blood system
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| percent of RBCs defined as (in lab) | hematocrit
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| plasma is 92% water plus . . . | proteins, solutes in this component of spun blood
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| plasma proteins gen made by | liver makes these
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| albumin is transporter pro and has this role also | osmotic pressure - part of bp contributed to by (this protein) and its attraction for water
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| if liver doesn't make plasma proteins, less osmotic pressure --> | water moves from bv into tissue (edema)
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| however we get to low protein state this symptom occurs | ascites (edema in abd cavity) is associated with dec. plasma pro bwo starvation, liver failure
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| globulins also transport things like | these proteins transport hormones, lipids, lipoproteins(LDL/HDL, immune fx (gamma globulins AKA antibodies)
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| fibrinogen helps with | coagulation, made by liver
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| plasma also contains nutrients Pro, CHO, LIP | nutrients carried by plasma
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| creatine, amonium and urea/uric acid also found in | plasma as waste products
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| formed elements contain | RBCs, some WBCs and platelets. Lab test is CBC to determine #/types of cells
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| If we want to know type of WBCs from CBC then need to order this lab | CBC with differential
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| WBCs = neutrophils, lymphocytes, monocytes, eosinophils, basophils nmeonic | never let monkeys eat bananas
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| neutrophils are phagocytic | yes
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| lymphocytes | increased in infection, make antibodies or are helpers or are able to attack infected cells
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| monoctyes | macrophages when in tissue space, eat dead, dying or infected cells. Usually see in chronic infections.
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| eosinophils | 2-4% of WBC are phagocytes that eat antigen/antibody complexes (as in allergies, autoimmune), parasites
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| basophil | a little bit of histamine (inflammatory chemical) --> bv vasodilation and inc permeability of capillaries
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| Hgb is a protein in RBC made by | bone marrow
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| bone marrow makes these cells | RBC, WBC and platelets (bwo megakaryocte)
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| pluripotent cells are undifferentiated stem cells in bone marrow can --> RBC, WBC or platelet depending on hormone or factors stimulate it. For RBC it is . . ..for platelets it is . . . | *erythropoeitin(from kidneys, some liver). Thrombopoeitin stimulates for platelet production (made in liver)
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| If you have liver failure, can't make thrombopoeitin-->platelets --> this type of disease | clotting disorders
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| Interleukins are stimulating factors for | WBC cell stimulation/proliferation
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| diseases of bone marrow interfere with homeostasis, --> | *can't make RBC, hypoxia
*can't make WBC, infectons
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| aplastic anemia | when bone marrow shuts down
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| leukemia | cancer of WBC lines(can be of any). mutation of pluripotent cell--> massive production of one in line (leukocyte, neutrophil, etc). Overproduction of cancer cell, underproduction of everything else
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| treatment of leukemia | chemotherapy and/or radiation to kill cancer cells, then bone marrow transplant. gen require protective isolation.
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| if decreased RBC and/or decreased Hgb and/or decreased Hct --> | anemia which results in hypoxia
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| anemia results in | hypoxia or decreased 02 carrying capacity of blood
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| if hypoxia then this hormone will stimulated bone marrow to increase RBCs | EPO (difficult to do if kidney diseased)
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| heme is made of | Fe and bilirubin(porphyrin ring)
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| bilirubin is byproduct of RBC degregation, which binds to albumin to liver then transported by transferrin to | liver, major storage, then to bile and/or
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| if pt presents with jaundice, this indicates | liver failure and/or hemolytic anemia (yellow pigment of bilirubin breakdown)
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| bilirubin (unconjugated) is destructive to this type of tissue | neural tissue affected by this byproduct of RBC degredation
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| Bilirubin --> liver for conjugation, then --> intestine (urobilinogen, makes feces brown) --> | urobiinogen to blood stream --> kidneys --> urobilinogen (sign of too much bilirubin conjugated indicates disease like hemolytic anemia
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| Hgb A1C measures what | this test measures glycosylation of the protein (how much sugar is on the Hgb)
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| hemostasis defn and process | stopping bleeding bwo spasm, platelet plug, coagulation (12 coagulation factors, no #6 so it looks like 13)
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| coagulation cascade factors arrive at site of hemostasis to form stable fibin clot | process of step 2 hemostasis
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| anticoagulants to break up clots in vessels | TPA, streptokinase, ASA,
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| Extrinsic cascade if vessel damaged from outside | Intrinsic pathway used if vessel damaged from inside (arteriosclerotic clot--> hydrostatic shearing of epithelial lining vessel)
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| hemophilia classification based upon what coagulation factor they are missing | how hemophilacs are treated . . .give them missing coagulation factor (synthetic)
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| ASA helps prevent | platelet plug formation
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| Heparin inhibits formation of . . . | thrombin and Vit K useage
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| coumadin interferes with | Vit K dependent factors (factors II, VII, IX and X)
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| coumadin -extrinsic - PT, INR as to | heparin, intrinsic pathway - APTT (thrombin)
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| what type of patient needs anticoagulation tx? | *pulmonary embolism (piece of thrombus that breaks off)
*post op
*mechanical heart valve (titanium is sticky for platelets)
*atrial fibrillation - cuz blood that's not flowing quickly is likely to clot
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| ASA effects | platelets with respect to clotting cascade
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| TPA = (used to inhibit thrombin) | tissue plasminogen activator, used for lysing clot when no longer needed (fibrinolysis pathway)
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| Blood Type A has surface Ag A | Type B has Ag B on it
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| Type AB has both A and B antigens | Type 0 has no antigens
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| Type A has these antibodies | Anti-B antibodies
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| Type B has these antibodies | Anti-A antibodies
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| Type AB has these types of antibodies | no antibodies
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| Type O has these antibodies | Anti-A and Anti-B
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| Rh antigen = D antibody therefore if Rh+ | no Anti-D antibody
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| Rh- can make antibody against D in the case of | 'sensitization' or exposure such as Rh+ transfusion OR Rh- mom exposed by Rh+ fetus during birth or late term abortion/miscarriage
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| Give Rhogam to prevent Ab production in | Rh- mom
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| If mom is Rh-, give her Rhogam in what pregnancy? | all pregnancies
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| Do we give Rhogam to Rh+ mom? | nope
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| transfusion reaction: Recipient is A+, donor is Type B+ | recipient has antibody to donated cell --> hemolysis (which is the transfusion reaction) --> globin etc clogs capillaries -->glomerular fxn decreases -> kidney failure --> dialysis or death may occur
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| universal donor type | O- (no antigens whatsoever, no transfusion reaction possible)
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| Universal recipient type | AB+ (has all possible antigens, so doesn't make ANY anti-antibodies to ANY antigen)
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