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154 Cards in this Set
- Front
- Back
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81 million people in US have one or more forms of Cardiovascular disease (CVD). Responsible for 35-40% of deaths. T or F?
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T
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what are the percentages of water in the human body? intracellular, extracellular, plasma
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2/3 (66%) intracellular
~1/3 (~33%) extracellular 5% plasma (approxamately 60% of lean body weight is water) |
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another name for ascites
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hydroperitoneum
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Edema in the body cavities. What are the regional names?
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Hydrothorax
Hydropericardium hydroperitoneum |
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how is normal flow of fluid conducted, thus avoiding edema?
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outflow from arteriolar end of microcirculation to interstitium is balanced by inflow at venular end.
small residual fluid within interstitium is drained by lymphatics. eventually returned to blood stream via thoracic duct |
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what would cause increased interstitial fluid?
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1. increased capillary pressure
2. decreased colloid osmotic pressure |
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what is transudate?
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protein poor fluid
caused by increased hydrostatic pressure or reduced plasma protein |
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What causes an increased hydrostatic pressure or reduced plasma protein edema?
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heart failure
renal failure hepatic failure malnutrition |
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in heart failure, what are the events that lead to edema?
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increased capillary hydrostatic pressure
decreased renal blood flow activation of renin-angiotensin system retention of Na and H2O increase in blood volume Leading to Edema |
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what is the pathway to edema from renal failure?
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retention of Na and H2O
increase in Blood Volume Edema |
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a PT presents with inflammation edema, what do you call this protein rich fluid?
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Exudate
protein rich exudate is a result of increased vascular permeability |
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what are the 4 noninflammatory causes of Edema?
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Increased hydrostatic pressure
Reduced plasma osmotic pressure Na and H2O retention Lymphatic obstruction |
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How do malnutrition, decrease in hepatic synthesis, and nephrotic syndrome lead to edema?
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pathway
decrease in plasma albumin decrease in osmotic pressure leads to edema |
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what are the 2 types of hydrostatic pressure increases?
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Regional
Generalized |
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How does regional HP increase function? example
|
focal impairment in venous return
ie. DVT causes localized edema in affected leg |
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how does generalized HP increase function? example
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congestive heart failure causes generalized edema
R ventricle failure leads to pooling of venous blood this increases venous pressure |
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a PT presents with until recently well managed liver disease. He has severe generalized edema. what should be done for him?
|
need to increase plasma osmotic pressure
give IV albumin |
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how does the decrease in plasma osmotic pressure affect the kidneys?
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net movement of fluid into interstitial tissues
subsequent plasma volume contraction reduced intravascular volume leads to decreased renal perfusion trigger renin production, angiotensin, and aldosterone salt and h2o retention in the kidneys are unable to correct the plasma volume deficit |
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what is an important cause in albumin loss?
|
nephrotic syndrome
glomerular capillaries become leaky PT presents with generalized edema |
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most important causes of renal hypoperfusion?
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congestive heart failure (CHF)
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what happens to hydrostatic pressure and colloid osmotic pressure with salt and subsequent h2o retention
|
hydrostatic pressure increases
vascular colloid osmotic pressure decreases |
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what causes salt retention?
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compromised renal function
decreased renal perfusion |
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a 65 yo m PT presents with worsening CHF. What should he do to manage his general edema?
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salt restriction
use diuretics take aldosterone antagonists |
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a 35 yo m PT returns from a year long trip abroad in Haiti with worsening localized edema in his thigh. On PE you note his genetalia are also affected. what could be causing this?
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Localized edema from filariais
Lymphatic Obstruction via lymphatic and lymph node fibrosis causing elephantiasis |
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what are other causes of lymphadema?
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chronic inflammation with fibrosis
invasive malignant tumors physical disruption radiation damage infectious agents |
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how is edema recognized microscopically?
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recognized as a clearing or separation of extracellular matrix and subtle cell swelling
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where is edema most commonly seen?
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subcutaneous tissues
lungs brain |
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what is dependent edema?
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distribution of edema is influenced by gravity
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common clinical consequences of edema
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impaired wound healing
impair clearance of infex bacterial infection brain herniation from edema in brain |
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what occurs when local blood volume increases?
