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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
What is the non-invasive test for peptic ulcers
1. Serological test 2. Breath test 3. Stool antigen testing (if test is positive then treatment ASAP)
26
When is an endoscopy used for Peptic ulcers
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
27
What are non-invasive H.pylori testing for diagnosis
1. Serology 2. C-Urea breath test 3. Stool antigen test
28
What are we trying to find in blood tests for H. pylori
1. Detects IgG antibodies (not useful for confirming eradication or present of current infection since IgG takes 1 year to fall by 50%)
29
Pros of C-urea breath test
1. Quick + Reliable test for H. Pylori
30
What is the C-urea breath test
Measures CO2 in breath after ingestion of C-urea 2. Used to monitor infection after eradication 3. Highly sensitive and specific 4. No antibiotics or PPIs before test
31
What is the stool antigen test
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
32
What is invasive H.pylori testing
ENDOSCOPY Biopsy urease test: H.pylori secrete urease so will cause colour change of yellow to red
33
Why do we not give PPIs or antibiotics in biopsy urease test
Will give false negatives
34
How do you treat Peptic ulcers
1. Reduce stress 2. Avoid irritating food 3. No smoking 4. Stop NSAIDS 5. H2 antagonist (CIMETIDINE) 6. Surgery
35
How is H.pylori eradicated
1. TRIPLE THERAPY: PPI (Lansoprazole or Omeprazole) 2. plus two of: 1. METRONIDAZOLE, CLARITHROMYCIN, AMOXICILLIN, TETRACYCLINE, BISMUTH 2. QUINOLONES (CIPROFLOXACIN, FUROZOLIDONE and RIFABUTIN)
36
What is a varices
A dilated vein which is at risk of rupture resulting in haemorrhage and in the GI system can result in GI bleeding
37
What veins form the Hepatic portal vein
Superior mesenteric and splenic veins
38
Role of the hepatic portal vein
Carries nutrient rich blood from GI tract, gallbladder, pancreas and spleen to the liver
39
What vein returns blood from the liver to the heart
Inferior vena cava
40
Pressure in the hepatic portal vein
5-8 mmHg
41
What is pre-hepatic portal hypertension
Blockage of the hepatic portal vein BEFORE the liver
42
What is intra-hepatic portal hypertension
Distortion of the liver architecture, either pre-sinusoidal (Schistosomiasis) or post-sinusoidal (cirrhosis)
43
What happens to the venous system when portal pressure rises above 10-12mmHg
Compliant venous system DILATES and varies form within the systemic venous system
44
When do gastro-oesophageal varies tend to rupture
When pressure exceeds 12mmHg
45
What condition usually causes gastro-oesophageal varices to form
1. Cirrhosis
46
When does gastro-oeosphagela varies result in bleeding other than pressure
1. If they are large 2. Red signs at endoscopy 3. Sevre liver disease
47
Where do varies tend to develop
Lower Oesophagus | Gastric Cardia
48
What are the main causes of varices
1. Alcoholism and viral cirrhosis = portal hypertension
49
What causes pre-hepatic portal hypertension
Thrombosis in portal or splenic vein
50
What causes intra=hepatic portal hypertension
1. Cirrhosis (most common cause) 2. Schistosomiasis 3. Sarcoidosis 4. Congenital hepatic fiborsis
51
What is sarcoidosis
Accumulation of inflammatory cells (forms granulomas)
52
Post-hepatic portal hypertension causes
1. Budd-Chiari syndrome 2. RHF 3. Constrictive Pericarditis
53
What is Budd-chiari syndrome
Hepatic vein obstruction by tumour or thrombosis
54
Risk factors for portal hypertension
1. Cirrhosis 2. Portal Hypertension 3. Schistosomiasis Infection 4. Alcoholism
55
How does liver injury and fibrogenesis result in portal hypertension
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
Clinical presentation of portal hypertension
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
What is Haematemesis
Vomiting blood
58
How is portal hypertension diagnosed
Endoscopy (allows us to find a source)
59
How is portal hypertension treated
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
What vasopressin is given for portal hypertension
IV TERLIPRESSIN IV SOMATOSTATIN
61
When is IV SOMATOSTATIN given instead of TERLIPRESSIN
During IHD (TERLIPRESSIN is contraindicated here)
62
What is vatical banding
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
Role of a Ballon tamponade
Reduces bleeding by placing pressure on avarice if banding fails
