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Yr3 Revision > MET3 Revision - Gastroenterology I > Flashcards

MET3 Revision - Gastroenterology I Flashcards

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1
Q
A
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2
Q

State 7 red flags for cancer w/ diarrhoea [7]

A
  1. Change in bowel habit
  2. Bleeding
  3. Weight loss, unintentional
  4. FH bowel or ovarian cancer
  5. > 50 and for >6 weeks
  6. Anaemia (anyone who doesnt have periods and has IDA has colorectal cancer until proven otherwise)
  7. Abdominal or rectal mass}
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3
Q

What causes secretory diarrhoea? [5]

A

Excess secretion of water:
- IBD
- Salmonella infection
- Enterotoxins: E. coli, V. cholera
- Bile salts
- Hormones

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4
Q

Give three examples of motility related diarrhoea [3]

A
  • Thyrotoxicosis
  • IBS
  • DM autonomic neuropathy
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5
Q

How do you distinguish between steatorrhoea from pancreatic insufficiency and small intestine disease? [4]

A

Pancreatic insufficiency:
- High faecal fat (rare to test now)
- High faecal elastase (more common to test)
- Normal red cell folate
- Pancreatic calcification on US

Small intestinal disease:
- low red cell folate (folate is absorbed higher up GI)
- anti-TTG: CD
- CT
- XR}

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6
Q

What would the following symptoms indicate about the infective cause of diarrhoea?

· Rapid onset of symptoms (within a few hours after eating) [1]

· Fever [1]

· Bloody diarrhoea [1]

· Abx [1]

A

Rapid onset of symptoms: (within a few hours after eating)
- this may be from a toxin-producing organism (i.e. reheated takeaways/rice from B.cereus, S.aureus from creamy products)

Fever
- is associated with invasive bacteria: such as campylobacter, salmonella, shigella), enteric viruses, and cytotoxic organisms such as C.dificile, E.histolytica.

Bloody diarrhoea
- is caused by invasive bacteria (is termed dysentery, bacillary dysentery).

Abx
- is associated with C.dificile

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7
Q

Which therapeutic drugs are associated with chronic diarrhoea? [8]

A
  1. Alcohol
  2. Antibiotics
  3. Anti-depressants (lithium, SSRIs)
  4. Anti-hypertensives
  5. Statins / Cholesterol-lowering agents
  6. GI drugs (Mg++, H2RA, PG analogs, 5-ASA)
  7. NSAIDs
  8. Oral hypoglycaemics like biguanides
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8
Q

Describe the blood tests for diarrhoea [7]

A
  • FBC: check for anaemia
  • WCC platelets, CRP: for signs of infection / inflammation
  • U&E: signs of AKI / dehydration
  • Albumin, Ca, P – give info on nutritional status
  • Haematinics: folate absorbed in proximal small bowel, B12 absorbed in stomach and distal small bowel
  • IgA TTG antibodies for coeliac disease
  • TFTs: undiagnosed thyrotoxicosis can cause chronic diarrhoea
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9
Q

Describe stool test for diarrhoea investigations [5]

A
  • Stool weight: useful but difficult to do in practice
  • Culture stool for infection: MC&S, cysts, ova, parasites, CDT
  • Faecal calprotectin: (protein produced by neutrophils so inflammation in bowel increases the amount of calprotectin shed so will show up in a stool specimen): easy test for infection and IBD, commonly used in follow-ups for IBD patients
  • Faecal immunochemical test for Hb: highly specific test for blood in the stool - colorectal cancer
  • Faecal elastase looks for pancreatic disease
  • Stool pH / electrolyte balance / reducing substances (see if patients are taking laxatives)
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10
Q

What is the gold standard for investigating diarrhoea? [1]

A

Colonoscopy & biopsy
(Also:
- Duodendal biopsy
- Small bowel MRI
- Video capsule endoscopy
- Cross sectional imaging)
}}

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11
Q

Which viruses commonly cause viral gastroenteritis? [3]

A

Rotavirus
Norovirus
Adenovirus (tends to cause respiratory symptoms)

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12
Q

E. coli produces which toxin? [1]
Which syndrome can it lead to and why? [2]

A

Produces Shiga toxin
Leads to haemolytic uraemic syndrome due to destruction of rbc

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13
Q

How do you treat Campylobacter jejuni infection? [3]

A
  • Clathromycin (1st line)
  • Azithromycin
  • Ciprofloxacin
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14
Q

A patient has recently eaten fried rice left at room temperature. They are reported vomitting and then diarrhoea.

