Functions of blood

- Transport - Regulation: ions/pH - Defense: immune - Hemostasis: prevent blood loss

Hematocrit

% of blood volume that is RBC's

Normal hematocrit

~45%

Anemic hematocrit

Low (less RBC's = less oxygen)

Polycythemic hematocrit

High (adapted to low oxygen = increased RBC's)

Plasma Proteins: Albumins Source and Function?

Source: liver Function: colloid osmotic pressure (pulls water in)

Plasma Proteins: Globulins Source and Function?

Source: liver and lymphoid tissue Function: antibodies

Plasma Proteins: Fibrinogen Source and Function?

Source: liver Function: clotting

Plasma Proteins: Transferrin Source and Function?

Source: liver Function: iron transport

What is Serum?

fraction of plasma where fibrinogen and clotting factors are removed

What and where is hematopoiesis

- formation of blood cells - prenatal: happens in yolk sac, liver, spleen - postnatal: bone marrow

How is hematopoiesis regulated

cytokines: hormone-like - growth factors - Erythropoietin: produces RBC's - Thrombopoietin: produces platelet's

What makes CO inhalation fatal?

Hemoglobin can bind to it more easily than binding to oxygen

Essential factors for RBC production

- cytokine - dietary factors: iron, folic acid, B12 - intrinsic factor

Which cells are involved in recycling RBC's

macrophages

Where does recycling of RBC's happen

spleen

What is anemia?

decreased oxygen-carrying capacity bc of RBC/Hb deficiency

What cause anemia

- decreased RBC production in bine marrow - destruction of RBC's: hemolytic anemia - blood loss: hemorrhagic anemia - abnormal Hb production: sickle cell - lack of iron - lack of IF or B12: pernicious anemia - damage of bone marrow: aplastic anemia

Non-specific defenses: innate immunity

skin, enzymes, tears, mucus - granulocytes and monocytes/macrophages - no memory - fast - complement system

Specific defenses: acquired immunity

- lymphocytes - has memory - slow - antibodies

What kind of response is inflammation

non-specific

Vascular events of inflammation

1. release histamine 2. vessels dilate 3. protein accumulation in extracellular spaces 4. inflammatory mediators released: bradykinin, prostaglandins (all cause pain)

Cellular events of inflammation

1. macrophages kill pathogens and release chemical signal 2. WBC's move into infected area 3. phagocytosis of non-self agent

What is chemotaxis

ability of WBC's to move against conc gradient in response to chemotactic factors

How do phagocytes recognize bacteria

PRR: patter recognition receptors

What are opsonin's

speed up phagocytosis - produced by host body

Oxygen dependent killing

uses free radicals

Oxygen independent killing

- lysozymes - lactoferrin - defensins

What are complement proteins

- inactive proteins in plasma Function: OIL opsonization, inflammatory mediators, lysis (of bacteria) - MAC: forming a pore

Primary lymphoid tissue

source: bone marrow and thymus function: B/T cells developed here

Secondary lymphoid tissue

source: lymph nodes function: where B/T cells mature and activate

What 3 things must all lymphocytes be able to do

- recognize antigens - respond to antigens - remember the antigen

Active immunity

- acquired through exposure or vaccine - self-generated - takes weeks to acquire immunity - lasts years

Passive immunity

- acquired through placenta or mothers milk - preformed - immediate immunity - lasts weeks

Key steps of hemostasis

1. vasoconstriction 2. primary hemostasis (platelet plug): white thrombus 3. secondary hemostasis (clotting): red thrombus

Where do platelets come from

Bone marrow/stem cells

T/F: platelets have a nucleus

False

Contents of platelet granules

1. alpha granules: vWF, cytokines 2. dense granules: ADP, serotonin, Ca

Steps of the platelet plug

1. adhesion: using vWF 2. activation: change shape 3. aggregation: stick together = plug

Why does the platelet plug not continuously expand

- signaling molecules (endothelial cells release chemical signal)

Aspirin: COX1 (platelets)

releases thromboxane A2: vasoconstriction, PRO hemostatic effect

Aspirin: COX2 (endothelial cells)

releases prostacyclin: vasodilation, ANTI hemostatic effect

Steps of blood clotting

prothrombin (active) uses prothrombinase = thrombin thrombin helps fibrinogen become fibrin

Intrinsic pathway

- internal trauma - cell injury, exposure to collagen, contact w/ foreign surfaces - factor XII in contact w. negatively charged surfaces In vivo: blood exposed w/ collagen In vitro: blood exposed w/ foreign surface

Extrinsic pathway

- external trauma: causes blood to leak out to surrounding tissues - exposure to TF Factor VII in blood encounter TF

What does thrombin do in clotting pathway

1. activate platelets 2. fibrinogen -> fibrin 3. activate clotting factors 4. activate protein C (anticoag)

Clinical anticoags

Ca chelators, heparin, vitamin K antagonists

What is agglutination

surface antigens on RBC bound to antibodies to form clumps = blood types not meant together

T/F: Type A blood can donate to Type O

False, Type O has anti A and B antibodies