Peptic ulcer Flashcards
What is a peptic ulcer?
a mucosal break penetrating the muscularis mucosa
What is an erosion?
a lesion superficial to the muscularis mucosa
difference between peptic ulcer & erosion
peptic ulcer penetrates muscularis mucosa but erosion is superficial to it
which one is more common, duodenal or gastric ulcer?
how many times more common?
dudeonal ulcer
5x
lifetime risk of peptic ulcer
10%
where is “duodenal bulb”?
the portion of the duodenum closest to the stomach (first 5cm of duodenum)
over 95% of peptic ulcers are in ___ and ___
duodenal bulb and antrum
peptic ulcer more in male of female?
slightly more in male
common age of duodenal ulcers and gastric ulcers
DU: 30 - 55 yrs
GU: 55 - 75 yrs
H. pylori is associated more with ___ ulcers
Aspirin and NSAIDs are associated more with ___ ulcers
H. pylori - duodenal
Aspirin and NSAIDs - gastric
2 main factors in the pathophysiology of peptic ulcers:
H. pylori and NSAIDs
helicobacter pylori microbiology
spiral-shaped, flagellated, Gram-negative bacillus with urease activity
H. pylori is seen in __% of DUs and __% of GUs
DU - 90%
GU - 70%
Urease changes ____ to ____ .
function:
Urease changes urea to ammonia
ammonia is alkaline, it helps resist acid
how and when is H. pylori transmitted?
orally, mostly during childhood
H. pylori is mostly in the ___
antrum
If H. pylori is in the duodenum, it is associated with
metaplastic gastric epithelium
Ulcer disease develops in __% of infected people
10%
H pylori GU tends to occur at the junction of ___ and ___
body and antrum
risk of GU and DU in long term NSAID use
GU: 10 - 20 %
DU: 2 - 5%
There is greater risk of ulcer from NSAIDs in:
first 3 months of therapy >60 yrs Hx of ulcer NSAIDs + aspirin steroids anticoagulants co-morbidities
Mucosal injury and, thus, peptic ulcer occur when the balance between the ____ factors and the ______ mechanisms is disrupted
aggressive defensive
Aggressive factors (factors that cause ulcers)
NSAIDs h. pylori alcohol bile salts acid pepsin
defensive mechanisms (protect against ulcers)
tight intercellular junctions mucus bicarbonate mucosal blood flow cellular restitution epithelial renewal
pathophysiolofy of H. pylori causing ulcers:
H pylori interact with G and D cells causing increased gastrin and hence acid production, mostly localized resulting in ulcer
In patients infected withH pylori,high levels of ___ and ____ and reduced levels of ____ have been measured
high: gastrin & pepsinogen
low: somatostatin
Virulence factors produced byH pylori:
urease
catalase
vacuolating cytotoxin
lipopolysaccharide
pathophysiology of H. Pylori causing duodenal ulcers:
increased gastric secretion + reduced duodenal bicarbonate secretion
= low pH
= gastric metaplasia
= duodenitis (predisposes to ulcers)
Non-selective NSAIDs inhibit __ synthesis
PG
Non-selective NSAIDs inhibit PG synthesis via _____ inhibition of ____
reversible
both cox1 and cox2
Aspirin causes _____ inhibition of __________
irreversible
cox1, cox2 and platelets aggregation
Coxibs are
selective cox2 inhibitors
the principal enzyme involved with cyto-protection in stomach and duodenum
Cox1
Coxibs reduce incidence of ___ by 75% compared with nsNSAIDs
ulcers
nsNSAIDS:
non-selective non-steroidal anti-inflammatory drugs
Coxibs reduce incidence of endoscopicallay visible ulcers by __% compared with nsNSAIDs
75
Coxibs result in __% reduction in incidence of serious complications of petic ulcers (obstruction, bleeding, perforation)
50%
risk of CVS complications (MI, CVA) with Coxib vs placebo
2 fold higher with coxibs
the only nsNSAIDs that do not increase risk of CV events:
Aspirin & naproxen
even low dose aspirin can increease risk of bleeding by:
2 fold
Risk factors for GIB
- Hx of PU/GIB
- Combining aspirin and NSAIDs or coxibs (10 fold increased PU complications than each alone)
- H.pylori + low dose aspirin (3 fold increased complications)
Less than 5-10 % of ulcers are caused by other conditions:
Acid hypersecretion/ZES Systemic mastocytosis CMV/transplant patients Crohn disease Lymphoma Medications/alendronates Chronic medical illness (cirrhosis, CKD…) Rarely idiopathic
clinical features of peptic ulcer
asymptomatic (20%, present with complications) (60% of NSAID ulcers)
epigastric pain (80 - 90 %) - not severe, dull, gnawing, aching, hunger-like
dyspepsia
Alarm features that warrant prompt gastroenterology referralinclude:
bleeding anemia early satiety unexplained weight loss progressive dysphagia or odynophagia recurrent vomiting FHx of GI cancer
Food aggravates or relieves pain?
