PUD - Peptic Ulcer Disease Flashcards

1
Q

Define PUD

A

Ulceration of the distal esophagus, stomach and/or duodenum secondary to excessive acid production or damaged barrier mechanisms

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2
Q

What are the most common sites for ulceration in PUD?

A

Duodenum > Gastric > oesophagus
1st part of duodenum > Gastric antrum > lesser curve of stomach

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3
Q

Compare the peak age of gastric and duodenal ulcers

A

Duodenal ulcers occur in younger patients than gastric
Duodenal = 25-50
Gastric >50

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4
Q

Compare the incidence of PUD based on gender

A

Male:Female 3:1. you only need to say male>female

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5
Q

State the 2 main RFs/causes of PUD
State 5 other RFs/causes of PUD

A

Main: H.Pylori and NSAID use
Other: Gastrinoma/Zollinger-Ellison Syndrome, Smoking, steroids, long-term use of PPIs, blood group O, Burns, Head injuries

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6
Q

H. Pylori is responsible for 70-80% of gastric ulcers and 90% of duodenal ulcers. How does H.Pylori lead to PUD?

A

It causes chronic Antral gastritis (inflammation in the antrum) => causing increased acid secretion and decreased mucosal resistance (definition of PUD)

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7
Q

NSAID use increases the risk of PUD by 40x for gastric ulcers and 8x for duodenal ulcers. How does chronic NSAID use lead to PUD?

A

NSAIDs such as Ibuprofen inhibit the COX 1 and 2 enzymes. COX 2 is responsible for inflammation and pain and hence this is the target. Inhibiting COX 1, however, leads to suppression of Prostaglandin responsible for acid homeostasis and hence this will lead to increased acid secretion (reduced inhibition of secretion)

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8
Q

What is Zollinger Ellison Syndrome? What is it caused by?
How is it screened for?

A

It is a syndrome of increased gastrin secretion (hypergastrinemia). This is typically caused by a neuroendocrine tumor in the duodenum and pancreas, a Gastrinoma, which hypersecretes gastrin.

Detected via fasting serum gastrin

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9
Q

Gastrinomas are one of the rarer causes of PUD. Most cases of Gastrinomas are sporadic but what gene is associated with it?
Where are Gastrinomas typically found? Where are their ulcers found
What syndrome can it cause?
How are they typically diagnosed?

A

MEN1 gene: MULTIPLE Endocrine Neoplasia Syndrome (3Ps)
Typically in the duodenum or pancreas. MULTIPLE ulcers in the stomach, duodenum and jejunum
The neuroendocrine tumour causes hypersecretion of gastrin which by definition is Zollinger-Ellison syndrome leading to increased acid secretion
Diagnosed typically via Gastric Antral Biopsy via OGD with MULTIPLE ulcers in the stomach duodenum and jejenum (must say this once)

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10
Q

A patient with PUD typically complains of pain in which region?

A

Epigastric

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11
Q

State the clinical features of UNCOMPLICATED PUD, while comparing duodenal and gastric ulcers.

A

Burning intermittent epigastric pain
Gastric: Non-cyclical pain, exacerbated by food, weight loss, nausea, vomiting , Fe anemia
Duodenal: Cyclical pain worse at night and early morning, impacting sleep, relieved by food,
less common weight loss, nausea, vomiting, Fe anemia

Heartburn, reflux, chest pain

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12
Q

What are the complications of PUD, stating the symptoms that arise from them

A

1) Bleeding/hemorrhage
=> Hematemesis and malaena
=> Shock: Tachycardia, tachypnea, hypotension and altered GCS
=> Anemia: Pallor, fatigue, lethargy, chest pain, SOB/dyspnea, dizziness, syncope
2) Perforation + Sepsis: Tachycardia, tachypnea, hypotension, diaphoresis, clammy sweaty cool peripheries, reduced urine output, altered GCS
3) Gastric outlet obstruction: episodic projectile vomiting unrelated to eating => often dehydrated and malnourished

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13
Q

What would you be looking for on an abdominal exam for a patient with suspected gastric outlet obstruction?

A

Succussion Splash: splash on auscultation of the stomach when moving the patient suddenly

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14
Q

Without comparing duodenal and gastric ulcers, state the general symptoms of COMPLICATED PUD.

