Pharmacy Infection Flashcards
(696 cards)
1
Q
SBA
What is the primary mechanism of action for PPIs in GORD management?
A
Irreversible inhibition of H/K-ATPase.
2
Q
EMQ
Select the most appropriate therapy for a patient with GORD who responds poorly to PPIs.
A
H2 Receptor Antagonist.
3
Q
SAQ
Outline a stepwise management plan for GORD, including lifestyle and pharmacological interventions.
A
Lifestyle changes (e.g., weight loss, smaller meals, avoid eating before bedtime).
Start antacids for immediate symptom relief.
Prescribe a PPI (e.g., Omeprazole 20 mg daily for 4 weeks).
For recurring symptoms, consider a step-down approach or H2RAs.
4
Q
SBA: What is the correct timing for taking a PPI for maximum efficacy in GORD?
A
Answer: 30 minutes to 1 hour before meals.
5
Q
SBA: What is the primary non-pharmacological management recommendation for patients with nighttime GORD symptoms?
A
Answer: Elevate the head of the bed.
6
Q
SBA: Why are gastro-resistant capsules used for omeprazole?
A
Answer: To protect the drug from degradation in the acidic stomach environment.
7
Q
SBA: What is the most common risk associated with long-term PPI use in older patients?
A
Answer: Chronic kidney disease.
8
Q
EMQ: Select the most appropriate treatment for a patient with mild GORD symptoms who has not improved with lifestyle changes.
A
Answer: Prescribe a PPI for 4 weeks.
9
Q
EMQ: Select the next step for a patient with GORD who has recurrent symptoms after 4 weeks of PPI therapy.
A
Answer: Continue PPI at the lowest effective dose.
10
Q
EMQ: Choose the best alternative treatment for a patient who responds poorly to PPIs.
A
Answer: Prescribe an H2 receptor antagonist.
11
Q
EMQ: Select the appropriate management for a patient presenting with water brash and regurgitation due to GORD.
A
Answer: Start antacids for immediate symptom relief.
12
Q
EMQ: For a patient with severe reflux symptoms persisting despite treatment, what is the appropriate next step?
A
Answer: Refer to a GP for further investigation.
13
Q
SAQ: Explain the mechanism of action of omeprazole and how it achieves long-term acid suppression.
A
Answer: Omeprazole irreversibly inhibits the H/K-ATPase proton pump in gastric parietal cells, blocking ~90% of acid secretion. This effect lasts beyond the plasma half-life because it requires new proton pumps to be synthesized.
14
Q
SAQ: Describe the risks and monitoring recommendations for long-term PPI use.
A
Answer: Risks include hypomagnesemia, chronic kidney disease, and possible acid rebound after discontinuation. Monitor serum magnesium in patients on long-term PPI therapy, especially those on ACE inhibitors or diuretics.
15
Q
SBA: What is the most common side effect associated with GORD?
A
Answer: Heartburn.
16
Q
SBA: Why are gastro-resistant capsules used for omeprazole?
A
Answer: To protect the drug from degradation in the acidic stomach environment.
17
Q
BA: What is the effect of antacids when taken on an empty stomach?
A
Answer: Effects last no longer than an hour due to rapid gastric emptying.
18
Q
SBA: What is the initial treatment duration for GORD using omeprazole 20 mg daily?
A
Answer: 4 weeks.
19
Q
SBA: What is a potential long-term risk of PPI therapy in older adults?
A
Answer: Chronic kidney disease.
20
Q
SBA: What should be monitored in long-term PPI use according to the BNF?
A
Answer: Serum magnesium.
21
Q
EMQ: Select the most appropriate non-pharmacological advice for a patient presenting with mild, intermittent GORD symptoms.
A
Answer: Advise smaller, more frequent meals and avoidance of eating 2–3 hours before bed.
22
Q
EMQ: Choose the most suitable therapy for a patient with uninvestigated dyspepsia and GORD symptoms.
A
Answer: Omeprazole 20 mg daily for 4 weeks.
23
Q
EMQ: Identify the best alternative therapy for a patient with GORD who does not respond to PPI therapy.
A
Answer: H2 receptor antagonist.
24
Q
EMQ: Select the best management for a patient reporting mild symptoms of acid reflux despite lifestyle changes.
A
Answer: Start antacids for immediate symptom relief.
25
EMQ: What is the next step for a patient whose symptoms return after stopping PPI therapy?
Answer: Initiate a step-down approach with the lowest effective PPI dose.
26
EMQ: Which pharmacological therapy is appropriate for a patient concerned about long-term PPI side effects but still requiring symptom control?
Answer: When-needed PPI therapy.
27
EMQ: Select the most suitable management for a patient with alarm symptoms (e.g., dysphagia or weight loss) after initial PPI therapy.
Answer: Refer to a GP for further investigation.
28
SAQ 1:
Describe pharmacological and non-pharmacological treatments for GORD. (10 marks)
Non-Pharmacological (2 marks):
Advise lifestyle changes: weight loss, smaller meals, avoid eating before bed.
Elevate the head of the bed for nighttime symptoms.
Pharmacological (8 marks):
Antacids for immediate relief (e.g., Gaviscon).
PPI (e.g., omeprazole 20 mg daily for 4 weeks) as first-line therapy.
H2 receptor antagonist (e.g., ranitidine) if PPI response is inadequate.
Step-down approach or on-demand PPI for long-term management.
29
SAQ 2:
Explain the role of gastro-resistant capsules in PPI therapy. (10 marks)
Prevents degradation of the drug in the stomach (2 marks).
Ensures release in the small intestine, where absorption is optimal (2 marks).
Helps maintain the biological effect of the PPI despite its short plasma half-life (2 marks).
Allows for sustained acid suppression by irreversibly inactivating proton pumps (4 marks).
30
Describe how to manage a patient with recurrent GORD symptoms after successful initial treatment with PPIs. (10 marks)
Restart PPI therapy at the lowest effective dose (2 marks).
Offer on-demand therapy as an alternative for intermittent symptoms (2 marks).
Address lifestyle factors and adherence to non-pharmacological measures (2 marks).
Consider H2 receptor antagonist if symptoms persist despite PPI (2 marks).
Refer to a GP if alarm symptoms (e.g., weight loss, dysphagia) appear (2 marks).
31
SBA: Which structure prevents food from entering the trachea?
Answer: Epiglottis.
32
SBA: Which layer of the alimentary canal is responsible for mucous secretion?
Answer: Mucosa.
33
SBA: Which vitamin requires intrinsic factor for absorption?
Answer: Vitamin B12.
34
SBA: What is the primary function of bile salts?
Answer: Emulsification of fats.
35
SBA: In what form are proteins absorbed into the bloodstream?
Answer: Amino acids.
36
SBA: What is the main function of the large intestine?
Answer: Absorption of water.
37
SBA: What hormone stimulates gastric juice secretion during the gastric phase?
Answer: Gastrin.
38
SBA: Where is vitamin B12 absorbed in the GI tract?
Answer: Terminal ileum.
39
SBA: What is the primary pharmacological target for reducing gastric acid secretion?
Answer: H+/K+ ATPase pump.
40
SBA: What is the first-line treatment for H. pylori-associated peptic ulcer disease?
Answer: Triple therapy with PPI, amoxicillin, and clarithromycin/metronidazole.
41
SBA: What is the main diagnostic test for H. pylori infection?
Answer: Urea breath test.
42
SBA: What is the pharmacological treatment for mild Crohn’s disease?
Answer: Budesonide (oral corticosteroid).
43
SBA: Which condition primarily involves inflammation of the rectum and colon?
Answer: Ulcerative colitis.
44
SBA: What supplementation is required after ileal resection in Crohn’s disease?
Answer: Vitamin B12.
45
SBA: What is the appropriate treatment for diarrhea in IBS?
Answer: Loperamide.
46
SBA: What is the most common risk associated with long-term PPI use in older adults?
Answer: Chronic kidney disease.
47
SBA: What side effect is commonly monitored during long-term PPI use?
Answer: Hypomagnesemia.
48
SBA: What is the primary action of alginates in GORD treatment?
Answer: Form a physical barrier to prevent reflux.
49
SBA: What red flag symptom requires urgent referral for further investigation in GORD?
Answer: Dysphagia.
50
SBA: What is the correct timing for taking a PPI for maximum efficacy?
Answer: 30 minutes to 1 hour before meals.
51
SBA: Why are gastro-resistant capsules used for omeprazole?
Answer: To protect the drug from degradation in the acidic stomach environment.
52
SBA: What non-pharmacological measure is most appropriate for patients with nighttime GORD symptoms?
Answer: Elevate the head of the bed.
53
SBA: How should GORD symptoms recurring after stopping PPI therapy be managed?
Answer: Restart PPI therapy at the lowest effective dose.
54
SBA: Which diagnostic tool is most appropriate for suspected esophageal cancer in a patient with alarm symptoms?
Answer: Endoscopy.
55
SBA: What condition is associated with long-term bile duct obstruction?
Answer: Steatorrhea.
56
SBA: What is the role of bile salts in fat digestion?
Answer: Facilitate the formation of micelles for fat absorption.
57
SBA: Which vitamin absorption would be impaired due to bile salt deficiency?
Answer: Vitamin A.
58
SBA: What is the primary role of the enteric nervous system in digestion?
Answer: Control of motility, secretion, and blood flow within the GI tract.
59
List the main features of GORD, peptic ulcers and H. pylori infection
Gastro-oesophageal reflux disease
* Usually caused by weakening/relaxation in lower oesophageal sphincter
* Acid from stomach leaks up into oesophagus, causing symptoms:
* Heartburn
* Acid reflux
* Bad breath
* Bloating / belching
* Nausea / vomiting
60
State how GORD, peptic ulcers and H. pylori infections are diagnosed
Diagnosis usually made solely on symptoms
* Should take a full drug history to identify any possible drug causes
* Calcium antagonists, nitrates, theophyllines, bisphosphonates, corticosteroids and
non-steroidal anti-inflammatory drugs
* Will unlikely perform any other tests to confirm GORD diagnosis
* May perform other tests to investigate other causes of symptoms
* Urea breath test for H. pylori infection
* Endoscopy for gastric cancers
61
Outline the pharmacological management of GORD, peptic ulcers and H. pylori
infection
Antacid: Pepto-Bismol®, Rennie®
* Alignate: Gaviscon Advance®
* Dual Product: Gaviscon Dual Action®, Peptac®
* PPI or H2 receptor antagonists
* Longer acting, but take longer to work than antacids
* Do not take both at same time, one or the other
* Quite strict criteria of who you can supply PPI to (recent POM to P switch)
* Max 2-4 weeks treatment, then refer to GP
62
What if any red flags exist for GORD referral?
Patients over 55 years with new onset symptoms
* Patients over 55 years with unexplained dyspepsia that hasn’t responded to 2 weeks of
treatment
* Patients who have continuously taken remedies for 4 weeks (risk of rebound indigestion)
* Pregnant or breastfeeding
* Not responded to OTC treatment
* Red flag symptoms:
* Unintentional weight loss
* Epigastric mass
* Stomach pain, pain/difficulty when swallowing
* Persistent vomiting
* Jaundice
* Signs suggestive of GI bleed
63
Sarah’s Pub Lunch Route:
Mouth → Pharynx → Esophagus → Stomach → Small Intestine (duodenum → jejunum → ileum) → Large Intestine (cecum → colon → rectum) → Anus.
64
Accessory Organs:
Liver, pancreas, gallbladder, salivary glands.
65
Four Layers of the GI Tract:
Mucosa → Submucosa → Muscularis externa → Serosa.
66
Location of the Oblique Muscle:
Found in the stomach’s muscularis externa, aiding in mechanical digestion.
67
Role of Mucus in the GI Tract:
Protects the lining from acidic and enzymatic damage.
Lubricates food passage.
68
Vomiting Center and Receptor Types:
Role: Coordinates emesis by activating GI and diaphragm muscles.
Receptors: Dopamine (D2), Serotonin (5-HT3), Histamine (H1), Acetylcholine (muscarinic), and Neurokinin-1 (NK1).
69
Pain Timing in Ulcers:
Duodenal Ulcers: Pain improves with eating.
Gastric Ulcers: Pain worsens with eating.
70
Gastroparesis Definition:
Partial paralysis of the stomach, delaying gastric emptying.
71
Symptoms and Treatment of Gastroparesis:
Symptoms: Nausea, vomiting, bloating, early satiety.
Treatment: Dietary changes, prokinetic agents (e.g., metoclopramide), and antiemetics.
72
Pathology of GORD:
Dysfunction of the lower esophageal sphincter (LES) → Acid reflux damages esophageal mucosa.
73
Features of GORD, Peptic Ulcers, H. pylori:
GORD: Heartburn, regurgitation, dysphagia.
Peptic Ulcers: Epigastric pain, hematemesis, melena.
H. pylori: Chronic gastritis, ulcer formation.
74
Diagnosis of GORD, Peptic Ulcers, H. pylori:
GORD: Clinical diagnosis, endoscopy if severe.
Peptic Ulcers: Endoscopy, urea breath test.
H. pylori: Urea breath test, stool antigen test, biopsy.
75
Pharmacological Management:
GORD: Antacids, PPIs, H2RAs.
Peptic Ulcers: PPIs + H. pylori eradication therapy.
H. pylori: Triple therapy (PPI, amoxicillin, clarithromycin/metronidazole).
76
Red Flags for GORD Referral:
Dysphagia, unintentional weight loss, GI bleeding, epigastric mass.
77
First-Line Treatment for GORD:
PPIs (e.g., omeprazole).
78
Sites of Action: Omeprazole vs. Ranitidine:
Omeprazole: Inhibits H+/K+ ATPase in parietal cells.
Ranitidine: Blocks H2 receptors in parietal cells.
79
PPI Drug Interactions:
PPIs inhibit CYP enzymes (e.g., CYP2C19), reducing metabolism of drugs like clopidogrel.
80
Role of H. pylori in Ulcers:
Produces urease, neutralizing stomach acid → Mucosal damage → Ulcer formation.
81
Treatment for H. pylori-Associated Ulcers:
Triple therapy: PPI + amoxicillin + clarithromycin/metronidazole.
82
Ulcers Without H. pylori:
Possible causes: NSAIDs, stress ulcers, Zollinger-Ellison syndrome.
83
Zollinger-Ellison Syndrome:
Gastrin-secreting tumor → Excess acid production → Refractory peptic ulcers.
84
IBD Symptoms:
Diarrhea (bloody in UC), abdominal pain, weight loss, fatigue, extraintestinal symptoms (e.g., joint pain).
85
Differential Diagnosis of UC:
Differentiated from Crohn’s by UC’s limitation to the colon/rectum and lack of skip lesions.
86
Term for UC + Crohn’s:
nflammatory Bowel Disease (IBD).
87
Recommended Treatment for Diarrhea:
Loperamide or oral rehydration therapy.
88
Role of Enteric Nervous System in IBS Treatment:
Regulates motility, secretion, and pain perception; targeted by antispasmodics (e.g., hyoscine).
