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Pharmacy - Year 2 > Pharm GI > Flashcards

Pharm GI Flashcards

1
Q

SBA: What legislative act primarily governs the control of poisons in the UK?

A

Answer: The Poisons Act 1972.

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2
Q

SBA: What was the purpose of the Deregulation Act 2015 in relation to the Poisons Act?

A

Answer: To respond to terrorism threats by introducing ‘regulated’ and ‘reportable’ substances.

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3
Q

SBA: What is required to supply regulated substances under the Poisons Act?

A

Answer: An Explosives Precursors and Poisons (EPP) licence or a recognised non-GB licence.

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4
Q

SBA: How must poisons be stored in retail premises?

A

Answer: In a cupboard or drawer reserved solely for poisons or partitioned from accessible areas.

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5
Q

SBA: What is the reporting timeframe for suspicious transactions involving reportable substances?

A

Answer: Within 24 hours.

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6
Q

SBA: Which organisation enforces the Poisons Act 1972?

A

Answer: The General Pharmaceutical Council (GPhC).

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7
Q

SBA: What is completely denatured alcohol (CDA) primarily used for?

A

Answer: Heating, lighting, cleaning, and general domestic use.

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8
Q

SBA: What is the mechanism of action of industrial denatured alcohol (IDA)?

A

Answer: Not for consumption; used in manufacturing (e.g., hand sanitizers).

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9
Q

SBA: What label must be included on chemicals classified as hazardous under GB CLP regulations?

A

Answer: Hazard pictograms, signal words, and precautionary statements.

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10
Q

SBA: Which category under drug precursor regulations includes substances like piperonal used to produce methamphetamine?

A

Answer: Category 1.

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11
Q

EMQ: Match the poison classification to its description.

A

Regulated substances: Require EPP licences for specific activities.
Reportable substances: Require monitoring and reporting of suspicious transactions.
Exempt substances: Medicinal and veterinary products.

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12
Q

EMQ: Match the requirement to its regulated substance.
Record of purchase:
Report suspicious transactions:
Storage:

A

Record of purchase: Name and address of purchaser, quantity, and purpose.
Report suspicious transactions: Within 24 hours to authorities.
Storage: Partitioned storage inaccessible to customers.

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13
Q

EMQ: Match the class of denatured alcohol to its use.

A

Completely denatured alcohol (CDA): General domestic use.
Industrial denatured alcohol (IDA): Manufacture of hand sanitizers.
Trade-specific denatured alcohol (TSDA): Industry-specific applications.

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14
Q

EMQ: Match the hazard classification to its example

A

Physical hazard: Flammable liquid.
Health hazard: Carcinogenic substances.
Environmental hazard: Harmful to aquatic life.

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15
Q

EMQ: Match the chemical regulatory requirement to its description.

A

Labelling: Signal words, hazard pictograms, and precautionary statements.
Safety Data Sheets: Provided to purchasers of hazardous chemicals.
Packaging: Child-resistant fastenings and tactile warnings.

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16
Q

What are the key requirements for the sale and supply of regulated poisons?

A

Answer: Must be sold through lawful retail pharmacy businesses under pharmacist supervision, with a record of purchaser details and purpose.

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17
Q

Describe the classification of denatured alcohols and their use cases.

A

Answer:
CDA: Heating, lighting, and cleaning.
IDA: Manufacturing (e.g., hand sanitizers).
TSDA: Trade-specific purposes. (2 marks)

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18
Q

What are the labelling requirements for hazardous chemicals under GB CLP?

A

Answer: Must include hazard pictograms, signal words (‘Warning’ or ‘Danger’), and precautionary statements. (2 marks)

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19
Q

Explain the reporting obligations for suspicious transactions involving reportable substances.

A

Answer: Suspicious transactions must be reported within 24 hours to the anti-terrorism hotline (0800 789321) or local authorities. (2 marks)

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20
Q

List two examples of drug precursors and their potential misuse.

A

Answer:
Piperonal (used to produce methamphetamine).
Acetic anhydride (used to produce heroin). (2 marks)

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21
Q

SBA: What are the four main functions of the gastrointestinal (GI) system?

A

Answer: Ingestion, digestion, absorption, and elimination.

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22
Q

SBA: What is the function of the pyloric sphincter in the stomach?

A

Answer: It prevents backflow of intestinal contents and regulates chyme movement into the small intestine.

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23
Q

SBA: What enzyme is secreted by the salivary glands for carbohydrate digestion?

A

Answer: Amylase.

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24
Q

SBA: What is the primary function of bile salts in digestion?

A

Answer: Emulsification of fats for absorption.

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25
Q

SBA: Which structure in the small intestine is specialized for nutrient absorption?

A

Answer: Villi.

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26
Q

SBA: What is the role of parietal cells in the stomach?

A

Answer: Secretion of hydrochloric acid and intrinsic factor.

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27
Q

SBA: What is the function of the enteric nervous system in the GI tract?

A

Answer: Regulates GI motility and secretion independently of the central nervous system.

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28
Q

SBA: What is the primary role of goblet cells in the intestines?

A

Answer: Secretion of mucus to protect the intestinal lining.

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29
Q

SBA: What triggers the cephalic phase of digestion?

A

Answer: Sensory stimuli such as the sight, smell, or thought of food.

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30
Q

SBA: Which hormone stimulates the gallbladder to contract and release bile?

A

Answer: Cholecystokinin (CCK).

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31
Q

EMQ: Match the GI structure to its primary function.

A

Stomach: Protein digestion via pepsin.
Small intestine: Nutrient and water absorption.
Large intestine: Water and electrolyte absorption.

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32
Q

EMQ: Match the GI secretion to its function.

A

Bicarbonate: Neutralizes stomach acid in the duodenum.
Pepsinogen: Converted to pepsin for protein digestion.
Intrinsic factor: Facilitates vitamin B12 absorption.

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33
Q

EMQ: Match the accessory organ to its contribution.

A

Liver: Bile production for fat digestion.
Pancreas: Secretion of digestive enzymes and bicarbonate.
Gallbladder: Storage and concentration of bile.

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34
Q

EMQ: Match the motility type to its description.

A

Peristalsis: Propels food forward through the GI tract.
Segmentation: Mixes chyme and digestive enzymes in the intestines.
Gastrocolic reflex: Triggers mass movement in the large intestine.

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35
Q

EMQ: Match the immune defense to its mechanism.

A

M cells: Transport antigens to immune cells in Peyer’s patches.
Lysozyme: Breaks down bacterial cell walls in saliva.
Gastric acid: Kills ingested pathogens.

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36
Q

What are the main anatomical regions of the GI tract?

A

Answer: Mouth, oral cavity, oesophagus, stomach, small intestine (duodenum, jejunum, ileum), large intestine, rectum, and anus. (2 marks)

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37
Q

Describe the key roles of the stomach in digestion.

A

Answer:
Secretes gastric acid and enzymes for protein digestion.
Mixes food into chyme using peristaltic movements.
Secretes intrinsic factor for vitamin B12 absorption. (2 marks)

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38
Q

What are the accessory organs of digestion, and what do they contribute?

A

Answer:
Liver: Produces bile.
Pancreas: Secretes digestive enzymes and bicarbonate.
Gallbladder: Stores and concentrates bile. (2 marks)

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39
Q

Explain the role of the enteric nervous system in regulating digestion.

A

Answer: Controls GI motility, secretion, and local reflexes independently of the CNS. (2 marks)

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40
Q

What protective mechanisms exist in the GI tract to prevent damage?

A

Answer:
Mucus secretion protects the lining.
Gastric acid kills pathogens.
Immune cells in Peyer’s patches initiate immune responses. (2 marks)

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41
Q

SBA: What is the primary site of drug absorption in the GI tract?

A

Answer: Small intestine.

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42
Q

SBA: What enzyme digests carbohydrates into monosaccharides?

A

Answer: Amylase.

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43
Q

SBA: What condition is caused by decreased lactase activity?

A

Answer: Lactose intolerance.

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44
Q

SBA: What is the primary mechanism for passive diffusion of drugs across membranes?

A

Answer: Movement down the concentration gradient.

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45
Q

SBA: Which vitamins are absorbed with dietary fats?

A

Answer: Fat-soluble vitamins (A, D, E, K).

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46
Q

SBA: What is the role of bile salts in fat digestion?

A

Answer: Emulsify lipids to form micelles for absorption.

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47
Q

SBA: What percentage of an acidic drug is unionized in the stomach (pH 1.5)?

A

Answer: Approximately 100%.

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48
Q

SBA: Which transporters mediate active absorption of hydrophilic drugs?

A

Answer: Organic anion and cation transporters (OATs and OCTs).

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49
Q

SBA: What determines the ionization of a drug in the GI tract?

A

Answer: The pH of the GI tract and the pKa of the drug.

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50
Q

SBA: What is the pharmacokinetic measure of oral drug absorption efficiency?

A

Answer: Bioavailability (F).

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51
Q

EMQ: Match the macronutrient to its site of absorption.

A

Carbohydrates: Small intestine (as monosaccharides).
Proteins: Small intestine (as amino acids and di/tri-peptides).
Fats: Small intestine (as fatty acids and monoglycerides).

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52
Q

EMQ: Match the factor to its effect on drug absorption.

A

Gastric emptying rate: Faster emptying increases absorption.
Presence of food: Can delay absorption of some drugs.
First-pass metabolism: Reduces bioavailability of some drugs.

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53
Q

EMQ: Match the nutrient to its absorption process.

A

Glucose: Sodium-glucose transporter (SGLT).
Fructose: GLUT5 transporter.
Vitamin B12: Requires intrinsic factor for absorption in the ileum.

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54
Q

EMQ: Match the GI pH to its drug absorption effect.

A

Stomach (pH 1.5): Favors absorption of weak acids.
Small intestine (pH 5.3-6): Optimal for weak bases.
Blood (pH 7.4): Maintains equilibrium for drug distribution.

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55
Q

EMQ: Match the digestion aid to its role.

A

Bile salts: Emulsify fats into micelles.
Pancreatic enzymes: Breakdown carbohydrates, proteins, and fats.
Mucosal enzymes: Final breakdown of disaccharides and peptides.

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56
Q

Describe the absorption process of carbohydrates, proteins, and fats in the GI tract.

A

Answer:
Carbohydrates: Broken into monosaccharides by amylase; glucose absorbed via SGLT2.
Proteins: Digested to amino acids and di/tri-peptides by proteases; absorbed via sodium-dependent transporters.
Fats: Emulsified by bile salts, digested by lipase into fatty acids/monoglycerides, absorbed via micelles. (3 marks)

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57
Q

What factors affect passive drug diffusion in the GI tract?

A

Answer:
Drug concentration gradient.
Lipid solubility of the drug.
Membrane thickness and surface area. (2 marks)

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58
Q

Explain the role of pH in drug absorption in different parts of the GI tract.

A

Answer:
Acidic drugs: Absorbed in the stomach.
Basic drugs: Absorbed in the small intestine.
Ionization depends on pKa and local pH. (2 marks)

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59
Q

What are the advantages of oral drug absorption?

A

Answer:
Large surface area of the small intestine.
Rich vascularization.
Long dwell time in the tract. (2 marks)

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60
Q

What is bioavailability, and how is it calculated?

A

Answer: The proportion of the administered dose that reaches systemic circulation; calculated as AUC (oral)/AUC (IV). (1 mark)

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61
Q

SBA: What is the main role of the gut-associated lymphoid tissue (GALT) in the GI tract?

A

Answer: Provides immune defense by stimulating IgA production and modulating inflammatory responses.

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62
Q

SBA: What is the primary function of bile salts in preventing GI infections?

A

Answer: Disrupt microbial membranes and aid in the elimination of pathogens.

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63
Q

SBA: Which bacterial pathogen is associated with pseudomembranous colitis?

A

Answer: Clostridium difficile.

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64
Q

Answer: Clostridium difficile.

A

Answer: Causes electrolyte and fluid loss, leading to watery diarrhea.

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65
Q

SBA: Which gut flora disruption is commonly caused by tetracycline use?

A

Answer: Microbiota dysbiosis.

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66
Q

SBA: Which component of the lipopolysaccharide (LPS) in Gram-negative bacteria is responsible for endotoxin activity?

A

Answer: Lipid A.

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67
Q

SBA: What is the first-line treatment for mild-to-moderate C. difficile infection?

A

Answer: Oral vancomycin.

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68
Q

SBA: What is the primary mechanism by which probiotics support gut health?

A

Answer: Compete with pathogens for colonization sites and enhance mucosal immunity.

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69
Q

SBA: Which diagnostic method detects C. difficile toxins in stool samples?

A

Answer: PCR-based assays.

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70
Q

SBA: What is the primary risk factor for C. difficile infection?

A

Answer: Prolonged use of broad-spectrum antibiotics.

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71
Q

EMQ: Match the pathogen to its associated infection.

A

Vibrio cholerae: Severe watery diarrhea (“rice-water stools”).
Clostridium difficile: Pseudomembranous colitis.
Norovirus: Acute viral gastroenteritis.

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72
Q

EMQ: Match the bacterial toxin to its mechanism of action.

A

Enterotoxin A: Disrupts tight junctions and causes cytoskeleton disruption.
Pore-forming toxin: Causes leakage of cellular contents.
Superantigen toxin: Overactivates T cells, leading to cytokine storm.

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73
Q

EMQ: Match the GI microbiota function to its description.

A

Structural function: Enhances the epithelial barrier lining.
Metabolic function: Synthesizes vitamins and ferments dietary fibers.
Protective function: Colonization resistance and immune activation.

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74
Q

EMQ: Match the treatment to its GI infection severity.

A

Mild C. difficile infection: Oral vancomycin.
Recurrent C. difficile infection: Oral fidaxomicin.
Life-threatening C. difficile infection: Oral vancomycin plus IV metronidazole.

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75
Q

EMQ: Match the toxin type to its properties.

A

Exotoxin: Heat-labile, secreted by living bacteria.
Endotoxin: Heat-stable, part of Gram-negative bacterial cell wall.

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76
Q

What are the key pathophysiological features of Clostridium difficile infection?

A

Answer:
Disruption of gut microbiota allows colonization by C. difficile.
Toxins A and B damage epithelial cells, leading to increased permeability, inflammation, and diarrhea.
Severe cases cause pseudomembranous colitis and toxic megacolon. (2 marks)

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77
Q

What are the primary risk factors for C. difficile infection?

A

Answer:
Prolonged broad-spectrum antibiotic use.
Hospitalization.
Advanced age or immunosuppression. (2 marks)

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78
Q

What diagnostic methods are used to confirm C. difficile infection?

A

Answer:
Stool PCR for toxin genes.
Detection of toxins A and B using immunoassays.
Colonoscopy to identify pseudomembranes in severe cases. (2 marks)

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79
Q

Describe the treatment options for mild-to-moderate and severe C. difficile infections.

A

Answer:
Mild-to-moderate: Oral vancomycin or fidaxomicin.
Severe: Oral vancomycin with IV metronidazole.
Discontinue causative antibiotics when possible. (2 marks)

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80
Q

What preventive measures can reduce the risk of GI infections?

A

Answer:
Judicious use of antibiotics.
Hand hygiene and infection control in healthcare settings.
Probiotics in high-risk patients (controversial). (2 marks)

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81
Q

SBA: What is the primary cause of GORD?

A

Answer: Weakening or relaxation of the lower oesophageal sphincter.

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82
Q

SBA: What is the main risk factor for GORD?

A

Answer: Obesity.

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83
Q

SBA: What is the first-line pharmacological treatment for GORD?

A

Answer: Proton Pump Inhibitor (PPI).

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84
Q

SBA: Which symptom requires urgent referral in GORD?

A

Answer: Unintentional weight loss.

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85
Q

SBA: What is the mechanism of action of PPIs?

A

Answer: Irreversible inhibition of the H+/K+ ATPase pump in gastric parietal cells.

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86
Q

SBA: What is the role of H2 receptor antagonists in GORD management?

A

Answer: Reduce gastric acid secretion by blocking histamine H2 receptors.

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87
Q

SBA: Which bacterium is most commonly associated with peptic ulcer disease?

A

Answer: Helicobacter pylori.

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88
Q

SBA: What is the key diagnostic test for H. pylori infection?

A

Answer: Carbon-13 urea breath test.

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89
Q

SBA: What antibiotics are commonly used in first-line triple therapy for H. pylori eradication?

A

Answer: Amoxicillin and clarithromycin.

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90
Q

SBA: What is a potential side effect of long-term PPI use?

A

Answer: Risk of fractures.

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91
Q

EMQ: Match the pharmacological therapy to its role in GORD management.

A

PPI: First-line therapy for reducing acid secretion.
H2RA: Alternative therapy when PPI is inadequate.
Antacids: Immediate symptom relief.

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92
Q

EMQ: Match the condition to the diagnostic test.

A

GORD: Clinical diagnosis based on symptoms.
H. pylori: Urea breath test.
Peptic ulcer: Endoscopy.

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93
Q

EMQ: Match the treatment regimen to the condition.

A

GORD with red flag symptoms: Refer for endoscopy.
H. pylori eradication: Triple therapy with PPI and two antibiotics.
NSAID-induced ulcer: Discontinue NSAID and start PPI.

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94
Q

EMQ: Match the complication to its cause.

A

Perforation: Peptic ulcer eroding through the stomach lining.
Gastrointestinal bleeding: Erosion of blood vessels at the ulcer site.
Gastric obstruction: Inflammation or scarring blocking food passage.

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95
Q

EMQ: Match the antibiotic to its key consideration in H. pylori treatment.

A

Clarithromycin: Avoid if recent macrolide use.
Metronidazole: Avoid alcohol due to disulfiram-like reaction.
Tetracycline: Avoid in children under 12 years old.

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96
Q

What are the key diagnostic methods for GORD, peptic ulcers, and H. pylori infection?

A

Answer:
GORD: Based on clinical symptoms, endoscopy for red flags.
Peptic ulcers: Endoscopy and urea breath test if H. pylori suspected.
H. pylori: Carbon-13 urea breath test or stool antigen test. (2 marks)

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97
Q

Outline the lifestyle modifications recommended for GORD management.

A

Answer:
Weight loss.
Avoid triggers like alcohol, coffee, and fatty foods.
Eat smaller, frequent meals and avoid eating before bedtime.
Elevate the head of the bed. (2 marks)

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98
Q

Describe the first-line pharmacological treatments for GORD and peptic ulcers.

A

Answer:
GORD: PPI for 4-8 weeks, H2RA if PPI ineffective.
Peptic ulcers: PPI or H2RA therapy, with eradication of H. pylori if present. (2 marks)

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99
Q

What are the complications of untreated peptic ulcers?

A

Answer:
Bleeding, perforation, gastric obstruction, and risk of peritonitis or sepsis. (2 marks)

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100
Q

What is the triple therapy for H. pylori eradication?

A

Answer: PPI + amoxicillin + clarithromycin or metronidazole for 7-14 days. (2 marks)

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101
Q

SBA: What is the main advantage of granules over powders in tablet formulation?

A

Answer: Granules have better flowability and uniformity.

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102
Q

SBA: What is the function of a filler in tablet formulations?

A

Answer: Provides sufficient bulk volume for compression.

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103
Q

SBA: Which excipient improves the flow of powders during tableting?

A

SBA: Which excipient improves the flow of powders during tableting?

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104
Q

SBA: What is the role of a disintegrant in a tablet?

A

Answer: Facilitates tablet breakup to release the active ingredient.

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105
Q

SBA: Which process involves the removal of void spaces during tablet compression?

A

Answer: Compression.

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106
Q

SBA: What is the purpose of wetting agents in tablet formulations?

A

Answer: Enhance water uptake and improve disintegration.

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107
Q

SBA: What is the most common lubricant used in tablet manufacturing?

A

Answer: Magnesium stearate.

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108
Q

SBA: What is capping during the tableting process?

A

Answer: Separation of the upper segment of a tablet from the main body.

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109
Q

SBA: What is the Heckel plot used to evaluate in tablet formulation?

A

Answer: The compressibility and deformation properties of a powder.

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110
Q

SBA: What causes mottling in tablet formulations?

A

Answer: Unequal distribution of colorants or dye migration during drying.

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111
Q

EMQ: Match the excipient to its role in tablet formulation.

A

Filler: Lactose, adds bulk for compression.
Binder: PVP or starch, provides cohesiveness.
Disintegrant: Croscarmellose sodium, promotes tablet breakup.

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112
Q

EMQ: Match the tablet defect to its cause.

A

Capping: Improper compression settings.
Sticking: Insufficient lubrication.
Mottling: Uneven dye distribution.

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113
Q

EMQ: Match the compaction step to its description.

A

Compression: Reduction in bulk volume by removing air.
Consolidation: Formation of interparticulate bonds.
Decompression: Pressure release during tablet ejection.

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114
Q

EMQ: Match the type of granulation to its description.

A

Wet granulation: Involves a liquid binder.
Dry granulation: Compresses powder without liquid.
Direct compression: Uses pre-compressed excipients.

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115
Q

EMQ: Match the additive to its purpose.

A

Antioxidant: Prevents drug oxidation (e.g., ascorbic acid).
Buffer: Maintains pH (e.g., sodium bicarbonate).
Sweetener: Improves taste (e.g., aspartame).

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116
Q

What are the main processes in tablet manufacture?

A

Answer: Compression (reducing bulk volume), consolidation (forming interparticulate bonds), and ejection (removing tablets from the die). (2 marks)

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117
Q

Describe the functions of three common excipients used in tablets.

A

Answer:
Filler: Provides bulk for compression (e.g., lactose).
Disintegrant: Promotes tablet breakup (e.g., starch).
Binder: Adds cohesiveness (e.g., PVP). (2 marks)

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118
Q

What are the advantages of granules over powders in tablet manufacturing?

A

Answer: Granules flow better, reduce dust, and provide uniformity. (2 marks)

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119
Q

What are the common defects in tablet manufacture, and how can they be addressed?

A

Answer:
Capping: Adjust compression force.
Sticking: Increase lubrication.
Mottling: Improve mixing of dyes. (2 marks)

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120
Q

xplain the role of the Heckel plot in tablet formulation.

A

Answer: Evaluates compressibility and deformation; larger Heckel constants indicate plastic deformation. (2 marks)

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121
Q

SBA: What is the British Pharmacopoeia (BP) acceptable friability limit for tablets?

A

SBA: What is the British Pharmacopoeia (BP) acceptable friability limit for tablets?

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122
Q

SBA: What test evaluates the resistance of a tablet to abrasion or mechanical stress?

A

Answer: Friability test.

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123
Q

SBA: Which factor primarily influences the hardness of a tablet?

A

Answer: Compression force during tableting.

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124
Q

SBA: What is the main purpose of the content uniformity (CU) test in tablets?

A

Answer: To ensure each dosage unit contains the intended amount of active ingredient.

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125
Q

SBA: What is considered a passing result for a tablet disintegration test?

A

Answer: All six tablets disintegrate within the specified time, except for insoluble fragments.

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126
Q

SBA: What media are typically used in dissolution testing to simulate gastric and intestinal fluids?

A

Answer: Hydrochloric acid (pH 1.5–3.5) for gastric and phosphate buffer (pH 6–7.4) for intestinal fluids.

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127
Q

SBA: At what temperature is the dissolution test typically performed?

A

Answer: 37°C.

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128
Q

SBA: What is the significance of determining disintegration time for a tablet?

A

Answer: It predicts how quickly the tablet will dissolve and release the drug for absorption.

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129
Q

SBA: What is the most common failure mode in a friability test?

A

Answer: Cracking, cleavage, or breakage of the tablet.

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130
Q

SBA: What is the key difference between the CU and mass variation (MV) tests?

A

Answer: CU measures the active ingredient, while MV focuses on weight consistency.

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131
Q

EMQ: Match the test to its purpose.

A

Content uniformity: Ensures consistent active ingredient content.
Friability: Assesses resistance to abrasion or mechanical stress.
Hardness: Measures resistance to crushing or breaking.

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132
Q

EMQ: Match the tablet defect to its cause.

A

Capping: Insufficient compression force.
Friability failure: Low binder concentration.
Mottling: Uneven dye distribution.

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133
Q

EMQ: Match the test outcome to its requirement.

A

Friability: Mass loss ≤1%.
Disintegration: Complete disintegration within specified time.
Dissolution: Predetermined percentage of drug released at specific intervals.

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134
Q

EMQ: Match the factor to its impact on tablet quality.

A

Binder concentration: Affects hardness and friability.
Lubricant concentration: Influences weight variation and disintegration.
Compression force: Impacts hardness and friability.

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135
Q

EMQ: Match the dissolution medium to its purpose.

A

Hydrochloric acid: Simulates gastric fluid.
Phosphate buffer: Simulates intestinal fluid.
Water: Neutral medium for dissolution.

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136
Q

Describe the friability test and its BP standard.

A

Answer: Friability assesses resistance to abrasion. Tablets are tumbled for 100 rotations, and mass loss should not exceed 1%. (2 marks)

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137
Q

What is the purpose of the content uniformity test?

A

Answer: Ensures each dosage unit has an active ingredient content within ±15% of the average dose. (2 marks)

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138
Q

How is tablet hardness evaluated, and why is it important?

A

Answer: Measures resistance to crushing using diametral compression. Affects tablet durability and handling. (2 marks)

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139
Q

xplain the dissolution test procedure and its relevance.

A

Answer: Tablets are placed in a dissolution medium at 37°C, with paddles rotating at 50 rpm. Samples are taken at specified intervals to ensure drug release meets specifications. (2 marks)

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140
Q

What are the consequences of a tablet failing the disintegration test?

A

Answer: Indicates poor bioavailability or delayed onset of therapeutic action. (2 marks)

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141
Q

SBA: What is the primary function of the myenteric plexus in the enteric nervous system?

A

Answer: Regulates GI motility, such as peristalsis.

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142
Q

SBA: Which neurotransmitter is primarily associated with the “rest-and-digest” response of the gut?

A

Answer: Acetylcholine.

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143
Q

SBA: What percentage of the body’s serotonin is synthesized in the gut?

A

Answer: 95%.

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144
Q

SBA: What is the role of ghrelin in the gut-brain axis?

A

Answer: Stimulates hunger by signaling the hypothalamus.

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145
Q

SBA: Which phase of digestion is initiated by the sight or smell of food?

A

Answer: Cephalic phase.

146
Q

SBA: What is the primary function of GLP-1 in digestion?

A

Answer: Enhances insulin secretion and promotes satiety.

147
Q

SBA: What type of reflex is triggered by local stimuli within the gut?

A

Answer: Short reflex.

148
Q

SBA: Which gut microbiota-derived metabolites influence brain function?

A

Answer: Short-chain fatty acids (SCFAs).

149
Q

SBA: What is the primary role of the vagus nerve in the gut-brain axis?

A

Answer: Facilitates bidirectional communication between the gut and brain.

150
Q

SBA: What triggers the release of CCK from the duodenum?

A

Answer: Presence of fats and partially digested proteins.

151
Q

EMQ: Match the reflex type to its characteristic.

A

Short reflex: Local control by the ENS.
Long reflex: Involves the CNS via the vagus nerve.

152
Q

EMQ: Match the GI hormone to its function.

A

Gastrin: Stimulates gastric acid secretion.
Secretin: Stimulates bicarbonate release and inhibits gastric acid secretion.
Motilin: Coordinates migrating motor complexes during fasting.

153
Q

EMQ: Match the gut-brain axis component to its role.

A

Microbiota: Produce neurotransmitters like serotonin.
ENS: Controls local GI motility and secretions.
Vagus nerve: Transmits signals between the gut and CNS.

154
Q

EMQ: Match the digestive phase to its activity.

A

Cephalic phase: Anticipatory mechanisms like salivation.
Gastric phase: Secretion of gastric acid and motility.
Intestinal phase: Coordination of intestinal motility and enzyme release.

155
Q

EMQ: Match the neurotransmitter to its function.

A

Substance P: Excites smooth muscle contraction.
Nitric oxide: Relaxes smooth muscle.
Vasoactive intestinal peptide (VIP): Inhibits smooth muscle contraction.

156
Q

Describe the primary components of the gut-brain axis.

A

Answer:
ENS (enteric nervous system): Controls local motility and secretion.
CNS: Modulates gut activity via long reflexes.
Microbiota: Influences mood and immunity via metabolites. (2 marks

157
Q

Explain the role of short and long reflexes in gut motility.

A

Explain the role of short and long reflexes in gut motility.

158
Q

What is the role of the gut microbiota in mood regulation?

A

Answer: Microbiota produce serotonin and SCFAs, which modulate brain function and emotional states. (2 marks)

159
Q

How do hormones regulate digestion in the gut-brain axis?

A

Answer:
CCK: Stimulates bile and enzyme secretion.
Secretin: Stimulates bicarbonate release.
GLP-1: Enhances insulin release and promotes satiety. (2 marks)

160
Q

What are the clinical implications of gut-brain axis dysfunction?

A

Answer: Associated with conditions like irritable bowel syndrome (IBS), anxiety, and neurodegenerative disorders. (2 marks)

161
Q

SBA: What is the primary action of antacids in the stomach?

A

Answer: Neutralization of stomach acid by reacting with hydrochloric acid (HCl).

162
Q

SBA: Which antacid component can cause constipation as a side effect?

A

Answer: Aluminium hydroxide.

163
Q

SBA: What is the mechanism of action of H2 receptor antagonists?

A

Answer: Block histamine H2 receptors on parietal cells, reducing cAMP and gastric acid secretion.

164
Q

SBA: Which PPI binds covalently to the H+/K+ ATPase pump?

A

Answer: Omeprazole.

165
Q

SBA: What is the primary risk associated with long-term use of PPIs?

A

Answer: Nutrient deficiencies such as B12, calcium, and magnesium.

166
Q

Answer: Nutrient deficiencies such as B12, calcium, and magnesium.

A

Answer: Gastro-oesophageal reflux disease (GORD).

167
Q

SBA: What is the recommended combination therapy for H. pylori eradication?

A

Answer: PPI with two antibiotics (e.g., amoxicillin and clarithromycin).

168
Q

SBA: Which enzyme is inhibited by cimetidine, potentially causing drug interactions?

A

Answer: Cytochrome P450.

169
Q

SBA: How long can a PPI inhibit gastric acid secretion following a single dose?

A

Answer: Up to 36 hours.

170
Q

SBA: What is the primary physiological stimulus for acid secretion in the stomach?

A

Answer: Gastrin, histamine, and acetylcholine.

171
Q

EMQ: Match the drug class to its primary action.

A

Antacids: Neutralizes stomach acid.
H2 antagonists: Blocks histamine receptors to reduce acid secretion.
PPIs: Irreversibly inhibit the proton pump.

172
Q

EMQ: Match the drug to its common side effect.

A

Aluminium hydroxide: Constipation.
Magnesium hydroxide: Diarrhea.
Calcium carbonate: Hypercalcemia.

173
Q

EMQ: Match the mechanism to the therapeutic outcome.

A

Neutralization of HCl: Rapid symptom relief in dyspepsia.
Blocking H2 receptors: Reduces basal and stimulated acid secretion.
Proton pump inhibition: Long-lasting acid suppression.

174
Q

EMQ: Match the therapy to its clinical application.

A

Antacids: Short-term relief of heartburn.
H2 receptor antagonists: Mild GORD symptoms.
PPIs: Peptic ulcer disease and erosive oesophagitis.

175
Q

EMQ: Match the long-term risk to the treatment.

A

Antacids: Electrolyte imbalances and rebound acid hypersecretion.
H2 antagonists: Drug interactions via P450 inhibition.
PPIs: Increased risk of fractures and infections.

176
Q

Describe the mechanism of action of antacids, H2 receptor antagonists, and PPIs.

A

Answer:
Antacids: Neutralize stomach acid to increase pH.
H2RAs: Block histamine receptors on parietal cells, reducing acid production.
PPIs: Irreversibly inhibit the H+/K+ ATPase pump, preventing acid secretion. (3 marks)

177
Q

What are the common side effects of these drug classes?

A

Answer:
Antacids: Constipation (aluminium), diarrhea (magnesium), hypercalcemia (calcium).
H2RAs: Drug interactions (e.g., cimetidine inhibiting P450).
PPIs: Nutrient deficiencies, increased infection risk. (2 marks)

178
Q

Outline the clinical indications for each therapy.

A

Answer:
Antacids: Rapid relief of mild dyspepsia.
H2RAs: GORD and mild peptic ulcer disease.
PPIs: Peptic ulcers, severe GORD, H. pylori eradication. (2 marks)

179
Q

Explain the risks of long-term PPI use.

A

Answer: Nutrient malabsorption (B12, calcium), bone fractures, infection risk, and possible drug interactions via CYP2C19 inhibition. (2 marks)

180
Q

What is the NICE-recommended treatment for H. pylori?

A

Answer: Triple therapy: PPI + amoxicillin + clarithromycin or metronidazole. (1 mark)

181
Q

SBA: What is the primary objective of tablet coating?

A

Answer: Protect the active pharmaceutical ingredient (API) and modify drug release.

182
Q

SBA: Which type of tablet coating is the most popular and involves spraying a liquid polymer-based formulation?

A

Answer: Film coating.

183
Q

SBA: What is the main purpose of enteric coatings?

A

Answer: To resist dissolution in the stomach and allow release in the intestines.

184
Q

SBA: Which polymer is commonly used for sustained-release film coatings?

A

Answer: Ethyl cellulose.

185
Q

SBA: What is the role of plasticizers in film coatings?

A

Answer: Reduce film brittleness and improve flexibility.

186
Q

SBA: Which type of coating involves successive applications of sucrose-based formulations?

A

Answer: Sugar coating.

187
Q

SBA: What is the key feature of compression coating?

A

Answer: Encases a preformed tablet with granular material for modified release.

188
Q

SBA: What is the purpose of colourants in film coatings?

A

Answer: Enhance appearance, identification, and uniformity.

189
Q

SBA: What is the main environmental concern with using organic solvents in film coatings?

A

Answer: Contribution to global warming and potential safety hazards.

190
Q

SBA: Which newer coating technology uses low energy and high coating efficiency?

A

Answer: Vacuum film coating.

191
Q

EMQ: Match the coating type to its purpose.

A

Film coating: Protects API and modifies release.
Sugar coating: Taste masking and appearance enhancement.
Enteric coating: Prevents stomach irritation by delaying release to the intestine.

192
Q

EMQ: Match the excipient to its role in tablet coating.

A

Plasticizer: Improves flexibility of the coating.
Colourant: Provides uniform appearance and identification.
Solvent: Dissolves polymers for spray application.

193
Q

EMQ: Match the polymer to its use in coatings.

A

Hydroxypropyl methylcellulose (HPMC): Immediate-release film coating.
Cellulose acetate phthalate (CAP): Enteric coating.
Ethyl cellulose: Sustained-release coating.

194
Q

EMQ: Match the coating defect to its cause.

A

Sticking: Over-wetting during spraying.
Chipping: Over-drying of the tablet surface.
Uneven colour: Improper mixing of colourants.

195
Q

EMQ: Match the coating process to its description.

A

Fluid-bed coating: Combines coating and drying in one step.
Conventional pan coating: Rotating tablet bed with liquid spray.
Compression coating: Encases tablet with granular material.

196
Q

Describe the main types of tablet coatings.

A

Answer:
Film coating: Polymer-based spray; protects API and modifies release.
Sugar coating: Multi-step process for taste masking and appearance.
Enteric coating: Prevents dissolution in the stomach.
Compression coating: Granular material encases the tablet. (3 marks)

197
Q

What are the key ingredients in film coating formulations?

A

Answer: Polymers, plasticizers, colourants, and solvents. (2 marks)

198
Q

Explain the role of enteric coatings.

A

Answer: Protect acid-sensitive drugs, prevent stomach irritation, and deliver API to the intestine. (2 marks)

199
Q

What are common defects in tablet coating, and how are they addressed?

A

Answer:
Sticking: Adjust spray rate.
Chipping: Optimize drying conditions.
Uneven colour: Improve mixing. (2 marks)

200
Q

What environmental and safety concerns exist with solvent-based coatings?

A

Answer: Solvents contribute to greenhouse effects and pose flammability risks. Alternatives like water-based coatings are preferred. (1 mark)

201
Q

SBA: What is the primary function of parietal cells in the stomach?

A

Answer: Secrete hydrochloric acid (HCl) and intrinsic factor for vitamin B12 absorption.

202
Q

SBA: Which phase of digestion involves the brain preparing the stomach for food by stimulating gastric secretions?

A

Answer: Cephalic phase.

203
Q

SBA: What is the role of gastrin in gastric physiology?

A

Answer: Stimulates gastric acid secretion and motility.

204
Q

SBA: Which type of diarrhea involves the presence of unabsorbed nutrients pulling water into the gut?

A

Answer: Osmotic diarrhea.

205
Q

SBA: What is the first-line pharmacological treatment for functional dyspepsia according to NICE guidelines?

A

Answer: Proton Pump Inhibitors (PPIs).

206
Q

SBA: What is the hallmark feature of gastroparesis?

A

Answer: Delayed gastric emptying in the absence of mechanical obstruction.

207
Q

Answer: Delayed gastric emptying in the absence of mechanical obstruction.

A

Answer: Mass movement contractions.

208
Q

SBA: What is the main side effect of stimulant laxatives like bisacodyl?

A

Answer: Cramping and abdominal pain.

209
Q

SBA: Which neurotransmitter is primarily involved in stimulating gut motility?

A

Answer: Acetylcholine.

210
Q

SBA: What is the primary diagnostic test for H. pylori in dyspeptic patients?

A

Answer: Urea breath test.

211
Q

EMQ: Match the GI condition to its primary symptom.

A

GORD: Heartburn and regurgitation.
Peptic Ulcer Disease: Epigastric pain relieved by eating.
Gastroparesis: Nausea, bloating, and early satiety.

212
Q

EMQ: Match the pharmacological agent to its primary use.

A

Omeprazole: Reduces gastric acid secretion in GORD.
Domperidone: Improves gastric emptying in gastroparesis.
Bisacodyl: Stimulates bowel movement in constipation.

213
Q

EMQ: Match the reflex to its mechanism.

A

Defecation reflex: Stretching of the rectal wall stimulates peristalsis.
Gastrocolic reflex: Food in the stomach triggers colon contractions.
Enterogastric reflex: Acid in the duodenum inhibits gastric secretion.

214
Q

EMQ: Match the treatment to the condition.

A

Antacids: Heartburn relief in GORD.
Prokinetic agents: Delayed gastric emptying in gastroparesis.
Osmotic laxatives: Constipation due to insufficient water retention.

215
Q

EMQ: Match the hormone to its role in digestion.

A

Secretin: Stimulates bicarbonate release to neutralize stomach acid.
Cholecystokinin (CCK): Stimulates bile and pancreatic enzyme secretion.
Motilin: Coordinates migrating motor complexes during fasting.

216
Q

Outline the structure of the alimentary canal.

A

Answer: Four layers: mucosa, submucosa, muscularis externa, and serosa. (2 marks)

217
Q

What are the phases of gastric acid secretion regulation?

A

Answer: Cephalic phase (vagal stimulation), gastric phase (stretch receptors and gastrin), intestinal phase (inhibitory hormones like secretin). (2 marks)

218
Q

Explain the role of the colon in water absorption and motility.

A

Answer: Absorbs water and electrolytes; uses segmental and mass movements for propulsion. (2 marks)

219
Q

Describe the pharmacological management of dyspepsia.

A

Answer: First-line therapy is a PPI; if symptoms persist, H. pylori eradication or lifestyle changes (smaller meals, avoiding trigger foods). (2 marks)

220
Q

What are the red flags in GI conditions that necessitate urgent referral?

A

Answer: Unintentional weight loss, blood in stools, persistent vomiting, difficulty swallowing, and anemia. (2 marks)

221
Q

SBA: What is the role of TPMT (thiopurine methyltransferase) testing before starting thiopurine therapy?

A

Answer: To identify patients at risk of myelosuppression and adjust dosage accordingly.

222
Q

SBA: What percentage of Caucasians have undetectable TPMT activity?

A

Answer: 0.3%.

223
Q

SBA: Which gene polymorphism affects the metabolism of PPIs like omeprazole?

A

Answer: CYP2C19 polymorphism.

224
Q

SBA: How does genetic variation in CYP2C19 affect PPI plasma levels?

A

Answer: Loss-of-function alleles increase plasma levels, while *17 alleles decrease plasma levels.

225
Q

SBA: Which drug class does azathioprine belong to?

A

Answer: Immunosuppressants.

226
Q

SBA: What is a potential side effect of azathioprine in patients with low or absent TPMT activity?

A

Answer: Severe myelosuppression.

227
Q

SBA: Which condition is most commonly associated with the use of azathioprine?

A

Answer: Inflammatory bowel disease (Crohn’s disease and ulcerative colitis).

228
Q

SBA: What enzyme system metabolizes most PPIs?

A

Answer: Cytochrome P450 (mainly CYP2C19 and CYP3A4).

229
Q

SBA: Which metabolite is responsible for the active immunosuppressive effects of azathioprine?

A

Answer: 6-thioguanine nucleotides (6-TGN).

230
Q

SBA: What is the primary genetic test recommended by NICE before azathioprine therapy?

A

Answer: TPMT activity test.

231
Q

EMQ: Match the enzyme to its role in drug metabolism.

A

TPMT: Metabolizes thiopurines to inactive metabolites.
CYP2C19: Metabolizes PPIs like omeprazole.
CYP3A4: Metabolizes a broad range of drugs, including azoles.

232
Q

EMQ: Match the pharmacogenomic application to its benefit.

A

Optimized dosage: Tailoring drug therapy to individual needs.
Avoiding adverse effects: Identifying patients at risk of myelosuppression.
Predicting efficacy: Determining response to PPIs based on CYP2C19.

233
Q

EMQ: Match the drug to its genetic consideration.

A

Azathioprine: TPMT polymorphism testing required.
Omeprazole: CYP2C19 polymorphism affects metabolism.
Thioguanine: Less commonly used due to severe myelosuppression risks.

234
Q

EMQ: Match the condition to its associated genetic factor.

A

IBS: Serotonin transporter gene polymorphisms.
IBD: TPMT enzyme activity variations.
GORD: CYP2C19 polymorphisms affecting PPI efficacy.

235
Q

EMQ: Match the drug interaction to its outcome.

A

Rifampin: Induces CYP2C19, reducing omeprazole plasma levels.
Voriconazole: Inhibits CYP2C19, increasing omeprazole plasma levels.
St John’s Wort: Induces CYP3A4, lowering PPI efficacy.

236
Q

Explain the role of CYP2C19 polymorphisms in PPI therapy.

A

Answer:
Loss-of-function alleles (2–9) increase PPI plasma levels, enhancing efficacy.
*17 alleles lead to rapid drug clearance, reducing efficacy. (2 marks)

237
Q

Why is TPMT testing recommended before starting azathioprine therapy?

A

Answer: Identifies patients with low or absent TPMT activity who are at risk of severe myelosuppression. (2 marks)

238
Q

What are the clinical implications of genetic testing for thiopurines in IBD management?

A

Answer:
Adjust doses for patients with reduced enzyme activity.
Use alternative treatments if TPMT activity is undetectable. (2 marks)

239
Q

Describe the role of pharmacogenomics in IBS treatment.

A

Answer: Variations in serotonin transporter genes (SLC6A4) affect response to serotonergic agents like SSRIs. (2 marks)

240
Q

What are the ethical considerations in implementing pharmacogenomics in clinical practice?

A

Answer:
Ensuring informed consent and patient privacy.
Addressing cost and accessibility of genetic testing. (2 marks)

241
Q

SBA: What is the most common subtype of IBS according to the Rome IV classification?

A

Answer: IBS-D (Diarrhoea predominant).

242
Q

SBA: Which laxative should be avoided in IBS due to its gas-producing effects?

A

Answer: Lactulose.

243
Q

SBA: What is the first-line pharmacological treatment for IBS-C?

A

Answer: Bulk-forming laxatives (e.g., Ispaghula).

244
Q

SBA: What is the gold standard test to confirm coeliac disease?

A

Answer: Positive coeliac serology followed by a small intestinal biopsy.

245
Q

SBA: Which drug is used to manage diarrhoea in IBS-D?

A

Answer: Loperamide.

246
Q

SBA: What is the only effective treatment for coeliac disease?

A

Answer: A strict gluten-free diet.

247
Q

SBA: What is the primary mechanism of action of Linaclotide in IBS?

A

Answer: Increases fluid secretion and promotes stool passage.

248
Q

SBA: What is the hallmark symptom of diverticulitis?

A

Answer: Severe abdominal pain, usually in the lower left quadrant.

249
Q

SBA: Which antidepressant class is used off-label to manage pain in IBS?

A

Answer: Tricyclic antidepressants (e.g., Amitriptyline).

250
Q

SBA: What dietary advice is recommended for patients with diverticular disease?

A

Answer: High-fibre diet, increased fluid intake, and regular exercise.

251
Q

EMQ: Match the condition to its primary diagnostic test.

A

IBS: Diagnosis of exclusion based on Rome IV criteria.
Coeliac disease: Coeliac serology and intestinal biopsy.
Diverticular disease: CT scan if complications suspected.

252
Q

EMQ: Match the drug to its primary use.

A

Linaclotide: Severe IBS-C unresponsive to other laxatives.
Loperamide: Diarrhoea in IBS-D.
Alverine citrate: Abdominal pain or spasm in IBS.

253
Q

EMQ: Match the GI disorder to its symptom.

A

IBS: Abdominal bloating and alternating stool frequency.
Diverticulitis: Fever, rectal bleeding, and severe LLQ pain.
Coeliac disease: Steatorrhoea, weight loss, and fatigue.

254
Q

EMQ: Match the treatment to its associated precaution.

A

Loperamide: Avoid in acute UC or conditions inhibiting peristalsis.
Lactulose: Avoid in IBS due to gas production.
Linaclotide: Contraindicated in GI obstruction or pregnancy.

255
Q

EMQ: Match the management approach to the condition.

A

IBS: Diet and lifestyle changes; avoid trigger foods.
Coeliac disease: Strict gluten-free diet and nutritional monitoring.
Diverticulitis: Oral antibiotics (e.g., co-amoxiclav) for uncomplicated cases.

256
Q

Outline the pharmacological and non-pharmacological management of IBS.

A

Answer:
Non-pharmacological: Diet and lifestyle changes, low-FODMAP diet, stress management.
Pharmacological:
IBS-C: Bulk-forming laxatives, Linaclotide if refractory.
IBS-D: Loperamide, antispasmodics (e.g., Mebeverine).
Pain: Tricyclic antidepressants. (3 marks)

257
Q

What are the steps in diagnosing coeliac disease?

A

Answer:
Persistent unexplained GI symptoms.
Coeliac serology: Check for IgA tTG and total IgA levels.
Small intestinal biopsy if serology positive. (2 marks)

258
Q

How is diverticular disease managed in uncomplicated cases?

A

Answer:
High-fibre diet and fluids.
Avoid NSAIDs and opioids.
Bulk-forming laxatives for symptom control. (2 marks)

259
Q

What red flags in IBS warrant further investigation?

A

Answer:
Unexplained weight loss, rectal bleeding, anemia, persistent vomiting, or family history of bowel cancer. (2 marks)

260
Q

What is the NICE-recommended management for diverticulitis?

A

Answer:
Mild: Oral antibiotics like co-amoxiclav, fluids, and rest.
Severe or complicated: Hospital admission and IV antibiotics. (1 mark)

261
Q

SBA: What is the hallmark histological feature of Crohn’s disease?

A

Answer: Skip lesions and transmural inflammation.

262
Q

SBA: What is the hallmark histological feature of ulcerative colitis?

A

Answer: Continuous mucosal inflammation starting from the rectum.

263
Q

SBA: What is a potential life-threatening complication of ulcerative colitis?

A

Answer: Toxic megacolon.

264
Q

SBA: Which test is used to differentiate between inflammatory bowel disease and irritable bowel syndrome?

A

Answer: Faecal calprotectin.

265
Q

SBA: What is the first-line treatment for mild to moderate ulcerative colitis?

A

Answer: Aminosalicylates (e.g., mesalazine).

266
Q

SBA: What is the recommended management for severe Crohn’s disease not responsive to corticosteroids?

A

Answer: Biologics (e.g., infliximab or adalimumab).

267
Q

SBA: Which extra-intestinal symptom is more common in Crohn’s disease than ulcerative colitis?

A

Answer: Erythema nodosum.

268
Q

SBA: What is the key risk factor for developing Crohn’s disease?

A

Answer: Smoking.

269
Q

SBA: Which thiopurine metabolizing enzyme should be tested before starting azathioprine in IBD patients?

A

Answer: Thiopurine methyltransferase (TPMT).

270
Q

SBA: What is the recommended treatment for maintaining remission in Crohn’s disease after surgical resection?

A

Answer: Azathioprine and 3 months of metronidazole.

271
Q

EMQ: Match the IBD subtype to its key feature.

A

Ulcerative colitis: Limited to the colon and rectum.
Crohn’s disease: Can affect any part of the GI tract.
Both: Associated with increased colorectal cancer risk.

272
Q

EMQ: Match the complication to its IBD subtype.

A

Toxic megacolon: Ulcerative colitis.
Fistula formation: Crohn’s disease.
Pyoderma gangrenosum: More common in Crohn’s disease.

273
Q

EMQ: Match the treatment to its indication.

A

Aminosalicylates: Mild to moderate ulcerative colitis.
Corticosteroids: Acute exacerbation of IBD.
Biologics: Severe or refractory IBD.

274
Q

EMQ: Match the test to its purpose.

A

Colonoscopy: Diagnosing IBD and assessing severity.
Faecal calprotectin: Differentiates IBD from IBS.
TPMT testing: Assessing suitability for azathioprine.

275
Q

EMQ: Match the drug to its primary side effect.

A

Azathioprine: Bone marrow suppression.
Corticosteroids: Cushing’s syndrome and weight gain.
Biologics: Increased infection risk.

276
Q

Describe the key symptoms of ulcerative colitis and Crohn’s disease.

A

Answer:
UC: Bloody diarrhoea, tenesmus, left lower quadrant pain.
CD: Abdominal pain, non-bloody diarrhoea, weight loss, perianal disease. (2 marks)

277
Q

What diagnostic tests are used to confirm IBD?

A

Answer:
Faecal calprotectin, colonoscopy with biopsy, imaging (CT/MRI for Crohn’s disease). (2 marks)

278
Q

Outline the first-line treatments for mild to moderate UC and CD.

A

Answer:
UC: Aminosalicylates (e.g., mesalazine).
CD: Budesonide or glucocorticoids. (2 marks)

279
Q

What are the common extra-intestinal manifestations of IBD?

A

Answer: Arthritis, erythema nodosum, uveitis, pyoderma gangrenosum. (2

280
Q

What is the recommended management for severe IBD?

A

Answer:
Corticosteroids, biologics (e.g., infliximab), or surgery for complications. (2 marks)

281
Q

SBA: What is the most common cause of acute diarrhoea in adults?

A

Answer: Viral gastroenteritis.

282
Q

SBA: What is the first-line treatment for cholestatic pruritus?

A

Answer: Colestyramine.

283
Q

SBA: Which laxative class is first-line for constipation in pregnancy?

A

Answer: Bulk-forming laxatives (e.g., Ispaghula husk).

284
Q

SBA: What is the gold standard treatment for symptomatic gallstones?

A

Answer: Laparoscopic cholecystectomy.

285
Q

SBA: Which dietary supplement is recommended alongside orlistat therapy to prevent deficiencies?

A

Answer: Vitamin and mineral supplements.

286
Q

SBA: What is the primary pharmacological treatment for acute anal fissures?

A

Answer: Bulk-forming laxatives.

287
Q

SBA: What is the mechanism of action of lactulose in constipation?

A

Answer: Osmotic effect increases water content in stools and decreases ammonia-producing organisms.

288
Q

SBA: What is the recommended non-drug management for haemorrhoids?

A

Answer: Increase dietary fibre and fluid intake.

289
Q

SBA: Which pancreatic enzyme replacement therapy is used in exocrine pancreatic insufficiency?

A

Answer: Pancreatin (lipase, amylase, protease).

290
Q

SBA: Which drug is used to manage severe pain in biliary colic if NSAIDs are contraindicated?

A

Answer: Intramuscular opioid (e.g., morphine).

291
Q

EMQ: Match the GI condition to its primary treatment.

A

Cholestasis: Colestyramine.
Gallstones: Laparoscopic cholecystectomy.
Exocrine pancreatic insufficiency: Pancreatic enzyme replacement therapy.

292
Q

EMQ: Match the laxative to its mechanism of action.

A

Bulk-forming: Absorbs water to form a gel-like mass.
Stimulant: Increases intestinal motility.
Osmotic: Draws water into the bowel lumen.

293
Q

EMQ: Match the drug to its precaution.

A

Orlistat: Avoid in pregnancy; monitor fat-soluble vitamin levels.
Lactulose: Avoid in patients with galactose intolerance.
Senna: Avoid near term in pregnancy.

294
Q

EMQ: Match the symptom to its GI condition.

A

Pruritus, jaundice, pale stools: Cholestasis.
Diarrhoea, steatorrhoea: Exocrine pancreatic insufficiency.
Severe LLQ pain: Diverticulitis.

295
Q

EMQ: Match the complication to its cause.

A

Toxic megacolon: Ulcerative colitis.
Gallstone pancreatitis: Gallstones obstructing the bile duct.
Anal fissures: Chronic constipation.

296
Q

Describe the primary treatment goals for acute diarrhoea.

A

Answer: Prevent dehydration, restore fluid and electrolyte balance, and manage symptoms (e.g., loperamide for rapid control). (2 marks)

297
Q

What are the pharmacological options for constipation?

A

Answer:
Bulk-forming laxatives for first-line treatment.
Osmotic laxatives (e.g., lactulose) if stools remain hard.
Stimulant laxatives (e.g., bisacodyl) for inadequate emptying. (2 marks)

298
Q

Outline the non-drug management for gallstones.

A

Answer: Dietary adjustments (low-fat meals), pain management (e.g., paracetamol), and monitoring for complications. (2 marks)

299
Q

What are the complications of untreated symptomatic gallstones?

A

Answer: Biliary colic, acute cholecystitis, pancreatitis, and obstructive jaundice. (2 marks)

300
Q

How is colestyramine used in cholestatic pruritus?

A

Answer: Binds bile acids in the intestine to form an insoluble complex, reducing serum bile acid levels and pruritus. (2 marks)

301
Q

SBA: What is the primary advantage of capsules over tablets?

A

Answer: Easier to swallow due to their smooth and slippery surface.

302
Q

SBA: What is the main material used in hard gelatin capsule shells?

A

Answer: Gelatin derived from animal bones and hides.

303
Q

SBA: Which type of capsule is typically used for hygroscopic drugs?

A

Answer: HPMC (vegetarian) capsules.

304
Q

SBA: What is the key difference between hard and soft capsules?

A

Answer: Hard capsules consist of two parts (cap and body), while soft capsules are one-piece and hermetically sealed.

305
Q

SBA: What is a common issue with hydrophobic drug particles in hard gelatin capsules?

A

Answer: Slow dissolution due to poor penetration of GI fluids.

306
Q

SBA: What is the primary advantage of suppositories in drug delivery?

A

Answer: They bypass first-pass metabolism and are useful when oral administration is not possible.

307
Q

SBA: Which condition is commonly treated with rectal suppositories containing 5-aminosalicylic acid?

A

Answer: Ulcerative colitis.

308
Q

SBA: What is the key quality control concern in suppository manufacturing?

A

Answer: Ensuring uniform drug dispersion in each unit.

309
Q

SBA: What type of base is used in suppositories that dissolve in the rectum?

A

Answer: Water-soluble bases such as polyethylene glycol (PEG).

310
Q

SBA: Which of the following is a common reason for a suppository breaking during manufacture?

A

Answer: Poured at too high a temperature.

311
Q

EMQ: Match the capsule type to its characteristic.

A

Hard gelatin capsules: Two-piece shells; suitable for powders and granules.
Soft gelatin capsules: One-piece shell; suitable for liquids or oils.
HPMC capsules: Vegetarian, suitable for moisture-sensitive drugs.

312
Q

EMQ: Match the capsule excipient to its function.

A

Plasticizers (e.g., glycerol): Increase flexibility of the capsule shell.
Colourants: Aid in product identification and appearance.
Hydrophilic diluents: Improve dissolution of hydrophobic drugs.

313
Q

EMQ: Match the suppository application to its benefit.

A

Local effect (e.g., haemorrhoids): Direct action at the application site.
Systemic effect (e.g., pain relief): Bypasses first-pass metabolism.
Prolonged effect (e.g., night pain relief): Slow drug release over time.

314
Q

EMQ: Match the manufacturing issue to its cause.

A

Broken suppository: Poured at too high a temperature.
Uneven drug distribution: Insufficient stirring during mixing.
Sticking to the mould: Inadequate lubricant application.

315
Q

EMQ: Match the quality test to its purpose.

A

Dissolution test: Ensures drug release in simulated GI conditions.
Weight variation: Confirms uniformity between units.
Content uniformity: Verifies consistent drug dosage.

316
Q

What are the advantages of capsules over tablets?

A

Answer: Easier to swallow, tasteless, can contain multiple dosage forms (e.g., granules, liquids), and allow modified drug release. (2 marks)

317
Q

Explain the differences between hard and soft capsules.

