L59, 60 Gastric disorders, CBDs Flashcards
(86 cards)
1
Q
59
What are the major gastric acid-related disorders?
A
Dyspepsia, Gastro-oesophageal reflux disease (GORD), peptic ulcers due to H. pylori, NSAIDs, stress, and Zollinger-Ellison syndrome.
2
Q
59
What are the symptoms of dyspepsia?
A
Indigestion, pain, discomfort, bloating, belching—linked to excess or leakage of acid and mucosal damage.
3
Q
59
What are major signs/symptoms of GORD?
A
Heartburn, acid reflux, dysphagia, dry cough, nausea, chest pain, sore throat.
4
Q
59
What causes GORD at the anatomical level?
A
Abnormal relaxation of the gastro-oesophageal sphincter; hiatal hernia increases reflux frequency.
5
Q
59
What factors contribute to peptic ulcer formation?
A
↑ Acid/pepsin secretion, ↓ mucus/bicarbonate protection, H. pylori, NSAIDs, stress.
6
Q
59
What cells and mechanisms regulate gastric acid secretion?
A
Parietal cells use H⁺/K⁺ ATPase (‘proton pump’); stimulated by histamine, gastrin, and ACh; inhibited by prostaglandins.
7
Q
59
What is Zollinger-Ellison syndrome?
A
Gastrin-secreting tumor → excessive gastric acid → ulcers.
8
Q
59
Name 4 strategies for treating acid-related disorders.
A
Lifestyle changes, antacids, acid secretion inhibitors, mucosal protection, and antibiotics (for H. pylori).
9
Q
59
How do antacids work? Give examples.
A
Neutralize acid & raise pH to inhibit pepsin. Examples: magnesium hydroxide, aluminium hydroxide, sodium bicarbonate.
10
Q
59
Name 3 classes of acid secretion inhibitors with examples.
A
H₂ antagonists (cimetidine, ranitidine)
PPIs (esomeprazole, lansoprazole)
Prostaglandin analogues (misoprostol)
11
Q
59
What drugs protect gastric mucosa?
A
Misoprostol, sucralfate (forms protective gel), bismuth chelate (antibacterial & protective).
12
Q
59
What is Helicobacter pylori and how is it spread?
A
Gram-negative bacterium, spread via faeco-oral route; linked to most duodenal and many gastric ulcers.
13
Q
59
How does H. pylori contribute to ulcer formation?
A
Damages mucosa with toxins, pepsin; increases gastrin → ↑ acid; leads to chronic gastritis, functional dyspepsia, and cancer risk.
14
Q
59
How is H. pylori infection diagnosed?
A
Urea breath test, blood antibody test, stool antigen test, biopsy during endoscopy.
15
Q
59
What is the standard eradication therapy for H. pylori?
A
Triple therapy: PPI + amoxicillin + metronidazole or clarithromycin; sometimes includes bismuth chelate.
16
Q
59
What role do prostaglandins play in gastric protection?
A
They inhibit acid secretion and stimulate mucus and bicarbonate production, maintaining mucosal integrity.
17
Q
59
How do NSAIDs cause peptic ulcers?
A
They inhibit COX enzymes → ↓ prostaglandin synthesis → ↓ mucus/HCO₃⁻ protection → mucosal injury.
18
Q
59
What are the long-term risks associated with chronic H. pylori infection?
A
Chronic gastritis, mucosal atrophy, duodenal/gastric ulcers, and increased risk of gastric cancer.
19
Q
59
Why are PPIs considered more effective than H₂ antagonists?
A
PPIs irreversibly block H⁺/K⁺ ATPase (the final step in acid secretion), offering longer-lasting and more profound acid suppression.
20
Q
59
What is the mechanism of action of sucralfate?
A
Forms a viscous, protective gel in acidic pH that binds ulcer craters and shields them from acid/pepsin.
21
Q
59
What is a hiatal hernia and how does it relate to GORD?
A
A portion of the stomach protrudes through the diaphragm; weakens sphincter function and worsens acid reflux.
22
Q
59
What lifestyle changes help manage GORD and dyspepsia?
A
Weight loss, avoiding trigger foods (spicy, fatty), elevating head during sleep, not eating late at night, smoking cessation.
23
Q
59
What is functional dyspepsia?
A
Chronic indigestion symptoms without identifiable structural cause; often linked to H. pylori or visceral hypersensitivity.
