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KINE 427: EXAM 2
Jv |
filtration/absorption flow |
Fc / v |
filtration constant (inc. by histamine)
|
S |
surface area (in skeletal muscle, S inc. 7x in exercise) |
Pc / v |
capillary / venule hydrostatic (pushing) pressure (mmHg) |
Pi |
interstitial hydrostatic (pushing) pressure (mmHg) |
PL |
lymphatic hydrostatic pressure (mmHg)
|
Pie c / v |
capillary / venule oncotic (sucking) pressure (mmHg) |
Pie i |
interstitial oncotic (sucking) pressure (mmHg) |
Jv lymph |
lymphatic flow rate (ml / min / 100 grams of tissue) |
C3a
C4a
C5a
subtypes |
inc vascular permeability
activate mast cells
histamine and heparin release
|
C3b
C4b |
Opsonization (mark foreign particles for phagocytosis)
|
C5a |
functions in chemotaxis |
C5b |
production of membrane attack complexes using C6-C9
membranes of antigen cells compromised = lysis (rupture of cell wall or membrane) |
Mediators of inflammation |
Compliment system
Histamine
Serotonin
Bradykinin
Eicosanoids
Free radicals
Cytokines
Nitric Oxide
Platelets |
Histamine |
-Primary mediator in early inflammation
-Synthesized in liver (in plasma when inactive)
-in mast cells(just below epithelial and around blood vessels), platelets, and basophils
-causes pain, vasodilation, bronchile constriction, secretion of gastric HCL, inc. capillary permeability, edema and swelling |
Serotonin |
-neurotransmitter
-known as 5-HT
-appetite, anger, aggression, mood, sleep, sexuality, ansxiety, and depression
-secreted by mast cells, GI mucosa, and PAF stimulated platelets
-excites pain recptors, inc. vasoconstriction, inc vascular platelet aggregation
-arachodonic acid production
|
Bradykinin |
-polypeptide in bld (inc vascular permeability)
-most powerful stimulator of pain receptors (most potent nociceptor agent) ex. bee venom
-Hageman factor (clotting factor XII), inc kallikrein, inc kininogen, inc bradykinin |
eicosanoids
|
-products of arachadonic acid cascade
-prostaglandins
-prostacyclin
-leukotrienes
-thromboxanes
|
prostaglandins |
-arachidonic acid metabolite
-released by damaged cells and macrophages
-dilation of bld vessels, leakage of fluid into surrounding tissue
-excites and enhances sensitivity of pain receptors
-slow suffering pain with tissue injury |
prostacyclin |
-arachidonic acid metabolite
-relaxes bld vessels and bronchial tubes
-prevents platelet aggregation
|
leukotrienes |
-arachidonic acid metabolite; released by neutrophils
-causes chemotaxis (summoning) of neutrophils
-inc. vascular permeability
-potent bronchoconstrictor and vasodilator (anaphylaxis)
-Asthma: inc bronchoconstrict., inc. mucous, inc. airway inflammation
-rheumatoid, psoriasis, inflammatory bowel disease
|
thromboxane |
-vasoconstriction
-inc platelet aggreagation
|
Free radicals |
-oxidizing agent
-removes electrons from substances (hydrogen peroxide, hydroxyl radical, superoxide anion)
-produced in metabolism
-produced by phagocytic cell (especially neutrophils) to kill antigens
-released in excess by macrophages in chronic inflammation
-normal by antioxidants
-production > neutralization = excess oxidation = cell death
-lipid peroxidation = atherosclerosis
-excess in DNA=mutation=cancer
-aging, alcoholic liver, smoking emphysema, parkinson's, alzheimers, schizophrenia, MS, ALS
|
Antioxidants |
endogenous
-gluthione peroxidase
-superoxide dismutase
-alphalipoic acid
-CoQ10
nutrient
-Vitamins C and D
-selenium
-bioflavinoids
|
Cytokines |
polypeptide produced by macrophages
-Tumor necrosis factor
-interlukins
-platelet derived growth factor
-interferons |
TNF |
released by macrophages
-pyrogen
-activates macrophages
-causes vascular endothelial cell retraction (inc vascular permeability = exudate)
- contributes to rheumation and others
|
Interlukins |
stimulates and enhances immune function
-inc monocyte activation/production and chemotaxis of neutrophils and lymphocytes
-causes vascular endothelial cell retraction (inc permeability) and is a pyrogen
-autoimmune diseases
|
platelet derived growth factor |
inc fibroblasts in area
inc angiogenesis
|
inteferons |
virus fighters
fight certain cancers |
Nitric Oxide (NO) |
EDFR
locally synthesized in endothelium and macrophages
-inc vascular dilation and permeability
-killing harmful bacteria
-product in coronary arteries as result of nitroglycerin
-E2 loss in menopause dec. amounts of endogenous NO = risk for CAD |
Platelets |
activated release...
