Wound Healing Process and Pathogenesis Quiz

Welcome to PPY400!

• Course name: Processes of Human Disease I
• Institution: Seneca College
• Program: BScN
• Year: Winter 2025

Instructor Information

• Instructor: Dr. David Anderson
• Email: [email protected]
• Office: Room 1128
• Office hours: available before and after class; email for specific time

Course Content

• Introduction to human disease and homeostatic mechanisms
• How alterations in homeostatic mechanisms disrupt the human body
• Cell injury, cell death, and wound healing
• Inflammation, immunity, and infection
• Pain mechanisms, theories, and bodily responses
• Fluids, electrolytes, and acid-base balance/imbalances
• Stress and disease
• Gastrointestinal (GI) disorders
• Cardiovascular disorders
• Respiratory disorders
• Endocrine system disorders
• Musculoskeletal disorders

Modes of Instruction

• One class per week, four hours per class
• Lecture-style classes
• Lecture power points posted on Blackboard under "Course Content"
• Lecture slides posted online before each class
• Optional: print lecture slides before class for better follow-along
• Students can add notes and extra information during class

Textbook

• Textbook: Gould's pathophysiology for the health professions (7th ed.) by Hubert, R.J. & VanMeter, K.C. (2023). Elsevier

Modes of Evaluation

• Test #1: 20%
• Test #2: 20%
• Test #3: 20%
• Test #4 (not comprehensive): 20%
• Assignments: 10%
• Quizzes: 10%
• Total: 100%
• All tests are written on-campus, at the beginning of class
• Quizzes may be online or in-class

Promotion

• Minimum grade of "C+" is required for promotion to PPY500
• C+ = final mark of at least 65%
• Students should contact instructor with concerns or questions about their mark

Hints to Succeed

• Do not miss quizzes or tests
• No rewrites for quizzes
• Acceptable documentation required for test absences
• Attend class regularly; material is covered extensively in each class
• If unable to attend, class notes are taken from a classmate
• Participate in class discussion
• Review notes and textbook before class
• Ask questions
• Turn off cell phones during class

Lecture #1

• Topics: Cell Injury, Aging, and Death
• Material from Chapters 1 and 5 of the textbook for the course.

Pathophysiology

• Definition: the study of abnormalities in physiologic functioning of living beings; examines disturbances of normal mechanical, physical, and biochemical function.
• 4 Key topics: etiology, pathogenesis, clinical manifestations, and treatment implications

Etiology (continued)

• Definition: the study of causes or reasons for the disease; identifies causal factors; examples: influenza virus for the flu.
• Types: idiopathic (causes unknown), iatrogenic (caused by medical treatment).
• Risk factors: factors that, if present during development, increase the probability of disease occurring; examples: diet, smoking, and lifestyle for coronary heart disease

Pathogenesis

• Definition: development or evolution of a disease
• Discusses the physiological events in response to an etiological factor (cause).
• Illustrates the progression from fat deposits to clogged arteries in coronary heart disease.

Clinical Manifestations

• Definition: indications that a disease exists in a person; the disease becomes evident.
• Examples: fever, observable symptoms.
• Diseases can be silently present until far advanced.

Manifestations

• Categories: signs and symptoms
• Signs = objective (observed through clinical exam, or lab tests)
• Symptoms = subjective (reported by the affected individual)

Definitions

• Complication: any unforeseen issue or problems encountered due to a disease or other condition
• Sequelae: predicted outcome from a disease or condition
• Epidemiology: source or origin of the disease or condition

Stages of a Disease

• Incubation period: the time between a tissue's exposure to harmful agent and the first appearance of signs or symptoms
• Prodromal period: onset of disease where mild signs and symptoms begin to appear
• Acute Phase: the most intense stage of a disease, characterized by a peak severity of signs and symptoms
• Convalescent period: when active symptoms begin to fade and the body recovers; signs and symptoms lessen
• Latent period: the time when there are few or no visible signs of the disease
• Subclinical: the disease is well established but patient functions normally; patient may not realize a disease exists
• Chronic: disease continues for months or years, often with repeated flare-ups and periods of remission.

More stages of a disease

• Alternating “attacks” or outbreaks of disease, signs and symptoms.
• Remissions: periods during a chronic disease where symptoms lessen or disappear.

Cell Response to Stressors

• Withstanding, adapting or failing in response to stressors
• Adaptability: increase in ability to handle a specific toxin
• Risk of mutation: a possible negative impact caused by excessive exposure to a toxin
• Hypertrophy: increase in cell/organ size
• Atrophy: decrease in cell/organ size
• Hyperplasia: increase in cell number
• Dysplasia: abnormal changes in size and shape of cells.
• Neoplasia: cancer

Cells

• Normal cell form and function
• Emphasizing cell receptors, transport mechanisms, and respiration.