24
Q
59
A 55-year-old man presents with epigastric pain relieved by eating, but returns a few hours later. Endoscopy confirms a duodenal ulcer. He is H. pylori positive. Which is the most appropriate first-line treatment?
A) Ranitidine alone
B) Omeprazole plus misoprostol
C) Esomeprazole + amoxicillin + clarithromycin
D) Sucralfate and antacids
A
✅ Answer: C
💡 Explanation: Triple therapy with a PPI + 2 antibiotics is standard for H. pylori eradication
25
# 59
Which mechanism most accurately explains NSAID-induced ulceration?
A) Direct cytotoxicity from acid-base imbalance
B) Overstimulation of H₂ receptors
C) Decreased prostaglandin synthesis → ↓ mucosal protection
D) Increased secretion of hydrochloric acid
✅ Answer: C
💡 Explanation: NSAIDs inhibit COX enzymes, reducing protective prostaglandin synthesis.
26
# 59
A patient with persistent heartburn and regurgitation is found to have a sliding hiatal hernia. Which of the following explains how this worsens GORD?
A) Enhances acid secretion
B) Delays gastric emptying
C) Weakens lower oesophageal sphincter competence
D) Stimulates vagal tone
✅ Answer: C
💡 Explanation: The sliding hernia alters diaphragm-sphincter alignment, allowing more reflux.
27
# 59
Which of the following statements about proton pump inhibitors is TRUE?
A) They competitively block histamine H₂ receptors
B) Their action lasts only 4–6 hours
C) They irreversibly inhibit H⁺/K⁺ ATPase in parietal cells
D) They neutralize gastric acid directly
✅ Answer: C
💡 Explanation: PPIs bind irreversibly to the proton pump, resulting in long-lasting acid suppression.
28
# 59
A 48-year-old woman is taking NSAIDs long-term for arthritis. What would be the best prophylactic agent to prevent NSAID-induced ulcers?
A) Ranitidine
B) Misoprostol
C) Sucralfate
D) Calcium carbonate
✅ Answer: B
💡 Explanation: Misoprostol is a prostaglandin E₂ analogue that protects mucosa from NSAID damage.
29
# 59
Which of the following diagnostic tests for H. pylori directly detects active infection rather than past exposure?
A) Blood antibody test
B) Urea breath test
C) Serological ELISA
D) IgG titre assay
✅ Answer: B
💡 Explanation: The urea breath test measures active urease activity, indicating current infection.
30
# 59
A patient presents with severe recurrent peptic ulcers and elevated gastrin levels. Which condition is most likely?
A) Hiatal hernia
B) Crohn’s disease
C) Zollinger-Ellison syndrome
D) Autoimmune gastritis
✅ Answer: C
💡 Explanation: Gastrin-secreting tumors (Zollinger-Ellison) cause extreme acid hypersecreti
31
# 59
Which drug forms a physical barrier over ulcer craters and protects them from acid and pepsin?
A) Omeprazole
B) Sucralfate
C) Misoprostol
D) Bismuth subsalicylate
✅ Answer: B
💡 Explanation: Sucralfate forms a viscous gel that adheres to ulcerated tissue in acidic pH.
32
# 59
Which combination is MOST effective for long-term remission of duodenal ulcers caused by H. pylori?
A) Sucralfate + ranitidine
B) Esomeprazole + amoxicillin + clarithromycin
C) Omeprazole + magnesium trisilicate
D) Bismuth chelate + misoprostol
✅ Answer: B
💡 Explanation: Triple therapy eradicates H. pylori and allows ulcer healing and remission.
33
# 59
A patient has refractory GORD despite maximal PPI therapy. What is the most appropriate next step?
A) Increase PPI dose
B) Add H₂ antagonist
C) Evaluate for surgical fundoplication
D) Prescribe misoprostol
✅ Answer: C
💡 Explanation: Surgical options are considered in refractory GORD cases not responding to medical therapy.
34
# 59
A 63-year-old patient is taking omeprazole for chronic reflux. He now presents with fatigue, pallor, and glossitis. Labs show macrocytic anemia. What is the most likely cause?
A) Iron deficiency due to occult GI bleeding
B) Vitamin B12 deficiency due to impaired absorption
C) Folic acid deficiency from dietary restriction
D) Autoimmune gastritis causing parietal cell loss
✅ Answer: B
💡 Explanation: Chronic PPI use ↓ gastric acid → ↓ intrinsic factor activation → impaired B12 absorption → macrocytic anemia.
