Pathophysiology concepts Exam 1

Disablement Model (Nagi)

A model for understanding the impact of disease, considering pathology, impairment, functional limitations, and disability.

Disability

A condition of the body or mind that makes it more difficult for a person to do certain activities and interact with the world.

ICF Model

A model adopted by the World Health Organization that considers contextual factors like environment, social factors, and individual goals in relation to health and disability.

Medical Model of Disease

A traditional approach focusing on identifying and correcting pathology to eliminate signs and symptoms.

Biopsychosocial Model

The clinical expression of pain encompasses psychological distress, attitudes, beliefs, and the social environment, beyond just physical dysfunction.

Social Model of Disability

The belief that societal barriers, attitudes, and environments create disability.

ICF Model = International Classification of Function, Disability, and Health Model

Focuses on function rather than disability, considering body function, activities, participation, environmental factors, and personal factors.

Clinical Decision Making

Clinical decisions about patient management require synthesis of information including the disease process, patient factors, signs and symptoms, interventions, values, and outcomes, all done with a degree of uncertainty.

Mental Agility

The ability to change course, respond to emerging data, explore alternative hypotheses, and incorporate barriers to treatment into the decision-making process.

Dual Process Model for Decision Making

A decision-making approach involving pattern recognition (Type 1) and analytical processing (Type 2).

Hypothetical-deductive reasoning

A systematic approach to clinical reasoning involving hypothesis generation, examination, and analysis.

Cognitive Load

The amount of thought required and the number of choices available influence decision-making.

Hypothesis-Oriented Algorithm for Clinicians (HOAC)

A structured approach to clinical decision-making involving problem statement generation, exam strategy, hypothesis generation, and intervention planning/reassessment.

Pathophysiology

An acute awareness of tissue healing, various clinical patterns, and healing pathways that can inform your clinical hypothesis and decision making.

IFOMPT, International Framework for Red Flags

A framework for identifying and responding to red flags that require immediate referral to other healthcare providers.

Social Determinants of Health (SDOH)

The major drivers of health and disparate health outcomes associated with social determinants.

Social Conditions

Conditions that occur in society due to systemic/structural barriers such as racism and discrimination, financial resources, education, occupation that influence wellness

Cultural Conditions

Customary beliefs, social norms, attitudes, values, practices shared by a group of people in a place and time

Environmental Conditions

Physical and social surroundings, encompassing natural environments, exposure to toxic substances, access to healthy foods, social interactions, and social capital.

Policies/Laws

Guidelines, principles, legislation, and activities that affect living conditions conducive to the welfare of individuals, communities, and societies.

Health Literacy

The degree to which individuals can obtain, process, and understand basic health information needed to make appropriate health decisions.

Pathology

A deviation or departure from a normal condition, including biochemical, structural, and functional changes in cells, tissues, and organs leading to a disease/condition.

Causes of Cell Injury

Oxygen deprivation (ischemia/anoxia, hypoxia), pulmonary compromise, transport deficiencies, physical agents, repetitive or forceful stress, chemical agents, infectious agents, immunologic reactions, genetic alterations/defects, and nutritional imbalances.

Incidence

The number of new occurrences/cases of a condition/disease/pathology or health-associated event in a group or population over time.

Risk

Factor or factors that increase the chance for developing a disease/condition; something that can contribute to harm.

Etiology/Pathogenesis

The cause of a disease or the process of disease development.

Signs and Symptoms / Clinical Manifestations

Signs are objective evidence of a disease (fever, rash, etc.); symptoms are subjective evidence (pain, fatigue, etc.).

Diagnosis

Identifying a disease or condition.

Treatment / Intervention

Direction of care and management options to battle disease or condition.

Prognosis

The chance(s) of recovery or recurrence and/or the likely outcome of a disease.

Prevention

Aims for prevention of a disease or condition (primary); reduction of disease impact or condition (secondary); moderate the impact of illness or injury that has lasting effects (tertiary prevention).

Atrophy

Decreased size of cells and often reduced function. Causes include decreased functional demand, disuse, denervation, ischemia, depletion of nutrition, interruption of hormonal signals, and persistent cell injury.

