Gastrointestinal (Including Liver) Flashcards

1
Q

Which hormone increases gastric motility and stimulates parietal maturity?

A

Gastrin

G cells from the antrium of stomach.

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2
Q

Which hormone delays gastric emptying?

A

Somatostatin.

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3
Q

Which parts of the duodenum are intraperitoneal and which are retroperitoneal?

A

The 1st part is intraperitoneal and the 2nd, 3rd, and 4th are retroperitoneal.

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4
Q

What is gastroparesis?

A

Ineffective peristalsis (neuromuscular issue) of the stomach, resulting in food and liquid remaining in the stomach for a prolonged period of time.

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5
Q

What is the most common known cause of gastroparesis?

A

Most common known cause is autonomic neuropathy of the vagus nerve, which innervates the stomach.

Uncontrolled diabetes mellitus is a frequent cause of this nerve damage, but trauma to the vagus nerve is also possible.

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6
Q

Symptoms of gastroparesis.

A

Nausea and vomiting.
Early satiety.
Bloating and abdominal pain.
Weight loss and malnutrition.
Blood sugar fluctuations.

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7
Q

Treatment for gastroparesis.

A

Dietary changes: e.g., eating 4-6 small meals a day, rather than 3 large meals.
Reducing the amount of insoluble fibre (e.g., wholegrain bread and beans).
Having a liquid diet.

Medicines: metoclopramide/domperidone.

Erythromycin is also listed by NICE as a possible treatment.

Other treatments depending on symptoms may include:

> A feeding tube for malnutrition.

> Botulinum toxin injections to help relax the pyloric sphincter.

> Gastro-electrical stimulation.

> Surgery to reshape the stomach.

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8
Q

What is Clostridioides difficile (C. difficile)?

Include type of bacteria

A

A gram-positive, spore-forming anaerobic bacterium causing antibiotic-associated colitis and diarrhoea.

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9
Q

What are common symptoms of C. difficile infection?

A

Common symptoms include watery diarrhea (>3 in 24 hrs), abdominal cramping, fever, nausea, and loss of appetite.

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10
Q

List 3 risk factors for C. difficile infection.

A
  • Recent antibiotic use,
  • PPI use due to suppression of gastric acid
  • Elderly, prolonged hospitalization, previous C. difficile infections.
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11
Q

How is C. difficile infection diagnosed?

A

Stool PCR – toxins A and B

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12
Q

What are the treatment options for C. difficile infection?

A

PO vancomycin 125mg QDS 10 d.
Fluids

2 Start when suspected due to risk of severe infection.

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13
Q

What complications can arise from C. difficile infection?

A

Complications can include severe dehydration/shock/AKI, bowel perforation, pseudomembranous colitis, and toxic megacolon.

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14
Q

What is the pathophysiology of C. difficile infection?

A

C. difficile produces toxins (Toxin A and Toxin B) that damage the intestinal lining, leading to inflammation and diarrhea.

Antibiotic use disrupts the normal gut flora, allowing C. difficile to proliferate and produce these toxins.

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15
Q

An elderly patient develops a profuse diarrhoeal illness after a long-hospital stay to treat bacterial pneumonia. What are your suspicions and next steps?

A

Probably C. Diff infection.

Investigate stool culture, start vancomycin, and treat symptoms e.g. IV fluid.

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16
Q

Are alcohol-based hand sanitisers effective against C. diff?

A

No. Use water and soap.

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17
Q

Where does C. difficile attack?

A

Colon.

Causes colitis and associated complications i.e. toxic megacolon, pseudomembranous colitis and perforation.

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18
Q

When is imaging indicated for patients with diarrhoeal illnesses?

A

When there is marked abdominal pain and distension.

X-ray for toxic megacolon
CT for colitis.

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19
Q

A C. diff patient’s colon was found to have damaged mucosa developing thickened, scab-like plaques, which are composed of dead cells, white blood cells, and cellular debris.

What is this describing?

A

Pseudomembranous colitis

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20
Q

What are common symptoms of GORD?

A

Common symptoms include heartburn, acid reflux (bad taste and cough), and dyspepsia (indigestion).

Worse after eating, and when lying down e.g. night time.

May be relieved by antacids.

Other: cough, halitosis, globus sensation

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21
Q

What lifestyle changes are recommended for managing GORD? List 4

A
  1. Weight loss if overweight
  2. Elevating the head of the bed
  3. Healthy dietary habits and avoiding triggering foods and drinks (e.g., caffeine, spicy foods, alcohol, fatty foods). No food 3 hours before bed.
  4. Smoking cessation
  5. Stress management
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22
Q

What are the first-line treatments for GORD?

A

First-line treatments include lifestyle modifications and medications i.e. PPIs and OTC medications like antacids and alginates.

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23
Q

When should a patient with GORD be referred for endoscopy?

A

Referral for endoscopy is recommended if there are alarm symptoms such as dysphagia (difficulty swallowing), persistent vomiting, gastrointestinal bleeding, or unexplained weight loss.

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24
Q

What is the role of Helicobacter pylori testing in GORD?

