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232 Cards in this Set
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a form of fluid loss, "blood where it doesn't belong", a name is give in reference to the site or organ affected
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hemorrhage
ex: cardiac hemorrhage, cerebral hemorrhage, arterial hemorrhage |
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"too much blood"
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hyperemia
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dilation of arterioles, usually a neural reflex
ex: blushing |
active hyperemia
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results from congestion, more sinister
ex: increase venous backflow ex: inflammation (erythema) |
passive hyperemia
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one sign of this disease is passive hyperemia, when blood backs up into distensible organs like the liver and spleen
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severe right-sided heart failure
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one sign of this disease is active hyperemia when blood backs up into the lung capillaries
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severe left-sided heart failure
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congested liver from passive hyperemia due to right-sided heart failure
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nutmeg liver
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the ability to preserved blood as a fluid and when necessary to form a clot (thrombus)
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normal hemostasis
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in blood, the transformation of a liquid to a solid to prevent leakage through vessels
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thrombus (clot) formation
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10 steps:
1.injury to endothelium of blood vessel 2.transient vasoconstriction via a neural reflex 3.release of endothelin (a vasoconstrictor) from damaged endothelial cells 4.release of von Willebrand factor by damaged endothelial cells so platelets will adhere to exposed basement membrane of injured site 5.von W. also mediates plat.-plat. adherence 6.platelets change shape and also release ADP and thromboxane A2 granules to stimulate more adherence 7.form a platelet plug 8.circulating prothrombin --> thrombin 9.thrombin polymerizes fibrinogen --> fibrin 10.form a secondary hemostatic plug |
10 steps to how blood vessels prevent or stop a leak
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what deactivates thromboxane A2
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aspirin
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this prevents widespread thrombus formation after endothelial injury
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plasminogen factor (t-PA)
Healthy endothelium at the edge of the hemostatic plug releases tissue plasminogen factor (t-PA) to block coagulation cascade |
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this is used to prevent further damage from occlusion in CHD and stroke
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(t-PA) tissue plasminogen factor
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where von Willbrand factor is stored
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Weibel-Palade bodies in endothelial cells
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the most common inherited bleeding disorder in humans; characterized by spontaneous bleeding from mucous membranes, excessive bleeding from wounds, prolonged bleeding times in the presence of a normal platelet count; usually seen with the first major dental procedure
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von Willebrand disease
from defective or absent von Willebrand factor |
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in blood, the ability to transform from a liquid to a solid; fibrin forms a meshwork that cements blood cells together
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coagulation
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slow process where blood is transformed into a solid, a cascade of clotting factors
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intrinsic system (pathway) of blood coagulation
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fast process of blood being transformed into a solid, initiated by trauma to a blood vessel or surrounding tissue which causes a cascade of clotting factors to form a secondary hemostatic plug
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extrinsic system (pathway)
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what clotting factor is common to both the intrinsic and extrinsic system?
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Factor Xa
*at the point where factor X is converted into Xa, the intrinsic and extrinsic pathways merge and the rest of the steps are the same |
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1.Factor X --> Factor Xa
2.prothrombin --> thrombin 3.fibrinogen --> fibrin |
final steps common to both the intrinsic and extrinsic pathways of secondary hemostatic plug formation
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which plasma factor is unstable and must be bound to vWF?
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Factor VIII
-activated factor VIII activates thrombin and accelerates coagulation 1/2 life of VIII is 2.4 hrs, but when bound to vWF it is 12 hrs (lasts much longer to cause effect) |
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what causes hemophilia A?
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deficiency or lack of factor VIII
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ionic calcium (aka factor IV)
vitamin K |
agents that promote coagulation
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this removes Ca from the blood
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chelator EDTA
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where are many of the coagulation factors produced?
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in the liver; vitamin K is often required
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warfarin (coumadin)
heparin antithrombin III |
agents that inhibit coagulation
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this coagulation inhibitor acts by decreasing prothrombin concetration and alters the availability of vitamin K
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warfarin (coumadin)
-by altering vitamin K, it impairs production of clotting factors -rat poison |
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this coagulation inhibitor acts by binding to antithrombin III to accelerate the deactivation of thrombin
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heparin
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this coagulation inhibitor binds to thrombin and deactivates it
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antithrombin III
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process by which a clot is dissolved; starts shortly after clot is formed.
fibrin activates plasminogen --> plasmin which dissolves the clot |
clot dissolution
*dissolution and formation is balanced |
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hemostasis in an exaggerated form; predisposes to thrombis formation
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hypercoagulability
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1. increased platelet function
2. increased clotting activity |
2 forms of hypercoagulability
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this results when distubances in blood flow occur, increasing endothelial damage, and increasing platelet sensitivity.
(from atherosclerosis, diabetes mellitus, smoking, elevated blood lipids and cholesterol, increased platelet levels) |
increased platelet function (a form of hypercoagulability)
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results from the stasis of blood flow, increases in coagulation factors, and/or decreases in anticoagulation factors.
conditions: pregnancy-increased clotting factors immobility-stasis oral contraceptives-enhance clotting factors smoking-enhances clotting factors malignancy-cancer cells release factors that stimulate production of clotting factors |
increased clotting activity (a form of hypercoagulability)
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these can form anywhere and are named in relation to location or distinctive appearance
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thrombi
intramural thrombi-heart, valvular thrombi-valves, arterial thrombi, venous thrombi also: red thrombi, white(or layered) thrombi |
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thrombi that form in small veins, contain RBCs. Due to stasis. "currant jelly"
ex: pulmonary embolism from DVT formation |
Red thrombi
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thrombi that form in arteries or in the wall of the heart (mural thrombi); from sedimentation
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White (layered) thrombi
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1.small ones can be lysed
2.narrow the lumen and reduces flow (causes ischemia and impedes organ function) 3.occlude the lumen; results in infarction 4.serve as the source of an embolism |
4 fates of thrombi
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a freely movable intravascular mass that is carried from one anatomical site to another in the blood
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embolism
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1.thromboemboli
2.liquid emboli 3.gaseous emobli 4.solid particle emboli |
4 types of embolism
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clinically the most important form of embolism; color will tell you where it originated
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thromboembolism
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forms in amniotic fluid
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liquid emboli
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forms from a needle stick
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gaseous emboli
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forms from bone marrow or tumor cells in blood
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solid particle emboli
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what is the net effect of an emboli?
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infarction
-color of thromboembolism will tell you where it originated |
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where are small emboli cleared from circulation?
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the lungs (with some enzymes)
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common cause of death in middle-age, overweight women
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pulmonary embolism from DVT in legs
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insufficiency of blood supply of sudden onset that results in an area of ischemic necrosis; 2 colors-white and red
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infarction
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these infarcts are due to venous obstruction
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red infarcts
shows up in organs with single venous drainage ex: testes, ovaries - something on a long stalk which can get twisted |
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these infarcts are due to arterial obstruction
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white infarcts
(blood can't get into organ, organ turns "white") |
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what infarction does to post mitotic tissue
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permanent tissue damage
ex: scar formation in the heart |
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what infarction does to mitotic or facultative mitotic tissue
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can heal with little permanent damage
ex: liver (but chronic state will cause scar formation anyway - like cirrhosis) |
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1.transportation
2.regulation 3.protection |
3 functions of blood (5-6L in adults)
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1.oxygen, nutrients to tissue
2.wastes, from tissue 3.hormones |
what the blood transports
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1.heat (via vasoconstriction/dilation)
2.pH 3.acid/base balance (buffering) |
what the blood regulates
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immune functions
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how the blood provide protection to the body
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1.albumin
2.immunoglobulins 3.fibrinogen 4.thrombin |
Major proteins of blood
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1.erythrocytes
2.leukocytes 3.neutrophils, basophils, eosinophils, monocytes, lymphocytes 4.platelets |
what are the blood cells?
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1.transport lipids, metals, acid/base balance, coagulation
2.provide capillary oncotic pressure (to bring fluid back into capillary) |
what plasma proteins do
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this is where almost all plasma proteins are synthesized (except immunoglobulins)
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Liver
(ex: people w/liver damage having bleeding problems from no coagulation factors getting produced) |
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production of blood cells
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hematopoeisis
-in red marrow |
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theory that stem cells divide into myelocyte stem cell line (which will populated the marrow) and lymphoid stem cell line
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stem cell theory
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this organ belongs to the reticuloendothelial system (with lymph nodes,liver) and is composes of red and white pulp
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spleen
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1.red pulp-where RBCs are removed from blood and destroyed
2.white pulp-where lymphocytes are produced 3.removal of bacteria and viruses |
what the spleen does
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formation of RBCs
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erythropoeisis
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1.vitamin B12
2.folic acid 3.iron |
3 dietary factors required for erythropoeisis
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hormone that regulates RBC production by stimulating marrow to produce more RBCs; secreted into blood by capillary endothelial cells in the kidney in response to low arterial O2 pressure
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erythropoietin
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the source is ferritin which is stored in the liver until needed, then it is transported to bone marrow via transporter protein (transferrin), where it moves into bone marrow cells
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iron
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this condition results from a lack of iron
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microcytic anemia (small erythrocytes)
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vitamin found in green leafy vegetables, yeast, liver; it is essential for the formation of thymine
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folic acid
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this results from a lack of folic acid
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-maturation failure anemia (aka megaloblastic anemia) - large immature RBCs
-neural tube defects in fetus |
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this is found only in animal products and is necessary for the action of folic acid; it is also required for normal myelin formation in the nervous system
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vitamin B12
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this results from a lack of vitamin B12
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pernicious anemia (another form of megaloblastic anemia) - spherical cells can't transport as much O2
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this is required by the intestines for absorption of vitamin B12
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intrinsic factor secreted by stomach cells
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term for too many RBCs
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polycythemia
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conditions that stimulate release of erythropoeitin
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high altitude living
kidney tumor COPD (hypoxia) athletes |
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what is the arterial blood partial pressure of O2?