89
Role and Types of PPI Drugs:
Block H+/K+ ATPase to reduce acid secretion (e.g., omeprazole, lansoprazole).
90
TPMT Analysis:
Required prior to azathioprine/mercaptopurine therapy to assess risk of myelosuppression.
91
SBA: What step in the viral lifecycle do HIV integrase inhibitors target?
Answer: HIV genome integration.
92
SBA: What is the primary mechanism of action of nucleoside reverse transcriptase inhibitors (NRTIs)?
Answer: Inhibition of genome replication via DNA chain termination.
93
SBA: Which class of drugs prevents HIV viral fusion with host cells?
Answer: HIV gp41 inhibitors.
94
SBA: What step in the influenza virus lifecycle do neuraminidase inhibitors block?
Answer: Viral release/exit.
95
SBA: What step in the influenza lifecycle do M2 blockers inhibit?
Answer: Viral uncoating.
96
SBA: Why are host proteins targeted in some antiviral drugs?
Answer: Host proteins mutate less frequently, reducing resistance risk.
97
SBA: What antiviral drug targets the CCR5 receptor to prevent HIV entry?
Answer: Maraviroc.
98
SBA: What is the oral prodrug of penciclovir?
Answer: Famciclovir.
99
SBA: How does acyclovir selectively target HSV-infected cells?
Answer: It requires phosphorylation by viral thymidine kinase for activation.
100
SBA: What makes cidofovir more stable than Antiviral A?
Answer: Cidofovir has a phosphonate bond (P-C), which is more stable than a phosphate bond (P-O).
101
SBA: What viral polymerase does remdesivir inhibit?
Answer: SARS-CoV-2 RNA-dependent RNA polymerase.
102
SBA: What technology is used to deliver monophosphate nucleotide inhibitors like remdesivir?
Answer: ProTide technology.
103
SBA: What is the key feature of tenofovir disoproxil that increases its absorption?
Answer: Masking of the phosphonate group with disoproxil groups.
104
SBA: Why is monotherapy ineffective for treating HIV?
Answer: High mutation rate leads to rapid emergence of resistance.
105
SBA: What is the active form of adefovir dipivoxil?
Answer: Adefovir diphosphate.
106
SBA: What is the role of NNRTIs in HIV therapy?
Answer: Allosteric inhibition of reverse transcriptase.
107
SBA: Which HIV drug class does not require intracellular activation?
Answer: NNRTIs (e.g., rilpivirine).
108
SBA: How does adefovir cause DNA chain termination?
Answer: It lacks a 3’-OH group required for DNA elongation.
109
SBA: Which viral infection can be cured with current antiviral therapies?
Answer: Hepatitis C virus (HCV).
110
SBA: What structural feature of remdesivir aids in intracellular delivery?
Answer: Masking of the negatively charged phosphate group.
111
EMQ: Match the drug class to its inhibited viral step in HIV replication.
Answer:
NRTIs: Genome replication.
NNRTIs: Reverse transcriptase allosteric inhibition.
Integrase inhibitors: HIV genome integration.
112
EMQ: Select the antiviral mechanism of acyclovir.
Answer: Inhibition of viral DNA polymerase by chain termination.
113
EMQ: Identify the correct antiviral therapy for influenza targeting viral uncoating.
Answer: M2 blockers.
114
EMQ: Choose the treatment targeting HSV that requires intracellular activation.
Answer: Acyclovir.
115
EMQ: Select the drug preventing HIV entry into host cells.
Answer: Maraviroc.
116
EMQ: Match the drug to its use: Famciclovir or Acyclovir for cold sores.
Answer: Acyclovir cream for cold sores (HSV-1).
117
EMQ: Choose the prodrug that enhances absorption of tenofovir.
Answer: Tenofovir disoproxil.
118
EMQ: Select the correct antiviral for HCV with a high mutation barrier.
Answer: Combination therapy with direct-acting antivirals (DAAs).
119
EMQ: Match ProTide technology to its role in remdesivir.
Answer: Facilitates intracellular delivery of monophosphate nucleosides.
120
EMQ: Identify the drug causing selective toxicity by viral thymidine kinase activation.
Answer: Acyclovir.
121
SAQ 1:
Explain the mechanism of action of acyclovir and its selective activity against HSV-infected cells.
Acyclovir is a nucleoside analog that inhibits viral DNA polymerase by causing chain termination. (3 marks)
It is phosphorylated into the active triphosphate form by viral thymidine kinase, ensuring activation only in infected cells. (4 marks)
It binds viral DNA polymerase with >100-fold affinity compared to human DNA polymerase, minimizing toxicity. (3 marks)
122
SAQ 2:
Describe the rationale for using combination therapy in HIV treatment.
Prevents resistance by targeting multiple steps of the viral lifecycle. (3 marks)
Provides a synergistic effect, improving antiviral efficacy. (2 marks)
Reduces drug toxicity by lowering individual drug dosages. (2 marks)
Addresses HIV’s high mutation and replication rates. (3 marks)
123
SAQ 3:
Outline the advantages of ProTide technology used in remdesivir.
Masks negatively charged phosphate group, enhancing membrane permeability. (3 marks)
Circumvents inefficient first phosphorylation step in nucleoside activation. (3 marks)
Protects the drug from hydrolysis until inside the target cell. (2 marks)
Increases delivery efficiency and antiviral potency. (2 marks)
124
SBA: What is the target of sulfonamides in bacterial cells?
Answer: Dihydropteroate synthetase (DHPS).
125
SBA: What family does ceftazidime belong to?
Answer: Cephalosporins.
126
SBA: What is the antibacterial effect of clavulanic acid?
Answer: No direct antibacterial effect (β-lactamase inhibitor).
127
SBA: Which bacterial target do fluoroquinolones inhibit?
Answer: Topoisomerases.
128
SBA: What is the key structural feature of methicillin responsible for β-lactamase resistance?
Answer: Bulky side chain on the acylamino group.
129
SBA: Which antibiotic is active against Mycoplasma pneumoniae?
Answer: Macrolides (e.g., erythromycin).
130
SBA: What is the mechanism of resistance in Mycoplasma pneumoniae to β-lactams?
Answer: Intrinsic resistance due to the absence of a cell wall.
131
SBA: Which family does doxycycline belong to?
Answer: Tetracyclines.
132
SBA: What is the minimum inhibitory concentration (MIC)?
Answer: The lowest concentration of an antibiotic that inhibits bacterial growth.
133
SBA: What family does levofloxacin belong to?
Answer: Fluoroquinolones.
134
SBA: What is the mode of action of aminoglycosides?
Answer: Inhibit bacterial protein synthesis by binding to the 30S ribosomal subunit.
135
SBA: Which penicillin has the narrowest spectrum of activity?
Answer: Penicillin G.
136
SBA: What is the mechanism of sulfonamide activity reduction by procaine?
Answer: Procaine hydrolyzes to release PABA, which competes with sulfonamides for binding to DHPS.
137
SBA: What is the effect of β-lactamase on penicillin?
Answer: Hydrolyzes the β-lactam ring, rendering the antibiotic inactive.
138
SBA: Which bacterial mechanism involves physical contact for horizontal gene transfer?
Answer: Conjugation.
139
SBA: What is the antibacterial effect of tetracyclines?
Answer: Bacteriostatic.
140
SBA: Why are bactericidal antibiotics preferred for immunocompromised patients?
Answer: They kill bacteria directly without relying on the immune system.
141
SBA: What is the role of β-lactamase inhibitors like clavulanic acid?
Answer: Prevent β-lactamase from hydrolyzing β-lactam antibiotics.
142
SBA: What family does piperacillin/tazobactam belong to?
Answer: Antipseudomonal penicillins combined with a β-lactamase inhibitor.
143
SBA: Which antibiotic family targets nucleic acid synthesis?
Answer: Fluoroquinolones.
144
EMQ: Match the bacterial target to the drug family.
Protein synthesis (50S ribosomal subunit): Macrolides.
Cell wall synthesis: Penicillins.
Nucleic acid synthesis: Fluoroquinolones.
145
EMQ: Select the appropriate drug for atypical pneumonia caused by Mycoplasma pneumoniae.
Answer: Azithromycin (Macrolides).
146
EMQ: Match the penicillins in order of spectrum of activity from narrowest to broadest.
Penicillin G → Flucloxacillin → Amoxicillin → Piperacillin-tazobactam.
147
EMQ: Choose the best treatment for a patient with Staphylococcus aureus producing β-lactamase.
Answer: Flucloxacillin.
148
EMQ: Select the antibiotic active against Pseudomonas aeruginosa.
Answer: Piperacillin-tazobactam.
149
EMQ: Choose the correct effect of sulfonamides on bacterial metabolism.
Answer: Inhibit folic acid synthesis.
150
EMQ: Match the β-lactamase inhibitor to its use.
Clavulanic acid: Used with amoxicillin.
151
EMQ: Select the drug that inhibits protein synthesis at the 30S ribosomal subunit.
Answer: Doxycycline (Tetracyclines).
152
EMQ: Choose the drug family requiring intracellular activation.
Answer: Nitroimidazoles (e.g., metronidazole).
153
EMQ: Match the antibacterial effect to the drug.
Amoxicillin: Bactericidal.
Sulfamethoxazole: Bacteriostatic.
154
SAQ 1:
Explain the mechanism of β-lactam resistance in bacteria.
β-lactamase production: Hydrolyzes the β-lactam ring, rendering the antibiotic inactive (4 marks).
Alteration of target site: Mutation in penicillin-binding proteins (PBPs) reduces drug binding (4 marks).
Efflux pumps: Bacteria actively pump out the antibiotic (2 marks).
155
SAQ 2:
Describe the role of clavulanic acid in combination therapy.
Prevents β-lactam hydrolysis by inhibiting β-lactamase enzymes (4 marks).
Extends the spectrum of β-lactam antibiotics (3 marks).
No direct antibacterial activity but enhances drug efficacy (3 marks).
156
SAQ 3:
Outline the difference between bacteriostatic and bactericidal antibiotics.
Bacteriostatic: Inhibit bacterial growth, rely on immune system for clearance (e.g., tetracyclines) (4 marks).
Bactericidal: Directly kill bacteria, preferred in immunocompromised patients (e.g., β-lactams) (4 marks).
Clinical Use: Choice depends on patient’s immune status and infection severity (2 marks).
157
SBA: What is the definition of epidemiology?
Answer: The study of how often diseases occur in different groups of people and why.
158
SBA: What is the role of epidemiology in healthcare?
Answer: To plan and evaluate strategies for disease prevention and guide patient management.
159
SBA: What is a biological agent of disease?
Answer: Bacteria, viruses, or fungi.
160
SBA: What is the primary transmission route of tuberculosis?
Answer: Airborne transmission.
161
SBA: What are fomites in the context of infection?
Answer: Objects that can facilitate pathogen transmission, such as handrails or utensils.
162
SBA: What is the natural reservoir for Clostridium tetani?
Answer: Soil.
163
SBA: Which pathogens are commonly transmitted through the faecal-oral route?
Answer: Cholera and hepatitis A.
164
SBA: What is a key feature of robust pathogens?
Answer: Ability to survive for long periods outside the host.
165
SBA: Which transmission route involves pathogens being carried by vectors?
Answer: Vector-borne transmission (e.g., malaria via mosquitoes).
166
SBA: What does the antimicrobial spectrum of activity describe?
Answer: The range of organisms targeted by an antimicrobial.
167
EMQ: Match the transmission route to the example of infection.
Airborne transmission: Tuberculosis.
Faecal-oral transmission: Cholera.
Vector-borne transmission: Malaria.
Direct contact transmission: Cold sores (HSV-1).
168
EMQ: Select the most appropriate prevention method for waterborne diseases.
Answer: Adequate sanitation and safe water supply.
169
EMQ: Match the pathogen to its primary reservoir.
Clostridium tetani: Soil.
Legionella pneumophila: Water.
Rabies virus: Infected animals.
170
EMQ: Identify the most likely mode of influenza transmission in an office setting.
Answer: Indirect contact via shared surfaces.
171
EMQ: Match the pathogen to its antimicrobial susceptibility.
Gram-positive bacteria: Penicillin V.
Gram-negative bacteria: Ceftriaxone.
172
Define epidemiology and its importance.
Answer: The study of disease occurrence and distribution in populations, used for prevention and management.
173
List three major modes of pathogen transmission.
Answer: Airborne, faecal-oral, and vector-borne.
174
Explain the term "fomites" and provide two examples.
Answer: Objects that facilitate transmission, e.g., handrails, used tissues.
175
What is the difference between droplet and airborne transmission?
Answer: Droplet transmission requires close contact, airborne pathogens remain infective for long periods in the air.
176
What factors make a pathogen "robust"?
Answer: Ability to survive outside a host, resistance to environmental changes, high transmissibility.
177
SBA: What is the definition of pathophysiology?
Answer: The study of disordered physiological processes associated with disease or injury.
178
SBA: What is the role of prostaglandin E2 (PGE2) in fever development?
Answer: Alters the hypothalamic set-point, leading to an elevated body temperature.
179
SBA: What is the systemic inflammatory response syndrome (SIRS) criterion for tachypnea?
Answer: Respiratory rate >20 breaths per minute.
180
SBA: Which immune cells are responsible for killing virus-infected cells?
Answer: Natural killer (NK) cells.
181
SBA: What defines sepsis in the context of infection?
Answer: SIRS caused by an infection.
182
SBA: What is the most common cause of bacterial sepsis in the hospital setting?
Answer: Staphylococcus aureus.
183
SBA: What type of molecular pattern triggers the inflammatory response in infection?
Answer: Pathogen-associated molecular patterns (PAMPs).
184
SBA: What is the hallmark cytokine associated with sepsis-induced organ dysfunction?
Answer: Tumor necrosis factor-alpha (TNF-α).
185
SBA: What is the primary diagnostic marker for sepsis?
Answer: Elevated lactate levels (>2 mmol/L).
186
SBA: Which organ dysfunction is commonly associated with severe sepsis?
Answer: Acute kidney injury.
187
EMQ: Match the pathogen to its disease association.
Staphylococcus aureus: Toxic shock syndrome.
Escherichia coli O157: Haemolytic uraemic syndrome.
Listeria monocytogenes: Meningitis in immunocompromised patients.
188
EMQ: Select the most likely systemic effect of infection in sepsis.
Answer: Vasodilation leading to hypotension.
189
EMQ: Identify the appropriate cytokine associated with systemic inflammation in infection.
Answer: Interleukin-1 (IL-1).
190
EMQ: Match the clinical sign to its systemic cause in infection.
Fever: Elevated hypothalamic set-point.
Hypotension: Systemic vasodilation.
Tachypnea: Increased metabolic demand.
191
EMQ: Match the infection to its primary mode of transmission.
Staphylococcus aureus: Direct contact.
Listeria monocytogenes: Ingestion of contaminated food.
Escherichia coli O157: Faecal-oral transmission.