A

Answer:
Hard capsules: Two-piece shells, used for powders or granules.
Soft capsules: Single-piece shells, used for liquids or oily drugs. (2 marks)

318
Q

What are the key quality control tests for capsules?

A

Answer: Dissolution, content uniformity, weight variation, and visual inspection. (2 marks)

319
Q

Describe the advantages of suppositories in drug delivery.

A

Answer: Bypass first-pass metabolism, suitable for patients with nausea/vomiting, and provide both local and systemic effects. (2 marks)

320
Q

What are the common issues in suppository manufacturing, and how can they be resolved?

A

Answer:
Broken suppositories: Avoid overheating during pouring.
Sticking: Proper application of lubricant to the mould.
Uneven drug distribution: Ensure continuous stirring during mixing. (2 marks)

321
Q

SBA: What is the primary mechanism of action of proton pump inhibitors (PPIs)?

A

Answer: Inhibit H+/K+-ATPase in parietal cells to reduce gastric acid secretion.

322
Q

SBA: What is the key use of antacids in GI disorders?

A

Answer: Neutralize stomach acid to relieve symptoms of heartburn and indigestion.

323
Q

SBA: Which receptor is targeted by H2 receptor antagonists?

A

Answer: Histamine H2 receptors on parietal cells.

324
Q

SBA: What is the primary mechanism of action of promotility agents like domperidone?

A

Answer: Enhance acetylcholine activity to increase GI motility.

325
Q

SBA: What is the first-line treatment for ulcerative colitis with mild-to-moderate disease?

A

Answer: Aminosalicylates (e.g., mesalazine).

326
Q

SBA: Which enzyme activates prodrugs like azathioprine in the treatment of IBD?

A

Answer: Thiopurine methyltransferase (TPMT).

327
Q

SBA: What is the mechanism of action of loperamide in managing diarrhoea?

A

Answer: Binds to opioid receptors in the gut to decrease motility.

328
Q

SBA: What is the primary purpose of using water-soluble bases in suppositories?

A

Answer: Facilitate dissolution in rectal fluids for drug absorption.

329
Q

SBA: Which component in antidiarrhoeals like atropine acts as an anticholinergic?

A

Answer: Atropine blocks acetylcholine receptors to reduce GI motility.

330
Q

SBA: What is the role of azoreductase in the activation of aminosalicylate prodrugs?

A

Answer: Cleaves azo bonds to release active 5-ASA in the colon.

331
Q

EMQ: Match the drug to its primary indication.

A

Omeprazole: Peptic ulcers and GORD.
Mesalazine: Ulcerative colitis.
Loperamide: Acute non-infectious diarrhoea.

332
Q

EMQ: Match the mechanism to the drug class.

A

Antacids: Neutralize gastric acid.
PPIs: Inhibit H+/K+-ATPase.
Promotility agents: Increase acetylcholine activity in GI smooth muscle.

333
Q

EMQ: Match the drug to its mechanism of action.

A

Loperamide: Opioid receptor agonist in the gut.
Domperidone: D2 receptor antagonist.
Scopolamine: Blocks muscarinic acetylcholine receptors.

334
Q

EMQ: Match the treatment to the GI condition.

A

Aminosalicylates: First-line for mild to moderate ulcerative colitis.
PPIs: Severe GORD or peptic ulcers.
Antibiotics (e.g., metronidazole): Bacterial overgrowth or anaerobic infections.

335
Q

EMQ: Match the drug to its side effect.

A

Loperamide: Constipation.
PPIs: Hypomagnesemia.
Aminosalicylates: Nephrotoxicity.

336
Q

What are the key drugs used in managing acid-peptic diseases?

A

Answer: PPIs (e.g., omeprazole), H2 receptor antagonists (e.g., ranitidine), and antacids. (2 marks)

337
Q

Outline the mechanism and use of promotility agents.

A

Answer: Enhance acetylcholine activity or block inhibitory neurotransmitters to treat gastroparesis and constipation. Examples: Domperidone, metoclopramide. (2 marks)

338
Q

What is the primary use of aminosalicylates in GI disease?

A

Answer: Treat mild-to-moderate ulcerative colitis by reducing inflammation in the colon. (2 marks)

339
Q

What are the mechanisms of action of antidiarrhoeals?

A

Answer:
Opioid receptor agonists (e.g., loperamide): Slow gut motility.
Anticholinergics (e.g., atropine): Reduce intestinal secretions and motility. (2 marks)

340
Q

What are the key differences between hard and soft gelatin capsules?

A

Answer: Hard capsules: Two-piece structure for powders/granules. Soft capsules: Single-piece, suitable for liquids/oils. (2 marks)

341
Q

SBA: What is the primary purpose of using protecting groups in drug synthesis?

A

Answer: To prevent unwanted side reactions and ensure chemoselectivity.

342
Q

SBA: What is a common protecting group for alcohols?

A

Answer: Silyl ethers (e.g., TBS, TBDMS).

343
Q

SBA: Which reagent is commonly used for the deprotection of benzyl ethers?

A

Answer: Hydrogenation with H₂ and Pd/C.

344
Q

SBA: Why are acetals commonly used to protect aldehydes and ketones?

A

Answer: They are stable under basic conditions and easily removed by acid hydrolysis.

345
Q

SBA: What is the preferred protecting group for primary amines in peptide synthesis?

A

Answer: Boc (tert-butyloxycarbonyl).

346
Q

SBA: What is the mechanism of protection for carboxylic acids using esters?

A

Answer: Conversion into less reactive esters to block electrophilicity.

347
Q

SBA: Which condition can deprotect carbamates like Boc?

A

Answer: Strong acids, such as HCl or TFA.

348
Q

SBA: What type of prodrug improves water solubility of a poorly soluble drug?

A

Answer: Carrier prodrug with a hydrophilic group.

349
Q

SBA: What is a key advantage of using Fmoc over Boc as a protecting group?

A

Answer: Fmoc is removed under basic conditions, avoiding acid-sensitive reactions.

350
Q

SBA: Which prodrug strategy can minimize GI bleeding caused by aspirin?

A

Answer: Esterification of aspirin into a prodrug form like acetylsalicylic acid.

351
Q

EMQ: Match the protecting group to its functional group.

A

Alcohols: Silyl ethers (e.g., TBDMS).
Aldehydes/Ketones: Acetals/Ketals.
Amines: Carbamates (e.g., Boc, Fmoc).

352
Q

EMQ: Match the deprotection method to the protecting group.

A

Boc: Strong acids like HCl or TFA.
Fmoc: Basic conditions (piperidine).
Benzyl ethers: Hydrogenation with H₂ and Pd/C.

353
Q

EMQ: Match the prodrug to its purpose.

A

Lipophilic carriers: Improve BBB penetration (e.g., for CNS drugs).
Ester prodrugs: Increase water solubility (e.g., enalapril).
Antibody-directed enzyme prodrug therapy: Target cancer cells.

354
Q

EMQ: Match the protecting group to its challenge.

A

Silyl ethers: Require specific reagents for removal (e.g., TBAF).
Acetals: Susceptible to acidic hydrolysis.
Carbamates: May require strong acids for deprotection.

355
Q

EMQ: Match the drug alliance to its mechanism.

A

Clavulanic acid: Inhibits β-lactamase to protect penicillins.
Ritonavir: Inhibits CYP3A4 to enhance lopinavir levels.
Adrenaline with procaine: Constriction of blood vessels to localize action.

356
Q

Why are protecting groups used in drug synthesis?

A

Answer: To prevent undesired reactions, guide chemoselectivity, and improve reaction yields. (2 marks)

357
Q

List examples of protecting groups for alcohols, aldehydes, and amines.

A

Answer:
Alcohols: Silyl ethers, acetals.
Aldehydes/Ketones: Acetals/Ketals.
Amines: Carbamates (e.g., Boc, Fmoc). (2 marks)

358
Q

Describe the deprotection conditions for Boc and Fmoc groups.

A

Answer:
Boc: Strong acids like HCl or TFA.
Fmoc: Basic conditions like piperidine. (2 marks)

359
Q

What are prodrugs, and what are their uses?

A

Answer: Inactive compounds converted into active drugs in the body. Used to improve solubility, stability, absorption, or reduce toxicity. (2 marks)

360
Q

Provide an example of a drug alliance and its mechanism.

A

Answer: Clavulanic acid protects penicillins by inhibiting β-lactamase enzymes. (2 marks)

Pharmacy - Year 2 (11 decks)

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