-lysozomes: contain digestive enzymes
-ADP, ATP, Serotonin, histamine
-Fibrinogen, thrombin, and clotting factor V
-Von willebrand factor (platelets bind to collagen)
-PAF and phospholipase A2 = thromboxane A2
-activate other platelets
-cytokines and chemokines = chemotaxis neutrophils
|
Platelet activation |
contact with
-collagen
-thrombin
-thromboxane A2
-ADP
-and each other
-adhere together by INTEGRINS
-adhere to endothelial cells in vessel walls
-form arms called pseudopods
-& fibrin form PLATELET PLUG and repair in damaged vessel wall
-contain myosin and actin to contract to re-enforce wall and close small wound
|
Acute inflammation resolved |
1. healing process takes place and tissue regenerates (rare) or scar forms (likely)
2. inflammation progresses and suppurative (pus) forming process starts
3. inflammation becomes chronic (subsides and returns)
|
Suppuartive process |
-toxins secreted from bacteria, neutrophils and macrophages + tissue ischemia
-excessive tissue destruction and necrosis
-when bacteria and immune cells die near dead tissue, pus forms (abscess: prevent antigens from spreading via fibrin, fibrnogen, and thrombin pocket)
-abscess may drain through skin, be absorbed by tissue, or surgically drained
|
Chronic inflammation |
Initiated by:
-excessive microtrauma to muscle or connective tissue
-asbestos and other non-living foreign material that cannot be dissolved by body
-bacteria and viruses that avoid and resist host defense (TB, mycobacteria, fungi)
-altered tissues or tissue displacement in or around tumors
-Possible fibroblast proliferation = fibrosis = inc risk of scarring and loss of tissue fxn
-exact cause not known (may have to do with immunological response)
|
Bleeding outside the body |
- 10-15% bld loss can be tolerated (bld donation=8-10%)
-Positive feedback: desanguination = hypovulemic shock
- blding = dec BP = activate barorecpetors = inc HR =inc bleeding
-hematoma (bld confined to limited tissue)
- bld under skin: subcutaneous hemmorage
- limit bld loss from injury
-can restimulate inflammation if not resolved
-inc risk with hemophilia, thrombocytopenia, and anti-coagulation
-subcutaneous hemorrhage eventually = ecchymosis
-bruises/contusions/capillaries rupture = bld into intestinal tissue
-associated with fracture, internal bleeding, compartment syndrome
-aging = thinner skin = dec fat under skin = more prone to bruises
-RICE and tylenol (NSAIDS within 24 hours inc blding) |
Bleeding inside the body |
Cause
-GI lesions: colon, rectal, or stomach cancer
-tissue malformation or dissection: aortic aneurysms, arteriovenous malformations
-ulcers
-Trauma
-head trauma
-extra-axial (outside brain; epidural, subdural, subarachnoid) vs. intra-axial (inside brain; c. hemorrhage or stroke)
- inc intracranial pressure = neurological function loss |
ulcers |
cause
-helicobacter pylori bacteria
-genetic predisposition
-overuse of NSAIDs
-stress
*smoking delays healing
Symptoms
-upper abdominal pain (relieved by eating, milk, antiacids)
-nause/vomiting of bld
-pain worse 2 hours after meal or when stomach is empty (middle of night)
|
Cessation of blood flow |
1. Vascular spasm
2. Formation of platelet plug
3. Coagulation |
1. vascular spasm |
Vessel rupture = vessel constriction due to...