192
SAQ: Explain the systemic effects of infection and their clinical markers. (10 marks)
Define sepsis and its progression to severe sepsis.
Answer: Sepsis is SIRS due to infection, characterized by dysregulated immune response. Severe sepsis includes organ dysfunction.
193
List the three major systemic effects of infection.
Answer: Fever, sepsis, and organ dysfunction
194
Describe the role of PGE2 in fever development.
nswer: PGE2 stimulates endogenous pyrogens (IL-1, IL-6, TNF-α), resetting the hypothalamic temperature set-point.
195
What is the clinical definition of septic shock?
Answer: Sepsis-induced hypotension persisting despite fluid resuscitation. (1 mark)
196
Explain the significance of lactate levels in sepsis diagnosis.
Answer: Elevated lactate (>2 mmol/L) indicates tissue hypoperfusion and metabolic dysfunction.
197
SBA: What is the definition of pneumonia?
Answer: Inflammation of the lungs caused by bacterial or viral infection, with pus-filled air sacs.
198
SBA: Which bacterial pathogen is the most common cause of community-acquired pneumonia (CAP)?
Answer: Streptococcus pneumoniae.
199
SBA: What scoring system is used to assess the severity of CAP in the hospital setting?
Answer: CURB-65.
200
SBA: What is the first-line antibiotic treatment for low-severity CAP in a non-penicillin-allergic patient?
Answer: Amoxicillin 500 mg TDS for 5 days.
201
SBA: What symptom in CAP is commonly associated with confusion in elderly patients?
Answer: Delirium.
202
SBA: What is a hallmark radiological finding in CAP?
Answer: New consolidation on chest X-ray.
203
SBA: What CRB-65 score suggests that a CAP patient can be managed at home?
Answer: CRB-65 score = 0.
204
SBA: Which risk factor increases susceptibility to CAP?
Answer: Smoking (active or passive).
205
SBA: What is the most common side effect of doxycycline?
Answer: Gastrointestinal upset (nausea, vomiting).
206
SBA: What antibiotic class does levofloxacin belong to?
Answer: Quinolones.
207
MQ: Match the antibiotic to the associated CAP severity and allergy status.
Amoxicillin: Low-severity CAP, non-penicillin-allergic.
Doxycycline: Low-severity CAP, penicillin-allergic.
Co-amoxiclav + Clarithromycin: High-severity CAP.
Levofloxacin: High-severity CAP, penicillin-allergic.
208
EMQ: Match the CURB-65 parameters to their thresholds.
Confusion: Abbreviated Mental Test (AMT) score ≤8.
Urea: >7 mmol/L.
Respiratory rate: >30 breaths/min.
Blood pressure: Systolic <90 mmHg or diastolic ≤60 mmHg.
209
EMQ: Match the pathogen to its associated CAP context.
Legionella spp.: Immunocompromised patients.
Haemophilus influenzae: Smokers or COPD patients.
Staphylococcus aureus: Post-influenza pneumonia.
210
EMQ: Identify the expected timeline for symptom resolution in CAP.
1 week: Fever resolution.
4 weeks: Reduction in chest pain and sputum production.
6 months: Return to normal energy levels.
211
EMQ: Match the diagnosis method to the relevant symptom or finding in CAP.
Chest X-ray: Consolidation.
CRP and WCC: Inflammatory markers.
Oxygen saturation: Hypoxia detection.
212
What are the common symptoms of CAP?
Answer: Fever, cough (productive with yellow/green sputum), dyspnea, chest pain, fatigue, confusion (in elderly).
213
Outline the CURB-65 parameters for severity classification.
Confusion (AMT ≤8).
Urea >7 mmol/L.
Respiratory rate >30 breaths/min.
Blood pressure (systolic <90 mmHg or diastolic ≤60 mmHg).
Age ≥65 years. (3 marks)
214
List first-line antibiotic options for low-severity CAP in non-penicillin-allergic and penicillin-allergic patients.
nswer:
Non-penicillin-allergic: Amoxicillin.
Penicillin-allergic: Doxycycline or Clarithromycin.
215
What investigations confirm the diagnosis of CAP?
Answer:
Chest X-ray (consolidation).
Blood tests: CRP, WCC.
Oxygen saturation. (2 marks)
216
How should CAP patients be counselled about symptom resolution?
Answer:
1 week: Fever resolves.
4 weeks: Chest pain and sputum reduce.
6 weeks: Cough and breathlessness improve.
3 months: Most symptoms resolve, fatigue may persist.
6 months: Full recovery expected.
217
SBA: What is the primary goal of antibiotic therapy?
Answer: To kill pathogenic bacteria while causing no harm to human tissue.
218
SBA: Which bacterial group is commonly associated with community-acquired pneumonia?
Answer: Streptococcus pneumoniae (Gram-positive).
219
SBA: What is the mechanism of action of penicillins?
Answer: Inhibition of bacterial cell wall synthesis.
220
SBA: Which antibiotic is contraindicated in children under 12 due to its effects on teeth and bone?
Answer: Tetracycline.
221
SBA: What is the definition of antimicrobial resistance (AMR)?
Answer: Loss of effectiveness of any anti-infective medicine.
222
SBA: What is the principal adverse effect of fluoroquinolones?
Answer: Tendon damage (e.g., tendinitis or tendon rupture).
223
SBA: Which parameter determines the efficacy of time-dependent antibiotics?
Answer: Time above the minimum inhibitory concentration (MIC).
224
SBA: What is the main side effect of aminoglycosides like gentamicin?
Answer: Nephrotoxicity and ototoxicity.
225
SBA: What is the role of beta-lactamase inhibitors like clavulanic acid?
Answer: Protect beta-lactam antibiotics from hydrolysis by beta-lactamases.
226
SBA: What is the primary benefit of using narrow-spectrum antibiotics over broad-spectrum antibiotics?
Answer: Reduced risk of Clostridium difficile infection and antimicrobial resistance.
227
EMQ: Match the antibiotic class to its mechanism of action.
Penicillins: Inhibit bacterial cell wall synthesis.
Macrolides: Inhibit protein synthesis at the 50S ribosomal subunit.
Fluoroquinolones: Inhibit bacterial DNA synthesis by targeting DNA gyrase.
228
EMQ: Match the bacterial infection with the likely causative pathogen.
Community-acquired pneumonia: Streptococcus pneumoniae.
Post-influenza pneumonia: Staphylococcus aureus.
Urinary tract infection: Escherichia coli.
229
EMQ: Match the patient scenario to the appropriate antibiotic choice.
Penicillin-allergic patient with mild CAP: Doxycycline.
Severe CAP requiring IV antibiotics: Co-amoxiclav + clarithromycin.
Skin infection caused by MRSA: Vancomycin.
230
EMQ: Match the mechanism of resistance to the bacterial adaptation.
Efflux pumps: Expels antibiotics from the cell.
Hydrolysis: Breaks down beta-lactam antibiotics.
Mutation of binding site: Prevents antibiotic binding.
231
EMQ: Select the principle of antimicrobial stewardship applied in these cases.
Avoiding broad-spectrum antibiotics in mild infections: Reduce AMR risk.
Reviewing IV antibiotics after 48 hours: Promote stepping down to oral therapy.
Counseling on completing the course: Prevent relapse and resistance.
232
What factors should be considered before starting antibiotic therapy?
Answer: History of allergy, renal/hepatic function, site of infection, likely pathogen, antibacterial sensitivity, patient age, comorbidities, and prior antibiotic use. (2 marks)
233
Explain the significance of reviewing IV antibiotics within 48 hours.
Answer: Ensures appropriateness of therapy, promotes stepping down to oral therapy, and reduces hospital-acquired infections. (2 marks)
234
List three common mechanisms of bacterial resistance to antibiotics.
Answer: Efflux pumps, beta-lactamase production, and target site mutations. (3 marks)
235
Why is it important to minimize broad-spectrum antibiotic use in community settings?
Answer: Broad-spectrum antibiotics increase the risk of resistant pathogens like MRSA and Clostridium difficile.
236
What advice should be given to patients prescribed antibiotics?
Answer: Complete the full course, avoid skipping doses, avoid alcohol if contraindicated (e.g., metronidazole), and report any adverse reactions immediately. (1 mark)
237
SBA: What is the primary function of the innate immune system?
Answer: Non-specific defense against pathogens, providing the first line of protection.
238
SBA: What is the key difference between innate and adaptive immunity?
Answer: Adaptive immunity involves specific antigen recognition and immunological memory.
239
SBA: Which component of the immune system is responsible for opsonization?
Answer: Complement system (e.g., C3).
240
SBA: What is the role of cytotoxic T cells in viral infections?
Answer: Induce apoptosis in virus-infected host cells.
241
SBA: Which immune cells produce antibodies?
Answer: B cells (Plasma cells).
242
SBA: What does the complement cascade form to induce microbial cell lysis?
Answer: Membrane attack complex (MAC).
243
SBA: What is the main immune response to extracellular bacterial infections?
Answer: Activation of phagocytes and complement-mediated opsonization.
244
SBA: Which type of T cell helps B cells differentiate into plasma cells?
Answer: Helper T cells (Th2 subtype).
245
SBA: How do NK cells recognize and target infected host cells?
Answer: Detect the absence of MHC-I molecules on the cell surface.
246
SBA: What cytokine is secreted by macrophages to induce antiviral states in neighboring cells?
Answer: Interferon (e.g., IFN-α/β).
247
MQ: Match the immune system component to its function.
Complement: Opsonization and lysis of pathogens.
Cytotoxic T cells: Induce apoptosis in infected cells.
Antibodies: Neutralization of extracellular pathogens.
248
EMQ: Match the pathogen type to the predominant immune response.
Extracellular bacteria: Phagocytosis and antibody response.
Viruses: T-cell-mediated immunity.
249
EMQ: Select the immune cells involved in each infection phase.
Early bacterial infection: Neutrophils.
Viral-infected host cells: Cytotoxic T cells and NK cells.
250
EMQ: Identify the stage of immune response from the description.
First exposure to an antigen: Primary response.
Faster and more robust response: Secondary response (memory cells).
251
EMQ: Match the complement function to the mechanism.
Opsonization: Binding of C3 to microbes.
Inflammation: C3a and C5a attract leukocytes.
Lysis: MAC formation by C5-C9.
252
What are the primary innate defenses against bacteria?
Answer: Complement activation, phagocytosis by macrophages and neutrophils, and inflammation. (2 marks)
253
Describe the adaptive immune response to extracellular bacteria.
Answer: Antigen-presenting cells activate helper T cells, which stimulate B cells to produce antibodies. Opsonization enhances phagocytosis.
254
How does the immune system respond to viruses during the extracellular phase?
nswer: Antibodies neutralize viral particles and promote phagocytosis. (2 marks)
255
What role do cytotoxic T cells play in intracellular viral infections?
Answer: Recognize viral antigens presented on MHC-I molecules and induce apoptosis in infected cells.
256
Explain the role of interferons in antiviral defense.
Answer: Induce antiviral states in neighboring cells, inhibiting viral replication. (2 marks)
257
SBA: What are the three necessary factors for an infection to occur?
Answer: Source, susceptible person, and transmission route.
258
SBA: What is the most effective method for preventing the spread of infection in healthcare?
Answer: Handwashing with soap and water.
259
SBA: Why is handwashing with soap preferred over alcohol gel for C. difficile?
Answer: Alcohol gel does not kill C. difficile spores.
260
SBA: What is the primary goal of personal protective equipment (PPE)?
Answer: To protect both healthcare workers and patients from cross-infection.
261
SBA: Which microorganism commonly causes healthcare-associated infections (HCAIs) via contact transmission?
Answer: Methicillin-resistant Staphylococcus aureus (MRSA).
262
SBA: What type of transmission is most associated with tuberculosis?
Answer: Airborne transmission.
263
SBA: What is the main objective of antibiotic prophylaxis in surgery?
Answer: To prevent surgical site infections.
264
SBA: Which patients are at the highest risk of Clostridium difficile infections?
Answer: Patients who have recently taken broad-spectrum antibiotics.
265
SBA: What does the term "bare below the elbow" refer to in infection control?
Answer: A policy to improve hand hygiene and reduce cross-infection.
266
SBA: What is the purpose of MRSA decolonization therapy?
Answer: To reduce colonization and prevent active infections and transmission.
267
EMQ: Match the transmission route to the infection example.
Contact transmission: C. difficile.
Droplet transmission: COVID-19.
Airborne transmission: Tuberculosis.
268
EMQ: Match the infection prevention measure to the purpose.
Handwashing: Remove microorganisms from hands.
Isolation: Prevent spread of infectious diseases.
PPE: Protect healthcare workers and patients.
269
EMQ: Match the HCAI pathogen to the clinical context.
MRSA: Contact transmission via healthcare worker hands.
C. difficile: Disruption of gut flora from broad-spectrum antibiotics.
Carbapenemase-producing organisms: Hospital admission abroad.
270
EMQ: Match the infection control procedure to its function.
Cleaning and decontamination: Reduce surface microorganisms.
Screening: Identify colonized patients before procedures.
Decolonization: Reduce MRSA colonization.
271
EMQ: Match the vaccination program to its primary goal.
Pneumococcal vaccine: Prevent invasive infections like sepsis and meningitis.
Influenza vaccine: Protect against seasonal flu strains.
MMR vaccine: Provide lifetime immunity against measles, mumps, and rubella.
272
Define healthcare-associated infections (HCAIs) and give examples.
Answer: Infections acquired during healthcare delivery (e.g., MRSA, C. difficile). (2 marks)
273
Describe the three components required for infection to occur.
Source: Place where microorganisms reside (e.g., surfaces, human skin).
Susceptible person: Individual with weakened immunity or entry points (e.g., IV lines).
Transmission route: Contact, droplet, airborne, or via medical equipment. (3 marks)
274
What are the key elements of standard precautions?
Answer:
Hand hygiene.
PPE use.
Respiratory hygiene/cough etiquette.
Cleaning and disinfecting surfaces. (2 marks)
275
How is Clostridium difficile prevented and managed in hospitals?
Answer:
Use soap and water for handwashing.
Avoid unnecessary antibiotics.
Isolate infected patients. (2 marks)
276
What is the role of vaccinations in infection prevention?
Answer: Prevent infections by inducing immunity (e.g., pneumococcal vaccine for sepsis, meningitis).
277
SBA: What is antimicrobial resistance (AMR)?
Answer: The ability of microorganisms to survive exposure to antimicrobial agents intended to kill or inhibit them.
278
SBA: What is the main goal of antimicrobial stewardship (AMS)?
Answer: To promote judicious use of antimicrobials to preserve their future effectiveness.
279
SBA: What does the ‘Start Smart then Focus’ approach advocate for in AMS?
Answer: Starting empirical broad-spectrum therapy only if needed, then streamlining to narrow-spectrum agents based on culture results.
280
SBA: What does the AWaRe classification tool developed by WHO categorize antibiotics into?
nswer: Access, Watch, and Reserve categories.
281
SBA: What is the leading factor contributing to AMR globally?
