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Year 2 > Gastric Diseases II > Flashcards

Gastric Diseases II Flashcards

1
Q

What is a peptic ulcer

A

Break in superficial epithelial lining that penetrates to the muscular mucosa of either the stomach or duodenum (fibrous base and increase in inflammatory cells)

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2
Q

Where are gastric ulcers commonly seen

A

Lesser curve of the stomach but can be found anywhere on the stomach

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3
Q

Are duodenal ulcers more or less common than gastric

A

More

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4
Q

What population do ulcers effect

A

Elderly and developing countries

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5
Q

What causes ulcers in the developing world

A

HELICOBACTER PYLORI

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6
Q

What gender is increainsgly getting ulcers

A

Women

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7
Q

Main causes of gastric ulcers

A
  1. Helicobacter pylori infection
  2. Drugs (NSAIDS, steroids and SSRI’s)
  3. Increased gastric acid secretion
  4. Smoking
  5. Delayed gastric emptying
  6. Blood group O
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8
Q

What disease can ulcers cause

A

Gastritis

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9
Q

What is the gastric mucosa protected by and what cells secrete it

A

Mucin

Gastric cells

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10
Q

Name two NSAIDS

A

Naproxen

Aspirin

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11
Q

What compound stimulates mucus secretion

A

Prostaglandins

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12
Q

What do NSAIDS inhibit

A

COX-1 (needed for prostaglandin synthesis)

So causes ulcers

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13
Q

IN what part of the stomach layer are helicobacter pylori found

A
  1. Mucous layer
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14
Q

How do helicobacter cause ulcers

A
  1. Destory mucin in mucosa
  2. Decreased duodenal HCO3- production increasing acidity of the stomach as there will be less alkali to buffer the acid
  3. Secretes urease, splitting yea into CO2 and ammonia
  4. Ammonia is toxic to gastric mucosa so less mucous is produced
  5. Secreted proteases, phospholipase and cytotoxin A attack gastric epithelium reducing mucous production
  6. Results in inflammatory response and less mucosal defence\7. Increases gastrin release (more HCL secretion by parietal cells + trigger release of histamine)
  7. Increases parietal cell mass = more acid production
  8. Decreased somatostatin
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15
Q

What three conditions are caused by H. pylori

A

Inflammation
Gastric cancer
Peptic ulcers

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16
Q

How does ischameia of gastric cells cause peptic ulcers

A
  1. Causes gastric cells to produce less mucin resulting in less protection from acid meaning acid is bale to damage mucosa resulting in an ulcer
  2. Cause day low pressure or atherosclerosis
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17
Q

How do we treat over production of HCL

A

PPI or H2 blockers

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18
Q

How does alcohol cause peptic ulcers

A

Direct toxic effect on gastric cells in high conc.

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19
Q

Clinical presentation of peptic ulcer disease

A
  1. Patient can point with one finger to the epigastrium as site of pain
  2. Pain of duodenal ulcers occurs at night and hunger
  3. Pain in both is relived by antacids
  4. Nausea, anorexia nd weight loss
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20
Q

red alarms for cancer and not PUD

A
  1. Unexplained weight loss
  2. Anaemia
  3. Evidence f GI bleeding
  4. Dysphagia
  5. Upper abdominal mass
  6. Persistent vomiting
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21
Q

Complications of a duodenal ulcer

A

Ulcer can get deeper and deeper unit lit hits an artery (gasproduodenal artery = massive haemorrhage)

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22
Q

Why can ulcers cause peritonitis

A

Acid enters the peritoneum

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23
Q

How do we diagnose for peritonitis

A

See air under the diaphragm on erect X-ray

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24
Q

How can an ulcer cause acute pancreatitis

A

If ulcer hits pancreas

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25
Q

What is the non-invasive test for peptic ulcers

A
  1. Serological test
  2. Breath test
  3. Stool antigen testing

(if test is positive then treatment ASAP)

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26
Q

When is an endoscopy used for Peptic ulcers

A

If gastric ulcer is present, needed for re-scope 6-8 weeks later to ensure no malignancy

Donen over 55 and red-alarm for cancer

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27
Q

What are non-invasive H.pylori testing for diagnosis

A
  1. Serology
  2. C-Urea breath test
  3. Stool antigen test
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28
Q

What are we trying to find in blood tests for H. pylori

A
  1. Detects IgG antibodies (not useful for confirming eradication or present of current infection since IgG takes 1 year to fall by 50%)
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29
Q

Pros of C-urea breath test

A
  1. Quick + Reliable test for H. Pylori
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30
Q

What is the C-urea breath test

A

Measures CO2 in breath after ingestion of C-urea

  1. Used to monitor infection after eradication
  2. Highly sensitive and specific
  3. No antibiotics or PPIs before test
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31
Q

What is the stool antigen test

A
  1. Immunoassay using monoclonal antibodies for detection of H.pylori
  2. Monitors efficacy of eradication therapy
  3. Patients should be off PPIs for 2 weeks before
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32
Q

What is invasive H.pylori testing

A

ENDOSCOPY

Biopsy urease test:

H.pylori secrete urease so will cause colour change of yellow to red

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33
Q

Why do we not give PPIs or antibiotics in biopsy urease test

A

Will give false negatives

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34
Q

How do you treat Peptic ulcers

A
  1. Reduce stress
  2. Avoid irritating food
  3. No smoking
  4. Stop NSAIDS
  5. H2 antagonist (CIMETIDINE)
  6. Surgery
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35
Q

How is H.pylori eradicated

A
  1. TRIPLE THERAPY:

PPI (Lansoprazole or Omeprazole)

  1. plus two of:
  2. METRONIDAZOLE, CLARITHROMYCIN, AMOXICILLIN, TETRACYCLINE, BISMUTH
  3. QUINOLONES (CIPROFLOXACIN, FUROZOLIDONE and RIFABUTIN)
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36
Q

What is a varices

A

A dilated vein which is at risk of rupture resulting in haemorrhage and in the GI system can result in GI bleeding

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37
Q

What veins form the Hepatic portal vein

A

Superior mesenteric and splenic veins

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38
Q

Role of the hepatic portal vein

A

Carries nutrient rich blood from GI tract, gallbladder, pancreas and spleen to the liver

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39
Q

What vein returns blood from the liver to the heart

A

Inferior vena cava

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40
Q

Pressure in the hepatic portal vein

A

5-8 mmHg

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41
Q

What is pre-hepatic portal hypertension

A

Blockage of the hepatic portal vein BEFORE the liver

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42
Q

What is intra-hepatic portal hypertension

A

Distortion of the liver architecture, either pre-sinusoidal (Schistosomiasis) or post-sinusoidal (cirrhosis)

43
Q

What happens to the venous system when portal pressure rises above 10-12mmHg

A

Compliant venous system DILATES and varies form within the systemic venous system

44
Q

When do gastro-oesophageal varies tend to rupture

A

When pressure exceeds 12mmHg

45
Q

What condition usually causes gastro-oesophageal varices to form

A
  1. Cirrhosis
46
Q

When does gastro-oeosphagela varies result in bleeding other than pressure

A
  1. If they are large
  2. Red signs at endoscopy
  3. Sevre liver disease
47
Q

Where do varies tend to develop

A

Lower Oesophagus

Gastric Cardia

48
Q

What are the main causes of varices

A
  1. Alcoholism and viral cirrhosis = portal hypertension
49
Q

What causes pre-hepatic portal hypertension

A

Thrombosis in portal or splenic vein

50
Q

What causes intra=hepatic portal hypertension

A
  1. Cirrhosis (most common cause)
  2. Schistosomiasis
  3. Sarcoidosis
  4. Congenital hepatic fiborsis
51
Q

What is sarcoidosis

A

Accumulation of inflammatory cells (forms granulomas)

52
Q

Post-hepatic portal hypertension causes

A
  1. Budd-Chiari syndrome
  2. RHF
  3. Constrictive Pericarditis
53
Q

What is Budd-chiari syndrome

A

Hepatic vein obstruction by tumour or thrombosis

54
Q

Risk factors for portal hypertension

A
  1. Cirrhosis
  2. Portal Hypertension
  3. Schistosomiasis Infection
  4. Alcoholism
55
Q

