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257 Cards in this Set
- Front
- Back
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what are the 2 forms of the "first line of defense"?
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1) physical and mechanical barriers
2) biochemical barriers |
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what are the 5 ways that the body rids itself of bacteria in the first line of defense?
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sloughing off of cells
coughing and sneezing flushing vomiting mucus and cilia |
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what is the physical barrier (first line of defense?
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skin
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what are the 3 bichemical barriers in the 1st line of defense?
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1) synthesized and secreted saliva, tears, ear wax, sweat, and mucus
2) antimicrobial peptides 3) normal bacterial flora |
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what is the mechanical barrier (first line of defense)?
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linings of the gastroinstestinal, genitourinary, and respiratory tracts
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antimicrobial peptides
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proteins that secrete a substansce to help fight bacteria
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what is the second line of defense?
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inflammatory response
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what are the cardinal LOCAL manifestations of the inflammatory response?
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redness, heat, pain, swelling, loss of function
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what microscopic changes occur in the inflammatory response? (3)
when do they occur |
vascular response (bleeding)
increased vascular permeabiltiy WBC adherence within seconds |
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what 3 things are included in the vascular response of inflammation?
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1) blood vessel dilation
2) increased vascular permeability and leakage 3) white blood cell adherence to the inner walls of the vessels and migration through the vessels |
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what are the 4 goals of inflammation?
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1) limit and control the inflammatory process
2) prevent and limit infection and further damage 3) initiate adaptive immune response 4) initiate healing |
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Acute inflammation is a....
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rapid and nonspecific protective response to cellular injury
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Acute inflammation can only occur in
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vascularized tissue
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what are the macroscopic hallmarks of acute inflammation? (5)
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rendess, swelling, heat, pain, loss of function
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what are the microscopic hallmarks of acute inflammation?
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accumulation of fluid and cells
(contributes to swelling) |
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what are the vascular responses to injury or pathogen invastion? (5)
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vasodilation
vascular permeability (edema) cellular infiltration (pus) throbmosis (clots) stimulation of nerve endings (pain) |
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what initiates the inflammatory response?
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Mast cells
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what are mast cells?
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cellular bags of granules
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where are mast cells located?
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loose connective tissues close to blood vessels
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what does histamine do?
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causes temproary, rapid constriction of the large blood vessels and the dilation of the postcapillary venules
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H1
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proinflammatory hitamine receptor
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H2
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anti inflammatory histamine receptor
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wwere are H1 receptors?
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present in smooth muscle cells of the bronchi
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where are H2 receptors?
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on parietal cells of the stomach mucosa
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Neurtophils respond to....
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bacteria
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eosinophils respond to...
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allergic reaction, parasitic invasion
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what are the two chemotactic factors?
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neutrophil chemotactic factor
eosinophil chemotactic factor |
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leukotrienes and prostaglandins
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mimic histamine in later stages
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prostaglandins
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mimics histamine in the later stages and induces pain
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platelet-activating factor
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similar effect to leukotrienes and platelet activation
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all the hallmarks of inflammation are cause by...
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mast cell products
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what are the 3 plasma protein systems
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complement
coagulation kinin |
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what is essential to an effective inflammatory response?
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protein
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complement system can destroy ______ directly
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pathogens
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which plasma protein system activates or collaberates with every component of the inflammatory response?
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complement system
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what is the purpose of the soagulation ( clotting) protein system? (4)
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1) prevents spread of infection
2) keep MO and foreign bodies at site of greatest inflammatory cell activity 3)forms a clot that stops bleeding 4) provides a meshwork for repair and healing |
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what is the main substance of the coagulation system?
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fibrin
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what is the end result of the coagulation system?
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fibrin
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fibrin
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insoluble protein`
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what is essential to the blood clotting mechanism?
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calcium
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what is the end result of the clotting mechanism?
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fibrin
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what is the function of the kinin system?
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activate and assist inflammatory cells and pain response
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what is the primary kinin?
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bradykinin
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phagocytes are...
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large molecules
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phagocytes...
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engulf and destroy microorganisms
think pacman |
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neutrophils are...
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a type of phagocyte
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neutrophiles arrive at the inflammatory site within....
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6-12 hours of injury
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what do neutrophils do?
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injest bacteria, dead cells, and cellular debris
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after dying, neutrophils become part of the...
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purulent exudate
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monocytes and macrophages are both what kind of cell?
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WBC
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what 2 cells are characteristic of CHRONIC inflammation?
