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lecture notes ptho 5
| Question | Answer |
|---|---|
| this cell releases: histamine platelet activating factors Leukotrienes (SRS-A) Prostaglandins (usally E2 | Mast cell |
| bv capillary dialate causing them to leak mucos cells begin 2 secrete bronchi contracts | histamine |
| increased vascular permeability emigration of leukocytes phagocytosis | Phases of imflammation |
| originate in bone marrow initiate inflammatory cascade by releasing chemicals. these are vasoactive or chemotactic chemicals. | mast cell |
| this cell releases their chemicals (granules) in responce to: physical injury chemical agents immunological mechanisms | Mast cell |
| factors that attract leukocytes 2 infected or inflamed areas: bacterial/cellular debris complement fragments cytokins | Chemotaxis |
| 1.recognition and adherence to phagocyte 2. engulfment of target 3. fusion of phagosome with intracellular lysosome. 4. destruction of target by lysosomal enzymes | 4 steps of phagocytosis |
| a lipid released from inflamed/damaged cells membrane. is further broken down into prostaglandins, thromboxane A2, & leukotrienes | Arachidonic acid |
| Is broken down to prostaglandins and thromboxane A2 | Cyclooxygenase enzyme pathway of arachidonic acid |
| results in leukotrienes. (bronchoconstriction of smooth muscle of lungs | Lipooxygenase enzyme pathway of arachidonic acid |
| inhibits cyclooxygenase. It stops production of prostaglandins (pain, fever and mucus production in stomach) | NSAIDS |
| arachidonic acid shifts toward lipooxygenase pathway: increases amount of leukotrienes (Bronchoconstriction) Reason y sum asthma pts cant take asprin or other " " | NSAIDS |
| can cause gastic ulceration | Cox 1 inhibition |
| Reduces prostaglandin that causes inflammation and pain. | Cox 2 Inhibition |
| causes increased capillary permeability and pain along with prostalglandin E2 INCREASES VASCULAR PERMEABILITY/MEDIATORS OF INFLAMMATION | PLasma Derived Bradykinin |
| histamine serotonin leukotrienes Platelet activation factor Nitric oxide | INCREASE VASCULAR PERMEABILITY/MEDIATORS OF INFLAMMATION |
| causes vasodialation and renal perfusion platelet clumping | Prostaglandin I2 AKA--prostacycline |
| works along with bradykinin(chemical mediator) and links to pain receptor | Prostaglandin E2 |
| Causes platelet activation platelets clump vasoconstriction | Thromboxane A2 |
| NON-steroidal anti-inflammatory drug | NSAID |
| an asprin or an a NSAID is considered | Cox inhibitor (Short for cyclooxygenase inhibitor) |
| high doses of NSAID, or asprin can cause increased BP due 2 vasoconstriction and decreased renal perfusion (thru the cox inhibitor) | cox inhibitor |
| causes bronchoconstriction | leukotrienes |
| Rubor-redness dialation of bv tumor-swelling calor-heat dolor-pain functio laesa-decrease funcion | 5 CARDINAL SIGNS OF INFLAMMATION "LOCAL SIGNS" |
| fever lathargy muscle catabolism increase in acute phase proteins in plasma | Systemic signs and symptoms of inflammation |
| critical for sustained on T-cell proliferation | IL2 |
| increases fever, anorexia, malaise and WBC count raises the "set point" of hypothalmus | IL1 & IL6 & TNFa |
| test that determines how fast it takes a rbc to sediment. the faster the rate the more fibrinogen. (causes inflammation) | ESR Erythrocyte Sedimentation Rate |
| non-specific indicator of inflammation: this level increases with inflammation. also used 2screen for coronary artery disease. | C-reactive protein |
| fluid that leaks out of the bv because of the endothelial cells hump up or contract, which allows more space at endothelial junction. | Inflammatory Exudates |
| 1.transport of leukocytes and antibodies 2.dilute toxins 3.transport nutrients for tissue repair | function of Exudates (3) |
| watery, low protein content, mild inflammation | Serous (exudate) |
| seen in greater inflammation/injury is very thick and sticky is a large protein molecule that can wall off infection so it wont spread. | Fibrinous exudate |
| seen in most severe inflammation causes severe leakage of bv after necrosis/breakdown of bv | Hemorrhagic exudate |
| pus accompanied by infection | Purulent exudate |
| 5,000-10,000 mm cubed | Normal WBC count |
| greater than 10,000 mm cubed | Leukocytosis |
| less than 5,000 mm cubed | leukopenia |
| never let monkeys eat bananas neutrophils, lymphocytes, monocytes eosinophils basophiles | differential WBC |
| is 70% of wbc count | neutrophils |
| is 30% of wbc count | lymphocytes |
| calculation of this number helps determine status of ability to fight off infection. | ANC:Absolute Neutrophil Count |
| ANC is 1000 or less mm cubed pt should have | Neutropenic precautions |
| begins at time of injury, prepares wound environment for healing | inflammatory phase of wound healing |
| begins at 2-3days can last for 3weeks focuses on building new tissue to fill wound space. granulation tissue forms | proliferation phase of wound healing |
| epithelial cells grow into the wound from surrounding tissue | epitheliazation phase of wound healing |
| begins approx 3weeks till 6months or longer. continued remodeling of scar. | Remodeling phase of wound healing |
| completed in 2yrs. at best tissue regains only 80% of original tensile strength | Maturation phase of wound healing |
| wound is clean straight line wound edges well approximated rapid healing minimal scar | Healing by primary intension |
| larger wound greater tissue loss wound not approximated healing takes longer | healing by 2ndary intension |
| wound is left open to drain out | healing by tertiary intention |
| these drugs blocks the conversion cyclooxygenase.cox inhibitor | asprin and nsaids |
| a medication that is a leukotriene receptor antagonist | singulair |
Created by:
tzagal
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