Membrane Transport Mechanisms

Also written as Cellular transport, Transmembrane transport.

Membrane transport moves substances across cell membranes via passive and active mechanisms, maintaining homeostasis and enabling drug action. Clinicians must recognise how transport defects cause disease and affect therapy.

Overview

Cell membranes are lipid bilayers with proteins that allow selective movement of ions, nutrients, and waste. Transport can be passive (diffusion, facilitated diffusion) or active (primary, secondary).

• Passive: follows concentration gradient, no energy.
• Active: requires ATP or ion gradients.

Key concepts

Understand the driving forces (concentration, electrical, electrochemical gradients) and the main transporter families (channels, carriers, pumps, exchangers).

• Serum electrolytes: Does the patient have a disturbance of ion gradients? Abnormal Na⁺/K⁺ suggests pump dysfunction or renal loss.
• Blood glucose: Is glucose transport impaired? Low glucose with normal insulin hints at GLUT‑1 deficiency.

• Channel: pore, fast, voltage‑ or ligand‑gated.
• Carrier: binds substrate, changes shape, slower.
• Pump: uses ATP, e.g., Na⁺/K⁺‑ATPase.

Clinical relevance

Transport defects underlie many common disorders and influence drug absorption, distribution, and toxicity.

• Sweat chloride test: Is CFTR function abnormal? >60 mmol/L confirms cystic fibrosis.
• Serum lactate: Is anaerobic metabolism due to impaired oxidative transport? >2 mmol/L suggests tissue hypoxia.

• Cystic fibrosis: CFTR channel defect → thick secretions, lung infection.
• Diabetic ketoacidosis: Na⁺/K⁺‑ATPase failure → cellular dehydration.
• Malaria: parasite uses host GLUT1 to import glucose.

Exam pearls

Focus on the link between transporter type and disease presentation, and on interpreting labs that reflect transport abnormalities.

• Channel vs carrier defects produce different time courses.
• Active transport requires ATP – think of energy‑dependent diseases.

Common mistakes

Students often list transport proteins without connecting to pathophysiology or ignore resource‑limited alternatives.

• Assuming normal labs mean normal transport – many values are compensatory.
• Prescribing drugs that rely on a defective transporter.

Questions an examiner may ask

• Explain how a defect in the Na⁺/K⁺‑ATPase contributes to the clinical features of diabetic ketoacidosis.
• Describe the diagnostic steps for cystic fibrosis and why the sweat chloride test is specific.
• List two ways malaria infection exploits host membrane transport and the clinical implications.

When to seek help

• Severe electrolyte imbalance causing cardiac arrhythmia
• Acute pulmonary edema from CFTR‑related lung failure
• Rapidly worsening metabolic acidosis in diabetic ketoacidosis

Quick questions

Why does cystic fibrosis cause salty sweat?

Defective CFTR cannot reabsorb Cl⁻ in sweat ducts, pulling Na⁺ with it, leading to high NaCl loss.

How does hypoxia affect Na⁺/K⁺‑ATPase?

Low ATP reduces pump activity, causing intracellular Na⁺ buildup and cellular swelling.

Can drug absorption be altered by transporter defects?

Yes; oral drugs that need GLUT or PEPT transporters may have reduced bioavailability if those proteins are impaired.