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monocytes and macrophages
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where are monocytes and macrophages produced?
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bone marrow
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when do monocytes and macrophages arrive at the inflammatory site?
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3-7 days after initial injury
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eosinophils control the vascular effects of what two things?
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serotonin and histimamine
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what do eosinophils do?
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help control vasodilation and dissolve surface membranes of parasites
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what are the 2 kinds of cytokines?
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interleukins and interferons
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what do cytokines do?
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govern effective inflammatory response
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what 3 things do interleukins do?
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1) alteration of adhesion molecule expresion on many types of cells
2) proliferation and maturation of leukocytes in the bone marrow 3) general enhancement or suppression of inflammation |
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what produces interluekins?
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macrophages and lymphocytes
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interleukins are...
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cytokines
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interferons are produced by
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macrophages, T cells and NK cells
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interferons defend the body against
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tumor cell growth and viruses, gram - bacteria
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interferons have no affect on...
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a cell that has been infected by a virus
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interferons are...
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cytokines
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what causes cytokines to arrive at a site?
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chemotaxis
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chemokines
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induce leukocyte chemotaxis
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what are the 5 local manifestations of inflammation?
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heat, redness, swelling, pain, loss of function
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what 2 local manifestations are caused by vasodiation?
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heat and redness
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what 2 local manifestations are caused by exudate?
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swelling and pain
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what are the 3 affects of exudates?
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1) dilute toxins produced by bacteria
2) carry plasma proteins and leukocytes to the site 3) carry away bacterial toxins, dead cells, debris and other products of inflammation |
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what does serous exudate indicate?
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early inflammation
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serous exudate
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watery exudate (blister)
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serosanguinous exudate
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watery exudate with a few red blood cells
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fibrinous exudate indicates...
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severe of more advanced inflammation
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what kind of exudate is walled off?
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fibrinous exudate and purulent/suppurative exudate
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fibrinous exudate
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thick, clotted
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purulent or suppurative exudate
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green/yellow coolor, has pus
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pus indicates...
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bacterial infection
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hemorrhagic exudate indicates....
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active bleeding
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hemorrahagic exudate
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contains multiple erythrocytes (blood)
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chronic inflammation occurs over an _____ length of time
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increased
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chronic inclammation lasts...
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weeks or longer, regardless of cause
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what are 4 causes of chronic inflammation?
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1) unsuccessful acute inflammatory response
2) not much of an acute response 3) high lipid content MO's 4)persistent irritation from chemicals, particulate matter, or physical agents |
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what could cause someone to have a poor acute response
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immunocompromised patients
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what are the characteristics of chronic inflammation?
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1) dense infiltration of lymphocytes and macrophages
2) walled off site forming a granuloma |
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resolution
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returning injured tissue to the original structure and function
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repair
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replacement of destroyed tissue with scar tissue
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scar tissue
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composed primarily of collagen to restore the tensile strength of the tissue
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bebridement
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cleaning up the dissolved clots, MO's, erythrocytes, and dead tissue cells
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healing consists of...(3)
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filling in the wound
epithelialization (sealing wound) contraction (shrinking wound) |
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epithelialization
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sealing the wound
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contraction
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shrinking the wound
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what is the 1st phase of healing?
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acute inflammatory response
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what is the second phase of healing?
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reconstruction
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recontruction
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development of granulation tissue
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fibroblasts
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synthesize and secretes collagen
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what is the most important cell during reconstruction?
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fibroblasts
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what is the 3rd phase of healing?
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maturation
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maturation
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scar tissue is remodeled and capillaries disappear
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collagen is
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avascular
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primary intention healing
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wounds that heal under condition of minimal tissue loss
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what is an ex of primary intention healing?
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surgical incisions
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secondary intention healing
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wounds that require a great deal more tissue replacement
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ex. of econdary intention healing
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open wound
burns, large surface wounds, infection decubitus (bed sores) |
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decubitus
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bed sores
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what must be removed before healing can occur?
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fibrin
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what can cause dysfunction during inflammatory response? (8)
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hemorrhage
fibrous adhesion infection excess scar formation wound sepsis hypovolemia hypoproteinemia anti-inflammatory steroids |
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what 3 things can cause dysnction during reconstructive phase?
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impaired collagen matrix assembly
impaired epithelialization impaired contraction |
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impaired collagen matrix assembly will cause....
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keloid scar
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impaired epithelialization can be caused by (3)
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anti-inflammatory steroids
hypoxemia nutritional deficiencies |
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the inflammatory phase occurs...