stomach -
duodenum -
stomach - aggravates
duodenum - relieves
50% of peptic ulcers are relieved with food,
pain recurds in __ - __ hours
2 - 4 hours
_/3 of DUs and _/3 of GUs cause nocturnal pain that awakens the patient
2/3 of DUs 1/3 of GUs
nausea and anorexia may occur with GU/DU?
GU
is significant vomiting and weight loss normal for peptic ulcer?
no, it could be GOO or malignancy
physical examination can show what in peptic ulcers?
deep epigastric tenderness
lab investigation results in uncomplicated ulcers:
normal
Lab. tests may be ordered to look for complications or other diagnoses like:
Anemia (blood loss)
Leukocytosis (penetration / perforation)
Raised amylase in severe epigastric pain (pancreatic penetration / perforation )
what test do we do if we suspect ZES?
fasting gastrin level
test of choice for peptic ulcers:
endoscopy
risk of malignancy is DU
0
when do u biopsy a gastric ulcer?
always
if ulcer doesnt heal after how long will u be suspicious its malignant?
3 months
CT for peptic ulcer can show what?
perforation
obstruction
penetration
CLO stands for _________ and is also known as __________
Campylobacter-like organism
Rapid Urease Test
explain how the CLO test is done:
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)
during what is the CLO test done?
gastroscopy
H pylori tests
CLO test histology urea breath test stool antigen serum antibody
what do u need to do before Urea breath and stool antigen test?
Stop PPI for 1-2 weeks and antibiotic for 2-4 weeks before
DDx of peptic ulcer
Dyspepsia Atypical GERD Biliary disease Chronic pancreatitis Abdominal malignancy/gastric, pancreatic in particular Carbohydrate malabsorption Chronic mesenteric ischemia
DDx for acute severe pain (instead of perforated/penetrated PU)
Acute pancreatitis Acute cholecystitis Choledaucholithiasis Esophageal rupture Gastric volvulus Ruptured aortic aneurysm
Treatment for PU involves doing what?
acid suppression
h pylori eradication
removing nsaid
what do PPIs do?
permenantly inhibit proton pump
after PPI, restoration of acid require new pump with half life of __ hours
18
PPIs have a half life of __ hours
60 min
24 hrs
24 hr acid secretion inhibition
PPI: %
H2R antagonists: %
PPI >90%
H2R antagonists <65%
with PPI, >90% of PUs heal within
GU:
DU:
GU: 8 weeks
DU: 4 weeks
when in the day are PPIs taken?
30 min before breakfast / long fasting
In 3% of patients on long term PPI ____ level increase considerably but normalizes in 2 weeks after stopping
gastrin
which ones better. H2R antagonists or PPIs?