How does liver injury and fibrogenesis result in portal hypertension

A
  1. Contraction of activated myofibroblasts increases resistance to blood flow
  2. Leads to portal hypertension
  3. Splanchnic vasodilatation
  4. Drop in BP
  5. Increased CO to compensate
  6. Retention of Na and water to increase water volume
  7. Hyperdynamic circulation
  8. Formation of collaterals between portal and systemic systems
56
Q

Clinical presentation of portal hypertension

A
  1. Haematemesis
  2. Abdo pain
  3. Shock (major blood loss)
  4. Fresh rectal bleeding (associated with shock in acute massive GI bleed)
  5. Hypotension and tachycardia
  6. Pallor
  7. Suspect varies as the cause of GI bleeding if there is alcohol abuse or cirrhosis
  8. Signs of chronic liver damage
  9. Splenomegaly
  10. Ascites
  11. Hyponaturaemia
57
Q

What is Haematemesis

A

Vomiting blood

58
Q

How is portal hypertension diagnosed

A

Endoscopy (allows us to find a source)

59
Q

How is portal hypertension treated

A
  1. Resus until haemodynamically stable
  2. If anaemic, blood transfusion to get Hb to 80g/l
  3. Correct clotting abnormalities (Vit K and platelet transfusion)
  4. Vasopressin (cause vasoconstriction)
  5. Prophylactic antibiotics
  6. Vatical banding
  7. Ballon tamponade
  8. TIPS
60
Q

What vasopressin is given for portal hypertension

A

IV TERLIPRESSIN

IV SOMATOSTATIN

61
Q

When is IV SOMATOSTATIN given instead of TERLIPRESSIN

A

During IHD (TERLIPRESSIN is contraindicated here)

62
Q

What is vatical banding

A

Where a band is put around avarice using an endoscope, after a few days the banded varix degenerates and falls off leaving a scar

63
Q

Role of a Ballon tamponade

A

Reduces bleeding by placing pressure on avarice if banding fails

64
Q

What is Transjugular intrahepatic portoclaval shunt

A

Shunt between systemic or portal systems which reduces sinusoidal and portal vein pressure

65
Q

When is TIPS done

A

Only when bleeding can’t be controlled

66
Q

How is portal hypertension prevented

A

Non-selective B-blocker

Variceal banding repeatedly

Liver Transplant

67
Q

What non-selective B-blocker is given

A

Propranolol

68
Q

What is achalasia

A
  1. Oesophagus can’t do peristalsis

2. Impaired relaxation of the lower oesophageal sphincter

69
Q

What happens to the lower oesophageal pressure in Achalasia

A

Elevated

70
Q

Why does the lower oesophageal sphincter fail to relax in achalasia

A

Degeneration of the mesenteric plexus of the oesophagus with reduction of ganglion cell numbers

71
Q

Clinical presentation of achalasia

A
  1. Dysphagia for fluid and solids
  2. Regurgitation of food particularly at night and aspiration pneumonia is a complication
  3. Substernal cramps
  4. Weight loss
  5. Spontaneous chest pains (oesophageal spasms) - could be misdiagnosed as cardiac pain
72
Q

How is Achalasia diagnosed

A
  1. CXR
  2. Barium swallow
  3. Manometry (DIAGNOSTIC)
  4. CT and oeosphagoscopy
73
Q

What would a CXR show in achalasia

A
  1. Dilated oesophagus

2. Fluid behind the heart

74
Q

What would a barium swallow show in achalasia

A
  1. Shows lack of peristalsis

2. Lower end shows birds beak due to failure of sphincter to relax

75
Q

What would a manometry show in achalasia

A
  1. Peristalsis of the oesophagus and failure of relaxation of the lower oesophageal sphincter
76
Q

Why is a CT and oeosphagoscopy done in achalasia

A

Rule out carcinoma at lower end of the oesophagus

77
Q

How is achalasia treated

A
  1. Relieve SYMPTOMS
  2. Medication to relax LOS
  3. Surgery
78
Q

What drugs would relax the lower oeopshageal sphincter

A
  1. NIFEDIPINE
  2. NITRATES
  3. SILDENAFIL
79
Q

What surgeries would be used to treat achalasia

A
  1. Endoscopic balloon dilatation to open sphincter
  2. Heller’s cardiomyotomy (surgical division of LOS and PPIs)
  3. Botox injections to relax sphincter TEMPORARILY
80
Q