A

Testing for Helicobacter pylori is recommended in patients with uninvestigated dyspepsia. Eradication therapy is advised if the test is positive.

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25
Q

What surgical option is available for GORD?

For refractory cases

A

Laparoscopic fundoplication is a surgical option considered for patients with severe GORD not responding to medical treatment.

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26
Q

PPI regime for GORD.

A

4-8 weeks full dose.

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27
Q

If reflux is persistent despite 4 weeks of PPIs, what are your next steps?

A

Endoscopy to look for oesophagitis and causes.

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28
Q

Management of severe oesophagitis.

A

Full dose/double dose PPI for 8 weeks and full-dose PPI long-term maintenance.

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29
Q

Alternative medication to PPI.

A

H2R antagonists e.g. ranitidine, famotidine

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30
Q

Complications of untreated GORD. List 4.

A
  • Oesophagitis
  • Barrett’s oesophagus (columnar changes)
  • Oesophageal stricture
  • Oesophageal ulcer/cancer (adenocarcinoma)
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31
Q

What is a peptic ulcer?

A

A peptic ulcer is an open sore that develops on the inner lining of the stomach (gastric ulcer) or the upper part of the small intestine (duodenal ulcer).

32
Q

What are the most common causes of peptic ulcers?

A

The most common causes are infection with Helicobacter pylori (H. pylori) and long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs).

33
Q

List 3 common symptoms of peptic ulcers.

Including associated symptoms

A

Burning or gnawing epigastric pain before (duodenal) or after (gastric) food, during night time,

Associated with bloating/early satiety, nausea/vomiting, melaena/bleeding.

May be relieved by antacids.

34
Q

How is H. pylori infection diagnosed?

A

A breath test, stool test (antigen), blood test, or endoscopy with biopsy.

35
Q

What are the primary treatment options for peptic ulcers? List 3.

A

Treatment includes antibiotics to eradicate H. pylori, proton pump inhibitors (PPIs) to reduce stomach acid, and lifestyle modifications.

36
Q

Name two common proton pump inhibitors (PPIs) used in the treatment of peptic ulcers.

A

Omeprazole, lansoprazole and Esomeprazole.

37
Q

What complications can arise from untreated peptic ulcers? List 3

A

Complications include bleeding, perforation, and gastric outlet obstruction.

38
Q

What lifestyle changes can help prevent peptic ulcers?

A

Avoiding NSAIDs, reducing alcohol consumption, quitting smoking, and managing stress.

39
Q

How does H. pylori contribute to the development of peptic ulcers?

A

H. pylori damages the protective mucous lining of the stomach and duodenum, leading to inflammation and ulcer formation.

40
Q

What is the role of endoscopy in the management of peptic ulcers?

A

Endoscopy is used to visualize the ulcer, take biopsies, and sometimes treat bleeding ulcers.

41
Q

How do NSAIDs contribute to gastric ulcers?

A

NSAIDs inhibit cyclooxygenase (COX) enzymes, reducing prostaglandin production, which compromises the protective mucus layer of the stomach and duodenum.

Include aspirin

42
Q

Lifestyle habits that increases the risk of developing gastric ulcers.

A

Smoking: Increases the risk of ulcer formation and impairs healing.

Alcohol consumption: Excessive intake can exacerbate mucosal damage.

Drugs: cocaine

Stress

43
Q

Where do peptic ulcers usually occur?

A

Stomach - gastric,
Duodenum - duodenal

44
Q

How might the symptoms of GORD differ from PUD?

A

GORD presents with heartburn, regurgitation, and chest pain, which may improve with proton pump inhibitors (PPIs).

Unlike PUD, GORD typically lacks the gnawing epigastric pain that improves with food.

45
Q

Investigations for PUD and related conditions. (List 3)

A
  • FBC - check for anaemia
  • H. pylori testing
  • Endoscopy - definitive but only if alarming symptoms present e.g. weight loss, dysphagia, malaena
46
Q

How is Zollinger-Ellison syndrome a risk factor of PUD?

A

Hypersecretion of gastrin: Increased gastric levels secreted by parietal cells.

47
Q

Management of H.pylori +ve PUD.

A

7 days of Triple-therapy - using a
PPI + 2 antibiotics
(first-line: Amoxicillin + Clarithromycin or metronidazole), no amoxicillin if penicillin allergic.

48
Q

How long should PPI therapy last for in treating PUD?

A

4-8 weeks — this is the amount of time it takes for an ulcer to heal.

49
Q

Which vessel is often the main culprit of GI bleeding associated with PUD? Where is it?

A

Gastroduodenal artery. Crosses at first part of the duodenum.

50
Q

What is gastric outlet syndrome? What is its predominant symptom with reference to its anatomy?

A

Scarring and narrowing of the pyloric channel from chronic ulceration/ tumour.

Presents with persistent vomiting and requires endoscopic or surgical management.

51
Q

What is a similar condition as PUD presenting and treated similarly?

A

Gastritis

Inflammation, irritation, or erosion of the stomach lining. It can be acute (sudden and short-term) or chronic (developing gradually and long-lasting)

52
Q

Which of the following findings is most characteristic of dermatitis herpetiformis on direct immunofluorescence?

