Term
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Definition
| weakness, fatigue, tired, poor oxygen delivery |
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Term
| two most common reasons for anemia |
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Definition
| decrease in blood cells and inefficiency of blood cells to pick up oxygen |
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Term
| where do all RBCs and WBCs grow? |
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Definition
| they grow and mature in the center of the long bone where there is bone marrow before being released into the blood stream |
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Term
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Definition
| a hormone released by the kidney tells bone marrow to produce more RBCs |
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Term
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Definition
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Term
| what occurs if hct is to high? |
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Definition
| the platelets begin to bump into each other and form clots |
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Term
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Definition
| have to get blood cells removed because hct is too high |
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Term
| pleura potential stem cells |
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Definition
| stem cells with embryonic message able to convert into any type of cell responsible for populating the whole body with RBC, WBC, and platelets |
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Term
| how does erythropoeitin work? |
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Definition
| it exposes its cell surface receptor and the ligand attaches to the receptor belonging to erythropoitin. causes the release of messenger to inc, the production of RBC. |
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Term
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Definition
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Term
| what happens when O2 oxidizes? |
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Definition
| it becomes methhemoglobin, it is the signal for the spleen and the liver to destroy the cell. |
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Term
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Definition
| the RBC dies before its lifetime expectancy. puts stress on stem cells who try to repopulate the body. |
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Term
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Definition
| made up of 2 alpha and 2 beta chains. iron and porphyrin(heme). your body cannor make iron you must consume it. when the spleen and kidney takes old RBCs it recycles the iron but if you bleed such as in menstruation or a cut the body loses iron. which then dec. hemoglobin causing a deficiency in the amnt of O2 in RBC's |
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Term
| which co-factors are needed to make hemoglobin? |
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Definition
| B12. B12 is absorbed in the wall of the stomach. needs a carrier molecule called intrinsic factor which is made by parietal cells. |
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Term
| B12 deficiency anemias are caused by what 2 reasons? |
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Definition
| 1. adequate intake of B12 but little intrinsic factor 2. inadequate intake of B12, intrinsic factor is perfectly fine. |
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Term
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Definition
| a lack of intrinsic factor |
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Term
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Definition
| inadequate B12 consumption |
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Term
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Definition
| plueropotential cells fails, results in a dec in RBC, WBC, Platelets = pancytopenia |
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Term
| causes of aplastic anemia |
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Definition
| exposure to therapeutic agents, also idiopathic |
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Term
| treatment of aplastic anemia |
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Definition
| give blood transfusion, the blood is fractioned into plasma, platelets, rbc, and wbcs the person will recieve w.e component they need |
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Term
| when does HCT drop? and what do you do? |
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Definition
| hct drops when large amounts of blood has been lost. Due to the body being quicker in restoring plasma and not RBC's. you must infuse w/ RBCs. |
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Term
| androgens in relation to anemia |
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Definition
| stimulate bone marrow like erythropoietin. |
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Term
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Definition
| not enough porfarin, which cannot make enough heme= dec hemoglobin. |
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Term
| 3 causes of sideroblastic anemia |
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Definition
1) genetic mutation, that cannot make porforin, can give pyroxidine which allows the making or porforin.
2) excessive alcohol intake can dec. porforin. pyroxidine does not work, must limit alcohol.
