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MBChB Surgery > Peptic ulcer disease > Flashcards

Peptic ulcer disease Flashcards

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1
Q

Define peptic ulcer disease

A

Ulceration of the UGI mucosa which may extend to and through the muscle layers

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2
Q

Name protective mechanisms in the mucosa

A

Bicarbonate
Blood flow
Prostaglandins
Mucus

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3
Q

Name injurious mechanisms of mucosa

A

H.pylori
Gastric acid
Pepsin
NSAIDs

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4
Q

Which substance is produced by the gastric parietal cells?

A

Hydrochloric acid

Intrinsic factor

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5
Q

Which substance is produced by the gastric chief cells?

A

Pepsinogen

Gastric lipase

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6
Q

Where are HCl and pepsinogen produced?

A

Gastric fundus and corpus

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7
Q

Discuss the formation of hydrochloric acid

A
  1. H20 and C02 catalysed by carbonic anhydrase in parietal cell cytoplasm to form H2CO3
  2. H+ derived from H2CO3 dissociation
  3. H+ transported against [ ] gradient into gastric lumen via H+/K+ pump
  4. Chloride follows H+ from blood into lumen to form HCl
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8
Q

What is the normal pH of gastric fluid?

A

2-3

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9
Q

Name the main actions of HCl

A
  1. Denaturation and unfolding of complex protein structures
  2. Activation of pepsinogen to pepsin to digest protein polypeptides
  3. Killing microbials ingested with food
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10
Q

Name the 3 phases of gastric stimulation

A

Cephalic
Gastric
Intestinal

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11
Q

Discuss the cephalic phase of gastric stimulation

A

Thought, smell, sight, taste, chewing, swallowing -> vagus nerve activation

  1. Acetylcholine and Ca2+ activate parietal cells -> H+
  2. Gastrin releasing peptide activates antral G-cells -> gastrin
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12
Q

Explain the role of gastrin

A

Stimulates parietal cells to secrete H+ via Ca2+

Activates enterochromaffin-like cells to secrete H+

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13
Q

Discuss the gastric phase of gastric stimulation

A

Distension of stomach by food

  1. Vago-vagal and local stretch receptors -> parietal Ach receptors
  2. Peptides and amino acids stimulated antral G-cells -> gastrin
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14
Q

Discuss the intestinal phase of gastric stimulation

A

10% HCl
Chyme enters the duodenum
1. Stretch receptors stimulate secretin by S-cells and D-cells -> somatostatin and cholecystokinin
2. Entero-oxyntin via hormonal stimulation

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15
Q

Discuss the intestinal phase of gastric stimulation

A

Chyme enters the duodenum

  1. Stretch receptors stimulate secretin by S-cells and D-cells -> somatostatin and cholecystokinin
  2. Entero-oxyntin via hormonal stimulation
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16
Q

Which phase of gastric stimulation produces the most HCl?

A

Gastric (60%)

Cephalic (30%)
Intestinal (10%)

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17
Q

Which mechanisms protect the GIT mucosa from acid-peptic damage?

A
  1. Bicarbonate (gastric mucus cells, pancreatic secretions, biliary secretions)
  2. Viscus mucus
  3. Prostaglandins
  4. Hormones inhibit secretion (somatostatin, secretin, cholecystokinin)
  5. Alkaline saliva
  6. Good blood flow
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18
Q

How does H.pylori increase acid production?

A

Bacteria produces urease
Urea -> ammonia
Mucosa -> alkaline
G-cells stimulated to produce gastrin

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19
Q

Name factors that increase acid production

A 
H.pylori 
G-cell hyperplasia
G-cell adenoma 
Diet
Alcohol
Smoking
Steroids
NSAIDs
Physiological stress
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20
Q

Name common sites of peptic ulceration

A

1st part of duodenum
Pyloric antrum
Lesser gastric curvature

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21
Q

Name uncommon sites of peptic ulceration

A

Distal oesophagus
Distal duodenum
Stomach at gastro-jejunal anastomosis
Meckel’s diverticulum

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22
Q

What should you suspect if there is ulceration at unusual GIT sites?

A

Zollinger-Ellison syndrome

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23
Q

Discuss the presentation of gastric vs duodenal ulcers

A

Dyspepsia for both

Gastric

  • postprandial epigastric pain
  • weight loss

Duodenal

  • epigastric pain on fasting
  • wake up in middle of the night
  • weight gain
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24
Q

Name complications of peptic ulcers

A 
Perforation 
Bleeding
Gastric outlet obstruction
Oesophageal stricture
Fistulas
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25
What may lower oesophageal strictures be associated with?
Development of epiphrenic diverticulum due to weakness in mm wall and increased intraluminal pressure
26
Discuss the presentation of perforated peptic ulcer
Acute abdomen! ``` Sudden onset of severe pain Lucid interval Shock Increased HR, temp, RR Decreased BP Generalised abdominal tenderness Board-like rigidity ```
27
What is the reason for the lucid interval in PUD perforation?
Initial chemical peritonitis diluted by inflammatory exudate
28
Name sites of pus collections after perforated peptic ulcer
``` Free peritoneal Subphrenic Subhepatic Paracolic Interloop Pelvic Pleural (rare) ```
29
How is perforated peptic ulcer diagnosed?
``` Erect CXR Erect AXR Abdominal U/S CT abdomen Bloods (WCC, CRP, lipase, amylase, Hb, UKE, Cr, ABG, lactic acid, culture, CMP) ```
30
Does absence of free air on CXR exclude perforation?
No!
31
Give a differential for free intra-abdominal gas
Perforated - peptic ulcer - colonic diverticulum - appendicitis - distal ileum (typhoid) - caecum
32
Discuss the management of perforated peptic ulcer
``` Resus - supplemental O2 - fluids - keep warm - urinary catheter - CVP - oesophageal temperature - inotropes - analgesics - dextrose Empirical broad spectrum antibiotics Surgical intervention ```
33
Name indications for non-surgical treatment of perforated peptic ulcer
Minimal abdominal signs | Severe shock with comorbidities
34
How do you perform non-surgical treatment of perforated peptic ulcer?
Multiple U/S percutaneous drains | Pus for MC&S
35
Discuss the surgical intervention in perforated peptic ulcer
Omentopexy with 6 biopsies of affected GIT | Rinse abdomen thoroughly with 6L warm water
36
Discuss the follow up of post surgical perforated peptic ulcer patients
Full PPI and H.pylori eradication | 6w F/U with endoscopy
37
What is the first line therapy for eradicating H. pylori?
7-14d - PPI - clarithromycin - amoxicillin/metronidazole
38
What is the second line therapy for eradicating H. pylori?
Bismuth quadruple OR PPI Levofloxacin Amoxicillin
39
Name scoring systems used for outcome prediction in perforated peptic ulcer
Boey PULP Mannheim peritonitis index ASA
40
Which parameters are evaluated in the Boey score?
Presentation within 24h Presence of pre-op shock Comorbidities
41
Which parameters are evaluated in the PULP score?
``` Presentation within 24h Presence of pre-op shock ASA Presence of - AIDS - malignancy - liver failure - Cr>30mmol/l ```
42
Which parameters are evaluated in the Mannheim Peritonitis Index?
``` Age Gender Organ failure Peritonitis duration Site of perforation Diffuse peritonitis Level of exudate ```
43
Discuss the interpretation of the Boey score
1 point - 8% mortality, 47% morbidity 2 points - 33% mortality, 75% morbidity 3 points - 38% mortality, 77% morbidity
44
Name investigations in suspected peptic ulcer bleeding
``` FBC UKE Cr Lactic acid ABG INR PPT Platelets ```
45
Discuss grade 1 of hemorrhagic shock
``` <750ml/15% blood loss HR<100 Normal BP RR 14-20 Urine output >30ml/hr ```
46
Discuss grade 2 of hemorrhagic shock
``` 750-1500ml/15-30% blood loss HR 100-120 Normal BP RR 20-30 Urine output 20-30ml/hr ```
47
Discuss grade 3 of hemorrhagic shock
``` 1500-2000ml/30-40% blood loss HR 120-140 Decreased BP RR 30-40 Urine output 5-20ml/hr ```
48
Discuss grade 4 of hemorrhagic shock
``` >2000ml/40% blood loss HR >140 Decreased BP RR >35 Negligible urine output ```
49
From what grade of hemorrhagic shock is blood used as fluid replacement?
Grade 3
50
Which fluids do we use in hemorrhagic shock?
Crystalloids
51
Discuss the management of hemorrhagic shock due to peptic ulcer
Resus NGT Lavage the stomach Gastroendoscopy within 24h
52
Which classification is used for bleeding peptic ulcer?
Forrest
53
Discuss the Forrest Classification of bleeding peptic ulcer
I (active hemorrhage) - Ia spurting - Ib oozing II (recent hemorrhage) - IIa non-bleeding vessel - IIb adherent clot - IIc coffee ground III (no hemorrhage) - clean ulcer base
54
What is the risk of rebleed in a Forrest 1a on medical management?
90%
55
What is the risk of rebleed in a Forrest 1b on medical management?
10-20%
56
What is the risk of rebleed in a Forrest 2a on medical management?
50%
57
What is the risk of rebleed in a Forrest 2b on medical management?
25-30%
58
What is the risk of rebleed in a Forrest 2c on medical management?
7-10%
59
What is the risk of rebleed in a Forrest 3 on medical management?
3-5%
60
Which Forrest class is most prevalent?
Forrest 3
61
Discuss haemostatic procedures for bleeding peptic ulcer
Endoscopic - saline/adrenaline - thermal coagulation - argon laser coagulation - clip application Surgical - underrun - figure of 8 Angiographic embolization
62
Name metabolic changes in protracted vomiting
``` Hypovolemia Renal insufficiency Alkalosis Hyponatremia Hypokalemia Hypochloremia Starvation ```
63
Why should you not infuse KCl via a CVP line?
Causes asystole and cardiac arrest
64
Discuss the definitive treatment of GOO due to peptic ulcer
TPN for 10-12d -> trial of clear fluid po -> mixed fluids -> fluid diet IV PPI for 10-12d Dilation/stoma Post-op triple therapy
65
Discuss the presentation of gastro-colic fistula
``` Faecal eructations (belch) Postprandial diarrhea with undigested food ```
66
How is gastro-colic fistula diagnosed?
Barium enema | Gastroscopy w/ biopsy
67
Discuss the definitive management of gastro-colic fistula due to peptic ulcer
Endoscopic fibrin gel plug Surgical resection Post-op triple therapy

MBChB Surgery (38 decks)

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