blood Flashcards
Components of blood
-also , what kind of tissue is blood
–blood is CT
Plasma = extracellular matrix
Formed elements = living cells
- Erythrocytes
- Leukocytes
- Platelets
how does oxygen affect blood color?
low O2 = dark red
high O2 = scarlet
Blood in centrifuge
Plasma on top 55%
Buffy layer = WBC and platelets <1%
Hematocrit = RBCs 45%
- 47% for men; 42% for femals
3 Func of blood
distributing substances
-O2, waste to lings and kidneys, hormones
regulating blood levels
-temp, pH (bicarbonate ion buffers), fluid volume
protection
- no blood loss (clots)
- no infection: antibodies, complement proteins, WBCs
Components of blood plasma
- 90% water
- a ton of dissolved solutes
- most solutes are plasma proteins which are made by the liver and stay in the blood
- 60% albumin; 36% globulins; 4% fibrinogen
Albumin
- main contributor to osmotic pressure
- substance carrier and blood buffer
- made by liver
Where do most blood cells originate?
How long do they last in the blood?
Do they divide?
- bone marrow
- a few days
- nah
What is the formation of blood cells called and how is it regulated?
hemopoiesis or hematopoiesis
regulated by negative feedback for RBC and as needed for WBCs
First two steps of hematopoiesis
!. Pluripotent stem cell
2. Myeloid cell or Lymphoid ell
-what helps push hematopoiesis in one way or another?
-can cells go backward in the process
-where do new blood cells enter the blood stream?
What is the exception to the no dividing rule?
- hormones and growth factors
- no
- blood sinusoids
- lymphocytes
Erythrocyte structure
- biconcave disk
- basically just a Hb filled sack
- has plasma membrane protein Spectrin so that it’s flecible enough to fit through small capillaries
How do Erythrocyte’s structural features compliment their functional tasks?
- biconcave shape = greater surface area for gas exchange
- no mitochondria = anaerobic atp production = no use of the O2 they’re carrying
Hemoglobin components and structure
how much hb per rbc?
- Globin = 4 polypep chains : 2 alpha and 2 beta
- Heme = red pigment bonded to each globin chain
- Heme’s central iron atom binds one O2
250 mil
How do changes in gas content affect Hb?
- O2 loading in lungs = oxyhemoglobin (ruby red)
- O2 unloading in tissues = deoxyhemoglobin (dark red) (reduced)
- CO2 loading in tissues = carbaminohemoglobin = 20% of CO2 in blood binds to Hb
Process of RBC production
-pluripotent stem cell –> myeloid stem cell ——–> reticulocytes enter blood stream –> 2 days later they’re RBCs
reticulocytes don’t have nuclei
Balance of Erythropoiesis
- too few = hypoxia
- too mmany = blood viscosity
- balance depends on hormonal regulation and adequate supplies of iron, AAs and B vits
Hormone that controls Erythropoiesis
- Erythropoietin (EPO)
- direct stimulus
- always some in blood to maintain basal rate of production
- released in kidneys in response to hypoxia
- triggers rapid maturation of COMMITTED marrow cells –> increases reticulocyte count in 1-2 days
- enhanced by testosterone
RESPONSE TO O2 CARRYING CAPACITY– NOT NUMBER OF RBCs
hypoxia causes
- low RBC bc of hemorrhage or increased destruction
- not enough Hb per RBC (e.g. iron deficiency)
- reduced O2 availability (high altitude)
Dietary requirements for erythropoiesis
Bonus: how and where is iron stored
- AA, lipid, carbs
- iron 65% in Hb, rest in liver spleen and bone marrow –> stored in cells as ferritin and hemosiderin–> transported in blood with prot transferrin
- Vit B12 and folic aid for DNA synth for rapidly dividing baby RBCs
Fate and destruction of Erythrocytes
- 100-120 days
- no prot synth, growth or division
- become fragile and Hb degenerates
- get trapped in small circulatory channels esp in spleen
- macrophages eat them
- heme and globin split and iron is saved
- heme makes bilirubin in bile to intestins –> urobilinogen –> stercobilin in fees
- globilin makes AA
Anemia
- low O2 carrying capacity
- not a disease in and of itself
- blood O2 levels can’t support normal metabolism
- fatigue, pallorm short breath, chills
Caused by
- blood loss
- low RBC productio
- high rbc destruction
Hemorrhagic anemia Chronic Hemorrhagic anemia Iron deficiency anemia Pernicious anemia Renal anemia Aplastic anemia Hemolytic anemia
- blood loss from stab wound
- slight perisstant blood loss like ulcer
- blood loss, low iron intake, or impaired absorption
