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Ch. 3 - Upper GI Surgery > PUD - Peptic Ulcer Disease > Flashcards

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

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

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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 (peak in 6th decade)

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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 4 Drug-related that are RFs
State 6 other RFs/causes of PUD

A

Main: H.Pylori and NSAID use
Drugs: Anticoagulants, Steroids, Long-term PPI-use, Polypharmacy in elderly
Other: Previous PUD, Stress/Cushing’s ulcers, Burns/Curling’s ulcers, Gastrinoma/Zollinger-Ellison Syndrome, Smoking, blood group O, 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? (Pathophysiology)

A

It causes chronic Antral gastritis => 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? (MOA of NSAIDs)

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 symptoms of UNCOMPLICATED PUD, while comparing duodenal and gastric ulcers.

A

Burning intermittent epigastric pain
+ Heartburn, reflux, chest pain
+ Waterbrash (reflux of acid into mouth)

Gastric: Non-cyclical pain, exacerbated by food, weight loss/anorexia, 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

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12
Q

What are the signs of dehydration?

A

Confusion/lethargy
Reduced skin turgor
Pulse = weak/tachycardiac
Prolonged cap refill time
Sunken eyes, absent tears
Dry oral mucous membranes
reduced urine output

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13
Q

What clinical signs on examination would you find in PUD?

A

Abdominal pain: epigastric tenderness

Shock/GI haemorrhage:
Vitals
Pulse: tachycardia (may also be weak pulse if haemorrhage)
BP: Hypotension secondary to shock
Tachypnoea
Reduced urine output
reduced consciousness (GCS)
Anaemia => pallor, pallor of palmer crease, koilonychia, angular stomatitis, conjunctival pallor

Perforation: Above + guarding + rigidity + sitting still + shallow breaths

Gastric outlet obstruction: Succusion splash, dehydration, malnutrition

Dehydration:
Confusion/lethargy
Reduced skin turgor
Pulse = weak/tachycardiac
Prolonged cap refill time
Sunken eyes, absent tears
Dry oral mucous membranes
reduced urine output

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14
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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15
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

Bonus: Patient also malnourished and dehydrated

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16
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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17
Q

Malignant ulcers as a cause of PUD is associated with what?

A

Gastric cancer

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18
Q

QUICK: A patient presents to you with epigastric pain. What are your ddx? (Give 10)

A

PUD
GORD
Cholelithiasis/biliary colic
Acute cholecystitis
Ascending cholangitis
AAA
Pancreatitis
Pancreatic neoplasm
Gastric neoplasm/Gastrinoma (malignant ulcers)
incarcerated paraesophageal hiatus hernia/gastric volvulus
Oesophagitis
Atypical MI

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19
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 H.pylori antigen testing
Seroloy (not used)

20
Q

How does the carbon 13 urea breath test work to detect H.pylori?

A

Fasting patient drinks a solution with carbon 13. H.Pylori metaboliszed the carbon-13 into CO2 which is radiolabelled and hence detected

21
Q

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

A

Triple Therapy (PAC500/PMC250)
PPI: 20mg Omeprazole PO
+ Clarithromycin 500/250mg
+ Amoxicillin 1g/Metronidazole 400mg respectiveley

All BD

22
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

23
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

24
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

25
Q

OGD + CLO testing is an important diagnostic investigation in PUD. What are the 3 main things it is used for in the setting of PUD?

A

1) CLO Diagnostic for H.Pylori
2) Cytology/histology for malignant cells
3) Ulcers: Screens for complications + therapeutic techniques

26
Q

CT abdomen is very useful in the workup for PUD. What information does it provide

A

CT Arterial phase to localize bleeding source and parenchymal phase to assess for complications such as pneumoperitoneum also

!+ Therapeutic if identified bleeding vessel to clip/coil/sclerose

27
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? Give the full list of investigation.

