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PHGY 209 > Blood part 3 > Flashcards

Blood part 3 Flashcards

1
Q

3 clinical indices of interest about blood

A

Number of RBC, amount of Hb and hematocrit

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2
Q

2 diseases associated with abnormal hematocrit and what hematocrit exactly

A

Ht < 45% (ex. 30%) -> Anemia. Can be caused by fluid retention.
Ht > 45% (ex. 70%) -> Polycythemia. Can be caused by dehydration.

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3
Q

Normal values and polycythemia values for RBC count per volume and Hb concentration

A

Normal : 5-5.5 x 10^6 RBC / microliter. 16g % Hb

Polycythemia : > 6x10^6 RBC / microliter. >18g % Hb

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4
Q

Relative vs Absolute polycythemia

A 
Relative = Due to lower plasma volume
Absolute = Physiological or Pathological
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5
Q

Physiological polycythemia 4 causes

A

1) High altitudes
2) Increased physical activity
3) Chronic lung disease
4) Heavy smoking

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6
Q

Pathological polycythemia 2 causes

A

1) Tumours of cells producing erythropoietin (kidney cells)

2) Unregulated production by bone marrow

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7
Q

What is polycythemia vera and values for RBC count per volume and Hematocrit

A

Blood cancer. Bone marrow does too many RBCs. 7-8 x 10^6 RBC / microliter. Ht approx. 70%

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8
Q

Problem with polycythemia

A

High blood viscosity -> sluggish blood flow and more risks of blood cloting

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9
Q

Anemia definition

A

Decrease in oxygen-carrying capacity of blood

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10
Q

F and M w/ Anemia -> RBC count and Hb content

A

M : 4x10^6 RBC/microliter and <11 g% Hb

F : 3.2 x 10^6 RBC/microliter and <9g %

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11
Q

Classifications of morphologic anemias

A

1) Microcytic (<80 u^3), Normocytic (80-94 u^3), Macrocytic (>94 u^3) (about volume so microcytic smaller diameter and macrocytic bigger diameter.
2) Normochromic (=33%) Hypochromic (<33%) (about % of RBC volume occupied by Hb)

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12
Q

On microscope, how to distinguish different morphologic anemias

A

Microcytic, normocytic and macrocytic -> sizes of RBCs

Normochromic or hypochromic -> colour of RBCs

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13
Q

3 etiologic anemias

A

1) Diminished (RBC) production 2) Increased (RBC) destruction 3) Ineffective (RBC) maturation

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14
Q

3 causes for diminished production of RBC (first etiologic anemia)

A

1) Abnormal site 2) Abnormal stimulus 3) Inadequate raw materials

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15
Q

Which anemia associated with diminished production of RBC due to abnormal site + causes (3) + morphologic classification

A

Aplastic (hypoplastic) anemia. a. uknown cause b. exposure to radiation c. chemicals or drugs.
Morph. class. of anemia : normocytic, normochromic

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16
Q

What causes anemia associated with diminished production due to abnormal stimulus + morphologic classification

A

Stimulation failure -> renal disease (EPO produced by kidneys)
Morph. class. of anemia : normocytic, normochromic

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17
Q

Which anemia associated with diminished production of RBC due to inadequate raw materials + causes (2) + morphologic classification

A

Iron deficiency anemia.
a. High requirements (infancy, adolescence, pregnancy)
b. Inadequate supplies due to 1) Failure to absorb Fe (gastrointestinal tract defficiency) 2) Dietary defficiency 3) Loss of Fe in hemorrhage (hemorrhage = loss of RBC + loss of Fe)
Morph. class. of anemia : microcytic, hypochromic

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18
Q

Total amount of iron in body and its % distribution

A

4g. 65% Hb. 30% stored. 5% myoglobin (muscle cells). 1% enzymes

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19
Q

Daily intake of iron and daily absorption from gut for M + F and what it depends on

A

15-20 mg daily. Gut absorbs 1 mg daily for males and 2 mg daily for females (depending on need).

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20
Q

Erythropoiesis iron requirement daily

A

25 mg

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21
Q

Iron that comes from RBC destruction and what happens with it

A

25 mg (24 mg recycled, 1 mg lost -sweat)

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22
Q

How much iron in 1 g of Hb

A

3.5 mg

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23
Q

Why women require 2 mg Fe daily

A

15g Hb/100 mL = 50 mg Fe (because 15 g * 3.5 mg Fe/1 g Hb)
Menstrual loss : 50 mL of blood so 25 mg Fe
25 mg + 28 mg (1 mg lost daily) = 50 mg/month = 2 mg daily

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24
Q

Second anemia type/etiology and names

A

Ineffective maturation. Maturation failure anemia

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25
Q

Cause of maturation failure anemia and morph. classification

A

Deficiencies in Vitamin B12 and folic acid (required for normal synthesis of DNA). Macrocytic RBCs, normochromic RBCs

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26
Q

What can cause lack of vitamin B12

A

Failure to absorb it

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27
Q

What can cause lack of folic acid

A

Dietary absence, overcooking vegetables

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28
Q

Vitamin B12 absorption mechanism

A

Vitamin B12 goes in digestive system. Joins intrinsic factor secreted by stomac cells in the stomac to form IF-B12 complex. IF-B12 complex absorbed in ileum by a receptor.

