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pr3154 > ic2 - rbc, platelets and hemostasis > Flashcards

ic2 - rbc, platelets and hemostasis Flashcards

1
Q

what are the components of blood and its proportions

A

plasma (55%), buffy coat (<1%), erythrocytes (45%)

plasma contains water (92%) and proteins (7%) and solutes (<1%)

buffy coat contains WBC and platelets

erythrocytes contains RBC

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2
Q

what are the proteins and its functions in our blood

A

albumin carries proteins that are lipid soluble and important in maintaining osmotic pressure, globulins important for immune function and clotting, fibrinogen is an inactive protein that needs to be activated into fibrin for clotting

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3
Q

where are proteins made

A

in our liver

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4
Q

what are the solutes

A

ions, nutrients, gases and waste

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5
Q

list the types of wbc in order of most to least abundant

A

neutrophils, leukocytes, monocytes, eosinophils, basophils

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6
Q

what is the function of wbc

A

important for immune defense

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7
Q

what are platelets and its function and another name for platelets

A

platelets are also known as thrombocytes and are fragments of cells produced in the bone marrow that play an important role in clotting and protection of vascular system

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8
Q

what is the function of rbc

A

transport of gases and to buffer the blood pH

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9
Q

what is the pH of blood

A

7.35-7.45

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10
Q

what is the weight of blood

A

8%

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11
Q

what is the volume of blood in males and females

A

males 5-6L, females 4-5L

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12
Q

what is the temperature of blood

A

38degC

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13
Q

what type of tissue is blood

A

connective tissue

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14
Q

what colour is blood

A

bright red if O2 rich from the artery, dark red if O2 poor from the vein

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15
Q

compare the structure of wbc, rbc and platelets

A

wbc are complete cells, rbc have no nuclei or organells, platelets are cell fragments

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16
Q

do rbc cell divide

A

no they are renewed by cells in bone marrow

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17
Q

what is the three main function of blood

A

transportation, regulation, protection

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18
Q

what does it mean to measure hematocrit and what is the average value for male and female

A

measuring rbc% of whole blood (46 for men, 42 for women)

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19
Q

what does hemoglobin consist and what are they

A

hemoglobin consist of heme and globin

globin is 4 folded polypeptide chains (2 alpha 2 beta) whose AA sequence determine affinity to O2 and each chain binds 1 heme group

heme is not a protein but a pigment and each heme group contains 1Fe which can bind to 1 O2 molecule (weak and reversible binding)

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20
Q

how many O2 can one Hb transport

A

4

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21
Q

what are the types of Hb

A

oxyhemoglobin, deoxyhemoglobin, carbaminohemoglobin

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22
Q

distinguish between pulmonary circuit (pulmonary arteries and pulmonary veins) VS systemic circuit (systemic arteries and systemic veins)

A

pulmonary circulation moves blood from heart to lungs while systemic circulation moves blood from heart to rest of body

artery vs vein differ in terms of direction (as long as from heart it is artery vs to the heart is vein)

pulmonary artery vs systemic artery differ in terms of gas content (pulmonary artery is O2 poor vs systemic artery is O2 rich)

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23
Q

which circulation has higher pressure

A

systemic circulation

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24
Q

what is erythropoiesis

A

generation of erythrocytes controlled by erythropoietin

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25
Q

where does erythropoiesis occur

A

for fetus, yolk sac then liver, spleen and lymph node

for <5yo, all bone marrow

5-20yo, bone marrow in ribs, sternum, vertebrae and proximal ends of long bones

> 20yo, bone marrow in ribs, sternum and vertebrae

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26
Q

where is erythropoietin produced

A

kidney

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27
Q

what happens when there is decreased O2 delivery to kidney and other tissues

A

cells in kidneys release more erythropoietin which increases rate of erythropoiesis and once O2 delivery is sufficient, the kidneys will decrease output of erythropoietin

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28
Q

what is the measurement that is indicative of erythropoiesis and what is the normal range of that measurement

