal pain that may generalize due to

A

chemical peritonitis

106
Q

what patients have no symptoms of perforated PU and present late with complications (bacterial peritonitis, sepsis and shock)

A

elderly

steroids

107
Q

signs of perforated PU

A

rigid & quiet abdomen

rebound tenderness

108
Q

HPO can occur when bacterial peritonitis develops therefore when HPO is present at the start think of:

A

Ruptured aortic aneurysm
Pancreatitis
Mesenteric ischemia

109
Q

lab signs of perforated PU

A

leukocytosis and increased serum amylase

110
Q

why does serum amylase increase in perforated PU?

A

Amylase leaks through perforation and get absorbed

111
Q

diagnosis of perforated PU is by

A

CT

112
Q

absence of free air in perforated PU leads to misdiagnosis of

A

pancreatitis / cholecystitic / appendicitis

113
Q

treatment of perforated PU is

A

surgery

114
Q

GOO occurs in

A

2

115
Q

GOO is caused by

A

edema or fibrosis of pylorus or bulb

116
Q

GOO is less from PU cuz we treat PUs better, now its mostly cuz of

A

gastric neoplasm and duodenal obstruction by extrinsic compression

117
Q

clinical features of GOO

A

early satiety
vomiting
weight loss (1 to several hours after eating, contains partially digested food)

118
Q

blood tests in GOO shows

A

Hypokalemia and alkalosis

119
Q

examination of patient with GOO shows

A

succussion splash

120
Q

management of GOO

A 
admission
IV fluid / saline and KCL
IV PPI
NG decompression
endoscopy after 1 - 3 days to diagnose
if benign: 
pneumatic balloon dilatation or surgery
vagotomy and antrectomy
vagotomy and pyloroplasty
truncal vagotomy
gastrojejunostomy

Internal medicine (7 decks)

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