o Contains DNA, site of transcription (mRNA synthesis).
o Nuclear envelope: double membrane with nuclear pores.
o ATP production via oxidative phosphorylation.
o Contains its own (maternal) DNA → basis for mitochondrial inheritance.
o Role in apoptosis (cytochrome c release).
o Rough ER: ribosome-studded; protein synthesis for secretion or membrane.
o Smooth ER: lipid synthesis, detoxification (especially in liver).
o Protein modification, sorting, packaging (glycosylation).
o Produces lysosomes.
o Acidic environment (pH ~5).
o Contain hydrolytic enzymes for degradation (e.g., in autophagy).
• Other:
o Peroxisomes: β-oxidation of very long-chain fatty acids, H₂O₂ breakdown.
• Phases
o G₁: cell growth, pre-DNA synthesis.
o S: DNA replication.
o G₂: preparation for mitosis.
o M: mitosis (prophase, metaphase, anaphase, telophase).
o G₀: quiescent phase.
• Checkpoints
o G₁/S and G₂/M critical for DNA integrity.
o p53 ("guardian of the genome"): halts cell cycle if DNA damaged; induces apoptosis if irreparable.
• Apoptosis (programmed cell death)
o Intrinsic (mitochondrial) and extrinsic (death receptor) pathways.
o Caspase activation → cell dismantling without inflammation.
• Phospholipid bilayer
o Hydrophilic heads, hydrophobic tails.
o Cholesterol: modulates fluidity.
• Membrane proteins
o Integral proteins: span membrane (e.g., channels, transporters).
o Peripheral proteins: attach to membrane surface.
• Transport mechanisms
o Passive diffusion: small, nonpolar molecules (e.g., O₂, CO₂).
o Facilitated diffusion: via channels/carriers; no energy (e.g., GLUT transporters for glucose).
o Active transport: against gradient, requires ATP (e.g., Na⁺/K⁺ ATPase).
o Secondary active transport: uses gradient (e.g., Na⁺-glucose cotransporter).
• Resting membrane potential
o ~–70 mV (neurons); maintained by Na⁺/K⁺ ATPase (3 Na⁺ out, 2 K⁺ in).
• Action potential (AP)
o Depolarisation: rapid Na⁺ influx (voltage-gated channels).
o Repolarisation: K⁺ efflux.
o Hyperpolarisation: transient overshoot due to continued K⁺ outflow.
• Ca²⁺ channels
o Important in muscle contraction, neurotransmitter release.
• Receptors
o G-protein coupled receptors (GPCRs): large family, involve heterotrimeric G proteins.
E.g., β-adrenergic receptors (activate adenylate cyclase → ↑cAMP).
o Tyrosine kinase receptors: e.g., insulin receptor.
• Second messengers
o cAMP: activates protein kinase A.
o IP₃: releases Ca²⁺ from endoplasmic reticulum.
o DAG: activates protein kinase C.
• Examples of downstream effects
o Smooth muscle relaxation: β₂ activation → ↑cAMP → MLCK inhibition.
o Platelet activation: thromboxane A₂ and ADP → Ca²⁺ mobilization.
Extra Revision Pearls
• Apoptosis vs necrosis: apoptosis = no inflammation; necrosis = cell lysis, inflammatory response.
• Oncogenes often activate growth signals (e.g., RAS), tumour suppressors inhibit them (e.g., p53, RB).
• GLUT4 translocation to cell surface (insulin-stimulated) is via vesicle fusion in muscle/adipose.
• Inhibition of Na⁺/K⁺ ATPase by digoxin increases intracellular Ca²⁺
(via Na⁺/Ca²⁺ exchanger), increasing cardiac contractility.
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Author & Educational Disclaimer
Author:
Dr Phillip Cockrell BM FRCP DipClinEd
Dr Phillip Cockrell is a UK Consultant Physician in Internal Medicine, currently working at Queen Alexandra Hospital, Portsmouth University Hospitals NHS Trust. He has previously worked as a registrar across Intensive Care Medicine, Gastroenterology, Cardiology, Stroke Medicine, Acute Medicine, and Respiratory Medicine.
He has held senior leadership roles including Associate Clinical Director of the Acute Medical Unit, Clinical Director of Internal Medicine, and Chief of Medicine. Dr Cockrell has over 15 years’ experience in postgraduate medical education, having lectured extensively across the MRCP syllabus and contributed to MRCP revision teaching and course development.
Dr Cockrell holds a Bachelor of Medicine (BM), Fellowship of the Royal College of Physicians (FRCP), and a Diploma in Clinical Education (DipClinEd). His teaching approach is based on structured consolidation of complex medical topics to support efficient and effective revision for postgraduate examinations.
Purpose of this content:
The material on this page is intended solely for educational purposes to support revision for the MRCP (UK) Part 1 examination. It reflects examination-relevant principles of internal medicine and is designed to aid learning and pattern recognition.
Medical disclaimer:
This content is designed for postgraduate medical examination revision and does not constitute medical advice, diagnosis, or treatment guidance and must not be used as a substitute for professional clinical judgement, local guidelines, or specialist consultation. Clinical decisions should always be made in the context of individual patient circumstances and current national guidance.