What is the most likely pathogen causing these symptoms? [1]

A

Bacillus cereus

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15
Q

What syndrome can Shigella cause? [1]
Name two treatments [2]

A

haemolytic uraemic syndrome:

Treatment of severe cases is with azithromycin or ciprofloxacin.

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16
Q

Which parasite is found in the small intestines of mammals and causes diarrhoea via a faecal-oral transmission? [1]

A

Giardia lamblia

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17
Q

How do you treat Giardia lamblia? [2]

A

tinidazole or metronidazole

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18
Q

[] is a severe inflammation of the inner lining of the large intestine, manifests as an antibiotic-associated colonic inflammatory complication.

What is the most common cause of this? [1]

How does this present? [1]

A

Pseudomembranous colitis, a severe inflammation of the inner lining of the large intestine, manifests as an antibiotic-associated colonic inflammatory complication.

The most common cause of this is clostridium difficile infection, which can present on sigmoidoscopy with yellow plaques on the intraluminal wall of the colon.

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19
Q

Which antibiotics are most likely to cause C. difficile infection? [2]

A

Second and third-generation cephalosporins are now the leading cause of C. difficile.

Clindamycin is historically associated with causing C. difficile but the aetiology has evolved significantly over the past 10 years.

C. difficile: think C!

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20
Q

First episode of C. difficile infection:

Oral [] is the first line antibiotic for use in patients with C. difficile infection
second-line therapy: oral []
third-line therapy: oral [] +/- IV []

A

Oral vancomycin is the first line antibiotic for use in patients with C. difficile infection
second-line therapy: oral fidaxomicin
third-line therapy: oral vancomycin +/- IV metronidazole

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21
Q

How do you differentiate between moderate and severe C. diff infection? [1]

A

A raised WBC count (but less than 15 * 109 per litre) is indicative of a moderate C. difficile infection.

If the WBC count is greater than 15 * 109 per litre, it is indicative of a severe infection.

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22
Q

State 7 red flag symptoms when asking about dyspepsia [7]

A
  • dysphagia
  • weight loss (unintentional)
  • persistent vomiting
  • epigastric mass
  • GI bleeding
  • iron deficiency
  • new/ persistent unexplained symptoms > 55y
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23
Q

A ptx presents with upper GI discomfort but after endoscopy there is no evidence of an ulcer. What is this called? [1]

A

Non-ulcer dyspepsia

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24
Q

State the 4 most common causes of dyspepsia [4]