A

Uncomplicated PUD (peptic)

Bloods:
FBC w differentials (anemia and platelets)
Coag screen (coagulopathy and INR)
!!Group and Cross-match 4 units

Imaging:
!Erect! CXR for perforation (pneumoperitoneum)

CT Arterial phase to localize bleeding source + guide management (clip/coil/sclerose)
and parenchymal phase to assess for complications such as pneumoperitoneum also

Gastric Antral Biopsy via OGD is the gold standard which will be used to
1) CLO urease test (alternatively carbon 13 urea breath test, or stool, H.Pylori antigen)
2) Gastric Antral Mucosal Histology to rule out malignancy (gastrinoma)
OR you can screen for hypergastrinemia via fasting serum gastrin
3) Screen for complications Diagnostic and therapeutic for ulcers

28
Q

What is your full management plan for a patient presenting with uncomplicated PUD

A

1) Preventative/lifestyle:
Dietician for:
1) Smaller meals at regular intervals
2) Avoid late night food intake
3) Avoid gastric irritants (caffeine, chocolate, spicy food)
4) Weight loss (RF)

Quit.ie = Smoking cessation

AAA, education, limit to 14U => Alcohol control

2) Medical:
Triple Therapy (PAC500/PMC250)
PPI: 20mg Omeprazole PO
+ Clarithromycin 500/250mg
+ Amoxicillin 1g/Metronidazole 400mg respectiveley
All BD

Mucosal protection: Sucralfate
Ant-acid: Gaviscon
PPI alternative: H2 blockers - Ranitidine

!Followup - Repeat OGD to ensure healing

29
Q

What is the surgical management for a PUD complicated with haemorrhage?

A

Oversewing of ulcer/artery which can be escalated to a gastrotomy or laparotomy

30
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?

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)

CT angiography -> clip/coil/sclerose

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.
Oversewing of ulcer/artery which can be escalated to a gastrotomy or laparotomy

!Followup - Repeat OGD to ensure healing

31
Q

How is Perforation diagnosed?

A

Pneumoperitoneum on erect CXR

32
Q

What is the surgical management of PUD complicated with perforation?

A

Laparoscopic/open graham patch repair

33
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?

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)

Peritonitis leading to sepsis => Surgical treatment:
Laparoscopic/open graham patch repair

!Followup - Repeat OGD to ensure healing

34
Q

What is Graham Patch repair?

A

It involves closure of the ulcer followed by omental patch and fixation.

35
Q

Chronic fibrosis from recurrent ulceration leads to gastric outlet obstruction. They are highly associated with malignancy but this complication is rare. How will a patient present with gastric outlet obstruction as a complication of PUD?

How is it diagnosed?

How is it surgically managed?

What differential may also present the same way?

A

Episodic projectile vomiting often unrelated to eating. They are typically dehydrated and undernourished.

Hx of projectile vomiting + PFA showing highly dilated stomach

Gastrojejunostomy +/- Truncal Vagotomy and Pyeloplasty

Ddx: Gastric malignancy

36
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)

Initially aggressive resus and feeding with NJ!! tube with monitoring for refeeding syndrome

Surgery: Gastrojejunostomy +/- Truncal Vagotomy and Pyelooplasty

!Followup - Repeat OGD to ensure healing

37
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

38
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)

39
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

40
Q

Where is Gastrin produced?

A

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

41
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

42
Q

PUD is an imbalance between the protective mechanisms of the gastric mucus later, bicarbonate, prostaglandins etc… against the damaging effects of H.Pylori, NSAIDs, alcohol, cigarette smoking etc… What is the most important risk factor in the elderly for PUD?

A

Polypharmacy (many of them on NSAIDs anyway)

43
Q

What is waterbrash?

A

Reflux of acid into mouth

44
Q

What are the main side effects of PPIs?

A

Hyponatremia
Risk of C.Diff
AKI +CKD
Nutrient deficiencies : B12, Mg, Ca
Long term use = risk of PUD
GI disturbances

45
Q

What type of ulcers are more likely to bleed?
Perforate?

A

Anterior ulcers are more likely to perforate

Posterior ulcers are more likely to erode into nearby structures (gastroduodenal artery)

Ch. 3 - Upper GI Surgery (7 decks)

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