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hyperemia and congestion
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is hyperemia an active or passive process?
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active process
arteriolar dilation leads to increased blood flow ex. inflammation; increase blood flow to skeletal mm. during exercise |
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is congestion active or passive in its process?
|
passive
occurs by reduced outflow from a tissue may be systemic; ie. cardiac failure local: venous obstruction |
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a patient presents with an inflamed erythmatous lesion on his left leg after a soccer match. Is this hyperemia or congestion?
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hyperimea
increased blood flow causes engorgement of vessels with oxygenated blood - erythematous |
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a PT presents with pallor in his conjunctiva, and you notice that his lips are cyanotic. He also has initial stages of clubbing. Would he have hyperemia or congestion?
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congestion
typically presents with dusky reddish blue color (cyanosis) due to red cell stasis accumulation of deoxygenated hemoglobin |
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chronic passive congestion leads to _____ and results in _____ tissue and scarring
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1. hypoxia
2. ischemic tissue injury and scarring |
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edema is a result commonly of long standing increased ____ and ______
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volumes and pressures
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catabolism of extravasated RBCs can lead to ________
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hemosiderin laden macrophages
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what is the microscopic appearance of acute pulmonary congestion?
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engorged alveolar capillaries
alveolar septal edema focal inra alveolar hemorrhage |
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what is the histological appearance of chronic pulmonary congestion?
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septa thickened and fibrotic
hemosiderin laden macrophages (ie. heart failure cells) |
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pt presents with acute hepatic congestion. what would the tissue look like microscopically?
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distended central vein and sinusoids
ischemic centrilobular hepatocytes fatty changes to periportal hepatocytes (receive better oxygen b/c of location) |
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pt presents with chronic passive hepatic congestion. what will she have when identifying tissues grossly/microscopically?
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gross inspection:
centrilobular regions red/brown and depressed (cell death) surrounding zones of tan uncongested liver (nutmeg liver) microscope: centrilobular hemorrhage heart failure cells degeneration of hepatocytes necrosis of centrilobular area due to its location at distal end of blood supply |
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define hemorrhage
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extravasation of blood into extravascular space
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define hemorrhagic diathesies
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increased tendency to bleed
usually with insignificant injury |
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examples of Arterial or venous rupture
|
vascular injury
trauma atherosclerosis inflammatory or neoplastic erosion of vessel wall |
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Tissue hemorrhage patterns, name them:
1. contained within a tissue 2. minute 1-2 mm on skin... 3. 3 mm or larger in size 4. 1 -2 cm subcutaneous 5. anatomical location |
1. hematoma
2. pettechiae 3. purpura 4. ecchymoses 5. hemothorax, hemopericardium, hemoperitoneum, hemarthrosis (joints) |
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pt. presents with petechiae from local increased intravascular pressure. what are other causes
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1. thrombocytopenia (low platelet count)
2. uremia (defective platelet function) 3. local increased intravascular pressure |
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purpura can be caused by the same problems in petechiae, what other causes?
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vascular fragility (eg. amyloidosis)
vascular inflammation secondary to trauma |
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characteristic color changes in ecchymoses...describe the sequence
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RBCs are degraded and phagocytosed by macrophages
hemoglobin (red/blue color) is enzymatically converted into bilirubin (blue-green color) eventually converted into hemosiderin (gold/brown color) |
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what is the difference in chronic/recurrent blood loss when bleeding into a body cavity or tissue vs. losing blood externally
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bleeding internally allows for the recycling of Iron
bleeding externally causes Iron deficiency anemia |
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pathologic counterpart to hemostasis is ______
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thrombosis (clot formation within vessels)
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three components of hemostasis and thrombosis
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endothelium of vascular wall, platelets, and coagulation cascade
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what are the stages of hemostasis at the site of vascular injury?
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vasoconstriction
primary hemostasis secondary hemostasis thrombus and antithrombotic events |
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describe vasoconstriction. what mediates this process
|
arteriolar vasoconstriction
mediated by: reflex neurogenic mecanisms endothelin (endothelium derived potent vasoconstrictor) |
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what would happen at the site of injury if only vasoconstriction occurred and the subsequent hemostatic events failed?
