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Gastro Theory Flashcards

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1
Q

Define GORD.

A

Prolonged or recurrent reflux of gastric contents –> oesophagus.

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2
Q

How does GORD clinically present?

A
  • Heartburn (related to lying down and meals)
  • Odynophagia
  • Regurgitation
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3
Q

What is the pathophysiology of GORD?

A
  • Tone of the LOS (lower esophageal sphincter) is reduced
  • Frequent transient relaxations of the LOS
  • Increased mucosal sensitivity to gastric acids
  • Hiatus hernia can cause increased reflux (but reflux can occur without hernia)
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4
Q

What are possible risk factors for GORD?

A
  • Smoking
  • Alcohol
  • Pregnancy
  • Obesity
  • Big meals
  • Complication of hiatus hernia
  • Any LOS dysfunction
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5
Q

Which patient group is more affected by GORD?

A

Mostly in men.

25% of adults experience heartburn.

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6
Q

Give a diagnostic test for GORD.

A

Endoscopy

Barium swallow

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7
Q

What is the treatment for GORD?

A

C: weight loss, avoid excess alcohol, stop smoking

M: Antacids if mild. If severe, PPI (omeprazole) or H2RA (cimetidine)

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8
Q

Give 2 possible complications of GORD?

A

Oesophageal stricture (worsening dysphagia)

Barrett’s Oesophagus (abnormal columnar epithelium replaces squamous epithelium of distal oesophagus) - irreversible and can develop into oesophageal cancer.

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9
Q

Which cell type changes to which in Barret’s Oesophagus?

A

Squamous epithelium -> Columnar epithelium (with goblet cells)

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10
Q

What are 3 possible causes of Upper GI bleeding?

A
  • Mallory Weiss Tear
  • Oesophago-gastric varices
  • Peptic ulcer
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11
Q

What is a Mallory-Weiss tear?

A

Mucosal laceration in the Upper GI tract —> leads to bleeding

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12
Q

How does a Mallory-Weiss tear clinically present?

A

Bout of retching or vomiting -> haemetesis

Blood volume loss:
Syncope
Light-headedness
Dizziness

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13
Q

What is the pathophysiology behind a Mallory-Weiss tear?

A

Sudden increased intragastric pressure within rigid LOS can cause tearing of the mucosa.

This then causes blood to leak out into the oesophagus and be vomited out.

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14
Q

What are risk factors/causes of Mallory-Weiss tears?

A

Trauma from frequent cough
Vomit
Retching
Hiccuping

RF: excess ETOH

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15
Q

In which groups of patients are Mallory-Weiss tears common in?

A
  • Bulimics
  • Alcoholics

*Comprises 4-8% of all UGIB

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16
Q

What is the diagnostic test for a Mallory-Weiss tear?

A

Endoscopy

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17
Q

What is the treatment for a Mallory-Weiss tear?

A

ABCDE (resuscitation)
Maintain airway
High flow oxygen
Correct fluid losses

Identify comorbidities

Tear tends to heal rapidly on its own

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18
Q

What are complications of a Mallory-Weiss tear?

A

Hypovolaemic shock
Re-bleeding
MI
Death

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19
Q

What are oesophago-gastric varices?

A

Dilated veins at the junction between the portal and systemic venous systems -> leading to variceal haemorrhage.

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20
Q

What is the clinical presentation of someone with oesophago-gastric varices?

A

Haematemesis

Liver disease

Pallor

Shock (low BP, high heart rate)

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21
Q

What is the pathophysiology behind oesophago-gastric varices?

A

Liver disease leads to high pressure in the portal vein –>

–>Veins at the junction with the systemic venous system distend (varices)

–> This causes damage and can lead to bleeding from the varices into the oesophagus, leading to haematemesis.

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22
Q

What is the main cause of oesophago-gastric varices?

A

Portal hypertension

majority of pt’s have chronic liver disease

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23
Q

What is the diagnostic test for oesophago-gastric varices?

A

Endoscopy

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24
Q

What are the treatments for oesophago-gastric varices?

A

C: ABCDE
Maintain airway
Treat shock

M: Vasoactive drugs, antibiotic prophylaxis

S: obturate with glue-like substances, endoscopic band ligation.

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25
What are complications of oesophago-gastric variceal tears?
70% chance of re-bleeding Death (high risk)
26
What is a peptic ulcer? What are the two types?
Break in the GI mucosa in or adjacent to acid bearing area 2 types: - Gastric - Duodenal
27
What is the clinical presentation of peptic ulcers? How does the presentation vary between gastric and duodenal ulcers?
- Burning epigastric pain - Nausea - Heartburn - Flatulence - Occasionally painless haemorrhage Differences: - Duodenal gives more pain when patient is hungry + at night
28
Which peptic ulcer type is more associated with H. pylori infection?
Duodenal (95% of cases) *Gastric is 80% of cases
29
What is the pathophysiology behind peptic ulcers?
Reduction in protective prostaglandins or increase in gastric acid secretions --> causes acidic contents of stomach/duodenum to break down the mucosa Pain varies with acid level of area affecting the ulcer H. pylori can then come and infect mucosa following this pH-induced damage --> further inflammation via proteases.
30
What are the 2 main causes of peptic ulcers?
H. pylori (increased gastric acid secretions, disruption of mucous protective layer, reduced duodenal bicarbonate production) NSAIDs (reduced production of prostaglandins which provide mucosal protection in the upper GI)
31
Which type of peptic ulcer is more common?
Duodenal is more common than gastric
32
What is the most common cause (50%) of Upper GI bleeds?
Peptic ulcers
33
What are diagnostic tests for peptic ulcers? List 3.
H. pylori tests - (carbon-13 urea breath test) - (stool antigen test) Endoscopy also possible
34
What is the treatment for peptic ulcers?
C: avoid NSAIDs, stop smoking M: Eradicate H.pylori via antibiotics and PPI (triple therapy*) *COM (clarithromycin, omeprazole, metronidazole)
35
What drugs are used in triple therapy when treating peptic ulcers?
Remember COM (abx and PPI) Clarithromycin Omeprazole Metronidazole
36
What is a possible complication of a peptic ulcer?
Upper GI bleed
37
What is the definition of gastritis?
Inflammation of the gastric mucosa
38
Which WBCs are involved in ACUTE gastritis?
Neutrophils (infiltrate into gastric mucosa)
39
Which WBCs are involved in CHRONIC gastritis?
Mononuclear cells (lymphocytes, plasma cells, macrophages)
40
What is the clinical presentation of gastritis?
Usually asymptomatic Sometimes functional dyspepsia (aka. non-ulcer dyspepsia) - indigestion!
41
What is the pathophysiology behind gastritis?
Local inflammatory response to H. pylori infection Can cause increase in gastric acid secretion (due to H. pylori presence)
42
What is the most common cause of gastritis? Give 2 other less common causes
Most common: H. pylori infection Less common: autoimmune gastritis (abs to parietal cells and IF) - viruses - duodeno-gastric reflux
43
What is the diagnostic investigation for gastritis?
Endoscopy +/- biopsy (appears reddened or normal on endoscopy) - can detect histological change with biopsy sample
44
What is the main treatment for gastritis?
Triple therapy (COM) to eradicate H. pylori Clarithromycin Omeprazole Metronidazole
45
What is a complication of gastritis?
Develops into peptic ulcer. | also pernicious anaemia if due to autoimmune gastritis attack on IF
46
What is the definition of gastropathy?
Injury to the gastric mucosa with epithelial cell damage and regeneration. LITTLE TO NO INFLAMMATION! (unlike gastritis)
47
What is the clinical presentation of gastropathy?
Indigestion (dyspepsia) Vomiting Haemorrhage
48
What is the pathophysiology of gastropathy?
Reduction in protective prostaglandins by NSAID use causes the acidic contents of the stomach/duodenum to break down the mucosa.
49
What is the most common cause of gastropathy? Give 2 other less common causes.
Most common: NSAID use Less common: severe stress - ETOH excess - CMV infection - HSV infection
50
What is the diagnostic investigation for gastropathy and what would be seen?
Endoscopy -> shows erosions and sub-epithelial haemorrhage
51
What is the treatment for gastropathy?
Remove causative agent (e.g. stop NSAID, quit ETOH, CMV, HSV) Give PPI
52
What is a complication of gastropathy?
Develops into peptic ulcer.
53
What is cholangitis?
Infection of the biliary tree
54
What is the clinical presentation of cholangitis?
Charcot's triad (fever, RUQ pain, jaundice) in most patients
55
What is Charcot's triad composed of?
Fever (with chills) RUQ pain Jaundice (pale stools, dark urine, pruritus)
56
What is the pathophysiology of cholangitis?
If CBD obstruction cause, then duct obstruction -> inflammation + susceptibility to infection If infective cause, infection ascends from junction with duodenum. Infection from GI flora causes inflammation and pain.
57
What is the most common cause of cholangitis? List 2 other less common causes.
Most common: gallstones Less common: infection (Klebsiella, E. coli) - Benign strictures - Malignancy of head of pancreas
58
In which patient group is cholangitis most commonly found?
History of gallstones Aged 50-60
59
Which bloods should you take for cholangitis (and what would they show)?
FBC (raised CRP) | LFT (raised ALP, AST, ALT)
60
What is the definitive investigation for cholangitis?