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at the onset of injury
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inflammatory phase constitutes what 2 stages of inflammation
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vascular and cellular
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reconstructive phase begins... lasts up to....
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3-4 days after injury and lasts up to 2 weeks
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main act in reconstructive phase
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fibroblasts synthesize/secretes collagen forming granulation tissue
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remodeling phase
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maturation phase
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proliferative phase
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recontructive phase
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maturation phase beings...lasts up to
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several weeks after injury, lasts up to 6 months-2 years
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main step in maturation phase?
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contraction of the wound and development of scar tissue
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allergy
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caused by environmental antigens
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autoimmunity
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self-antigens
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SLE
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systemic lupus erythematosus
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systemic lupus erythematosus
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chronic multisystem inflammatory disease
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SLE creates autoantibodies against: (7)
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nucleic acids, erythrocytes, coagulation proteins, phospholipids, lymphocytes, platelets,
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90% of SLE pateints show:
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arthralgias or arthritis
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70-80% of SLE pateints show:
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vasculitis and rash
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40-50% of SLE pateints show:
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Renal disease
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50% of SLE pateints show:
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hematologic changes
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30-50% of SLE pateints show:
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cardiovascular disease
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To be diagnosed with SLE you must present with:
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at least four of 11 common findings
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11 findings of SLE
FDPONSRNHIP Friends Don't Put On Nice Shoes Right Next to Homely, Impoverished People |
Facial rash
Discoid rash photosensitivity oral or nasopharyngeal ulcers nonerosive arthritis serositis renal disorder neurologic disorder hematologic disorders immunologic disorders presssence of antinuclear antibodies |
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AIDS is a syndrome caused by
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Human immunodeficiency Virus (HIV)
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AIDS depletes...
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the body's T helper cells
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HIV is a...
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retrovirus
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retrovirus
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genetic information is carried on RNA instad of DNA
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How does HIV infect cells?
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by binding to the surface of a traget cell through a receptor and inserting their RNA into the target cell
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what acts as the primary receptor for HIV?
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CD4
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CD4
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an antigen on the T helper Cell
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you can be diagnosed with HIV in 4 ways:
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serologically negative
serologically positive but asymptomatic early stages of HIV AIDS |
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what are you looking for in a test of HIV?
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antibodies against HIV
decreased number of Helper T cells |
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to be diagnosed with HIV your CD4 needs to be...
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<200
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normal CD4
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800-1000
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you may be dianosed with AIDS even if you have - serogology if...
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lymphoma of brain and younger than 60
lymphoid interstitial pneumonia <13 |
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If you have positive serology, AIDS diagnosis is made....
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in association to clinical symptoms
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window period
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period between infection and appearance of antibody
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window period for AIDS
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blood exposure- 4-7 weeks
sexual exposre-6-14 months |
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what causes agining in the skin?
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changes from genetic and evironmental factors
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capillary loops....
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chorten and decrease in number with aging
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# of melanocytes and langerhans cells _______ with age
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decrease
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pruritis
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itching
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what is the most common cymptom of primary skin disorders?
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pruritus
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what causes the itch sensation?
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specific unmyelinated nerve fibers triggered by itch mediators
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what cause pressure ulvers?
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pressure and shearing forces that occlude capillary blood flow with resultant ischemia and necrosis
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where are the areas of greatest risk for pressure ulcers?
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pressure points over bony prominences
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who are high risk individuals for pressure ulcers?
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immobilized with fractures and or neuroloical deficits
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what are the clinical manifestations of pressure ulcers?
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inflammatory response (pain, fever, leukocytosis) hyperemia
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large pressure ulcers run the risk of...
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toxicity and pain leading to loss of appetite, debility, and renal insufficiency
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what are the 4 stages of pressure ulcers
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1) nonblanchable erythema of intact skin
2) partial thickness skin loss involving epidermis or dermis 3) full-thickness skin loss involving damage or loss of subcutaneous tissue 4) full-thickness skin loss with damage to muscle, bone, or supporting structures |
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what is the most common inflammatory disorder of the skin
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eczema
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what causes eczema?
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endogenous and exogenous agents
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what are the 4 clinical manifestations of eczema?