A

uncomplicated PUD:
Burning, intermittent epigastric pain
Nausea, vomiting
mild weight loss
heartburn, reflux, chest pain
+ complications:
1) Bleeding/hemorrhage
=> Hematemesis and malaena
=> Shock: Tachycardia, tachypnea, hypotension and altered GCS
=> Anemia: Pallor, fatigue, lethargy, chest pain, SOB/dyspnea, dizziness, syncope
2) Perforation + Sepsis: Tachycardia, tachypnea, hypotension, diaphoresis, clammy sweaty cool peripheries, reduced urine output, altered GCS
3) Gastric outlet obstruction: episodic projectile vomiting unrelated to eating => often dehydrated and malnourished

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15
Q

QUICK: A patient presents to you with epigastric pain. What are your ddx?

A

PUD
GORD
Cholelithiasis/biliary colic
Acute cholecystitis
Pancreatitis
Gastric neoplasm
Pancreatic neoplasm

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16
Q

Give 3 ways to detect the presence of an active H.Pylori infection as the cause of PUD

A

Antral biopsy via OGD -> CLO urease test
Carbon 13 urea breath test
Stool antigen testing
Seroloy (not used)

17
Q

What is the direct treatment of an active H.Pylori infection?

A

Triple Therapy
20mg Omeprazole PO BD + Clarithromycin BD + Amoxicillin/Metronidazole BD

18
Q

What drug can be used to increase mucosal protection for patients suffering from PUD?

A

Sucralfate. Reacts with HCL to form paste-like substance which acts as a buffer

19
Q

Why is serology not typically used to confirm the presence of an active H. Pylori infection as the cause of PUD?

A

Not performed since antibodies persist 6-12 months after eradication

20
Q

How would you screen for Gastrinoma/Zollinger-Ellison syndrome?
How would you confirm the presence of a gastrinoma or malignancy causing gastrin hypersecretion?

A

Screen: Fasting serum gastrin
Diagnostic: Gastric Antral Mucosal histology from OGD biopsy

21
Q

A patient presents to you with the following symptoms Burning, intermittent epigastric pain, Nausea, vomiting, mild weight loss, and heartburn.
What is your most likely diagnosis?
What is the Gold standard to confirm your diagnosis?
How would you treat this patient?

A

Uncomplicated PUD

Gastric Antral Biopsy via OGD is the gold standard which will be used to
1) CLO urease test (alternatively carbon 13 urea breath test)
2) Gastric Antral Mucosal Histology for ulcer staging and to rule out malignancy (gastrinoma)
OR you can screen for hypergastrinemia via fasting serum gastrin

Treatment:
1) Triple Therapy: 20mg Omeprazole PO BD + Clarithromycin BD + Amoxicillin/Metronidazole BD
2) Mucosal protection: Sucralfate
3) Non-pharmacological: Stop NSAIDs, smoking, dietician consult

22
Q

A patient with complicated PUD presents to the ED and is deteriorating rapidly.
What investigations would you perform?

A

Bedside: ECG

Bloods:
FBC w differentials (anemia and platelets)
Coag screen (coagulopathy and INR)
ABG - Rule out Ischemia (via lactate)
Group and Cross-match 4 units

Imaging:
!Erect! CXR for perforation
Gastric Antral Biopsy via OGD is the gold standard which will be used to
1) CLO urease test (alternatively carbon 13 urea breath test)
2) Gastric Antral Mucosal Histology for ulcer staging and to rule out malignancy (gastrinoma)
OR you can screen for hypergastrinemia via fasting serum gastrin
CT/CT angio to localize bleeding source

23
Q

What would you prescribe as broad spectrum antibiotics in an emergency situation?

A

Coamoxiclav/Pip-taz + Metronidazole/Gentamicin

24
Q

FULL STATION: A patient with complicated PUD presents to the ED and is deteriorating rapidly. You have performed the necessary investigations and have determined the complication of hemorrhage to be the cause of his deterioration.
What is your Full management plan? (include difference between duodenal and gastric)

A

1) Admit to hospital
2) ABCDE: Send out FBC w/differentials, U&E, CRP, LFTs, and coag profile, ABG
3) NPO for all, NG tube if vomiting, Intubate if GCS 8 or under or if vomiting
4) O2 if in doubt until ABG becomes available (15L 100% O2 via non-rebreather mask)
5) 2x large bore cannulas, IV fluids at 100ml/hr until losses worked out via intake/output chart +/- urinary catheter
6) Type and save, group and hold, Group and cross match 4 units of blood (10 for AAA). If needed give in 1:1:1 aiming for Hb>8 and >10 in CVD
7) Analgesia (Paracetamol, NSAIDS, Morphine/oxynorm/oxycontin)
8) Antiemetics if needed (Ondansetron)
9) Antibiotics: Coamox/pip taz + Gent/Metronidazole
10) DVT prophylaxis (TEDs, Clexane, LMWH)

OGD with techniques (adrenaline injection, thermal coagulation, argon plasma coagulation)

Medications:
Correct Coagulation (vit K > FFP > PCC)
PPI: Bolus IV 80mg Omeprazole followed by 40mg BD or IV 8mg/hr for 72hrs if active bleeding
IV 1g Tranexamic Acid TDS

If patient is still hemodynamically unstable despite >6-8 units in <24 hours and all has failed => surgery.
Gastric: Wedge Resection OR biopsy/over sewing of ulcer to exclude malignancy
Duodenal: Duodenotomy with over sewing of ulcer

25
Q

How is Perforation diagnosed?

