Ch. Nine: Blood Flashcards
1
Q
Functions of the Blood
A
- transport, defense, and hemostasis
2
Q
Blood Characteristics
A
- 8% of body weight
- makes up 25% of extracellular fluid
- blood is thicker than water: contains 3 cell types and suspended in plasma
3
Q
Types of Cell Types
A
- erthrocytes: RBCs
- leukocytes: WBCs (immune system’s mobile defence units)
- platelets: thrombocytes (cell fragments and important in hemostasis)
4
Q
Haematocrit
A
- centrifuge blood to separate cells from plasma
- 99% are RBCs
- hematocrit (packed cell volume) is 42% for women and 45% for men
5
Q
Plasma
A
- fluid portion of blood
- 92% water and 7% proteins
- remaining 1%: dissolved organic molecules, ions, and trace elements, vitamins, dissolved o2 and co2
6
Q
Plasma Proteins
A
- remain in the blood; most made in liver and colloid osmotic pressure (remember bulk flow)
- 3 major groups: Albumins, Globulins, and Fibrinogen
7
Q
Albumin
A
- most prevalent: 60% of total, contribute to colloid osmotic pressure
- bind many substances: bilirubin and drugs
8
Q
Globulins
A
- alpha, beta, and gamma
- alpha and beta: transport hormones and cholesterol, and involved in blood clotting
- are inactive before regulatory inputs: Angiotensinogen
- y= immunoglobulins (antibodies)
9
Q
Fibrinogen
A
- forms fibrin threads essential to blood clotting
10
Q
Erythrocytes
A
- transport O2 to tissues and remove CO2
- thin, biconcave disks which provides large surface area for diffusion of oxygen
- very flexible can squeeze into capillaries
- no nucleus nor organelles
- glycolytic enzymes
- carbonic anhydrase
- hemoglobin (binds oxygen and carbon dioxide)
11
Q
Hemoglobin (Hb)
A
- found only in red blood cells
- pigment containing iron: appears reddish when oxyengenated
- molecule consists of 2 parts:
1. Globin portion: protein composed of four highly folded polypeptide chains
2. Heme groups: 4 iron groups per Hb molecule, each is bound to one of the polypeptides
12
Q
Primary Role of Hemoglobin
A
- carry O2
- also combines with CO2, H+ from CO2 reaction (not on heme group), carbon monoxide, and nitric oxide
13
Q
Erythrocytes Enzymes
A
- glycolytic enzymes: anaerobic respiration, and rely on glycolysis for ATP formation
- carbonic anyhdrase: critical in CO2 transport, catalyzes reaction that leads to conversion of metabolically produced CO2 into bicarbonate ion (primary form in which CO2 is transported in blood)
14
Q
Erythropoiesis
A
- erythrocyte production
- RBCs survive about 120 days
- spleen removes most of old erythrocytes from circulation (1% per day)
- must be replaced at rate of 2 million to 3 million cells/second
- erythropoiesis occurs in red bone marrow: stem cells in red bone marrow differentiate into the different types of blood cells
- production controlled by erthropoitin from kidney on demand
- cells committed to becomes RBCS proliferation and maturation
15
Q
Erythropoiesis in Age
A
- intrauterine: first by yolk sac, developing liver and spleen, and bone marrow when developed
- childhood: most bones have red bone marrow
- adulthood: sternum, ribs, upper ends of long bones
16
Q
Blood Types
A
- special case of active immunity
- ABO blood types are named for presence of antigens on surface of erythrocytes
- type A: contains A antigens
- type B: contains B antigens
- type AB: contains both A and B antigens
- type O: neither A or B antigens
17
Q
Blood Groups
A
- antibody binds with the specific antigen against which its produced
- type A has anti-B antibodies (plasma)
- type B has anti-A antibodies (plasma)
- type AB has no antibodies related to the ABO system
- type O has both anti-A and anti-B antibodies (plasma)
18
Q
Blood Groups: transfusion
A
- transfusion reaction occurs when blood of incompatible type is given
- type O is “universal donar”
- type AB is “universal recipient’
19
Q
Transfusion Reaction
A
- most dangerous is AB in recipient’s plasma for incoming donor RBCs
- high HB my cause kidney failue
20
Q
Rh Blood Group
A
- people who have Rh factor have Rh-positive blood
- no naturally occurring antibodies develop against Rh factor
- anti-Rh antibodies are produced only by Rh-negative people if exposed to Rh-positive blood
21
Q
Rh Factor
A
- erythroblastosis fetalis (hemolytic disease of newborn) in subsequent pregnancies
- rH-negative mother develops antibodies against the erythrocytes of an Rh-positive fetus
22
Q
Other Blood Group Systems
A
- cross-matched blood: mix donor RBCs with plasma of recipient
- approx. 12 other minor human erythrocyte antigen systems
23
Q
Filtering and Destruction of Erythrocytes
A
- spleen filters and removes old erythrocytes
- liver metabolizes byproducts from breakdown of erythrocytes
- iron is recycled for synthesis for new hemoglobin and transported bound to transferrin to red bone marrow
