Physio quiz 5

What is blood important for?

maintaining homeostasis

What is function of blood?

move nutrients and waste around the body, regulate pH levels, prevent infections

do different species have different blood volumes?

yes

Why is there variation in blood volume across species?

reflects physiological adaptions related to metabolism,body size, and cardiovascular efficiency

what are the 3 components of blood? what is in each?

plasma-water,proteins,solutes

buffy coat-platlets and WBC

erthrocytes-RBS

what is hematocrit?

the precentage of blood volume occupied by red blood cells

what can the clinical measurement of hematocrit do?

asses oxygen carrying capacity and hydration

what does a low hematocrit suggest?

anemia

what may a high hematocrit suggest?

dehydration

how read hematocrit?

put the tube up against chart (bottom lined up at 0 and top at 100) and read what number erthrocytes go to (0 to ___ and thats the percentage (ex:45%)

what are 3 formed elements in blood?

leukocytes

erthrocytes

platelets

what are 2 main components of plasma?

water

proteins

what is albumin?

a transporter and is important for many bodily processes

what is main function of erythrocytes?

carry oxygen

what is lifespan of erythrocyte like?

short (100 to 120 days)

do erythrocytes have nuclei?

no

WHta is biconcave shape of erythrocytes goof for?

-increase surface area

-flexibility so can move through capillaries

what does erythrocytes contain a large number of?

hemoglobin

what call the process of making erythrocytes?

erythropoesis

what is needed for RBC production? where get?

Iron

-diet

what is the process of erythropoesis?

iron from diet reaches the intestine where it is converted from ferric iron to ferrous iron which is easier to absorb. The iron is transported into the enterocyte by DMT1 transporter where inside the cell in can be stored as ferritin or it can be transported out of the enterocyte into blood using ferroportin where it is converted back into ferrous form that will bind transferrin and travel to bone marrow

what is primary regulator of erythropoiesis?

erythropoietin

what is erythropoietin produced by?

kidneys

what does erythropoietin do?

bind pronormoblast to stimulate production of more RBS

is there a step in erythropoesis where eject nucleus?

yes

when see erythropoietin secretion increase?

When oxygen delivery to tissues decreases in situations like anemia, blood loss, high altitude exposure or reduced renal perfusion

what is hemolysis?

the breakdown of RBC

are hemolysis and erythropoesis occuring at same time in body?

yes

what is process of physiological hemolysis?

old RBCs get caught in spleen where macrophages recognoze and break them down into globin and heme. Globin is degraded into amino acids while heme is converted into biliverdin by heme oxygenase and then into bilirubin which is conjugated with glucuronic acid and secreted into bile. The iron from heme goes back to bone marrow to be used in new RBCs. Bilirubin in intestine is mad einto urobilirubin then either sterocobilin which is in feces and gives feces their color or uroblin in urine giving urine its color

what is the summarized pathway of hemolysis?

old rbc → hemoglobin → heme → biliverdin → unconjugated bilirubin → liver → conjugated bilirubin → bile → intestine → stercobilin (feces) and urobilin (urine)

when does anemia occur?

when theres a decrease in RBCs or hemoglobin

what is polycythemia?

increase in RBS that can thicken blood and impair ciculation

what is main function of platlets?

hemostasis (detect vascular injurt and initiate clot formation)

what do platelets come from?

Mature megakaryocytes in blood that then fragment into platlets

are megakaryocytes mature in bone marrow?

no

what are the 4 phases of hemostasis?

1. primary hemostasis (platlet plug)

2. secondary hemostasis (coagulation cascade generating fibrin)

3. clot retraction

4. fibrinolysis (clot removal)

What are the 5 general steps of primary hemostasis? whats the goal?

goal: close hole

1.endothelial injury

2.exposure

3.adhesion

4.activation

5.aggregation

what needs to occur for primary hemostasis to begin?

endothelial injury that exposes underlying structures

why do endothelial cells secrete nitric oxide and prostaglandins when not injured?

rpomote vasodilation and inhibit platelet activation

what occurs in endothelial injury step in primary hemostasis in detail?

-injury occurs to endothelium

-reflex vasoconstriction occurs mediated by neural reflexes where smooth muscle contracts and endothelin is released from endothelial cells while at the same time endothelial cells stop producing nitric oxide so that there isnt any vasodilation signals (normal uninjured endothelial cells release nitric oxide and prostaglandins to promote vasodilation and inhibit platelet activation)

what occurs in exposure step in primary hemostasis in detail?