Cell Metabolism

• Catabolism and Anabolism
• Anabolism is the constructive of molecules within cells.
• Catabolism breaks down molecules that provide energy.

Cell Injury and Aging

• Diseases affect cells first, not the whole body
• General characteristics of cellular injury, adaptation, aging, and death
• Types of cell injury: reversible/irreversible; nutritional deficiencies, toxic chemicals, physical or mechanical stress (temperature, pressure, injury).

Cellular Adaptation and Transformation

• Cells adapt to stimuli and environment, such as Atrophy, Hypertrophy, Hyperplasia, Dysplasia and Neoplasia

Reversible Cell Injury

• If the cell can withstand the injury or is short lived, the cell returns to the normal state of activity.

Hydropic Swelling

• Cellular swelling due to water accumulation

Cell in Stress Phase

• Hydropic swelling can lead to the malfunctioning of cellular structures

Intracellular Accumulations

• Excessive substance within cells can cause cell damage due to obstruction of normal cell functions

Fatty Liver

• Accumulation of lipids in the liver; symptoms includes jaundice, swollen liver (enlarged), abdominal pain

Intracellular Accumulations continued

• Common accumulated substances like inorganic particles and mineral deposits (affect lung tissue)
• Calcium deposits are common (affects blood vessels, eyes and can cause obstruction)

Cellular Adaptation

• Adaptation to persistent stress/stimulus
• Adaptive cell changes (atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia)

Atrophy

• Cells decreasing in size
• Examples: denervation, ischemia (inadequate blood supply), nutrient starvation, disruption of endocrine signals, persistent cell injury

Atrophy (continued)

• Consequences of disuse or lack of exercise
• Muscle atrophy example when limb is immobilized such as in a cast
• Tissue size may return to normal after activity

Hypertrophy

• Increased cell/organ size due to increased physiological demands or pathophysiological demands
• Example, from exercise such as increasing skeletal muscle mass and strength

Hypertrophy Continued

• Other examples; left ventricular hypertrophy of the heart
• Occurs when there is an increase in size of the left ventricle of the heart

Hyperplasia

• Increased cell number due to increased physiological demands or pathophysiological demands
• Example occurrence of calluses and corns

Metaplasia

• Replacement of one cell type with another

Dysplasia

• Abnormal changes in size and shape, primarily in cells (increase in size, shape, and arrangement)
• Commonly seen in hyperplastic squamous epithelium
• Possibly, precancerous condition

Dysplasia (continued)

• Varying sizes and types of cells
• Signs of cellular abnormalities that are considered precancers

Irreversible Cell Injury

• Cell death may occur, with necrosis and apoptosis being two processes that contribute to cell death

Necrosis

• Cell death and breakdown or disintegration of cells
• Characteristics of necrosis include: the change of shape and color of necrotic cells, disruption of cellular membranes, and cellular swelling

Necrosis (continued)

• Release of cellular content into the extracellular fluid.
• In the event of necrosis, the cellular contents are released into the extracellular fluid; the body may experience inflammatory responses, such as fever, an increase in heart rate.

Types of Necrosis

• Coagulative, liquefactive, fat, and caseous necrosis.

Coagulative Necrosis

• Cellular swelling and breakdown of cellular elements (plasma membrane and nucleus)
• Formation of a hard, solid, and denatured proteins area.
• The area is slowly dissolved by enzymes
• Ischemic injury; typical for solid organs like the heart, kidney and liver.

Liquefactive Necrosis

• Dissolution and liquefaction of cells and tissues
• Usually from bacterial infection
• Common in the brain due to the presence of abundant enzymes

Fat Necrosis

• Death of adipose tissue; usually from trauma or pancreatitis (inflammation of the pancreas)
• Activated digestive enzymes break down fat cells.

Caseous Necrosis

• Characteristic of damaged lung tissue due to tuberculosis
• White, soft, fragile, clumpy, abnormal lung tissue that is commonly walled off by white blood cells (WBCs).

Gangrene

• Death of tissues due to severe blood supply disruption
• Dry gangrene: coagulative necrosis characterized by black, dry, wrinkled tissue
• Wet gangrene: liquefactive necrosis characterized by black, foul-smelling tissue; usually found in internal organs

Gangrene (continued)

• Gas gangrene: formation of gas bubbles in muscle tissues cause by anaerobic bacteria

Apoptosis

• Cell death or removal; cellular suicide
• Occurs in a neat, orderly manner without causing inflammation
• Common in development and maintenance of cell populations.
• Examples include neuronal development, immune system functions, and tissue homeostasis

Types of Cell Injury; Ischemia and Hypoxia

• Living cells require constant oxygen to produce ATP
• Hypoxia: lack of oxygen
• Ischemia: interruption of blood flow to a tissue
• Ischemia is dangerous to cells due to disruption of blood supply and loss of nutrients
• ATP production stops/ Na+/K+ cannot regulate/ Hydropic swelling occurs

Ischemia and Hypoxia (continued)

• Some cells are highly sensitive to oxygen deprivation; particularly critical in situations with abnormal metabolism and limited oxygen supply.
• Excessive glutamate (neurotransmitter) may build up causing injury in the brain or nervous system.

Ischemia and Hypoxia (continued)

• Re-uptake systems for glutamate are impaired when blood supply is interrupted or limited, excessive glutamate binds to NMDA receptors; this can trigger further injury (nitric oxide production and reactive nitrogen species formation damage cellular components).
• Excess free radicals will damage cellular components.

Calcium Overload Injuries

• Influx of calcium (disrupts mitochondrial function) decreases the ability of mitochondria to bind calcium and sequester further calcium → further overload.
• Excess calcium activates enzyme cascade (phospholipase activation → free radical formation) that leads to cell death(apoptosis)

Reperfusion Injury

• When blood supply resumes, cells exposed to reactive oxygen products and inflammatory chemicals can suffer further damage
• Leads to damage in the damaged cell structures

More Types of Cell Injury

• Nutritional imbalances (excess or deficiency)
• Toxic chemicals/poisons
• Bacteria/viruses
• Physical/mechanical forces (temperature, pressure, deformation, electricity, radiation).

Cellular Aging and Death

• The decline in cell's proliferative and reparative capacity combined with environmental factors damage to the cells.
• Programmed senescence: aging is due to an internal genetic program that causes cell division to stop; studies show that cells from older individuals divide less frequently.
• Cellular DNA (telomeres) shortens with cell division eventually, the cell stops replicating.

Oxidative Stress

• Accumulation of reactive oxygen species (free radicals) caused by metabolic processes.
• High metabolic rate = production of greater oxygen free radicals leading to damage of the cell membrane
• Oxidative stress is an imbalance of free radicals and antioxidants in the body; oxidative stress can occur naturally and is associated with aging.

Wound Healing

• Goal: restoration of damaged tissue.
• Two possible outcomes: regeneration (replacement by same type of cell) or replacement (damaged cells replaced by connective tissue).
• Possible when cells can divide (mitosis)
• Tissue regeneration is ideal outcome for healing and is characteristic of cells that retain the ability for regeneration.

Factors Affecting Healing

• Adequate nutrition/Vitamins/Minerals/CHO/Pro
• Blood flow: delivers nutrients and removes wastes
• Age: reduces the capacity to heal and resistance to infection; increased vulnerability to chronic and severe wound damage
• Stress: can reduce response from inflammatory processes.

Fibrous Repair (Replacement)

• When cells do not have capacity to undergo mitosis, replacement of damaged cells by connective tissue occurs.
• Steps: mast cell degranulation (release of chemicals to signal injury), granulation tissue formed (initially disorganized collection of capillaries and fibroblasts), angiogenesis (formation new blood vessels), fibrogenesis (fibroblasts migrate to healing site to deposit ECM deposits), scarring (fibrous tissue is built on granulation tissue, with less vascularity afterward).

Healing Process

• Stage 1: fill the space and restore continuity; regeneration is the ideal outcome.
• Stage 1 Intention Healing: no loss of tissue
• Stage 2 Intention Healing: loss of tissue
• Three stages: inflammation, proliferation, and remodeling

Inflammatory Phase

• In response to injury, blood clotting occurs; vasodilation, and leaking of plasma and WBCs into injured tissues.
• Removal of foreign bodies
• Formation of new blood vessels; arrival of fibroblasts

Proliferative Phase

• Formation of granulation tissue
• Epithelialization (cells migrating to form new surface layer)

Remodeling Phase

• Lasts for months to more than six months after the injury.
• Lysis and synthesis of collagen to increase the organization and strength of the tissue; results in scarring.
• Second intention healing often leaves obvious scarring and loss of function.

Test your knowledge on the intricacies of wound healing and the underlying pathogenesis of diseases. This quiz covers key concepts such as the role of mast cells, chemical mediators, and the stages of repair. Challenge yourself with questions about signs, symptoms, and healing intentions.