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Health.2 > Haemorrhage, Homeostasis, Coag, Thromb > Flashcards

Haemorrhage, Homeostasis, Coag, Thromb Flashcards

1
Q

PART I…
I. Haemorrhage

What is a haemorrhage?

A

bleeding from a ruptured blood vessel

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2
Q

What is haemostasis?

A

the stopping of bleeding

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3
Q

What is thrombosis?

A

formation of a clot inside a blood vessel

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4
Q

When is thrombosis beneficial?

A

in the case of trauma/injury to stop bleeding

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5
Q

When is thrombosis detrimental?

A

in DCT or other pathological conditions

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6
Q

What types of drugs inhibit detrimental thrombosis?

A

anti-thrombotic drugs

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7
Q

What are the 2 types of haemorrhage?

A
  • internal: leaky blood vessels inside body

- external: natural opening/break in skin

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8
Q

What are 2 causes of haemorrhage?

A
  • trauma: different types of injury

- medical condition: intravascular, intramural, extravascular

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9
Q

What is meant by the medical conditions capable of causing a haemorrhage:

  • intravascular
  • intramural
  • extravascular
A
  • defects in the blood
  • defects in the vessel wall
  • defects outside blood vessels
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10
Q

What are 6 risk factors for a haemorrhage?

A
  • congential (haemophilia)
  • medication (anti-coagulants)
  • age (poorly tolerated by elderly)
  • trauma (burns/punctures/ballistic)
  • disease (liver disease
  • infection (gastroenteritis)
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11
Q

What are the 4 classes of haemorrhage according to the American College of Surgeons database?

A
  • class I
  • class II
  • class III
  • class IV
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12
Q

What are the characteristics of a class I haemorrhage (loss percentage of blood volume, vital signs)?

A
  • loss of <15% blood volume

- no change in vital signs

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13
Q

What are the characteristics of a class II haemorrhage (loss percentage of blood volume, vital signs)?

A
  • loss of 15-30% blood volume

- tachycardia, vasoconstriction

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14
Q

What are the characteristics of a class III haemorrhage (loss percentage of blood volume, vital signs)?

A
  • loss of 30-40% blood volume
  • ↓ BP, ↑ HR, shock, confusion
  • volume expander or transfusion necessary
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15
Q

What are the characteristics of a class IV haemorrhage (loss percentage of blood volume, vital signs)?

A
  • loss of >40% blood volume
  • limit of body’s compensation mechanisms, possible death
  • aggressive resuscitation required
    most severe
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16
Q

Haemorrhage grading scle of bleeding?

A 
0: no bleeding
1
2: sometimes clinically significant
3: severe
4: possible death- too much blood lost
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17
Q

What is observed with haemorrhagic shock? (3)

A
  • hypovolemia (decreased blood volume)
  • reduced cardiac output
  • reduced organ perfusion
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18
Q

What are the physiological/clinical responses to stop further blood loss in a haemorrhage?

A
  • vasoconstriction (req mechanical pressure)
  • haemostasis/thrombosis (amplified by haemostatic agents)
  • fibrinolysis (dissolution of blood of clots - antifibrinolytic agents)
  • surgery (to inhibit bleeding)
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19
Q

What are the physiological/clinical responses to replace lost blood volume in a haemorrhage?

A
  • volume expanders containing crystalloids (aqueous sols of mineral salts + other water-soluble molecules) and colloids (containing larger insoluble molecules like gelatine)
  • blood transfusion
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20
Q

II. compensatory mechanisms
III. haemostatic agents

What is the body’s first reaction to a haemorrhage?

A

Activation of compensatory mechanisms that regulate blood loss to restore haemostasis

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21
Q

What is the first consequence of blood loss that can activate compensatory mechanisms for a haemorrhage?

A
  • ⬇ arterial pressure
  • altered blood gases
    activate baroreceptor reflex + chemoreceptor reflex respectively

= cardiac stim, systemic vasoconstr, flow+vol redistribution

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22
Q

What is the kidney’s trigger to activate compensatory mechanisms for a haemorrhage?

A

RAAS activation (kidneys, adrenal, liver, lungs)

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23
Q

What is the pituitary’s trigger to activate compensatory mechanisms for a haemorrhage?

A

vasopressin (ADH) release

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24
Q

What is the sympathetic nerves’ trigger to activate compensatory mechanisms for a haemorrhage?

A

catecholamine release (sympathetic nerves, adrenal)

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25
Q

RAAS system diagram p89 and 90…

A
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26
Q

What are the two main aims of the body when responding to a haemorrhage?

A
  • increase blood pressure

- increase blood volume

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27
Q

What are the two ways the body increases blood pressure?

A
  • vasoconstriction

- tachycardia

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28
Q

What are 3 mechanisms resulting in vasoconstriction to increase BP in response a haemorrhage? (hint: think about the kidney’s, sympathetic nerves’ and pituitary triggers)

A
  • AngII formation – ↓ BP → ↑renin (kidney) → ↑Ang II
  • baroreceptor reflex - ↓ BP → ↑NAd (sympathetic nerves) tachycardia
  • vasopressin (ADH) - ↓ blood volume → antidiuretic effect
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29
Q

What are the four ways the body increases blood volume?

A
  • vasopressin baroreceptor reflex (⬇ water excretion + thirst)
  • Ang II formation (↑vasopressin → ↑aldosterone.. antidiuretic effect)
  • aldosterone
    (Na+ and water retention)
  • erythropoietin production - ↓O2 (kidney) → ↑Epo → ↑erythrocytes
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30
Q

What is the prognosis of a haemorrhage (3 peaks of death)?

A
  • minutes: exsanguination (severe blood loss)
  • hours: progressive decompensation (due to failure of compensation mechanisms)
  • days-weeks: sepsis and organ failure
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31
Q

signs and symptoms - haemorrhage?

A

tachycardia
rapid breathing, ⬇ pulse pressure, pale, anxiety
⬇ systolic pressure, confusion, agitation
loss peripheral pulses, ⬇ urine, loss of consciousness

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32
Q

what may some symptoms of haemorrhage be masked by?

A

use of drugs- b blockers

.. inhib effects e.g. tachycardia

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33
Q

Blood loss reduction summary diagram

page95

A
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34
Q

III. haemostatic agents

What are 3 haemstatic agents?

A
  • Recombinant factor VIIa (FVIIa)
  • desmopressin (DDAVP)
  • fibrinogen
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35
Q

how does recombinant factor 7a VIIa (FVIIa) work?

A

⬆ formation of factors IXa and Xa

to ⬆ thrombin generation and fibrin formation

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36
Q

What is desmopressin (DDAVP) an analogue of?

A

vasopressin

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37
Q

What does desmopressin (DDAVP) stimulate the release of? How does it do this?

A

release of VWF from endothelial cells by acting on V2 receptor

-> results in a secondary increase in factor VIII levels

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38
Q

What does DDAVP increase?

A

fibrin formation and platelet deposition

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39
Q

What does fibrinogen enhance the formation of?

A

fibrin

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40
Q

What are 3 antifibrinolytic agents?

A
  • tranexamic acid (TXA)
  • epsilon aminocaproic acid (EACA)
  • aprotinin (Trasylol)
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41
Q

What are TXA (tranexamic acid) and EACA
and what do they inhibit the conversion of?
affect?

A

synthetic lysine analogues.

:plasminogen to plasmin
= ⬇ fibrinolysis -> ⬆ clot stability

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42
Q

What type of inhibitor is aprotinin (trasylol)? What does it inhibit

A
  • serine protease inhibitor

- inhibits plasmin

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43
Q

What does aprotinin (trasylol) reduce?

A

fibrinolysis, leading to an increased clot stability

same as EACA and TXA

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44
Q

PART II…
I. Haemostasis: primary and coagulation

major components of haemostasis- stages?

A

vasc injury… collagen-> platelet formn
tissue factor-> coagulation cascade

primary haemostasis: platelet plu
secondary haemostasis: blood clot from fibrin

plasmin
–> finbinolysis+ clot degradation

pic on p101

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45
Q

Primary hemostasis occurs at the site of vascular injury. What happens in primary hemostasis?

A

weak platelet plug formed due to vasoconstriction and platelet activation to limit blood loss

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46
Q

What happens in secondary hemostasis?

A

Activation of coagulation cascade in plasma generates thrombin.
Thrombin converts fibrinogen to fibrin which then polymerizes.
Fibrin strands strengthen the primary hemostatic plug.

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47
Q

Name platelet activator and platelet inhibitor?

A

activator

  • collagen
  • thrombin
  • fibrinogen

inhibitor

  • nitric oxide
  • PGI2
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48
Q

what 2 things form a thrombus/blood clot?

A

platelets-haem plug from primary
+
fibrin- clot coagulation, from secondary

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49
Q

what are platelets?

A

v reactive blood cells…

after agonist, theyre activated

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50
Q

in which state are platelets unable to react with fibrinogen?

A

resting state

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51
Q

What is the difference between activated and resting state platelets?

A

resting shape: discoid and granular with inactive integrins.

Activated have different shape, degranulated and integrin activated

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52
Q

what can activated platelets do?

A

aggregation
adhesion
spreading on endothelium surface
procoagulant

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53
Q

3 steps to forming a platelet plug? to recruit to sit?

p105

A
  1. transloacation
    - signalling inside platelets, secrete molecules, allow…
  2. adhesion to sub endothelium
  3. aggregation- after recruiting others.
    = thrombus formation (after binding w fibrinogen molecule and bridging platelets)
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54
Q

what factor on a platelet is important for aggregation and when is it inactive?

A

integrin aIIbb3

inactive on resting platelet… thus cant interact w fibrinogen for aggregaton

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55
Q

when are granules secreted from platelets?

A

after activation

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56
Q

thrombin= activates platelets, what can the integrin aIIbb3 now do?

A

converted into active form, can bind fibrinogen and bridge to platelets together
= form a platelet plug!!

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57
Q

what 2 types of granules are found within resting platelet?

A

dense granules
alpha granules

after activation, theyre released

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58
Q

name some alpha granules found within a resting platelet

A 
coagulation factors
P-selectin for immune response
anti-bac 
angiogenic
chemo-attractants
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59
Q

name some dense granules found within a resting platelet

A 
ADP: mojor sec mediator for platelet activation
Ca2+
serotonin
CD63
LAMP1/2
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60
Q

what do platelets do once activated? w granules and generating something…

A 
ADP released from dense granules
generate TxA2 (Thromboxabe A2)

= ADP and TxA2 = 2 sec mediators of platelet activation

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61
Q

what are the 2 sec mediators of platelet activation and when are they released and where?

A

once platelet activated…
to autocrine pathway, platelet activation, at + feedback loop
(as ADP will go sit in another resting platelet)

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62
Q

what do anti platelet drugs target?

A

ADP and TxA2 = the 2 sec mediators of platelet activation…

= target amplification loop of platelet activation and not first initial steps of platelet activation

63
Q

classical haemostasis is XX dependant?

A

GPIIbIIIa (aIIbb3)

64
Q

summary of 3 steps of classical haemostasis

A
  1. rolling
    at site of vasc injury
    dependant on GPIb interaction w prothrombin? factor
  2. Activation
    platelets firmly adhere, secrete molecules in thrombin, ADP, TxA2 (sec mediators) recruit other platelets, form pluf
  3. stable adhesion, thrombus growth
    plug must be solidified by fibrin and activation of coagulation- allow stabilation of clots ☺
65
Q

sec haemostasis: coagulation happens at site of tissue damage/injury …

main aim of coagulation=?

A 
generate thrombin 
(enzyme that gen by coag cascade. fibrinogen-> fibrin clot... allow integration and stabilation of clot) ☺
66
Q

what may inc risk of embolism and bleeding? (sec haemostasis: coagulation)

A

any defects in fibrin generation from fibrinogen… cant form clot
thrombus formed not stable! :(

67
Q

what 3 things may thrombin do other than help form fibrin clot in coagulation cascade?

A
  1. amplify coagulation cascade
  2. vasoconstriction (directly)
  3. platelet activation

thrombin= key thing in reg of whole process of haemostasis!!

68
Q

what are the 2 pathways to generate thrombin?

when activated?

A

intrinsic: activated on polyanions surfaces (tissue damage) not activated in healthy donors. mainly infection as bacteria can activate. stents, heart disease…
extrinsic: site of injury

69
Q

What is the common phase between the intrinsic and extrinsic pathway leading to the formation of a fibrin clot?

A

converge to activation of factor Xa which cleaves prothrombin (II) -> thrombin (IIa) (key molecule of coag) then this changes fibrinogen -> fibrin-> form blood clot

70
Q

what form are all the coagulation factors in, in intrinsic pathway of thrombin formation?

A

inactive, and can be activated by: A/ same factor in active form.
cascade effect as XIIa activates XI, XIa activates IX…

71
Q

hows extrinsic pathway activated?

A

exposure of TF (tissue factor) in sub-endothelium, and gets upregulated in endothelial cells-> can bind to factor VIIa

TF: VIIa changes X-> Xa

72
Q

what do TF: VIIa and IXa factors have in common?

A

TF: VIIa is in extrinsic pathway
and IXa in in intrinsic

both change factor X to XA which converges into common pathway and converts prothrombin to thrombin -> fibrinogen to fibrin… form fibrin clot ☺

73
Q

central role of thrombin in coagulation- what are the 3 phases?

A
  1. initiation: exposure of TF, little thrombin formed (NOT enough to support fibrin gener, but enough to….
  2. amplification: of coag cascade and activate others… burst of thrombin and propagation
  3. propogation: lot of thrombin, can now gen fibrin and XIII, TAFI, enough to cross link fibrin and stabilise it
74
Q 
prothrombotic activity of platelets:
wheres PS (phosphatidylserine) uaully located and role?
A

inside of inner memb of platelet surface

platelet activated, PS exposed, allows assembly of coag factors on surface: Xa enzyme, cofactor Va and Ca2+

= prothrombinase complex

75
Q

what does activation of prothrombinase complex from PS allow?

A

inactive zymogen: prothrombin –> active serine protease: Thrombin

76
Q

PS complex… what will thrombin formation from prothrombin allow?

A

thrombin: convert

fibrinogen-> fibrin polymers

77
Q

3 potential pathways involved in change form prothrombin -> thrombin?

A

intrinsic pathway: X->Xa
extrinsic pathway: X->Xa

then… Va, PS, Ca2+, Xa = prothr-> thrombin

78
Q

whys generation of thrombin a positive feedback loop?

A

can go back and generate other coag factors on diagram… make more thrombin
= amplify its own generation

little platelet= make lots of thrombin

79
Q

how will thrombin also trigger negative feedback loop? that will limit formation + coag cascade

A

gen thrombin binds to thrombomodulin (receptor on endothelial cells), complex will activate powerful anticoag pathway APC.
APC (activated protein C) inhib co factors of coag: 8 and 5.

powerful!!
limits!!

80
Q

after coag cascade triggeres, what system used to limit?

A

natural anti coagulant system

81
Q

3 natural anti coagulant system?

A
  1. activation of TFPI
  2. Anti thrombin AI
  3. APC (most powerful)
82
Q

hows natural anti coagulant system: APC (most powerful one) generated?

A

thrombin binding to thrombomodulin…
transforms PC-> APC
inhibit co factors Va and VIIIa

83
Q

2 stages of haemostasis?

summary in detail

A 
primary hemostasis (platelet plus)
- platelets activated, secrete sec med: ADP, TAx2, recruit others to form plug. not stable. needs....

sec haemostasis: coag cascade
- 3 phases: initiation with bit of thrombin, amplification, propogate= thrombin burst…
gen fibrin.-> deposits on platelet plug, stabilise clot formation

clot formed, bleeding stopped

84
Q

II. fibrinolysis

what is it?

A

degradation of a fibrin clot

85
Q

fibrinolysis cascade formed by?

A

cleavage of plasminogen-> plasmin… which degrades fibrin into small pieces (FDPs)
resolve clot

86
Q

how can fibrinolysis be inhibited?

A

factors formed by thrombin:
TAFI -> TAFIa

inhib/block fibrin degradation of the clot!

87
Q

aim of fibrinolytic system?

A

limit clot growth- by degrading the fibrin

88
Q

key protease formed in fibrinolysis and how activated?

A

plasmin (from plasminogen- inactive form is zymogen)

activated by tPA and uPA from kidney

plasmin can now degrade fibrin- degrade clot ☺

89
Q

3 main pathways to inhibit the coag pathway?

A

TFPI (TF-> X)
antithrombin (X -> Xa)
APC (VIIIa, Va)

90
Q

3 main pathways to inhibit the fibrinolytic pathway?

and what they each inhibit

A

PAI-1: tPA
a2 antiplasmin: plasmin
TAFIa: plasmin

91
Q

how does TAFIa reduce fibrin clot degradation? detail pathway

A

thrombin made, neg feedback loop
binds to thrombomodulin…
activate TAFI into active TAFIa
inhib clot degradation by inhib plasminogen formation to plasmin (fibrin clot + plasminogen)

= inc clot stability

92
Q

Anticoagulant, antithrombotic drugs
PART I…
Antiplatelets, anticoag drugs

what is an embolus?

A

‘stopper’

detached blood clot

93
Q

whats coagulation

and role of anticoagulants?

A

process by which blood-> solid

AC: prevent blood from clotting… no affect on platelets/ fibrinolysis

94
Q

what does antithrombotic do?

A

prevent thrombus (clot) from forming

95
Q

whats a thrombolytic?

A

clot buster

drug that dissolves blood clots

96
Q

platelet adhesion and activation more valid in what system?

A

arterial (not venous)

97
Q

what stage of haemostasis do antiplatelets target?

A

primary haemostasis- platelet plug

98
Q

what stage of haemostasis do anticoagulants target?

A

secondary: coagulation cascade

reduce fibrin and thrombin generation

99
Q

what stage of haemostasis do thrombolytics target?

A

final:clot stabilisation

dissolve thrombi by degrading fibrin by increasing fibrinolysis

100
Q

what 2 things can be targetted when targetting (reducing) thrombosis via drugs?

A

coagulation: fibrin clot
platelets: haem plug rish in platelets

–> both form thrombus/ blood clot

reducing fibrin… destroy clot bc not stable and solidified (bricks and mortar!!) need both fibrin + platelets

101
Q

why may we differ between treating clot w antiplatelets/ anticoagulants

A

as some drugs rich in platelets… and some in fibrin

102
Q

what plays a critical role in arterial system?

and what type of system is this?

A

HIGH shear system

platelets (thrombi rich in)

103
Q

What is the difference between red and white thrombi?

A

red thrombi: RBC and fibrin

white thrombi: platelets

104
Q

What is the difference between the treatment of white and red thrombi?

A

white thrombi is treated with anti platelets:aspirin and clopidogrel.

red thrombi is treated with anti coagulants: heparin and warfarin

105
Q

what system has white thrombi and why?

A

arterial

as predom platelets

106
Q

what system has red thrombi and why?

A

venous

as predom RBC

107
Q

What are the 3 factors of virchows triad that contribute to thrombosis?

A

blood flow: immobile, AF
endothelial injury: trauma, atherosclerosis
hypercoagulation: inherited preg meds

108
Q

when is thrombosis:

  • good
  • bad
A

stops bleeding: at site of vasc injury, forms clot
must be transient and non-occlusive

blocks blood supply, at site of vasc aterosc injury- arteries!
chronic, occlusive, embolise

109
Q

where are bad thrombi: blocks blood supply, usually formed?

how treates?

A

in arteries, at site of atherosclerotic plaques.

use antiplatelet drugs to treat

110
Q

what does high shear rate of arterial system allow?

A

platelets to interact w exposed cell endothelium at site of injury w collagen,
esp VWF and GPIb

allows platelets to roll on VWF and get activated… secrete sec mediators: ADP, TXA2 = form WHITE thrombi. platelets.

aim: ⬇ platelet activation and use antiplatelets to ⬇ thrombosis

111
Q

why anticoags not used to treat arterial thrombosis?

A

as thrombi not rich in fibrin

112
Q

most common antiplatelet: COX inhibitors- example and MoA?

A 
aspirin.
blocks cyclooxygenase (COX)
inhib formation of TxA2 from arachidonic acid
113
Q

common antiplatelet: P2Y12 inhibitors- examples and MoA?

A

clopidogrel, prasugrel, ticagrelor, cangrelor

block ADP receptor (second mediator of platelet activation)= reduction

114
Q

antiplatelet: Phosphodiesterase inhibitors- examples and MoA?

A

dipyridamole
cilostazol
trifusal

block platelet activation+ aggregation…
stop cAMP –> 5’AMP

115
Q

how do aIIbb3 inhibitors (antiplatelets) work?

e.g. abciximab

A

inhib platelet aggregation by inhibitiing interaction of platelets with fibrinogen

116
Q

Name an antiplatelet drug that is an antagonist for alpha II beta 3 and is a monoclonal antibody?

A

abciximab

117
Q

integrillin is an example of an alpha II beta 3 receptor blocker. Why were these trials stopped?

A

lack of efficacy and increased mortality due to risk of excessive bleeding

were restricted for use in acute hospital care- unstable angina..
snake venom peptide analogue

118
Q

which two drugs are excellent anti thrombotic drugs and block secondary mediator activation and amplification loop of platelets?

A

aspirin: block COX, stop-> TxA2
clopidogrel: block P2Y12 rec for ADP

119
Q

Aspirin has an irreversible effect for around the same life as a platelet half life. What length of time is this?

A

approx 10 days

120
Q

Two things that aspirin and clopidogrel inhibit the action of?

A

TxA2 and ADP (receptor) positive feedback mediators

121
Q

what venous thrombosis mainly mediated by?
(hows it diff to arterial)

what does this allow?

A

by turbulent shear- observed at level of valve in veins

allows coag cascade and RED thrombus formn (RBC + fibrin)

122
Q

another way to reduce clots in venous system (and arterial)

A 
increaase fibrinolysis...
inc tPA, uPA (from kidneys)...
inc plasmin gen
and fibrin degradation
into small peptides

thrombin activates TAFIa- inhib fibrinolysis by inhib fibrin degradation..
balance in pro and anti coagulant activated

123
Q

how can natural pathways of coagulation be used as drugs to inhib coagulation
drug targets: 4 classes? anticoags

A

heparins: UFH/LMWH
Vit K antagonists
direct thrombin inhibitors
Factor Xa inhibitors

124
Q

What is the first line drug class of choice to increase venous thrombosis?

A

anticoagulants

125
Q

What degrades fibrin clots?

A

plasmin

126
Q

what coag factors will be targetted by: Vit K antagonists?

A 
vitK dependant coagulation factors:
VII (7)
IX (9)
X (10)
II (2)
127
Q

what coag factors will be targetted by: Heparins: LMW/UFH?

A 
Extrinsic: VIIa (7a)
Intrinsic:
XIIa (12a)
XIa (11a)
Xa (10a)
IXa (9a)
IIa (2a)
128
Q

what coag factor will be targetted by: direct thrombin inhibitor?

A

IIa (2a)

129
Q

antithrombin III is a v powerful inhibitor and also used as…

A

physiological suicide inhibitor

130
Q

What does antithrombin III (serpin) do?

A

inhibits coagulation by inhibiting thrombin (binds to active site).. forms thrombin:AT complex (inactive)

131
Q

first choice anti coag: heparin: role in antithrombin III MoA?

A

binds to AT (antithrombin), increasing efficacy 1000x, as cofactor… which binds to thrombin

doesnt act directly on thrombin but inc capacity to bind to AT and thrombin

132
Q

What does heparin act as a co factor and bind to in order to inactivate thrombin?

A

antithrombin (serpin)

133
Q

what type of anticoag is anti-thrombin?

A

broad as can also inhib other coag factors in cascade

134
Q

What is the drug class of warfarin? (anticoagulants)

A

Vitamin K analogue.

inhib vitK dep factors II, VII, IX, X

135
Q

warfarin MoA?

A

Warfarin competitively inhibits vitamin K epoxide reductase complex 1 (VKORC1), an essential enzyme for activating vitamin K available in body
…depletes functional vitamin K reserves and reduces synthesis of active clotting factors (II, VII, IX, X)

136
Q

what enzyme converts inactive II, VII, IX, X into active form in liver (Vit K recycling) warfarin MoA role?

A

vit K-dependant carboxylase

warfarin indirectly inhibits

137
Q

commonly used anti coag drug:

IIa inhibitors target only …

A

thrombin (IIa)

138
Q

what heparin is more specific and what coag factors does it target?

A

LMW

XIa, IIa… 11a, 2a (thrombin)

139
Q

what drug class are thrombin inhibitors and give examples of

  • direct
  • indirect
A

anticoags for venous thromb

  • argatroban, dabigatran, desirudin
  • enoxaparin, dalteparin, fondaparinux, UFH
140
Q

4 examples of direct Xa inhibitors (anticoags)

A

apixaban, betrixaban, edoxaban, rivaroxaban

141
Q

examples of thrombolytics

A

plasminogen activators

  • reteplase
  • streptokinase
  • tenecteplase
  • tissue plasminogen activator

inhib through inc fibrinolysis

142
Q

PART II…
I. Thrombolytic agents
II. Anti thrombotic agents choice

aim of arterial thrombosis?

A

reduce pla activation by using antiplatelets

143
Q

P2Y12 inhibs do what?

A

inhib ADP effect on platelets

144
Q

The aim of thrombolytics is to activate another process to degrade fibrin clots. What is this process called?

A

fibrinolysis

144
Q

The aim of thrombolytics is to activate another process to degrade fibrin clots. What is this process called?

A

fibrinolysis

145
Q

why are thrombolytics not commonly used?

A

stroke

limited time to use, then inc risk of bleeding

146
Q

How can the activation of fibrinolysis be reduced?

A

red factors/ haemostatic agents prevent plasmin generation

146
Q

fibrinolytic system: whats the common agent used?

A

tPA (endothelial cells)… also have uPA (kidney)

146
Q

what does tPA (fibrinolytic agent) do?

A

inc formn of plasmin from plasminogen…. –> fibrin degradation into fibrin.

146
Q

haemostatic agents that inhibit fibrinolytic system by inhib plasmin?

A

transexamic acid

aminocaproid acid

147
Q

commonly used thromolytics (clot busters)? + examples of each

A

recombinant tPA: alteplase, reteplase, tenecteplase

urokinase: abbokinase, kinlytic
streptokinase: sec by streptococci

148
Q

List 5 indications for thrombolytics?

A
  • acute stemi
  • acute ischaemic stroke
  • peripheral artery occlusion
  • DVT
  • PE
149
Q

Is arterial thrombosis due to platelet rich thrombi or a fibrin rich clot?

A

platelet rich thrombi

150
Q

Is arterial or venous thrombosis due to fibrin rich clots?

A

venous thrombosis

Health.2 (19 decks)

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