Damage to endothelial cells exposes collagen and von willebrand factor in the underlying tissue.

why exposure step important?

Makes sticky place for platelets to bind as platelets dont stick to intact endothelium

what occurs in adhesion step in primary hemostasis in detail?

Circulating platelets encounter the exposed collagen and von willebrand factors and the platelets will use GP1B receptor to bind the von willebrand factor which begins platelet involvement

what occurs in activation step in primary hemostasis in detail?

Platelets undergo a conformational change where develop pseudopodia extensions that allow them to interact physically with other platelets nearby and the vessel wall. While the shape change occurs the platelets being to release granule contents including serotonin which contributes to vasoconstriction, von wiilebrand factor to maintain the response locally and calcium ions which are used as a cofactors during secondary hemostasis, Adenosine diphosphate and thromboxane are also released and act on nearby platelets to stimulate their activation creating a positive feedback loop.

In response to ADP and thromboxane A2 platelets expresses receptor GPIIb/IIIa on surface and are now fully activated and functional.

what occurs in aggregation step in primary hemostasis in detail?

GPIIb/IIIa receptors on platelets bind fibrinogen which acts as a bridge between active platelets connecting them to one another. They can bind many other platelets at once building a large collection of platelets linked together making the platelet plug

whats the goal of secondary hemostasis?

form a fibrin mesh

What are the 3 steps to secondary hemostasis?

intrinsic or extrinsic pathway

factor x activation

coagulation cascade

where are factors that activate intrinsic pathway? extrinsic pathway?

in: factors found in blood

ex: tissue factor outside of blood

when is extrinsic pathway activated?

when damage occurs outside blood vessel

when is intrinsic pathway activated?

when damage occurs inside blood vessel exposing collagen or other negatively charged surfaces to circulating blood

which part of secondary hemostasis is responsible for producing thrombin?

common pathway

What are the steps of secondary hemostasis starting with extrinsic pathway?

1. exposed tissue factor III is bound by circulating factor VII and calcium forming a complex on damaged surface

2. Complex activates factor X into factor Xa, transitioning to common pathway

3. Factor Xa binds Factor Va and calcium ions forming prothrombinase complex on surface of activated platelets

4. prothrombinase complex converts prothrombin (factor III) into active thrombin (factor IIa)

5. Thrombin then converts fibrinogen (factor I) into insoluble fibrin chains that forms mesh around platelet plug

6. Thrombin then activated Factor XIII to crosslink fibrin fibers and strengthen mesh making it less likely to breakdown

7. Thrombin also amplifies coagulation by activating factors V,VIII, and XI

8. Thrombin also further enhances platelet activation

what is the major amplification point in coagulation cascade?

Activation of prothrombin into thrombin and is a transition point

what is process of secondary hemostasis using intrinsic pathway?

1. Activated factor XII activates factor XI

2. factor XI binds calcium and activates factor IX

3. factor IX binds calcium and activates factor VIII

4. Factor VIII binds calcium and factor IX to form complex which activates factor X into factor Xa

5. Factor Xa binds Factor Va and calcium ions forming prothrombinase complex on surface of activated platelets

6. prothrombinase complex converts prothrombin (factor III) into active thrombin (factor IIa)

7. Thrombin then converts fibrinogen (factor I) into insoluble fibrin chains that forms mesh around platelet plug

8. Thrombin then activated Factor XIII to crosslink fibrin fibers and strengthen mesh making it less likely to breakdown

9. Thrombin also amplifies coagulation by activating factors V,VIII, and XI

10. Thrombin also further enhances platelet activation

How do intrinsic and extrinsic pathways compare when talking about thrombin?

intrinsic produces more thrombin to ensure the formation of a stable clot

what is the main role of the intrinsic pathway in secondary hemostasis?

sustain coagulation rather than initiate it

where do the intrinsic and extrinsic processes converge?

at the activation of factor x

what is anticoagulation?

the prevention of blood clot from growing to large and blocking blood flow

when does anticoagulation and fibrinolysis occur?

after primary and secondary hemostasis

what do anticoagulation and fibrinolysis prevent?

bleeding and thrombosis

what is the central control point of regulation? why?

Thrombin as its generated in large amounts during coagulation and want to avoid excess clotting

how does anticoagulation/fibrinolysis occur?