- iron is stored to ferritin in the liver, spleen, and small intestines
24
Q
Spleen
A
- spleen macrophages filter blood by phagocytosis of old fragile RBCs
- hemoglobin broken down and the iron is removed
- converted into bilirubin (yellow colour)
- further metabolism in liver: secreted in bile to the intestinal tract or released into the blood stream and excreted in the urine
25
Q
Anaemia
A
- below-normal O2-carrying capacity
- nutritional anaemia: iron deficiency in diet
- pernicious anaemia: vitamin B12 deficiency (required for action of folic acid), dietary (only form animal products), and lack of intrinsic factor from stomach lining
- aplastic anaemia: insufficient RBC production, or destruction of bone marrow (radiation, cancer, or chemotherapy)
- renal anaemia: kidney disease or failure
- hemorrhagic: wound or menstral flow
Hemolytic anaemia: rupture of RBCs caused by infections (malaria) or sickle cell disease (fragile and production unable to keep up with removal)
26
Q
Polychthaemia
A
- primary polycthaemia: erythropoiesis at excessive and uncontrolled rate and viscosity of blood increased
- secondary polychthaemia: adaptive mechanism- reduced O2 due to high altitude or chronic lung disease or heart failure
27
Q
Leukocytes
A
- mobile units of body’s immune defense system
- immune system: made up of leukocytes and variety of plasma proteins; recognizes and destroys material within body that are foreign to “normal self”
28
Q
Leukocytes Functions
A
- defends against invading pathogens
- identifies and destroys cancer cells that arise in body
- functions as “cleanup crew” that removes worn-out cells and tissue debris
29
Q
Leukocytes Characteristics
A
- colourless, lack hemoglobin
- vary in structure, function and number
- somewhat larger than RBCs
- 5 different types: neutrophils, eosinophils, basophils, monocytes, and lymphocytes
- characterized by appearance of nuclei and granules
- names based on granuole-staining dyes
30
Q
Leukocytes Production
A
- ultimately originate form same undifferentiated multipotent stem cells in red bone marrow
- granulocytes and monocytes are produced only in bone marrow
- most new lymphocytes are actually produced by lymphocytes already in lymphoid tissues such as lymph nodes and tonsils
31
Q
Granulocytes
A
- ctyoplasmic granules: neutrophils, eosinophils, and basophils
- many shaped nucleus
32
Q
Agranulocytes
A
- no ctyoplasmic granules: monocytes, and lymphocytes
- single nucleus
33
Q
Polymorphonucleur granulocytes
A
- neutrophils: granules are neutral and show no dye preference
- eosinophils: granules have an affinity for the red dye eosin
- basophils: granules have an affinity for a basic blue dye
34
Q
Mononuclear Agranulocytes
A
- monocytes: have an oval or kidney-shaped nucleus
- lymphocytes: smallest of the leukocytes; usually have large spherical nucleus that occupies most of the cell
35
Q
Leukopoiesis
A
- chemical messages from damaged or invaded tissues
- colony-stimulating factors from endothelial cells, marrow fibroblasts, activated WBCs
ex. granulocyte colony-stimulating factor: increased replication of granulocytes, especially neutrophils
36
Q
Neutrophils
A
- phagocytic specialists: destroy bacteria by phagocytosis and also release bacteria-killing chemicals
- functions: first defenders on scene of bacterial invasion, important in inflammatory response, scavenge to clean up debris, and increased cell count may point to bacterial infection
37
Q
Eosinophils
A
- increase in circulating eosinophils is associated with:
- allergic conditions such as asthma and hay fever
- internal parasite infestations such as worms (attach to worms and secrete substances to kill it)
38
Q
Basophils
A
- least numerous and most poorly understood
- quite similar and functionally to mast cells
- synthesize and store histamine (release in allergic reactions) and heparin (anti-clotting agent of blood samples drawn for chemical analysis, used extensively as anticoagulant drug)
39
Q
Monocytes
A
- phagocytic:
- migrate to tissues and become macrophages
- also for antigen presentation, cytokine production and cytotoxicity
- emerge from bone marrow while still immature and circulate for day or two before settling down in various tissues in body
- mature and enlarge in resident tissue and become known as macrophages (life span from several months to years)
40
Q
Lymphocytes
A
- B cells: produce antibodies and responsible to antibody-mediated or humoral immunity
- T cells: bind to antigens and destroys cells (virus infected, cancer cells, tissue transplant) by releasing chemicals to punch holes in victim cell (cell-mediated immunity)
- provide immune defense against targets for which they are specifically programmed
- live about 100-300 days
41
Q
Platelets
A
- from megakaryocytes
