A&pii Blood Jkjkhardcore

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Functions of blood 5

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Transport dissolved casses wastes nutrients hormones
Regulate the pH/Ion [ ] Eliminating excess Ca or K
Restrict fluid loss at injury sites
Defend against toxins and pathogens
Stabilization of Temperature.

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Plasma

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Fluid CT matrix of blood

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Formed elements and 3 types

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RBC, platelets WBC

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Hemopoiesis

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Process of making formed elements.

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Percent formed elements

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1%- WBC&Platelets 99.9% RBC
37-54% of blood is the formed elements

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% plasma

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46-63% is the Plasma
7% plasma proteins
other solutes 1%
Water 92%

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5 wbc

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Neutrophils 50-70%
Lymphocytes 20-30%
Monocytes 2-8%
Eosinophils 2-5%
Basophils less than 1%

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Plasma proteins

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Albumins 60%
Globulins 35%
Fibrinogen- 4%
Regulatory proteins less than 1%

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Blood
pH
Compared to water
Temperature

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pH 7.35-7.45
5xs everything as water
38 Celcius

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Two components that make up whole blood

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Venous and artierial blood

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Plasma vs interstitial fluid

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levels of respiratory gasses o2 co2 and [ ] and types of dissolved proteins as they cannot cross capillary walls.

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Albumins

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60% of plasma proteins
osmotic pressure of plasma
transport fatty acids thyroid hormones some steroids hormones

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Globulins

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35% of pretins in plasma
antibodies aka imunoglobulins
and transport globulins that bind things so that they are not lost at kidneys ie Fe and Thyroid hormone Steriod binding apolipoproteins.

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Fibrinogen

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clotting 4 percent of plasma proteins. Leaves serum.

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Hematocrit

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% of whole blood volume contributed by formed elements
the WBC RBC and platelets.

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3 advantages of biconcave

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squeeze through b/c of flexibility
stacking
Large surface area to volume enabling more carrying of o2 & stuff

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Hemoglobin
(Hb)

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95% intracellular proteins in RBC's
Cantain heme and bind with iron to make oxyhemoglobin HbO2

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Deoxyhemoglobin and oxyhemoglobin

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Blood who's iron (Fe) is bound to oxygen either bright or dark red.

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In preggo women using drugs like Hydroxyurea or butyrate help simulate fetal hemoglobin why is this important

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It is tx for conditions like sickle cell anemia

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aenemia

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Hb content is reduced or hematocrit is low, interfering with oxygen delivery to peripheral tissues

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Removal of Heme units

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heme unit stripped of iron converted to > biliverdin>bilirubin>out the bile

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myeloid tissue found at?

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Sternum (menubrium, ribs skull scapulae pelvis and proximal limbs of bones

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RBC maturation

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Proehtroblast>erythroblasts>Reticulocytes>Mature red blood cell

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Myeloid stem cells

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make RBC and WBC

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lymphoid stem cells

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make lymphocytes

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pernicious anemia

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B12 deficiency, normal stem cell devisions of RBC cannot accor.

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Estrogens vs Androgens w/ respect to Erythropoiesis

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Estrogens don't stimulate RBC production Androgens do. Males have more RBCs

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EPO erythropoeitin ESH

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glycoprotein formed in kidneys when Low o2
Stimulates RBC
stimulates inc cell division rates, speeds up maturation, by accelerating rate of Hb synthesis.

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Conditions for Hypoxia

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during anemia, blood flow to kidneys declines, low oxygen in air (disease or high altitutdes) lungs are damaged

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Hemoglobin

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Protein with four globular units that each contain a heme group that binds an iron that binds oxygen

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Renal arteries blocked...

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Then the kidneys will not have sufficient o2 causing them to produce EPO hormone that will stimulate RBC production and thus increase hematocrit levels

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Diseases that damage the liver such as hepatitis does what to bilirubin in the blood

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When RBCs are broken down the globulins are converted into biliverdins > bilirubin>thrown out of the body with bile. if the liver is dmg'd bilirubin is unable to be excreted and thus levels will increase.

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Type A blood

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Antigen for A only
2nd most in us
anti b

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Type B blood

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Antigens for B only
anti a

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Type AB blood

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both A & B antigens
least amount in pop of usa

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Type O blood

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neither A or B antigens
most dominant in the us
both anti A and anti B

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agglutination

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Clump together and hemolysis of foreign RBCs or opposing surface antigen of the resident antibodies

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Rh factor

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Person with Rh and a person without it, an Rh negative person does not have antibodies against RH however if a person is sensitized by previous exposure to Rh positive blood then those antibodies will form.

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cross reaction

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agglutination

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surface antigens

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determines blood types and identifies rbcs of each person

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WBC functions

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defend against pathogins removetoxins wasts and abnormal or damaged cells

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positive chemotaxis

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guides wbs to dmg'd tissues, and pathogens, attraction to specific chem. stimuli

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WBC movement

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migrate ouf of the bloodsteam, have amoeboid movement, positive chemotaxis, and (some) phagocytosis

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Phagocytosis

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Neutrophils, eosionphils and monocytes, they eat stuff

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granulocytes

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neutrophils eosinophils basophils

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Basophils

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histamine, inflammation

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eiosinophils

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virus, exotoxc

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platelets 3 functions

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Release enzymes and chem. that help clot
Formation of a patch on dmg'd blood vessels
Active contraction after clot has formed to shrink the clots size, pulling it together.

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Agranular leukocytes

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monocytes lymphocytes: Tcells(atk foreign cells and go into peripheral tissue)
b-cells (antibodies)
NK cells destroy abnormal tissue

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Differential count

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Counts the number/types of wbc
Leukemia can be show from leukocytosis

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myeloid stem cells

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Make granulocytes and monocytes, from the bone marrow

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Life span of platelets

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about 9-12 days phagocytes remove them

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Thrombocytopoiesis

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making platelets
Megakaryocytes in bone release platelets Multi csf TSF and inerleukin-6 regulates the rate at platelet formation

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Hematostasis

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stop blood. clotting process
vascular phase
platelet phase
coagulation phase

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vascular phase

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local blood vessel constriction vascular spasm

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Platelet phase

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follows as platelets are activatged adhere to the damaged surfaces

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coagulation phase

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platelets inter act with clotting factors either extrinsic or intrinsic pathway to form a blood clot
fibrinogen>fibrin

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clot retraction

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platelets pull the clot together making it smaller AFTER CLOT FORMS

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fibrinolysis

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fibrin breaks down dissolving through plasmin (a form of plasminogen)