64
What is Transjugular intrahepatic portoclaval shunt
Shunt between systemic or portal systems which reduces sinusoidal and portal vein pressure
65
When is TIPS done
Only when bleeding can't be controlled
66
How is portal hypertension prevented
Non-selective B-blocker Variceal banding repeatedly Liver Transplant
67
What non-selective B-blocker is given
Propranolol
68
What is achalasia
1. Oesophagus can't do peristalsis | 2. Impaired relaxation of the lower oesophageal sphincter
69
What happens to the lower oesophageal pressure in Achalasia
Elevated
70
Why does the lower oesophageal sphincter fail to relax in achalasia
Degeneration of the mesenteric plexus of the oesophagus with reduction of ganglion cell numbers
71
Clinical presentation of achalasia
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
How is Achalasia diagnosed
1. CXR 2. Barium swallow 3. Manometry (DIAGNOSTIC) 4. CT and oeosphagoscopy
73
What would a CXR show in achalasia
1. Dilated oesophagus | 2. Fluid behind the heart
74
What would a barium swallow show in achalasia
1. Shows lack of peristalsis | 2. Lower end shows birds beak due to failure of sphincter to relax
75
What would a manometry show in achalasia
1. Peristalsis of the oesophagus and failure of relaxation of the lower oesophageal sphincter
76
Why is a CT and oeosphagoscopy done in achalasia
Rule out carcinoma at lower end of the oesophagus
77
How is achalasia treated
1. Relieve SYMPTOMS 2. Medication to relax LOS 3. Surgery
78
What drugs would relax the lower oeopshageal sphincter
1. NIFEDIPINE 2. NITRATES 3. SILDENAFIL
79
What surgeries would be used to treat achalasia
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
Complications of achalasia treatment
Incidence of squamous carcinomas increased risk
81
What is scleroderma
Multi-system disease that effects the body by hardening connective tissues
82
In what gender does Scleroderma effect
Females
83
Risk factors of Scleroderma
Vinyl Chloride | Silica dust
84
Why is there diminished peristalsis and oesophageal clearance in scleroderma
Replacement of smooth muscle by fibrous tissue LOS pressure decreased = GORD and mucosal damage Strictures may develop
85
Clinical presentation of achalasia
1. Initially no symptoms | 2. Dysphagia and heartburn occur as the oesophagus becomes more severely involved
86
How is achalasia diagnosed
1. Barium swallow 2. CXR 3. Manometry
87
Role of barium swallow in achalasia diagnosis
Confirms impaired oesophageal motility
88
How is achalasia treated
Same as GORD (PPI for lansoprazole)
89
What is gastritis
Inflammation that is associated with mucosal injury
90
What is gastropathy
Epithelial cell damage and regeneration WITHOUT inflammation - NSAIDs and Aspirin caused
91
Causes of gastritis
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
How does helicobacter pylori cause gastritis
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
What parts of the stomach is effected by autoimmune gastritis
Affects funds and body of the stomach
94
How does autoimmune gastritis effect the stomach
1. Leads to atrophic gastritis | 2. Loss of parietal cells with intrinsic factor deficiency resulting in pernicious anaemia
95
How do aspirin and NSAIDs result in gastritis
Inhibit COX-1 and less mucus is produced
96
Clinical presentation of gastritis
1. Nausea 2. Abdo bleeding 3. Epigastric pain 4. Vomiting 5. Indigestion 6. Haematemesis
97
Differential diagnosis of gastritis
1. PUD 2. GORD 3. Non-ulcer dyspepsia 4. gastric lymphoma 5. Gastric carcinoma
98
How is gastritis diagnosed
1. Endoscopy 2. Biopsy 3. H. pylori urea breath test 4. H. pylori stool antigen test
99
How is gastritis treated
1 . Remove causative agents such as alcohol 2. Reduce stress 3. H. pylori eradication (7-14 days)
100
How is H.pylori eradication confirmed
Urea breath or faecal antigen test
101
How is H.pylori eliminated
TRIPLE TEHRAPY: PPI (Lansopraozle or Omeprazole) and TWO of: 1. METRONIDAZOLE, CLARITHROMYCIN, AMOXICILLIN, TETRACYCLINE, BISMUTH 2. Quinolones (CIPROFLOXACIN, FUROZOLIDONE and RIFABUTIN)
102
What drugs are given to treat gastritis
H2 antagonist (RANITIDINE or CIMETIDINE) PPIs (LANSOPRAZOLE or OMEPRAZOLE) Antacids
103
How is gastritis prevented
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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