PPIs
All H2R antagonists can inhibit nocturnal acid but not _____ acid
post prandial
when in the day are H2R antagonists given?
once at bedtime
they suppress nocturnal acid, not post prandial like PPIs so not given before meals
with H2R antagonists,85 - 90% of PUs heal within
GU:
DU:
GU: 8 weeks
DU: 6 weeks
Agents enhancing mucosal defenses:
Bismuth
misoprostol
antacids
general regimen for H pylori eradication is ___ + ___
PPI + antibiotics (1 or more)
how does misoprostol work? (in the context of PUs)
Misoprostolis a synthetic prostaglandin E1 analog that stimulates prostaglandin E1 receptors on parietal cells in the stomach to reduce gastric acid secretion
duration of H pylori eradicatio is
1 - 2 weeks
Confirm h pylori eradication _ weeks after stopping antibiotics and _ weeks after stopping PPI
4
2
UBT:
urea breath test
explain the UBT
- urea capsule is swallowed
- h pylori urease breaks down the later to produce ammonia and CO2
- CO2 is detected in breath
re infection rate of h. pylori after eradication:
1 - 2 % per year
when an ulcer recurs, we should exclude
NSAIDs and hypoer-secretory states
if patient has ulcer but u cant stop NSAIDs
concomitant PPI once daily results in ulcer healing in __% in _ weeks
80% 8
All NSAID-associated ulcers should be tested for
H pylori
how to reduce NSAID induced ulcers
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
All patients who require aspirin and anticoagulants should be given a
PPI
what percentage of ulcers don’t heal by 8 weeks of 1 PPI / day?
2 PPI / day?
< 5%
almost all heal with 2
most common cause of refractory ulcers:
non compliance
causes of refractory ulcers
noncompliance NSAIDs, aspirin, iron, biphosphonates H pylori ZES malignancy (adenocarcinoma or lymphoma) Crohn infection (CMV, HSV, mucormycosis, TB, syphilis, candida) ischemia
50% of UGIB are cuz of
peptic ulcers
UGIB from PU is significant in __%
10
what percent of PU bleeding stops spontaneously?
80%
mortality rate of bleeding PU
7%
mortality from bleeding PU is higher in:
elderly comorbidities hospital associated persistent HPO bright red blood in vomit / NGT severe coagulopathy
H2RA for bleeding peptic ulcer
useless
Recurrent PU bleeding occur in _/3 within _ years if no specific treatment is given
1/3 in 3 yrs
if there is recurrent bleeding from PU and everything else failed, we do
surgical treatment endoscopically (<5%)
surgical mortality for bleeding PU is 6% but higher if:
> 60 years
Comorbidities
Renal failure
Requiring >10 pints of blood
alternative surgical treatment to endoscopy in bleeding PU is
angiographic embolization
perforated peptic ulcer is usually in the
anterior wall of stomach and duodenum
in perforated PU, sudden severe abdominal pain that may generalize due to
chemical peritonitis
what patients have no symptoms of perforated PU and present late with complications (bacterial peritonitis, sepsis and shock)
elderly
steroids
signs of perforated PU
rigid & quiet abdomen
rebound tenderness
HPO can occur when bacterial peritonitis develops therefore when HPO is present at the start think of:
Ruptured aortic aneurysm
Pancreatitis
Mesenteric ischemia
lab signs of perforated PU
leukocytosis and increased serum amylase
why does serum amylase increase in perforated PU?
Amylase leaks through perforation and get absorbed
diagnosis of perforated PU is by
CT
absence of free air in perforated PU leads to misdiagnosis of
pancreatitis / cholecystitic / appendicitis
treatment of perforated PU is
surgery
GOO occurs in
2
GOO is caused by
edema or fibrosis of pylorus or bulb
GOO is less from PU cuz we treat PUs better, now its mostly cuz of
gastric neoplasm and duodenal obstruction by extrinsic compression
clinical features of GOO
early satiety
vomiting
weight loss (1 to several hours after eating, contains partially digested food)
blood tests in GOO shows
Hypokalemia and alkalosis
examination of patient with GOO shows
succussion splash
management of GOO
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
