Cardiovascular System Flashcards
functions of blood
- transport: gas, nutrients, wastes, processed molecules, regulatory molecules
- regulate pH (7.35-7.45) and osmosis
- maintain internal body temp
- protect against foreign substances
- clot formation
production of formed elements
- hematopoiesis: to make blood cells
- stem cells: all formed elements derive from here
- proerythroblasts -> erythrocytes
- myeloblasts -> basophils, neutrophils, eosinophils
- lymphoblasts -> lymphocytes
- monoblasts -> monocytes
- megakaryoblasts -> platelets (not cells but fragments)
erythropoiesis
production of red blood cells
-decreased O2 = kidney release erythropoietin = red bone marrow make more RBC = release more RBC
- stem cell –> proerythrocytes –> early erythrocytes –> intermediate erythrocytes –> late erythrocytes–> reticulocytes
erythropoietin
A hormone produced and released by the kidney that stimulates the production of red blood cells by the bone marrow.
hemoglobin breakdown
1) Hemoglobin is split into heme and globin
2) Globin’s amino acids are recycled to the blood
3) Heme’s iron is stored in the liver for future use (to spleen and bone marrow to make RBC)
4)Heme’s pigment, now bilirubin, is used in bile production
WBCs function and movement
protect body against microorganisms; remove dead cells and debris
- ameboid: pseudopod
- diapedesis: stretch to fit btwn cells or thru capillaries
- chemotaxis: attraction and mvmnt toward foreign material or injured cells
hemostasis
stoppage of bleeding by one of 3 ways:
- vascular spasm
- platelet plug formation
- clot formation / coagulation
vascular spasm
vasocontraction of the smooth muscle in the wall of a damaged blood vessel to prevent blood loss
- form of hemostasis
- caused by thromboxane from platelets and endothelin
platelet plug formation
platelet adhesion: when von Willebrand factor connects collagen and platelets
platelet release rxn: release ADP, thrombaxanes, other chemicals to activate platelets in cascade effect
platelet aggregation: activated platelets give out receptors to bind to fibrinogen to make a plug/bridge btwn platelets
expression of factor V and phospholipids
coagulation
blood clotting (hemostasis)
- activate prothrombinase > prothrombin to thrombin > fibrinogen to fibrin
- factors are proteins in plasma that circulate inactively until tissues are damaged; when platelets adhere the activations begin
- blood clot: fibrin fibers, trapped blood cells, platelets and fluid
extrinsic clotting pathway
- begin w chemicals outside of blood
stage 1: damaged tissues release TF3; Ca present makes TF3 + TF7 = TF 10; form prothrombinase
stage 2: prothrombinase turn prothrombin > thrombin
stage 3: thrombin turn fibrinogen > fibrin
and thrombin activate TF13 to stabilize clot
intrinsic clotting pathway
- begin with chemicals part of blood
stage 1: in damaged vessels TF12 comes in contact w collagen to activate TF12; TF11 is stimulated to turn on TF9; TF9 joins with TF8, platelets, Ca, to make TF10; prothrombinase made
stage 2: prothrombinase turn prothrombin > thrombin
stage 3: thrombin turn fibrinogen > fibrin
and thrombin activate TF13 to stabilize clot
control of clot formation
- anticoagulants: prevent coagulation factors from starting clot
- coagulation factors need to meet threshold
anticoagulants
prevent blood clot formation
- antithrombin: made in liver, slowly inactivates thrombin
- heparin: made from basophils and endothelial cells; increases antithrombin effectiveness
- prostacyclin: prostaglandin from endothelial cells,, cause vasodilation and inhibit release of coagulating factors from platelets
fibrinolysis
Breakdown and removal of a clot; how stop blood leave body
- fibrin threads of clot attach to vessel walls
- platelet processes attach to fibrin threads
- actin and myosin in platelets contract to pull edges in and allow serum to exit
clot dissolved by plasmin (enzyme that hydrolyzes fibrin)
antibodies
Specialized proteins that aid in destroying infectious agents by attaching to antigens
antigens
foreign substances that trigger the attack of antibodies in the immune response.
blood types
A: has B antibodies and A antigens
B: has A antibodies and B antigens
AB: no antibodies; A and B antigens
O: has A and B antibodies but no antigens
Rh blood group
Rh (+) : have these antigens on surface of RBCs
Rh (-) : do not have these antigens on RBCs
mean arterial pressure (MAP)
average BP in aorta
- MAP = CO x PR = (SV x HR) x PR
- low HR at rest = greater SV
- PR: total resistance blood pumped against
Decreased BP causes
1.) Decreased blood pressure, decreased blood pH, increased blood carbon dioxide, decreased blood oxygen, exercise, and emotions
↓
2.) Increased sympathetic stimulation, decreased parasympathetic stimulation, and increased epinephrine and norepinephrine secretion from the adrenal medulla
↓
3.) Increased heart rate
↓
4.) Increased cardiac output
↓
5.) Increased mean arterial pressure
increased BP causes
1.) increased BP, exercise, change sit/stand–>
2.) increased venous return increases end diastolic volume –>
3.) increased force of contraction and end diastolic volume –>
4.) increase SV –> increase CO–> increase MAP
intrinsic heart regulation
Normal heart functions (not neural or hormonal)
- preload: (Sterling’s Law) amount of stretch of ventricular walls; more stretch = more force contraction
- afterload: pressure contracting ventricles overcome to aortic pressure to move blood into heart
extrinsic heart regulation
neural and hormonal control of heart
- parasympathetic: vagus nerve decreases HR, ACh repolarizes heart
- sympathetic: cardiac nerves SA and AV nodes, increase HR, epinephrine and norepinephrine released.
increased HR = increase CO = low end diastolic = less refill
- hormonal: epinephrine and norepinephrine when increased PA, emotions and stress