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pruritus
lesions with indistinct borders epidermal changes thick, leathery, hyperpigmentation |
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psoriasis
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chronic, relapsing, proliferating skin disease
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what occurs in psoriasis
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thickening of both epidermis and dermis. scaly, erythematous pruritic plaques
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acne rosacea
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hypertrophy and inflammation of the sebaceous glands, dvelos middle third of the face
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Lupus erythematosus
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inflammatory lesions in sun-exposed areas with a butterfly distribution over the nose and cheeks
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erythema multiforme
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acute inflammation of skin and mucous membranes with lesions
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erythema multiforme is often associated with....
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allergic reactions
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what are the 2 types of erythema multiforme?
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stevens-johnson syndrome
toxic epidermal necrolysis (TEN) |
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Folliculitis
|
bacterial infection of the hair follicle
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furuncles
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infection of hair folicle that extends to the surrounding tissue
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carbuncles
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collection of infected hair follicles that forms a draining abscess
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cellulitis
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diffuse infection of the dermis and subcutaneous tissue
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erysipelas
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superficial streptococcal infection of skin
commonly on face, ears, and lower legs |
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impetigo
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bullous or ulcerative lesions caused by staph or strept
|
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HSV 1
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causes cold sores, can affect cornea, mouth, labia
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HSV 2
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genital lesions; usually spread by sexual contact
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Herpes Zoster (shingles)
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cuased by varicella zoster virus
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Warts
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benign, rough, elevated lesions caused by papillomavirus
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condylomata acuminata
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venereal warts (genital warts)
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urticari
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wheals, hives welts
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urticari is associate with...
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Type I hypersensitivity reactions to drugs, systemic diseases, or physical agents
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scleroderma
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sclerosis of the skin
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scleroderma is more common in.....
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women
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seborrheic keratosis
|
benign proliferation of basal cells
|
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what does seborrheic keratosis look like?
|
smooth or warty in appearance, tan to waxy yellow, flwesh-colored, dark-brown; oval and greasy
|
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keratoacanthoma
|
benign, self-limiting; arises from hair follicles
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deratoacanthoma looks like...
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dome shaped, crusty lesion filled with keratin on face, back of hands, forearms, neck and legs
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actinic keratosis
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premalignant lesion found on skin surface exposed to UV radiation
|
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actinic keratosis looks like...
|
pgmented patch of ouch, adherent scale
|
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Nevi
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pigmented or non-pigmented lesions that form from melanocytes beginning at age 3 to 5
pre malignant |
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basal cell carcinoma originates in what 3 places?
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interfollicular basal cells
hair follicles sebaceous glands |
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what is the most common human cancer
|
basal cell carcinoma
|
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|
what is the most common skin cancer
|
basal cell carcinoma
|
|
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what does basal cell carcinoma look like?
|
depressed centers and rolled borders
grow by direct extension gernerally doesn't invade blood or lymph |
|
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squamous cell carcinoma
|
tumor of epidermis either localized (in situ) or invasive lesions
|
|
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squamous cell carcinoma looks like
|
firm, red, scaling, keratotic, slightly elevated lesion with irrecultar border, crusty ulcerations, raised erythematous borders
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malignant melanoma
|
rapidly progressing malignant tumor of the melanocytes
|
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metastsis of malignant melanoma occurs through the...
|
lymph nodes
|
|
|
ABCDE rule
|
asymmetry
border irregularity color variation diamter > 6 mm evolving or rapid enlargement |
|
|
kaposi sarcoma
|
vascular malignancy associatied with immunodeficiency and herpes virus
|
|
|
kaposi sarcoma looks like...
|
purplish brown macules that develop into plaque and nodules with angioproliferation
|
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|
first degree burn
|
involve supreficial skin without loss of protective function
|
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second degree burn
partial thickness |
blister formation
|
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second degree burn
deep thickness |
involve entire dermis sparing skin app.
appear waxy white and take weeks to heal |
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third degree burn
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destruction of entire epi, dermis, and underlying subcutaneous tissue
|
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cardiovascular response to burn
|
fluid and protein move out of the vascual compartment
|
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what results from fluid and protein leaving vascular system after a burn? (4)
|
decreased cardiac output
elevated hematocrit elevated WBC count hypoproteinemia |
|
|
cellular impact of burns
|
impairments of sodium potassium pump
|
|
|
normal color of urine
|
abmer yellow
|
|
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normal pH of urine
|
4.6-8
|
|
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specific gravity of urine
|
density of water
1.010-1.025 |
|
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blood in urine test
|
negative
|
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crystals/fat in urine
|
negative
|
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creatinine men
|
.6-1.5
|
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creatinine women
|
.6-1.0
|
|
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creatinine clearance
|
.8-2.1
|
|
|
what are 4 complications of a urinary tract obstruction?