Answer: Overprescribing of antibiotics for viral or self-limiting infections.
282
SBA: Which pathogen is a common cause of healthcare-associated infections and is often resistant to multiple antibiotics?
Answer: Methicillin-resistant Staphylococcus aureus (MRSA).
283
SBA: What is the purpose of de-labeling penicillin allergies in patients?
Answer: To avoid unnecessary broad-spectrum antibiotic use and reduce AMR risk.
284
SBA: What is a key benefit of switching from IV to oral antibiotics when clinically appropriate?
Answer: Reduces the risk of line-related infections and improves patient comfort.
285
SBA: What are the two major sources of AMR according to the AMS lecture?
Answer: Overuse in human medicine and use in domestic animals.
286
SBA: What is a critical strategy to combat AMR in the general public?
Answer: Public awareness campaigns emphasizing appropriate antibiotic use.
287
EMQ: Match the AMS principle to its description.
Start Smart then Focus: Start empirical treatment only if necessary and de-escalate based on culture results.
Selective Reporting: Provide susceptibility results for antibiotics consistent with guidelines.
IV to Oral Switch: Transition to oral antibiotics when clinically appropriate.
288
EMQ: Match the AWaRe category to its characteristics.
Access: First-line treatment options for most infections.
Watch: Higher resistance potential and reserved for specific infections.
Reserve: Last-resort antibiotics for multidrug-resistant pathogens.
289
EMQ: Match the pathogen to the consequence of AMR.
MRSA: Increased hospital stays and treatment costs.
E. coli: Urinary tract infections resistant to first-line antibiotics.
Pseudomonas aeruginosa: Complicated respiratory infections in immunocompromised patients.
290
EMQ: Match the AMS action to its goal.
De-labeling penicillin allergies: Reduce unnecessary use of broad-spectrum antibiotics.
Monitoring prescribing data: Assess compliance with guidelines and AMR trends.
Empirical therapy review: Narrow-spectrum therapy selection based on culture results.
291
EMQ: Match the cause to the inappropriate use of antibiotics.
Overprescription: Physicians prescribing antibiotics for viral infections.
Patient pressure: Expectations for antibiotics despite no bacterial infection.
Time constraints: Quick prescribing decisions without diagnostic confirmation.
292
Define AMR and explain why it is a global health threat.
Answer: AMR is the ability of microorganisms to resist antimicrobials. It threatens effective infection treatment and could result in 10 million deaths per year by 2050. (2 marks)
293
What are the key principles of the 'Start Smart then Focus' approach?
Answer:
Start empirical treatment only if indicated.
Base treatment on clinical signs, severity, and culture results.
De-escalate to narrow-spectrum antibiotics when possible. (3 marks)
294
Describe the AWaRe classification of antibiotics and its purpose
Answer:
Access: First-line antibiotics for common infections.
Watch: For infections needing second-line agents.
Reserve: Last-resort antibiotics for resistant infections.
Helps monitor antibiotic use and resistance trends. (2 marks)
295
Why is IV to oral switching an essential part of AMS?
Answer:
Reduces line-related infections and nursing workload.
Improves patient satisfaction and reduces costs.
Facilitates earlier hospital discharge. (2 marks)
296
What public health strategies can help combat AMR?
Answer:
Public awareness campaigns (e.g., "Keep Antibiotics Working").
Education on appropriate antibiotic use.
Encouraging vaccination to reduce infection prevalence. (1 mark)
297
SBA: What is the primary target of beta-lactam antibiotics?
Answer: Bacterial transpeptidases (penicillin-binding proteins).
298
SBA: What is the main difference between Gram-positive and Gram-negative bacteria cell walls?
Answer: Gram-positive bacteria have a thick peptidoglycan layer, while Gram-negative bacteria have a thin peptidoglycan layer with an outer membrane.
299
SBA: What is the mechanism of resistance to beta-lactam antibiotics in some bacteria?
Answer: Production of beta-lactamases that cleave the beta-lactam ring.
300
SBA: Which test measures bacterial susceptibility to antibiotics using diffusion on an agar plate?
Answer: Disk diffusion test (Kirby-Bauer method).
301
SBA: What is the purpose of the E-test in microbiology?
Answer: To determine the minimum inhibitory concentration (MIC) of an antibiotic.
302
SBA: What type of antibiotic effect relies on the immune system to clear bacteria?
Answer: Bacteriostatic.
303
SBA: What is the MBC/MIC ratio for a bactericidal antibiotic?
Answer: Less than 4.
304
SBA: What class of antibiotics is typically used for intracellular pathogens like Mycoplasma pneumoniae?
Answer: Macrolides.
305
SBA: Which antibiotic class disrupts DNA replication by targeting DNA gyrase?
Answer: Fluoroquinolones.
306
SBA: What does selective toxicity mean in the context of antimicrobial therapy?
Answer: Targeting microbial processes or structures that differ from those in the host.
307
EMQ: Match the bacterial classification to its features.
Gram-positive: Thick peptidoglycan layer, teichoic acids.
Gram-negative: Thin peptidoglycan layer, outer membrane with lipopolysaccharides.
308
EMQ: Match the antibiotic to its mechanism of action.
Beta-lactams: Inhibit cell wall synthesis by blocking transpeptidation.
Tetracyclines: Inhibit protein synthesis at the 30S ribosomal subunit.
Aminoglycosides: Cause misreading of mRNA by binding to 30S ribosomes.
309
EMQ: Match the bacterial growth requirement to its oxygen preference.
Obligate aerobes: Require oxygen (e.g., Pseudomonas aeruginosa).
Obligate anaerobes: Harmed by oxygen (e.g., Clostridium spp.).
Facultative anaerobes: Can grow with or without oxygen (e.g., Escherichia coli)
310
EMQ: Match the bacterial test to its result type.
Disk diffusion: Zone of inhibition.
E-test: MIC as an intersection of inhibition zone with the strip gradient.
Dilution test: MIC and MBC determined from bacterial growth in liquid media.
311
EMQ: Match the resistance mechanism to its description.
Beta-lactamase production: Inactivates beta-lactam antibiotics.
Efflux pumps: Actively remove antibiotics from bacterial cells.
Target modification: Mutations in penicillin-binding proteins reduce drug binding.
312
Describe the difference between bacteriostatic and bactericidal antibiotics.
Answer: Bacteriostatic antibiotics inhibit growth and rely on the immune system, while bactericidal antibiotics kill bacteria directly. (2 marks)
313
What are the key structural differences between Gram-positive and Gram-negative bacteria?
Answer: Gram-positive bacteria have a thick peptidoglycan layer; Gram-negative bacteria have a thin layer and an outer membrane with LPS and porins. (2 marks)
314
List two common mechanisms of antibiotic resistance.
Answer: Beta-lactamase production and efflux pumps. (2 marks)
315
Explain how the disk diffusion test measures antibiotic susceptibility.
Answer: Antibiotic-impregnated disks are placed on an agar plate with bacteria, and the diameter of the inhibition zone is measured to determine susceptibility. (2 marks)
316
What is the significance of the therapeutic index in antimicrobial therapy?
Answer: It is the ratio of the toxic dose to the therapeutic dose, indicating the safety margin of the antibiotic. (2 marks)
317
SBA: What is the mechanism of action of beta-lactam antibiotics?
Answer: Inhibit bacterial cell wall synthesis by binding to transpeptidases and preventing peptidoglycan cross-linking.
318
SBA: Which penicillin is effective against Pseudomonas aeruginosa when combined with a beta-lactamase inhibitor?
Answer: Piperacillin-tazobactam.
319
SBA: What is the primary adverse effect of vancomycin when infused too rapidly?
Answer: Red man syndrome (histamine-mediated flushing and rash).
320
SBA: What structural feature allows aminopenicillins like amoxicillin to target Gram-negative bacteria?
Answer: Hydrophilicity enables passage through porins in the outer membrane of Gram-negative bacteria.
321
SBA: What is the key adverse effect associated with aminoglycosides?
Answer: Nephrotoxicity and ototoxicity.
322
SBA: What is the primary mechanism of action of macrolides?
Answer: Inhibit protein synthesis by binding to the 50S ribosomal subunit, preventing translocation.
323
SBA: Which antibiotic class is most associated with photosensitivity as a side effect?
Answer: Tetracyclines.
324
SBA: What distinguishes carbapenems from other beta-lactam antibiotics?
Answer: Their broad-spectrum activity, including effectiveness against many beta-lactamase-producing bacteria.
325
SBA: Which antibiotic is contraindicated in children under 8 years due to its effect on teeth and bone growth?
Answer: Tetracycline.
326
SBA: What is the recommended route of administration for vancomycin in systemic infections?
Answer: Intravenous (IV).
327
EMQ: Match the beta-lactam subclass to its primary use.
Natural penicillins: Streptococcus spp. infections.
Antistaphylococcal penicillins: Methicillin-sensitive Staphylococcus aureus (MSSA).
Antipseudomonal penicillins: Pseudomonas aeruginosa infections.
328
EMQ: Match the mechanism of action to the antibiotic class
Beta-lactams: Inhibit cell wall synthesis.
Aminoglycosides: Cause mRNA misreading by binding to 30S ribosomal subunit.
Tetracyclines: Block tRNA attachment at the ribosomal A site.
329
EMQ: Match the antibiotic to its adverse effect.
Tetracyclines: Photosensitivity.
Aminoglycosides: Nephrotoxicity and ototoxicity.
Chloramphenicol: Aplastic anemia.
330
EMQ: Match the generation of cephalosporins to their activity.
First-generation: Primarily Gram-positive bacteria.
Third-generation: Enhanced Gram-negative coverage.
Fifth-generation: Effective against MRSA.
331
EMQ: Match the antibiotic to its clinical use
ancomycin: Severe Gram-positive infections, including MRSA.
Clindamycin: Anaerobic infections and bone/joint infections.
Amoxicillin: Mild-to-moderate respiratory tract infections.
332
Describe the mechanism of action of beta-lactam antibiotics.
Answer: Inhibit transpeptidases, preventing peptidoglycan cross-linking in bacterial cell walls, leading to cell lysis. (2 marks)
333
Outline the spectrum and clinical use of antipseudomonal penicillins
Answer: Broad-spectrum against Gram-negative bacteria, including Pseudomonas aeruginosa; used in sepsis, hospital-acquired pneumonia, and severe UTIs. (2 marks)
334
List the adverse effects of aminoglycosides and explain the importance of monitoring.
Answer: Nephrotoxicity, ototoxicity, and neuromuscular blockade; therapeutic drug monitoring prevents toxicity due to the narrow therapeutic index. (2 marks)
335
Compare the mechanisms of action of macrolides and tetracyclines.
Answer:
Macrolides: Bind to the 50S ribosomal subunit, inhibiting translocation.
Tetracyclines: Bind to the 30S ribosomal subunit, blocking tRNA attachment. (2 marks)
336
What is the clinical importance of beta-lactamase inhibitors like clavulanic acid?
Answer: Protect beta-lactam antibiotics from enzymatic degradation, extending their spectrum of activity against beta-lactamase-producing bacteria. (2 marks)
337
SBA: What is the mechanism of action of fluoroquinolones?
Answer: Inhibit bacterial DNA replication by targeting DNA gyrase and topoisomerase IV.
338
SBA: Which two enzymes are primarily targeted by fluoroquinolones in bacterial DNA replication?
Answer: DNA gyrase and topoisomerase IV.
339
SBA: What is the primary clinical use of co-trimoxazole?
Answer: Treatment of urinary tract infections and Pneumocystis jirovecii pneumonia in immunocompromised patients.
340
SBA: Which side effect is most commonly associated with sulfonamides?
Answer: Hypersensitivity reactions, such as rash.
341
SBA: What is the key structural feature of rifampicin that allows it to inhibit RNA polymerase?
Answer: Its ability to bind to the beta subunit of bacterial RNA polymerase.
342
SBA: Which group of bacteria are nitroimidazoles primarily effective against?
Answer: Anaerobic bacteria.
343
SBA: What is the major adverse effect of fluoroquinolones related to the musculoskeletal system?
Answer: Tendonitis and tendon rupture.
344
SBA: Which antibiotic combination is referred to as "RIPE" for tuberculosis treatment?
Answer: Rifampicin, Isoniazid, Pyrazinamide, and Ethambutol.
345
SBA: Why is rifampicin-associated discoloration of body fluids harmless?
Answer: It is due to the drug's excretion and has no toxic implications.
346
SBA: What is the primary mechanism of resistance to rifampicin in Mycobacterium tuberculosis?
Answer: Mutation in the rpoB gene encoding RNA polymerase.
347
MQ: Match the antibiotic to its mechanism of action.
Fluoroquinolones: Inhibit DNA gyrase and topoisomerase IV.
Rifampicin: Inhibit bacterial RNA polymerase.
Sulfonamides: Compete with PABA to inhibit dihydropteroate synthase.
348
EMQ: Match the clinical use to the antibiotic.
Co-trimoxazole: Pneumocystis jirovecii pneumonia in immunocompromised patients.
Fluoroquinolones: Complicated urinary tract infections.
Rifampicin: Tuberculosis treatment.
349
EMQ: Match the tuberculosis drug to its target.
Isoniazid: Inhibits mycolic acid synthesis.
Rifampicin: Inhibits RNA polymerase.
Pyrazinamide: Interferes with fatty acid synthesis.
350
EMQ: Match the antibiotic to its major side effect.
Fluoroquinolones: Tendon rupture.
Nitroimidazoles: Disulfiram-like reaction with alcohol.
Rifampicin: Orange discoloration of body fluids.
351
EMQ: Match the resistance mechanism to the antibiotic.
Rifampicin: rpoB gene mutation.
Sulfonamides: Overproduction of PABA.
Fluoroquinolones: Mutation in DNA gyrase or topoisomerase IV.
352
What are the primary targets of fluoroquinolones in bacteria?
Answer: DNA gyrase in Gram-negative bacteria and topoisomerase IV in Gram-positive bacteria. (2 marks)
353
List two common clinical uses of fluoroquinolones.
Answer: Complicated urinary tract infections and respiratory tract infections. (2 marks)
354
What is the mechanism of action of rifampicin, and why is it effective in tuberculosis?
Answer: Binds to the beta subunit of bacterial RNA polymerase, preventing transcription; effective because it penetrates the mycobacterial cell wall. (2 marks)
355
Explain the mechanism of resistance to sulfonamides.
Answer: Overproduction of PABA, mutations in dihydropteroate synthase, or decreased drug uptake. (2 marks)
356
Why is combination therapy essential in tuberculosis treatment?
Answer: Prevents the development of drug resistance and targets bacteria at different stages of replication. (2 marks)
357
SBA: What is antimicrobial resistance (AMR)?
Answer: The ability of microorganisms to survive exposure to antimicrobial agents that were previously effective.
358
SBA: What is the primary mechanism of resistance to beta-lactam antibiotics in bacteria?
Answer: Production of beta-lactamases, which hydrolyze the beta-lactam ring.
