Peptic Ulcers Flashcards

1
Q

What is the definition of a peptic ulcer?

A

A defect in gastric or duodenal mucosa with a diameter of at least .5cm and depth that penetrates through the muscularis mucosae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the definition of as gastric ulcer?

A

A peptic ulcer of the gastric mucosa, typically located along the lesser curvature in the transitional portion between corpus and antrum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the definition of a duodenal ulcer?

A

A peptic ulcer of the duodenal mucosa, usually located on the anterior or posterior wall of the duodenal bulb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the median age for developing a peptic ulcer?

A

18-30 years of age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the 2 most common causes of peptic ulcer disease?

A

Helicobacter pylori
Chronic NSAID use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How many cases of duodenal and gastric ulcers is H pylori associated with?

A

Duodenal - 40-70%
Gastric - 25-50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the associated risk factors for peptic ulcer disease?

A

Smoking
Heavy alcohol use
Glucocorticoids
Caffeine
Diet
Anxietysgtress
PTSD
Genetic factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are some rare causes of PUD?

A

Acid hypersecretory state (gastrinoma for example)
Non NSAID medication eg acetaminophen, chemo
Infections eg EBV, CMV
Radiation
Illicit drug use eg cocaine
Systemic inflammatory disease eg chrons disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is gastric juice composed of?

A

HCL
Peposinogen

Intrinsic factor
Mucus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What prevents the gastric juice from damaging the stomach lining?

A

Secretion of mucus and HCO3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What can cause the ulcer formation?

A

When either the protective mechanisms are disrupted and or excessive acids or pepsin are secreted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the function of the parietal cells?

A

Secrete HCl and intrinsic factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What stimulates the parietal cells?

A

Acetylcholine, histamine and gastrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What inhibits parietal cells?

A

Prostaglandins
Somatostatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the function of the mucosal cells?

A

Secrete protective mucus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What stimulates the mucosal cells?

A

Acetylcholine, prostaglandin (which inhibits HCl production) and Secretin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the purpose of chief cells?

A

Secrete pepsinogen

18
Q

What stimulates the chief cells

A

Acetylcholine, gastric, secretin and vasoactive intestinal polypeptide

19
Q

How does H pylori infection cause a gastric ulcer formation?

A

Hpylori secretes urease -> conversion of urea to Ammonia -> alkalinisation of acidic environment -> survival of bacteria in the gastric lumen. Bacterial colonisation and attachment to epithelial cells -> release of cytotoxins -> disruption of the mucosal barrier and damage to underlying cells

20
Q

How does H pylori infection cause a duodenal ulcer formation?

A

Hpylori inhibits somatostatin secretion -> increased gastrin secretion -> increased acid production ->? Excess acid delivery to duodenum. Direct spread of Hpylori to duodenum -> Inhibition of duodenal HCO3 secretion -> acidification and insufficient neutralisation off duodenal contents

21
Q

How do NSAID’s lead to peptic ulcer formation? (Pathophysiology)

A

Inhibits COX1 and COX2 -> decrease in prostaglandin production -> erosion of the gastric mucosa. Decrease mucosal blood flow. Inhibit mucosal cell proliferation.

22
Q

How does acid hypersecretioon lead to peptic ulcer formation? (Pathophysiology)

A

Acid hypersecretion and increased gastrin production -> increased acid secretion and parietal cell mass -> delivery of excessive acid to the duodenum

23
Q

Clinical features of peptic ulcer?

A

Up to 70% asymptomatic (more common in those who are due to NSAID use)
Epigastric abdominal pain - gnawing or burning in nature. Related to meal intake depending on location of ulcer
Belching
Indigestion
GER
Nausea and or vomiting
Bloating/abdominal fullness

24
Q

Which clinical features are common in gastric and peptic ulcer? §

A

Dyspepsia - postprandial heaviness, early satiety, gnawing aching burning epigastric pain
Pain relief with antacids
Potential signs of internal bleeding eg anemia, hematemesis
Stool sample p=positive for occult blood

25
Q

What are the differences in clinical features of gastric and duodenal ulcer?

A

Gastric - pain increases shortly after eating -> weight loss. Nocturnal pain less common
Duodenal - pain is relieved with foods intake -> weight gain. Pain increases after 2-5 hours of food ingestion. Nocturnal pain more common

26
Q

What is a subtype of a peptic ulcer?

A

Stress ulcer

27
Q

What is a stress ulcer associated with?

A

Erosive gastritis

28
Q

What is the initial diagnosis approach for peptic ulcer?

A

Look for underlying cause eg NSAID’s.
CBC and BMP (basic metabolic panel) if suspicion for occult bleeding

29
Q

What does a basic metabolic panel check?

A

Serum concentrations of -
Sodium
Potassium
Chloride
Bicarbonate
Urea nitrogen
Creatinine
Glucose

30
Q

What is the diagnosis approach for patients <60 and without red flags for dyspepsia

A

Begin with non invasive testing for H pylori infection - urea breath test and stool antigen test

31
Q

What is the diagnosis approach for patients >60/45 years with high gastric cancer prevalence, patients with red flags for dyspepsia and patients unresponsive to empiric medical therapy eg hpylori eradication therapy

A

Refer directly for esopaghogastroduiodenoscopy

32
Q

What is Ruthie most accurate test to confirm peptic ulcer diagnosis?

A

Esophagogastroduodenoscopy

33
Q

What are the other purposes of an EGD?

A

Malignancy screening - to differentiate between PUD and gastric cancer
Invasive hpylori testing
Hemostasis treatment

34
Q

What are the differences between benign and malignant gastroduodenal ulcers?

A

(Look at picture in gallery)

35
Q

What are the objectives of treatment of a peptic ulcer?

A

Removing symptoms
Healing the ulcerous cratere
Preventing reoccurrence
Preventing complications
Treatment of complications

36
Q

What are the treatments for peptic ulcer?

A

Dietary management - Quit smoking and alcohol. Stoop NSAID us. 8 hours of sleep and small regular meals

37
Q

What is the medical treatment of Peptic ulcer?

A

Duodenal ulcer and Hpylori - eradicate HP and antisecretory drugs
Duodenal ulcer and HP and NSAID - eradicate HP and antisecretory drugs and prostaglandins
DU and NSAID - antisecretory drugs and prostaglandins

38
Q

Which antibiotics are used for the treatment of HP?

A

Amoxicillin 500mg x4/day
Clarithromycin 500-1500mg/day
Tetracycline 500mg x4/day
Metronidazole 2500mg x4/day

39
Q

What are the antisecretory drugs used?

A

PPI’s - omeprazole 40mg/dauy
Pantoprazole 40mg/day
Rabeprazole 40mg/day
Lansoprazole 40mg/day

40
Q

What are some Histamine receptor blocking drugs?

A

Ranitidine 150mg x2/day
Famotidine 20mg x2/day
Nizatidine 150mg x2/day

41
Q

What is the modified Johnson classification of peptic ulcers?

A

Type 1 - ulcer along body of stomach, most often along lesser curvature at inciusra angularis along locus minoris resistantiae

Type 2 - ulcer in body in combination with duodenal ulcers. Associated with acid hypersecretion

Type 3 - in pyloric channel within 3cm of pylorus. Associated with acid hypersecretion

Type 4 - proximal gastroesophageal ulcer

Type 5 - can occur throughout stomach. Associated with chronic NSAID use eg aspirin