A

reticulocyte count, normal range 0.8-1%

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29
Q

what are hematopoietic stem cells

A

immature cell that can develop into all types of blood cells incl wbc, rbc and platelets

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30
Q

explain the step by step process of erythropoiesis

A

hematopoietic stem cells in bone marrow give rise to proerythroblasts

proerythroblasts develop into erythroblasts in three phases: ribosome synthesis in early erythroblasts, Hb accumulation in late erythroblasts and normoblasts, ejection of nucleus from normoblasts and formation of reticulocytes which are preRBC

reticulocytes continue Hb synthesis and leave the bone marrow and complete differentiation into mature erythrocytes in blood

old RBC self destructs as the lack of protein synthesis makes membranes fragile and Hb degrades

they become ruptured in tiny vessels of spleen and these dying RBC and components are taken up by macrophages (in liver and bone marrow also)

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31
Q

what does the heme and globin give upon destruction of rbc

A

from heme, the Fe binds to transferrin and is recycled and reused in bone marrow or stored in liver

from heme, heme can also degrade into yellow pigment bilirubin which is excreted via liver and bile into urine and feces

from globin, it metabolises into AA and released into circulation

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31
Q

what is the lifespan of a rbc

A

100-120 days

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32
Q

how long does erythropoiesis take

A

about 7days

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33
Q

what triggers erythropoietin release by the kidneys

A

hypoxia due to decr RBC number or function, decreased O2 availability, increased tissue demand for O2, anemia, reduced blood flow to kidney, blood donation

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34
Q

is erythropoietin enhanced be androgen or estrogen

A

androgen thus men have higher RBC concentration than women

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35
Q

what condition does elevated hematocrit suggest and what condition does depressed hematocrit suggest

A

elevated suggests polycythemia while depressed suggests anemia

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36
Q

what condition does elevated reticulocyte count suggest and what condition does depressed reticulocyte count suggest

A

elevated suggest reticulocytosis while depressed suggests defect erythropoiesis

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37
Q

what condition does elevated rbc count suggests and what condition does depressed rbc count suggest

A

elevated suggest erythrocytosis or polycythemia while depressed suggests anemia

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38
Q

what does depressed Hb suggests

A

anemia

39
Q

what is mean corpuscular volume (MCV)

A

average volume or size of RBC

40
Q

what is mean corpuscular hemoglobin (MCH)

A

average amount of Hb in RBC

41
Q

what is mean corpuscular hemoglobin concentration (MCHC)

A

average conc of Hb in RBC (amount/vol)

42
Q

what is red cell distribution width (RCW)

A

how RBC size varies

43
Q

what does elevated RCW suggest

A

anisocytosis (may be an early indicator of anemia)

44
Q

what is anemia

A

reduction below the normal capacity of the blood to carry O2 due to reduction of erythrocyte numbers and/or reduction in Hb function

45
Q

what determines viscosity of the blood

A

RBC conc in blood

46
Q

what happens to O2 distribution into tissues when there is reduction in RBC

A

RBC reduction causes blood to become very liquid and if blood rushes too fast through the tissues they release too little O2 thus causing hypoxia which will widen blood vessels and eventually effect is reinforced and the widening of vessels and blood rushing greatly increases the workload for the heart and may potentially result in cardiac arrest

47
Q

what are the sx of anemia

A

fatigue, paleness, sob, chills

48
Q

what are the types of anemia

A

nutritional - caused by dietary deficiencies

aplastic - failure of bone marrow to make sufficient RBC (maybe due to chemotx)

renal - due to kidney disease resulting in lack of erythropoietin

hemorrhagic - loss of significant amounts of blood

malaria - plasmodium falciparum amplifies in RBC thus rupturing them and offspring invades new RBC

sickle cell - mutation in beta-globin gene causing Hb to aggregate in low O2 conditions to crescents which rupture RBC membranes

erythroblastosis fetalis - Rh+ RBC of fetus destroyed by anti-Rh Ab of a Rh-mother

thalessemia - low production of Hb (hereditary in nature)