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resume bleeding
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what occurs to platelets during primary hemostasis?
what forms with this process? |
platelets activated by exposure to subendothelial ECM
platelets become more adherent and activated undergo shape change - round to flat with increase surface area release of secretory granules Product: hemostatic plug from platelet aggragation |
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what is tissue factor?
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TF is aka factor III, and Thromboplastin
membrane bound procoagulant synthesized by endothelial cells |
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in addition to TF what other factor is needed to promote thrombin generation?
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TF acts in conjunction with factor VII to generate thrombin
|
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what does thrombin do? 3 things
|
1. circulating fibrinogen into insoluble fibrin
2. creates fibrin meshwork 3. induces platelet recruitment and activation |
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what does secondary hemostasis do?
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consolidates initial hemostatic platelet plug
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what does t-PA do at the site of injury? what is t-PA
|
t-PA; aka tissue plasminogen activator
counter-regulatory mechanism limits hemostatic plug |
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what feature is normally exhibited by endothelial cells?
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antiplatelet, anticoagulant, and fibrynolytic properties
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what causes endothelial cells to acquire procoagulant properties?
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activation by:
trauma infectious agents hemodynamic forces plasma mediators cytokines |
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how does the endothelium cause antiplatelet activity?
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prevents platelets from engaging with subendothelial ECM (collagen)
EVEN if platelets are ACTIVATED: endothelial cells produce PGI2 and NO inhibitors of platelet aggregation promotors of vasodilation |
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how is endothelium anticoagulant
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endothelial membrane associated heparin-like molecules inactivate thrombin INDIRECTLY
also... endothelium produces: protein S; a cofactor for protein C TFPI - tissue factor pathway inhibitor TFPI is a cell surface protein that DIRECTLY inhibits VIIa and Xa activities |
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how do the heparin like molecules act indirectly?
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heparin like molecules are cofactors that enhance inactivation of thrombin and other coag factors by Antithrombin III
Thrombomodulin binds to thrombin to convert it to anticoagulant via activation of Protein C Protein C inhibits cloting by inactivating Va and VIIIa |
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three effects of prothrombosis
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platelet effects
procoagulant effects antifibrinolytic effects |
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describe platelet effects in the endothelial response
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contact of platelets to the ECM
adhesion through interactions with von Willebrand Factor (vWF) |
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what is vWF?
|
von willebrand factor is a product of normal epithelial cells
cofactor for platelet binding to Matrix elements |
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describe endothelial procoagulant effects
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1. Tissue Factor (TF) is synthesized by endothelial cells in response to cytokines (TNF or IL-1) or bacterial endotoxin
TF activates clotting cascade 2. activated endothelial cells augment activated coag factors IXa and Xa |
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how does the endothelium prevent fibrinolysis?
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secrete Inhibitors of plasminogen activators (PAI's)
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where do platelets come from?
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shed from megakaryocytes
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what are the factors in platelet function
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glycoprotein receptors
contractile cytoskeleton (2) cytoplasmic granules: α-granules δ -granules - aka dense granules |
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what are a-granules?
surface molocule 7 contents |
p-selectin on their membranes
contain: fibrinogen fibronectin factor V factor VIII platelet factor 4 (heparin binding chemokine) PDGF (platelet derived growth factor) transforming factor ß |
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(Dense granules) δ-granules contain
6 contents |
ADP and ATP
ionized Ca++ histamine seratonin epinephrine |
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when platelets encounter collagen in the ECM and vWF, what happens?
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1. adhesion and shape change
2. secretion (release action) 3. aggregation |
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how do von Willebrand disease and Bernard Soulier syndrome genetic deficiencies interrupt platelet adhesion?
|
1. vW disease - deficiency of vWF
causes lack of the necessary linkage of vWF to GpIb this linkage overcomes the shearing forces of flowing blood 2. Bernard Soulier syndrome deficiency of receptor glycoprotein IB (GpIb) also presents as a problem with overcoming shearing forces |
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do platelets adhere to anything else?
|
yes
adherence to other components of ECM eg. fibronectin |
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what causes the secretion of granule types α & δ
|
secretion occurs soon after adhesion
agonists bind to platelet surface receptors and initiate a protein phosphorylation cascade this leads to degranulation |
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importance of secretion (release reaction)
|
Ca++ in dense bodies is required for the coag cascade
ADP is potent activator of Platelet aggregation ADP also causes additional ADP release - amplification Platelet activation leads to negatively charged phospholipids on surface of platelet |
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what do the neg. charged phospholipids do?
