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124 Cards in this Set
- Front
- Back
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Functions of Defense Mechanisms |
- protection from pathogens: Microbes, parasites, exogenous cells & molecules - removal of dead/damaged cells - removal of abnormal cells (self, nonself) |
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First line of defense |
- non-specific - mechanical barrier: unbroken skin and mucous membranes - biochemical barriers: exocrine secretions such as tears and gastric juices, normal flora on surfaces (symbiotic relationships) - no memory created |
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Second line of defense |
- non-specific - phagocytosis (WBC) - eat stuff in CT damaging you - inflammation - immediate - no memory created |
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Third line of defense (immune response) |
- specific defense - production of specific antibodies or cell-mediated immunity - delayed response - memory created |
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Inflammation:2nd line of defense |
- protective, coordinated response of the body to an injurious agent - intensity of the inflammatory reaction is usually proportional to the extent of tissue injury (in healthy individual) |
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Goals of inflammation |
- wall-off the area of injury - prevent spread of the injurious agent - bring the body's defenses to the region under attack - inflammation increases if response isn't balanced |
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Cardinal Signs and Symptoms of Inflammation |
- Rubor (redness) - blood flow to site of inflammation - Tumor (swelling) - Calor (heat) = energy - Loss of function - symptom - Dolor (pain) - pressure on your sensory neurons tell CNS to take care of it = promotes healing |
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Tumor (swelling) |
Edema, ↓Blood flow out of area by building up pressure that squeeze off capillary bed |
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Acute Inflammation |
Occurs rapidly in reaction to cell injury - rids the body of the offending agent - enhances healing - terminates after a short period (hours/few days) |
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Chronic Inflammation |
Inflammatory reaction persists - weeks to months - inhibits healing - causes continual cellular damage and organ dysfunction - One of the #1 causes of heart attacks - Reasons: autoimmune disease, don't get rid of damage (acute inflammation doesn't work) |
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Local Effects of Inflammation: Functions of Acute Inflammation |
1) Limit tissue damage: dilute toxins 2) Prevent infection: destroy pathogens 3) Initiate adaptive response (3rd tier): macrophages & lymphocytes to area 4) Initiate healing: removal of dead/damaged cells (Phase 2 promotes and affects phase 1) |
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3 Main Stages of Acute Inflammatory Reaction |
1) Vascular permeability: formation of exudate 2) Cellular Chemotaxis 3) Systemic Responses |
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Cellular Chemotaxis |
Large numbers of WBCs move into damaged space - release many different chemicals from cells that bring more WBC to area of inflammation and promote inflammatory response - capable of changing blood flow |
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Systemic Responses |
- Fever - Malaise - Fatigue (using energy for inflammatory response) - Headache (edema pressure on brain) - Loss of appetite (body doesn't want to expend energy digesting food) |
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Vascular Permeability Stage: Inflammatory Mediators |
- Histamine, bradykinin - enable the blood vessels to dilate and become more permeable - permeability change permits fluids, WBCs and platelets to travel out of BV to the site of injury or infection - Vasodilation of the arterioles is followed by enhanced capillary permeability |
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Enhanced permeability allows... |
...fluid to flow out of the blood vessels to the injured tissues - more blood into capillary beds = ↑ BP = enhances movement of stuff from vessels into tissues |
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Process of Changing Vascular Permeability |
- Formation of Exudate: Ultimate goal 1: Arterioles constrict in response to damage 2: Arterioles dilate 3: Formation of transudate shifts to exudate 4: Stasis |
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Exudate |
Effusion if inflammation occuring in 3rd space |
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Arterioles constrict in response to damage: |
Transient vasospasm (very quick) metarterioles expand instantly = turbulence - quick contraction and relaxation |
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Arterioles Dilate: |
Hyperemia: Increased blood flow |
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Formation of transudate shifts to exudate: |
- capillary endothelium changes permeability - WBC infiltration: for phagocytosis - Swelling (edema) and pain (↑transudate) |
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Stasis: |
Stoping of blood flow |
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Capillary Endothelial + histamine → |
Change shape of cells = more space in between = WBC can get through without damage |
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Benefits of Exudate Formation |
- dilution of toxins - increased pain - antibodies(made by B lymph); proteins - proteins that amplify the response (can shut down when needed) |
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Transudate |
Fluid that contains little protein and is mainly a watery filtrate of blood - fluid found in body tissues - fluid in blister - fluid in edema without infection |
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Purulent Exudate |
Fluid that is rich in protein from WBCs, microbial organisms, and cellular debris - also called pus |
