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Cardiovascular > 13. > Flashcards

13. Flashcards

1
Q

what is the CESSATION (stopping) of BLOOD known as

A

HAEMOSTASIS

  • PREVENTS BLOOD LOSS through the WALLS of DAMAGED VESSELS and establishes a framework for tissue repair

like a chain reaction

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2
Q

HAEMOSTASIS consists of 3 PHASES:

A
  1. VASCULAR PHASE
  2. PLATELET PHASE
  3. COAGULATION PHASE
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3
Q

VASCULAR PHASE occurs when the WALL of a BLOOD VESSEL is CUT, which TRIGGERS…

A

CONTRACTION of SMOOTH MUSCLE Fibres in the wall

  • VASCULAR SPASM
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4
Q

what is the purpose of the VASCULAR SPASM (smooth muscle cells in wall contract) in VASCULAR PHASE

A

DECREASES DIAMETER or vessel at injury site

which SLOWS / STOPS the FLOW OF BLOOD through the wall

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5
Q

VASCULAR SPASM lasts approx how long

A

30 MINUTES

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6
Q

what CHANGES OCCUR in the vessel ENDOTHELIUM during the VASCULAR PHASE

A

-endothelial cells CONTRACT and EXPOSE UNDERLYING BASEMENT MEMBRANE to the bloodstream

  • RELEASE CHEMICAL FACTORS and LOCAL HORMONES such as
    ADP, TISSUE FACTOR (factor 3), and PROSTACYCLIN (PROSTAGLANDIN I2)
  • also RELEASE ENDOTHELINS (peptide hormones)
  • endothelial cell membranes become ‘STICKY’ so cells on opposite sides STICK TOGETHER and CLOSE OFF PASAGEWAY
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7
Q

in VASCULAR PHASE, what do ENDOTHELIAL CELLS RELEASE

A
  • ADP, TISSUE FACTOR (3), PROSTACYCLIN (prostaglandin I2)
  • ENDOTHELINS (peptide hormones)
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8
Q

VASCUALAR PHASE
what do ENDOTHELINS do

A
  • Stimulate smooth muscle Contraction, PROMOTE VASCULAR SPASMS
  • Stimulate the DIVISION / PROLIFERATION of Endothelial cells, Smooth Muscle Fibres, Fibroblasts to ACCELERATE REPAIR PROCESS
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9
Q

VASCULAR PHASE
ENDOTHELIAL CELL MEMBRANES CONTRACT to EXPOSE.. to the bloodstream
(pull themselves back)

A

UNDERLYING BASEMENT MEMBRANE

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10
Q

VASCULAR PHASE
how can ENDOTHELIAL CELLS CLOSE off the passageway

A

MEMBRANES BECOME STICKY

so in small capillaries the endothelial cells on opposite sides stick together

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11
Q

what are PLATELETS

A

SMALL, NON-NUCLEATED bodies that are PINCHED OFF FROM MEGAKARYOCYTES in the BONE MARROW

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12
Q

wat is PLATELET HALF LIFE

A

approx 10 DAYS

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13
Q

how is PLATELETS NUCLEUS

A

NO NUCLEUS

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14
Q

PLATELETS are formed as they are PINCHED OFF from which CELLS in the BONE MARROW

A

MEGAKARYOCYTES

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15
Q

the PLATELET PHASE BEGINS within …. SECONDS AFTER INJURY

A

within 15 SECONDS

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16
Q

what are the 3 MAIN STEPS of the PLATELET PHASE

A
  1. platelet ADHESION
  2. platelet ACTIVATION
  3. platelet AGGREGATION
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17
Q

PLATELET PHASE
in ADHESION, what do PLATELETS STICK TO

A
  • STICKY ENDOTHELIAL SURFACES
  • BASEMENT MEMBRANES
  • EXPOSED COLLAGEN FIBRES beneath endothelium via collagen receptor - glycoprotein Ia / IIa
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18
Q

name of COLLAGEN RECEPTOR that allows PLATELETS to ADHERE to EXPOSED COLLAGEN FIBRES

A

GLYCOPROTEIN Ia / IIa

(2 separate proteins resting on the cell membrane)

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19
Q

ADHESION between PLATELET and COLLAGEN via GLYCOPROTEIN Ia / IIa (receptor) happens by BRIDGING WITH which factor

A

VON WILLEBRAND’S FACTOR

(formed by endothelial cells)

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20
Q

VON WILLEBRAND’S FACTOR CIRCULATE in PLASMA COMPLEXED with with factor

A

FACTOR VIII (8)

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21
Q

VON WILLEBRAND’S FACTOR is FORMED BY..