49
Q

what is pernicious anemia

A

refers to lack of vitB12 or intrinsic factor

50
Q

what is Rh and why might it be dangerous in pregnancy and is it first pregnancy

A

Rh is a protein that can be found on surface of RBC (if you are Rh+ means it is present)

dangerous only in second or later pregnancies if the anti-Rh Ab in a mother of Rh negative passes into Rh positive baby as the Ab will then attack Rh positive RBC in the baby

51
Q

what is polycythemia/ erythremia

A

excess in circulating erythrocytes, causing elevated hematocrit

52
Q

what can polycythemia cause

A

polycythemia causes very viscous blood and potentially plugging of capilarries resulting in insufficient O2 delivery to tissues

53
Q

what are the types of polycythemia

A

primary - tumor or tumor like condition in bone marrow

secondary - erythropoietin induced, adaptive mechanism to improve O2 carrying capacity of blood

others - dehydration

54
Q

what is the range of RBC count that differentiates primary and secondary polycythemia

A

primary has 7-8x10^9 RBC/mL while secondary has 6-7x10^9 RBC/ml

55
Q

what are the types of disorders related to leukocytes

A

leukopenia - too few leukocytes (includes lymphopenia, neutropenia etc)

leukocytosis - elevated wbc count

leukemia/ lymphoma - cancers of wbc

56
Q

what does leukopenia pose as a risk to and what is it caused by

A

leukopenia increases risk of opportunistic infections and can be caused by chemo tx, radiation, chemicals, viral infections

57
Q

what is the likely wbc count indicative of leukocytosis and what is it caused by

A

> 1.1x10^7 wbc/ml and is a normal response to bacterial or viral invasion, may indicate cancer of wbc

58
Q

what is the likely wbc count indicative of leukemia/ lymphoma

A

up to 5x10^8 wbc/ ml (normal count is 4-11 x10^6 wbc/ml)

59
Q

what can leukemia/ lymphoma cause and what are its tx options

A

can cause immune deficiency and many infections, anemia and hemorrhage as bone marrow can become completely occupied by cancerous leukocytes and the wbc produced are not functional and will displace the remaining healthy ones

tx include irradiation, chemotx and bone marrow transplantation

60
Q

what is hemostasis

A

natural reaction to an injury whereby there are processes aimed at closing a leak in the vascular system with an aim to prevent loss of blood

61
Q

how long does clot retraction take and what is it mediated by

A

20mins to an hr and is mediated by platelets

after a few hrs, clot is dissolved or is invaded by fibroblasts

62
Q

what are fibroblasts

A

type of cell that contributes to the formation of connective tissue

63
Q

how long does healing take

A

1-2w whereby fibrous tissues replaces blood clot

64
Q

what are the three main phases part of hemostasis

A

vasoconstriction, formation of platelet plug and fibrin clot

65
Q

explain what happens during vasoconstriction as part of the

A

damage to blood vessel wall causes constriction of smooth muscle to limit the amount of blood going through thus limiting the amount of blood that may be left from the damage in the wall –> reduces blood loss but most of the times insufficient

immediate and lasts for approx 30mins or maybe hrs

indicated by sympathetic nerves and mediated by vascular smooth muscle cells

correlates with damage and provides time for platelet and coagulation phase

endothelial cells of opposite sides may stick together, and contract which exposes basal lamina

66
Q

explain what happens during platelet plug formation

A

damage to blood vessel wall causes collagen fibers to be exposed which serve as little flags to platelets moving through the blood vessel

platelets will recognise and adhere to collagen mediated by von willebrand’s factor (vWF) which is a plasma protein produced by platelets

adhesion activates morphological changes in platelets which triggers the release of granules that contain platelet agonists such as ADP and TXA2