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Empyema |
Pleural effusion - triggered ARDS |
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ARDS |
Acute Respiratory Distress Syndrome - inflammatory response in lungs happen so fast, capillary beds dissolve = blood into pleural space = coagulated = blood clot = lungs can't inflate/deflate |
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Cellular Chemotaxis |
Using chemicals to pull things to an area - during the cellular phase of inflammation, a chemical signal from microbial agents, endothelial cells, and WBCs attracts platelets and other WBCs to the site of injury - WBCs release inflammatory mediators that amplify the inflammatory process; some attract more WBCs to the area of injury, and others dampen the inflammatory process |
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Mast Cells |
- found in loose connective tissue near body surfaces (below basement membrane) - filled with histamine granules, sit and wait →tissue damage→signal to release at once |
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Mast Cells release chemicals via: |
1 - degranulation: released all granules at once, chemotaxic agent 2 - synthesis of mediators |
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Degranulation |
Immediate response - rapid release of histamine: vasodilation → hyperemia and increased capillary permeability: fluid dilutes toxins, allows globulins and other proteins to travel to injury site - other chemotactic chemicals |
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Other chemotactic chemicals that are released during degranulation |
- diffuse away from injury site, forming a chemotactic gradient - attract neutrophils to area Leukotrienes, prostaglandins, PAF |
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Synthesis of mediator chemicals |
Delayed response - leukotrienes: vasodilation, ↑ permeability, chemotaxis - WBC get pulled towards it (enhance chemotaxis |
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Prostaglandins |
vasodilation, ↑ permeability, pain (ache) - sensitize nerve endings |
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Platelet-activating factor (PAF) |
- activates platelets for hemostasis - form blood clots to stop bleeding |
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3 Separate Plasma Protein Systems |
1 - Clotting system: shut down inflammatory response when needed 2 - Complement System: ramp up inflammation/immune response 3 - Kinin System: enhance pain and inflammation |
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All systems involve the... |
activation of inactive proteins in a cascade |
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Cascade |
sequential activation of chemicals using chemical reactions |
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Clotting Cascade Functions |
- stop bleeding (hemostasis) - trap pathogens: barrier, stop pathogens from entering blood vessels (scab) - repair and healing |
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Scab |
Dried out blood clot to promote healing underneath (dehydrate) |
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Clotting Cascade # of steps |
12 steps |
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Basics of clotting cascade |
- prothrombin → Thrombin → Thrombin acts to convert fibrinogen → Fibrin → Fibrin forms a net to trap RBCs and activated platelets (cells secreting PAF at same time = makes platelets sticky and stick to fibrin nets |
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Prothrombin |
circulating in bloodstream - convert through chemical reaction/enzymes |
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Fibrin |
sticky, long protein (fiber) - stick to each other and stick/adhere to ragged edges of blood vessel endothelium |
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Blood Clotting |
Positive feedback that enhances blood clotting until shut down blood flow |
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Occlusion in coronary artery |
- everything downstream is cut off from O2 = ischemia = infarction = death by MI |
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Occlusion evokes... |
clotting cascade = ↑ clot size until completely shut down blood flow |
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Embolism |
anything solid/big circulating in bloodstream that shouldn't be there - bone marrow pieces (broken bone) - broken off clot - tumor → metastasize |
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Pulmonary Embolism |
- Embolism from systemic → heart → lungs - blue line across chest or back |
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Emboli lodging commonly occur in |
- lungs - liver: hepatic portal system: emboli in digestive system - brain |
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Kinin System |
- Kinin System activates cells used in inflammation (damaged cells produce kinins) - produces bradykinin (found in bee stings) - potent vasodilator - increases capillary permeability - induces chemotaxis - stimulates pain sensations using sensory nerve endings |
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Why do pain levels differ? |
Pain interpretation happens in brain: |
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Fibromyalgia: |
defects in kinin (microinflammation) being released at insignificant times when not needed |
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Complement System |
Activated by fibrinolytic cascade(control system): take place to control size of blood clot - creates active proteins (chemicals) that complement (aid) the inflammatory response, and/or healing - Opsonins - Chemotactic factors - Anaphylatoxins - MAC |
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Opsonins |
warning sign = cause chemotaxis (attract WBC) - coat bacteria to aid phagocytosis (bind to receptors on foreign cells, red flags) |
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Chemotactic factors |
attract phagocytes |
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Anaphlatoxins |