A

ENDOTHELIAL CELLS

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22
Q

when COLLAGEN and VON WILLEBRAND’S FACTOR INTERACT with GP Ia / IIa, the receptor form a COMPLEX that BINDS with…..

A

FIBRINOGEN from PLASMA

-> platelet is now ACTIVATED and ready to bind other platelets and cause PLATELET AGGREGATION (STICK TOGETHER)

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23
Q

what does PLATELET AGGREGATION FORM

A

PLATELET PLUG which CLOSES SMALL BREAKS

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24
Q

other PLATELETS need to be ACTIVATED in order to BIND, so ACTIVATED PLATELETS RELEASE CLOTTING COMPOUNDS to promote FURTHER PLATELET ACTIVATION AND …

A

VASOCONSTRICTION

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25
Q

what are the CLOTTING COMPOUNDS that ACTIVATED PLATELETS in aggregation RELEASE?
in order to promote VASOCONSTRICTION and further Platelet ACTIVATION

A
  • ADENOSINE DIPHOSPHATE (ADP)
  • THROMBOXANE A2 and SEROTONIN
  • CLOTTING FACTORS
  • PLATELET DERIVED GROWTH FACTOR (PDGF)
  • CALCIUM IONS Ca2+
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26
Q

what is COMPLEXED WITH FACTOR VIII (8) in PLASMA

A

VON WILLEBRAND’S FACTOR

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27
Q

what causes PLATELETS to be ACTIVATED which then allows them to BIND to others and cause PLATELET AGGREGATION (STICK together)

A

when PLATELETS ADHERE to COLLAGEN, COLLAGEN and VON WILLEBRAND’S FACTOR INTERACT with GLYCOPROTEIN Ia / IIa,
GP Ia/IIa FORM A COMPLEX that BINDS FIBRINOGEN

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28
Q

what is the ROLE of ADP in HAEMOSTASIS and blood clotting

A

it is a CLOTTING COMPOUND
that is RELEASED FROM ACTIVATED PLATELETS

promotes VASOCONSTRICTION and further PLATELET ACTIVATION

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29
Q

what FACTORS LIMIT the GROWTH of the PLATELET PLUG so that it doesn’t keep growing

A
  • PROSTACYCLIN (from endothelial cells) inhibits platelet aggregation
  • INHIBITORY COMPOUNDS RELEASED by other WHITE BLOOD CELLS
  • Circulating ENZYMES BREAK DOWN ADP
  • NEGATIVE FEEDBACK from SEROTONIN
  • Development of BLOOD CLOT ISOLATES the AREA (stops activating factors getting there)
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30
Q

what help BREAK DOWN ADP in order to LIMIT PLATELET PLUG GROWTH

A

Circulating ENZYMES

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31
Q

what is RELEASED by ENDOTHELIAL CELLS that INHIBITS PLATELET AGGREGATION

A

PROSTACYCLIN

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32
Q

INHIBITORY COMPOUNDS that LIMIT GROWTH of PLATELET PLUG are RELEASED by other..

A

WHITE BLOOD CELLS

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33
Q

NEGATIVE FEEDBACK to LIMIT / INHIBIT GROWTH of PLATELET PLUG is from…

A

SEROTONIN

(released from activated platelets as clotting compound)

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34
Q

when does the COAGULATION PHASE begin after injury

A

after 30 SECONDS or MORE

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35
Q

what is COAGULATION

A

BLOOD CLOTTING

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36
Q

COAGULATION occurs by …. reactions

A

CASCADE REACTIONS

  • chain reactions of enzymes and proenzymes
  • form 3 pathways
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37
Q

what is the RESULT of the COAGULATION PHASE

A

to COVERT circulating FIBRINOGEN -> insoluble FIBRIN

38
Q

CLOTTING FACTORS are also CALLED..