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bind calcium
nucleation site for assembly of coagulation factor complexes |
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what follows platelet adhesion and granule release?
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platelet aggregation
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what molecules are needed to form the platelet plug via platelet aggregation?
|
ADP - activator of platelet aggregation
Thromboxane - TxA2 amplifies platelet aggregation |
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is the initial aggregation of platelets reversable?
|
yes
|
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what are the two mechanisms for stabilizing the platelet plug?
|
1. secondary hemostatic plug creation
-thrombin binds protease activated receptor (PAR) on platelet membrane ADP and TxA2 cause further platelet aggregation Platelet cytoskeleton causes platelet contraction -result: irreversibly fused platelets 2. fibrinogen converted to fibrin by thrombin - cements platelets in place |
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is the initial aggregation of platelets reversable?
|
yes
|
|
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why is fibrinogen an important part of platelet aggregation? what does it have to do with GpIIb-IIIa?
|
-ADP triggers conformational change in platelet GpIIb-IIIa receptors
-induces binding to fibrinogen -fibrinogen (large protein) forms bridges between platelets; promotes platelet aggregation |
|
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is the initial aggregation of platelets reversable?
|
yes
|
|
|
is the initial aggregation of platelets reversable?
|
yes
|
|
|
what are the two mechanisms for stabilizing the platelet plug?
|
1. secondary hemostatic plug creation
-thrombin binds protease activated receptor (PAR) on platelet membrane ADP and TxA2 cause further platelet aggregation Platelet cytoskeleton causes platelet contraction -result: irreversibly fused platelets 2. fibrinogen converted to fibrin by thrombin - cements platelets in place |
|
|
what if there is a deficiency in GpIIb-IIIa?
|
causes Glanzmann thrombasthenia
bleeding disorder |
|
|
what are the two mechanisms for stabilizing the platelet plug?
|
1. secondary hemostatic plug creation
-thrombin binds protease activated receptor (PAR) on platelet membrane ADP and TxA2 cause further platelet aggregation Platelet cytoskeleton causes platelet contraction -result: irreversibly fused platelets 2. fibrinogen converted to fibrin by thrombin - cements platelets in place |
|
|
what are the two mechanisms for stabilizing the platelet plug?
|
1. secondary hemostatic plug creation
-thrombin binds protease activated receptor (PAR) on platelet membrane ADP and TxA2 cause further platelet aggregation Platelet cytoskeleton causes platelet contraction -result: irreversibly fused platelets 2. fibrinogen converted to fibrin by thrombin - cements platelets in place |
|
|
what therapeutic agents are available for blocking platelet aggregation?
|
clopidogrel - block ADP binding
Synthetic antagonists or Monoclonal antibodies - bind to GpIIb-IIIa receptors |
|
|
why is fibrinogen an important part of platelet aggregation? what does it have to do with GpIIb-IIIa?
|
-ADP triggers conformational change in platelet GpIIb-IIIa receptors
-induces binding to fibrinogen -fibrinogen (large protein) forms bridges between platelets; promotes platelet aggregation |
|
|
why is fibrinogen an important part of platelet aggregation? what does it have to do with GpIIb-IIIa?
|
-ADP triggers conformational change in platelet GpIIb-IIIa receptors
-induces binding to fibrinogen -fibrinogen (large protein) forms bridges between platelets; promotes platelet aggregation |
|
|
why is fibrinogen an important part of platelet aggregation? what does it have to do with GpIIb-IIIa?
|
-ADP triggers conformational change in platelet GpIIb-IIIa receptors
-induces binding to fibrinogen -fibrinogen (large protein) forms bridges between platelets; promotes platelet aggregation |
|
|
what if there is a deficiency in GpIIb-IIIa?
|
causes Glanzmann thrombasthenia
bleeding disorder |
|
|
what if there is a deficiency in GpIIb-IIIa?
|
causes Glanzmann thrombasthenia
bleeding disorder |
|
|
are RBC's or leukocytes found in hemostatic plugs?
|
yes
leukocytes adher to platelets via P-selectin contribute to inflammation Thrombin causes neutrophil and monocyte adhesion through chemotactic Fibrin Split Products |
|
|
what therapeutic agents are available for blocking platelet aggregation?
|
clopidogrel - block ADP binding
Synthetic antagonists or Monoclonal antibodies - bind to GpIIb-IIIa receptors |
|
|
what if there is a deficiency in GpIIb-IIIa?
|
causes Glanzmann thrombasthenia
bleeding disorder |
|
|
what therapeutic agents are available for blocking platelet aggregation?
|
clopidogrel - block ADP binding
Synthetic antagonists or Monoclonal antibodies - bind to GpIIb-IIIa receptors |
|
|
is the initial aggregation of platelets reversable?
|
yes
|
|
|
are RBC's or leukocytes found in hemostatic plugs?
|
yes
leukocytes adher to platelets via P-selectin contribute to inflammation Thrombin causes neutrophil and monocyte adhesion through chemotactic Fibrin Split Products |
|
|
what are the two mechanisms for stabilizing the platelet plug?
|
1. secondary hemostatic plug creation
-thrombin binds protease activated receptor (PAR) on platelet membrane ADP and TxA2 cause further platelet aggregation Platelet cytoskeleton causes platelet contraction -result: irreversibly fused platelets 2. fibrinogen converted to fibrin by thrombin - cements platelets in place |
|
|
are RBC's or leukocytes found in hemostatic plugs?
|
yes
leukocytes adher to platelets via P-selectin contribute to inflammation Thrombin causes neutrophil and monocyte adhesion through chemotactic Fibrin Split Products |
|
|
why is fibrinogen an important part of platelet aggregation? what does it have to do with GpIIb-IIIa?
|
-ADP triggers conformational change in platelet GpIIb-IIIa receptors
-induces binding to fibrinogen -fibrinogen (large protein) forms bridges between platelets; promotes platelet aggregation |
|
|
what therapeutic agents are available for blocking platelet aggregation?
|
clopidogrel - block ADP binding
Synthetic antagonists or Monoclonal antibodies - bind to GpIIb-IIIa receptors |
|
|
what if there is a deficiency in GpIIb-IIIa?
|
causes Glanzmann thrombasthenia
bleeding disorder |
|
|
are RBC's or leukocytes found in hemostatic plugs?
|
yes
leukocytes adher to platelets via P-selectin contribute to inflammation Thrombin causes neutrophil and monocyte adhesion through chemotactic Fibrin Split Products |
|
|
what therapeutic agents are available for blocking platelet aggregation?
|
clopidogrel - block ADP binding
Synthetic antagonists or Monoclonal antibodies - bind to GpIIb-IIIa receptors |
|
|
is the initial aggregation of platelets reversable?
|
yes
|
|
|
is the initial aggregation of platelets reversable?
|
yes
|
|
|
is the initial aggregation of platelets reversable?
|
yes
|
|
|
is the initial aggregation of platelets reversable?
|
yes
|
|
|
is the initial aggregation of platelets reversable?
|
yes
|
|
|
is the initial aggregation of platelets reversable?
|
yes
|
|
|
is the initial aggregation of platelets reversable?
|
yes
|
|
|
are RBC's or leukocytes found in hemostatic plugs?
|
yes
leukocytes adher to platelets via P-selectin contribute to inflammation Thrombin causes neutrophil and monocyte adhesion through chemotactic Fibrin Split Products |
|
|
what are the two mechanisms for stabilizing the platelet plug?
|
1. secondary hemostatic plug creation
-thrombin binds protease activated receptor (PAR) on platelet membrane ADP and TxA2 cause further platelet aggregation Platelet cytoskeleton causes platelet contraction -result: irreversibly fused platelets 2. fibrinogen converted to fibrin by thrombin - cements platelets in place |
|
|
what are the two mechanisms for stabilizing the platelet plug?
