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72 Cards in this Set
- Front
- Back
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- send messages from one leukocyte to another to enhance inflammation
- produced in response to antigen stimulation or by products of inflammation |
Interleukins
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affect neighboring host cells and help them talk to one another (inflammation)
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Cytokines
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biochemical mediators produced by T cells
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Lymphokines
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- prevents viruses from infecting healthy cells
- has no effect on cells already infected |
Interferon
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- after cell injury, arterioles in the area briefly undergo vasoconstriction
- vessels dilate after the release of histamine and other chemicals by the injured cells |
Vasular Response of Inflammation
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- endothelial cell retraction
- increased capillary permeability - movement of fluid from capillaries into tissue spaces |
Vasodilation
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pulls leukocytes
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Chemotaxis
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-chemotaxis
- directional migration of WBCs along concentration gradient of chemotactic factors - mechanism for accumulating neutrophils and monocytes at site of injury |
Cellular Response of Inflammation
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the engulfment and destruction of microorganisms, dead cells and foreign particles
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Phagocytosis
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What are the 2 main classes of leukocytes that carry out inflammatory processes?
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Granulocytes and Monocytes/Macrophages
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3 types of Granulocytes
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Neutrophils
Eosinophils Basophils |
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immature form of phagocytes in the blood
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monocytes
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mature phagocytes in the tissues
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Macrophages
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- 1st leukocytes to arrive(6-12 hours)
-phagocytize bacteria, other foreign material and damaged cells -short life span -die and are removed as pus |
Neutrophils
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What is pus composed of?
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dead neutrophils
digested bacteria other cell debris |
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-2nd type of phagocytic cells
- attracted to site by chemotactic factors - arrive within 3-7 days after the onset of inflammation |
Monocytes
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largest blood cells
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monocytes
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transform when they enter the tissue spaces
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monocytes
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important in cleaning the area before healing can occur
long life span can multiply may stay in damaged tissue for weeks |
Macrophage
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released in large quantities during an allergic reaction
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Eosinophils
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release chemicals that act to control the effects of histamine and serotonin
- phagocytosis of allergen-antibody complex - act directly against parasites by dissolving their surface membranes |
Eosinophils
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similar to mast cells, but found in blood instead of tissues
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basophils
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carry histamine and heparin in their granules which they release during inflammation
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basophils
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What are the local manifestations of acute inflammation?
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swelling-as exudate accumulate
pain- pressue from swelling & ppresence of mediators heat and redness- from vasodilation and increased perfusion |
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fluid and leukocytes that move from the circulation to the site of injury to facilitate tissue repair and healing
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exudate
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3 functions of exudate
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1- dilute toxins produced by bacteria and dying cells
2- carry plasma proteins (antibodies and leukocytes) to the site 3- carry away toxins, dead cells and debris-occurs via channels through the epithelium(sinuses) or through lymph nodes(stimulating B and T cells) |
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watery, indicates early or mild inflammation, contains very few plasma proteins or leukocytes
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serous exudate
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fluid in a blister is an example of this type of exudate
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serous
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thick and clotted, indicates more severe or advanced inflammation
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fibrinous exudate
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lungs in patients with pneumonia are an example of this type of exudate
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fibrinous
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consists of pus, large # of leukocytes, indicates persistent bacterial infection (cyst or abscess)
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Purulent exudate
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bloody exudate
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hemorrhagic exudate
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clinical manifestations of systemic response of inflammation
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-leukocytosis
-fever - increase in circulating proteins |
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-induced by IL-1 released from neutrophils and macrophages
-endogenous pyrogen acts directly on the hypothalamus |
Fever
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the replacement of destroyed tissue with scar tissue
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repair
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the cleanup of a lesion
(dissolution of fibrin clots by fibrinolytic enzymes) - begins with phagocytosis |
Debridement
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granulation tissue, epithelialization- occurs within 3 days to 2 weeks
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reconstructive phase
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continued scar formation and remodeling
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Maturation phase
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raised scar that extends beyond the orginial boundaries of the wound
(caused by excessive production of collagen) |
Keloid scar
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decreased blood volume
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hypovolemia
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essential for healing
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protein, iron and calcium
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Factors that cause impaired wound healing in the elderly
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-chronic illness(diabetes)
- immobility - age related skin changes - medications -decreased immune system |
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immune response exaggerated against environmental antigens
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allergy
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immune response is misdirected against host's own cells- body against self
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autoimmunity
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immune response directed against beneficial foreign tissues(transplants or transfusions)
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alloimmunity
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immune response insufficient for protection due to a disease or drugs such as chemo
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immune deficiency
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pathologic immune response to an antigen after reexposure (immediate or delayed)
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hypersensitivity
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antibodies against self antigens
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auto-antibodies
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occurs in susceptible persons who are highly sensitized to specific allergens
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Type I reaction (IgE mediated reaction)
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most potent mediator
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histamine
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most rapid and severe hypersensitivity reaction
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anaphylaxis
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individuals prone to allergies, produce higher concentrations of IgE (often genetically linked)
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Atopic individuals
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localized release of histamine causing areas of edema, wheal and flare reaction and itching
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Urticaria
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maternal immune system becomes sensitized against antigens expressed by the fetus
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transient neonatal diseases
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number one cause of death worldwide
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infectious diseases
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greatly enhances the probability of graft acceptance
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HLA matching
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transplant rejection or transfusion reaction
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alloimmunity
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most classic autoimmune diseases
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Endocrine- Thyroiditis and Grave's disease
Hematologic system- hemolytic and pernicious anemias Nervous- myasthenia gravis Musculoskeletal- rheumatoid arthritis |
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most common auto immune disorder
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Systemic Lupus Erythematosus
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hallmark of infectious disease
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fever
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-induce primary and secondary immune responses
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vaccines
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reasons for antibiotic resistance
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-over use of antibiotics
- non-compliance |
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tinea and yeast
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fungal infections
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take over host cells and use them for their own survival and replication (common cold, cold sores-herpes simplex)
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Viral
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septicemia
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bacterial infection
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occurs when an immunodeficient patient is transfused or transplanted with immunocompentent cells
- 7-30 days after transplant - little can be done after reaction starts |
Graft V. Host disease
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a virus that infects cells by inserting RNA into the cell
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retrovirus
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Stages of Selye theory
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1- alarm
2- adaptive or resistance phase 3- exhaustion phase |
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when the stressor triggers activation of the pituitary gland and the sympathetic nervous system
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Alarm phase of Selye
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begins with the actions of the cortisol and the catecholamines
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resistance or adaptation phase of selye
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occurs if stress continues and adaptation is not achieved.
-impaired immune response, heart failure, kidney failure or death |
exhaustion phase of selye
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examples of catecholamines
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epinephrine and norepinephrine
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