359
SBA: How is rifampicin resistance in Mycobacterium tuberculosis commonly acquired?
Answer: Mutation in the rpoB gene encoding RNA polymerase.
360
SBA: Which resistance mechanism involves the active removal of antibiotics from bacterial cells?
Answer: Efflux pumps.
361
SBA: What is the main feature of multidrug-resistant (MDR) bacteria?
Answer: Resistance to multiple classes of antibiotics.
362
SBA: What is the mechanism of resistance in vancomycin-resistant Enterococcus (VRE)?
Answer: Alteration of the terminal amino acids in peptidoglycan precursors (D-Ala-D-Lac).
363
SBA: What test measures the minimum inhibitory concentration (MIC) of an antibiotic?
Answer: Dilution susceptibility test or E-test.
364
SBA: Which method of horizontal gene transfer involves plasmid exchange via direct cell-to-cell contact?
Answer: Conjugation.
365
SBA: What is the role of extended-spectrum beta-lactamases (ESBLs)?
Answer: Hydrolyze a wide range of beta-lactam antibiotics, including cephalosporins.
366
SBA: What is the role of biofilms in antibiotic tolerance?
Answer: Biofilms act as a physical barrier, reducing antibiotic penetration and housing dormant, slow-dividing bacteria.
367
EMQ: Match the resistance mechanism to the description.
Efflux pumps: Active removal of antibiotics from bacterial cells.
Drug target modification: Mutations that reduce drug binding to its target.
Enzymatic degradation: Beta-lactamase production to hydrolyze antibiotics.
368
EMQ: Match the resistance mechanism to the pathogen example.
MRSA: Acquisition of mecA gene encoding modified transpeptidase.
VRE: Altered D-Ala-D-Lac target in peptidoglycan precursors.
Pseudomonas aeruginosa: Efflux pump-mediated resistance.
369
EMQ: Match the gene transfer method to the description.
onjugation: Plasmid exchange via direct cell-to-cell contact using sex pili.
Transduction: DNA transfer mediated by bacteriophages.
Transformation: Uptake of free DNA from the environment.
370
EMQ: Match the test to its resistance evaluation.
Disk diffusion: Qualitative measurement of susceptibility or resistance.
E-test: Quantitative MIC determination using a strip gradient.
Dilution test: Quantitative MIC and MBC determination in liquid media.
371
EMQ: Match the resistance term to its definition.
Intrinsic resistance: Natural resistance due to inherent bacterial properties.
Acquired resistance: Resistance gained via mutations or horizontal gene transfer.
Tolerance: Ability to survive antibiotics without genetic resistance.
372
Define AMR and explain its significance in healthcare.
Answer: AMR is the ability of microorganisms to resist antimicrobials. It leads to treatment failure, increased mortality, and healthcare costs. (2 marks)
373
What are the four main mechanisms of drug resistance in bacteria?
Answer:
Alteration of drug target sites (e.g., mecA gene in MRSA).
Drug inactivation (e.g., beta-lactamases).
Reduced drug uptake (e.g., porin loss in Gram-negative bacteria).
Efflux pumps. (3 marks)
374
Explain the difference between intrinsic and acquired resistance.
Answer:
Intrinsic: Natural resistance inherent to a bacterial species.
Acquired: Resistance gained through mutations or horizontal gene transfer. (2 marks)
375
How does horizontal gene transfer contribute to AMR?
Answer: Bacteria acquire resistance genes via conjugation, transformation, or transduction, spreading resistance within and between species. (2 marks)
376
What is the impact of biofilms on antibiotic resistance?
Answer: Biofilms reduce antibiotic penetration, harbor dormant bacteria, and enhance tolerance, making infections more persistent. (1 mark)
377
SBA: What is the primary mechanism of action of sulfonamides?
Answer: Competitive inhibition of dihydropteroate synthetase, blocking folic acid synthesis.
378
SBA: What type of inhibition is exhibited by penicillin on transpeptidase enzymes?
Answer: Irreversible inhibition (suicide substrate).
379
SBA: What distinguishes Gram-negative bacteria from Gram-positive bacteria in terms of cell wall structure?
Answer: Gram-negative bacteria have a thin peptidoglycan layer and an outer membrane containing lipopolysaccharides.
380
SBA: Which structural feature is essential for the activity of beta-lactam antibiotics?
Answer: The strained beta-lactam ring.
381
SBA: What is the mechanism of action of fluoroquinolones?
Answer: Inhibition of bacterial DNA gyrase and topoisomerase IV.
382
SBA: Which antibiotic is most commonly associated with a disulfiram-like reaction when alcohol is consumed?
Answer: Metronidazole.
383
SBA: Which antibiotic class is typically used for treating MRSA infections?
Answer: Glycopeptides, such as vancomycin.
384
SBA: Why is clavulanic acid combined with beta-lactam antibiotics?
Answer: To inhibit beta-lactamases and extend the antibiotic’s spectrum.
385
SBA: What structural feature allows aminopenicillins like amoxicillin to act against Gram-negative bacteria?
Answer: The presence of a hydrophilic amino group.
386
SBA: What is the main adverse effect associated with tetracycline use in children?
Answer: Permanent discoloration of teeth.
387
EMQ: Match the drug to its mechanism of action.
Sulfonamides: Inhibit dihydropteroate synthetase.
Fluoroquinolones: Inhibit DNA gyrase and topoisomerase IV.
Beta-lactams: Inhibit transpeptidase, preventing cell wall cross-linking.
388
EMQ: Match the bacterial property to its antibiotic target.
Peptidoglycan layer: Beta-lactams.
DNA replication: Fluoroquinolones.
Ribosomes: Tetracyclines.
389
EMQ: Match the antibiotic resistance mechanism to its description.
Beta-lactamase production: Hydrolyzes beta-lactam antibiotics.
Efflux pumps: Actively remove antibiotics from bacterial cells.
Alteration of target site: Mutations reduce drug binding.
390
EMQ: Match the antibiotic to its spectrum of activity.
Amoxicillin: Broad-spectrum against Gram-positive and Gram-negative bacteria.
Metronidazole: Effective against anaerobic bacteria and protozoa.
Ciprofloxacin: Primarily active against Gram-negative bacteria.
391
EMQ: Match the antibiotic to its major side effect.
Fluoroquinolones: Tendonitis and tendon rupture.
Tetracyclines: Photosensitivity.
Metronidazole: Disulfiram-like reaction with alcohol.
392
List the five main mechanisms by which antibiotics target bacterial infections.
Inhibition of bacterial metabolism (e.g., sulfonamides).
Inhibition of cell wall synthesis (e.g., beta-lactams).
Disruption of protein synthesis (e.g., tetracyclines).
Inhibition of nucleic acid synthesis (e.g., fluoroquinolones).
Alteration of cell membrane permeability (e.g., polymyxins).
393
What is the mechanism of action of beta-lactam antibiotics, and why are they bactericidal?
Answer: Inhibit transpeptidase, preventing peptidoglycan cross-linking. This weakens the cell wall, causing bacterial lysis and death.
394
Describe the role of clavulanic acid in combination therapy.
Answer: Clavulanic acid inhibits beta-lactamases, protecting beta-lactam antibiotics from enzymatic degradation and extending their spectrum of activity. (2 marks)
395
What are the clinical applications of sulfonamides and trimethoprim, and why are they often used together?
Answer: Sulfonamides treat urinary tract infections, and trimethoprim is used for respiratory infections. Together, they inhibit sequential steps in folic acid synthesis, increasing efficacy (e.g., co-trimoxazole). (2 marks)
396
Explain how bacterial resistance mechanisms can undermine antibiotic efficacy.
Answer:
Beta-lactamase production hydrolyzes beta-lactams.
Efflux pumps remove antibiotics from cells.
Mutations in drug targets reduce antibiotic binding. (2 marks)
397
SBA: What is the primary mechanism of action of nucleoside reverse transcriptase inhibitors (NRTIs)?
Answer: Mimic natural nucleotides, get incorporated into viral DNA, and cause chain termination.
398
SBA: What is the target of oseltamivir in influenza treatment?
Answer: Neuraminidase enzyme, preventing viral release.
399
SBA: Which antiviral drug is effective against herpes simplex virus by inhibiting DNA polymerase?
Answer: Acyclovir.
400
SBA: What is the main advantage of host-targeting antivirals?
Answer: Reduced risk of viral resistance.
401
SBA: Which HIV drug targets the CCR5 receptor to prevent viral entry?
Answer: Maraviroc.
402
SBA: What is the role of protease inhibitors in antiviral therapy?
Answer: Prevent cleavage of viral polyproteins into functional proteins.
403
SBA: Which step of the viral life cycle is inhibited by enfuvirtide?
Answer: Fusion of the viral envelope with the host cell membrane.
404
SBA: What is the suffix common to integrase inhibitors used in HIV treatment?
Answer: -tegravir.
405
SBA: What is the main limitation of nucleoside analogues like acyclovir?
Answer: Requires activation by viral kinases.
406
SBA: Which hepatitis C antiviral is a nucleotide analog that inhibits RNA polymerase?
Answer: Sofosbuvir.
407
EMQ: Match the antiviral drug to its mechanism of action.
Acyclovir: Inhibits viral DNA polymerase.
Oseltamivir: Blocks neuraminidase activity.
Enfuvirtide: Inhibits fusion between the viral envelope and the host cell.
408
EMQ: Match the virus to the corresponding drug class.
HIV: Integrase inhibitors.
Influenza: Neuraminidase inhibitors.
Herpes simplex virus: Nucleoside analogs.
409
EMQ: Match the antiviral mechanism to the viral life cycle stage.
Fusion inhibitors: Viral penetration.
NRTIs: Genome replication.
Protease inhibitors: Protein maturation.
410
EMQ: Match the drug to its viral target.
Maraviroc: CCR5 receptor.
Zanamivir: Neuraminidase.
Raltegravir: Integrase enzyme.
411
EMQ: Match the limitation to the antiviral drug.
Acyclovir: Requires viral kinase activation.
Ribavirin: Broad-spectrum toxicity.
Oseltamivir: Effectiveness limited to early treatment.
412
ist the six key stages of the viral replication cycle targeted by antivirals.
Answer:
Attachment (e.g., maraviroc).
Penetration (e.g., enfuvirtide).
Uncoating (e.g., amantadine).
Genome replication (e.g., sofosbuvir).
Protein synthesis and maturation (e.g., protease inhibitors like atazanavir).
Viral release (e.g., oseltamivir). (2 marks)
413
Explain the mechanism of action of nucleoside analogs and give one example.
Answer: Mimic natural nucleotides, get incorporated into viral DNA/RNA, and terminate the chain. Example: Acyclovir. (2 marks)
414
Describe how neuraminidase inhibitors work and provide a clinical use.
Answer: Block neuraminidase to prevent release of viral progeny. Used in influenza treatment.
415
What are the advantages of host-targeting antivirals?
Answer: Reduced risk of resistance and potential broad-spectrum activity. (2 marks)
416
Identify one limitation for each antiviral mechanism.
Answer:
Attachment inhibitors: May not work for all viral strains.
Nucleoside analogs: Require activation and may have resistance.
Neuraminidase inhibitors: Limited efficacy if treatment is delayed. (2 marks)
417
SBA: What is the primary goal of microbial identification in clinical diagnostics?
Answer: Rapidly and accurately identify pathogens responsible for infection or confirm their absence.
418
SBA: Which staining technique is used to differentiate Mycobacterium tuberculosis?
Answer: Acid-fast (Ziehl-Neelsen) staining.
419
SBA: What is the purpose of selective media in microbial culture?
Answer: Suppress unwanted microbes and encourage the growth of desired microbes.
420
SBA: Which method is used to amplify a specific fragment of microbial DNA?
Answer: Polymerase Chain Reaction (PCR).
421
SBA: What is a key requirement for primers in PCR?
nswer: They must be complementary to the 3’ ends of the DNA target strand.
422
SBA: What diagnostic system uses antigen-antibody specificity to identify pathogens?
Answer: Immunoassays (e.g., ELISA).
423
SBA: Why is a positive control used in PCR?
Answer: To confirm that the reagents and PCR conditions work as expected.
424
SBA: Which diagnostic technique allows quantitative detection of microbial DNA in real-time?
Answer: Real-Time PCR.
425
SBA: What feature makes Taq polymerase suitable for PCR?
Answer: Its resistance to high temperatures (up to 100°C).
426
SBA: Which medium is commonly used to differentiate lactose-fermenting bacteria?
Answer: MacConkey agar.
427
EMQ: Match the staining technique to its diagnostic use.
Gram staining: Distinguish Gram-positive from Gram-negative bacteria.
Acid-fast staining: Identify Mycobacterium tuberculosis.
Fluorescence staining: Detect mycolic acids in TB.
428
EMQ: Match the diagnostic method to its purpose.
PCR: Amplify specific DNA fragments.
Immunoassay: Detect antigens or antibodies.
Culture: Obtain pure colonies for biochemical profiling.
429
EMQ: Match the culture medium to its application.
Blood agar: Differentiate hemolytic bacteria.
Sabouraud's agar: Isolate fungi.
MacConkey agar: Differentiate Gram-negative lactose fermenters.
430
EMQ: Match the PCR cycle step to its function.
Denaturation: Separate DNA strands.
Annealing: Primers bind to target DNA sequences.
Extension: DNA polymerase synthesizes new strands.
431
EMQ: Match the feature of a good diagnostic system to its description.
Sensitivity: Correctly identify true positives.
Specificity: Correctly identify true negatives.
Simplicity: Allow efficient use in routine testing.
432
What are the primary objectives of microbial diagnostics?
Answer: Identify pathogens, determine susceptibility to antibiotics, confirm absence of infection, and exclude other diagnoses. (2 marks)
433
Explain the steps in PCR and their significance.
Answer:
Denaturation: DNA strands are separated by heating.
Annealing: Primers bind to target sequences.
Extension: DNA polymerase synthesizes complementary strands. (3 marks)
434
List three features of a good diagnostic test and explain their importance.
Answer:
Sensitivity: Detect all true positives, reducing false negatives.
Specificity: Minimize false positives.
Simplicity: Ensure routine applicability and efficiency. (2 marks)
435
What is the purpose of selective and differential media in microbial culture?
Answer:
Selective media: Suppress unwanted microbes and promote target growth (e.g., Sabouraud's agar for fungi).
Differential media: Distinguish microbes based on their metabolic properties (e.g., MacConkey agar for lactose fermenters). (2 marks)
436
What role do immunoassays play in diagnostics, and how do they differ from molecular techniques like PCR?
Answer: Immunoassays detect antigens or antibodies, whereas PCR amplifies specific nucleic acid sequences. Both are used for rapid pathogen detection but have different sensitivities and applications. (1 mark)
437
SBA: What is the main goal of highly active antiretroviral therapy (HAART) for HIV?
Answer: Suppress viral replication and maintain immune system function.
438
SBA: What is the mechanism of action of integrase inhibitors in HIV therapy?
Answer: Prevent the integration of viral DNA into the host genome.
