Exam 2 Flashcards
Cardinal signs of inflammation
Erythema (redness), Edema (swelling), heat, pain, loss of function
Local edema
effective host defense: leukocytes recruitment, bacterial containment, bacterial killing, limited damage to host tissues
systemic edema
Organ injury: hypotension, acute lung injury, acute kidney injury, DIC (Dissemination intravascular coagulation), death
Chronic inflammation
result of prolonged stimulus, destructive, fibrous tissue proliferation (impacts function, body thinks its helping)
tissue repair
vascular endothelial cells (form new blood vessels), myofibroblasts (shrink and contract the wound site) and fibroblasts (produces collagen) proliferate within the wound
Fibronectin
early protein to promote formation of scaffolding to provide tensile strength and “glue” to hold extracellular matrix substances and cells together.
Collagen
most important fibrous protein for structural and tensile strength, glue producer
Type I collagen
the main component of mature scars and also predominant in strong tissues such as tendons and bones
Type II collagen
assembled into thin supporting filaments and predominant collagen type found in cartilaginous tissue
Type III collagen
prevalent in newborns & early scar formation that is progressively remodeled into Type I with cross links to provide greater strength to scar tissue
Type IV collagen
not assembled into fibers, form basement membrane to which epithelial, endothelial, & mesenchymal cells are anchored
Tissue contractures
normal process that contributes to approximation of wound edges, excessive shrinkage results in contractures
Remodeling Phase
remodeling or maturation phase may be initiated as early as 14 days post injury, relatively slow process in connective tissues and may last up to a year or more, shift from type III to type I
Inflammation
protective response to injury, process in which liquid, chemicals, and cells are brought into an injured area to remove stimuli, cellular debris, and initiate the healing process. If prolonged, damage/death to healthy tissue
Contusion
muscle is subject to a sudden, heavy compressive force
Strain
excessive tensile forces lead to overstraining of the myofibers most commonly at the myotendinous junction
lethal injury
regeneration only if basement membrane is intact
Excessive scar tissue
mechanical barrier for muscle fiber regrowth
muscle regeneration (after transection)
muscle fibers regenerate by growth from undamaged stumps or by growth of new independent fibers
muscle regeneration (contused or strained muscle)
capable of self-repair, process is slow and often incomplete. Results in loss of strength and high rate of reinjury
Muscle remodeling
14 days post injury, regenerating myofibers and maturation of new myofibers, revascularization
Tendon and Ligaments
78% water, 20% collagen, 2% glycosaminoglycans (proteins), sustain high unidirectional tensile loads, transfer forces, provide flexible support. Greatest risk when forces are rapid and oblique, presence of degenerative changes. Thicker tendon = greater tensile strength
Inflammation & Proliferation of tendons and ligaments
Hemostasis (clot formation), proliferation begins 2-3 weeks after injury
Maturation and remodeling of tendons and ligaments
begins around week 3 after the initial injury, type III collagen is replaced with type I collagen, fibers realign with tensile forces
Natural and remodeling of tendons and ligaments timeline
Healing lasts 12-16 weeks to manage basic stressors, 24 weeks strength is 40% to 60% of healthy tendon, 40 to 50 weeks to gain normal strength.
Ligament injuries
grade 1 is stretching and small tears, grade 2 is a larger tear, grade 3 is a complete rupture. Ligaments have poor healing response
Healing of bone phases
- Hematoma formation
- fibrocartilaginous callus formation
- Bony callus formation
- Bone remodeling
Bone inflammatory stage
bleeding occurs resulting in hematoma formation
Bone reparative stage
begins next few weeks after Injury, repair lasts between 6-12 weeks, osteoclasts (bone macrophages), osteoblasts (produce bone matrix). poor nutrition, smoking, and immobilization can delay healing time.
bone remodeling phase
begins once union has occurred, no movement. Ends when bone returns to normal
Rehab of repaired soft tissue (tendon or muscle rupture)
During the proliferation phase (usually 5 to 28 days after tendon injury/repair), controlled passive movement is allowed
4-8 weeks after injury/repair active range of motion is initiated with controlled movements
at 8 weeks, resistance with weights, rubber tubing, elastic bands can begin
at the end of 12 weeks, if there has been no complications, full force muscle contraction can be tolerated
Rehab of repaired soft tissue (muscle strain)
As soon as pain and swelling subside, a program can be initiated to recover range of motion, strength, and endurance
return to sports is considered safe when there is an 80% return of strength compared to noninvolved side.
Phases of an immune response
- Recognition (immune system recognizes an intruder)
- Amplification (complement cascades, production of soluble factors, recruitment of WBC “army”)
- Effector phase (Removal of antigens by various means)
- Termination phase (The immune system stands down)
- Memory (generation of long-lived T- & B-lymphocytes)
Innate Immunity
organs, tissues, and cells of the immune system that you are born with, first line of defense, managing most threats. Non-specific (does not recognize one pathogen form another) non adaptive (does not remember encounter)
Acquired immunity
immunity that develops during your lifetime
Active immunity
develops in response to an infection or vaccination
Passive immunity
develops after you receive antibodies from someone or somewhere else
Natural active immunity
antibodies developed in response to an infection
Artificial active immunity
antibodies developed in response to a vaccination
Natural passive immunity
Antibodies received from mother through breast milk
Artificial passive immunity
antibodies received from a medicine, ex: from a gamma globulin injection or infusion
complement system
biochemical network of more than 30 plasma proteins
5 major types of leukocytes
Neutrophils, eosinophils, basophils, monocytes & lymphocytes (pacman of the body)
Neutrophils, eosinophils, and basophils are the first line of defense
Neutrophils
1st to arrive at site of infection & significantly increase in number during a response, attract monocytes. They die following phagocytosis = pus
Monocytes
clean up debris and kill any remaining damaged or large bacteria
Eosinophils
derived from bone marrow, respond during allergic reactions or when organisms are too large for neutrophils & macrophages (like parasites)
Basophils and mast cells
circulate close to blood vessels, important in allergic response
Lymphocytes
Circulate in tissues, peripheral blood and lymphatic system, respond to viral infections. Three major types are natural killer cells, B cells, T cells
Dendritic cells
messenger between innate and adaptive immune system
Adaptive Immunity
specific, recognizes threat, promotes effective response, destroys threat & establishes memory
B-cells
Arise & mature in bone marrow, fight bacteria and viruses by making Y-shaped proteins - antibodies
Antibodies
Presented to T-cell, are pathogen specific, & mark a cell for destruction
T-cells
Originate in bone marrow, travel to thymus for maturation
4 types of T-cells
Helper T cells, killer T cells, memory T cells, Regulator/supressor T cells
Antibodies/Immunoglobulins IgA
found in mucous, saliva, tears, and breast milk. Protects against pathogens
Antibodies/Immunoglobulins IgD
part of the B cell receptor. activates basophils and mast cells
Antibodies/Immunoglobulins IgE
Protects against parasitic worms. Responsible for allergic reactions
Antibodies/Immunoglobulins IgG
Secreted by plasma cells in the blood. able to cross the placenta into the fetus
Antibodies/Immunoglobulins IgM
may be attracted to the surface of a B cell or secreted into the blood. Responsible for early stages of immunity
Steps to acquired immunity
Precursor: Phagocytosis of pathogen by monocytes
A: T cells and B cells released
B: Helper T cells promote B cells to make antibodies
C: Plasma cell produced by the B cell forms and releases antibodies
D: Memory B cells lay in wait for next attack
Factors that alter immune system
Aging, medications, nutrition, environmental pollution, exposure to toxic chemicals, trauma, burns, sleep disturbance/stress, presence concurrent illness/disease, splenectomy
Factors that increase exposure to pathogens
Urinary catheters
Nasogastric tubes
Endotracheal tubes
Chest tubes
PICC line
External fixation devices
Implanted prostheses
Iatrogenic factors
Social & sexual practices
Aging - Changes to innate immunity
exterior defenses are affected by thinning of the skin, phagocytes decrease function with age, eosinophils accumulate in fewer sites of infection with age, basophils have reduced degranulation with aging
Aging - Changes to acquired immunity
Difficulty mounting protective immune responses to newly encountered antigens, such as coronavirus. Such responses depend on naive T and B cells, and aging is associated with a decline in their production.
Moderate exercise, resistance training, and long lasting endurance can…
Induce pro inflammatory reactions
Brisk exercise can…
increase the WBC count in proportion to the effort
Lymphocytes increase during exercise but…
decrease below the normal levels for several hours after intense exercise
Strenuous/High intensity exercise can…
suppress immune function & damage tissues inducing acute-phase responses in humans
Immunodeficiency
immune response is absent or depressed
primary immunodeficiency diseases
congenital (from birth), rare genetic diseases
secondary immunodeficiency diseases
acquired, result from an underlying disease or factor that depresses the immune response, most prevalent
severe combined immunodeficiency (SCID)
defect of lymphoid stem cells, nearly absent immune system
Isolated deficiency of IgA
most common, 1: 700, often asymptomatic, may have intestinal infections
Human Immunodeficiency Virus Diseases (HIV)
infection of the immune system, resulting in progressive & ultimately profound immune suppression. Acquired immune deficiency syndrome (AIDS) is advanced HIV
Incidence of HIV/AIDS
1 in 5 are unaware, greater among racial and ethnic minority groups. In US, most are diagnosed with AIDS 20 to 49
Transmission of HIV/AIDS
transfer of body fluids containing infected cells, high risk behaviors, unprotected sex, non sterile needles
Pathogenesis of HIV/AIDS
Replication of the virus leads to cell death, although the person remains asymptomatic.
Symptomatic HIV begins when virus enters blood to affect remaining lymphocytes.
Clinical Presentation of HIV stage 1
Stage 1: Acute infection, flu-like symptoms, 1 to 6 weeks after exposure
Clinical Presentation of HIV stage 2
Stage 2: Asymptomatic infection, Positive antibody test, fatigue and lymphadenopathy
Clinical Presentation of HIV stage 3
Stage 3: Symptomatic HIV, immune system is compromised, lymphadenopathy and generalized symptoms
Clinical Presentation of HIV stage 4
Stage 4: Advanced HIV, neurological involement, dementia, skin conditions
Distal sensory polyneuropathy
most common, seen in advanced HIV due to damaging effects, affects feet and legs initially.
Athletes Foot
Tinea Pedis, fungal infection
Kaposi Sarcoma
cancerous patches of abnormal tissue under the skin
HIV treatment
highly active antiretroviral therapy (HAART), decreases amount of virus in blood to very low and even undetectable levels. lifelong therapy is needed.
Prognosis of HIV
HAART drug combinations have decreased mortality rates by more than 80%, 9 out of 10 people with AIDS can expect to live at least 10 years after infection. Improves survival rate but results in metabolic effects.
Physical Therapy and HIV
management of neurological involvement to optimize functional ability, strength training, joint and soft tissue mobilization or stretching, gait/balance training
Exercise and HIV/AIDS early stages
exercise is considered safe for people with HIV, encourage people to exercise both aerobic and resistance components
Exercise and HIV/AIDS advanced stages
strenuous exercise training is not recommended, 20 minutes of aerobic exercise 3 to 4x per week may lead to cardiopulmonary fitness and improved psychology status. Longer rest periods
