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Greek Pharmacist License study materials
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Greek Pharmacist License: Pharmacy Legislation, Ethics and Professional Practice in Greece

Greek Pharmacist License · Work through your exam, one topic at a time.

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Pharmacy Legislation, Ethics and Professional Practice in Greece

This domain tests the legal framework of pharmacy practice in Greece and the ethical duties that attach to the profession: licensing, ownership, the competences of the national regulator, advertising, controlled substances, confidentiality and professional conduct.

The legal layers

  • European Union law sets the frame: Directive 2001/83/EC on medicinal products for human use, Regulation 726/2004 on the centralised procedure and the European Medicines Agency, Directive 2011/62/EU on falsified medicines, and the GMP and GDP guidelines.
  • National law transposes and supplements these, defines pharmacy licensing and ownership, sets prescription requirements and governs reimbursement through the national health insurance organisation (EOPYY).
  • The EOF (Εθνικός Οργανισμός Φαρμάκων) is the national competent authority: marketing authorisations for national, mutual-recognition and decentralised procedures, pharmacovigilance, inspection, and approval of advertising for non-prescription medicines.
  • Professional bodies: the Panhellenic Pharmaceutical Association and the regional Pharmaceutical Associations maintain registers and professional discipline.

Ownership, establishment and conduct

  • A community pharmacy may be owned and operated only by a licensed pharmacist, and the general rule is one pharmacy per pharmacist; partnerships are permitted only among pharmacists.
  • The pharmacist is personally responsible for the pharmacy's operation and must be physically present or represented by a qualified deputy.
  • Professional secrecy covers all patient information obtained in practice and is reinforced by data-protection law; information may be shared only within the care team and with consent or legal obligation.
  • Advertising of prescription-only medicines to the public is prohibited; advertising of OTC medicines requires prior authorisation, must be factual and balanced, and may not suggest a diagnosis or guarantee a cure.
  • Controlled substances require secure storage, a dedicated register, and compliance with the narcotics legislation and its reporting duties.

Ethics in practice

Core duties: primacy of the patient's health, competence and continuing education, honesty in commercial dealings, refusal to dispense only on legitimate and stated grounds, and no self-prescribing or dispensing to oneself outside defined exceptions.

Worked example

A customer asks for an antibiotic for a sore throat without a prescription. Reasoning: the medicine is prescription-only, so supply is unlawful regardless of the request; the pharmacist also has an antimicrobial stewardship duty. The correct response is a clear and courteous refusal, explanation that a prescriber must assess the infection, and offering symptomatic advice and appropriate OTC options with a safety-netting instruction to seek medical review if warning signs appear.

Traps that cost marks

Confusing EOF with the EMA; assuming any commercial company may own a pharmacy; believing substitution requires the prescriber's prior consent; failing to keep records for controlled drugs.

Pharmacovigilance, Drug Safety and Regulatory Affairs

This domain tests the detection, assessment, reporting and regulatory handling of adverse drug reactions: definitions, seriousness criteria, causality assessment, reporting timelines, periodic reports and risk management. Items often present a case and ask whether and how it must be reported.

Definitions you must know precisely

  • An adverse drug reaction is a noxious and unintended response to a medicinal product at any dose, including reactions from off-label use, overdose, medication error and occupational exposure.
  • Seriousness is a regulatory category. A reaction is serious if it results in death, is life-threatening, requires hospitalisation or prolongation of hospitalisation, results in persistent or significant disability, is a congenital anomaly, or is another medically important condition.
  • Severity is the clinical intensity of the reaction and is not the same as seriousness. A severe headache is not a serious reaction if it does not meet any criterion.
  • Expectedness is judged against the product information, not against the reporting clinician's experience.

Causality and reporting

  • WHO-UMC categories: certain, probable/likely, possible, unlikely, conditional/unclassified, unassessable/unclassifiable. The Naranjo algorithm gives a numeric score.
  • In the EEA, health professionals and patients report suspected reactions to the national authority - in Greece the EOF through the yellow card (Κίτρινη Κάρτα) system, with data flowing into EudraVigilance.
  • Marketing authorisation holders must report serious valid ICSRs within 15 days and non-serious ones within 90 days; periodic safety update reports are submitted according to the EURD list, with PSUSA procedures for substances requiring harmonised review.
  • Risk management plans describe identified and potential risks, missing information, pharmacovigilance activities and risk-minimisation measures, including additional measures such as educational materials or pregnancy prevention programmes.
  • Type A reactions are dose-related and predictable; Type B are idiosyncratic and unpredictable.

Worked example

Naranjo scoring for a suspected reaction: previous conclusive reports (+1), appeared after the drug was given (+2), improved when the drug was discontinued (+1), did not recur on rechallenge (0, not performed), alternative causes present (−1), placebo response not tested (0), drug concentration not measured (0), dose-response suggested (+1), previous exposure to a similar reaction (+1), confirmed by objective evidence (+1). Total = 6, which corresponds to probable. Reasoning: even though rechallenge was not performed, a score of 5 to 8 places the case in the probable category, and the reaction must still be reported regardless of causality.

Traps that cost marks

Treating severe as serious; failing to report a reaction because it is already in the SmPC (expectedness affects assessment, not the duty to report); confusing causality with reportability; missing congenital anomaly or medically important events as seriousness criteria.

Biochemistry

Biochemistry underpins drug action and laboratory interpretation: energy metabolism, enzyme kinetics, cofactors and vitamins, lipoprotein metabolism and the inborn errors that produce classic examination vignettes. Expect numerical enzyme-kinetics items and cofactor-matching items.

Energy metabolism

  • Glycolysis yields a net 2 ATP and 2 NADH per glucose; phosphofructokinase-1 is the rate-limiting enzyme and is activated by AMP and fructose-2,6-bisphosphate, inhibited by ATP and citrate.
  • Pyruvate dehydrogenase converts pyruvate to acetyl-CoA, requiring thiamine pyrophosphate, lipoic acid, CoA, FAD and NAD.
  • The TCA cycle generates NADH and FADH₂; oxidative phosphorylation yields approximately 2.5 ATP per NADH and 1.5 ATP per FADH₂.
  • Anaerobic glycolysis regenerates NAD⁺ via lactate dehydrogenase, producing lactate.

Enzyme kinetics

  • Km is the substrate concentration at half of Vmax and is inversely related to affinity; Vmax reflects enzyme amount.
  • Competitive inhibition raises Km with unchanged Vmax; non-competitive inhibition lowers Vmax with unchanged Km; uncompetitive inhibition lowers both.
  • A Lineweaver–Burk plot shows 1/v against 1/[S], with the x-intercept equal to −1/Km and the y-intercept equal to 1/Vmax.

Cofactors and vitamins

  • Thiamine (B1): pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, transketolase.
  • Riboflavin (B2): FAD and FMN. Niacin (B3): NAD and NADP. Pyridoxine (B6): transamination and aminolevulinate synthase.
  • Cobalamin (B12): methylmalonyl-CoA mutase and methionine synthase; folate: one-carbon transfer.
  • Biotin: carboxylases; vitamin C: prolyl and lysyl hydroxylase in collagen; vitamin K: gamma-carboxylation of clotting factors.

Lipoproteins and inborn errors

  • Chylomicrons carry dietary triglyceride with apoB-48; VLDL becomes LDL (apoB-100) through lipoprotein lipase; HDL (apoA-I) mediates reverse cholesterol transport.
  • Statins inhibit HMG-CoA reductase, the rate-limiting enzyme of cholesterol synthesis.
  • HbA1c is formed by non-enzymatic glycation and reflects average glycaemia over about two to three months.
  • Phenylketonuria results from phenylalanine hydroxylase deficiency; G6PD deficiency reduces NADPH and glutathione regeneration, causing haemolysis after oxidative drugs or fava beans.