439
SBA: Why does monotherapy in HIV treatment lead to drug resistance?
Answer: High mutation rate of HIV combined with selective pressure from a single drug.
440
SBA: What is the common backbone of first-line HAART regimens?
Answer: Two nucleoside reverse transcriptase inhibitors (NRTIs) combined with a protease inhibitor or integrase inhibitor.
441
SBA: What is the mechanism of action of ribavirin in antiviral therapy?
Answer: Inhibits viral RNA synthesis by acting as a guanosine analog.
442
SBA: Which antiviral drug is commonly used for HCV treatment and targets NS5B polymerase?
Answer: Sofosbuvir.
443
SBA: What is a significant limitation of direct-acting antivirals (DAAs) for HCV treatment?
Answer: High cost and limited global access.
444
SBA: What does the term "pan-genotypic" refer to in the context of HCV therapy?
Answer: Antiviral activity against all HCV genotypes.
445
SBA: What is the main barrier to curing HIV despite effective HAART?
Answer: Persistent viral reservoirs in the host genome.
446
SBA: How is the effectiveness of HCV treatment commonly assessed?
Answer: By achieving a sustained virological response (SVR) after therapy.
447
EMQ: Match the drug to its mechanism of action.
Maraviroc: Blocks CCR5 receptor to inhibit HIV entry.
Sofosbuvir: Inhibits HCV NS5B polymerase.
Raltegravir: Prevents integration of HIV DNA into the host genome.
448
EMQ: Match the therapy to its advantage.
HAART: Reduces risk of resistance by targeting multiple stages of HIV replication.
DAA therapy for HCV: Short treatment duration with >95% cure rates.
Combination HIV therapy: Minimizes viral replication and delays progression to AIDS.
449
EMQ: Match the resistance mechanism to the virus.
HIV: High mutation rate during reverse transcription.
HCV: Rapid replication with no proofreading activity in RNA polymerase.
Influenza: Point mutations in neuraminidase and hemagglutinin.
450
EMQ: Match the therapeutic goal to its rationale.
Suppress viral replication: Reduce viral load to undetectable levels.
Prevent drug resistance: Use combination therapy to target multiple pathways.
Enhance patient adherence: Simplify regimens with fixed-dose combinations.
451
EMQ: Match the HCV drug class to its target.
NS5B polymerase inhibitors: Block RNA replication.
NS5A inhibitors: Disrupt viral assembly.
Protease inhibitors: Prevent cleavage of HCV polyproteins.
452
Describe the primary goals of HAART in HIV treatment.
Answer: Suppress viral replication, maintain CD4+ T-cell counts, prevent opportunistic infections, and improve survival. (2 marks)
453
Explain why combination therapy is preferred over monotherapy in HIV and HCV treatments.
Answer: Prevents drug resistance by targeting multiple viral pathways and reduces viral replication more effectively. (2 marks)
454
What are the advantages of direct-acting antivirals (DAAs) in HCV treatment?
Answer: High cure rates (>95%), short duration (8-12 weeks), oral administration, and pan-genotypic activity. (2 marks)
455
List two key challenges in global access to HCV therapy.
Answer: High cost of DAAs and limited healthcare infrastructure for diagnosis and treatment. (2 marks)
456
Why can’t HAART cure HIV infection completely?
Answer: Latent viral reservoirs in immune cells allow HIV to persist and reignite replication if therapy is stopped. (2 marks)
457
SBA: What is the primary definition of sepsis?
Answer: A life-threatening organ dysfunction caused by a dysregulated host response to infection.
458
SBA: What is the most common bacterial cause of meningitis in young children?
Answer: Neisseria meningitidis (meningococcus).
459
SBA: Which key diagnostic test is used to confirm bacterial meningitis?
Answer: Lumbar puncture with cerebrospinal fluid (CSF) analysis.
460
SBA: Which antibiotic is used empirically for suspected bacterial meningitis in adults without penicillin allergy?
Answer: Ceftriaxone.
461
SBA: What is the primary purpose of the "Sepsis Six" protocol?
Answer: To initiate critical treatments within the first hour of sepsis diagnosis.
462
SBA: What clinical sign strongly suggests meningitis in children?
Answer: Non-blanching rash.
463
SBA: What is the mechanism of action of gentamicin in sepsis treatment?
Answer: Inhibition of bacterial protein synthesis by binding to the 30S ribosomal subunit.
464
SBA: Why is therapeutic drug monitoring essential for vancomycin use?
Answer: To avoid nephrotoxicity and ensure therapeutic levels.
465
SBA: What is the hallmark complication of meningitis leading to permanent deficits?
Answer: Neurological complications, such as hearing loss.
466
SBA: In the context of sepsis, what is a red flag symptom that necessitates urgent care?
Answer: Systolic blood pressure <90 mmHg.
467
EMQ: Match the diagnostic test to its purpose in sepsis or meningitis.
Blood cultures: Identify causative pathogen.
Lumbar puncture: Confirm bacterial meningitis.
CT scan: Rule out other conditions like stroke or subarachnoid hemorrhage.
468
EMQ: Match the antibiotic to its clinical use in sepsis or meningitis.
Ceftriaxone: Empirical treatment for meningitis.
Gentamicin: Covers Gram-negative bacilli in sepsis.
Metronidazole: Anaerobic coverage in abdominal sepsis.
469
EMQ: Match the step of the Sepsis Six to its rationale.
High-flow oxygen: Address hypoxia.
IV fluids: Prevent circulatory collapse.
Measure lactate: Monitor for tissue hypoperfusion.
470
EMQ: Match the symptom to its associated condition.
Non-blanching rash: Meningitis.
Mottled skin: Sepsis.
Photophobia: Meningitis.
471
EMQ: Match the complication to its condition.
Hearing loss: Bacterial meningitis.
Disseminated intravascular coagulation (DIC): Sepsis.
Skin scarring: Meningitis with septicaemia.
472
What is the "Sepsis Six" protocol, and why is it critical in sepsis management?
Answer: High-flow oxygen, IV antibiotics, IV fluids, blood cultures, measure lactate, monitor urine output. It ensures early intervention and reduces mortality. (2 marks)
473
List three red flag symptoms of sepsis that require urgent action.
Answer:
Systolic BP <90 mmHg.
Respiratory rate >25 breaths/min.
Mottled or ashen skin. (2 marks)
474
Explain the empirical antibiotic regimen for suspected bacterial meningitis in a patient aged <60 years.
Answer: Ceftriaxone 2 g IV once daily. If penicillin allergic, chloramphenicol 25 mg/kg every 6 hours. (2 marks)
475
What diagnostic tests are performed to confirm sepsis or meningitis, and what do they detect?
Answer:
Blood cultures: Identify pathogen.
Lumbar puncture: Detect bacteria in CSF.
Lactate levels: Indicate tissue hypoperfusion. (2 marks)
476
What are the major complications of meningitis, and how can they be mitigated?
Answer:
Hearing loss, cognitive impairment, amputations.
Mitigation: Early diagnosis and appropriate antibiotics. (2 marks)
477
SBA: What is the mechanism of action of chloroquine in malaria treatment?
Answer: Inhibits heme detoxification in Plasmodium food vacuoles, leading to toxic heme accumulation.
478
SBA: What is the main structural feature of quinoline antimalarials that allows their action?
Answer: Aromatic quinoline scaffold enabling interaction with heme.
479
SBA: Which enzyme is inhibited by proguanil after conversion to its active form, cycloguanil?
Answer: Dihydrofolate reductase (DHFR).
480
SBA: What is the primary target of atovaquone in Plasmodium?
Answer: Mitochondrial ubiquinone reductase, disrupting the electron transport chain.
481
SBA: Which Plasmodium species is responsible for the most severe cases of malaria?
Answer: Plasmodium falciparum.
482
SBA: What is the role of the sulfonamide-pyrimethamine combination in malaria treatment?
Answer: Inhibits sequential steps in folic acid synthesis.
483
SBA: What is the mechanism of action of azole antifungal agents?
Answer: Inhibit 14α-demethylase, disrupting ergosterol biosynthesis.
484
SBA: Which antifungal agent forms pores in fungal cell membranes by binding to ergosterol?
Answer: Amphotericin B.
485
SBA: What is the mechanism of action of echinocandins?
Answer: Inhibit β-1,3-glucan synthase, weakening the fungal cell wall.
486
SBA: What is the mechanism of griseofulvin in treating fungal infections?
Answer: Binds to tubulin, disrupting microtubules and inhibiting mitosis.
487
EMQ: Match the antimalarial drug to its mechanism of action.
Chloroquine: Inhibits heme detoxification.
Proguanil: Inhibits dihydrofolate reductase.
Atovaquone: Disrupts mitochondrial electron transport.
488
EMQ: Match the antifungal drug to its target.
Amphotericin B: Binds to ergosterol, forming membrane pores.
Azoles: Inhibit 14α-demethylase.
Echinocandins: Inhibit β-1,3-glucan synthase.
489
EMQ: Match the antimalarial drug to its clinical use.
Chloroquine: First-line treatment for uncomplicated malaria.
Atovaquone-proguanil: Malaria prophylaxis and treatment.
Artemisinin: Severe malaria and artemisinin-resistant strains.
490
EMQ: Match the drug class to its example.
Quinoline: Chloroquine.
Biguanide: Proguanil.
Naphthoquinone: Atovaquone.
491
EMQ: Match the mechanism to the fungal drug.
DNA synthesis inhibition: Flucytosine.
Membrane disruption: Amphotericin B.
Microtubule disruption: Griseofulvin.
492
Describe the life cycle stages of Plasmodium targeted by antimalarial drugs.
Answer:
Erythrocytic stage: Chloroquine, quinine.
Exo-erythrocytic stage: Primaquine.
Mitochondrial function: Atovaquone.
493
What is the role of combination therapy in malaria treatment?
Answer: Prevents resistance, enhances efficacy (e.g., atovaquone-proguanil).
494
Explain the mechanism of action of azole antifungal drugs.
Answer: Inhibit 14α-demethylase, preventing ergosterol synthesis, disrupting fungal membrane integrity.
495
What are the key adverse effects of amphotericin B?
Answer: Nephrotoxicity, infusion-related reactions, electrolyte imbalance.
496
Differentiate between echinocandins and azoles in their mechanism of action.
Answer:
Echinocandins: Inhibit β-1,3-glucan synthase, weakening the fungal cell wall.
Azoles: Inhibit ergosterol biosynthesis via 14α-demethylase.
497
SBA: What is the primary target of HIV in the human immune system?
Answer: CD4+ T cells, macrophages, and dendritic cells.
498
SBA: What is the mechanism of action of integrase inhibitors in HIV treatment?
Answer: Prevent integration of viral DNA into the host genome.
499
SBA: Which co-receptors are required for HIV entry into host cells?
Answer: CCR5 and CXCR4.
500
SBA: What is the primary goal of antiretroviral therapy (ART)?
Answer: Achieve an undetectable viral load to preserve immune function and prevent transmission.
501
SBA: What is the standard backbone of first-line ART regimens?
Answer: Tenofovir and emtricitabine.
502
SBA: What is a key factor that contributes to HIV resistance to antiretroviral drugs?
Answer: High mutation rate of the virus during replication.
503
SBA: What CD4 count indicates significant immunosuppression and increased risk of opportunistic infections?
Answer: <200 cells/mm³.
504
SBA: Which class of ART is bictegravir categorized under?
Answer: Integrase inhibitors.
505
SBA: What diagnostic test is used to measure viral load in HIV patients?
Answer: Polymerase chain reaction (PCR) test.
506
SBA: What is the most common mode of HIV transmission worldwide?
Answer: Sexual contact through the exchange of sexual fluids.
507
EMQ: Match the drug class to its mechanism of action.
NRTIs: Mimic natural nucleotides, causing chain termination during reverse transcription.
Integrase inhibitors: Block integration of viral DNA into the host genome.
Protease inhibitors: Prevent cleavage of viral polyproteins into functional proteins.
508
EMQ: Match the diagnostic marker to its clinical significance.
CD4 count: Reflects immune suppression and risk of opportunistic infections.
Viral load: Measures viral replication and treatment efficacy.
HIV antibody test: Confirms HIV infection.
509
EMQ: Match the ART regimen component to its role.
Tenofovir: NRTI used as part of the backbone therapy.
Bictegravir: First-line integrase inhibitor.
Emtricitabine: NRTI that complements tenofovir.
510
EMQ: Match the mode of transmission to its description.
Vertical transmission: From mother to child during delivery or breastfeeding.
Bloodborne: Via sharing of contaminated needles or transfusions.
Sexual contact: Exchange of sexual fluids during intercourse.
511
EMQ: Match the HIV stage to its clinical features.
Stage 1: Flu-like symptoms.
Stage 2: Asymptomatic or mild symptoms.
Stage 3: AIDS with opportunistic infections.
512
What diagnostic tests are used to confirm HIV infection?
Answer: HIV antibody test and polymerase chain reaction (PCR) for viral RNA. (2 marks)
513
What is the role of CD4 count and viral load in monitoring HIV?
Answer:
CD4 count: Reflects immune function and risk of opportunistic infections.
Viral load: Indicates level of viral replication and ART efficacy. (2 marks)
514
What are the key components of first-line ART regimens?
Answer: Two NRTIs (e.g., tenofovir and emtricitabine) and an integrase inhibitor (e.g., dolutegravir or bictegravir). (2 marks)
515
List three challenges associated with ART adherence and how they can be addressed.
Answer:
Long-term adherence: Addressed through patient education.
Drug-drug interactions: Managed by reviewing medications.
Side effects: Monitored and mitigated with specialist support. (2 marks)
516
What prevention strategies are available for HIV transmission?
Answer:
Primary: Pre-exposure prophylaxis (PrEP), condom use, safer injecting practices.
Secondary: Early diagnosis, ART initiation, treatment as prevention (U=U). (2 marks)
517
SBA: What is the mechanism of action of oseltamivir in influenza treatment?
Answer: Inhibits neuraminidase, preventing the release of viral progeny.
518
SBA: Which type of influenza virus is most responsible for seasonal epidemics?
Answer: Types A and B.
519
SBA: What is the incubation period for influenza?
Answer: Approximately 2 days.
520
SBA: Which antiviral is recommended for severe influenza and is administered via inhalation or IV?
Answer: Zanamivir.
521
SBA: What is the target of dexamethasone in COVID-19 management?
Answer: Reduces inflammation by suppressing pro-inflammatory cytokines.
522
SBA: What is the primary risk associated with rifampicin in tuberculosis treatment?
Answer: Hepatotoxicity.
523
SBA: Which test is used to confirm active tuberculosis?
Answer: Sputum culture or PCR.
524
SBA: What are the two phases of tuberculosis treatment?
Answer: Initial phase (2 months with four drugs) and continuation phase (4 months with two drugs).
525
SBA: How is COVID-19 diagnosed in hospitalized patients?
Answer: PCR testing of respiratory samples.
526
SBA: What is the primary indication for the use of tocilizumab in COVID-19?
