Gastric conditions Flashcards

1
Q

What is dyspepsia (7)

A
AKA INDIGESTION
Is a collective name for a group of symptoms:
Upper abdo pain/retrosternal pain
Anorexia - appetite loss
Nausea
Vomiting
Bloating
Fullness/early satiety
Heartburn
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2
Q

When is an UGIE indicated (6)

A
If they have ALARM features:
Anorexia 
Loss of weight
Anaemia - iron deficiency anaemia
Recent onset - >55yrs age
Melaena/haematamesis & Masses
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3
Q

What drugs can cause dyspepsia (7)

A
NSAIDs
Steroids
Bisphosphonates
CCBs
Nitrates
Theophyllines
OTC
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4
Q

Peptic ulcer MOST COMMON cause

A

H. pylori infection

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5
Q

Duodenal ulcers are more likely caused by H. pylori infection but what are gastric ulcers more commonly caused by

A

NSAIDs

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6
Q

Peptic ulcer pathophysiology (2)
+ 2 types of peptic ulcers
+ is acid secretion high or normal or low in the respective types

A

Imbalance between acid secretion and level of mucous protection –> epithelial damage and subsequent mucosal/submucosal damage

DU - acid hyper secretion
GU - normal/low acid secretion

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7
Q

Peptic ulcer risk factors

A

H pylori infection
NSAIDs
Smoking

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8
Q

Peptic ulcer symptoms (5) + signs (1)

-location of pain + 3 characteristics of the pain

A

Symptoms:
Dyspepsia - epigastric pain
-pain worsen after eating in GU/better after eating in DU
-pain often worsens at night
-pain can radiate to back in DU perforated

Nausea + vomiting

Signs:
Epigastric tenderness

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9
Q

Peptic ulcer investigations (3)

A

Urea breath test/H.pylori faecal antigen test
UGIE
FBC (ordered if anaemic or evidence of GI bleed)

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10
Q

Peptic ulcer treatment (4)

  • if due to H. pylori (3)
  • medical measures (2)
  • triggers to avoid
  • when is surgery indicated
A

If caused by H. pylori then eradication therapy - amoxycillin (or metronidazole if penicillin allergic) + clarithromycin + omeprazole

PPI - omeprazole
OR Hydrogen receptor blocker - ranitidine

Stop NSAIDs if being used

Surgery if ulcer –> complicated peptic ulcer disease

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11
Q

Initial treatment for acute bleeding ulcer (2)

A

Blood transfusion

Endoscopic ligation

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12
Q

Complications of peptic ulcer (4)

A

Acute bleed (haemorrhage) - haematemesis (coffee ground vomit) or melaena

Chronic bleed - iron deficiency anaemia

Perforation - ulcer can erode through stomach wall into peritoneum –> peritonitis

Stricture –> gastric outlet obstruction

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13
Q

Where can you get peptic ulcers (3)

A

Lower oesophagus
Stomach (body and antrum)
Duodenum (1st/2nd part)

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14
Q

3 types of gastritis

A

Type A - autoimmune
Type B - bacterial
Type C - chemical

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15
Q

What is gastritis

A

Gastric mucosal lining inflammation

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16
Q

Type A (autoimmune) gastritis pathophysiology (4)

A

Autoantibodies attack parietal cells + intrinsic factor –> atrophy of parietal cells –> decreased acid secretion + loss of intrinsic factor –> vit B12 deficiency

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17
Q

Type A gastritis risk factors (2)

A

Existing autoimmune diseases

Critically ill

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18
Q

Gastritis symptoms (4)

A

Dyspepsia - epigastric pain
Nausea
Vomiting
Loss of appetite

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19
Q

Type A gastritis investigations (6)

  • 2 investigations to rule out H. pylori
  • imaging
  • bloods (for a certain vitamin and 2 autoantibodies)
A

Urea breath test - to exclude H. pylori
H pylori faecal antigen test - to exclude H. pylori

Endoscopy + biopsy

Serum vitamin B12
Parietal cell autoantibodies
Intrinsic factor autoantibodies

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20
Q

Type A gastritis treatment (3)

A

CORRECT VITAMIN DEFICIENCY
-Vit B12 injection

Hydrogen receptor blocker - ranitidine
PPI - omeprazole

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21
Q

Type B gastritis cause

A

H pylori infection

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22
Q

Type B (bacterial) gastritis pathophysiology

A

H pylori causes inflammation of gastric mucosa –> increased mucosal permeability

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23
Q

Difference between H. pylori infection in upper stomach and lower stomach
(describe if the acid secretion is increased or decreased and what disease it is more likely to progress on to)

