General concepts in pathophysiology & inflammatory responses - study notes

General concepts in pathophysiology & inflammatory responses

• Source context: Lecture by Ong Hwee Kuan on general pathophysiology concepts, cellular responses to stress, inflammation, and healing; aims to define pathology concepts, explain cellular adaptations vs necrosis, describe inflammation effects, and discuss inflammation management.

• Core aim: Build foundational understanding for clinical pathophysiology and host defense mechanisms.

Pre-reading terminology and core definitions

• Pathology: the study and diagnosis of disease; encompasses cause, mechanism of disease development, morphological changes, and clinical manifestations.

• Pathogenesis: mechanism of disease development.

• Pathophysiology: functional or physiologic changes that result from a disease process.

• Signs: objective indicators of disease.

• Symptoms: subjective feelings reported by the patient.

• Syndrome: a collection of signs and symptoms.

• Prognosis: likelihood of a specific outcome (recovery, mortality, etc.).

• Remission: signs/subsides in disease course.

• Exacerbation: signs worsen or intensify.

• Complications: new or additional problems arising after the original disease.

• Sequelae: potential unwanted outcomes following the primary condition.

Body defence systems

• Two broad categories of defense:

  • Non-Specific defence system / Innate immunity

  • Mechanical barrier

  • Non-specific phagocytosis

  • Inflammation

  • Interferons

  • Specific defence system / Adaptive immunity

  • Production of unique antibodies or cell-mediated immunity via sensitized lymphocytes

• Figure reference (conceptual): Types of defence system (VanMeter KC, 2014, p67).

Common causes of cellular injuries

• Ischemic and hypoxic injury: lack of blood supply leading to insufficient oxygen for cell homeostasis and metabolism.

• Microorganisms: infection.

• Immune reactions: hypersensitivity and autoimmune disease.

• Genetic factors: chromosomal changes or gene mutations.

• Nutritional factors: protein malnutrition, abnormal vitamin/mineral levels.

• Physical factors: blunt trauma, hypo/hyperthermic injury, ionizing radiation, electricity.

• Chemical agents: air pollutants, toxic substances (e.g., ethanol, heavy metals).

Cellular responses to stress and injurious stimuli

• Concept map (described): Cellular response to stress and injurious stimuli includes adaptive changes and potential injury progression.

• Cellular adaptations (types):

  • Atrophy

  • Hypertrophy

  • Hyperplasia

  • Metaplasia

  • Dysplasia

  • Anaplasia

  • Neoplasia

• Note: These adaptations reflect the cell’s ability to adjust growth and differentiation to new conditions; they can be reversible or precursors to further pathology.

Cellular death: necrosis vs apoptosis

• Irreversible cell injury leads to cell death, which can be:

  • Necrosis: rapid loss of plasma membrane integrity, organelle swelling, mitochondrial dysfunction; typically a pathological process.

  • Apoptosis: programmed cell death, a regulated physiologic process; part of normal development and turnover.

• Visual cue (concept): Necrosis vs apoptosis represent two distinct morphologic and mechanistic pathways of cell demise.

Inflammation: overview and mediators

• Definition: A protective response involving host cells, blood vessels, and proteins/mediators intended to eliminate the initial injury and necrotic tissue and to initiate repair.

• Inflammatory response & mediators (conceptual steps):

  • Vascular event: Bradykinin and histamine cause capillary dilation (↑ blood flow) and ↑ capillary permeability.

  • Cellular event: Neutrophils and macrophages (mature monocytes) exit blood via chemotaxis and phagocytose microbes.

• Local vs systemic inflammatory features:

  • Local: redness (erythema), heat, swelling, pain, loss of function.

  • Systemic: low-grade fever, malaise, fatigue, headache, anorexia.

Acute vs chronic inflammation

• Acute inflammation: a healthy, protective response to injury; hallmark signs include pain, swelling, redness, and warmth.

• Chronic inflammation: follows an acute episode with ongoing tissue destruction; characteristic features include:

  • Less swelling and exudate compared to acute phase

  • More lymphocytes, macrophages, and fibroblasts

  • More severe tissue destruction

  • More collagen and fibrous scar formation

• Visual reference: The course of inflammation and healing (conceptual model).

Management of inflammation

• RICE principle: Rest, Ice, Compression, Elevation.

• Pharmacological measures: anti-inflammatory medications and related therapies (as part of standard care).

Healing processes after injury

• Healing sequence:

  • Blood clot forms to seal the area.

  • Inflammatory cleaning removes debris and pathogens.

  • Granulation tissue formation develops.

  • Epithelial regeneration restores surface.

  • Fibroblasts lay down collagen fibers (scar matrix).

  • Angiogenesis supplies blood vessels for new tissue.

  • Cross-linking and realignment of collagen fibers consolidate the repair.

Types of healing

• First intention (primary intention):

  • Wound is clean, free of foreign material and necrotic tissue.

  • Wound edges are held closely together, promoting rapid healing with minimal scar.

• Second intention (secondary intention):

  • Wound is large, with more inflammation, greater scar tissue, and a longer healing process.

Factors promoting or delaying healing

• Promoting healing:

  • Youth

  • Good nutrition (protein, vitamins A & C)

  • Adequate hemoglobin

  • Effective circulation

  • Clean, undisturbed wound

  • No infection or further trauma

• Delaying healing:

  • Advanced age

  • Poor nutrition, dehydration

  • Anemia

  • Circulatory problems

  • Chronic disease or comorbidities

  • Irritation, bleeding, or excessive wound movement

  • Infection or foreign material

  • Chemotherapy treatment

  • Prolonged use of glucocorticosteroids

References and study resources (contextual)

• VanMeter KC, & Hubert RJ. Gould's Pathophysiology for the Health Professions (5th Ed.).

• Huether SE, & McCance KL. Understanding Pathophysiology (7th Ed.).

• Focus areas include: Introduction to Pathophysiology; Inflammation & Healing; Altered cellular and tissue biology; Innate Immunity: Inflammation and wound healing.