Answer: Severe COVID-19 requiring oxygen and dexamethasone treatment.
527
EMQ: Match the condition to its diagnostic test.
nfluenza: PCR from respiratory samples.
COVID-19: Lateral flow or PCR tests.
Tuberculosis: Chest X-ray and sputum culture.
528
EMQ: Match the antiviral to its condition.
Oseltamivir: Influenza.
Paxlovid: COVID-19.
Rifampicin: Tuberculosis.
529
EMQ: Match the vaccine type to its condition.
Seasonal influenza: Annual vaccine based on global strain predictions.
COVID-19: Pfizer or Moderna for primary and booster doses.
Tuberculosis: BCG vaccine for high-risk individuals.
530
EMQ: Match the drug to its common side effect.
Oseltamivir: Nausea and dizziness.
Dexamethasone: Hyperglycemia.
Rifampicin: Orange discoloration of body fluids.
531
EMQ: Match the treatment phase to its tuberculosis management.
Initial phase: Rifampicin, isoniazid, pyrazinamide, ethambutol.
Continuation phase: Rifampicin and isoniazid.
Latent TB treatment: Isoniazid for 6 months.
532
List two pharmacological treatments for influenza and their mechanisms.
Answer:
Oseltamivir: Inhibits neuraminidase to prevent viral release.
Zanamivir: Similar mechanism, available as an inhaled or IV formulation. (2 marks)
533
What are the main components of COVID-19 management in patients requiring oxygen?
Answer:
Dexamethasone: Reduces inflammation.
Tocilizumab: Monoclonal antibody against IL-6 receptor.
VTE prophylaxis: Prevents thrombotic complications. (2 marks)
534
Explain the role of vaccination in preventing each condition.
Answer:
Influenza: Annual vaccine tailored to predicted strains.
COVID-19: mRNA or vector vaccines, with boosters.
Tuberculosis: BCG vaccine for high-risk groups. (2 marks)
535
Describe the standard treatment regimen for active tuberculosis.
Answer:
Initial phase: Rifampicin, isoniazid, pyrazinamide, ethambutol for 2 months.
Continuation phase: Rifampicin and isoniazid for 4 months. (2 marks)
536
What counseling points should be given to a patient on rifampicin?
Answer:
Avoid alcohol to reduce hepatotoxicity risk.
Expect orange discoloration of bodily fluids.
Adhere strictly to dosing schedule to prevent resistance. (2 marks)
537
SBA: What is the first-line antibiotic for uncomplicated cystitis in women aged 16-64 according to local guidelines?
Answer: Nitrofurantoin or trimethoprim.
538
SBA: What is the primary mechanism of action of nitrofurantoin?
Answer: Inhibits bacterial enzymes involved in DNA synthesis.
539
SBA: What symptom necessitates referral for suspected cystitis?
Answer: Haematuria or persistent symptoms beyond 2 days.
540
SBA: What is the first-line treatment for pyelonephritis in patients without penicillin allergy?
Answer: Cefalexin.
541
SBA: Which UTI antibiotic is contraindicated near term in pregnancy due to the risk of neonatal haemolysis?
Answer: Nitrofurantoin.
542
SBA: What is the most common pathogen causing UTIs?
Answer: Escherichia coli (E. coli).
543
SBA: What defines a complicated UTI?
Answer: UTI associated with underlying conditions that increase the risk of therapy failure (e.g., diabetes, renal impairment).
544
SBA: What antibiotic is recommended for UTI prophylaxis in recurrent infections?
Answer: Nitrofurantoin or methenamine hippurate.
545
SBA: Which antibiotic is reserved for complicated UTIs and taken as a single 3g dose?
Answer: Fosfomycin.
546
SBA: What is the primary management for urosepsis in patients with CrCL >30 mL/min?
Answer: IV gentamicin for up to 5 days.
547
EMQ: Match the UTI classification to its description.
Simple UTI: Confined to the bladder without systemic symptoms.
Complicated UTI: Associated with structural or functional abnormalities.
Pyelonephritis: Infection involving the kidneys with systemic symptoms.
548
EMQ: Match the drug to its clinical use.
Nitrofurantoin: First-line treatment for uncomplicated cystitis.
Fosfomycin: Single-dose treatment for complicated UTIs.
Cefalexin: Treatment for pyelonephritis in pregnancy.
549
EMQ: Match the patient group to the recommended antibiotic for cystitis.
Pregnant women: Nitrofurantoin (1st and 2nd trimesters).
Children: Cefalexin.
Men: Nitrofurantoin for 7 days.
550
EMQ: Match the symptom to the condition.
Dysuria and frequency: Cystitis.
Fever and flank pain: Pyelonephritis.
Confusion and low urine output: Urosepsis.
551
EMQ: Match the antibiotic to its side effect.
Nitrofurantoin: Yellow-brown urine discoloration.
Ciprofloxacin: Tendon rupture.
Trimethoprim: Hyperkalemia.
552
What are three red flags in UTI presentation that warrant referral?
Answer: Haematuria, flank pain with fever, persistent symptoms beyond 48 hours. (2 marks)
553
Describe the empirical management of uncomplicated cystitis in women.
Answer:
Nitrofurantoin 100 mg MR BD for 3 days.
Trimethoprim 200 mg BD for 3 days (if low resistance). (2 marks)
554
What is the standard treatment for pyelonephritis in primary care?
Answer:
First-line: Cefalexin 500 mg TDS for 7-10 days.
Second-line: Co-trimoxazole or ciprofloxacin. (2 marks)
555
Explain why nitrofurantoin is avoided in renal impairment.
Answer: Requires renal secretion for antibacterial activity; accumulation in renal impairment increases toxicity risk. (2 marks)
556
What are the complications of untreated UTIs?
Answer: Progression to pyelonephritis, urosepsis, kidney damage, and chronic UTIs. (2 marks)
557
SBA: What is the first-line therapy for dehydration in gastroenteritis?
Answer: Oral rehydration therapy (e.g., Dioralyte).
558
SBA: Which symptom warrants referral in acute diverticulitis?
Answer: Rectal bleeding or constant severe abdominal pain.
559
SBA: What is the recommended antibiotic for giardiasis?
Answer: Tinidazole 2 g as a single dose.
560
SBA: What is the primary cause of bacterial gastroenteritis from undercooked poultry?
Answer: Campylobacter.
561
SBA: Which eye condition requires urgent referral if accompanied by photophobia and discharge?
Answer: Gonococcal conjunctivitis.
562
SBA: What is the first-line treatment for anterior blepharitis?
Answer: Warm compresses and gentle cleaning with diluted baby shampoo.
563
SBA: What is the key red flag symptom of dental abscess requiring emergency referral?
Answer: Airway compromise or spreading infection.
564
SBA: What class of drugs should be stopped in cases of severe diarrhoea and dehydration?
Answer: DAMN drugs (Diuretics, ACEi/ARB, Metformin, NSAIDs).
565
SBA: What is the most common mode of transmission for Shigella infections?
Answer: Faecal-oral route, particularly in households and nurseries.
566
SBA: Which bacteria is associated with antibiotic-associated diarrhoea and requires treatment with vancomycin?
Answer: Clostridioides difficile (C. difficile).
567
EMQ: Match the condition to the recommended first-line treatment.
Acute diverticulitis: Dietary fibre and analgesics.
Giardiasis: Tinidazole.
Bacterial conjunctivitis: Chloramphenicol.
568
EMQ: Match the pathogen to its transmission route.
Campylobacter: Undercooked poultry.
Cryptosporidium: Contaminated water.
Shigella: Faecal-oral spread.
569
EMQ: Match the clinical symptom to the condition.
Sudden abdominal pain with pyrexia: Diverticulitis.
Burning and itching of eyelids: Blepharitis.
Painful, throbbing gum swelling: Dental abscess.
570
EMQ: Match the drug to its clinical use.
Vancomycin: C. difficile infection.
Amoxicillin: Dental abscess.
Tinidazole: Giardiasis.
571
EMQ: Match the contraindication to the therapy.
Antimotility agents: Diarrhoea with blood or mucus in stools.
Oral rehydration therapy: No contraindications.
Nitrofurantoin: CrCL <45 mL/min.
572
What are the diagnostic features of gastroenteritis?
Answer:
Sudden-onset diarrhoea and abdominal cramping.
Nausea/vomiting, fever, or malaise.
Risk factors: contaminated water, recent foreign travel, antibiotic use. (2 marks)
573
What is the first-line treatment for dehydration in gastroenteritis?
Answer: Oral rehydration therapy (e.g., Dioralyte). Monitor for risk of dehydration, especially in children or the elderly. (2 marks)
574
What red flags in dental abscesses warrant immediate referral?
Answer:
Airway compromise.
Spreading infection or systemic symptoms (fever, trismus).
Difficulty opening the eye due to swelling. (2 marks)
575
Explain the management of anterior blepharitis.
Answer:
Gentle lid cleaning twice daily with warm water and baby shampoo.
Warm compresses.
Topical antibiotics (e.g., chloramphenicol) if severe. (2 marks)
576
What antibiotics are used for confirmed C. difficile infection and why?
Answer: Vancomycin, as it targets the bacteria in the colon with minimal systemic absorption. (2 marks)
577
SBA: Which Plasmodium species is most likely to cause severe disease in healthy individuals?
Answer: Plasmodium falciparum.
578
SBA: What is the first-line chemoprophylaxis for malaria in regions with chloroquine resistance?
Answer: Atovaquone/proguanil.
579
SBA: What is the mechanism of action of doxycycline in malaria prophylaxis?
Answer: Inhibits protein synthesis by binding to ribosomal RNA.
580
SBA: When should atovaquone/proguanil prophylaxis be started before entering a malaria-endemic area?
Answer: 1-2 days before travel.
581
SBA: What is a key adverse effect associated with mefloquine?
Answer: Neuropsychiatric effects.
582
SBA: Which non-pharmacological intervention is the most effective first-line defense against malaria?
Answer: Insecticide-treated mosquito nets.
583
SBA: Why are pregnant women at higher risk for malaria?
Answer: Increased attractiveness to mosquitoes and altered immune response.
584
SBA: What is the preferred treatment for uncomplicated Plasmodium falciparum malaria?
Answer: Artemisinin-based combination therapy (ACT).
585
SBA: What is the primary action of chloroquine in malaria treatment?
Answer: Inhibits heme detoxification in the parasite's food vacuole.
586
SBA: What temperature range is most suitable for malaria transmission?
Answer: 20-30°C.
587
EMQ: Match the chemoprophylactic drug to its appropriate region of use.
Chloroquine: Central America north of the Panama Canal.
Atovaquone/proguanil: Regions with chloroquine resistance.
Mefloquine: Parts of Southeast Asia.
588
EMQ: Match the intervention to its mechanism of prevention.
DEET repellent: Prevents mosquito bites.
Insecticide-treated nets: Kills resting mosquitoes.
Long-sleeved clothing: Reduces mosquito accessibility to skin.
589
EMQ: Match the adverse effect to the drug.
Doxycycline: Photosensitivity.
Mefloquine: Neuropsychiatric effects.
Chloroquine: GI disturbances and headache.
590
EMQ: Match the Plasmodium species to its clinical features.
P. falciparum: Severe disease with microvascular effects.
P. vivax: Relapses due to liver hypnozoites.
P. malariae: Chronic infection with low-grade symptoms.
591
EMQ: Match the diagnostic approach to its purpose.
Thick blood film: Detects parasite presence.
Thin blood film: Identifies Plasmodium species.
PCR: Confirms diagnosis with high sensitivity.
592
What are the ABCD principles for malaria prevention?
Answer:
Awareness of risk.
Bite prevention.
Chemoprophylaxis.
Diagnosis of symptoms early. (2 marks)
593
List two key bite-prevention strategies for travelers.
Answer:
Use of 50% DEET repellents on exposed skin.
Sleeping under insecticide-treated mosquito nets. (2 marks)
594
What are the indications for atovaquone/proguanil use?
Answer: Prophylaxis in regions with chloroquine resistance; start 1-2 days before travel and continue for 7 days after leaving. (2 marks)
595
Explain the role of thick and thin blood films in malaria diagnosis.
Answer:
Thick film: Detects parasite presence.
Thin film: Identifies Plasmodium species. (2 marks)
596
What are the key counseling points for travelers taking mefloquine?
Answer:
Start 2-3 weeks before travel to assess tolerability.
Avoid in individuals with a history of neuropsychiatric disorders.
Continue for 4 weeks after leaving the endemic area. (2 marks)
597
SBA: What is the most common bacterial sexually transmitted infection in the UK?
Answer: Chlamydia.
598
SBA: What is the first-line treatment for chlamydia in non-pregnant adults?
Answer: Doxycycline 100 mg twice daily for 7 days.
599
Answer: Doxycycline 100 mg twice daily for 7 days.
Answer: Nucleic acid amplification tests (NAATs).
600
SBA: Which STI can cause neonatal conjunctivitis during delivery?
Answer: Gonorrhoea.
601
SBA: What antibiotic is recommended for gonorrhoea treatment according to current guidelines?
Answer: Ceftriaxone 500 mg IM plus azithromycin 1 g orally.
602
SBA: What is the primary diagnostic symptom of primary syphilis?
Answer: A painless chancre.
603
SBA: What is the most common complication of untreated gonorrhoea in women?
nswer: Pelvic inflammatory disease (PID).
604
SBA: Which STI is caused by the spirochete Treponema pallidum?
Answer: Syphilis.
605
SBA: What is the first-line treatment for syphilis?
Answer: Benzathine benzylpenicillin.
606
SBA: Which STI is strongly associated with increased HIV transmission risk?
Answer: Syphilis.
607
EMQ: Match the STI to its most common symptom.
Chlamydia: Asymptomatic in most cases.
Gonorrhoea: Purulent urethral discharge.
Syphilis: Painless chancre.
608
EMQ: Match the diagnostic test to its STI.
NAAT: Chlamydia and gonorrhoea.
Dark field microscopy: Syphilis.
Viral culture: Herpes simplex virus.
609
EMQ: Match the STI to its complication.
Chlamydia: Epididymo-orchitis.
Gonorrhoea: Disseminated gonorrhoea.
Syphilis: Neurosyphilis.
610
EMQ: Match the antibiotic to its condition.
Ceftriaxone: Gonorrhoea.
Doxycycline: Chlamydia.
Benzathine benzylpenicillin: Syphilis.
611
MQ: Match the STI to its mode of transmission.
Chlamydia: Genital-genital contact.
Gonorrhoea: Direct mucous membrane contact.
Syphilis: Direct contact with infectious lesions.
612
What are the diagnostic methods for chlamydia and gonorrhoea?
Answer:
NAATs from vulvovaginal swabs or first-catch urine (women and men).
Culture for gonorrhoea in suspected antimicrobial resistance cases. (2 marks)
613
hat are the first-line treatments for chlamydia and gonorrhoea?
Answer:
Chlamydia: Doxycycline 100 mg BD for 7 days.