A

If H. pylori infects upper stomach –> gastritis of body –> DECREASED ACID PRODUCTION –> gastric cancer

If H. pylori infects lower stomach –> antral gastritis –> INCREASED ACID PRODUCTION –> duodenal disease

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24
Q

Type B gastritis/H. pylori investigations (4)

  • tests to confirm H. pylori
  • imaging + histological diagnosis
A

Urea breath test - to confirm H. pylori

H. pylori faecal antigen test - to confirm H. pylori

Endoscopy + biopsy

Serology - IgG against H. pylori

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25
Q

Type B gastritis treatment (H.pylori eradication therapy)

A

Eradication therapy for 14 days (2 antibiotics + 1 PPI):

  • Clarithromycin
  • Amoxycillin (or metronidazole if penicillin allergic)
  • Omeprazole
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26
Q

Type C gastritis risk factors (3)

A

Long term use of

  • NSAIDs
  • alcohol

Chronic bile reflux

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27
Q

Type C (chemical) gastritis pathophysiology

A

Caused by Drugs (NSAIDs), alcohol, bile reflux

NSAIDs reduce prostaglandin production (which protects stomach) –> inflammation

28
Q

Type C gastritis investigations (4)

  • 2 investigations to rule out H. pylori
  • imaging
  • bloods
A

Urea breath test - to rule out H .pylori
H pylori faecal antigen test - to rule out H .pylori
Endoscopy + biopsy
FBC

29
Q

Type C gastritis treatment

A

Stop NSAIDs/alcohol
Hydrogen receptor blockers - ranitidine
PPI - omeprazole

30
Q

Complications of gastritis

A

Chronic gastritis
Peptic ulcer disease
Vitamin B deficiency
Achlorhydria - decreased/absent gastric acid production

31
Q

What is gastric outlet obstruction

A

Obstruction of pylorus –> DELAYED gastric emptying

32
Q

Gastric outlet obstruction causes (3)

A

Fibrotic stricture from healing of gastric ulcer
Tumour - gastric cancer, pancreatic cancer (in the head)
Pyloric stenosis

33
Q

Gastric outlet obstruction symptoms (3) and signs (2)

A

Symptoms:
Postprandial nausea/vomiting –> alkalosis
Epigastric pain
Early satiety

Signs:
Abdominal distension/bloating
Weight loss

34
Q

Gastric outlet obstruction investigations

  • bloods (2)
  • imaging (3)
A

U+Es - low K+ due to prolonged vomiting
RFTs (impaired) - creatine may be high due to abnormal renal function, low albumin

UGIE - to see any mechanical obstruction, i.e. pyloric stenosis or tumour
Abdo XR - to see if there’s any SI obstruction
Gastric emptying scintigraphy - assesses for how much food is retained in stomach after 4 hours; would indicate GASTROPARESIS

35
Q

Gastric outlet obstruction treatment

  • medical (2)
  • surgical (2)
A

Pro-kinetics - promote GI motility so faster gastric emptying
Anti-emetics

Endoscopic balloon dilation - if stricture present from a healed ulcer or pyloric stenosis
Surgery - antrectomy/gastrectomy/gastrojejunostomy if serious

36
Q

Gastric cancer is usually what type of tumour

A

Adenocarcinoma

37
Q

Gastric cancer pathophysiology (3)

A

From chronic gastritis, cancer can develop through phases of intestinal metaplasia –> intestinal dysplasia –> carcinoma

Loss of tumour suppressor genes (e.g. p53)/ Overexpression of oncogenes

38
Q

Gastric cancer risk factors (5)

A

Chronic H pylori infection
Pernicious anaemia - from B12 deficiency
High nitrate diet

Smoking
Family history of gastric cancer

39
Q

Gastric cancer symptoms (3) and signs (4)

-usually asymptomatic until ADVANCED

A

Symptoms:
Dyspepsia - epigastric pain
Nausea/vomiting
Dysphagia - not as common; more so if proximal tumour

Signs:
Weight loss/anorexia
Acute bleeding
-haematamesis
-melaena
Chronic bleeding
-Iron deficiency anaemia
40
Q

Gastric cancer diagnostic investigation + staging investigations (4)