Complications of achalasia treatment

A

Incidence of squamous carcinomas increased risk

81
Q

What is scleroderma

A

Multi-system disease that effects the body by hardening connective tissues

82
Q

In what gender does Scleroderma effect

A

Females

83
Q

Risk factors of Scleroderma

A

Vinyl Chloride

Silica dust

84
Q

Why is there diminished peristalsis and oesophageal clearance in scleroderma

A

Replacement of smooth muscle by fibrous tissue

LOS pressure decreased = GORD and mucosal damage

Strictures may develop

85
Q

Clinical presentation of achalasia

A
  1. Initially no symptoms

2. Dysphagia and heartburn occur as the oesophagus becomes more severely involved

86
Q

How is achalasia diagnosed

A
  1. Barium swallow
  2. CXR
  3. Manometry
87
Q

Role of barium swallow in achalasia diagnosis

A

Confirms impaired oesophageal motility

88
Q

How is achalasia treated

A

Same as GORD (PPI for lansoprazole)

89
Q

What is gastritis

A

Inflammation that is associated with mucosal injury

90
Q

What is gastropathy

A

Epithelial cell damage and regeneration WITHOUT inflammation - NSAIDs and Aspirin caused

91
Q

Causes of gastritis

A
  1. Helicobacter pylori infection
  2. Autoimmune gastritis
  3. Viruses (cytomegalovirus + herpes simplex)
  4. Dudoenogastric reflux (bile salts enter stomach and damage mucin protection resulting in gastritis)
  5. Crohns
  6. Mucosal ischaemia (reduced blood supply to mucosal cells means less mucin produced so acid can induce gastritis)
  7. Increased acid (destroy mucin) - increased by stress
  8. Aspirin and NSAIDs
  9. Alcohol
92
Q

How does helicobacter pylori cause gastritis

A
  1. Gastric mucus degradation and increased mucosal permeability which is cytotoxic to gastric epithelium (since H. pylori urease converts urea to ammonia and CO2 which is toxic since ammonia and H+ form ammonium which is toxic to mucosa)
93
Q

What parts of the stomach is effected by autoimmune gastritis

A

Affects funds and body of the stomach

94
Q

How does autoimmune gastritis effect the stomach

A
  1. Leads to atrophic gastritis

2. Loss of parietal cells with intrinsic factor deficiency resulting in pernicious anaemia

95
Q

How do aspirin and NSAIDs result in gastritis

A

Inhibit COX-1 and less mucus is produced

96
Q

Clinical presentation of gastritis

A
  1. Nausea
  2. Abdo bleeding
  3. Epigastric pain
  4. Vomiting
  5. Indigestion
  6. Haematemesis
97
Q

Differential diagnosis of gastritis

A
  1. PUD
  2. GORD
  3. Non-ulcer dyspepsia
  4. gastric lymphoma
  5. Gastric carcinoma
98
Q

How is gastritis diagnosed

A
  1. Endoscopy
  2. Biopsy
  3. H. pylori urea breath test
  4. H. pylori stool antigen test
99
Q

How is gastritis treated

A

1 . Remove causative agents such as alcohol

  1. Reduce stress
  2. H. pylori eradication (7-14 days)
100
Q

How is H.pylori eradication confirmed

A

Urea breath or faecal antigen test

101
Q

How is H.pylori eliminated

A

TRIPLE TEHRAPY:
PPI (Lansopraozle or Omeprazole)

and TWO of:

  1. METRONIDAZOLE, CLARITHROMYCIN, AMOXICILLIN, TETRACYCLINE, BISMUTH
  2. Quinolones (CIPROFLOXACIN, FUROZOLIDONE and RIFABUTIN)
102
Q

What drugs are given to treat gastritis

A

H2 antagonist (RANITIDINE or CIMETIDINE)

PPIs (LANSOPRAZOLE or OMEPRAZOLE)

Antacids

103
Q

How is gastritis prevented

A

Give PPIs alongside NSAIDs - prevents bleeding from acute stress ulcers and gastritis which is often seen with ill patients - especially burns patients

Year 2 (155 decks)

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