35
# 59
Which of the following best explains why bismuth chelate is used in H. pylori eradication regimens?
A) It directly inhibits the proton pump
B) It neutralizes gastric acid and inhibits pepsin
C) It enhances mucosal prostaglandin production
D) It has antibacterial properties and forms a protective barrier
✅ Answer: D
💡 Explanation: Bismuth has bactericidal action against H. pylori and coats ulcers to protect mucosa.
36
# 59
A patient with no history of H. pylori or NSAID use develops multiple gastric ulcers. Gastrin levels are elevated. What diagnostic test should be done next?
A) Urea breath test
B) Endoscopic biopsy
C) Serum chromogranin A
D) Secretin stimulation test
✅ Answer: D
💡 Explanation: A positive secretin stimulation test helps confirm Zollinger-Ellison syndrome by paradoxically raising gastrin levels further.
37
# 59
Why are prostaglandin analogues contraindicated in pregnancy?
A) They reduce fetal renal perfusion
B) They impair folate metabolism
C) They stimulate uterine contractions
D) They cross the placenta and cause teratogenicity
✅ Answer: C
💡 Explanation: Misoprostol (PGE1 analogue) can cause uterine contractions → miscarriage/preterm labor.
38
# 59
Which drug combination is LEAST effective in eradicating H. pylori and may promote resistance?
A) Clarithromycin + metronidazole
B) PPI + amoxicillin + clarithromycin
C) PPI + tetracycline + bismuth + metronidazole
D) PPI + sucralfate + antacids
✅ Answer: D
💡 Explanation: Sucralfate and antacids provide symptomatic relief but lack antibacterial activity — ineffective for H. pylori.
39
# 59
A patient reports black stools while taking multiple antacids. He is not bleeding. Which compound most likely caused this?
A) Magnesium hydroxide
B) Aluminium hydroxide
C) Bismuth subsalicylate
D) Calcium carbonate
✅ Answer: C
💡 Explanation: Bismuth darkens stool (harmlessly), often confused with melena (GI bleeding).
40
# 59
A patient on long-term PPI therapy develops rebound acid hypersecretion after abrupt cessation. Why?
A) Acid-neutralizing enzymes increase in response
B) Parietal cell mass increases during PPI use
C) Upregulation of H₂ receptors
D) Hypergastrinemia during PPI therapy stimulates parietal cells
✅ Answer: D
💡 Explanation: Chronic acid suppression → ↑ gastrin → rebound hypersecretion when PPIs are stopped.
41
# 59
Which of the following would most likely reduce the bioavailability of a concurrently administered oral ketoconazole?
A) Aluminium hydroxide
B) Ranitidine
C) Sucralfate
D) Omeprazole
✅ Answer: D
💡 Explanation: Ketoconazole requires acidic pH for absorption — omeprazole raises pH and reduces its bioavailability.
42
# 59
A 34-year-old man has peptic ulcer symptoms but tests negative for H. pylori. He occasionally uses ibuprofen. What test will best confirm NSAID-related ulceration?
A) Gastrin level
B) Endoscopic biopsy
C) Trial of misoprostol
D) Fecal occult blood test
✅ Answer: C
💡 Explanation: Misoprostol protects against NSAID-induced ulcers — symptom resolution supports NSAID causality.
43
# 59
What is the best explanation why antacids may impair the absorption of tetracycline antibiotics?
A) Antacids neutralize tetracycline
B) Tetracyclines chelate with metal ions (e.g., Mg²⁺, Al³⁺) in antacids
C) Antacids alter gut motility
D) Antacids stimulate bacterial resistance
✅ Answer: B
💡 Explanation: Divalent/trivalent cations in antacids bind tetracyclines, forming insoluble complexes → ↓ absorption.
44
# 60
What are the key roles of gut microflora in health and disease?
Aid digestion, influence immunity, and may trigger inflammation in IBD; also involved in drug metabolism.
45
# 60
Where are most gut bacteria located, and what percentage of faecal mass do they represent?
Mostly in the large bowel; ~60% of faecal mass is bacterial.
46
# 60
How can microflora composition be altered?
Diarrhoeal illness, antibiotic use, and other environmental factors.
47
# 60
What are the hallmark symptoms of IBD?
Bloody diarrhoea, abdominal pain, anaemia, fever, weight loss, and fatigue.
48
# 60
How does ulcerative colitis (UC) differ anatomically from Crohn’s disease (CD)?
UC affects only the colon and rectum; CD can affect any part of the GI tract (mouth to anus), sparing the rectum.
49
# 60
What pathological features distinguish Crohn’s disease?
Fistulae, strictures, peri-anal disease, transmural inflammation, and patchy lesions.
50
# 60
What are the main drug classes used in IBD?
Aminosalicylates, corticosteroids, immunosuppressants, biologics, antibiotics.
51
# 60
What is the role of 5-aminosalicylates (5-ASA) in IBD?
Anti-inflammatory agents, mainly used to maintain remission in UC.
52
# 60
Why is sulfasalazine associated with side-effects?
It's broken down in the colon to 5-ASA and sulfapyridine; the latter causes nausea and infertility.
53
# 60
Name newer aminosalicylate formulations that avoid sulphonamides.
Mesalazine (Pentasa®, Asacol®), olsalazine (Dipentum®), balsalazide (Colazide®).
54
# 60
What is the advantage of budesonide over prednisolone?
Modified release → local GI effect with fewer systemic side-effects.
55
# 60
Name two immunosuppressants used in IBD.
Azathioprine and ciclosporin.
56
# 60
What are biologics and when are they used in IBD?
Monoclonal antibodies (e.g., infliximab, vedolizumab), used in moderate to severe cases unresponsive to standard treatment.
57
# 60
What is vedolizumab's mechanism of action?
Inhibits 'gut-homing' T-cells → reduces GI inflammation.
58
# 60
Why are antibiotics used in Crohn’s disease?
To reduce bacteria-driven inflammation, especially in peri-anal disease.
59
# 60
Name two antibiotics commonly used in Crohn’s colitis.
Metronidazole and ciprofloxacin.
60
# 60
What is the purpose of faecal microbiota transplant (FMT)?
Re-colonise the gut to treat refractory Clostridium difficile infection and possibly IBD.
61
# 60
What are key features of IBS?
Abdominal pain, altered bowel habits (diarrhoea or constipation), no identifiable pathology.
62
# 60
What are common non-GI symptoms associated with IBS?
Lethargy, anxiety, depression.
63
# 60
What are the treatment strategies for IBS?
Symptomatic control: laxatives, anti-diarrhoeals, antispasmodics, antidepressants, and 5-HT receptor agents.
64
# 60
Name two anti-spasmodic agents used in IBS.
Alverine (Spasmonal®), mebeverine (Colofac®).
65
# 60
What is the role of tricyclic antidepressants in IBS?
Used in low doses for abdominal pain—not for mood.
66
# 60
How do 5-HT receptor agents help IBS?
Alosetron (5-HT₃ antagonist): for diarrhoea-predominant IBS
Tegaserod (5-HT₄ agonist): for constipation-predominant IBS
67
# 60
Why are NSAIDs generally avoided in IBD?
NSAIDs can exacerbate inflammation in IBD patients, potentially triggering disease flares.
68
# 60
What is a common surgical indication in Crohn’s disease?
Strictures, fistulae, or refractory disease may require bowel resection or fistula repair.
69
# 60
Why is mesalazine more effective in UC than Crohn’s disease?
UC is confined to the colon, where 5-ASA acts topically; CD often affects the small intestine, where standard mesalazine isn’t released effectively.
70
# 60
What are the differences between acute, chronic, and maintenance treatment objectives in IBD?
Acute attacks: corticosteroids ± immunosuppressants
Maintenance: 5-ASA
Chronic active disease: 5-ASA, corticosteroids, or azathioprine
71
# 60
What makes budesonide preferable in mild-moderate Crohn’s disease?
It has high first-pass metabolism → fewer systemic corticosteroid effects.
72
# 60
What is the benefit of enteric-coated 5-ASA formulations?
Delayed release ensures the drug reaches the large bowel, where inflammation occurs in UC.
73
# 60
Why might IBS be considered a functional GI disorder?
IBS presents with symptoms but no identifiable structural abnormality on investigation.
74
# 60
What psychological factors influence IBS?
Anxiety, stress, and depression can exacerbate gut sensitivity and motility, contributing to IBS flares.
75
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What is a fistula and what causes it in Crohn’s disease?
An abnormal connection between bowel and other structures, due to transmural inflammation.
76
# 60
How do anti-TNFα agents like infliximab work in IBD?
They neutralise TNF-alpha, a key pro-inflammatory cytokine in IBD pathogenesis.