- do not leave blood as WBCs do but (1/3) are stored in blood-filled spaces in spleen and released when needed by sympathetically induced splenic contraction
- thrombopoietin: liver hormone increases number of megakaryocytes and more platelets per cell (mechanism unknown)
- cytoplasmic fragments derived from megakaryocytes (1000 platelets/cell and last 10 days)
- no nuclei, some organelles and enzymes
- have granules important in blood clotting
- granules contain secretory products: ADP, sertonin, and epinephrine
42
Q
Haemostasis
A
- stoppage of bleeding from broken blood vessel
- haemostasis is a 3 step process:
1. vascular spams
2. formation of platelet plug
3. blood coagulation
43
Q
Vascular Spasm
A
- results from damage to the blood vessel; damaged tissue secretes factors that cause contraction
- vessels constrict to minimize blood loss (maintains BP)
- endothelial layer becomes sticky to aid in the clotting process
44
Q
Formation of Platelet Plug
A
- platelet aggregate on contact with exposed collagen in damaged wall of the vessel
- forms a sticky endothelium and exposed collagen- platelet activation
- release ADP which causes platelets to become sticky- platelet aggregation
- thromboxane A2 synthesis from activated platelets stimulate further platelet aggregation
- the plug results in a decreased blood loss (maintains BP)
- plug formation is important for production of a blood clot
45
Q
Formation of Blood Clot
A
- clotting= coagulation
- blood converted into solid gel called clot or thrombus
- occurs around platelet plug
- dominant hemostatic defence mechanism: can take place in absence of all cells except platelets
46
Q
Clot Formation
A
- reinforces platelet plug and converts blood in the vicinity of vessel injury into a nonflowing gel
- clotting factors are always present in blood plasma in inactive precursor form; activated in a cascade
47
Q
Clotting Cascade
A
- 12 plasma proteins produced mainly in the liver:
- designated with roman numerals (and names) and act as proteolytic enzymes or co-factors
- series of steps lead to final conversion of fibrinogen into a stabilized fibrin mesh
- may be triggered by intrinsic or extrinsic pathway
- fibriogen converted to fibrin by thrombin
48
Q
Clotting Cascade: Summary
A
- intrinsic pathway: all elements present in blood:
- involves seven separate steps
- factor XII (Hageman factor) is activated by coming into contact with exposed collagen in injured vessel
- or foreign surface such as glass test tube
- extrinsic pathway:
- requires only 4 steps
- requires contact with tissue factors external to the blood
- tissue thromboplastin released from traumatize tissue directly activates factor X
49
Q
Clot Retraction and Dissolution
A
- clot retraction: contraction of platelets shrinks fibrin mesh, squeezing fluid from the clot
- clot dissolution: enzyme plasmin dissolves clot and plasmin formed from plasminogen
50
Q
Dissolving Blood Clots- Factor XII
A
- plasminogen converted to plasmin; fibrinolytic enzyme
- breaks down the fibrin meshwork
51
Q
Plasminogen Activators
A
- plasminogen activators convert plasminogen to plasmin:
ex. tissue plaminogen activator (tPA); secreted by endothelial cells especially in lungs, plasminogen and tPA bind to fibrin - recombinant tissue plasminogen activator (tPA):
- dissolve clots that are obstructing flow in coronary arteries, pulmonary arteries and cerebral arteries
- used to treat stroke patients if they arrive soon enough to the hospital
52
Q
Clot Controllers
A
- swift removal of clotting factors and inhibition of active clotting factors:
- most of the thrombin is bound to the fibrin threads thus prevents systemic clotting
- unbound thrombin is inactivated
- endothelial cells:
- nitric oxide, prostacyclin, endothelial dysfunction
53
Q
Inappropriate Clotting
A
- thrombus:
- abnormal intravascular clot attached to a vessel wall
- can eventually completely occlude the vessel
- ischemia and tissue death downstream from the clot ex. fatal heart attacks
- emboli:
- freely floating clots
- can suddenly block blood flow
- pulmonary embolism impair the body’s ability to get enough oxygen
- cerebral embolisms cause strokes
54
Q
Thromboembolic Conditions
A
- factors that can cause thromboembolism:
- roughened vessel surface associated with atherosclerosis
- imbalances in the clotting-anticlotting systems
- slow-moving blood
55
Q
Role of Coagulation Factors in Clot Formation Disorders
A
- impaired liver function: reduced protein production including clotting factors
- vitamin K deficiencies: decreased synthesis of clotting factors
56
Q
Hemophillia: FYI
A
- genetic X-linked disorders seen primarily in men
- Hemophilia A is a lack of factor VIII
- hemophillia B is lack of factor IX
- hemophillia C can be seen in both sexes and is milk; kacks factor XI
- symptoms occur early in life and can be disabling