1. Nitric oxide and prostglandins are secreted by neighboring uninjured endothelial cells to keep platlets inactivated by making activated platlets produce less thromboxane A2. These healthy cells also express thrombomodulin

2. thrombin binds to thrombomodulin loosing its pro coagulant activity

3. the thrombin-thrombomodulin complex activates circulating protein c which works with circulating protein s to act as strong anticoagulant by cleaving and inactivating factor V and factor VIII

4. Antithrombin iii produced in liver binds directly and inactivates thrombin and factor Va. It also inhibits factors VII, IX, XA, and XII

what is the result of the inactivation of factor V and factor VIII?

the intrinsic and common pathway slows down and coagulation is significantly reduced ensuring the clot stays localized and doesnt get too big

where are protein c and s produced?

in liver but circulate in plasma

what is function of thromboxane A2? why in fibrinolysis make platelets produce less?

Thromboxane A2 makes platelets express GPIIB/IIIA proteins

-GPIIB/IIIA proteins used in original clot formation to make platlelts stick together so by making these expressed les sget less platelet sticking together which is goal of fibrinolysis

how does clot retraction occur?

1. llamellipodia on platelets have actin and myosin protrusions that attach to fibrin fibers and other platleets using integin aIIbB3 (GPIIb/IIIa)

2. actin and myosin in platelets use calcium dependent mechanisms to generate force

3. contraction pulls on fibrin strands pulling sides of wound towards each other

4. the fibrin network becomes tighter and more compact which stabilizes clot and facilitates tissue repair and endothelial regeneration

5. serum is squeezed out of clot

what is fibrinolysis?

the gradual degradation of fibrin mesh

when does fibrinolysis occur?

starts a few days after injury

what inactive protein binds during clot formation and becomes trapped in fibrin mesh?

plasminogen

What occurs during fibrinolysis that involves plasminogen?

as vessel heals thrombin and facotr x stimulate release of plasminogen activator tPA from endothelial cells signaling clot has formed and clot removal should begin. tPA binds plasminogen and converts it into active plasmin. Plasmin acts as proteolytic enzyme that cuts fibrin strands into smaller fragments breaking down the integrity of the clot and weakens the clot.

how does body prevent plasmin from degrading fibrin uncontrollably?

Antiplasmin (a2-antiplasmin) binds free plasmin in bloodstream to inactivate it

what call low amount of platlets?

thrombocytopenia

what call high number of platelets?

trombocytosis

if start bleeding immediately after clot formation what does that indicate a problem with?

primary hemostasis

if get delayed bleeding after clot formation has started (like 30 minutes to a few hours later) what does this indicate a problem with?

secondary hemostasis problem (fibrin formation is defective)

if get delayed bleeding after clot formation has ended (like days later) what does this indicate a problem with?

fibrinolysis abnormalities

what happens in von willebrand disease?

Animal inherits a bleeding disorder in which they dont have von willebrand factor so cant/struggle to form platelet plug and start hemostasis since they dont have the factor to initiate platelets

what is one dog breed where see von willibrand disease more often?

Dobermans (not all dobermans have but a lot do)

what 3 things are immune cells responsible for?

defense

inflammation

immune regulation

what else found in buffy coat besides platelets?

leukocytes

what are 5 leukocytes?

neutrophil

lymphocytes

monocytes

eosinophils

basophils

what are the 3 granluocytes?

neutrophils

eosinophils

basophils

what call leukocytes that are not granulocytes?

agranulocytes

which leukocyte responds first to infection?

neutrophils

what is function of neutrophils?

preform phagocytosis

accute inflammation

what is an increase in neutrophil count often associated with?

bacterial infection

What are eosinophils specialized in combating? how do so?

combat parasites and mediate allergic responses by releasing toxic granules

What do basophils contribute to? how?

contribute to hypersensitivity reactions by releasing histamine

what are the 3 lymphocytes?

b cells

t cells

nk cells

what is function of b cell? t cell? nk cells?

b-produce antibodies

t-destroy infected cells

nk-target abnormal or tumor cells

what is an increase in lymphocytes commonly associated with?

viral infections

what do monocytes differentiate into in tissue?

macrophages

what is function of monocyte? what essential for?

they preform phagocytosis and are essential in chronic inflammation and tissue repair

how do monocytes link innate and adaptive immunity?

they present antigens to lymphocytes

what is diapedisis?

cell move from blood into tissues

when do monocytes act?

during innflammation

what is epistaxis?

bleeding from nose