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Gastro Theory Flashcards

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
Q

What are complications of oesophago-gastric variceal tears?

A

70% chance of re-bleeding

Death (high risk)

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26
Q

What is a peptic ulcer? What are the two types?

A

Break in the GI mucosa in or adjacent to acid bearing area

2 types:

  • Gastric
  • Duodenal
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27
Q

What is the clinical presentation of peptic ulcers?

How does the presentation vary between gastric and duodenal ulcers?

A
  • Burning epigastric pain
  • Nausea
  • Heartburn
  • Flatulence
  • Occasionally painless haemorrhage

Differences:
- Duodenal gives more pain when patient is hungry + at night

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28
Q

Which peptic ulcer type is more associated with H. pylori infection?

A

Duodenal (95% of cases)

*Gastric is 80% of cases

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29
Q

What is the pathophysiology behind peptic ulcers?

A

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.

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30
Q

What are the 2 main causes of peptic ulcers?

A

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)

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31
Q

Which type of peptic ulcer is more common?

A

Duodenal is more common than gastric

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32
Q

What is the most common cause (50%) of Upper GI bleeds?

A

Peptic ulcers

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33
Q

What are diagnostic tests for peptic ulcers?

List 3.

A

H. pylori tests

  • (carbon-13 urea breath test)
  • (stool antigen test)

Endoscopy also possible

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34
Q

What is the treatment for peptic ulcers?

A

C: avoid NSAIDs, stop smoking

M: Eradicate H.pylori via antibiotics and PPI (triple therapy*)

*COM (clarithromycin, omeprazole, metronidazole)

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35
Q

What drugs are used in triple therapy when treating peptic ulcers?

A

Remember COM (abx and PPI)

Clarithromycin
Omeprazole
Metronidazole

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36
Q

What is a possible complication of a peptic ulcer?

A

Upper GI bleed

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37
Q

What is the definition of gastritis?

A

Inflammation of the gastric mucosa

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38
Q

Which WBCs are involved in ACUTE gastritis?

A

Neutrophils (infiltrate into gastric mucosa)

39
Q

Which WBCs are involved in CHRONIC gastritis?

A

Mononuclear cells (lymphocytes, plasma cells, macrophages)

40
Q

What is the clinical presentation of gastritis?

A

Usually asymptomatic

Sometimes functional dyspepsia (aka. non-ulcer dyspepsia) - indigestion!

41
Q

What is the pathophysiology behind gastritis?

A

Local inflammatory response to H. pylori infection

Can cause increase in gastric acid secretion (due to H. pylori presence)

42
Q

What is the most common cause of gastritis?

Give 2 other less common causes

A

Most common: H. pylori infection

Less common: autoimmune gastritis (abs to parietal cells and IF)

  • viruses
  • duodeno-gastric reflux
43
Q

What is the diagnostic investigation for gastritis?

A

Endoscopy +/- biopsy

(appears reddened or normal on endoscopy) - can detect histological change with biopsy sample

44
Q

What is the main treatment for gastritis?

A

Triple therapy (COM) to eradicate H. pylori

Clarithromycin
Omeprazole
Metronidazole

45
Q

What is a complication of gastritis?

A

Develops into peptic ulcer.

also pernicious anaemia if due to autoimmune gastritis attack on IF

46
Q

What is the definition of gastropathy?

A

Injury to the gastric mucosa with epithelial cell damage and regeneration.

LITTLE TO NO INFLAMMATION! (unlike gastritis)

47
Q

What is the clinical presentation of gastropathy?

A

Indigestion (dyspepsia)
Vomiting
Haemorrhage

48
Q

What is the pathophysiology of gastropathy?

A

Reduction in protective prostaglandins by NSAID use causes the acidic contents of the stomach/duodenum to break down the mucosa.

49
Q

What is the most common cause of gastropathy?

Give 2 other less common causes.

A

Most common: NSAID use

Less common: severe stress

  • ETOH excess
  • CMV infection
  • HSV infection
50
Q

What is the diagnostic investigation for gastropathy and what would be seen?

A

Endoscopy

-> shows erosions and sub-epithelial haemorrhage

51
Q

What is the treatment for gastropathy?

A

Remove causative agent (e.g. stop NSAID, quit ETOH, CMV, HSV)

Give PPI

52
Q

What is a complication of gastropathy?

A

Develops into peptic ulcer.

53
Q

What is cholangitis?

A

Infection of the biliary tree

54
Q

What is the clinical presentation of cholangitis?

A

Charcot’s triad (fever, RUQ pain, jaundice) in most patients

55
Q

What is Charcot’s triad composed of?

A

Fever (with chills)
RUQ pain
Jaundice (pale stools, dark urine, pruritus)

56
Q

What is the pathophysiology of cholangitis?

A

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
Q

What is the most common cause of cholangitis?

List 2 other less common causes.

A

Most common: gallstones

Less common: infection (Klebsiella, E. coli)

  • Benign strictures
  • Malignancy of head of pancreas
58
Q

In which patient group is cholangitis most commonly found?

A

History of gallstones

Aged 50-60

59
Q

Which bloods should you take for cholangitis (and what would they show)?

A

FBC (raised CRP)

LFT (raised ALP, AST, ALT)

60
Q

What is the definitive investigation for cholangitis?

A

ERCP (reveals gallstones and can remove the blockage too)

61
Q

What are investigations for cholangitis?

A

Bloods (CRP, LFT)

Abdo USS

Blood cultures (if septic)

ERCP *gold-standard

Culturing of ERCP-collected specimens

62
Q

How is cholangitis treated?

A

C: fluid resuscitation

M: Antibiotic therapy

S: ERCP to clear obstruction

63
Q

What is the most dangerous complication of cholangitis?

64
Q

What is the definition of primary sclerosing cholangitis?

A

Chronic inflammation + fibrosis of the bile ducts

65
Q

What is the clinical presentation of primary sclerosis cholangitis?

A
  • May be asymptomatic (incidentially found after LFTs)
  • Charcot’s triad (fever, RUQ pain, jaundice)
  • Hepatomegaly
66
Q

Which form of IBD is primary sclerosis cholangitis usually associated with?

A

Ulcerative colitis

67
Q

What is the pathophysiology behind primary sclerosing cholangitis?

A

Progressing fibrosis in intra/extra-hepatic ducts –> ducts become strictured –> cholestatic jaundice + RUQ pain

Eventually –> CIRRHOSIS

68
Q

What are causes of primary sclerosing cholangitis?

A 
?Unknown generally
Genetic
Lymphocyte recruitment
Portal bacteraemia
Bile salt toxicity

(can also be secondary to infection, thrombosis or iatrogenic/trauma)

69
Q

Which gender and age group is primary sclerosing cholangitis most common in?

A

Males

30-40s

70
Q

What investigations are needed to diagnose primary sclerosing cholangitis?

A

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
Q

How is primary sclerosing cholangitis managed?

A

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
Q

What is the final outcome of primary sclerosing cholangitis?

A

Eventual liver failure

also 15% can get cholangiocarcinoma - cancer of bile ducts

73
Q

Define achalsia

A

Lack of peristalsis in the oesophagus and failure of LOS to relax impairs oesophageal emptying

74
Q

What is the clinical presentation of achalsia?

A
  • Onset at any age
  • Long history of dysphagia for solids and liquids
  • Retrosternal chest pain (non-cardiac)
  • Weight loss
75
Q

What is the pathophysiology of achalasia?

A

Decrease in the ganglionic cells in the nerve plexus of the oesophageal wall + degeneration in the vagus nerve

76
Q

Is achalasia common in children?

77
Q

Give 2 diagnostic investigations for achalasia?

What would these show?

A

Barium swallow: aperistalsis + beak deformity (oesophagus tapers to a point)

Oesophageal manometry: aperistalsis and failure of LOS to relax on swallowing.

78
Q

What is the treatment of achalasia?

A

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
Q

What is a dangerous complication of achalasia?

A

If untreated, asphyxiation of material in oesophagus —> choking.

Can also result in oesophageal cancer.

80
Q

What is systemic sclerosis scleroderma? (SSc)

A

It is a multi-system autoimmune disease.

Caused by increased fibroblast activity —> abnormal growth of connective tissue.

81
Q

What are the 2 types of Systemic Sclerosis Scleroderma?

A

Limited cutaneous (CREST syndrome)

Diffuse cutaneous

82
Q

What does CREST syndrome stand for? (in systemic sclerosis)

A 
Calcinosis
Raynaud’s phenomenon
Esophageal dysmotility
Sclerodactyly
Telangiectasia
83
Q

What is the clinical presentation of Diffuse Cutaneous subtype of systemic scleroderma?

A

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
Q

What proportion of people with SSC do the following affect?

a) Limited cutaneous (CREST)
b) Diffuse cutaneous

A

a) Limited cutaneous affects 70% of SSc

b) Diffuse cutaneous affects 30% of SSc

85
Q

Which parts of the body does limited cutaneous SSc usually affect?

A

Face
Forearms
Lower legs (up to knee)

86
Q

Which part of the body does Diffuse cutaneous SSc usually affect?

A

Widespread

Face
Entire arm
Thighs + Legs
Trunk

87
Q

What is the pathophysiology behind systemic scleroderma?

A

Excessive collagen produced and deposited —> vascular damage and inflammation then results.

88
Q

What is the prevalence of systemic scleroderma in the UK?

More common in which gender?

A

88 in 1 million (very rare) in UK

More common in women

(Rare in children)

89
Q

What is the definition of ulcerative colitis?

A

Continuous chronic inflammation of only the colon

90
Q

How does ulcerative colitis usually present?

A
  • Recurrent diarrhoea - blood/mucus

- Extra-gastrointestinal symptoms - arthralgia, fatty liver and gall stones

91
Q

In which form of IBD is smoking protective?

A

Ulcerative colitis

92
Q

What is the pathophysiology behind ulcerative colitis?

A

Mucosal inflammation that starts in the anus and continues proximally, affecting only the large colon.

No granulomata.

Goblet cell depletion and crypt abcesses.

93
Q

How does Crohn’s usually present?

A

Symptoms depend on region affected.

Small bowel:

94
Q

What are the 4 types of laxatives?

A

Bulk-forming
Stimulants
Osmotics
Stool softeners

Gastroenterology (3 decks)

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