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100+ Free CMSA FCP(SA) Part I Practice Questions

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Sample CMSA FCP(SA) Part I Practice Questions

Try these sample questions to test your CMSA FCP(SA) Part I exam readiness. Each question includes a detailed explanation. Start the interactive quiz above for the full 100+ question experience with AI tutoring.

1Which cell type resorbs mineralised bone matrix by creating an acidic microenvironment beneath a ruffled border?
A.Osteoclast
B.Osteoblast
C.Osteocyte
D.Chondrocyte
Explanation: Osteoclasts are multinucleated cells of monocyte–macrophage lineage that attach to bone, form a sealing zone, and secrete acid and proteases under the ruffled border to dissolve mineral and organic matrix. Osteoblasts synthesise osteoid; osteocytes sense mechanical load; chondrocytes maintain cartilage.
2In rheumatoid arthritis synovium, which cytokine is most central to driving pannus formation and joint destruction and is a major biologic therapy target?
A.Interleukin-5
B.Erythropoietin
C.Tumour necrosis factor-alpha
D.Insulin-like growth factor-1
Explanation: TNF-α is a key proinflammatory cytokine in rheumatoid synovitis that promotes synovial hyperplasia, angiogenesis, and osteoclast activation leading to pannus-mediated cartilage and bone damage. Anti-TNF biologics exploit this pathway. IL-5 mainly drives eosinophils; EPO stimulates red-cell production; IGF-1 is anabolic growth signalling.
3Parathyroid hormone (PTH) raises serum calcium primarily by which coordinated renal and skeletal effects?
A.Increased renal calcium excretion and decreased osteoclast activity
B.Increased renal calcium reabsorption and increased osteoclast-mediated bone resorption
C.Decreased 1,25-dihydroxyvitamin D synthesis and increased osteoblast mineralisation
D.Increased phosphate reabsorption and decreased intestinal calcium absorption
Explanation: PTH increases distal tubular calcium reabsorption, stimulates renal 1α-hydroxylase to raise 1,25-(OH)₂D (enhancing gut calcium absorption), and increases osteoclast-mediated bone resorption via osteoblast RANKL signalling. Net effect is higher plasma ionised calcium with phosphaturia.
4According to the Frank–Starling mechanism, increasing left-ventricular end-diastolic volume (within physiologic limits) primarily increases stroke volume because of:
A.Reduced afterload from aortic dilation
B.Reflex bradycardia prolonging diastolic filling only
C.Coronary steal diverting flow to the right ventricle
D.Greater sarcomere stretch increasing length-dependent contractile force (including increased myofilament Ca²⁺ sensitivity)
Explanation: Frank–Starling describes how greater preload stretches cardiomyocyte sarcomeres and increases length-dependent force generation—largely via increased myofilament Ca²⁺ sensitivity and cross-bridge recruitment—so stroke volume rises for a given afterload and inotropic state. It is an intrinsic myocardial length–tension property, not primarily an afterload or heart-rate effect.
5Mean arterial pressure (MAP) is best approximated by which relationship?
A.MAP = cardiac output × systemic vascular resistance (neglecting central venous pressure)
B.MAP = heart rate × stroke volume only
C.MAP = systolic pressure − diastolic pressure
D.MAP = pulse pressure ÷ 3
Explanation: Ohm’s law analogue for the circulation states MAP − CVP ≈ CO × SVR. With low CVP, MAP is largely the product of cardiac output and systemic vascular resistance. Pulse pressure is SBP−DBP; MAP is often estimated clinically as DBP + 1/3 pulse pressure, not pulse pressure alone.
6Myocardial oxygen supply is most dependent on which phase of the cardiac cycle for left-ventricular subendocardium?
A.Systolic ejection only
B.Isovolumetric contraction exclusively
C.Diastole, when intramural compressive forces fall and coronary perfusion pressure drives flow
D.Atrial systole alone
Explanation: Left-ventricular coronary flow, especially to the subendocardium, occurs mainly in diastole because systolic wall tension compresses intramural vessels. Tachycardia shortens diastole and can critically reduce supply. Systolic flow contributes more in the right ventricle with lower wall stress.
7In systolic heart failure with reduced ejection fraction, which neurohormonal change is most characteristic and contributes to adverse ventricular remodelling?
A.Suppressed renin–angiotensin–aldosterone system activity
B.Sustained sympathetic and RAAS activation with elevated natriuretic peptides
C.Isolated ADH deficiency
D.Primary suppression of endothelin release only
Explanation: Low effective arterial blood volume in HFrEF activates sympathetic nerves and RAAS, promoting vasoconstriction, salt retention, and fibrosis, while natriuretic peptides rise secondarily but often inadequately oppose these effects. Chronic neurohormonal activation drives adverse remodelling—the rationale for ACE inhibitors, ARNI, beta-blockers, and mineralocorticoid antagonists.
8Which ion-channel change primarily underlies phase 0 rapid depolarisation of ventricular myocytes?
A.Outward potassium current through delayed rectifier channels
B.Inward chloride current through CFTR
C.Outward calcium current through L-type channels
D.Inward sodium current through voltage-gated Na⁺ channels
Explanation: Phase 0 of the ventricular action potential is driven by a rapid inward Na⁺ current (I_Na) through voltage-gated sodium channels, producing the steep upstroke. Potassium currents dominate repolarisation; L-type Ca²⁺ current sustains the plateau (phase 2), not the initial rapid depolarisation.
9A rise in arterial PCO₂ most directly increases cerebral blood flow through which mechanism?
A.CO₂-mediated reduction in perivascular pH causing cerebral arteriolar vasodilation
B.Hypocapnic vasoconstriction of cerebral arterioles
C.Exclusive dependence on carotid baroreceptor unloading
D.Coronary steal diverting flow from brain to heart
Explanation: Hypercapnia lowers perivascular/extracellular pH, relaxing cerebral arteriolar smooth muscle and raising cerebral blood flow—a key physiologic coupling of ventilation and brain perfusion. Hypocapnia does the opposite (vasoconstriction). Baroreceptors mainly regulate systemic pressure, not this local CO₂ response.
10In aortic stenosis, left-ventricular stroke work increases mainly because the ventricle must generate higher pressure to overcome:
A.Reduced preload from mitral stenosis physiology
B.Acute decrease in systemic vascular resistance
C.Increased afterload from the stenotic valve orifice
D.Complete loss of atrial contribution only
Explanation: Valvular aortic stenosis imposes a high pressure gradient, markedly increasing left-ventricular afterload and wall stress; concentric hypertrophy develops to maintain stroke volume. Preload may be altered secondarily, but the defining haemodynamic burden is obstructive afterload.