- automimmune – destroys stomach mucosa, so no intrinsic factor, so can’t absorb B12, so RBCs can’t divide (macrocytes)
- lack of EPO often accompanies renal disease
- destruction or inhibition or red marrow by drugs, chems, radiation, viruses
- premature RBC lysis (weird Hb, bad transfusions, infections, large spleen)
How do Leukocytes exit cappilaries
- through diapedesis
- moe through tissue spaces by ameboid motion and positive chemotaxis
Leukocytosis and Leukopenia
- WBC over 11,000 (normal if infection)
- WBC less that 4000
5 types of WBC in order of most numerous
Neutrophils Lymphocytes (t and b) Monocytes Eosinophils Basophils
2 categories of lymphocytes
Granulocytes : neutrophils, eosinophils, and basophils
Aranulocytes = lymphocytes and monocytes
Granulocytes
- bigger than RBCs, but don’t live as long
- lobed nuclei
- all phagocytic to some degree
- Wright’s stain
Neutrophils
50-70% of WBCs
- “Polymorphonuclear leukocytes”
- Granules have hydrolytic enxymes/ defensins
- 3-6 lobes in nucleas
- 2x RBC size
- VERY phagocytic “bacteria slayers”
Eosinophils
- bilobed nucleus
- granules similar to lysozomes –> release enzymes to digest paracytic worms
- alleries and asthma –> granular proteins promote inflamation
- modulate immune response
Basophils
- Granules have histamine
- Histamine = inflammatory chem that acts as vasodilator to attract WBC to inflamed sites
- similar to mast cells
Lymphocytes
- mostly in lyphoid tissue (lymph nodes and spleen) –> few circulate in blood
- crucial to immunity
- T lymphocytes act against virus-infected cells and tumor cells
- B lymphocytes give rise to plasma cells which make antibodies
- Natural killer cells func in innate, non-specific immunity
Monocytes
- biggest leukocyte
- leave circulation, entering tissues and differentiate into macrophages
- Macrophages = actively phagocytic cells
- Activate lymphocytes to mount an immune response
Leukopoisis
- where?
- what stimulates it
- what is the cellular CA
- red bone marrow
- interleikins and colony stimulating factors
- hemocytoblasts
Leukopoiesis
- 2nd step
- progression of granulocytes
- where are granulocytes stored
- which type of blood cell does the body make more of?
- Lymphoid stem cell = lymphocytes; Myeloid stem cells = all the others
- myeloblast–>promyelocyte–>myelocyte–>band–>mature cell
- bone marrow
- 3x more WBCs, but shorter life; die in battle
progression of agranulocytes
Monocytes (last several months)
- common precurser with neutrophils
- monoblast–>promonocyte–>monocyte
Lymphocytes (few hours to decades)
-Lymphoid stem cell–>T lymph precurser (thymus) and B lymph precurser
Platelets
- what is it?
- granular or agranular?
-cytoplasmic fragments of megakaryocytes
-granules with sratonin, Ca, enzymes, ADP, and platelet derived growth factors
150000-400000
Main function of platelets
- lifespan
- hormone regulating their production
- derive from
- form plugs that help seal breaks in blood vessels
- kept inactive in circulation by Nitric oxide and prostacyclin from endothelial cells
- live 10 days
- homrone = thrombopoietin from liver and kidney
- from megakaryoblast
Hemostasis
- definition
- required elements
- steps
- series of reactions to stop bleeding
- need clotting factors and substances released by platelets/injured tissue
- vascular spasm
- platelet plug formation
- coagulation
Hemostasis: vascular spasm
- what is it?
- what triggers it?
- where is it most effective?
-vasoconstriction of damaged blood vessel
triggered by
- direct injury to vascular smooth muscle
- chems released by endothelial cells and platelets
- pain reflexes
effective in small blood vessels
Hemostasis: Platelet Plug Formation
- feedback
- process
- chems
- positive feedback
- damaged skin exposes collagen fibers
- platelets stick to collagen via plasma protein von Willebrand factor
- Platelets swell, and get stick and release cham messengers
- ADP makes moreplatelets stick and release chems
- seratonin and thromboxane A2 enhance vascular spasm and platelet aggregation
Hemostasis: Coagulation
- Reinforces platelet plug with fibrin threads (fibrinogin)
- blood turns to gel
- series of rxns using clotting factors (procoagulants)
- vit K needed to synthesize 4 of the 13 clotting factors
3 stages of clotting
- Extrinsic or intrinsic pathways lead to formation of prothrombinase
- Prothrombinase converts prothrombin into thrombin
- Thrombin converts fibrinogen (soluble) into fibrin (insoluble) forming the threads of the clot