|
1. secondary hemostatic plug creation
-thrombin binds protease activated receptor (PAR) on platelet membrane ADP and TxA2 cause further platelet aggregation Platelet cytoskeleton causes platelet contraction -result: irreversibly fused platelets 2. fibrinogen converted to fibrin by thrombin - cements platelets in place |
|
|
why is fibrinogen an important part of platelet aggregation? what does it have to do with GpIIb-IIIa?
|
-ADP triggers conformational change in platelet GpIIb-IIIa receptors
-induces binding to fibrinogen -fibrinogen (large protein) forms bridges between platelets; promotes platelet aggregation |
|
|
what are the two mechanisms for stabilizing the platelet plug?
|
1. secondary hemostatic plug creation
-thrombin binds protease activated receptor (PAR) on platelet membrane ADP and TxA2 cause further platelet aggregation Platelet cytoskeleton causes platelet contraction -result: irreversibly fused platelets 2. fibrinogen converted to fibrin by thrombin - cements platelets in place |
|
|
what are the two mechanisms for stabilizing the platelet plug?
|
1. secondary hemostatic plug creation
-thrombin binds protease activated receptor (PAR) on platelet membrane ADP and TxA2 cause further platelet aggregation Platelet cytoskeleton causes platelet contraction -result: irreversibly fused platelets 2. fibrinogen converted to fibrin by thrombin - cements platelets in place |
|
|
what are the two mechanisms for stabilizing the platelet plug?
|
1. secondary hemostatic plug creation
-thrombin binds protease activated receptor (PAR) on platelet membrane ADP and TxA2 cause further platelet aggregation Platelet cytoskeleton causes platelet contraction -result: irreversibly fused platelets 2. fibrinogen converted to fibrin by thrombin - cements platelets in place |
|
|
what are the two mechanisms for stabilizing the platelet plug?
|
1. secondary hemostatic plug creation
-thrombin binds protease activated receptor (PAR) on platelet membrane ADP and TxA2 cause further platelet aggregation Platelet cytoskeleton causes platelet contraction -result: irreversibly fused platelets 2. fibrinogen converted to fibrin by thrombin - cements platelets in place |
|
|
what are the two mechanisms for stabilizing the platelet plug?
|
1. secondary hemostatic plug creation
-thrombin binds protease activated receptor (PAR) on platelet membrane ADP and TxA2 cause further platelet aggregation Platelet cytoskeleton causes platelet contraction -result: irreversibly fused platelets 2. fibrinogen converted to fibrin by thrombin - cements platelets in place |
|
|
why is fibrinogen an important part of platelet aggregation? what does it have to do with GpIIb-IIIa?
|
-ADP triggers conformational change in platelet GpIIb-IIIa receptors
-induces binding to fibrinogen -fibrinogen (large protein) forms bridges between platelets; promotes platelet aggregation |
|
|
why is fibrinogen an important part of platelet aggregation? what does it have to do with GpIIb-IIIa?
|
-ADP triggers conformational change in platelet GpIIb-IIIa receptors
-induces binding to fibrinogen -fibrinogen (large protein) forms bridges between platelets; promotes platelet aggregation |
|
|
what if there is a deficiency in GpIIb-IIIa?
|
causes Glanzmann thrombasthenia
bleeding disorder |
|
|
why is fibrinogen an important part of platelet aggregation? what does it have to do with GpIIb-IIIa?
|
-ADP triggers conformational change in platelet GpIIb-IIIa receptors
-induces binding to fibrinogen -fibrinogen (large protein) forms bridges between platelets; promotes platelet aggregation |
|
|
why is fibrinogen an important part of platelet aggregation? what does it have to do with GpIIb-IIIa?
|
-ADP triggers conformational change in platelet GpIIb-IIIa receptors
-induces binding to fibrinogen -fibrinogen (large protein) forms bridges between platelets; promotes platelet aggregation |
|
|
why is fibrinogen an important part of platelet aggregation? what does it have to do with GpIIb-IIIa?
|
-ADP triggers conformational change in platelet GpIIb-IIIa receptors
-induces binding to fibrinogen -fibrinogen (large protein) forms bridges between platelets; promotes platelet aggregation |
|
|
what if there is a deficiency in GpIIb-IIIa?