A
  • No lesions / non-ulcer dyspepsia (75%)
  • Peptic ulcer disease (10-15%)
  • Oesphagitis (15%)
  • Cancer (2%)
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25
Name 4 factors that increase the likelyhood of GORD [4]
- **Obesity** (BMI > 30; increases intra-abdominal pressure) - **Smoking, alchohol and coffee** - **Drugs** (relax LOS): tricyclics, anticholinergics, nitrates, calcium channel blockers - **Fatty foods** - **Pregnancy** NB: no association with H. pylori. }
26
Describe the pathophysiology of GORD [3]
- **High intra-abdominal pressure** combined with **LOS relaxation and / or abnormalities** causes **gastric** **acid**, **bile**, **pepsin** and **pancreatin** enzymes are able to **reflux** back into the **oesophagus**, causing **mucosal injuries** - Often combined with **decreased** **oesophageal motility**, causing **decreased oesophageal clearance** - **The gastric acid levels are normal, just in the wrong place**
27
Describe a cause of LOS dysfunction [1]
**Hiatus hernia**: **herniation** of the **stomach up through the diaphragm.** Causes the opening from the oesophagus to the stomach to be wider, and more **stomach content can reflux into the oesophagus**
28
Describe the 4 different types of hiatus hernia [4]
**Type 1**: Sliding **Type 2**: Rolling **Type 3:** Combination of sliding and rolling **Type 4:** Large opening with additional abdominal organs entering the thorax
29
GORD can lead to macroscopic oesophagitis. Define macroscopic oesophagitis [1]
Ulcerations of the oesophagus
30
Why is GORD developing macroscopic oesophagitis clinically signfiicant? [3]
- **Causes strictures** - Can cause **Barrett**'s **oesophagus**: can lead to cancer
31
Describe diagnostic investigations for GORD [3]
**Therapeutic trial of PPI:** - i.e. 40mg of omeprazole for 2 weeks and if the symptoms are completely resolved on that and no alarm symptoms, this may be a reasonable diagnostic tes **Endoscopy** (NB: ~ 50% have no lesions); - used to create **Los Angeles scoring system** for oesophagitis **Oesophageal function testing**: - can **monitor pH over 24 hours** using a small sensor
32
Describe the LA Classification of oesophagitis [4]
**Grade A** - At least one mucosal break, up to 5 mm, that does not extend between the tops of two mucosal folds **Grade B:** - At least one mucosal break, more than 5 mm long, that does not extend between the tops of two mucosal folds **Grade C:** - At least one mucosal break that is continuous between the tops of two or more mucosal folds but which involve less than 75% of the circumference **Grade D:** - At least one mucosal break which involves at least 75% of the esophageal circumference
33
State the therapeutic management for GORD - Therapeutics [4] - Surgery [1]
Drugs: If no red flags: **4 week PPI course**: - **omeprazole** **Antiacids**: **Mg trisilicate** **Alginates**: **Gaviscon** **Acid suppression**: - PPIs: **omeprazole** and **lansoprazole** - or H2 receptor antagonists: **famotidine** or **ranitidine** Surgery: - **laparoscopic fundoplication:** tying the fundus of the stomach around the lower oesophagus to narrow the lower oesophageal sphincter
34
Describe the pathophysiology of H. pyorli cause gastritis, uclers and stomach cancer [3]
H. pylori goes into gastric mucosa; exposing epithelial cells below to stomach acid H. pylori produces ammonium hydroxide; neutralises the acid around the bacteria and also produces toxins Ammonia & toxins causes gastric mucosal damage
35
Describe the treatment regime if a patient tests postive for H. pylori [6] How long is treatment for? [1]
7 Day treament plan of triple therapy: **PPI**: - **omeprazole** **Antibiotics** (**two** required): - **amoxicillin** - **clathromyocin** - **metronidazole** (increasing resistance has limited its usefulness) - **Bismuth** - **Metoclopramide** - **Vasopressin** 7 days
36
Describe the pathophysiology of Barrett's oesophagus (BO) [2]
**Chronic** **oesophageal** **injury** from **chronic reflux of gatstric contents**; causes a change from s**quamous to columnar epithelium** (process is called metaplasia)
37
Describe why BO is a clincially significant disease [2]
**BO is pre-malignant**; high risk of deveoping **oesophageal adenocarcinoma** (via reflux associated DNA damage) There can be a **stepwise progression from no dysplasia to low-grade dysplasia, high-grade dysphasia, and adenocarcinoma**.
38
Describe the treatment for non-dysplastic BO [2] low-grade dysplasia BO [2] high-grade dysplasia [3]
non-dysplastic BO: - **PPI** (omeprazole) - **Anti-reflux surgery** (Nissen fundoplication) low-grade dysplasia BO - **radiofrequency ablation** - **consider PPI** high-grade dysplasia - **radiofrequency ablation** - **consider PPI** - **oesophagectomy**
39
Describe what Eosinophilic oesophagitis (EoO) is [2]
Chronic, immune-mediated/allergen-mediated clinicopathological condition: - **oesophageal dysfunction** (e.g., dysphagia and food impaction in adolescents and adults, and vomiting, regurgitation, heartburn, abdominal pain) **AND** - Histologically: **eosinophilic infiltration** of the oesophageal epithelium of ≥15 eosinophils
40
How do you diagnose EoO? [1] How do you treat? [2]
Diagnose: **biopsy** Tx: **swallow inhaled steroids; exclusion diet**
41
Describe two motility disorders that can cause dysphagia [2]
**Achalasia**: increased tone of LOS; can't relax **Presbyoesophagus**: elderly; peristalsis ineffective
42
How do PPIs work? [1]
PPIs form the cornerstone of GORD treatment. PPIs **prevent acid production** within the stomach through **inhibition of H+/K+ ATPases in parietal cells.**
43
What is the name of the surgery for GORD? [1]
