{[ promptMessage ]}

Bookmark it

{[ promptMessage ]}

Heart disease lysis of clots clots may be liquefied

Info iconThis preview shows page 1. Sign up to view the full content.

View Full Document Right Arrow Icon
This is the end of the preview. Sign up to access the rest of the document.

Unformatted text preview: spholipid + Ca++ will convert Prothrombin to Thrombin •  fibrinogen--------------->fibrin Heparin- activates antithrombin which prevents the conversion of fibrinogin to fibrin Extrinsic Pathway •  Tissue thromboplastin + Factor VII + Ca++ will activate Factors X & V •  Activated X & V + Phospholipid + Ca++ will convert Prothrombin to Thrombin Final Common Steps •  Once Fibrinogen has been converted to Fibrin by Thrombin it is changed from the soluble monomer to the insoluble polymer by the activated Factor XIII •  Factor XIII is activated by Thrombin and Ca++ TPA - can be used in strokes (non hemorhhagic) & heart attacks TPA prevents clotting by activating plasmin which is used to liquefy the clot Risk factors in Heart Disease Lysis of Clots •  Clots may be liquefied by (fibrinolysis) by a proteolytic enzyme plasmin •  It circulates in the blood in an inactive form known as plasminogen •  Activators are found in tissues, plasma, and urine •  It can also be activated by exogenous activators such as tPA, or streptokinase TPA - activates the bodies plasmin •  •  •  •  •  •  •  •  •  •  Increasing age Male gender Heredity (including race) Tobacco Smoke High blood cholesterol High blood pressure Physical inactivity Obesity/overweight Diabetes Mellitus High blood homocysteine 5 Homocysteine •  Amino acid in the blood that may irritate blood vessels promoting atherosclerosis •  Can also cause cholesterol to change into oxidized LDL •  Can make blood more likely to clot •  High levels in blood (> 12 µmol/L) can be reduced by increasing intake of folic acid, B6 and B12 Heart muscle •  Atrial & Ventricular –  striated enlongated grouped in irregular anatamosing columns –  1-2 centrally located nuclei •  Specialized excitatory & conductive muscle fibers (SA node, AV node, Purkinje fibers) Either autonomic rhythmical electrical discharge or conduction of action potemtials through the heart –  contract weakly –  few fibrils AP are not conducted from atrial sync to ventricular syncinstead AP goes bt in a Specialized conductive system called a AV bundle Allows atria to contract for a short time before the ventrical Syncytial nature of cardiac muscle •  Syncytium = many acting as one •  Due to presence of intercalated discs –  low resistance pathways connecting cardiac cells end to end –  presence of gap junctions Intercalated discs- cell membranes that seperate individual cardiac muscle cells from one another The gap jxns formed buy the binding of the discs allow for rapid diffusion of ions Action potentials in cardiac muscle •  Duration of action potential is from .2-.3 sec •  Channels –  fast Na+ channels –  slow Ca++/Na+ channels –  K+ channels K channels not slow or fast •  Permeability changes –  Na+ sharp increase at onset of depolarization –  Ca++ increased during the plateau –  K+ increased during the resting polarized state Action potentials travel peasily from one cardiac muscle cell to the next- as one cell becomes excited the AP easily travels to the next- syncytium Membrane physiology •  In excitable tissue an action potential is a pulse like change in membrane permeability •  In cardia...
View Full Document

{[ snackBarMessage ]}

Ask a homework question - tutors are online