A

Granular IgA deposition at the dermal papillae.

53
Q

Dermatitis Herpetiformis

A

Inflammatory, immunobullous (caused by antibody mediated reactions), intensely pruritic skin condition characterised by clusters of erythematous, vesicular, and papular lesions.

54
Q

Haplotype most commonly associated with coeliac disease.

A

HLA DQ2.5

55
Q

What is coeliac disease? Which part of the bowel does it affect?

A

Gluten leads to damage in the small intestine.

56
Q

List 4 symptoms and 1 extra-intestinal symptom of coeliac disease.

A
  • Symptoms: Chronic, intermittent diarrhea, abdominal pain, bloating, weight loss.
  • Extra-intestinal symptom: fatigue, dermatitis herpetiformis (itchy, blistery, vescicular skin rash).
57
Q

Which foods are common culprits? When is it therefore worse?

A

Common culprits include foods containing wheat, barley, and rye. Symptoms worsen after consuming these gluten-containing foods.

58
Q

When will coeliac disease be suspected in a child/young teen?

A

If the child has symptoms like chronic diarrhea, abdominal distension, abdominal pain, failure to thrive, weight loss, or delayed puberty.

59
Q

Which other non-digestive organ may coeliac disease affect?

A

Coeliac disease can affect the spleen, leading to reduced spleen function (hyposplenism).

60
Q

What blood tests are used for coeliac disease diagnosis and any specific requirements?

A
  1. Total igA,
  2. TGA (tissue transglutaminase antibodies)

It’s important to be on a gluten-containing diet for accurate results for at least 6 weeks.

61
Q

Which gene is coeliac disease most commonly linked to?

A

Coeliac disease is most commonly linked to the HLA-DQ2 and HLA-DQ8 genes.

62
Q

What are the endoscopy findings in coeliac disease?

A

Endoscopy may show villous atrophy, crypt hyperplasia, and increased intraepithelial lymphocytes.

63
Q

Most common complication of coeliac disease

A

Anaemia: iron, folate and vitamin B12 deficiency (folate deficiency is more common than vitamin B12 deficiency in coeliac disease)

Risk of other auto-immune diseases.

64
Q

What are the 4 main types of gastric cancer?

A

The main types include:
- Adenocarcinoma: The most common type, originating in the parietal cells of the stomach lining.
- Lymphoma
- Gastrointestinal stromal tumor (GIST): A rare type that starts in the stomach’s connective tissue.
- Neuroendocrine tumors: Rare tumors that originate from hormone-producing cells.

65
Q

Most important RFs to ask for when suspecting gastric cancer.

List 3

A
  • Infections: Helicobacter pylori infection (adenocarcinoma), EBV
  • Smoking
  • Diet: high in salty and smoked foods
  • FH of gastric cancer
  • Obesity
  • Certain genetic conditions (e.g., Lynch syndrome).
66
Q

What are the common symptoms of gastric cancer?

A
  • Early stages are non-specific: e.g. indigestion, mild epigastric discomfort/early satiety.
  • Late stages: epigastric mass, persistent pain, Loss of appetite, unintentional weight loss, fatigue, anaemia
  • Dysphagia
  • Black, tarry stools (indicative of bleeding).
67
Q

What are the treatment options for gastric cancer?

A
  • Surgery: Partial or total gastrectomy.
  • Chemotherapy/radiotherapy/targeted/immunotherapy.
68
Q

List a strong risk factor for gastric cancers.

A

Helicobacter pylori infection.

Mainly includes MALT (mucosa-associated lymphoid tissue) lymphoma and diffuse large B-cell lymphoma.

69
Q

Signs of gastric cancer metastasis found on clinical exam.

A
  • Virchow’s node (left supraclavicular lymph node enlargement)
  • Sister Mary Joseph node (periumbilical nodule - on belly button).
  • Hepatomegaly
  • Ascites
70
Q

How is the pain associated with gastric cancer different from PUD?

A

PUD presents with epigastric pain often relieved by food or antacids, whereas gastric cancer pain is typically persistent and progressive.

71
Q

Next steps upon suspecting gastric cancer.

A

Suspected cancer pathway and urgent upper GI endoscopty.

Diagnosis:
- Endoscopy and biopsy
- Imaging tests: Such as CT scans.
- Blood tests: To check for anemia, LFTs

72
Q

Most common type of gastric cancer

A

Adenocarcinoma (90%)

Adenocarcinomas: Originates in the glandular cells of the stomach lining. Often found in the antrum or body of the stomach.

73
Q

Which cancers do H. pylori typically cause?

A

Adenocarcinomas and MALT lymphomas.

74
Q

Where do gastrointestinal stromal tumors (GISTs) originate from?

A

GISTs are rare tumors that originate from the interstitial cells of Cajal in the gastrointestinal tract.

Produce slow electrical waves that cause smooth muscles to contract at a steady pace. From stomach to colon. 'Pacemakers' of the gut.
75
Q

What is a mucinous cell type found in gastric and colon adenocarcinomas that indicates poor differnetiation and aggressive behaviour?

A

Signet ring cell, (mucin filled cells that push the nucleus to the side)