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MBChB Surgery > Peptic ulcer disease > Flashcards

Peptic ulcer disease Flashcards

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
Q

What may lower oesophageal strictures be associated with?

A

Development of epiphrenic diverticulum due to weakness in mm wall and increased intraluminal pressure

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26
Q

Discuss the presentation of perforated peptic ulcer

A

Acute abdomen!

Sudden onset of severe pain
Lucid interval
Shock
Increased HR, temp, RR
Decreased BP 
Generalised abdominal tenderness
Board-like rigidity
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27
Q

What is the reason for the lucid interval in PUD perforation?

A

Initial chemical peritonitis diluted by inflammatory exudate

28
Q

Name sites of pus collections after perforated peptic ulcer

A 
Free peritoneal
Subphrenic
Subhepatic
Paracolic
Interloop
Pelvic
Pleural (rare)
29
Q

How is perforated peptic ulcer diagnosed?

A 
Erect CXR 
Erect AXR 
Abdominal U/S
CT abdomen
Bloods (WCC, CRP, lipase, amylase, Hb, UKE, Cr, ABG, lactic acid, culture, CMP)
30
Q

Does absence of free air on CXR exclude perforation?

A

No!

31
Q

Give a differential for free intra-abdominal gas

A

Perforated

  • peptic ulcer
  • colonic diverticulum
  • appendicitis
  • distal ileum (typhoid)
  • caecum
32
Q

Discuss the management of perforated peptic ulcer

A 
Resus 
- supplemental O2
- fluids
- keep warm
- urinary catheter
- CVP
- oesophageal temperature 
- inotropes
- analgesics
- dextrose 
Empirical broad spectrum antibiotics
Surgical intervention
33
Q

Name indications for non-surgical treatment of perforated peptic ulcer

A

Minimal abdominal signs

Severe shock with comorbidities

34
Q

How do you perform non-surgical treatment of perforated peptic ulcer?

A

Multiple U/S percutaneous drains

Pus for MC&S

35
Q

Discuss the surgical intervention in perforated peptic ulcer

A

Omentopexy with 6 biopsies of affected GIT

Rinse abdomen thoroughly with 6L warm water

36
Q

Discuss the follow up of post surgical perforated peptic ulcer patients

A

Full PPI and H.pylori eradication

6w F/U with endoscopy

37
Q

What is the first line therapy for eradicating H. pylori?

A

7-14d

  • PPI
  • clarithromycin
  • amoxicillin/metronidazole
38
Q

What is the second line therapy for eradicating H. pylori?

A

Bismuth quadruple

OR

PPI
Levofloxacin
Amoxicillin

39
Q

Name scoring systems used for outcome prediction in perforated peptic ulcer

A

Boey
PULP
Mannheim peritonitis index
ASA

40
Q

Which parameters are evaluated in the Boey score?

A

Presentation within 24h
Presence of pre-op shock
Comorbidities

41
Q

Which parameters are evaluated in the PULP score?

A 
Presentation within 24h
Presence of pre-op shock
ASA
Presence of 
- AIDS
- malignancy
- liver failure
- Cr>30mmol/l
42
Q

Which parameters are evaluated in the Mannheim Peritonitis Index?

A 
Age
Gender
Organ failure
Peritonitis duration
Site of perforation
Diffuse peritonitis
Level of exudate
43
Q

Discuss the interpretation of the Boey score

A

1 point - 8% mortality, 47% morbidity
2 points - 33% mortality, 75% morbidity
3 points - 38% mortality, 77% morbidity

44
Q

Name investigations in suspected peptic ulcer bleeding

A 
FBC
UKE
Cr
Lactic acid
ABG
INR
PPT
Platelets
45
Q

Discuss grade 1 of hemorrhagic shock

A 
<750ml/15% blood loss
HR<100
Normal BP 
RR 14-20
Urine output >30ml/hr
46
Q

Discuss grade 2 of hemorrhagic shock

A 
750-1500ml/15-30% blood loss
HR 100-120
Normal BP
RR 20-30
Urine output 20-30ml/hr
47
Q

Discuss grade 3 of hemorrhagic shock

A 
1500-2000ml/30-40% blood loss
HR 120-140
Decreased BP
RR 30-40 
Urine output 5-20ml/hr
48
Q

Discuss grade 4 of hemorrhagic shock

A 
>2000ml/40% blood loss
HR >140 
Decreased BP
RR >35 
Negligible urine output
49
Q

From what grade of hemorrhagic shock is blood used as fluid replacement?

A

Grade 3

50
Q

Which fluids do we use in hemorrhagic shock?

A

Crystalloids

51
Q

Discuss the management of hemorrhagic shock due to peptic ulcer

A

Resus
NGT
Lavage the stomach
Gastroendoscopy within 24h

52
Q

Which classification is used for bleeding peptic ulcer?

A

Forrest

53
Q

Discuss the Forrest Classification of bleeding peptic ulcer

A

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
Q

What is the risk of rebleed in a Forrest 1a on medical management?

A

90%

55
Q

What is the risk of rebleed in a Forrest 1b on medical management?

A

10-20%

56
Q

What is the risk of rebleed in a Forrest 2a on medical management?

A

50%

57
Q

What is the risk of rebleed in a Forrest 2b on medical management?

A

25-30%

58
Q

What is the risk of rebleed in a Forrest 2c on medical management?

A

7-10%

59
Q

What is the risk of rebleed in a Forrest 3 on medical management?

A

3-5%

60
Q

Which Forrest class is most prevalent?

A

Forrest 3

61
Q

Discuss haemostatic procedures for bleeding peptic ulcer

A

Endoscopic

  • saline/adrenaline
  • thermal coagulation
  • argon laser coagulation
  • clip application

Surgical

  • underrun
  • figure of 8

Angiographic embolization

62
Q

Name metabolic changes in protracted vomiting

A 
Hypovolemia
Renal insufficiency
Alkalosis
Hyponatremia 
Hypokalemia 
Hypochloremia 
Starvation
63
Q

Why should you not infuse KCl via a CVP line?

A

Causes asystole and cardiac arrest

64
Q

Discuss the definitive treatment of GOO due to peptic ulcer

A

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
Q

Discuss the presentation of gastro-colic fistula

A 
Faecal eructations (belch) 
Postprandial diarrhea with undigested food
66
Q

How is gastro-colic fistula diagnosed?

A

Barium enema

Gastroscopy w/ biopsy

67
Q

Discuss the definitive management of gastro-colic fistula due to peptic ulcer

A

Endoscopic fibrin gel plug
Surgical resection
Post-op triple therapy

MBChB Surgery (38 decks)

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