- induce mast cell degranulation - anaphylaxis: appropriate sized |
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Membrane Attack Complex (MAC) |
- protein complex assembled, used to form pores in bacterial membranes - proteins instantly create/assembled into machine by chemicals in cells that can attack/punch holes in membranes of foreign cells - complements inflammation |
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Proteins that form MAC complex, triggered by... |
foreign antigen (epitope) |
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Epitope |
tiny spot that is most identifiable piece - highly reactive to distinguishA self from nonself |
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Antigen used for... |
identifiable purposes |
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Inflammation/complement system activated by: |
- foreign epitope |
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Opsonization |
Opsonins are present in exudate - chemicals that bind antigenic substances: antibodies, C reactive proteins, Collectins(proteins that bind to bacterial cell walls) - Enhance WBC attraction and binding - aid in phagocytosis |
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Cytokines |
Some of the inflammatory mediators released by WBCs are referred to as cytokines
Examples: Tumor Necrosis Factor (TNF-alpha) and interleukins (ILs), interferons: redirect growth for new blood vessels - amplify or deactivate inflammation |
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Interleukins |
- enhance or supress inflammation - chemotaxis - proliferation and maturation of WBCs - produce fever - enhance acquired immunity (creation of B cells stuff) |
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Interferons |
- anti-viral activity - go after your cells (self) but screwed up because it has a virus infection - MHC - interferons recognize MHC and amp up immune system to destroy cell |
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MHC |
Major Histocompatibility Complex - virus leaves remnant on surface of cell it is infecting |
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Inflammation: Cellular Component - Goal |
leukocyte immigration out of vessels - Vasospasm sets it off, chemotactic factors keeps it going |
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3 steps of Inflammation: Cellular Component |
1 - Margination 3 - Transmigration |
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Margination |
A change in normal axial blood flow (vasospasm) |
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Pavementing |
- WBCs have receptors for chemicals released and on damaged endothelial cells (receptors activated by complement, clotting, etc due to damage) - They move to the edges of vessels and "pavement" or stick to the sides |
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Transmigration |
WBCs migrate out of vessels (and basement membrane) and into tissues |
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Cellular Responders for acute inflammation |
- Neutrophils - Monocytes/macrophages - Eosinophils - Natural killer cells - Platelets |
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Antimicrobial proteins |
NETs constructed around area of tissue damage/pathogens |
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NETS |
Neutrophil Extracellular Traps |
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MRSA and NETs |
release chemical toxins so fast they disable neutrophils ability to make NETs |
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What can change pH in area of inflammation |
- functional group on highly reactive chemicals - enzymes dying - shift to the acidic side |
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Axial Blood Flow |
denser/solid portions (RBC, Platelets, WBC) are circulating through vessels in center |
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Vasospasm |
disrupt normal axial blood flow and create turbulence - WBCs move to outer edge |
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Reasons for change in cell type |
- neutrophils are most numerous but undergo apoptosis (pH) - macrophages can survive for long time - chemotactic agents change - delayed response (pulls macrophages in) - macrophages may be able to replicate, neutrophils can't |
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Mononucleosis |
Tons of monocytes in blood |
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Histaminase |
Enzyme that breaks down histamine - control vasoactivity, inflammation |
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What causes fever? |
All act as pyrogens - microbial organisms - bacterial products - cytokines |
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Pyrogens activate... |
prostaglandins to reset the hypothalamic temperature-regulating center in the brain to a higher level |
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Antipyretic Agent |
drug that brings down fever by inhibiting prostaglandin formation - block the effect of endogenous pyrogens (prostaglandins) - NSAIDS |
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Hypothalamus has no... |
astrocytes that form a BBB around it - therefore direct contact with hypothalamic neurons and blood (chemotactic agents in blood act upon hypothalamus and reset set points |
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Endogenous Pyrogens |
- reset set point - associated with your cells - prostaglandins |
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Exogenous pyrogens |
- toxins that cause reset of set points - ex: bacterial toxins, metabolic waists |
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Fever can reach levels high enough to cause... |
seizures and brain damage - temp to high = denature proteins/unravel to primary structure = permanent in body |
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It is recommended to keep fever below... |
102 F through the use of antipyretic medications such as aspirin, ibuprofen, or acetaminophen |