3) idiopathic |
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Term
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Definition
| microcytic anemia, caused by the loss of to much iron. leads to symptoms of: koilonychia, glossitis, cheliosis (cracking of the lips) |
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Term
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Definition
| test to see if it is a pernicious anemia or a B12 deficient anemia |
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Term
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Definition
| macrocytic anemia. if a pregnant mother does not consume enough folic acid, the mother may have children with anencephaly (an infant w. no brain) caused by chroni alcholism, chemotherapy. |
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Term
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Definition
| a genetic disorder. due to the shape of the cells the RBC lacks the pumps that pump out water from the cells they cause the cell to inc in size with H2O and becomes a sphere shaped disk. it is a hemolytic anemia bc it is taken out of the cell before the 120 days. when it gets to the spleen it is trapped in the reticulo endothelial tissue. |
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Term
| how to treat spherocytosis |
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Definition
| they remove the spleen and it inc the lifespan of the cell. |
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Term
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Definition
| genetic mutation. preserves hgb to protect RBC against oxidation. If you lack this enzyme the RBC will oxidize sooner and have a hemolytic anemia. need to avoid aspirin, antimalrial drugs, and sulfonimides. |
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Term
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Definition
| genetic mutation (recessive). when the cells sickle they are more likely to get caught in the spleen and develop and aplastic crisis. as the sickle cells try to pass the narrowing of the capillaries the cells get caught and clot against each other and O2 cannot get through may lead to ischmia of the muscle and a thrombotic crisis. person must stimulate the pleuropotential membrane to make more RBCs. |
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Term
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Definition
| must push fluids to inc orthostatic pressure which breaks up the clot. not RBC's bc it would make the congestion worse. |
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Term
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Definition
Hh=no sickle cell but you are a carrier
HH= no sickle no carrier
hh=sickle cell |
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Term
| thalassemia AKA cooleys anemia |
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Definition
| genetic mutation. affect adequate quantities of alpha chains OR adequate quantities of Beta chains. symptoms are the same: cells do not produce enough HGB. If you have the disease= thalassemia major. if you are a carrier of the disease thalassemia minor. a pregnant woman w. thalassemia minor is a highrisk pregnancy. |
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Term
| how do you removes Fe from the body? |
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Definition
| chelating agent, it binds to iron and is excreted regularly through the digestive tract. |
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Term
platelets
1) how much in the body?
2) avg lifespan? |
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Definition
1) 150k-350k/mm3
2) 10 days |
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Term
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Definition
| blood stops flowing. can lead to the formation of clots. legs are at most risk can get DVT (deep vein thrombus). |
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Term
| risk of clots w. atrial fibrilation |
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Definition
| occurs due to electrical damages to the heart and causes the atrium to not pump fully but quiver. 15% of the blood stays n the atrium and the blood sits there and pools, this may form clots which can eventually be pushed into the circulation and cause an embolli travelling into the blood stream. |
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Term
| chronic atrial fibrillation |
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Definition
| must give them a constant dose of anticoagulant such as heparin (in the hospital) and coumadin (at home). |
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Term
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Definition
| platelets are sticky when there is a break in the B.V. a nerve message is sent to the nearest B.V. to vasoconstrict. the platelets then stick to the jagged areas a platelet plug is formed. |
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Term
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Definition
| platelets are water soluble, it allows for stopping of RBC spilling, but it cont to spill plasma, in order to stitch the spaces between the platelets with fibrin and the plug then becomes an actual clot. |
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Term
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Definition
| clotting factor made by the liver are always formed and circulating the body in the inactive form. when factor 12 bumps into a broken B.V. it acts as a signal to convert 12 to 12a then activates 11 to 11a, then activates 8 to 8a, 8a activates 5 to 5a makes prothrombin to thrombin which converts fibrinogen to fibrin. |
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Term
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Definition
| are activated when blood is found on the outside of the B.V. both pathways need calcium to work if the person has hypocalcemia they will not be able to form clots. |
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Term
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Definition
| lack factor 8 throws off the intrinsic pathway but does not affect extrinsic branch. you are able to inject factor 8 into blood stream |
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Term
| anticoagulants vs. fibrinoytics/thrombolytics |
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Definition
anticoagulants stop clots from forming (heparin and coumadin) it blocks the intrinsic pathway as an anti-coagulant.