ERCP (reveals gallstones and can remove the blockage too)
61
What are investigations for cholangitis?
Bloods (CRP, LFT) Abdo USS Blood cultures (if septic) ERCP *gold-standard Culturing of ERCP-collected specimens
62
How is cholangitis treated?
C: fluid resuscitation M: Antibiotic therapy S: ERCP to clear obstruction
63
What is the most dangerous complication of cholangitis?
Sepsis
64
What is the definition of primary sclerosing cholangitis?
Chronic inflammation + fibrosis of the bile ducts
65
What is the clinical presentation of primary sclerosis cholangitis?
- May be asymptomatic (incidentially found after LFTs) - Charcot's triad (fever, RUQ pain, jaundice) - Hepatomegaly
66
Which form of IBD is primary sclerosis cholangitis usually associated with?
Ulcerative colitis
67
What is the pathophysiology behind primary sclerosing cholangitis?
Progressing fibrosis in intra/extra-hepatic ducts --> ducts become strictured --> cholestatic jaundice + RUQ pain Eventually --> CIRRHOSIS
68
What are causes of primary sclerosing cholangitis?
``` ?Unknown generally Genetic Lymphocyte recruitment Portal bacteraemia Bile salt toxicity ``` (can also be secondary to infection, thrombosis or iatrogenic/trauma)
69
Which gender and age group is primary sclerosing cholangitis most common in?
Males 30-40s
70
What investigations are needed to diagnose primary sclerosing cholangitis?
USS (may show bile duct dilatation) ERCP LFTs (elevated ALP or GGT) AST/ALT can be normal to several times above normal. Serum albumin drops with progression of disease.
71
How is primary sclerosing cholangitis managed?
C: Manage symptoms of liver failure M: High dose ursodeoxycholic acid can slow progression. S: ERCP can dilate some extra-hepatic structures to slow progression. Eventual liver transplant needed.
72
What is the final outcome of primary sclerosing cholangitis?
Eventual liver failure | also 15% can get cholangiocarcinoma - cancer of bile ducts
73
Define achalsia
Lack of peristalsis in the oesophagus and failure of LOS to relax impairs oesophageal emptying
74
What is the clinical presentation of achalsia?
- Onset at any age - Long history of dysphagia for solids and liquids - Retrosternal chest pain (non-cardiac) - Weight loss
75
What is the pathophysiology of achalasia?
Decrease in the ganglionic cells in the nerve plexus of the oesophageal wall + degeneration in the vagus nerve
76
Is achalasia common in children?
No.
77
Give 2 diagnostic investigations for achalasia? What would these show?
Barium swallow: aperistalsis + beak deformity (oesophagus tapers to a point) Oesophageal manometry: aperistalsis and failure of LOS to relax on swallowing.
78
What is the treatment of achalasia?
No cure C: Treat symptoms. M: Nitrates (if surgery is contraindicated. Can also use botox for elderly where surgery is not an option.) S: Surgical division of LOS and endoscopic balloon dilatation.
79
What is a dangerous complication of achalasia?
If untreated, asphyxiation of material in oesophagus —> choking. Can also result in oesophageal cancer.
80
What is systemic sclerosis scleroderma? (SSc)
It is a multi-system autoimmune disease. Caused by increased fibroblast activity —> abnormal growth of connective tissue.
81
What are the 2 types of Systemic Sclerosis Scleroderma?
Limited cutaneous (CREST syndrome) Diffuse cutaneous
82
What does CREST syndrome stand for? (in systemic sclerosis)
``` Calcinosis Raynaud’s phenomenon Esophageal dysmotility Sclerodactyly Telangiectasia ```
83
What is the clinical presentation of Diffuse Cutaneous subtype of systemic scleroderma?
Same as CREST syndrome but with more RAPID and WIDESPREAD onset GI: indigestion, reflux, oesophagitis. Delayed gastric emptying Resp: pulmonary fibrosis, pulmonary artery hypertension
84
What proportion of people with SSC do the following affect? a) Limited cutaneous (CREST) b) Diffuse cutaneous
a) Limited cutaneous affects 70% of SSc | b) Diffuse cutaneous affects 30% of SSc
85
Which parts of the body does limited cutaneous SSc usually affect?
Face Forearms Lower legs (up to knee)
86
Which part of the body does Diffuse cutaneous SSc usually affect?
Widespread Face Entire arm Thighs + Legs Trunk
87
What is the pathophysiology behind systemic scleroderma?
Excessive collagen produced and deposited —> vascular damage and inflammation then results.
88
What is the prevalence of systemic scleroderma in the UK? More common in which gender?
88 in 1 million (very rare) in UK More common in women (Rare in children)
89
What is the definition of ulcerative colitis?
Continuous chronic inflammation of only the colon
90
How does ulcerative colitis usually present?
- Recurrent diarrhoea - blood/mucus | - Extra-gastrointestinal symptoms - arthralgia, fatty liver and gall stones
91
In which form of IBD is smoking protective?
Ulcerative colitis
92
What is the pathophysiology behind ulcerative colitis?
Mucosal inflammation that starts in the anus and continues proximally, affecting only the large colon. No granulomata. Goblet cell depletion and crypt abcesses.
93
How does Crohn’s usually present?
Symptoms depend on region affected. Small bowel:
94
What are the 4 types of laxatives?
Bulk-forming Stimulants Osmotics Stool softeners

Gastroenterology (3 decks)

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