77
# 60
A 35-year-old man presents with chronic diarrhoea, weight loss, and peri-anal abscesses. Endoscopy reveals patchy inflammation and deep ulcers in the terminal ileum. What is the most appropriate long-term maintenance therapy to prevent relapse?
A) Prednisolone
B) Sulfasalazine
C) Azathioprine
D) Ciprofloxacin
✅ Answer: C
💡 Explanation: Azathioprine is used to maintain remission in Crohn’s. Corticosteroids induce remission, but aren’t suitable long-term.
78
# 60
A patient with ulcerative colitis is in remission on mesalazine. She becomes pregnant and reports mild lower rectal bleeding. Which change in therapy is most appropriate?
A) Start oral corticosteroids
B) Add rectal mesalazine
C) Switch to sulfasalazine
D) Begin azathioprine
✅ Answer: B
💡 Explanation: Rectal mesalazine is effective and safe in pregnancy for distal/rectal flares.
79
# 60
A 44-year-old man with longstanding Crohn’s disease develops shortness of breath, fatigue, and elevated MCV. He has been on omeprazole and sulfasalazine. What is the most likely cause of his anaemia?
A) Iron deficiency from occult bleeding
B) Folate deficiency due to sulfasalazine
C) Vitamin B12 deficiency due to PPI use
D) Bone marrow suppression from azathioprine
✅ Answer: B
💡 Explanation: Sulfasalazine impairs folate absorption → megaloblastic (macrocytic) anaemia.
80
# 60
A 29-year-old female with diarrhoea-predominant IBS is anxious and reports frequent cramps. Which drug could relieve symptoms while also targeting the underlying psychogenic component?
A) Alverine
B) Amitriptyline
C) Ranitidine
D) Mesalazine
✅ Answer: B
💡 Explanation: Low-dose TCAs like amitriptyline reduce visceral pain and anxiety — effective in IBS.
81
# 60
A patient with Crohn’s disease affecting the ileum and colon has failed treatment with mesalazine and corticosteroids. What is the next step in moderate-to-severe disease unresponsive to conventional therapy?
A) Increase mesalazine dose
B) Start vedolizumab
C) Switch to balsalazide
D) Start sucralfate
✅ Answer: B
💡 Explanation: Vedolizumab (anti-integrin) is a second-line biologic for moderate-severe IBD unresponsive to first-line therapy.
82
# 60
Which of the following best explains why mesalazine is more effective in ulcerative colitis than Crohn’s disease?
A) It’s better absorbed in the colon than the small intestine
B) UC has more bacterial colonisation
C) It acts topically in the colon and doesn’t reach the small bowel
D) Crohn’s patients metabolise 5-ASA too quickly
✅ Answer: C
💡 Explanation: Standard formulations release 5-ASA in the colon, not useful in small bowel CD.
83
# 60
A 30-year-old man with Crohn’s colitis presents with elevated liver enzymes. He is currently taking azathioprine. Which metabolic complication is most concerning?
A) Cholestasis
B) Pancreatitis
C) Portal hypertension
D) Hepatic steatosis
✅ Answer: B
💡 Explanation: Azathioprine may cause idiosyncratic pancreatitis, especially in early treatment.
84
# 60
Why is budesonide preferred over prednisolone in mild to moderate ileal Crohn’s disease?
A) Budesonide has higher anti-inflammatory potency
B) Budesonide acts systemically
C) Budesonide has extensive first-pass metabolism → lower systemic effects
D) Budesonide is better absorbed in the stomach
✅ Answer: C
💡 Explanation: Budesonide’s first-pass metabolism limits systemic exposure, reducing side effects.
85
# 60
A patient with IBS is given alosetron. What is the key safety concern associated with this drug?
A) Hepatic necrosis
B) Ischaemic colitis
C) Renal stones
D) QT prolongation
✅ Answer: B
💡 Explanation: Alosetron (5-HT₃ antagonist) is effective in IBS-D but has a rare risk of ischaemic colitis.
86
# 60
Which mechanism best explains how peppermint oil (Colpermin®) relieves symptoms in IBS?
A) Increases serotonin release
B) Inhibits prostaglandin synthesis
C) Blocks H₂ receptors
D) Acts as a smooth muscle relaxant via calcium channel blockade
✅ Answer: D
💡 Explanation: Peppermint oil reduces GI spasm by blocking calcium channels in smooth muscle.