fibrinolytics dissolve clots that have already formed. |
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Term
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Definition
| as the fibrin strands contract it pulls platelets together along with the edges of the blood vessel. |
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Term
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Definition
| plasmin dissolves blood clots. we have plasminogen in the body (the inactive form of plasmin) activated by several enzymes: if its from the plasma we have plasma activator, if its from the tissue we have tissue plasminogen activator, if its from the kidney we have urine activator, if its from the blood we have clot activator. |
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Term
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Definition
| releases streptokinase which acts as blood dissolving enzymes and causes the clots to be dissolved before time, and the wound has not fully healed yet and causes bleading. Must use an antibiotic in order to get rid of strep bacteria. |
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Term
| disseminated intravascular coagulation (DIC) |
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Definition
| tirggered by: sepsis, bacteremia, massve trauma, burns, cancer, shock, lood transfusion reactions, pre-eclampsia, alter clotting mechanism and forms micro-emboli throughout the body and the micro-emboli circulate the body it may: 1. become larger and block circulation 2. they are useless clots and when you actually need to form a clot all of the clotting factors have been used. |
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Term
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Definition
1) classic hemophilia- cannot produce factor VIII 80%
2) hemophilia B (x-mas disease)- cannot produce factor IX 15%
3) hemophilia C- cannot produce factor XI 5%
MEN ARE MORE LIKELY TO GET IT |
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Term
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Definition
| essential within normal limits for myelinating sheaths also for sex hormones and other steroids. |
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Term
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Definition
| carbon bonds where it is fully packed with hydrogen |
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Term
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Definition
| tend to be liquids at room temp. are not packed with hydrogen ions. |
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Term
| how does the liver react to saturated and unsaturated fats? |
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Definition
| when you eat saturated fats the liver tends to turn it into cholesterol. when you eat unsaturated fats the liver does no to make cholesterol (good thing! :) ) |
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Term
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Definition
| man made. partially hydrogenated found that they were more unhealthy than saturated fats b/c transfatty acid were converted to cholesterol much sooner than saturated fats. they also increase LDLs AND lower HDLs. |
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Term
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Definition
| is a lipid (fat, oil), must be transported in the blood stream to the cells by proteins. when it is taken to the cell the protein is called LDL's, when taken from the cell back to the liver to be metabolized it is called HDL's. |
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Term
| which lipo protein is involved with atherogenesis? |
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Definition
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Term
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Definition
| usually they are proportionate. is better if u have more HDLS than LDLs. |
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Term
| estrogen in relation to cholesterol |
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Definition
| estrogen increases the evel of HDL's in the body when menopause kicks in they loose the cardiprotective effect. more women after menopause have alot of increased LDLs. estrogen also protects bone breakdown. |
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Term
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Definition
| the more receptors you have the better because the cell can pull the cholesterol in, if you dont have enough receptors they end up in the arteries. 1 out of 250,000 ppl cannot produce any receptors at all. |
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Term
| meds to lower cholesterol |
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Definition
1) cholestyramine: bile acid sequesterin. the drug binds to bile and cannot emulsify fat and causes the liver to use cholesterol to make more bile and then lower cholesterol in the blood stream. a major symptom was bloating alot and indigestion.
2) statins like lipitor work by going to the liver and inhibiting enzymes that make cholesterol. lowers LDLs and does not affect HDLs. a major symptom is muscle necrosis.
3) omega 3 fatty acids decreases LDLs, in nuts and fish. |
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Term
process of atherosclerosis
(formation of fatty streaks) |
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Definition
| when there is an injury to the endothelial cells a monocyte comes and attaches to the wall of the B.V. now called macrophage it is able to put out LDL receptors, the LDLs attach to the macrophage and stay there, they bring in more and more cholesterol they become larter and larger they are renamed foam cells, and form a streak called a fatty streak. this is the beginning of atherosclerosis. |
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Term
process of atherosclerosis
(formation of raised fibrous plaques) |
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Definition
| platelets begin to be drawn to the area of fat and begin to release a growth factor and trickles down to smooth muscle and connective tissue and causes it to grow and form a cap over the foam cells. causes them to die and leaves just a pure amnt of cholesterol. the cap is called raised fibrous plaque. as the RFP grows it takes up more space and less blood can flow through. at 60% you loose the ability to vasodilate in the event that you are exerting yourself and need more O2 flow to the heart. your heart must then depend more on anaerobic respiration, which is not ideal. the body releases lactic acids and sends a message of pain to the brain and causes u to stop movement. |
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Term
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Definition
| occurs if tissue death occurs in the myocardium. |
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Term
| atheroslerosis (plaque cracking) |
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Definition
| if the plaque cracks a clot may form to stop bleading and can grow so fast it fills the lumen in seconds. give TPA to clear the B.V. |
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Term
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Definition
| if you have a clot on top of the crack/plaque and causes the smooth muscle to spasm causing vasoconstriction. then the muscle spasms it causes unstable angina. if coronary artery is 60% occluded or you have symptoms of angina you have C.A.D |
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Term
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Definition
| measures how much the heart can take before it hurts ex: running on treadmill. |
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Term
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Definition
| injects dye into coronary artery to see how much is occluded done when a stent is going to be inserted. we then have to worry about clots because it is not a human object. |
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Term
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Definition
| use the saphenous vein and stitch the veins in the areas where there is an occlusion. |
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Term
| what happens during systole? and what else is it refered as? |
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Definition
| the blood is being pumped into the arteries and the ventricles contract. also refered as surged pressure |
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Term
| what happens during diastole? and what else is it refered as? |
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Definition
| the ventricles relax and the atria empties into the ventricles. also known as maintenance pressure. |
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Term
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Definition
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Term
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Definition
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Term
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Definition
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Term
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Definition
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Term
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Definition
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Term
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Definition
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Term
| which reading is an indicator of HTN |
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Definition
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Term
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Definition
| the B.P. readings come up higher than usual due to nervousness. cannot make diagnosis of HTN w. just one reading if they are boarderline. must have atleast 3 readings on diff visits indicating HTN. |
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Term
| what are the two types of HTN? |
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Definition
1) essential HTN or idiopathic
2) secondary HTN |
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Term
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Definition
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Term
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Definition
| amnt of blood the heart pumps in a minute. |
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Term
| how many liters of blood do you need at rest and during exercise to meet perfusion needs? |
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Definition
at rest: 5-7 Liters
during exercise: 10-12 Liters |
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Term
| what makes cardiac output? |
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Definition
|
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Term
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Definition
| the amnt of blood pumped out everytime your heart contracts |
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Term
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Definition
| by inc. the force of contraction. epinephrine controls the force by which the heart contracts. |
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Term
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Definition
| affect the amnt of times the heart contracts. has a (+) effect on epinephrine and (-) effect on digoxin. |
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Term
| what is the normal heart rate? |
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Definition
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Term
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Definition
| affects the strength by which the heart contracts. has a (+) effect on epi and (+) effect of digoxin. |
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Term
| which drugs have a (-) inotropic effect? |
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Definition
| calcium channel blockers and beta blockers. |
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Term
| what does the parasympathetic N.S. do? |
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Definition
| it works to digest food, maintain homeostasis and works w. a hormone called ACH (acetylcholine) |
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Term
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Definition
| it is an anticholinergic that blocks salivary secretion during surgeries. |
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Term
| what does the sympathetic N.S. do? |
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Definition
| works with the fight or flight response. its main nuero trasmitter is epinephrine. epinephrine is made in the adrenal glands norepinephrine is made in the nerve endings. |
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Term
| where do B1 and B2 receptors work? |
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Definition
| B1 works in the heart and B2 works in the lungs. |
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Term
| what kind of reaction would you want after a heart attack and what medication would you give? |
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Definition
| give a beta blocker bc it has a (-) inotropic effect. therfore dec force of contraction and allowing the heart to rest. |
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Term
| what would you do in relation to the heart with someone who has HTN? |
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Definition
| u would dec CO in order to dec BP bc BP=CO x TPR if you lower CO you lower BP |
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Term
| what happens when you release epinephrine in relation to BP? |
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Definition
| the peripheral BV constricts and causes the TPR to go up and therefore inc. BP |
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Term
| how can you inc. after load |
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Definition
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Term
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Definition
| the amount of blood being pushed forward at rest. it is the amnt of total blood in the heart divided by the amnt of blood that leaves the heart. |
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Term
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Definition
| idiopathic. risk factors include smoking, obesity, and excess alc consumption. occurs most common in adults |
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Term
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Definition
| cause is known. organic causes, if fixed it will correct HTN. occurs most common in children |
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Term
| what meds are given to HTN |
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Definition
beta blockers: dec S.V. and HR
vasodilators: dec TPR
calcium channel blockers: (-) chro and (-) inotropic effect.
ACE inhibitors |
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Term
| how does the kidneys react to hypotension? |
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Definition
| if the kidney senses a dec in BP due to a dec amnt of fluid going into the kidney it will release renin. which would then stimulate angiotensin I which is a powerful vasoconstrictor, ang 1 turns into ang II, it keeps water in and SV goes up which inc. BP |
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Term
| how can you stop BP from going up in relation to angiotensin? |
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Definition
| if u block enzymes which convert ang 1 to ang II you can dec overall BP. |
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Term
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Definition
| a tumor, develops in the adrenal gland and releases epinephrine. the tumor causes the inc. release of epinephrine which will inc BP really high. causes sweating, palpatations, and headaches. |
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Term
| what does the medulla release? |
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Definition
|
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Term
| what does the cortex release? |
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Definition
| aldosterone, cortisol and male and female sex hormones. |
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Term
| how can you test for phachromocytoma? |
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Definition
| epinephrine is broken down into a waste product called VMA (vandilmandelic acid) if this product is elevated they have the tumor. you then get a CT scan and remove tumor. |
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Term
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Definition
| max amnt of blood in the ventricles. which is at the very end of diastole. if you inc preload you will inc the pressure of the ventricles. |
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