|
causes Glanzmann thrombasthenia
bleeding disorder |
|
|
why is fibrinogen an important part of platelet aggregation? what does it have to do with GpIIb-IIIa?
|
-ADP triggers conformational change in platelet GpIIb-IIIa receptors
-induces binding to fibrinogen -fibrinogen (large protein) forms bridges between platelets; promotes platelet aggregation |
|
|
what if there is a deficiency in GpIIb-IIIa?
|
causes Glanzmann thrombasthenia
bleeding disorder |
|
|
what if there is a deficiency in GpIIb-IIIa?
|
causes Glanzmann thrombasthenia
bleeding disorder |
|
|
what therapeutic agents are available for blocking platelet aggregation?
|
clopidogrel - block ADP binding
Synthetic antagonists or Monoclonal antibodies - bind to GpIIb-IIIa receptors |
|
|
what if there is a deficiency in GpIIb-IIIa?
|
causes Glanzmann thrombasthenia
bleeding disorder |
|
|
what if there is a deficiency in GpIIb-IIIa?
|
causes Glanzmann thrombasthenia
bleeding disorder |
|
|
what if there is a deficiency in GpIIb-IIIa?
|
causes Glanzmann thrombasthenia
bleeding disorder |
|
|
what therapeutic agents are available for blocking platelet aggregation?
|
clopidogrel - block ADP binding
Synthetic antagonists or Monoclonal antibodies - bind to GpIIb-IIIa receptors |
|
|
what therapeutic agents are available for blocking platelet aggregation?
|
clopidogrel - block ADP binding
Synthetic antagonists or Monoclonal antibodies - bind to GpIIb-IIIa receptors |
|
|
are RBC's or leukocytes found in hemostatic plugs?
|
yes
leukocytes adher to platelets via P-selectin contribute to inflammation Thrombin causes neutrophil and monocyte adhesion through chemotactic Fibrin Split Products |
|
|
are RBC's or leukocytes found in hemostatic plugs?
|
yes
leukocytes adher to platelets via P-selectin contribute to inflammation Thrombin causes neutrophil and monocyte adhesion through chemotactic Fibrin Split Products |
|
|
what therapeutic agents are available for blocking platelet aggregation?
|
clopidogrel - block ADP binding
Synthetic antagonists or Monoclonal antibodies - bind to GpIIb-IIIa receptors |
|
|
what therapeutic agents are available for blocking platelet aggregation?
|
clopidogrel - block ADP binding
Synthetic antagonists or Monoclonal antibodies - bind to GpIIb-IIIa receptors |
|
|
are RBC's or leukocytes found in hemostatic plugs?
|
yes
leukocytes adher to platelets via P-selectin contribute to inflammation Thrombin causes neutrophil and monocyte adhesion through chemotactic Fibrin Split Products |
|
|
what therapeutic agents are available for blocking platelet aggregation?
|
clopidogrel - block ADP binding
Synthetic antagonists or Monoclonal antibodies - bind to GpIIb-IIIa receptors |
|
|
what therapeutic agents are available for blocking platelet aggregation?
|
clopidogrel - block ADP binding
Synthetic antagonists or Monoclonal antibodies - bind to GpIIb-IIIa receptors |
|
|
are RBC's or leukocytes found in hemostatic plugs?
|
yes
leukocytes adher to platelets via P-selectin contribute to inflammation Thrombin causes neutrophil and monocyte adhesion through chemotactic Fibrin Split Products |
|
|
are RBC's or leukocytes found in hemostatic plugs?
|
yes
leukocytes adher to platelets via P-selectin contribute to inflammation Thrombin causes neutrophil and monocyte adhesion through chemotactic Fibrin Split Products |
|
|
are RBC's or leukocytes found in hemostatic plugs?
|
yes
leukocytes adher to platelets via P-selectin contribute to inflammation Thrombin causes neutrophil and monocyte adhesion through chemotactic Fibrin Split Products |
|
|
are RBC's or leukocytes found in hemostatic plugs?
|
yes
leukocytes adher to platelets via P-selectin contribute to inflammation Thrombin causes neutrophil and monocyte adhesion through chemotactic Fibrin Split Products |
