Applied Bioscience for Health – Cellular Injury & Death (Key Vocabulary)

Vocabulary flashcards covering key terms, causes, mechanisms, and outcomes of cellular injury and death as outlined in the lecture notes.

Adenosine Triphosphate (ATP)

The major intracellular energy source; depletion is an early step in cell injury.

Aerobic Respiration

ATP production in the presence of oxygen, yielding large ATP amounts plus CO₂ and H₂O.

Anaerobic Respiration

ATP production without oxygen by carbohydrate breakdown, generating lactic acid as a by-product.

Cellular Injury

State in which normal cellular homeostasis is not maintained due to hypoxia, toxins, trauma,

Reversible Cell Injury

Damage from which the cell can recover (e.g., early ischaemia), often marked by cell swelling or lipid accumulation.

Irreversible Cell Injury

‘Point of no return’ after which the cell dies, exemplified by apoptosis and necrosis.

Apoptosis

Programmed, energy-dependent cell self-destruction occurring in normal (skin turnover) and pathological states (elimination of infected cells).

Necrosis

Uncontrolled cellular death with enzymatic dissolution (autolysis); follows severe irreversible injury (e.g., myocardial infarction).

Hypoxia

Lack of sufficient cellular oxygen, frequently caused by ischaemia; forces anaerobic metabolism and Na⁺/K⁺ pump failure.

Ischaemia

Reduced blood flow to tissue, most common cause of hypoxia; may result from arteriosclerosis or thrombus.

Anoxia

Total absence of oxygen delivery, often from complete arterial blockage, leading to rapid infarction.

Infarction

Tissue death due to prolonged ischaemia or anoxia (e.g., myocardial infarction, pulmonary embolus).

ATP Depletion

Early biochemical event in injury; decreased energy halts active transport mechanisms such as the Na⁺/K⁺ pump.

Free Radicals

Highly reactive oxygen species that damage membranes, proteins, and DNA during cellular injury.

Intracellular Calcium Overload

Loss of calcium homeostasis that activates destructive enzymes and exacerbates cell damage.

Sodium–Potassium Pump Failure

Energy-dependent transport breakdown causing intracellular Na⁺/water accumulation and cell swelling in reversible injury.

Coagulative Necrosis

Form of necrosis with protein denaturation, typically in solid organs like the heart and kidneys.

Liquefactive Necrosis

Tissue becomes liquid; characteristic of brain infarcts and abscesses.

Caseous Necrosis

Cheese-like necrosis seen in tuberculosis lesions.

Fat Necrosis

Destruction of adipose tissue with saponification, common in pancreatitis and breast trauma.

Gangrenous Necrosis (Gangrene)

Large-scale tissue necrosis from hypoxia plus bacterial invasion, often in extremities.

Ischaemic Cascade

Sequence: ischaemia → ↓O₂ → ↓ATP → pump failure → swelling → membrane rupture → necrosis.

What are the common causes (aetiology) of reversible cellular injury? 

Reversible cell injury is typically caused by early ischaemia, leading to decreased ATP and subsequent sodium–potassium pump failure. The cell can recover from this damage.

What are the key pathophysiological mechanisms underlying cellular injury? 

ATP depletion, halting active transport mechanisms. - Damage from highly reactive free radicals. - Loss of calcium homeostasis leading to intracellular calcium overload and enzyme activation. - Sodium–potassium pump failure, causing intracellular Na⁺/water accumulation and cell swelling.

How does reversible cell injury manifest pathophysiologically? 

Pathophysiological hallmarks of reversible cell injury include: - Cell swelling due to Na⁺/water accumulation. - Lipid accumulation within the cell.

What are the main causes (aetiology) leading to irreversible cell injury? 

Irreversible cell injury, or the 'point of no return' after which a cell dies, is often caused by prolonged ischaemia or anoxia. Examples include myocardial infarction.