13. Flashcards
(92 cards)
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
2
Q
HAEMOSTASIS consists of 3 PHASES:
A
- VASCULAR PHASE
- PLATELET PHASE
- COAGULATION PHASE
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
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
5
Q
VASCULAR SPASM lasts approx how long
A
30 MINUTES
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
7
Q
in VASCULAR PHASE, what do ENDOTHELIAL CELLS RELEASE
A
- ADP, TISSUE FACTOR (3), PROSTACYCLIN (prostaglandin I2)
- ENDOTHELINS (peptide hormones)
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
9
Q
VASCULAR PHASE
ENDOTHELIAL CELL MEMBRANES CONTRACT to EXPOSE.. to the bloodstream
(pull themselves back)
A
UNDERLYING BASEMENT MEMBRANE
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
11
Q
what are PLATELETS
A
SMALL, NON-NUCLEATED bodies that are PINCHED OFF FROM MEGAKARYOCYTES in the BONE MARROW
12
Q
wat is PLATELET HALF LIFE
A
approx 10 DAYS
13
Q
how is PLATELETS NUCLEUS
A
NO NUCLEUS
14
Q
PLATELETS are formed as they are PINCHED OFF from which CELLS in the BONE MARROW
A
MEGAKARYOCYTES
15
Q
the PLATELET PHASE BEGINS within …. SECONDS AFTER INJURY
A
within 15 SECONDS
16
Q
what are the 3 MAIN STEPS of the PLATELET PHASE
A
- platelet ADHESION
- platelet ACTIVATION
- platelet AGGREGATION
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
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)
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)
20
Q
VON WILLEBRAND’S FACTOR CIRCULATE in PLASMA COMPLEXED with with factor
A
FACTOR VIII (8)
21
Q
VON WILLEBRAND’S FACTOR is FORMED BY..
A
ENDOTHELIAL CELLS
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)
23
Q
what does PLATELET AGGREGATION FORM
A
PLATELET PLUG which CLOSES SMALL BREAKS
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
25
what are the CLOTTING COMPOUNDS that ACTIVATED PLATELETS in aggregation RELEASE?
in order to promote VASOCONSTRICTION and further Platelet ACTIVATION
- ADENOSINE DIPHOSPHATE (ADP)
- THROMBOXANE A2 and SEROTONIN
- CLOTTING FACTORS
- PLATELET DERIVED GROWTH FACTOR (PDGF)
- CALCIUM IONS Ca2+
26
what is COMPLEXED WITH FACTOR VIII (8) in PLASMA
VON WILLEBRAND'S FACTOR
27
what causes PLATELETS to be ACTIVATED which then allows them to BIND to others and cause PLATELET AGGREGATION (STICK together)
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
28
what is the ROLE of ADP in HAEMOSTASIS and blood clotting
it is a CLOTTING COMPOUND
that is RELEASED FROM ACTIVATED PLATELETS
promotes VASOCONSTRICTION and further PLATELET ACTIVATION
29
what FACTORS LIMIT the GROWTH of the PLATELET PLUG so that it doesn't keep growing
- 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)
30
what help BREAK DOWN ADP in order to LIMIT PLATELET PLUG GROWTH
Circulating ENZYMES
31
what is RELEASED by ENDOTHELIAL CELLS that INHIBITS PLATELET AGGREGATION
PROSTACYCLIN
32
INHIBITORY COMPOUNDS that LIMIT GROWTH of PLATELET PLUG are RELEASED by other..
WHITE BLOOD CELLS
33
NEGATIVE FEEDBACK to LIMIT / INHIBIT GROWTH of PLATELET PLUG is from...
SEROTONIN
(released from activated platelets as clotting compound)
34
when does the COAGULATION PHASE begin after injury
after 30 SECONDS or MORE
35
what is COAGULATION
BLOOD CLOTTING
36
COAGULATION occurs by .... reactions
CASCADE REACTIONS
- chain reactions of enzymes and proenzymes
- form 3 pathways
37
what is the RESULT of the COAGULATION PHASE
to COVERT circulating FIBRINOGEN -> insoluble FIBRIN
38
CLOTTING FACTORS are also CALLED..
PROCOAGULANTS
39
MOST PROTEIN CLOTTING FACTORS are SYNTHESISED by the ...
LIVER
40
which CLOTTING FACTORS are NOT SYNTHESISED by the LIVER
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
what are the 3 COAGULATION PATHWAYS
1. EXTRINSIC pathway
2. INTRINSIC pathway
3. COMMON pathway
42
what is the COMMON END RESULT of EXTRINSIC and INTRINSIC PATHWAYS needed to begin COMMON pathway
ACTIVATE FACTOR X (10)
(stuart-prower factor)
43
EXTRINSIC PATHWAY BEGINGS WHERE
OUTSIDE BLOODSTEAM (extrinsic)
in VESSEL WALL
44
how does EXTRINSIC PATHWAY lead to ACTIVATION of FACTOR X
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
which FACTOR is RELEASED by DAMAGED ENDOTHELIUM in EXTRINSIC PATHWAY
FACTOR III (3) - TISSUE FACTOR
46
in EXTRINSIC PATHWAY,
FACTOR III / TISSUE FACTOR is associated with which CLOTTING FACTORS to form TISSUE FACTOR ENZYME COMPLEX that activates factor x
CA 2+ IONS (factor IV)
CLOTTING FACTOR VII (7)
47
WHERE does INTRINSIC PATHWAY BEGIN
WITHIN BLOODSTREAM (intrinsic_
begins with CIRCULATING PROENZYMES
48
what happens in INTRINSIC PATHWAY to cause ACTIVATION of FACTOR X
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
3. FORM FACTOR X ACTIVATOR COMPLEX
49
in INTRINSIC PATHWAY what associates with ACTIVATED FACTOR XII (12) to form FACTOR X ACTIVATOR COMPLEX
* PF-3
CA2+
CLOTTING FACTORS VIII (8) and IX (9)
50
what is the END RESULT / FORMATION from the COMMON PATHWAY
FIBRIN
- will form scaffold for platelets to form a clot
51
how does COMMON PATHWAY form FIBRIN
1. FACTOR X CONVERTED into PROTHROMBINASE
2. prothrombinase CONVERTS PROTHROMBIN -> THROMBIN
3. thrombin converts FIBRINOGEN -> FIBRIN
52
in COAGULATION PHASE, the COMMON PATHWAY what causes the CONVERSION of FIBRINOGEN TO FIBRIN
THROMBIN
53
how is THROMBIN FORMED in COMMON PATHWAY
PROTHROMBINASE CONVERTS PROTHROMBIN -> THROMBIN
54
in COMMON PATHWAY what is FACTOR X CONVERTED INTO
PROTHROMBINASE
which converts prothrombin -> thrombin
which converts fibrinogen -> fibrin
55
in PLATELET PHASE what INHIBITS PLATELET AGGREGATION
PROSTACYCLIN
56
what is the ROLE of CA2+ IONS in HAEMOSTASIS
(factor IV)
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
when is FACTOR VIII (8) used
in EXTRINSIC PATHWAY CONVERTS TISSUE FACTOR (3) into ENZYME COMPLEX which activated factor X
58
when is FACTOR XII (12) USED
INTRINSIC PATHWAY
as the activated proenzyme
59
why is THROMBIN important
- CONVERTS FIBRINOGEN -> FIBRIN
fibrin forms clot
- & forms POSITIVE FEEDBACK LOOP and ACCELERATES CLOTTING
- & plays role in FIBRINOLYSIS (slow dissolving of a clot)
60
how does THROMBIN also form a POSITIVE FEEDBACK LOOP and ACCELERATE CLOTTING
- 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
which FACTORS RESTRICT BLOOD CLOTTING as part of NEGATIVE FEEDBACK LOOP
- ANTICOAGULANTS
- HEPARIN
- ASPIRIN
- PROTEIN C
- PROSTACYLIN
62
which ANTICOAGULANTS are part of the NEGATIVE FEEDBACK LOOP that RESTRICT BLOOD CLOTTING and what do they do
- ANTITHROMBIN-III : INACTIVATES several clotting factors including thrombin
- ALPHA-2-MACROGLOBULIN: INHIBITS THROMBIN
63
what does HEPARIN do as part of the NEGATIVE FEEDBACK LOOP that RESTRICTS BLOOD CLOTTING
COFACTOR that ACCELERATES the ACTIVATION of ANTITHROMBIN-III
- an ANTICOAGULANT that INACTIVATES THROMBIN and other clotting factors
64
besides being given CLINICALLY as DRUG to RESTRICT BLOOD CLOTTING, how do we have HEPARIN naturally
RELEASED by BASOPHILS and MAST CELLS
65
what does ASPIRIN do as part of the NEGATIVE FEEDBACK LOOP that RESTRICTS BLOOD CLOTTING
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
what does PROTEIN C do as part of the NEGATIVE FEEDBACK LOOP that RESTRICTS BLOOD CLOTTING
INACTIVATES several CLOTTING FACTORS
& STIMULATES FORMATION of PLASMIN
- ENZYME that BREAKS DOWN FIBRIN,FIBRINOLYSIS (dissolving clot)
67
what is FIBRINOLYSIS is the the slow process of DISSOLVING CLOT. how does it take place
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
what is PROTEIN C ACTIVATED BY
THROMBOMODULIN
69
what does PROSTACYCLIN do as part of the NEGATIVE FEEDBACK LOOP that RESTRICTS BLOOD CLOTTING
(released in PLATELET PHASE)
INHIBITS PLATELET AGGREGATION
and OPPOSED STIMULATORY THROMBIN, ADP and other factors
70
what ENZYME DIGESTS FIBRIN STRANDS (fibrinolysis)
PLASMIN
71
in FIBRINOLYSIS what ACTIVATE PLASMINOGEN which PRODUCES PLASMIN
THROMBIN and PLASMINOGEN ACTIVATOR (t-PA)
72
what does THROMBOMODULIN ACTIVATE
PROTEIN C
73
what ACCELERATES ACTIVATION of ANTITHROMBIN-III (anticoagulant, inactivates thrombin) to reduce blood clotting
HEPARIN
74
which ANTICOAGULANT INHIBITS THROMBIN
ALPHA-2-MACROGLOBULIN
75
what BLOCKS FORMATION of THROMBOXAN A2 and thus has an INHIBITORY EFFECT on PLATELET AGGREGATION to restrict blood clotting
ASPIRIN
76
what INACTIVATES CLOTTING FACTORS and STIMULATES PLASMIN FORMATION for FIBRINOLYSIS
PROTEIN C
77
what OPPOSES THROMBIN, ADP and other factors to restrict blood clotting
PROSTACYCLIN
78
besides CA2+ what is also ESSENTIAL to the CLOTTING PROCESS
VITAMIN K
(Fat soluble vitamin present in green vegetables, grains, organ meats and is absorbed with dietary lipids)
79
how is VITAMIN K OBTAINED
- half in DIET
- rest MANUFACTURED BY BACTERIA in the LARGE INTESTINE
80
any disorders that LOWER ... CONC will IMPAIR CLOTTING
PLASMA CA2+ conc
81
adequate amounts of VITAMIN K must be present for the LIVER to be able to SYNTHESIS which CLOTTING FACTORS
- PROTHROMBIN (factor II)
- FACTOR VII (7)
- FACTOR IX (9)
- FACTOR X
82
how does VITAMIN K DEFICIENCY affect CLOTTING system
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
what does CLOT RETRACTION do
REDUCES SIZE of DAMAGED AREA
- making it EASIER for FIBROCYTES, SMOOTH MUSCLE CELLS, ENDOTHELIAL CELLS to COMPLETE REPAIRS
- smaller surface area to cover
84
how does CLOT RETRACTION OCCUE
(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
VIRCHOW'S TRIAD consists of 3 broad categoraries of factors that influence the occurence of THROMBOSIS (CLOT)
what are the 3 categories
- HYPERCOAGULABILITY
-VASCULAR DAMAGE
- CIRCULATORY STASIS
86
VIRCOW'S TRIAD
examples of conditions that can cause HYPERCOAGULABILITY
- 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
VIRCOW'S TRIAD
examples of conditions that can cause VASCUALAR DAMAGE
- THROMBOPHLEBITIS (inflamed vein)
- CELLULITIS (infection in skin)
- ATHEROSCLEROSIS
- Indwelling CATHETER / HEART VALVE
- VENEPUNCTURE
- physcal Trauma, Strain, Injury
- Microtrauma to vessel wall
88
VIRCOW'S TRIAD
examples of conditions that can cause CIRCULATORY STASIS
- IMMOBILITY
- VENOUS OBSTRUCTION
- VARICOSE VEINS
- ATRIAL FIBRILLATION (quiver) or LEFT VENTRICULAR DYSFUNCTION
- Congenital Abnormalities
- Low Heart Rate (bradycardia) and Low Blood Pressure
89
extra...
pt (prothrombin time) blood test should be how long
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
a prolonged prothrombin time in pt test is assessing which pathways and what does it indicate
assessing Extrinsic and Common pathways
- indicates deficiency in either factor VII, X, V, Prothrombin or Fibrinogen
91
an APTT -activated partial thromboplastin time test should be how long
normally around 35 seconds
(blood decalcified, separated, add calcium and activating substances Kaolin which activates factor 12 and Cephalin which substitutes platelet phospholipids)
92
aptt test measures integrity of which pathways and factors
intrinsic and common pathways
factors 12, 11, 8, 9 and 10, prothrombin, fibrinogen