Hypertrophy

Increased size of cells (cell mass) and often augmented functional capacity. Causes include increased cellular protein content, increased functional demand, enhancements in nutrition, increases of hormonal signals, and persistent cell stimulation.

Hyperplasia

Increased number of cells. Causes include increased endocrine stimulation and persistent normal or abnormal cell stimulation or stress.

Metaplasia

The reversible replacement of one cell type with another mature differentiated cell type due to persistent cell stimulation or stress.

Dysplasia

Abnormality in maturation of cells within a tissue due to persistent cell stimulation or stress (not necessarily a cancer, but it may become a cancer).

Necrosis

Changes produced by enzymatic digestion of dead cellular elements.

Apoptosis

Vital process that helps eliminate unwanted cells--an internally programmed series of events effected by dedicated gene products.

Tissue Injury (Vascular Phase)

The vascular phase initiated after tissue injury.

Inflammation

Consists of vascular, proliferation, and maturation phases.

Healing/Repair

Consists of proliferation and maturation phases.

Anoxia

Oxygen deprivation

Phases of Healing

Includes vascular (hemostasis), inflammation, cell migration, chemical mediators, proliferation, cell propagation, and maturation/remodeling.

Things a PT might want to know after an injury

Response normal, type of tissue injured, pain levels, swelling/edema present, impact interventions, and return to participation.

Vascular Reaction

Platelets are activated and form an initial plug

Clotting Cascade

A series of biochemical reactions that result in a fibrin clot and leads to increased activation of platelets.

Red Blood Cells

Adds to the clot and are trapped by fibrin strands.

Platelet Activation

Platelets secrete proteins needed for soft tissue healing and homeostasis

Platelets

Traps exudate and foreign materials, localizes by-products for removal, prevents spread of infection.

Platelets (Continued)

Induces endothelial cell activation and production of collagen and glycosaminoglycans (GAG). Initiates formation of blood clot and forms lattice or matrix at bleeding site.

Vascular Damage

Platelets are activated and will be a part initial clot formation at the site of vascular damage.

Hemostasis Duration

Generally resolves in 6-8 hours - Highly vascular tissues bleed more and for a longer duration

Inflammation Phase Duration

Begins at the time of injury and commonly persists up to 10 days, may last longer.

Vasoconstriction

Decreases blood loss and collects inflammatory cells and initial chemical mediators, decreases the surface area for initial clot formation if vessels are disrupted.

Vasodilation

Provides increased oxygen and nutrients for cell function; allows delivery of inflammatory cells and chemical mediators (increase in vessel permeability occurs as well).

Red Blood Cells (Cellular Reaction)

Provide oxygen and nutrients

Platelets (Cellular Reaction)

Stimulate inflammation and activate leukocytes

Leukocytes

Fight infection

Macrophages

Take up and kill microbial agents or dead cells by phagocytosis

White Blood Cells

Remove and eliminate, kill and engulf microbial agents and degrade necrotic tissue

Neutrophils

Bacteria and fungi

Macrophages - Inflammatory Stage

Arrive at injury site and release Death cytokines that trigger cell death (apoptosis) of the other WBCs, perform phagocytosis on damaged tissue and apoptotic WBC, digestion of cell debris prevents chronic inflammation and fibrosis

Macrophages - Transition from Inflammatory to Proliferative Stage

After phagocytosis of tissue debris, Macrophages switch phenotype and release anti-inflammatory mediator(s) that suppress previously secreted pro-inflammatory signals

Redness and heat from inflammtion

Vasodilation increases blood flow to area, local delivery of chemical mediators trigger inflammatory response

Edema

Vasodilation and increased capillary permeability along with leakage of intravascular fluid

Loss of Function

Due to either simple loss of mobility due to either edema or pain or replacement of the cells with scar tissue

Vasoconstriction - Mediators of Inflammation

Thromboxane A2 synthesized in platelets that also stimulates platelet aggregation

Platelet Activation - Mediators of Inflammation

Platelet Activating Factor (PAF) facilitates platelet activation. Produced in platelets, neutrophils, mast cells, endothelial cells, monocytes, macrophages, basophils, etc

Intrinsic Clotting

Damage to the blood vessel

Extrinsic Clotting

Damage to tissue outside the vessel tissue thromboplastin (enzyme) found in tissue cells and platelets

Vasodilation - Mediators of Inflammation

Prostaglandins are autacoids (locally produced hormones) produced in virtually every cell of the body including platelets and leukocytes. Histamine is a vasoactive amine. Serotonin is a vasoactive amine, and Bradykinin is a peptide.

Increased Vascular Permeability - Mediators of Inflammation

Histamine, Serotonin, C3a and C5a, Bradykinin, Leukotrienes C4, D4, E4, and PAF

Chemotaxis and Leukocyte Activation

C5a, Leukotrienes B4, PAF, Cytokines (IL-8, TNF-α)

Pain

Prostaglandins, Bradykinin, Histamine, Serotonin, Tissue damage, and Swelling

Fever

Cytokines (IL-1, IL-6, TNF) and Prostaglandins

Acute Inflammation

Inflammation is an immediate, adaptive response specificity caused different kinds of noxious stimuli, such as infection and tissue damage

Cardinal signs of Acute Inflammation

Redness (rubor), heat (calor), swelling (tumor), pain (dolor), and loss of function (functio laesa)

Chronic inflammation - Etiology

Failure of eliminating the agent causing an acute inflammation such as infectious organisms that can resist host defenses and remain in the tissue for an extended period

Chronic Inflammation - Signs and Symptoms

Body pain, arthralgia, myalgia, Chronic fatigue and insomnia, Depression, anxiety and mood disorders, Gastrointestinal complications like constipation, diarrhea, and acid reflux, Weight gain or weight loss, Frequent infections

Inflamed Wound Characteristics

Serous, serosanguinous exudate with no odor that decreases with time and present erythema and edema that decreases with time with no induration and temperature decreases with time

Infected Wound Characteristics

Purulent, seropurulent exudate with possible odor that increases over time with present erythema that does not resolve or increases over time, present edema does not resolve or increases over time, induration can develop, and temperature does not resolve and may increase over time

Proliferation

Distinguished by proliferation of fibroblast, production of ECM, and cell regeneration, laying down of collagen and ECM

ECM Prodution during Proliferation

Fibroblasts produce large amounts of ECM composed of 30% type III collagen, then type I

Angiogenesis

Vascular remodeling and neovascularization

Collagen Deposition

Collagen fibers, elastic fibers, glycosaminoglycans, proteoglycans, etc

Tissue Contraction

Mainly piloted by myofibroblasts

Tissue Regeneration

Cells in GI tract are continuously dividing, epidermal cells are actively divided in skin

Remodeling

Early collagen fibrils are cleaved and degraded, newly deposited collagen increases in thickness, organization and tensile strength

Ligament Remodeling timeline

Ligament Matrix strength at one week is 3% of normal tissue comprised of 30% Type III Collagen

tissue Approximation

The ability to closely approximate uninjured tissue is dependent upon size, depth, location and type of injury, type of tissue, the patient's nutritional status and overall health,reorganization/functional remodeling of tissues requires physiologic movement

PT Implications

Early in the inflammatory and proliferation phases and continue through the remodeling phase based on tissue type in injury

Normal Tissue Organization

Interventions for function and mobility and load tissue with function in mind

Innate Immunity

Nonspecific or natural immunity; first-line defenses without memory.

Exterior Defenses

Skin, mucosa, secretions, nasal hair, and ear wax.

Cellular Defenses (Leukocytes)

Neutrophils, eosinophils, basophils, mast cells, monocytes/macrophages, cytokines, interferons, complement, and natural killer cells.

External Immune Defenses

Limit the ability of an organism to penetrate the body.

Physical Barriers

Skin and Mucus.

Mechanical Barrier

Peristalsis, coughing and sneezing.

Chemical Barrier

Hydrochloric acid, cerumen, tears and saliva.

Adaptive Immunity

Immunity that recognizes threats, promotes an immune response, destroys/removes invading pathogens, and establishes long-term memory.