-reflexes
-myogenic response: stretch = inc Ca in smooth muscle =vasoconstriction
-platelets release thromboxane A2 (vasoconstrict. and platelet aggregator)
-2 endothelial surfaces causes them to stick together
more cross-sectional area of vessel damaged = greater the spasm
-knife cute=more bld than crush injury
|
2. Formation of platelet plug |
-seal small breaks in small vessels that occur hundreds of time/day
-exposed collagen has (-) charge : (+) platelets attracted
-Von willebrand factor helps bind platelets to collagen = platelet adhesion
-adhered platelets become activated = swell and form irradiating processes
-platelets release THRA2 and ADP = inc activation of nearby platelets
-activated platelets are "sticky" and adhere to each other = platelet aggregation
-high actin and myosin in platelets contract = platelet plug formed
-activated platelets exude substance important in coagulation and healing (phospholipids, PDGF, IGF-1, platelet factor IV) |
3. Coagulation |
initiated by
-trauma to vascular wall and adjacent tissue (extrinsic)
-traumitized tissue releases thromboplastin = coagulation initiated
-exposed collagen (endothelium damage) - (intrinsic)
- activation of Hageman factor = coagulation initiated |
Extrinsic pathway |
begins with substances extrinsic to the blood (completed in 15 seconds)
-damaged tissue releases tissue thromboplastin (tissue factor)
-thromboplastin activates Factor X
-Factor X + platelet phospholipids form prothrombinase
-Prothrombinase activates prothrombin to form thrombin
-thrombin causes fibrinogen to form long "hair-like" structures called fibrin
-firbrin strands form "web" - plasma turns gel-like and traps other elements = clot |
Intrinsic pathway |
injury (collagen exposure) within vessel (completed in 3-6 minutes)
-hageman factor comes in contact with collagen and activates Factor X
-factor X + platelet phospholipids form prothrombinase
-Prothrombinase activates prothrombin to form thrombin
-thrombin causes fibrinogen to form long "hair-like" structures called fibrin
-firbrin strands form "web" - plasma turns gel-like and traps other elements = clot |
clotting factors and fibrinogen |
formed by liver
hepatitis, cirrhosis, etc = inc bleeding and bruising
|
Vitamin K |
necessary for formation of 5 of the clotting factors
deficiency = inc blding and bruising |
Clot contraction |
within 20-60 mins, clots undergo syneresis (pulling wound together)
-actomyosin protein complex contracts like skeletal muscle
-pull created on fibrin strands = edges of injury drawn together |
Clot lysis |
after healing, clot is lysed
-injured tissue releases PLASMINOGEN and TISSUE PLASMINOGEN ACTIVATOR (TPA)
-those are in the clot and activated after days
-TPA converts plasminogen to plasmin (proteolytic enzyme that dissolves clot)
-TPA (& steptokinase) can be used to dissolve clots in MI's, strokes (up to 4.5 hours after onset), and embolisms
|
Coagulation time |
time required for capillary tube of blood to clot
-tube of bld broken off at 30 second intervals
-bld coagulated when fibrin threads appear at broken tube ends
-normal = 6-10 mins |
thrombus |
bld clot in cardiovascular system |
embolus |
circulating plug (solid, liquid, or gas) composed of thrombus or other material that may occlude a bld vessel
-Thromboemolic conditions...
roughened endothelial surface = collagen exposed to bld = coagultation
dec. bld flow = excess thrombin not eliminated by liver = coagulation
stagnant bld = small quantities of thrombin formed = coagulation
atrial fibrilation = dec bld flow in left atria = thrombus formation |
prothrombin time (PT time or pro time) |
coagulation time for mixture of thromboplastin (tissue facctor), calcium, and decalcified plasma
-PT time mean = 12-15 seconds
|
International Normalized Ratio (INR) |
PT time ratio which normalizes for different thromboplastin reagents and equipment
-INR mean = 2-3
-used to monitor effect of anticoagulant drugs (Heparin, Coumadin) to ensure nominal anticoagulation
-used to prevent thromboembolic conditions (stroke, MI, TIA) or keep IV patent
- heaparin, lovonox, coumadin, rivaroxaban, dabigatran |
Haparin |
inactivates factor X
inhibits conversion of prothrombin to thrombin
-LOVONOX=low molecular weight heparin
|
Coumadin |
depresses clotting factor formation in liver (especially with vitamin K related factors)
-results in 50% reduction in coagulation activity after 12 hrs, 80% after 24 hrs
*drug of choice |
Rivaroxaban |
inhibits Factor Xa
no monitoring required
|
dabigatran |
inhibits thrombin
no monitoring required |