A

UGIE + BIOPSY

Staging

  • EUS,
  • CXR,
  • CT chest/abdo/pelvis,
  • PET CT (more sensitive than plain CT for metastases)
41
Q

Gastric cancer treatment

  • curative (1)
  • non-surgical candidate (1)
  • palliative for advanced/metastatic
A

Gastrectomy
+/- perioperative/postoperative chemotherapy (given depending on stage of cancer at diagnosis)

Non-surgical - chemoradiotherapy

Chemoradiotherapy

42
Q

Complications of gastric cancer (4)

A

Malnutrition
Gastric obstruction - may obstruct pylorus
GI bleed
Gastric perforation - tumour can erode through wall –> peritonitis

43
Q

4 ways that gastric cancer can spread

A

Direct
Lymphatic
Blood
Transcoelomic (spreads into peritoneal cavity)

44
Q

5 places gastric cancer spreads to

A

Lymph nodes
Liver
Peritoneum

Lungs
Bone marrow

45
Q

Prognosis of gastric cancer

A

5 year survival rate less than 20%

46
Q

Differentials of haematemesis (5)

A

Peptic Ulcer
Gastric/oesophageal carcinoma
Oesophageal varices
Mallory Weiss Tear

47
Q

Benign disorders of the oesophagus (3)

A

GORD
Peptic ulceration (can get this in lower oesophagus)
Barrett’s oesophagus

48
Q

Does H. pylori increase or decrease gastric acid secretion in patients with

  • duodenal ulcers
  • gastric cancer
A

DU - increases acid secretion

Gastric cancer - decreases acid secretion

49
Q

Organic v functional dyspepsia

A

Organic - definitive pathological cause

Functional - abnormal function but normal structure

50
Q

If ALARM features indicate dyspepsia, what investigation should be done

A

UGIE

51
Q

Describe the characteristics of H.pylori (4)

A

Gram negative, spiral shaped, microaerophilic, flagellated

52
Q

H. pylori only resides where

A

Gastric surface MUCOSA layer, doesn’t penetrate epithelium below

53
Q

What characteristics of H.pylori allows it to escape from the toxic gastric acid around it (2)

A

Its tail (flagellated) allows it to burrow into the mucous layer (but doesn’t burrow through epithelium)

It produces urease which creates a halo of alkalinity around the bacteria

54
Q

H. pylori typically has to to chronically infect what part of the stomach to cause gastric cancer

A

Body

55
Q

H. pylori typically has to to chronically infect what part of the stomach to cause duodenal disease

A

Antrum

56
Q

How does the urea breath test detect H.pylori

A

swallow urea labelled with radioactive carbon

If isotope-labelled CO2 detected in exhaled breath then indicates that the urea swallowed was split by urease (produced by H pylori) into ammonia and CO2 (UREASE DEPENDENT TEST)

57
Q

What enzyme does H.pylori produce

A

Urease

58
Q

Invasive investigations of H.pylori (non invasive = serology, urea breath test, faecal H.pylori antigen test) (2)

A

Gastric biopsy
Rapid slide urease test - gastric biopsy placed onto gel, the urease produced by H pylori (if present) will break down the yellow gel and turn it pink (UREASE DEPENDENT TEST

59
Q

What is a fundoplication + what is it done for

A

Wrapping fundus of stomach around lower oesophagus to create a valve around the LOS to tighten it –> reduces reflux

Done for severe GORD

60
Q

Name a common approach used in total gastrectomy

A

Roux en Y

61
Q

Treatment of acute bleeding peptic ulcer (4)

A

Endoscopic therapy

  • injecting adrenaline - constricts ulcer area
  • cautery to burn/scar bleeding vessel
  • endoclip

PPI

62
Q

Duodenal ulcers are relieved after what

A

Meals

Gastric ulcers tend to WORSEN after meals

63
Q

If peptic ulcer has perforated and caused bleeding, what are the 2 signs of the bleeding

A

Overt bleeding (visible)

  • Haematemesis - coffee ground vomit
  • Melaena - dark foul smelling stool

Occult bleeding
-stool haem test +ve

64
Q

What is gastroparesis (similar to gastric outlet obstruction but not exactly the same)

A

NON-MECHANICAL OBSTRUCTION of pylorus (i.e. not due to a physical abnormality like pyloric stenosis or a tumour or ulcer) –> DELAYED gastric emptying

65
Q

Paraneoplastic complication/manifestation of gastric cancer on the skin

A

SEBORRHOEIC KERATOSES (‘stuck on’ lesions)