TXA2 promotes aggregation and further vasoconstriction, fibrinogen links platelets through glycoprotein receptors but links are weak thus need reinforcement from factor XIII

platelet aggregation also releases prothrombin activator which activates prothrombin into thrombin

as more platelets stick together, platelet plug is form and results in a positive feedback cascade

occurs within seconds

67
Q

where is prothrombin produced and what does it require

A

prothrombin is produced in the liver and requires vitK

68
Q

what is thrombin and what is its function

A

thrombin is a molecular scissors that cuts protein fibrinogen into fibrin and activates factor XIII into XIIIa which is the fibrin stabilising factor, and along with fibrin, forms fibrin mesh

69
Q

what are the main functions of the platelet plug formation

A

closure of leak by formation of temporary patch, release of chemical mediators to regulate blood clotting and contraction of blood clot

70
Q

how do intact endothelial cells prevent unintentional platelet activation and aggregation

A

intact endothelial cells release No and prostacyclins that inhibits unintentional platelet activation and aggregation

71
Q

explain what happens during the coagulation phase

A

platelets and fibrin are present at site of damage and reinforces the clot, remodelling occurs after this to fix the damaged wall by fitting in connective tissues

occurs within mins

72
Q

what happens in secondary hemostasis

A

coagulation cascade and formation of final stable fibrin clot

platelets arriving at site of injury and the coagulation cascade is activated along with various coagulation factors which involves the intrinsic, extrinsic and common pathway

73
Q

where does extrinsic path take place and explain what happens in the extrinsic path

A

extrinsic path is when tissue damage occurs outside the blood circulation

damaged tissue releases tissue factor/ thromboplastin which converts factor VII to VIIa through formation of a complex and the presence of Ca2+ will activate factor X into Xa then Xa with Ca2+ and Va will activate prothrombin into thrombin

thrombin either activates fibrinogen into fibrin then form fibrin meshwork with factor XIIa or directly forms fibrin meshwork with factor XIIa

74
Q

explain what happens in the intrinsic path

A

exposure to collagen fibers or exposure to foreign surface causes conformational change in platelet phospholipids leading to activation of factor XII into XIIa then XIIa activates XI into XIa then XIa in presence of Ca2+ activates factor IX into IXa and IXa in presence of Ca2+ and VIIa activates X into Xa then Xa with Ca2+ and Va will activate prothrombin to thrombin

75
Q

explain what happens in the intrinsic path

A

exposure to collagen fibers or exposure to foreign surface causes conformational change in platelet phospholipids leading to activation of factor XII into XIIa then XIIa activates XI into XIa then XIa in presence of Ca2+ activates factor IX into IXa and IXa in presence of Ca2+ and VIIa activates X into Xa then Xa with Ca2+ and Va will activate prothrombin to thrombin

76
Q

explain what happens in the intrinsic path

A

exposure to collagen fibers or exposure to foreign surface causes conformational change in platelet phospholipids leading to activation of factor XII into XIIa then XIIa activates XI into XIa then XIa in presence of Ca2+ activates factor IX into IXa and IXa in presence of Ca2+ and VIIa activates X into Xa then Xa with Ca2+ and Va will activate prothrombin to thrombin ……..

77
Q

is extrinsic or intrinsic path faster

A

extrinsic bc intrinsic has alot of enzymes and enzymatic reactions involved

78
Q

which is the point where extrinsic path meets intrinsic path

A

factor Xa

79
Q

what does large amounts of thrombin cause

A

it causes further activation of platelets and the enhanced formation of fibrin

fibrin then form strands which makes up the mesh that stabilises the platelet plug in an arterial clot and holds together rbc in a venous clot

80
Q

what are the factors involved in extrinsic path

A

VII, X, II (thrombin), I (fibrinogen), Va, XIIIa, IV (Ca2+)

81
Q

what are the factors involved in intrinsic path

A

XII, XI, IX, X, II (thrombin), I (fibrinogen), Va, XIIIa, IV (Ca2+)