A

PROCOAGULANTS

39
Q

MOST PROTEIN CLOTTING FACTORS are SYNTHESISED by the …

A

LIVER

40
Q

which CLOTTING FACTORS are NOT SYNTHESISED by the LIVER

A

FACTOR III (3) - TISSUE FACTOR
(damaged tissue and activated platelets)

FACTOR IV (4) - CALCIUM IONS
(bone, diet, platelets)

FACTOR VIII (8) - ANTIHEMOPHILIC
(platelets, endothelial cells)

41
Q

what are the 3 COAGULATION PATHWAYS

A
  1. EXTRINSIC pathway
  2. INTRINSIC pathway
  3. COMMON pathway
42
Q

what is the COMMON END RESULT of EXTRINSIC and INTRINSIC PATHWAYS needed to begin COMMON pathway

A

ACTIVATE FACTOR X (10)

(stuart-prower factor)

43
Q

EXTRINSIC PATHWAY BEGINGS WHERE

A

OUTSIDE BLOODSTEAM (extrinsic)

in VESSEL WALL

44
Q

how does EXTRINSIC PATHWAY lead to ACTIVATION of FACTOR X

A
  1. DAMAGED ENDOTHELIUM RELEASES TISSUE FACTOR (factor III)
  2. Tissue Factor + other compounds = ENZYME COMPLEX
    (with help of CA2+ and CLOTTING FACTOR VII (7) )

activated factor X

45
Q

which FACTOR is RELEASED by DAMAGED ENDOTHELIUM in EXTRINSIC PATHWAY

A

FACTOR III (3) - TISSUE FACTOR

46
Q

in EXTRINSIC PATHWAY,
FACTOR III / TISSUE FACTOR is associated with which CLOTTING FACTORS to form TISSUE FACTOR ENZYME COMPLEX that activates factor x

A

CA 2+ IONS (factor IV)

CLOTTING FACTOR VII (7)

47
Q

WHERE does INTRINSIC PATHWAY BEGIN

A

WITHIN BLOODSTREAM (intrinsic_

begins with CIRCULATING PROENZYMES

48
Q

what happens in INTRINSIC PATHWAY to cause ACTIVATION of FACTOR X

A
  1. ACTIVATION of FACTOR XII (12) exposed to COLLAGEN
    (activated proenzyme is usually factor 12)
  2. PLATELETS RELEASE FACTORS - PLATELET FACTOR 3 (PF-3)

+ CA2+ IONS

+ CLOTTING FACTORS 8 and 9

  1. FORM FACTOR X ACTIVATOR COMPLEX
49
Q

in INTRINSIC PATHWAY what associates with ACTIVATED FACTOR XII (12) to form FACTOR X ACTIVATOR COMPLEX

A
  • PF-3

CA2+

CLOTTING FACTORS VIII (8) and IX (9)

50
Q

what is the END RESULT / FORMATION from the COMMON PATHWAY

A

FIBRIN

  • will form scaffold for platelets to form a clot
51
Q

how does COMMON PATHWAY form FIBRIN

A
  1. FACTOR X CONVERTED into PROTHROMBINASE
  2. prothrombinase CONVERTS PROTHROMBIN -> THROMBIN
  3. thrombin converts FIBRINOGEN -> FIBRIN
52
Q

in COAGULATION PHASE, the COMMON PATHWAY what causes the CONVERSION of FIBRINOGEN TO FIBRIN

A

THROMBIN

53
Q

how is THROMBIN FORMED in COMMON PATHWAY

A

PROTHROMBINASE CONVERTS PROTHROMBIN -> THROMBIN

54
Q

in COMMON PATHWAY what is FACTOR X CONVERTED INTO

A

PROTHROMBINASE

which converts prothrombin -> thrombin

which converts fibrinogen -> fibrin

55
Q

in PLATELET PHASE what INHIBITS PLATELET AGGREGATION

A

PROSTACYCLIN

56
Q

what is the ROLE of CA2+ IONS in HAEMOSTASIS
(factor IV)

A
  1. PLATELET PHASE:
    CLOTTING COMPOUND RELEASED from ACTIVATED PLATELETS to FURTHER ACTIVATE and promote VASOCONSTRICTION
  2. COAGULATION PHASE:

EXTRINSIC PATHWAY - associates with TISSUE FACTOR to form TISSUE FACTOR / ENZYME COMPLEX

INTRINSIC PATHWAY - associates with activated FACTOR XII (12) along with PF-3 and factors 8&9 to form FACTOR X ACTIVATOR COMPLEX

57
Q

when is FACTOR VIII (8) used

A

in EXTRINSIC PATHWAY CONVERTS TISSUE FACTOR (3) into ENZYME COMPLEX which activated factor X

58
Q

when is FACTOR XII (12) USED

A

INTRINSIC PATHWAY
as the activated proenzyme

59
Q

why is THROMBIN important

A
  • CONVERTS FIBRINOGEN -> FIBRIN
    fibrin forms clot
  • & forms POSITIVE FEEDBACK LOOP and ACCELERATES CLOTTING
  • & plays role in FIBRINOLYSIS (slow dissolving of a clot)
60
Q

how does THROMBIN also form a POSITIVE FEEDBACK LOOP and ACCELERATE CLOTTING

A
  • STIMULATES FORMATION of TISSUE FACTOR (3)
    (Extrinsic pathway, released from damaged endothelium)
  • STIMULATES RELEASE of PF-3
    (Intrinsic pathway, associates with factor XII)

so more factor X activated, more fibrin

61
Q

which FACTORS RESTRICT BLOOD CLOTTING as part of NEGATIVE FEEDBACK LOOP

A
  • ANTICOAGULANTS
  • HEPARIN
  • ASPIRIN
  • PROTEIN C
  • PROSTACYLIN
62
Q

which ANTICOAGULANTS are part of the NEGATIVE FEEDBACK LOOP that RESTRICT BLOOD CLOTTING and what do they do

A
  • ANTITHROMBIN-III : INACTIVATES several clotting factors including thrombin
  • ALPHA-2-MACROGLOBULIN: INHIBITS THROMBIN
63
Q

what does HEPARIN do as part of the NEGATIVE FEEDBACK LOOP that RESTRICTS BLOOD CLOTTING

A

COFACTOR that ACCELERATES the ACTIVATION of ANTITHROMBIN-III

  • an ANTICOAGULANT that INACTIVATES THROMBIN and other clotting factors
64
Q

besides being given CLINICALLY as DRUG to RESTRICT BLOOD CLOTTING, how do we have HEPARIN naturally

A

RELEASED by BASOPHILS and MAST CELLS

65
Q

what does ASPIRIN do as part of the NEGATIVE FEEDBACK LOOP that RESTRICTS BLOOD CLOTTING

A

Irreversibly BLOCKS the FORMATION of THROMBOXANE A2
(clotting compound released from activated platelets in platelet phase aggregation)

  • INHIBITORY EFFECT on PLATELET AGGREGATION

(does NOT affect clotting cascade / coagulant phase therefore not an anticoagulant)

66
Q

what does PROTEIN C do as part of the NEGATIVE FEEDBACK LOOP that RESTRICTS BLOOD CLOTTING

A

INACTIVATES several CLOTTING FACTORS

& STIMULATES FORMATION of PLASMIN
- ENZYME that BREAKS DOWN FIBRIN,FIBRINOLYSIS (dissolving clot)

67
Q

what is FIBRINOLYSIS is the the slow process of DISSOLVING CLOT. how does it take place

A
  1. THROMBIN and TISSUE PLASMINOGEN ACTIVATOR (t-PA)
    ACTIVATE PLASMINOGEN
  2. plasminogen PRODUCES PLASMIN
    (formation also stimulated by protein C)
  3. plasmin DIGESTS FIBRIN STRANDS
68
Q

what is PROTEIN C ACTIVATED BY

A

THROMBOMODULIN

69
Q

what does PROSTACYCLIN do as part of the NEGATIVE FEEDBACK LOOP that RESTRICTS BLOOD CLOTTING

A

(released in PLATELET PHASE)
INHIBITS PLATELET AGGREGATION

and OPPOSED STIMULATORY THROMBIN, ADP and other factors

70
Q

what ENZYME DIGESTS FIBRIN STRANDS (fibrinolysis)

A

PLASMIN

71
Q

in FIBRINOLYSIS what ACTIVATE PLASMINOGEN which PRODUCES PLASMIN

A

THROMBIN and PLASMINOGEN ACTIVATOR (t-PA)

72
Q

what does THROMBOMODULIN ACTIVATE

A

PROTEIN C

73
Q

what ACCELERATES ACTIVATION of ANTITHROMBIN-III (anticoagulant, inactivates thrombin) to reduce blood clotting

A

HEPARIN

74
Q

which ANTICOAGULANT INHIBITS THROMBIN

A

ALPHA-2-MACROGLOBULIN

75
Q

what BLOCKS FORMATION of THROMBOXAN A2 and thus has an INHIBITORY EFFECT on PLATELET AGGREGATION to restrict blood clotting

A

ASPIRIN

76
Q

what INACTIVATES CLOTTING FACTORS and STIMULATES PLASMIN FORMATION for FIBRINOLYSIS

A

PROTEIN C

77
Q

what OPPOSES THROMBIN, ADP and other factors to restrict blood clotting

A

PROSTACYCLIN

78
Q

besides CA2+ what is also ESSENTIAL to the CLOTTING PROCESS

A

VITAMIN K

(Fat soluble vitamin present in green vegetables, grains, organ meats and is absorbed with dietary lipids)

79
Q

how is VITAMIN K OBTAINED

A
  • half in DIET
  • rest MANUFACTURED BY BACTERIA in the LARGE INTESTINE
80
Q

any disorders that LOWER … CONC will IMPAIR CLOTTING

A

PLASMA CA2+ conc

81
Q

adequate amounts of VITAMIN K must be present for the LIVER to be able to SYNTHESIS which CLOTTING FACTORS

A
  • PROTHROMBIN (factor II)
  • FACTOR VII (7)
  • FACTOR IX (9)
  • FACTOR X
82
Q

how does VITAMIN K DEFICIENCY affect CLOTTING system

A

lead to eventual BREAKDOWN of COMMON PATHWAY due to LACK of CLOTTING FACTORS (prothrombin, 7, 9, 10)

entire CLOTTING SYSTEM will be INACTIVATED

(factor 7 associated with tissue factor 3 in extrinsic
factor 9 associated with factor 12 in intrinsic,
factor 10 converts to prothrombinase
prothrombin converted to thrombin)

83
Q

what does CLOT RETRACTION do

A

REDUCES SIZE of DAMAGED AREA

  • making it EASIER for FIBROCYTES, SMOOTH MUSCLE CELLS, ENDOTHELIAL CELLS to COMPLETE REPAIRS
  • smaller surface area to cover
84
Q

how does CLOT RETRACTION OCCUE

A

(1. platelets contract after platelets and rbcs have stuck to fibrin strands)

PULLS TORN EDGES of VESSEL CLOSER TOGETHER (like sewing a hole by pulling a thread)

REDUCING Residual BLEEDING and STABILIZING injury site

85
Q

VIRCHOW’S TRIAD consists of 3 broad categoraries of factors that influence the occurence of THROMBOSIS (CLOT)

what are the 3 categories

A
  • HYPERCOAGULABILITY

-VASCULAR DAMAGE

  • CIRCULATORY STASIS
86
Q

VIRCOW’S TRIAD

examples of conditions that can cause HYPERCOAGULABILITY

A
  • major SURGERY / TRAUME
  • MALIGNANCY (cancer)
  • PREGANCY (3rd trimester and post-partum)
  • INHERITIS THROMBOPHILIA
  • INFECTION and SEPSIS
  • INFLAMMATORY BOWEL DISEASE
  • AUTOIMMUNE CONDITION
  • Estrogen Therapy
  • Inflammation
  • Dehydration
87
Q

VIRCOW’S TRIAD

examples of conditions that can cause VASCUALAR DAMAGE

A
  • THROMBOPHLEBITIS (inflamed vein)
  • CELLULITIS (infection in skin)
  • ATHEROSCLEROSIS
  • Indwelling CATHETER / HEART VALVE
  • VENEPUNCTURE
  • physcal Trauma, Strain, Injury
  • Microtrauma to vessel wall
88
Q

VIRCOW’S TRIAD

examples of conditions that can cause CIRCULATORY STASIS

A
  • IMMOBILITY
  • VENOUS OBSTRUCTION
  • VARICOSE VEINS
  • ATRIAL FIBRILLATION (quiver) or LEFT VENTRICULAR DYSFUNCTION
  • Congenital Abnormalities
  • Low Heart Rate (bradycardia) and Low Blood Pressure
89
Q

extra…
pt (prothrombin time) blood test should be how long

A

11-15 seconds

time from addition of calcium chloride until plasma clots

(blood decalcified, separate, add tissue factor to convert prothrombin to thrombin and add calcium chloride)

90
Q

a prolonged prothrombin time in pt test is assessing which pathways and what does it indicate

A

assessing Extrinsic and Common pathways

  • indicates deficiency in either factor VII, X, V, Prothrombin or Fibrinogen
91
Q

an APTT -activated partial thromboplastin time test should be how long

A

normally around 35 seconds

(blood decalcified, separated, add calcium and activating substances Kaolin which activates factor 12 and Cephalin which substitutes platelet phospholipids)

92
Q

aptt test measures integrity of which pathways and factors

A

intrinsic and common pathways

factors 12, 11, 8, 9 and 10, prothrombin, fibrinogen

Cardiovascular (16 decks)

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