Worked example

An enzyme has Km = 5 mM. What is the reaction velocity at [S] = 15 mM? Using v = Vmax × [S]/(Km + [S]) = Vmax × 15/(5 + 15) = 0.75 Vmax, that is 75% of maximal velocity. Reasoning: at [S] = Km the velocity is 50% of Vmax; at 3 × Km it is 75%; the relationship is hyperbolic, so large substrate increases give diminishing returns.

Traps that cost marks

Treating Km as a rate rather than a concentration; reversing the effects of competitive and non-competitive inhibition on Km and Vmax; forgetting that vitamin K is required for gamma-carboxylation, not for synthesis of the clotting factors themselves.

Physiology and Pathophysiology

This domain tests normal physiology and the mechanisms of disease that pharmacological decisions depend on: membrane transport, cardiac and renal function, acid-base balance, endocrine regulation and electrolyte disorders. Vignettes ask you to calculate and then interpret.

Membranes, heart and circulation

  • The Na⁺/K⁺-ATPase pumps 3 Na⁺ out and 2 K⁺ in per ATP, maintaining the resting membrane potential; secondary active transport, as in SGLT2, uses the sodium gradient.
  • Cardiac output = heart rate × stroke volume; stroke volume follows preload, afterload and contractility (Frank–Starling relationship).
  • The renin–angiotensin–aldosterone system raises blood pressure through angiotensin II vasoconstriction and aldosterone-mediated sodium retention; ACE inhibitors and ARBs interrupt this axis, and ARBs avoid the bradykinin-mediated cough.
  • Natriuretic peptides (ANP, BNP) are released on atrial and ventricular stretch and promote natriuresis; BNP is a diagnostic marker in heart failure.

Renal function

  • Clearance = (urine concentration × urine flow)/plasma concentration; inulin clearance measures GFR, creatinine clearance estimates it.
  • Chronic kidney disease is staged by eGFR: G1 ≥ 90, G2 60–89, G3a 45–59, G3b 30–44, G4 15–29, G5 < 15 mL/min/1.73 m².
  • Acute kidney injury follows KDIGO criteria based on a creatinine rise or urine output fall.
  • Hyperkalaemia produces peaked T waves, a widened QRS and a sine-wave pattern; calcium gluconate stabilises the myocardium first.

Acid-base and electrolytes

  • Henderson–Hasselbalch: pH = 6.1 + log([HCO₃⁻]/(0.03 × pCO₂)).
  • Anion gap = Na⁺ − (Cl⁻ + HCO₃⁻), normally 8–12 mmol/L; a raised gap indicates unmeasured anions (lactate, ketones, urea, salicylate, methanol, ethylene glycol).
  • Winter's formula for metabolic acidosis: expected pCO₂ = 1.5 × HCO₃⁻ + 8 ± 2.
  • Hyponatraemia is assessed by serum osmolality and volume status; hypotonic hyponatraemia is further divided by urine osmolality and urine sodium.

Worked example

A patient has Na⁺ 138, Cl⁻ 102, HCO₃⁻ 12 mmol/L, pH 7.25 and pCO₂ 25 mmHg. Anion gap = 138 − (102 + 12) = 24 mmol/L, a high-anion-gap metabolic acidosis. Expected pCO₂ by Winter's formula = 1.5 × 12 + 8 = 26 ± 2 mmHg; the measured 25 mmHg lies inside that range, so respiratory compensation is appropriate and no second acid-base disorder is present. Reasoning: calculate the gap first, then check whether the measured pCO₂ matches the predicted value.

Traps that cost marks

Reporting an eGFR as a measured GFR in acute kidney injury; forgetting to apply Winter's formula and so missing a mixed disorder; attributing hyponatraemia to sodium loss without checking osmolality and volume status.