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PO2 100 mmHg (corresponds to 95% saturation of hemoglobin)
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what is the venous blood partial pressure of O2?
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PO2 40 mmHg (corresponds to 70% saturation of hemoglobin)
*true everywhere except heart, which extracts 70% of O2 from hemoglobin; little reserve capacity |
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CO2 diffuses into erythrocytes:
1.25% gets bound to hemoglobin 2.75% of CO2 combines with water in the cell and forms carbonic acid --> carbonic acid dissociates into bicarbonate ion and hydrogen a.bicarbonate ion diffuses into plasma, gets replaced by chloride ion in the cell to maintain electrical neutrality b.H+ binds to hemoglobin (acts as buffer) *Reactions reversed in the lungs and CO2 is lost |
How CO2 is transported
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what is the way RBCs produce ATP?
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glycolysis
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why do RBCs need ATP?
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to produce enzymes, for Na/K pump
*ability wears out at about 120 days |
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what happens to old RBCs?
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cleared by phagocytes in the spleen and liver
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if RBC ruptures in plasma it releases hemoglobin and binds to this circulating plasma protein:
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haptoglobin (which prevents renal excretion so it is preserved in the body);
hemoglobin-haptoglobin complex is taken up by phagocytes in the liver and hemoglobin is recycled |
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an increase in erythrocytes secondary to a known stimulus, such as renal cell cancer, or high altitude living; hypoxia causes overproduction of erythropoeitin
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erythrocytosis
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increase in #of circulatig RBCs from a primary myeloproliferative disorder (in bone marrow) from an unknown stimulus; symptoms include light-headedness, visual disturbances, headaches, enlarged liver & spleen r/t increased blood volume, increased hematocrit, increased viscosity, increased cardiac workload, & thrombosis
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polycythemia vera
*not from overproduction of erythropoeitin! |
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1.not enough RBCs
2.not enough hemoglobin 3.both |
the 3 causes of anemia
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results from reduced bone marrow function from genetic failure or trauma to stem cells; causes weakness, dyspnea, headaches, impaired immune function & bleeding
Tx: bone marrow transplant, discontinue use of causative agent |
aplastic anemia
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1.radiation
2.chemitherapy 3.antimicrobials 4.anticonvulsants 5.anti-inflammatories |
agents that can cause trauma to bone marrow stem cells, resulting in aplastic anemia
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this results in shortened RBC life-span from:
1.abnormalities of cell membrane and shape 2.hemoglobinopathies 3.physical injury |
hemolytic anemia
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abnormality of RBC membrane that results in premature lysis of cell; inherited autosomal dominant (need 1 copy from 1 parent to express, not x-linked); molecular defect on membrane
Sx:jaundice, splenomegaly, anemia |
hereditary spherocytosis
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destruction of RBCs by immune system - IgG or complement fixed to surface of RBC-->cell gets opsonized-->phagocytized
*a type 2 hypersensitivity rxn Dx: positive Coombs test associated with lymphoma, lupus, certain drug rxns |
acquired immune hemolysis
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caused by blood transfusion rxns, incompatibility of the ABO system
-IgM binds causing lysis and removal of RBCs |
secondary immune hemolysis
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a type of hemoglobinopathy: an inherited disorder with structural defects of hemoglobin globin beta protein chains
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sickle cell trait and disease
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cell sickling is brought on by severe hypoxia; these people are heterozygous
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sickle cell trait
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sickling of cells is much worse; homozygous individuals
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sickle cell disease (nearly all hemglobin is HbS)
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at what age will sickle cell become evident?
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at 6 months: when fetal Hb changes to adult Hb
10% african americans have trait with 0.2% expressing the disease |
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a type of hemolytic anemia hemoglobinopathy:
this is a group of disorders that results in lack of or defective globin protein |
alpha, beta thalassemia
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total lack of the 2 beta proteins or they are defective; autosomal codominant disorder (2 different genes, both have to express themselves); more common and more severe
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beta thalassemia
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heterzygotes - asymptomatic or mild
homozygotes - severe hemolytic anemia (thalassemia major) appears a 6 mos. of age-->need repeated blood transfusions or bone marrow transplant |
relevant features of alpha and beta thalassemia
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extended trauma
turbulent blood flow prolonged exercise artificial cardiac valves extracorporeal circulation devices |
hemolytic anemia resulting from direct physical trauma to RBCs
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monocytes are released into blood from bone marrow and migrate into tissues (36 hrs) to become these
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macrophages
(live for many years) |
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lymphocytes differentiate and mature here; they live for hrs to years
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lymphoid tissue
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which cell lives longer, T-lymphocytes or B-lymphocytes?
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T-lymphocytes
(and they circulate about every 10 hours) B-lymphocytes don't circulate, plasma cells live 2-3 days |
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where eosinophils are seen
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inflammatory and allergic reactions
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histamine
heparin bradykinin serotonin receptors for IgE - may give rise to mast cells |
what basophils contain
*type I hypersensitivity? |
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this system is composed of fixed and mobiles phagocytes present in the liver, spleen, GI tract and lymph nodes; function to remove and recycle substances from the blood such as antigen-antibody complexes, iron, worn out RBCs
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mononuclear phagocyte system (reticuloendothelial system)
*type III hypersensitivity? |
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>7500 per mcl blood - neutrophilia
<2500 per mcl blood - neutropenia |
neutrophil disorders
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the appearance of increased numbers of immature neutrophils indicates what?
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acute infection ("shift to the left")
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toxic granulations of neutrophils indicate this
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acute bacterial infection
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what tissue factors released by the inflammatory process stimulate bone marrow to release addition neutrophils?
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cytokines
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a lymphocyte disorder; lymphocytes are proliferating
Sx: cervial lymphadenopathy, fever, sore throat, splenomegaly, fatigue, malaise Caused by epstein-barr virus *may have more elevated risk for Hodgkins disease later |
infectious mononucleosis
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-qualitative and quantitative alterations in circulating leukocytes
-classified according to course & duration &/or the abnormal type of cells/tissues |
malignant WBC disorders - Leukemia
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rare leukemia with rapid onset, massive #of immature leukocytes, rapid progression,
too many leukocytes, low RBCs and platelets bone pain seen in children |
acute leukemia
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50% of all leukemia cases, adults and elderly, slow progression
granulocytic lymphocytic -bone marrow is infiltrated with malignant cells caused by genes & chemical/physical agents |
chronic leukemia
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in chronic granulocytic (myeloid) leukemia, 90% of all cases have this
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Philadelphia chromosome
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solid neoplasms that contain cells of lymphoreticular origin
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malignant lymphoma
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white males 20-30 yrs., and again over 50 most prone to this disease; presence of giant multinucleated Reed-Sternberg cells
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malignant lymphoma - Hodgkin's disease
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like Hodgkin's but more diffuse and diagnosed later with poor prognosis
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Non-Hodgkin's lymphoma
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plasma cell myeloma, damages bone marrow and skeletal structuresm tumors arise from a single clone of plasma cells
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multiple myeloma
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blood traveling from right heart --> pulmonary artery --> pulmonary capillaries --> pulmonary veins --> left heart
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pulmonary circulation
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blood traveling from left heart --> aorta --> capillaries --> systemic veins --> vena cava --> right heart
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systemic circulation
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if output of left heart < right heart, where does blood accumulate?
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pulmonary circulation
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if output of right heart < than left heart where does blood accumulate?
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systemic circulation
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the physical principles governing pressure, flow, and resistance as they relate to the cardiovascular system
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hemodynamics
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64% of blood is found where?
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in the veins and venules
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16% of blood is found where?
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in arteries and arterials
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what do arteries have that veins don't?
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smooth muscle
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what do veins have that arteries don't?
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"check" valves to prevent backflow
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period of ventricular contraction and ejection of blood
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Systole
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period of ventricular relaxation in order to fill with blood (atria contract and push blood into ventricles at this time)
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diastole
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this sound is heard when atrioventricular valves close (tricuspid, mitral)
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1st (Lub) sound
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this sound is heard when semilunar valves close (pulmonic, aortic)
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2nd (Dub)
3rd & 4th sounds are not heard in health adults |
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an electrical measurement of the action of the heart
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ECG Electrocardiogram
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Stroke volume X Heart Rate =
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cardiac output
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the maximum percentage of increase in CO possible beyond the normal resting level
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cardiac reserve
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the volume of blood heart must pump out of ventricles with each beat determined by venous return and muscular stretch
(before contraction) |
preload
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increased stretch (from increased end diastolic volume) causes increased force of contraction
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Frank-Starling law
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pressure the heart needs to push blood into the aorta, AFTER the contraction
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afterload
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this increases with Congestive Heart Failure
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Preload
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this increases with Hypertension
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afterload
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contractility; heart can change its force of contraction while maintaining the resting (diastolic) myocardial muscle length (it adjusts at the molecular level)
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inotropic
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heart rate; how many beats per minute; frequency ejection
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chronotropic
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reflects changes in the radius of arterioles and the viscosity of the blood
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total peripheral resistance
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1. slow contraction rate
2. high contractile forces for long time 3. low energy requirement |
characteristics of vascular smoot muscle
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calmodulin instead of troponin
less SR for storage influx of Ca for depolarization |
differences between cardiac and skeletal muscle
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alpha adrenergic receptors are excitatory and cause Ca channels to open, resulting in
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vasoconstriction
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beta adrenergic receptors are inhibitory and cause Ca channels to close, resulting in
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vasodilation
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what is commonly used for HTN and arrthmia management?
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Ca channel blockers
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what is the relationship?
F=Flow P=Pressure difference between 2 ends R=Resistance |
F=P/R
*flow decreases further from the heart |
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SVR
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systemic vascular resistance
-the total resistance of systemic circulation; relates to afterload=total resistance |
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PVR
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peripheral vascular resistance
-the total resistance of systemic circulation; relates to afterload=total resistance |
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TPR
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total peripheral resistance
-the total resistance of systemic circulation; relates to afterload=total resistance |
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P wave – deplorization of atria
(atria push blood into ventricles) Space – delay in AV node QRS – depolarization ventricles (larger wave, ventricles push blood out) T repolarization ventricles (wipes out repolarization of resting atrium) |
basics of an ECG
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What is the relationship where
P=difference between aortic or mean arterial pressure and the right atrial pressure CO=cardiac output SVR=systemic vascular resistance |
SVR=P/CO
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the smaller the vessel, the slower the
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velocity
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why is velocity flow slower in capillaries than other vessels?
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to allow for exchange of gas and nutrient
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blood flows through vessels in "layers" with plasm next to endothelium to reduce the imact of molecule or particle resistance
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laminar flow
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blood moving crosswise and lengthwise in blood vessels with conditions of high velocity, changes of vessel diameter, and low blood viscosity
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turbulant flow
*risk of clot with platelets and other molecules contact endothelium |
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force in vessel wal opposing distending pressure of fluid
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vessel wall tension
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what is the relationship when
T=wall tension r=vessel radius P=intraluminal pressure |
P=T/r
LAPLACE'S LAW *wall tension is inversely proportional to wall thickness (like a balloon) |
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What is the relationship where
C=compliance V=change in volume P=change in distending pressure |
C=V/P
Compliance is the total quantity of blood stored in a given portion of circulation for each mmHg rise in pressure |
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ability of a vessel to accomodate an increase in blood volume
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distensibility
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blood pressure from the periodic ejection of left ventricular blood into aorta at systole
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atrial pulse pressure
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What is the relationship where
BP=blood pressure CO=cardiac output TPR=total peripheral resistance |
BP=CO x TPR
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Height of pulse pressure
About 120 mmHg Function of stroke volume and stretch of aorta |
Systolic pressure
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Lowest pulse pressure
About 80 mmHg Function of the stored energy (systolic stretch) and rest tension that resists the “runoff” of blood from aorta without causing an increase in P |
diastolic pressure
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Difference between systolic and diastolic P
About 40 mmHg Increases with increased volume ventricular ejection into arterial circ. Decreases with decreased resistance to outflow Decreases in shock (decrease in Stroke vol, decrease in syst BP) even with compensatory increase in TPR |
pulse pressure
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Average pressure in the arterial systemic circulation during ventricular contraction and relaxation
About 90-100 mmHg MABP=CO/PVR Estimate by: (Diastolic BP)+ (Pulse Pressure/3) = MABP |
Mean Arterial Pressure
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Forced expiration against closed glottis leads to increased preload and afterload
Intrathoracic pressure increase can cause decrease venous return - triggers baroreceptor reflex. Upon release of pressure, venous return occurs on top of the baroreceptor triggered increase HR and arterial resistance. This leads to transient vagal slowing of heart. (heart attack on the toilet) |
Valsalva's maneuver
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baroreceptors in carotids and aorta (close to heart) --> to brain --> adjust BP
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autonomic nervous system regulation of BP - short term
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renin (from kidney):so kidney is a sensor of pressure and RBC count
angiotensin: blood (lungs) aldosterone (from pituitary): regulate fluid retention and salt balance |
humoral regulation of blood pressure - RAA system - short and long term
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1. renal-body fluid system
2. increase in fluid volume |
long-term regulation of blood pressure
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tissue vasodilators
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histamine
kinins prostaglandins |
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serotonin from platelets
nitric oxide prostacyclin |
vasodilators
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predominant innervation of coronary arteries is
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sympathetic
alpha receptors - constrict beta receptors - dilate *parasympathetic role is very minor |
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predominant innervation of veins is
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sympathetic
alpha - constrict beta - dilate |
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alpha receptors are
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postsynaptic
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beta receptors are
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presynaptic
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Complex of apoproteins, cholesterol esters, triglycerides, phosopholipids, nonesterified cholesterol esters
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lipoprotein
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intestinal biosynthesis – transport dietary lipids to fat and muscle
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Classes of lipoproteins: Chylomicrons
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transport endogenous liver triglycerides to fat and muscle
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Classes of lipoproteins: VLDL
very low density lipoproteins |
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source of LDL
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Classes of lipoproteins: IDL
intermediate density lipoproteins |
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liver, carries cholesterol from tissues (also atheromatous plaques) to liver
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Classes of lipoproteins: HDL
high density lipoproteins |
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main carrier of cholesterol, receptor mediated endocytosis, or nonreceptor uptake. A problem if arterial wall macrophages takes up LDL.
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Classes of lipoproteins: LDL
low density lipoproteins |
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abnormal lipids in the blood (excess of some lipid)
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DYSLIPIDEMIA
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what causes dyslipidemia in genetic forms?
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defects with enzymes or receptors can cause dyslipidemia
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process of forming atheromas in arteries, anywhere, not just heart
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ATHEROSCLEROSIS
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Hyperlipidemia (cholesterol)
Genetics: multifactorial, inherited Men>45 yrs Women>55 yrs, premature menopause Hypertension Diabetes mellitus HDL<40 mg/dL Smoking stress emotional weight diet |
dependent risk factos for atherosclerosis
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excess C-reactive Protein (CRP)-a marker of systemic inflammation
Homocysteine Serum lipoprotein (a) Infections |
independent risk factors for atherosclerosis (not associated with genes or environment)
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Acute inflammatory phase protein that interacts with complement to increase
inflammation marker of atherosclerosis marker of inflammation indicator of CV risk (3-4X increase risk) |
C-Reactive Protein
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Breakdown metabolite of the amino acid methionine
Methionine breakdown requires folate, B6, B12, riboflavin(insufficient vitamins increase homocysteine) >15 µmol/L Homocysteine is dose-dependent risk factor Inhibits parts of anticoagulation cascade Trigger of endothelial damage |
homocysteine
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Similar structure to LDL
Mechanism in atherogenesis not clear |
SERUM LIPOPROTEIN (a)
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Chlamydia pneumoniae
Herpes hominis Cytomegalovirus |
infections that are risk factors for atherosclerosis
|
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NCEP ATP III guidelines
ideal LDL:? too-low HDL:? Ideal triglycerides:? |
NCEP ATP III guidelines
ideal LDL:<100 mg/dl too-low HDL:<40 mg/dl Ideal triglycerides:<150 mg/dl |
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Still controversial whether these lead to atherosclerotic lesions
In the lumina Thin and yellow Contain macrophages Contain distended smooth muscle cells of lipid – foam cells |
fatty streaks
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1.Endothelial injury
2.Lipid infiltration 3.Inflammation 4.Smooth muscle proliferation |
steps to atherosclerotic lesion formation
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1. Injury to endothelial cells (triggers of inflammation)
2a. Platelets respond to injury and are recruited to area 2b. Injury recruits monocytes (macrophage) adhere and stimulate growth of SM and cause cell damage 2c. C-reactive protein released from endothelial cells 3. LDL deposit (trapped) on the damaged site 3b. macrophages fill with oxidized LDL - foam cells 4. Smooth muscle proliferation triggered by various factors as a result of above. 5. Atheroma forms (bump with hardened fibrous cap) 6. Weak arterial wall 7. Calcification of atheroma (dystrophic) and possible necrosis |
detailed hypothesis of atheroma formation
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Leaks or rupture of SM wall - hemorrhage
Thrombosis Occlusion Sudden obstruction due to plaque hemorrhage or rupture platelet aggregation abnormal vasoconstriction heart attack, stroke |
possible outcomes of atheroma formation
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Collateral circulation to maintain blood flow
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Compensatory Mechanisms
like development anastomoses |
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Inflammatory injury and necrosis of blood vessel wall from:
Direct injury to vessel Infectious agent Secondary to another disease process Cold – e.g. frostbite Irradiation – e.g. sunburn Mechanical injury toxins |
Vasculitis
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Sudden interruption of blood flow to tissue or organ
Usually from thrombus or embolus Dx:Signs of impaired blood flow Visual, palpation, instrument measure blood flow |
Acute Arterial Occlusion
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ATHEROSCLEROTIC OCCLUSIVE DISEASE OF LOWER EXTREMITY
Common location: superficial femoral and popliteal arteries Risk factors same as for atherosclerosis manifestations: pain (lack of oxygen, interferes w/krebs, lactic acid, triggers nerve pain) coldness or sensitivity impaired arterial pulsations color changes ulceration and gangrene edema sexual dysfunction superficial thrombophlebitis (nonvaricose veins) |
Ateriosclerosis obliterans
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Inflammatory arterial disorder that causes thrombus
Medium size arteries: plantar and digital vessels foot and lower leg; arm and hand Etiology not sure: associated with cigarette smoking in men Common Manifestations: Ischemic Pain Sensitivity to cold Peripheral pulses decrease or absent Coloration Skin- thin, shiny, altered hair and nutrition Nails- could be thick if ischemia is severe |
Thromboangiitis obliterans (Buerger’s disease)
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“functional disorder” – intense vasospasm of arteries and arterioles to fingers and sometimes toes. These body parts have only sympathetic vasoconstrictor vessels.
Triggers: cold stress Manifestations: Skin color:palor to cyanosis Cold numb, tingle Rebound hyperemia Could lead to ulceration or gangrene Dx: history Tx: prevention, vasodilator med. (Ca channel blockers, or alpha blockers), surgery (sympathectomy) |
Raynaud’s Disease and Phenomenon
Phenomenon is secondary to other disease such as: Previous vessel injury Collagen diseases Neurologic disorders Chronic arterial occlusive disorders |
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Localized abnormal dilation of a vessel
Can occur in arteries and veins, MORE COMMON in arteries CLASSIFIED according to cause, location, anatomic features |
aneurysm
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Small, spherical at a bifurcation
Often- circle of Willis in cerebral circulation |
Berry aneurysm
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Entire circumference with gradual and progressive dilation
Could be large in thoracic and abdominal aortas |
Fusiform aneurysm
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Part of circumference with saclike appearance
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Saccular aneurysm
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False aneurysm
Tear in inner wall, with blood separating the layers to form cavity |
Dissecting aneurysm
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Vessel wall weakness
Congenital defects Trauma Infections Atherosclerosis Tension = pressure x radius |
Causes of aneurysms
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Rupture
Pressure on adjacent tissue Block adjacent vessel blood flow |
manifestations of aneurysms
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Location: any part of aorta (ascending, descending, aortic arch, thoracoabdominal, abdominal)
Common Causes:Atherosclerosis, Degeneration of vessel media Usually after 50 yrs; men > women Manifestations:Often asymptomatic, Depend on location Thoracic:Pain of substernal, back and neck; Dyspnea, stridor, brassy cough from trachea pressure; Hoarseness from pressure on laryngeal nerve; Difficulty swallow from esophageal pressure Abdominal aorta:Often asymptomatic, Pulsating mass, Possible pain mid-abdominal or lumbar |
aortic aneurysm
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Acute and life threatening
Anywhere along aorta length Caused by conditions that lead to vessel wall weakness or degeneration Hypertension Degeneration of medial layer vessel wall Connective tissue disease Pregnancy induced chemical changes MANIFESTATIONS: (depend on location) Abrupt and severe pain Change in BP Interruption blood flow to extremities Syncope hemiplagia paralysis of lower extremeties |
DISSECTING ANEURYSMS
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1.Superficial veins collect and drain to deep venous channels; Thin walled, easily distensible
2.Return blood flow Valves prevent retrograde flow Require skeletal muscle contraction Low pressure system |
anatomy and physiology of veins
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Distended veins usually lower extremities
Primary- superficial saphenous veins > 50 yrs, obese, hereditary? Secondary- deep venous channels due to obstruction ( e.g. DVT, tumor, defect, pregnancy) |
varicose veins
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Prolonged standing
Increased intra-abdominal pressure: The valves in external iliac or femoral need to support (prevent retrograde) blood flow. Example of situations: after pregnancy, heavy lifting, prolonged increase pressure, obesity effects on superficial fascia and tissues |
mechanisms of primary varicose veins
(faulty valves) |
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Mx:Appearance, Ache, Edema, Venous insufficiency, Once stretched, not reversible on own
Dx:Physical inspection, Techniques to assess extent, Trendelengburg’s test, Doppler ultrasound, Contrast angiography Tx: Avoid activities that aggravate, Elastic support stockings, Scleotherapy, Surgery for deep venous channels |
manifestations, diagnosis, treatment of varicose veins
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Consequence of:DVT, Valvular incompetence
MANIFESTATIONS Impaired blood flow and associated signs and symptoms(if arterial flow in place, the oxygenation occurs) Tissue edema Impaired tissue nutrition Subcutaneous fat necrosis RBC breakdown hemosiderin deposits (brown pigment) Secondary lymphatic insufficiency (backs up because lymph drains into veins) Severe:Stasis dermatitis, Venous ulcers |
CHRONIC VENOUS INSUFFICIENCY
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Thrombus in Vein with inflammation of in vessel wall
Superficial veins or deep veins An example of acute vessel obstruction: (DVT) most common lower extremity Virchow triad Stasis blood Increase blood coagulability Vessel wall injury |
VENOUS THROMBOSIS
(Thrombophlebitis) |
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(tissue acts as a tourniquet ex:snakebite)
Localized pressure increase in “surrounding tissues” that restricts blood flow and can lead to ischemia Usually in the muscle compartment Normal P is 6 mmHg Elevated to cause damage is 30-40 mmHg MANIFESTATIONS:Tissue circulation decreased, Necrosis of tissue and nerves, Loss of limb function Time/location are factors |
COMPARTMENT SYNDROME
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External pressure that impairs blood and lymph flow to tissue (skin and underlying) can lead to ischemic lesions.