|
impeded flow proximal to the blockage
dilates urinary system increases risk for infection compromises renal function |
|
|
the severity of consequences for a urinary tract obstruction is based on what 5 things?
|
location of obstructive lesion
whether 1 or both upper tracts involved severity of blockage duration nature of the obstructive lesion |
|
|
3 most common renal calculi
|
70% calcium oxalate or phosphate
15% struvite 7% uric acid |
|
|
Bladder neck dyssynergia
|
fails to funnel during micturition
|
|
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urthral stricture
|
narrowing of urethral lumen
|
|
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pelvic organ prolapse
|
cystocele descends below the urethral outlet; bladder protrudes into vagina
|
|
|
neurogenic bladder dysfunction
|
urinary incontinence or low bladder wall compliance
|
|
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what could cause neurogenic bladder dysfunction
|
r/t lesions of CNS and spinal cord
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vesicosphincter dyssynergia
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lesions of spinal cord causing incoordination between the detrusor contraction and urethral sphincter
|
|
|
UTI can be caused by:
|
inflammation of urinary epithelium from pathogen (ex. e.choli)
inflammation of bladder (cystitis) |
|
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Interstitial cystitis UTI
|
nonbacterial, cause obscure..often sexual
|
|
|
acute pyelonephritis
|
infection of renal pelvis and interstitium, one or both kidneys
|
|
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what can cause acute pyelonephritis?
|
kidney stones, pregnancy, neurenic bladder, female sex trauma, reflux, e coli
|
|
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what is the patho of acute pyelonephritis?
|
infiltration of WBC in renal medulla resulting in renal inflammation, renal edema and purulent urine
|
|
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chronic pyelonephritis
|
persistent recurrent infeciton of the kidney leading to scarring
|
|
|
acute glomerulonephritis
|
begins adruptly 7-10 days after a strep infection
|
|
|
clinical acute glomerulonephritis
|
hematuria, RBC casts, proteinuria, decreased GFR oliguria
|
|
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Good pasture syndrome
|
rapidly progressive glmerulonephritis
idiopathic...poor prognosis if untreated early |
|
|
chronic glomerulonephritis
|
several diseases leading ot chronic renal failure ass. with hypercholesterolemia and proteinuria
|
|
|
nephrotic syndrome
|
excretion of 3.5 g or more of protein in the urine per day
|
|
|
what disease will see hypoalbuminemia, edema, hyperlipidemia, lipiduriria and a vitaimin D definiciency?
|
nephrotic syndrome
|
|
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what disease will see hematuria and proteinuria?
|
chronic glomerulonephritis
|
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|
what are the 3 types of actue renal failure
|
prerenal
intrarenal postrenal |
|
|
prerenal
|
impaired renal blood flow
GFR declines due to decreased filtration pressure |
|
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intrarenal
|
tubular necrosis, surgery sepsis, obstruction
|
|
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postrenal
|
urinary tract obstruction (bilateral)
|
|
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Chronic Renal Failure
|
progressive and irreversible loss of nephrons
|
|
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what happens to the GFR during chronic renal failure?
|
decreases dramatically
|
|
|
when does chronic renal failure become apparent
|
not until renail function <25%
|
|
|
End stage renal Disease
|
< 10% renal funcion remains, progressive chronic renal failure
|
|
|
what is necessary to sustain life with ESRD?
|
dialysis
transplant |
|
|
what is the hematologic affect of ESRD?
|
anemia
|
|
|
what causes anemia in ESRD
|
decreased erythropoetin secretion by diney leads to decreased RBC production in bone marrow
|
|
|
Cardiopulmonary in ESRD
|
hypertension
|
|
|
what causes hypertension in ESRD?
|
fluid overload
|
|
|
what is the affects on the reproductive system of ESRD?
|
infertility
decreased libido impotence |
|
|
what is the affect of ESRD on the integumentary system
|
pruritus
uremic frost |
|
|
what is the affect of ESRD neurology?
|
fatigue
|
|
|
what is the affect of ESRD on the skeletal system
|
bone demineralization
|
|
|
what is the affect of ESRD on the gastrointestinal system
|
diarrhea
nausea vomiting |
|
|
what is the affect of ESRD on the renal system
|
retainment of wastes
oliguria/anuria BUN elevated Creatinine elevated |
|
|
what is the affect of ESRD on the endocrine system
|
hyperglycemia
|