Nissen fundoplication.
44
State five drug classes that can cause GORD [5]
* **tricyclic** * **anticholinergics** * **nitrates** * **CCBs** * **NSAIDs**
45
Describe symptoms of GORD [5]
**Heartburn** **Retrosternal discomfort after meals** **Belching** **Halitosis** **Acid brash** **Increased salivation** (mouth fills with saliva)
46
State 3 extra-oesophageal symptoms of GORD [3]
**Nocturnal asthma** **Chronic cough** **Laryngitis** Sinusitis
47
Which form of testing for H. pylori is used for **post-eradication therapy**? [1]
**Urea breath test** is the only test recommended for H. pylori post-eradication therapy
48
Which form of Which form of testing for H. pylori is used for **diagnosis**? [1]
The **stool** **test** is often used to **diagnose** Helicobacter pylori, but cannot be used to test for eradication as there is insufficient evidence for this.
49
Which form of testing for H. pylori is used for **during endoscopy**? [1]
**CLO testing** is a **rapid urease test** that is done during endoscopy to detect Helicobacter pylori and relies on the fact that the bacteria contain the urease enzyme . It is approximately 90% sensitive, however it is an invasive test and is not recommended for eradication testing unless a patient requires an endoscopy.
50
What is the NICE first line treatment for H. pylori? [3]
A **proton pump inhibitor**, plus **amoxicillin**, and either **clarithromycin** or **metronidazole**
51
Achalasia is associated with which type of oesophageal cancer? [1] Name a significant risk factor for this cancer [1]
**Squamous cell cancer** **Smoking**
52
What is the difference in location of adenocarcinoma and squamous cell carcinoma of oesophagus? [2]
**Adenocarcinoma**: Lower third - near the gastroesophageal junction **SSC**: Upper two-thirds of the oesophagus
53
Describe the blood results for a patient with Coeliac [4]
**normocytic anaemia:** causes malabsorption of iron, folate and B12 - compensates to make normocytic Raised **WCC** and **CRP** Positive for **IgA-tTG** Positive for **endomysial antibody (EMA)**: a more expensive alternative to IgA-tTG
54
Why can patients have false negatives on a celiac disease antibody test when investigating for coeliac?
**May be suffering from IgA deficiency**: so **IgA-tTG** may not be positive **IgA deficiency** is **significantly** **more** **common** in people with **coeliac disease than in the general population.**
55
What is the seroligcal test of choice for a coeliac patient with IgA defiency? [1]
**IgG DGP** (deamidated gliadin peptide)
56
Explain why you would perfom a skin biopsy for a coeliac patient? [1] Explain the pathophysiology of this disease [1]
test initially in any patient with skin lesions suggestive of **dermatitis herpetiformis**: - caused by **granular** **deposits** of **IgA** at the **dermal** **papillae** of **lesional** **and perilesional skin** by direct immunofluorescence
57
Which three antibodies are related to coeliac? [3]
Anti-tissue transglutaminase antibodies (anti-TTG) Anti-endomysial antibodies (anti-EMA) Anti-deamidated gliadin peptide antibodies (anti-DGP)
58
Which HLAs is coliac particularly associated with? [2]
HLA-DQ2 HLA-DQ8
59
The first line blood test is for Anti-tissue transglutaminase antibodies (anti-TTG) and what else? [1]
**Total immunoglobulin A levels** (to **exclude IgA deficiency**)
60
Coeliac disease can effect which organ? [1] Why is this clinically significant? [3]
Causes **hyposplenism**: means that patients are at risk of: - **Pneumococcus** - **Haemophilus influenzae** - **meningococcus**
61
Name [1] and explain [3] an MSK complication of coeliac.
**Osteoporosis**: **Reduced bone mineral density** is common in coeliac disease and often improves significantly within 1 year of gluten withdrawal. Occurs due to: * **release of pro-inflammatory cytokines** * **calcium malabsorption** * **activation of osteoclasts**
62
Which cancer is associated iwth coeliac? [1]
Enteropathy associated T cell lymphoma of smal intestine
63
Why may coeliac disease lead to fat malabsorption? [2]
Decrease in absorptive surface area Decrease in absorption of fat soluble vitamins: **ADEK**
64
Describe what is meant by refractory coeliac disease [1] Describe the two classifcations [2]
**Refractory coeliac disease:** **persistent** or **recurrent** **symptoms** and signs of malabsorption **despite** **adherence** to a **strict gluten-free diet for at least 12 months**. Believed to be **independent** of **gluten** since the gluten-free diet is not effective in preventing the lymphocytes from increasing. **Type I**: - Have < 20% abnormal lymphocytes **Type II:** - Have >20% abnormal lymphocytes
65
State why and explain which type of refractory coeliac disease is more prone to cancers [2]
**Type II:** - Type II have a greater than 50 percent chance of the **abnormal lymphocytes spreading outside the gut** - Causes: developing **enteropathy-associated T-cell lymphoma (EATL)**
66
Which type of cancer in the GI tract do coelaic patients suffer a risk of developing? [1]
**Small bowel adenocarcinoma**
67
Describe two neuorogical complications of coeliac disease [2]
*Anti-gluten antibodies created by the immune system of patients with celiac disease in response to gluten are thought to damage nerves* **Peripheral neuropathy**: Coeliac disease can be associated with peripheral neuropathy, presenting as numbness, tingling, or burning sensations in the extremities. **Gluten ataxia:** This rare neurological complication is characterized by gait disturbances, dysarthria, and nystagmus. A gluten-free diet may improve symptoms in some cases.

Yr3 Revision (37 decks)

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