Often over bony prominence Prolonged lack of movement MECHANISMS External pressure to compress vessels 2 hours is possible Shearing that tears and injures vessels Sliding of one tissue layer over another with angulation of blood vessels to cause injury and thrombosis e.g. elevation head of bed to cause torso to slide PREVENTION: Identify persons at risk, Keep tissue healthy to improve tolerance to pressure, Protect against external forces |
PRESSURE ULCERS
(Decubitus ulcers, bedsores) |
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JNC7
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Diagnostic and Treatment Guidelines from The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7)
Printed by the National Heart Lung and Blood Institute (NHLBI) of the National Institutes of Health (NIH). |
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HTN
Normal:? PreHTN:? HTN1:? HTN2:? |
HTN
Normal:<120 PreHTN:120-139 HTN1:140-149 HTN2:160 and up *Diabetes Mellitus: goal <130/80 |
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obesity
hypercholesterolemia atherosclerosis high sodium diet diabetes hyperinsulinemia (associated insulin resistance) stress Type A personality familial history (race -Blacks) smoking lack of exercise Excess alcohol consumption Decreased Intake K, Ca, Mg Oral contraceptives |
related conditions to the pathophysiology of primary (essential, idiopathic) HTN
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SNS activity increase
RAA system activity increase ANP activity increase Nitric Oxide decrease Pressure Natriuresis Neural and Hormonal control of kidney low Mg, K, Ca Insulin resistance Genes |
what causes increase peripheral resistance and/or blood volume
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Activation of Sympathetic nervous system – effects CO and TPR, renal sodium retention
Insulin stimulated vascular SM growth –increase TPR Kidney salt and water retention Changes in Na and Ca cell membrane transport- sensitization of blood vessels to vasopressor stimuli |
proposed mechanism of increased BP
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Renovascular hypertension - atherosclerotic or fibrous dypslastic stenosis of renal artery(ies)
Renal parenchymal disease - renin or sodium dependent failure Cushing's disease (adrenal)- increase adrenocorticotropic hormone, increase vol Primary aldosteronism (adrenal) - increase aldosterone, increase vol Pheochromocytoma (adrenal medulla) - increase sympathetic tone Coarctation of the aorta - congenital constriction of aorta Estrogen-induced hypertension Sleep Apnea Drug induced/related Thyroid/parathyroid disease |
secondard HTN is due to a known cause
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∑ elevated systolic increases risk of stroke and heart disease
∑ elevated diastolic increases risk of stroke and heart disease ∑ systolic pressure puts greatest stress on blood vessels and heart ∑ both systolic and diastolic pressures matter, but systolic matters more ∑ not normal for systolic pressure to increase with age - elevated systolic pressure in elderly indicated arterial damage has begun |
PATHOPHYSIOLOGY OF HYPERTENSION
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∑ high systolic with normal diastolic reading
∑ most common form of hypertension in >65yr ∑ incidence increases with age ∑ treatment has been shown to reduce risk stroke and heart disease ∑ Decreased elastic properties of the arteries ∑ CV complications associated with increased Systolic BP ∑ CV complications associated with increased pulse pressure |
ISOLATED SYSTOLIC HYPERTENSION (ISH)
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often asymptomatic
headache, nosebleed, dizzy, tinnitus, blurred vision target organ damage |
physiological effects of HTN
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increased afterload * heart
compensatory systems try to regulate (RAA, SNS, etc.) damage small arterioles (single cell layer thick) target organ dysfunction (TOD) primarily: brain, eyes, kidneys, heart |
Pathologic sequelae: series of events in steps of physiological effects of HTN
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Upon standing, a sudden and abnormal drop in BP that does not adequately correct with compensatory mechanisms.
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ORTHOSTATIC HYPOTENSION
(Postural Hypotension) |