About the CMSA FCP(SA) Part I Exam

FCP(SA) Part I is the Colleges of Medicine of South Africa primary examination for the Fellowship of the College of Physicians. It tests applied physiology and pathophysiology across the physician systems blueprint rather than clinical management. Candidates who pass Part I proceed toward registrar training requirements and later FCP(SA) Part II.

Assessment

One written SCA/MCQ paper of 150 best-of-4 items covering basic sciences for physicians. Official blueprint splits the paper approximately evenly between pathophysiology and physiology and allocates items by organ-system discipline (cardiology, endocrinology, nephrology, pulmonology, infectious diseases, haematology, neurology, immunology, cell biology/cancer, metabolism/nutrition, gastroenterology, hepatology, therapeutics/toxicology, research/statistics, geriatrics, genetics, bones and joints, pregnancy and skin).

Time Limit

4 hours (July 2025 FCP(SA) regulations). Earlier regulation editions stated 3 hours — check your acceptance letter for the diet you are sitting.

Passing Score

Cohen’s method of standard setting (example formula used by the College: about 65% of the 95th percentile of scores for that paper). No negative marking, but a correction-for-guessing formula is applied. CMSA does not publish a single fixed percentage pass mark for all diets.

Exam Fee

R 12 950 including VAT for FCP(SA) Part I (written only) on the CMSA SS2026/FS2027 fee schedule. The prior SS2025/FS2026 schedule listed R 12 150 — confirm the payable amount on the examination portal for your sitting. (Colleges of Medicine of South Africa (CMSA), College of Physicians)

CMSA FCP(SA) Part I Exam Content Outline

3%

Bones and Joints

Bone/joint physiology and arthropathy pathophysiology.

7%

Cardiology

Cardiac physiology, blood-pressure control and cardiovascular pathophysiology.

6%

Cell Biology / Cancer

Cell cycle, signalling, apoptosis and cancer biology.

7%

Endocrinology

Hormone axes, feedback and endocrine disease mechanisms.

5%

Gastroenterology

GI physiology and gut pathophysiology.

5%

Hepatology

Liver physiology and hepatic pathophysiology.

3%

Genetics

Inheritance patterns and molecular genetics relevant to adult medicine.

3%

Geriatrics

Ageing physiology and age-related homeostatic change.

7%

Haematology

Haemopoiesis, coagulation and haematological pathophysiology.