Gonorrhoea: Ceftriaxone 500 mg IM plus azithromycin 1 g orally. (2 marks)
614
List three complications of untreated syphilis.
Answer: Neurosyphilis, cardiovascular syphilis, gummatous syphilis. (2 marks)
615
What is the recommended treatment for syphilis?
Answer: Benzathine benzylpenicillin IM in a single dose for early syphilis. (2 marks)
616
What preventive measures can reduce STI transmission?
Answer:
Consistent condom use.
Regular STI testing for high-risk individuals.
Prompt partner notification and treatment. (2 marks)
617
SBA: What is the mechanism of action of azole antifungal drugs?
Answer: Inhibit 14α-demethylase, disrupting ergosterol biosynthesis in fungal cell membranes.
618
SBA: What is the first-line treatment for oral thrush in adults?
Answer: Miconazole oral gel.
619
SBA: What is the primary antifungal used for the treatment of aspergillosis?
Answer: Voriconazole.
620
SBA: Which antifungal drug is commonly used for vaginal candidiasis?
Answer: Clotrimazole pessary or cream.
621
SBA: What is the mechanism of action of polyene antifungals such as amphotericin B?
Answer: Bind to ergosterol, forming pores in the fungal cell membrane.
622
SBA: Which antifungal agent is used prophylactically in immunocompromised patients to prevent fungal infections?
Answer: Micafungin or oral triazoles.
623
SBA: What is the treatment for systemic candidiasis?
Answer: First-line: Caspofungin; Alternative: Fluconazole or amphotericin B.
624
SBA: Which antifungal drug is contraindicated in liver disease due to its hepatotoxicity risk?
Answer: Itraconazole.
625
SBA: What is the most common side effect associated with nystatin?
Answer: Mild gastrointestinal disturbances such as nausea.
626
SBA: What is the treatment of choice for cryptococcal meningitis?
Answer: Amphotericin B with flucytosine.
627
EMQ: Match the drug to its fungal infection treatment.
Voriconazole: Aspergillosis.
Clotrimazole: Vaginal candidiasis.
Amphotericin B: Cryptococcal meningitis.
628
EMQ: Match the antifungal drug to its mechanism of action.
Polyenes (e.g., amphotericin B): Bind to ergosterol, disrupting membranes.
Azoles: Inhibit ergosterol biosynthesis.
Echinocandins: Inhibit β-1,3-glucan synthase, weakening fungal cell walls.
629
EMQ: Match the fungal infection to its risk factor.
Aspergillosis: Stem cell transplantation.
Vaginal candidiasis: Antibiotic use or pregnancy.
Systemic candidiasis: Central venous catheter use.
630
EMQ: Match the antifungal to its primary toxicity.
Amphotericin B: Nephrotoxicity.
Itraconazole: Hepatotoxicity.
Flucytosine: Bone marrow suppression.
631
EMQ: Match the infection to its diagnostic features.
Oral thrush: White plaques that can be wiped off, leaving erythematous areas.
Vaginal candidiasis: Thick, cottage cheese-like discharge with pruritus.
Systemic candidiasis: Fever, tachycardia, and tachypnoea in an immunocompromised host.
632
What are the first-line treatments for oral and vaginal candidiasis?
Answer:
Oral candidiasis: Miconazole oral gel or nystatin suspension.
Vaginal candidiasis: Clotrimazole pessary or fluconazole oral capsule. (2 marks)
633
Describe the mechanism of action of echinocandins.
Answer: Inhibit β-1,3-glucan synthase, impairing fungal cell wall synthesis and leading to osmotic instability. (2 marks)
634
What are the key risk factors for fungal infections in immunocompromised patients?
Answer:
Prolonged neutropenia.
Use of central venous catheters.
High-dose steroids or chemotherapy. (2 marks)
635
Explain the management of systemic candidiasis.
Answer:
First-line: Caspofungin or micafungin.
Alternative: Amphotericin B or fluconazole.
Duration depends on resolution of symptoms and negative cultures. (2 marks)
636
What preventive measures can reduce the incidence of fungal infections?
Answer:
Maintain proper hygiene (e.g., cleaning dentures or preventing skin moisture).
Use antifungal prophylaxis in high-risk patients (e.g., micafungin or posaconazole).
Educate on proper inhaler use to prevent oral candidiasis. (2 marks)
637
SBA: What is the defining feature of a heterocyclic compound?
Answer: A cyclic compound containing at least one atom other than carbon (e.g., nitrogen, oxygen, sulfur) in the ring.
638
SBA: What is the mechanism of action of azole antifungals such as ketoconazole?
Answer: Inhibits 14α-demethylase, disrupting ergosterol biosynthesis in fungal membranes.
639
SBA: Which heterocycle is present in penicillins?
Answer: Thiazolidine ring.
640
SBA: What is the importance of amide bonds in biological systems?
Answer: They form peptide bonds, linking amino acids in proteins.
641
SBA: Which reagent is commonly used to form acid halides for amide bond synthesis?
Answer: Thionyl chloride (SOCl₂).
642
SBA: What type of bond is a β-lactam ring?
Answer: A cyclic amide bond.
643
SBA: What is the primary structural feature of quinoline?
Answer: A fused aromatic ring system containing nitrogen.
644
SBA: What is the risk associated with using carbodiimides (e.g., DCC) for amide bond formation in peptide synthesis?
Answer: Epimerization of chiral centers in amino acids.
645
SBA: What is the role of β-1,3-glucan synthase inhibitors such as echinocandins?
Answer: Inhibit fungal cell wall biosynthesis.
646
SBA: What is the function of additives in coupling reactions involving carbodiimides?
Answer: Reduce epimerization and increase reaction yield.
647
EMQ: Match the heterocycle to its clinical application.
Pyrimidine: Found in nucleotides and antimetabolites like trimethoprim.
Thiazolidine: Present in penicillins, inhibits transpeptidase enzymes.
Quinoline: Used in antimalarials such as chloroquine.
648
EMQ: Match the coupling reagent to its role in amide bond formation.
Thionyl chloride: Generates acid halides.
DCC: Forms activated esters for direct amide formation.
Phosphorus pentachloride: Converts acids into acid chlorides.
649
EMQ: Match the heterocycle to its biological significance.
Imidazole: Found in histamine and antifungals.
Pyrrole: Forms tetrameric derivatives in heme and chlorophyll.
Piperazine: Common in drug salts to enhance solubility.
650
EMQ: Match the heterocycle to the drug example.
Thiazole: Sulphamethoxazole.
Triazole: Fluconazole.
Pyrimidine: Cytosine (component of DNA).
651
EMQ: Match the reaction condition to its role in amide bond formation.
Acid halides: Generated with thionyl chloride or oxalyl chloride.
Anhydrides: Used for efficient amide bond formation.
Coupling reagents: Activate acids for peptide synthesis.
652
What are heterocycles, and why are they important in drugs?
Answer: Cyclic compounds with at least one non-carbon atom (e.g., nitrogen, oxygen, sulfur). Found in antibiotics (e.g., penicillins), antifungals (e.g., azoles), and antimalarials (e.g., quinolines). (2 marks)
653
List two examples of drugs containing heterocyclic structures and their uses.
Answer:
Penicillins: Antibacterial, inhibit transpeptidase.
Ketoconazole: Antifungal, inhibits ergosterol biosynthesis. (2 marks)
654
Describe the role of amide bonds in biological systems.
Answer: Amide bonds form peptide bonds in proteins and are critical in enzyme-substrate interactions. (2 marks)
655
What are the challenges in synthesizing amide bonds, and how are they overcome?
Answer: Poor electrophilicity of carboxylic acids; overcome using activating reagents like thionyl chloride or DCC. (2 marks)
656
Explain the significance of reducing epimerization during peptide synthesis.
Answer: Maintains the correct stereochemistry of amino acids, critical for biological activity of peptides. (2 marks)
657
SBA: When was the NHS in England and Wales established?
Answer: 5th July 1948.
658
SBA: What significant change occurred to the NHS in Wales in 1969?
Answer: Legislation separated the Welsh NHS from the English NHS under the Welsh Office.
659
SBA: Which Act governs the NHS in Wales?
Answer: National Health Service (Wales) Act 2006.
660
SBA: What are the responsibilities of devolved healthcare authorities in Wales?
Answer: Organisation, funding of the NHS, family planning, and prevention/treatment of diseases.
661
SBA: How many Local Health Boards (LHBs) are there in Wales?
Answer: Seven.
662
SBA: Which NHS trust in Wales provides ambulance services?
Answer: Welsh Ambulance Services NHS Trust.
663
SBA: What is the role of the Primary Care Services Division of the NHS Wales Shared Services Partnership?
Answer: Reimbursement services to pharmacies, GPs, and appliance contractors.
664
SBA: Which body oversees education and workforce development in NHS Wales?
Answer: Health Education and Improvement Wales (HEIW).
665
SBA: When did Wales legally establish Community Pharmacy Wales as a negotiating body?
Answer: April 2004.
666
SBA: What key difference exists between NHS Wales and NHS England regarding prescriptions?
Answer: Wales no longer charges for NHS prescriptions.
667
EMQ: Match the organisation to its role.
Public Health Wales NHS Trust: Public health promotion and disease prevention.
Velindre NHS Trust: Cancer services and specialist palliative care.
Welsh Ambulance Services NHS Trust: Ambulance and emergency response services.
668
EMQ: Match the health authority to its area.
Aneurin Bevan Health Board: South East Wales.
Betsi Cadwaladr University Health Board: North Wales.
Swansea Bay University Health Board: South West Wales.
669
EMQ: Match the legislative framework to its application.
NHS Act 2006: Applies to England and Wales.
National Health Service (Wales) Act 2006: Governance of the Welsh NHS.
Welsh Language Standards (Schedule 5, 2020 Regulations): Welsh language use in pharmacy.
670
EMQ: Match the responsibility to the NHS Wales body.
Health Education and Improvement Wales: Training and workforce development.
Community Pharmacy Wales: Negotiation on reimbursement and national services.
NHS Wales Shared Services Partnership: Reimbursement for NHS prescriptions.
671
EMQ: Match the pharmacy service to its jurisdiction.
Wales: Discharge Medicine Review Service.
England: New Medicine Service (NMS).
Both: Essential and advanced services under the community pharmacy framework.
672
Describe the role of Local Health Boards (LHBs) in Wales.
Answer: Manage and deliver primary, secondary, and community care services across defined regions. (2 marks)
673
What NHS Trusts provide national services in Wales, and what do they do?
Answer:
Public Health Wales: Disease prevention and health promotion.
Velindre NHS Trust: Cancer care and specialist services.
Welsh Ambulance Services NHS Trust: Emergency medical services. (2 marks)
674
What is the role of Health Education and Improvement Wales (HEIW)?
Answer: Oversee education, training, and workforce development; improve healthcare workforce retention and development. (2 marks)
675
What are key differences in pharmacy services between Wales and England?
Answer:
Wales: Free NHS prescriptions, discharge medicine review service.
England: Charges for prescriptions, New Medicine Service (NMS). (2 marks)
676
What provisions exist under the Welsh Language Standards for pharmacy services?
Answer: Bilingual signage, Welsh versions of documents, and training on Welsh language use in healthcare. (2 marks)
677
SBA: What is the mechanism of action of penicillins?
Answer: Inhibition of peptidoglycan synthesis by targeting transpeptidase enzymes.
678
SBA: How is the minimum inhibitory concentration (MIC) defined?
Answer: The lowest drug concentration that prevents visible bacterial growth.
679
SBA: When is an antibiotic considered bactericidal?
Answer: When the MBC/MIC ratio is ≤4.
680
SBA: What is the mechanism of action of rifampicin?
Answer: Inhibits bacterial RNA polymerase.
681
SBA: Which antibiotic class includes glycopeptides such as vancomycin?
Answer: Inhibitors of cell wall synthesis.
682
SBA: What is the main mechanism of action of fluoroquinolones?
Answer: Inhibit bacterial DNA gyrase and topoisomerase IV.
683
SBA: What mechanism does metronidazole use to kill anaerobic bacteria?
Answer: Generates reactive oxygen species (ROS), causing DNA fragmentation.
684
SBA: What is the primary cause of resistance to β-lactam antibiotics?
Answer: Bacterial production of β-lactamases.
685
SBA: Which diagnostic test is used to determine antibiotic susceptibility?
Answer: Disk diffusion test (Kirby-Bauer method).
686
SBA: What is the purpose of combination therapy in HIV treatment?
Answer: To reduce the viral load, delay resistance, and achieve synergistic antiviral effects.
687
EMQ: Match the drug to its target.
Rifampicin: Bacterial RNA polymerase.
Fluoroquinolones: DNA gyrase and topoisomerase IV.
Glycopeptides: Peptidoglycan precursors.
688
EMQ: Match the resistance mechanism to the example.
Drug efflux: Tetracycline resistance.
Target site alteration: MRSA and penicillin resistance.
Enzymatic inactivation: β-lactamase production in E. coli.
689
EMQ: Match the antibiotic to its spectrum of activity.
Penicillin G: Gram-positive cocci.
Metronidazole: Anaerobic bacteria and protozoa.
Ciprofloxacin: Broad-spectrum, including Gram-negative bacteria.
690
EMQ: Match the diagnostic test to its purpose.
MIC test: Determine the lowest concentration of antibiotic that prevents bacterial growth.
Kirby-Bauer method: Measure zones of inhibition for susceptibility testing.
PCR: Detect specific resistance genes.
691
EMQ: Match the infection to its treatment.
Tuberculosis: RIPE regimen (Rifampicin, Isoniazid, Pyrazinamide, Ethambutol).
Gonorrhoea: Ceftriaxone plus azithromycin.
Clostridioides difficile: Vancomycin or fidaxomicin.
692
List four main mechanisms of action for antibiotics and provide an example for each.
Inhibition of cell wall synthesis (e.g., penicillins).
Inhibition of protein synthesis (e.g., aminoglycosides).
Inhibition of nucleic acid synthesis (e.g., fluoroquinolones).
Disruption of metabolic pathways (e.g., sulfonamides).
693
What are the key mechanisms of antibiotic resistance?
Answer:
Enzymatic degradation (e.g., β-lactamase).
Alteration of target sites (e.g., MRSA resistance to penicillin).
Efflux pumps (e.g., tetracycline resistance).
Reduced permeability (e.g., porin loss in Gram-negative bacteria).
694
Describe the difference between bactericidal and bacteriostatic antibiotics.
Answer:
Bactericidal: Actively kill bacteria (e.g., penicillins).
Bacteriostatic: Inhibit bacterial growth, relying on the immune system for clearance (e.g., tetracyclines). (2 marks)
695
What tests are used to determine antibiotic susceptibility?
Answer:
Disk diffusion test (Kirby-Bauer method).
MIC testing via dilution methods.
E-tests for gradient diffusion. (2 marks)
696
Explain why combination therapy is preferred in tuberculosis treatment.
Answer: Prevents resistance, targets multiple pathways, and ensures complete bacterial eradication. (2 marks)