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29
Q

What can cause a failure to absorb B12 and what pathology would occur

A

Intrinsic Factor deficiency or ileum disease -> Pernicious anemia

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30
Q

Anemia type/etiology other than increased RBC destruction. different names and what may come with it

A

Survival disorders/Hemolytic anemias - may be accompanied by jaundice

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31
Q

Survival disorders/Hemolytic anemias etiology (2)

A

1) Congenital

2) Acquired

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32
Q

Congenital survival disorders causes (3)

A

1) Abnormal membrane structure (less flexible, more fragile) ex. hereditary spherocytosis (spherical RBCs)
2) Abnormal enzyme systems (abnormal metabolism)
3) Abnormal hemoglobin structure ex. sickle cell anemia (half moon shape) ex. Thalassemia - deficient synthesis of globin amino acid chains

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33
Q

Acquired hemolytic anemia causes (3)

A

Toxins, drugs, antibodies. Kill RBCs

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34
Q

Name for blood loss. 2 types and name of accumulation of blood in tissues

A

Hemorrhage. External and internal (into tissues). Hematoma = acccum. of blood in tissues

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35
Q

Hemostasis def.

A

Arrest of bleeding following vascular injury

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36
Q

3 overlaping mechanisms in hemostasis and which part of hemostasis they’re involved in

A

Vascular response. Platelet response. Clot formation. Vascular resp. and Plat. response = primary hemostasis. Platelet resp. and clot formation = secondary hemostasis

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37
Q

Time for primary hemostasis to occur

A

couple seconds after injury

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38
Q

4 general hemostasis step

A

Vascular injury, vasoconstriction, platelet plug formation (temporary), blood clot formation (there until healing)

39
Q

Vascular response name and 3 levels of response

A

Vasoconstriction. 1. Nervous reflex (larger vessels) 2. Myogenic response (muscle cells in vessel wall contract) 3. Chemical vasoconstrictors (local release of agents)

40
Q

Platelet response

A

Platelet plug (white thrombus - means clot) blocks blood flow

41
Q

Platelets size, life span and amount

A

2-4 micrometers diameter. 7-10 days life span. 250 000 per microliter

42
Q

Platelet structure (composition)

A

No nucleus, granules, mitochrondion, tubule, submembranous filaments (platelet contractile protein)

43
Q

What are granules in platelet

A

Factors for vasoconstriction, platelet aggregation, clotting, growth, etc.

44
Q

Platelet production name and general scheme

A

Thrombopoiesis -> pluripotential stem cell -> committed stem cell ….. Megakaryocytes -> release of platelets in blood

45
Q

Thrombopoiesis committed stem cell size vs megakaryocyte size

A

15-20 micrometers vs 60-80 micrometers.

46
Q

When thrombopoiesis process becomes in blood stream

A

Megakaryocytes in bone marrow but platelets released in blood stream

47
Q

Name of what regulates thrombopoiesis, what secretes it and what kind of molecule it is

A

Thrombopoietin. Liver. Cytokine

48
Q

Platelet plug formation 4 general steps

A

Adhesion, Activation and release of cytokines, Aggregation, Consolidation.

49
Q

Name 8 substances that can be related to platelet plug formation

A

Prostacyclin, NO (nitric oxyde), von Willebrand factor, collagen, PF3, Serotonin, ADP, Thromboxane A2 (TXA2)

50
Q

What prostacyclin and nitric oxyde do and where come from

A

Released by endothelial cells and discourage platelets aggregation

51
Q

What von Willebrand Factor does

A

grabs platelet at one end and endothelial cells at other end

52
Q

What collagen does

A

has affinity with platelets

53
Q

What is TXA2 and what it does

A

Thromboxane A2 -> promotes vasoconstriction and promotes aggregation

54
Q

What ADP does

A

promotes aggregation

55
Q

What serotonin does

A

facilitates hemostasis mechanism

56
Q

what is PF3 and what it does

A

platelet factor 3. source of phospholipid activity which participates in coagulation.

57
Q

First steps in platelet plug formation

A

Vascular injury -> collagen exposure and von Willebrand Factor facilitate platelet adhesion.

58
Q

2nd steps in platelet plug formation

A

Activation and release of cytokines (TX A2, ADP, PF3) and platelet aggregation.

59
Q

Important things that platelet factors released do

A

Attract more platelets

60
Q

Last steps in platelet plug formation

A

Thrombin (which is critical for clot formation) and the coagulation pathway also promotes platelet plug (white thrombus) adhesion, aggregation, formation. POSITIVE FEEDBACK

61
Q

Platelets function (5)

A

1) Release vasoconstricting factors
2) Form white thrombus (platelet plug)
3) Release clotting factors
4) Participate in clot retraction
5) Promote maintenance of endothelial integrity

62
Q

What is the consequence of an abnormal hemostatic response

A

prolonged bleeding

63
Q

What can cause abnormal primary hemostatic response

A

1) Failure of blood vessels to constrict

2) Platelet defficiencies

64
Q

Different platelet deficiencies

A

1) Numerical (less than 75 000 per microliter)
2) Functional (congenital or acquired)
3) Caused by drugs, toxins, antibodies

65
Q

Exemple of drug than can cause platelet deficiency and what it does

A

Aspirin (in small doses) inhibits synthesis and release of TX A2 and this inhibits ability of platelets to come together (TX A2 stimulates vasoconstriction but also aggregation of platelets, just like all factors released by platelets)

66
Q

Blood clot : what do we name it

A

thrombus

67
Q

Clot formation is a function ___________. What it involves and what it doesn’t involve.

A

Function of PLASMA. RBCs and WBCs are bystanders and are not necessary for the process

68
Q

Clotting def

A

Sequential activation and interaction of plasma proteins or clotting factors (some act as enzymes and some act as co-factors), in presence of calcium and phospholipid agents

69
Q

3 stages of clotting -> which stage is visible and which is not

A

stage 1 -> beginning. stages 1 and 2 molecular changes that aren’t visible. stage 3 : final form

70
Q

How protein factors in cloting were named

A

Roman numerals I to XIII in order of discovery

71
Q

Stage 1 of clotting 2 pathways involved, the time they take and what induces them

A

Intrinsic pathway activated by blood vessel damage (3-6 minutes)
Extrinsic pathway activated by tissue outside vessel (15-20 seconds)

72
Q

Stage 3 of clotting what happens

A

Fibrinogen is converted into fibrin (some a.a removed) in presence of thrombin

73
Q

Stage 2 of clotting what happens (2)

A

1) Prothrombin is converted into thrombin in presence of prothrombinase and Ca 2+.
2) Thrombin activates factor XIII (becomes XIIIa) which consolidates/cross-links fibrin molecule to make the network they form more compact

74
Q

Stage 1 of clotting how intrinsic pathway starts, what it uses and what it leads to

A

Starts with collagen exposure. Uses plasma factors, Ca 2+ and PF3. Leads to prothrombinase formation (complex of Va, Xa, PF, Ca 2+)

75
Q

Stage 1 of clotting what extrinsic pathway uses and what it leads to

A

Uses tissue factors (protein and phospholipid), plasma factors, Ca 2+ and tissue phospholipid. Leads to prothrombinase formation

76
Q

Why extrinsic AND intrinsic pathway

A

Small amounts of thrombin generated rapidly by extrinsic scheme trigger strongly positive feedback on intrinsic scheme to generate more thrombin

77
Q

3 things thrombin does

A

1) Catalyzes formation of fibrin from fibrinogen
2) Activates factor XIII into XIIIa
3) Positive feedback on intrinsic pathway

78
Q

What downregulates clotting (2)

A

1) Inhibitors of platelet adhesion

2) Anticoagulants (naturally occuring chemicals that block reactions in coagulation scheme)

79
Q

Exemples of coagulants and what they do

A

Heparin and antithrombin III work together to block IX, X, XI and XII
Protein C inhibits factors V and VIII

80
Q

3 factors in coagulation and if we can lack them

A

Ca 2+, phospholipid (always present sufficiently) and protein plasma factors (can be deficient - congenital)

81
Q

Congenital cloting factor deficiencies

A

Heredity deficiencies of a single factor (ex. VIII -> hemophilia)

82
Q

Acquired cloting factor deficiencies and 2 exemples

A

Multifactor deficiencies (ex. liver disease, vitamin K deficiency)

83
Q

Clot retraction meaning

A

Clot moves away from vessel walls/sides

84
Q

Obtaining serum in vitro

A

Induce cloting in presence of plasma, cloting factors get involved in cloting and liquid left is plasma

85
Q

What clot retraction depends on

A

Platelets. (release a contractile protein named thrombosthenin which influences clot retraction)

86
Q

How clot helps healing

A

Tends to shrink after it retracts and this pulls walls of damaged vessel together

87
Q

Clot lysis what it means and other name for it

A

Clot dissolution/destruction. Fibrinolysis

88
Q

Scheme of fibrinolysis

A

Plasmin dissolves fibrin into fibrin fragment. Plasmin derives from plasminogen. Plasminogen activator transforms plasminogen into plasmin.

89
Q

2 types of plasminogen activators

A

1) Intrinsic proactivators (ex. XIIa) and endothelial cell factors.
2) Extrinsic proactivators (ex. tissue factors)

90
Q

Anticoagulants 3 types

A

1) Inhibitors of platelet adhesion
2) Anticoagulant drugs (interfere with clot formation)
3) Thrombolytic drugs (promote clot lysis)

91
Q

Exemple of inhibitor of platelet adhesion

A

aspirin

92
Q

2 exemples of anticoagulant drugs

A

1) Coumarin (blocks synthesis of functional prothrombin, VII, IX, X)
2) Heparin (inhibits thrombin activation and action)

93
Q

2 exemples of thrombolytic drugs

A

1) Tissue plasminogen activator (t-PA)

2) Streptokinase

PHGY 209 (17 decks)

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