82
Q

what are platelets

A

fragments of megakaryotes that are bone marrow boned wbc

83
Q

what is the life span of platelets

A

5-7days

84
Q

what do platelets have

A

contractile proteins actin and myosin that allows them to move

organelles like mitochondria for release of ADP and ER, and golgi for storage of Ca2+ and synthesis of enzymes

enzyme systems for synthesis of PG

growth factors PDGF and VEGF
factor XIII (fibrin stabilising factor)

85
Q

what is the function of thrombin

A

key regulator of hemostasis

activator of XIII and platelets

release of PF3 from platelets to activate intrinsic path

enhances own generation (positive feedback loop)

86
Q

which are the clotting factors produced in the liver and which clotting factors requires vitK

A

produced in liver: I, II, V, VII, IX, X, XI, XII, XIII

requires vitK: II, VII, IX, X

87
Q

what is clot retraction and why does it occur

A

clot retraction is the stabilisation of clot by squeezing serum from the fibrin clot which serves to give further closure to the leak

88
Q

how does clot repair occur

A

through stimulation of vascular smooth muscle cells by platelet derived growth factor (PDGF) to build new vessel wall and the stimulation of endothelial cells by vascular endothelial growth factor (VEGF) to multiply and restore inner endothelial lining

89
Q

how is blood clotting regulated normally

A

prostaglandin produced by intact endothelial cells inhibits platelet activation and thus limits the spread of blood clotting

at high concentrations, serotonin inhibits ADP activity thus helping to regulate blood clotting

90
Q

differentiate pro and anticoagulants

A

procoagulants are tissue factors, collagen while anticoagulants can come in the form of artificial (citrate, EDTA, VKA, DOAC) or endogenous (smoothness of endothelial surface, antithrombin III, heparin, thrombomodulin, tissue plasminogen activator tPA)

91
Q

what is meant by the term fibrinolysis

A

dissolution of clots

92
Q

explain the process of fibrinolysis

A

during clot formation, plasminogen (plasma protein and protease precursor made by liver) is trapped inside the clot

surrounding tissue and vascular endothelial cells slowly release tissue plasminogen activator (tPA) which cleaves the inactive plasminogen into protease plasmin

plasmin digests the fibrin thus dissolving the clot and macrophages remove the remains of the clot

93
Q

does fibrinolysis occur constantly

A

yes it does at low levels and is balanced by equilibrium of thrombin and plasmin

94
Q

what are the types of blood clotting disorders

A

hemophilia - in men, excessive bleeding after an injury, hereditary and caused by lack of clotting factors (hemophilia A is deficiency of VIII and is more common while hemophilia B is deficiency of IX while hemophilia C is deficiency of XI)

liver disease - inability to synthesise procoagulants as most clotting factors are produced by the liver and cannot produce bile to absorb fat and vitK

vitK deficiency - essential for synthesis of several clotting factors, half comes from gut half from diet

thrombocytopenia - low circulating platelet count (<50million/ml)

thrombosis - inappropriate clotting caused by roughened surface of vessel, endothelial cell injury, disturbed blood flow (stasis)

thromboembolism - results from DVT, embolus is a thrombus freely flowing in the blood stream

95
Q

list the blood coagulation tests and explain what they test for

A

aPPT/PPT - measures efficacy of intrinsic and common pathway (I, II, V, VIII, IX, X, XI, XII)
citrated plasma and Ca2+ and phospholipid and kaolin
used to monitor heparin tx
normal range is 25-39sec

PT - measure efficacy of extrinsic and common pathways (I, II, V, VII, X)
citrated plasma and Ca2+ and tissue factor
used to monitor warfarin tx
normal range 12-15sec

INR - ratio of patient PT to healthy PT
normal range is 0.9-1.3

96
Q

what is thrombocytopenia caused by and what can thrombocytopenia result in and what can you use to tx it

A

caused by damage or destruction of bone marrow (eg. malignancy or chemotx), results in spontaneous widespread hemorrhage visible by small purple spots on skin, treat with fresh whole blood transfusion or platelet transfusion

pr3154 (20 decks)

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