A

Pneumoperitoneum on erect CXR

26
Q

FULL STATION: A patient with complicated PUD presents to the ED and is deteriorating rapidly. You have performed the necessary investigations and have determined the complication of Perforation to be the cause of his deterioration.
What is your Full management plan? (include difference between duodenal and gastric)

A

1) Admit to hospital
2) ABCDE: Send out FBC w/differentials, U&E, CRP, LFTs, and coag profile, ABG
3) NPO for all, NG tube if vomiting, Intubate if GCS 8 or under or if vomiting
4) O2 if in doubt until ABG becomes available (15L 100% O2 via non-rebreather mask)
5) 2x large bore cannulas, IV fluids at 100ml/hr until losses worked out via intake/output chart +/- urinary catheter
6) Type and save, group and hold, Group and cross match 4 units of blood (10 for AAA). If needed give in 1:1:1 aiming for Hb>8 and >10 in CVD
7) Analgesia (Paracetamol, NSAIDS, Morphine/oxynorm/oxycontin)
8) Antiemetics if needed (Ondansetron)
9) Antibiotics: Coamox/pip taz + Gent/Metronidazole
10) DVT prophylaxis (TEDs, Clexane, LMWH)

Perforation => sepsis workup included with antibiotics (Coamoxiclav/Pip-taz + Metronidazole/Gentamicin)
=> Surgical treatment:
Gastric: Wedge Resection to exclude malignancy
Duodenum: Laparoscopic/open Graham Patch Repair (Ommental patch repair)

27
Q

What is Graham Patch repair?

A

It is a laparoscopic or open Ommental patch repair for treatment of perforated ulcer
It involves omental patching and peritoneal debridement

28
Q

FULL STATION: A patient with complicated PUD presents to the ED and is deteriorating rapidly. You have performed the necessary investigations and have determined the complication of Gastric outlet obstruction to be the cause of his deterioration.
What is your Full management plan?

A

Initially aggressive resuscitation with NG tube feed as these patients are often dehydrated and undernourished followed by surgery.

1) Admit to hospital
2) ABCDE: Send out FBC w/differentials, U&E, CRP, LFTs, and coag profile, ABG
3) NPO for all, NG tube if vomiting, Intubate if GCS 8 or under or if vomiting
4) O2 if in doubt until ABG becomes available (15L 100% O2 via non-rebreather mask)
5) 2x large bore cannulas, IV fluids at 100ml/hr until losses worked out via intake/output chart +/- urinary catheter
6) Type and save, group and hold, Group and cross match 4 units of blood (10 for AAA). If needed give in 1:1:1 aiming for Hb>8 and >10 in CVD
7) Analgesia (Paracetamol, NSAIDS, Morphine/oxynorm/oxycontin)
8) Antiemetics if needed (Ondansetron)
9) Antibiotics: Coamox/pip taz + Gent/Metronidazole
10) DVT prophylaxis (TEDs, Clexane, LMWH)

Surgery: Gastrojejunostomy +/- Truncal Vagotomy and Pyelooplasty

29
Q

What is a Gastrojejunotomy

A

It is a procedure used in the treatment of complicated PUD due to gastric outlet obstruction.
It involves bypassing the duodenum therefore connecting the stomach to the jejenum
This procedure may be performed along with truncal vagotomy and pyeloplasty

30
Q

What is a Truncal Vagotomy

A

It is conducted along with Gastrojejunostomy and pyeloplasty in the treatment of complicated PUD due to gastric outlet obstruction.
It involved cutting off part of the Vagus nerve at the gastroesophageal junction which reduces HCl secretion (through acetylcholine but doesnt matter)

31
Q

What is Pyeloplasty

A

It is a procedure conducted to reduce the thickness of the pyloric sphincter. This is used in the treatment of pyloric stenosis and gastric outlet obstruction in Chronic complicated PUD

32
Q

Where is Gastrin produced?

A

Pancreas => why Gastrinoma is a neuroendocrine tumour of the duodenum and pancreas

33
Q

What finding is displayed in this image?

A

Pneumoperitoneum. You can see it on the right side with diaphragm then gas then diaphragm again