6%

Immunology

Innate/adaptive immunity and immune dysregulation.

7%

Infectious Diseases

Host–pathogen biology, sepsis, HIV/TB and antimicrobial mechanisms.

6%

Metabolism / Nutrition

Intermediary metabolism, nutrition and metabolic disease.

7%

Nephrology

Renal physiology, acid–base/electrolytes and kidney pathophysiology.

7%

Neurology

Neurophysiology and neurological disease mechanisms.

2%

Pregnancy

Maternal physiological adaptations in pregnancy.

7%

Pulmonology

Respiratory physiology and lung pathophysiology.

5%

Research / Statistics

Biostatistics and evidence-based medicine for physicians.

2%

Skin

Cutaneous physiology and selected dermatopathology.

5%

Therapeutics / Toxicology

PK/PD principles and toxicology mechanisms.

How to Pass the CMSA FCP(SA) Part I Exam

What You Need to Know

  • Passing score: Cohen’s method of standard setting (example formula used by the College: about 65% of the 95th percentile of scores for that paper). No negative marking, but a correction-for-guessing formula is applied. CMSA does not publish a single fixed percentage pass mark for all diets.
  • Assessment: One written SCA/MCQ paper of 150 best-of-4 items covering basic sciences for physicians. Official blueprint splits the paper approximately evenly between pathophysiology and physiology and allocates items by organ-system discipline (cardiology, endocrinology, nephrology, pulmonology, infectious diseases, haematology, neurology, immunology, cell biology/cancer, metabolism/nutrition, gastroenterology, hepatology, therapeutics/toxicology, research/statistics, geriatrics, genetics, bones and joints, pregnancy and skin).
  • Time limit: 4 hours (July 2025 FCP(SA) regulations). Earlier regulation editions stated 3 hours — check your acceptance letter for the diet you are sitting.
  • Exam fee: R 12 950 including VAT for FCP(SA) Part I (written only) on the CMSA SS2026/FS2027 fee schedule. The prior SS2025/FS2026 schedule listed R 12 150 — confirm the payable amount on the examination portal for your sitting.

Keys to Passing

  • Complete 500+ practice questions
  • Score 80%+ consistently before scheduling
  • Focus on highest-weighted sections
  • Use our AI tutor for tough concepts

CMSA FCP(SA) Part I Study Tips from Top Performers

1Study to the CMSA Part I systems blueprint and recommended texts (for example Ganong for physiology and McPhee/Ganong Pathophysiology of Disease for mechanisms), not to clinical management algorithms.
2Split revision time roughly evenly between physiology and pathophysiology within each organ system, matching the 50/50 paper split.
3Practise calculator-friendly quantitative physiology (cardiac output, A–a gradient, clearance, anion gap, NNT) because candidates may bring an ordinary calculator.
4Use research/statistics items as easy marks: master sensitivity, specificity, PPV/NPV dependence on prevalence, absolute risk reduction and number needed to treat.

Frequently Asked Questions

What is the format of the CMSA FCP(SA) Part I examination?

Part I is a single written paper of 150 multiple-choice questions in best-of-4 format, assessing basic sciences for physicians. The July 2025 College of Physicians regulations describe it as an SCA paper of 4 hours with no negative marking. The paper is blueprinted at roughly 50% pathophysiology and 50% physiology by organ-system discipline.

How is the FCP(SA) Part I pass mark set?

The pass mark is set using Cohen’s method of standard setting rather than a fixed national percentage. CMSA materials describe determining the pass mark as a percentage derived from the cohort’s score distribution (for example, about 65% of the 95th percentile). There is no negative marking, but a correction-for-guessing formula is applied, so candidates should answer all items. Confirm details for your sitting on the CMSA website and candidate communications.

How much does FCP(SA) Part I cost?

The CMSA examination fee schedule for Second Semester 2026 and First Semester 2027 lists FCP(SA) Part I (written only) at R 12 950 including VAT. The prior SS2025/FS2026 schedule listed R 12 150 — always confirm the amount payable on the CMSA examination portal for your diet.

What topics does the official FCP(SA) Part I blueprint cover?

The published MCQ/SCA blueprint allocates items across bones and joints, cardiology, cell biology/cancer, endocrinology, gastroenterology, hepatology, genetics, geriatrics, haematology, immunology, infectious diseases, metabolism/nutrition, nephrology, neurology, pregnancy, pulmonology, research/statistics, skin, and therapeutics/toxicology, with approximately half the paper pathophysiology and half physiology.