Royal College of Veterinary Surgeons Membership Exam (RCVS) Diagnostic and Foundational Veterinary Sciences Flashcards

24 sample cards from the Diagnostic and Foundational Veterinary Sciences deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. Explain the difference between a competitive and non-competitive (irreversible) antagonist on a dose-response curve.

   A competitive antagonist binds reversibly at the agonist site, shifting the agonist dose-response curve to the right (higher $EC_{50}$) but the maximal effect ($E_{max}$) is preserved and surmountable. A non-competitive/irreversible antagonist reduces the maximal response ($E_{max}$) and cannot be overcome by increasing agonist concentration.

2. Describe the mechanism of action of beta-lactam antibiotics and the basis of bacterial resistance.

   Beta-lactams (penicillins, cephalosporins) inhibit bacterial cell wall synthesis by binding penicillin-binding proteins and blocking peptidoglycan cross-linking, causing lysis (bactericidal, time-dependent). Resistance arises mainly from beta-lactamase enzymes that hydrolyse the beta-lactam ring, altered PBPs, or reduced permeability.

3. What is the mechanism of action of fluoroquinolones and a key adverse effect in growing animals?

   Fluoroquinolones (e.g. enrofloxacin, marbofloxacin) inhibit bacterial DNA gyrase (topoisomerase II) and topoisomerase IV, blocking DNA replication (bactericidal, concentration-dependent). A key adverse effect is cartilage damage/arthropathy in young growing animals; enrofloxacin can cause retinal degeneration/blindness in cats at high doses.

4. Explain how aminoglycosides kill bacteria and their two main toxicities.

   Aminoglycosides (e.g. gentamicin, amikacin) bind the 30S ribosomal subunit, causing misreading of mRNA and inhibition of protein synthesis (bactericidal, concentration-dependent). Main toxicities are nephrotoxicity (proximal tubular damage, reversible) and ototoxicity/vestibulotoxicity (often irreversible). They are inactive in anaerobic/low-oxygen environments.

5. What is the basis for prudent (responsible) antimicrobial use and the concept of antimicrobial stewardship classification (e.g. EMA categories)?

   Prudent use minimises selection of resistance by using antimicrobials only when justified, ideally guided by culture and sensitivity, with the narrowest effective spectrum and correct dose/duration. The EMA categorises antibiotics A (Avoid), B (Restrict, e.g. fluoroquinolones/3rd-4th gen cephalosporins), C (Caution), D (Prudence) to prioritise first-line agents and reserve critically important antimicrobials for human medicine.

6. Describe the mechanism of action of NSAIDs and the rationale behind COX-2 selectivity.

   NSAIDs inhibit cyclo-oxygenase (COX), reducing prostaglandin synthesis from arachidonic acid, producing analgesic, anti-inflammatory and antipyretic effects. COX-1 produces protective prostaglandins (GI mucosa, renal flow, platelets); COX-2 is induced at inflammation. COX-2-selective/sparing NSAIDs (e.g. carprofen, meloxicam, robenacoxib) aim to retain efficacy while reducing GI and renal adverse effects.

7. What are the main classes of analgesics used in the multimodal analgesia approach in veterinary medicine?

   Multimodal analgesia combines drugs acting at different points of the pain pathway: opioids (e.g. methadone, buprenorphine), NSAIDs, local anaesthetics (lidocaine, bupivacaine), alpha-2 agonists (medetomidine), NMDA antagonists (ketamine), and adjuncts (gabapentin, paracetamol in dogs only). This improves efficacy and lowers individual drug doses and side effects.

8. Why is paracetamol (acetaminophen) contraindicated in cats, and what is the toxic mechanism?

   Cats have deficient glucuronyl transferase (glucuronidation), so they cannot adequately conjugate paracetamol. The toxic metabolite NAPQI accumulates, causing oxidative damage: methaemoglobinaemia, Heinz body haemolytic anaemia and hepatotoxicity. The antidote is N-acetylcysteine, which replenishes glutathione.

9. Classify adverse drug reactions into Type A and Type B with examples.

   Type A (Augmented): dose-dependent, predictable extensions of pharmacological action, common (e.g. NSAID-induced GI ulceration, sedation from opioids). Type B (Bizarre): dose-independent, unpredictable, idiosyncratic or immune-mediated, rare (e.g. sulphonamide hypersensitivity, idiosyncratic hepatotoxicity).

10. What is the antidote and mechanism for ethylene glycol (antifreeze) toxicity?

    Ethylene glycol is metabolised by alcohol dehydrogenase to glycolic and oxalic acid, causing severe metabolic acidosis and calcium oxalate crystal-induced acute kidney injury. Antidotes competitively inhibit alcohol dehydrogenase: fomepizole (4-MP) or ethanol, which slow toxic metabolite formation. Treatment is most effective when given early.

11. Describe the toxic mechanism of anticoagulant rodenticides and their treatment.

    Anticoagulant rodenticides (e.g. warfarin, brodifacoum) inhibit vitamin K epoxide reductase, preventing recycling of vitamin K needed to activate clotting factors II, VII, IX and X. This causes coagulopathy after a delay of 3–5 days. Treatment is vitamin K1 supplementation (weeks for second-generation products) plus plasma/blood for active bleeding.

12. What is chocolate (methylxanthine) toxicity's mechanism and which methylxanthines are responsible?

    Theobromine and caffeine are methylxanthines that competitively antagonise adenosine receptors, inhibit phosphodiesterase (raising cAMP) and increase intracellular calcium. This causes CNS stimulation, tachyarrhythmias, hyperexcitability and seizures. Dark/baking chocolate is most dangerous due to high theobromine content.

13. Compare the basic structure and function of cardiac, skeletal and smooth muscle.

    Skeletal muscle: striated, multinucleated, voluntary, no gap junctions. Cardiac muscle: striated, branched, single nucleus, involuntary, joined by intercalated discs with gap junctions allowing syncytial contraction and intrinsic rhythmicity. Smooth muscle: non-striated, spindle-shaped, single nucleus, involuntary, slow sustained contraction (GI, vessels).

14. Describe the key anatomical differences in the digestive tract between ruminants and monogastric animals.

    Ruminants have a four-compartment stomach: rumen, reticulum, omasum (forestomachs lined by non-glandular epithelium for microbial fermentation) and abomasum (true glandular stomach). Monogastrics (e.g. dog, horse) have a single glandular stomach; horses are hindgut fermenters relying on the large colon and caecum.

15. What is the equation describing alveolar gas exchange (the alveolar gas equation) in simplified form?

    $P_AO_2 = FiO_2 (P_{atm} - P_{H_2O}) - \frac{P_aCO_2}{R}$, where $FiO_2$ is inspired oxygen fraction, $P_{atm}$ atmospheric pressure, $P_{H_2O}$ water vapour pressure, and $R$ the respiratory quotient (~0.8). It predicts alveolar oxygen tension and helps assess the A-a gradient.

16. State the formula for glomerular filtration rate's relationship to renal clearance and name the endogenous marker used to estimate it.

    GFR is estimated by the clearance of a freely filtered substance: $GFR = \frac{U \times V}{P}$, where U and P are urine and plasma concentrations and V is urine flow rate. Creatinine is the classic endogenous marker; symmetric dimethylarginine (SDMA) is a more sensitive early marker, rising with ~40% loss of renal function.

17. Explain the Frank-Starling law of the heart.

    The Frank-Starling mechanism states that within physiological limits, the force of cardiac contraction (stroke volume) increases as end-diastolic volume (preload/myocardial fibre stretch) increases. Greater venous return stretches sarcomeres to a more optimal overlap, increasing contractile force and matching cardiac output to venous return.

18. What is the basal/resting energy requirement (RER) formula used in clinical veterinary nutrition?

    $RER\ (kcal/day) = 70 \times (BW_{kg})^{0.75}$ (allometric formula, valid across all body weights). A linear approximation for animals 2–45 kg is $RER = (30 \times BW_{kg}) + 70$. Maintenance energy requirement is then obtained by multiplying RER by a life-stage/illness factor.

19. Which amino acid and fatty acid are essential in cats but not dogs, and what deficiency results?

    Taurine is an essential amino acid in cats (they cannot synthesise enough from cysteine); deficiency causes dilated cardiomyopathy and feline central retinal degeneration. Arachidonic acid is an essential fatty acid in cats because they lack sufficient delta-6-desaturase activity to synthesise it from linoleic acid.

20. In clinical nutrition, how is the body condition score (BCS) scale interpreted and what is the ideal?

    BCS is most commonly a 9-point scale where 1 = emaciated and 9 = grossly obese; the ideal is 4–5/9, where ribs are easily palpable with minimal fat cover and there is an obvious waist and abdominal tuck. Each point above ideal corresponds to roughly 10–15% over ideal body weight.

21. Define evidence-based veterinary medicine (EBVM) and its three/four core components.

    EBVM is the integration of the best available scientific evidence with individual clinical expertise, patient/animal factors, and client values/circumstances to make decisions about the care of individual patients. It emphasises critically appraised research evidence rather than tradition or anecdote alone.

22. Rank the levels of the evidence hierarchy from highest to lowest quality in EBVM.

    From highest to lowest: systematic reviews and meta-analyses of randomised controlled trials; individual randomised controlled trials; cohort studies; case-control studies; case series and case reports; and finally expert opinion, anecdote and bench/in-vitro research. Higher levels minimise bias and confounding.

23. Define sensitivity and specificity of a diagnostic test and their formulas.

    Sensitivity is the proportion of truly diseased animals correctly identified: $Sensitivity = \frac{TP}{TP + FN}$ (rule-out test when high, SnNout). Specificity is the proportion of truly healthy animals correctly identified: $Specificity = \frac{TN}{TN + FP}$ (rule-in test when high, SpPin).

24. What are positive and negative predictive values, and how does disease prevalence affect them?

    $PPV = \frac{TP}{TP + FP}$ (probability disease is present given a positive test); $NPV = \frac{TN}{TN + FN}$ (probability disease is absent given a negative test). Unlike sensitivity/specificity, predictive values depend strongly on prevalence: PPV rises and NPV falls as disease prevalence increases in the tested population.

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