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Lymphadenopathy (Lymphadenitis) |
The enlargement of lymph nodes caused by inflammatory processes |
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Lymph Nodes |
small bean-sized masses of tissues located in various regions of the body including the neck, axillary region, central thoracic region, inguinal areas, and GI tract |
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During inflammatory responses, lymph nodes become... |
enlarged and tender - chemicals associated with inflammation and caused by pathogen → lymph nodes turn on, swell up, and begin to hurt/ache → turn on WBCs to fight pathogen |
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Acute Inflammation will result in one of 3 outcomes |
1 - complete resolution 2 - healing by connective tissue 3 - chronic, persistent inflammation that does not recede |
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Healing by connective tissue |
- take care of what caused tissue damage but can't completely heal tissue = develop scar tissue |
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Scar Tissue |
- not tissue/alive → masses of collagen densely packed - looks white |
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Sarcoidosis |
- autoimmune disease where fibroblasts out of control/highly active - fibrosis occurs in healthy tissues |
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Chronic Inflammation Causes: |
- follows acute inflammation if its cause is not eradicated - develops from chronic irritation |
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Chronic Inflammation Characteristics |
- less swelling and exudate - more lymphocytes, macrophages, fibroblasts - more tissue destruction - more collagen = more fibrous scarring - granuloma development may occur around area/foreign object |
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Granuloma |
An area where macrophages have aggregated and are transformed into epithelial-like cells - epithelioid cells are surrounded by lymphocytes, fibroblasts, and connective tissue - multinucleated giant cells and necrotic tissue may be present |
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Principle Components of Granuloma (walled off) |
- collagen fibers - multinucleated giant cell - epithelioid cell - macrophage - fibroblast - lymphocytes |
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Tuberculosis; Chronic Inflammation |
- lose functioning of lung tissue = caseous necrosis - crumbly bits = granulomas |
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The Cell Cycle |
G0 → G1 → G2 → S → M |
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G0 Phase |
Cells are resting or quiescent and not undergoing mitotic division |
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G1 Phase |
Cells enter the cell cycle during this stage, where they make preparations for mitosis and then continue on to the S phase |
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G2 Phase |
Cells continue to undergo necessary activities before mitosis |
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S Phase |
Cells undergo chromosomal (DNA) duplication in preparation for mitotic division |
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M Phase |
Cell completes mitosis and divides to regenerate itself |
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What cells give you brain tumors? |
Glial cells (oligodendrocytes, astrocytes, ependymal cells, Schwann cells, microglia, satellite cells) - Classified as epithelial |
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Adult "stem cells" can be stimulated to... |
regenerate permanent cells |
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3 Phases of wound healing |
1 - Inflammation 2 - Proliferation, granulation tissue formation, and epithelialization 3 - Wound contraction and remodeling |
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Wound contraction and remodeling |
Wound contraction = gets progressively smaller, heal edges → inward Remodeling = scar tissue structurally refined and reshaped by fibroblasts |
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Proliferation, Granulation tissue formation, and Epithelialization |
- fibroblasts and vascular endothelial cells form the granulation tissue → The granulation tissue then secrete growth factors and cytokines (EX: VEGF) - Epithelial cells also migrate and proliferate to form a new surface/fill in the gap between wound edges |
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Skin Wound Healing (less severe → more severe) |
- primary intention - secondary intention - tertiary intention |
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Angiogenesis |
The development of new blood vessels |
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Possible Complications of Wound Healing |
- Keloid - Contractures - Dehiscence - Evisceration - Stricture - Fistula - Adhesions |
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Keloid |
Hyperplasia of scar tissue - genetic predisposition |
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Contractures |
Inflexible shrinkage of wound tissue that pulls the edges toward the center of the wound |
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Dehiscence |
Opening of a wound's suture line |
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Evisceration |
Opening of a wound with extrusion of tissue and organs |
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Stricture |
An abnormal narrowing of a tubular body passage from the formation of scar tissue |
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Fistula |
An abnormal connection between two epithelium-lined organs or vessels (usually organs closely related to one another) - Ex: Common with childbirth at young age. Tissue damage repaired = forms so much scar tissue → create passageway between bladder and uterus |
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Adhesions |
Internal Scar tissue between tissues or organs - scarring on organ near wall of a cavity - Ex: Ovaries after C-section or laparoscopy |
