Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Gastroenterology > Gastro Theory > Flashcards

Gastro Theory Flashcards

1
Q

Define GORD.

A

Prolonged or recurrent reflux of gastric contents –> oesophagus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does GORD clinically present?

A
  • Heartburn (related to lying down and meals)
  • Odynophagia
  • Regurgitation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are possible risk factors for GORD?

A
  • Smoking
  • Alcohol
  • Pregnancy
  • Obesity
  • Big meals
  • Complication of hiatus hernia
  • Any LOS dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Which patient group is more affected by GORD?

A

Mostly in men.

25% of adults experience heartburn.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Give a diagnostic test for GORD.

A

Endoscopy

Barium swallow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

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

A

Squamous epithelium -> Columnar epithelium (with goblet cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are 3 possible causes of Upper GI bleeding?

A
  • Mallory Weiss Tear
  • Oesophago-gastric varices
  • Peptic ulcer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is a Mallory-Weiss tear?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does a Mallory-Weiss tear clinically present?

A

Bout of retching or vomiting -> haemetesis

Blood volume loss:
Syncope
Light-headedness
Dizziness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

Trauma from frequent cough
Vomit
Retching
Hiccuping

RF: excess ETOH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A
  • Bulimics
  • Alcoholics

*Comprises 4-8% of all UGIB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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

A

Endoscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are complications of a Mallory-Weiss tear?

A

Hypovolaemic shock
Re-bleeding
MI
Death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are oesophago-gastric varices?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A

Haematemesis

Liver disease

Pallor

Shock (low BP, high heart rate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the main cause of oesophago-gastric varices?

A

Portal hypertension

majority of pt’s have chronic liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the diagnostic test for oesophago-gastric varices?

A

Endoscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are complications of oesophago-gastric variceal tears?

A

70% chance of re-bleeding

Death (high risk)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

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

A

Duodenal (95% of cases)

*Gastric is 80% of cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Which type of peptic ulcer is more common?

A

Duodenal is more common than gastric

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

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

A

Peptic ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

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

A

Remember COM (abx and PPI)

Clarithromycin
Omeprazole
Metronidazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is a possible complication of a peptic ulcer?

A

Upper GI bleed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the definition of gastritis?

A

Inflammation of the gastric mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?

A

Sepsis

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?

A

No.

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions