Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is haemostasis?

A

the stopping of bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is thrombosis?

A

formation of a clot inside a blood vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

When is thrombosis beneficial?

A

in the case of trauma/injury to stop bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

When is thrombosis detrimental?

A

in DCT or other pathological conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What types of drugs inhibit detrimental thrombosis?

A

anti-thrombotic drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the 2 types of haemorrhage?

A
  • internal: leaky blood vessels inside body

- external: natural opening/break in skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are 2 causes of haemorrhage?

A
  • trauma: different types of injury

- medical condition: intravascular, intramural, extravascular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is observed with haemorrhagic shock? (3)

A
  • hypovolemia (decreased blood volume)
  • reduced cardiac output
  • reduced organ perfusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

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

A

RAAS activation (kidneys, adrenal, liver, lungs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

A

vasopressin (ADH) release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

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

A

catecholamine release (sympathetic nerves, adrenal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
RAAS system diagram p89 and 90...
26
What are the two main aims of the body when responding to a haemorrhage?
- increase blood pressure | - increase blood volume
27
What are the two ways the body increases blood pressure?
- vasoconstriction | - tachycardia
28
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)
- AngII formation – ↓ BP → ↑renin (kidney) → ↑Ang II - baroreceptor reflex - ↓ BP → ↑NAd (sympathetic nerves) tachycardia - vasopressin (ADH) - ↓ blood volume → antidiuretic effect
29
What are the four ways the body increases blood volume?
- vasopressin baroreceptor reflex (⬇ water excretion + thirst) - Ang II formation (↑vasopressin → ↑aldosterone.. antidiuretic effect) - aldosterone (Na+ and water retention) - erythropoietin production - ↓O2 (kidney) → ↑Epo → ↑erythrocytes
30
What is the prognosis of a haemorrhage (3 peaks of death)?
- minutes: exsanguination (severe blood loss) - hours: progressive decompensation (due to failure of compensation mechanisms) - days-weeks: sepsis and organ failure
31
signs and symptoms - haemorrhage?
tachycardia rapid breathing, ⬇ pulse pressure, pale, anxiety ⬇ systolic pressure, confusion, agitation loss peripheral pulses, ⬇ urine, loss of consciousness
32
what may some symptoms of haemorrhage be masked by?
use of drugs- b blockers | .. inhib effects e.g. tachycardia
33
Blood loss reduction summary diagram | page95
34
III. haemostatic agents What are 3 haemstatic agents?
- Recombinant factor VIIa (FVIIa) - desmopressin (DDAVP) - fibrinogen
35
how does recombinant factor 7a VIIa (FVIIa) work?
⬆ formation of factors IXa and Xa | to ⬆ thrombin generation and fibrin formation
36
What is desmopressin (DDAVP) an analogue of?
vasopressin
37
What does desmopressin (DDAVP) stimulate the release of? How does it do this?
release of VWF from endothelial cells by acting on V2 receptor -> results in a secondary increase in factor VIII levels
38
What does DDAVP increase?
fibrin formation and platelet deposition
39
What does fibrinogen enhance the formation of?
fibrin
40
What are 3 antifibrinolytic agents?
- tranexamic acid (TXA) - epsilon aminocaproic acid (EACA) - aprotinin (Trasylol)
41
What are TXA (tranexamic acid) and EACA and what do they inhibit the conversion of? affect?
synthetic lysine analogues. :plasminogen to plasmin = ⬇ fibrinolysis -> ⬆ clot stability
42
What type of inhibitor is aprotinin (trasylol)? What does it inhibit
- serine protease inhibitor | - inhibits plasmin
43
What does aprotinin (trasylol) reduce?
fibrinolysis, leading to an increased clot stability same as EACA and TXA
44
PART II... I. Haemostasis: primary and coagulation major components of haemostasis- stages?
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
45
Primary hemostasis occurs at the site of vascular injury. What happens in primary hemostasis?
weak platelet plug formed due to vasoconstriction and platelet activation to limit blood loss
46
What happens in secondary hemostasis?
Activation of coagulation cascade in plasma generates thrombin. Thrombin converts fibrinogen to fibrin which then polymerizes. Fibrin strands strengthen the primary hemostatic plug.
47
Name platelet activator and platelet inhibitor?
activator - collagen - thrombin - fibrinogen inhibitor - nitric oxide - PGI2
48
what 2 things form a thrombus/blood clot?
platelets-haem plug from primary + fibrin- clot coagulation, from secondary
49
what are platelets?
v reactive blood cells... | after agonist, theyre activated
50
in which state are platelets unable to react with fibrinogen?
resting state
51
What is the difference between activated and resting state platelets?
resting shape: discoid and granular with inactive integrins. Activated have different shape, degranulated and integrin activated
52
what can activated platelets do?
aggregation adhesion spreading on endothelium surface procoagulant
53
3 steps to forming a platelet plug? to recruit to sit? | p105
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)
54
what factor on a platelet is important for aggregation and when is it inactive?
integrin aIIbb3 | inactive on resting platelet... thus cant interact w fibrinogen for aggregaton
55
when are granules secreted from platelets?
after activation
56
thrombin= activates platelets, what can the integrin aIIbb3 now do?
converted into active form, can bind fibrinogen and bridge to platelets together = form a platelet plug!!
57
what 2 types of granules are found within resting platelet?
dense granules alpha granules after activation, theyre released
58
name some alpha granules found within a resting platelet
``` coagulation factors P-selectin for immune response anti-bac angiogenic chemo-attractants ```
59
name some dense granules found within a resting platelet
``` ADP: mojor sec mediator for platelet activation Ca2+ serotonin CD63 LAMP1/2 ```
60
what do platelets do once activated? w granules and generating something...
``` ADP released from dense granules generate TxA2 (Thromboxabe A2) ``` = ADP and TxA2 = 2 sec mediators of platelet activation
61
what are the 2 sec mediators of platelet activation and when are they released and where?
once platelet activated... to autocrine pathway, platelet activation, at + feedback loop (as ADP will go sit in another resting platelet)
62
what do anti platelet drugs target?
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
classical haemostasis is XX dependant?
GPIIbIIIa (aIIbb3)
64
summary of 3 steps of classical haemostasis
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
sec haemostasis: coagulation happens at site of tissue damage/injury ... main aim of coagulation=?
``` generate thrombin (enzyme that gen by coag cascade. fibrinogen-> fibrin clot... allow integration and stabilation of clot) ☺ ```
66
what may inc risk of embolism and bleeding? (sec haemostasis: coagulation)
any defects in fibrin generation from fibrinogen... cant form clot thrombus formed not stable! :(
67
what 3 things may thrombin do other than help form fibrin clot in coagulation cascade?
1. amplify coagulation cascade 2. vasoconstriction (directly) 3. platelet activation thrombin= key thing in reg of whole process of haemostasis!!
68
what are the 2 pathways to generate thrombin? | when activated?
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
What is the common phase between the intrinsic and extrinsic pathway leading to the formation of a fibrin clot?
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
what form are all the coagulation factors in, in intrinsic pathway of thrombin formation?
inactive, and can be activated by: A/ same factor in active form. cascade effect as XIIa activates XI, XIa activates IX...
71
hows extrinsic pathway activated?
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
what do TF: VIIa and IXa factors have in common?
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
central role of thrombin in coagulation- what are the 3 phases?
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
``` prothrombotic activity of platelets: wheres PS (phosphatidylserine) uaully located and role? ```
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
what does activation of prothrombinase complex from PS allow?
inactive zymogen: prothrombin --> active serine protease: Thrombin
76
PS complex... what will thrombin formation from prothrombin allow?
thrombin: convert | fibrinogen-> fibrin polymers
77
3 potential pathways involved in change form prothrombin -> thrombin?
intrinsic pathway: X->Xa extrinsic pathway: X->Xa then... Va, PS, Ca2+, Xa = prothr-> thrombin
78
whys generation of thrombin a positive feedback loop?
can go back and generate other coag factors on diagram... make more thrombin = amplify its own generation little platelet= make lots of thrombin
79
how will thrombin also trigger negative feedback loop? that will limit formation + coag cascade
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
after coag cascade triggeres, what system used to limit?
natural anti coagulant system
81
3 natural anti coagulant system?
1. activation of TFPI 2. Anti thrombin AI 3. APC (most powerful)
82
hows natural anti coagulant system: APC (most powerful one) generated?
thrombin binding to thrombomodulin... transforms PC-> APC inhibit co factors Va and VIIIa
83
2 stages of haemostasis? | summary in detail
``` 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
II. fibrinolysis | what is it?
degradation of a fibrin clot
85
fibrinolysis cascade formed by?
cleavage of plasminogen-> plasmin... which degrades fibrin into small pieces (FDPs) resolve clot
86
how can fibrinolysis be inhibited?
factors formed by thrombin: TAFI -> TAFIa inhib/block fibrin degradation of the clot!
87
aim of fibrinolytic system?
limit clot growth- by degrading the fibrin
88
key protease formed in fibrinolysis and how activated?
plasmin (from plasminogen- inactive form is zymogen) activated by tPA and uPA from kidney plasmin can now degrade fibrin- degrade clot ☺
89
3 main pathways to inhibit the coag pathway?
TFPI (TF-> X) antithrombin (X -> Xa) APC (VIIIa, Va)
90
3 main pathways to inhibit the fibrinolytic pathway? | and what they each inhibit
PAI-1: tPA a2 antiplasmin: plasmin TAFIa: plasmin
91
how does TAFIa reduce fibrin clot degradation? detail pathway
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
Anticoagulant, antithrombotic drugs PART I... Antiplatelets, anticoag drugs what is an embolus?
'stopper' | detached blood clot
93
whats coagulation | and role of anticoagulants?
process by which blood-> solid AC: prevent blood from clotting... no affect on platelets/ fibrinolysis
94
what does antithrombotic do?
prevent thrombus (clot) from forming
95
whats a thrombolytic?
clot buster | drug that dissolves blood clots
96
platelet adhesion and activation more valid in what system?
arterial (not venous)
97
what stage of haemostasis do antiplatelets target?
primary haemostasis- platelet plug
98
what stage of haemostasis do anticoagulants target?
secondary: coagulation cascade | reduce fibrin and thrombin generation
99
what stage of haemostasis do thrombolytics target?
final:clot stabilisation | dissolve thrombi by degrading fibrin by increasing fibrinolysis
100
what 2 things can be targetted when targetting (reducing) thrombosis via drugs?
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
why may we differ between treating clot w antiplatelets/ anticoagulants
as some drugs rich in platelets... and some in fibrin
102
what plays a critical role in arterial system? | and what type of system is this?
HIGH shear system | platelets (thrombi rich in)
103
What is the difference between red and white thrombi?
red thrombi: RBC and fibrin | white thrombi: platelets
104
What is the difference between the treatment of white and red thrombi?
white thrombi is treated with anti platelets:aspirin and clopidogrel. red thrombi is treated with anti coagulants: heparin and warfarin
105
what system has white thrombi and why?
arterial | as predom platelets
106
what system has red thrombi and why?
venous | as predom RBC
107
What are the 3 factors of virchows triad that contribute to thrombosis?
blood flow: immobile, AF endothelial injury: trauma, atherosclerosis hypercoagulation: inherited preg meds
108
when is thrombosis: - good - bad
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
where are bad thrombi: blocks blood supply, usually formed? | how treates?
in arteries, at site of atherosclerotic plaques. | use antiplatelet drugs to treat
110
what does high shear rate of arterial system allow?
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
why anticoags not used to treat arterial thrombosis?
as thrombi not rich in fibrin
112
most common antiplatelet: COX inhibitors- example and MoA?
``` aspirin. blocks cyclooxygenase (COX) inhib formation of TxA2 from arachidonic acid ```
113
common antiplatelet: P2Y12 inhibitors- examples and MoA?
clopidogrel, prasugrel, ticagrelor, cangrelor block ADP receptor (second mediator of platelet activation)= reduction
114
antiplatelet: Phosphodiesterase inhibitors- examples and MoA?
dipyridamole cilostazol trifusal block platelet activation+ aggregation... stop cAMP --> 5'AMP
115
how do aIIbb3 inhibitors (antiplatelets) work? | e.g. abciximab
inhib platelet aggregation by inhibitiing interaction of platelets with fibrinogen
116
Name an antiplatelet drug that is an antagonist for alpha II beta 3 and is a monoclonal antibody?
abciximab
117
integrillin is an example of an alpha II beta 3 receptor blocker. Why were these trials stopped?
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
which two drugs are excellent anti thrombotic drugs and block secondary mediator activation and amplification loop of platelets?
aspirin: block COX, stop-> TxA2 clopidogrel: block P2Y12 rec for ADP
119
Aspirin has an irreversible effect for around the same life as a platelet half life. What length of time is this?
approx 10 days
120
Two things that aspirin and clopidogrel inhibit the action of?
TxA2 and ADP (receptor) positive feedback mediators
121
what venous thrombosis mainly mediated by? (hows it diff to arterial) what does this allow?
by turbulent shear- observed at level of valve in veins allows coag cascade and RED thrombus formn (RBC + fibrin)
122
another way to reduce clots in venous system (and arterial)
``` 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
how can natural pathways of coagulation be used as drugs to inhib coagulation drug targets: 4 classes? anticoags
heparins: UFH/LMWH Vit K antagonists direct thrombin inhibitors Factor Xa inhibitors
124
What is the first line drug class of choice to increase venous thrombosis?
anticoagulants
125
What degrades fibrin clots?
plasmin
126
what coag factors will be targetted by: Vit K antagonists?
``` vitK dependant coagulation factors: VII (7) IX (9) X (10) II (2) ```
127
what coag factors will be targetted by: Heparins: LMW/UFH?
``` Extrinsic: VIIa (7a) Intrinsic: XIIa (12a) XIa (11a) Xa (10a) IXa (9a) IIa (2a) ```
128
what coag factor will be targetted by: direct thrombin inhibitor?
IIa (2a)
129
antithrombin III is a v powerful inhibitor and also used as...
physiological suicide inhibitor
130
What does antithrombin III (serpin) do?
inhibits coagulation by inhibiting thrombin (binds to active site).. forms thrombin:AT complex (inactive)
131
first choice anti coag: heparin: role in antithrombin III MoA?
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
What does heparin act as a co factor and bind to in order to inactivate thrombin?
antithrombin (serpin)
133
what type of anticoag is anti-thrombin?
broad as can also inhib other coag factors in cascade
134
What is the drug class of warfarin? (anticoagulants)
Vitamin K analogue. | inhib vitK dep factors II, VII, IX, X
135
warfarin MoA?
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
what enzyme converts inactive II, VII, IX, X into active form in liver (Vit K recycling) warfarin MoA role?
vit K-dependant carboxylase warfarin indirectly inhibits
137
commonly used anti coag drug: | IIa inhibitors target only ...
thrombin (IIa)
138
what heparin is more specific and what coag factors does it target?
LMW | XIa, IIa... 11a, 2a (thrombin)
139
what drug class are thrombin inhibitors and give examples of - direct - indirect
anticoags for venous thromb - argatroban, dabigatran, desirudin - enoxaparin, dalteparin, fondaparinux, UFH
140
4 examples of direct Xa inhibitors (anticoags)
apixaban, betrixaban, edoxaban, rivaroxaban
141
examples of thrombolytics
plasminogen activators - reteplase - streptokinase - tenecteplase - tissue plasminogen activator inhib through inc fibrinolysis
142
PART II... I. Thrombolytic agents II. Anti thrombotic agents choice aim of arterial thrombosis?
reduce pla activation by using antiplatelets
143
P2Y12 inhibs do what?
inhib ADP effect on platelets
144
The aim of thrombolytics is to activate another process to degrade fibrin clots. What is this process called?
fibrinolysis
144
The aim of thrombolytics is to activate another process to degrade fibrin clots. What is this process called?
fibrinolysis
145
why are thrombolytics not commonly used?
stroke | limited time to use, then inc risk of bleeding
146
How can the activation of fibrinolysis be reduced?
red factors/ haemostatic agents prevent plasmin generation
146
fibrinolytic system: whats the common agent used?
tPA (endothelial cells)... also have uPA (kidney)
146
what does tPA (fibrinolytic agent) do?
inc formn of plasmin from plasminogen.... --> fibrin degradation into fibrin.
146
haemostatic agents that inhibit fibrinolytic system by inhib plasmin?
transexamic acid | aminocaproid acid
147
commonly used thromolytics (clot busters)? + examples of each
recombinant tPA: alteplase, reteplase, tenecteplase urokinase: abbokinase, kinlytic streptokinase: sec by streptococci
148
List 5 indications for thrombolytics?
- acute stemi - acute ischaemic stroke - peripheral artery occlusion - DVT - PE
149
Is arterial thrombosis due to platelet rich thrombi or a fibrin rich clot?
platelet rich thrombi
150
Is arterial or venous thrombosis due to fibrin rich clots?
venous thrombosis

Health.2 (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions