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Medical Studies 1 > Haem Week 12 > Flashcards

Haem Week 12 Flashcards

1
Q

Describe the structure of platelets

A

Formed from the cytoplasm of giant megakaryocytes

Nucleus lacking

Packed w chemicals

Contains mitochondria, microtubules, dense granules, surface membrane receptors

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2
Q

What is haemostasis

A

Process by which blood clots

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3
Q

What are the 3 major components of haemostasis and provide a brief description of each

A

Vasoconstriction - constriction of blood vessels to reduce blood flow and limit bleeding

Primary haemostasis - platelets adhere to injured blood vessel wall and aggregate to form a temporary plug

Coagulation - formation of stable blood clot through a cascade of biochemical reactions involving clotting factors and fibrin

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4
Q

Describe the role of the endothelium in the process of platelet adhesion

A

Endothelial cells prevent binding of platelets

It acts as a mechanical barrier, secretes small anti-aggregation molecules that prevent clotting, expresses surface anticoagulant proteins, enables fibrinolysis

However, it also produces von Willebrand Factor which promotes coagulation during infection/inflammation

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5
Q

What is von willebrand factor (vWF)

A

Long, sticky protein that allows platelets to adhere to damaged endothelium

Plays role in extending the lifespan of coagulation factors VIII within the plasma

It is produced by endothelial cells, megakaryocytes and sub endothelial CT

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6
Q

Describe the process of platelet plug formation

A

Vessel injury leads to exposure of collagen fibres beneath the endothelium

Then, there is adhesion of platelet GPIb-V-IX to matrix vWF and platelet GPIa/IIb and GP VI bind to collagen

Then, adhered platelets become activated, changing shape, and releasing certain chemical signals such as ADP and thromboxane which attract more platelets to the site

Then, GPIIb/IIIa on platelets binds to fibrinogen irreversibily, forming a temporary plug that helps prevent excessive bleeding

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7
Q

What are 3 factors that activate platelets

A

ADP - secreted by activated platelets, activates itself and platelets in vicinity

Thomboxane A2 - diffuses out of activated platelets, activates itself and other platelets

Thrombin - formed from the coagulation cascade; enables coagulation to occur

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8
Q

Outline the process of platelet aggregation

A

Activated platelets release ADP to attract more platelets

Activated platelets synthesise thromboxane which further promotes platelet activation and aggregation

Platelets have specific receptors for ADP and thromboxane, which, when bound, enhance platelet activation and aggregation

GP IIb/IIIa receptors on platelet surface play a crucial role in platelet aggregation by binding to fibrinogen and other platelets

Fibrinogen is a plasma protein that bridges platelets via their GPIIb/IIIa receptors, facilitating the formation of stable platelet aggregates

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9
Q

What are 4 anti platelet drugs

A

COX inhibitor

ADP receptor antagonist

Phosphodiesterase inhibitor

GPIIb/GPIIIa inhibitor

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10
Q

What is the mechanism of action of COX inhibitor

A

Blocks cyclooxygenase (COX) enzymes to reduce the synthesis of prostaglandins, which play a role in inflammation and pain

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11
Q

What is the mechanism of action of ADP receptor antagonist

A

Blocks ADP receptors on platelets, preventing platelet activation and aggregation

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12
Q

What is the mechanism of action of phosphodiesterase inhibitor

A

Inhibits phosphodiesterase enzymes to increase cyclic AMP levels, leading to vasodilation and reduced platelet aggregation

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13
Q

What is the mechanism of action of GPIIb/GPIIIa inhibitors

A

Blocks the GPIIb/IIIa receptors on platelets, preventing fibrinogen binding and inhibiting platelet aggregation

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14
Q

What are 3 contraindications of using antiplatelet medication

A

Active bleeding g

Thrombocytopenia

Bleeding disorders

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15
Q

What does GP Ia/IIb and GP VI bind to and what is its function

A

Binds to collagen

Function is adhesion

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16
Q

What does GP Ib/V/IX bind to and what is its function

A

Binds Von willebrand factor

Function is adhesion

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17
Q

What does GP IIb/IIIa bind to and what is its function

A

Binds to fibrinogen

Function is aggregation (as it is an integrin)

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18
Q

What are the 3 interconnected pathways of coagulation

A

Intrinsic

Extrinsic

Common

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19
Q

Outline the intrinsic pathway of coagulation

A

Factors XII, XI, IX and VIII contribute to the formation of factor X

Factor XII is converted into XIIa using collagen, then this allows fro XI to be converted into XIa, then this allows IX to be converted into IXa which then leads to the formation of factor X

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20
Q

Outline the extrinsic pathway of coagulation

A

Factors V and VII contribute to the formation of factor X

Factor III is converted into IIIa when there is damage to endothelial tissue, then this is used to convert factor VII into factor X

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21
Q

Outline the common pathway of coagulation

A

Active factor X contributes to the activation of fibrinogen to form fibrin

Active factor Xa is used to convert factor II into IIa (thrombin) which is then used to convert factor I into Ia (fibrin)

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22
Q

Describe the mechanism of action of the drug class Activated C Protein

A

Inactivates coagulation factors Va and VIIIa by cleaving them

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23
Q

Describe the mechanism of action of antithrombin drug class

A

Inhibits multiple coagulation factors, including factors IIa (thrombin), IXa, Xa, and XIa

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24
Q

Describe the mechanism of action of the drug class Vitamin K antagonist

A

Interferes w the synthesis of vitamin K-dependent coagulation factors (II, VII, IX, X) and proteins C and S

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25
Describe the mechanism of action of heparins
Enhances the activity of antithrombin, which inhibits multiple coagulation factors, including IIa, IXa, Xa, XIa, XIIa
26
Describe the mechanism of action of LMWH
Low molecular weight heparin acts similarly to heparin, but it has a greater effect on factor Xa and less on factor IIa (thrombin)
27
Describe the mechanism of action of DOACs
Direct-acting oral anticoagulants inhibit specific coagulation factors directly Include factor Xa inhibitors (e.g apixaban) and direct thrombin inhibitors (e.g dabigatran)
28
What is fibrinolysis
Process by which the body dissolves blood clots, preventing them from becoming too big or lingering longer than necessary It is crucial for maintaining blood vessel potency, preventing the formation of obstructive blood clots, and promoting tissue repair after injuries
29
Outline the process of fibrinolysis
Plasminogen is converted into its active form of plasmin which is an enzyme This then cleaves the fibrin into soluble fragments, thereby dissolving the clot
30
Describe the role of tranexamic acid in inhibiting fibrinolysis
TXA is an antifibrolytic medication used to inhibit fibrinolysis Works by blocking enzymatic activity of plasmin Exerts its inhibitory effect on plasmin by binding to the lysine-binding sites on plasminogen, preventing conversion of plasminogen to plasmin By inhibiting plasmin activity, TXA helps maintain stability of blood clots, preventing their premature dissolution Commonly used in surgical procedures, especially in settings where there is a risk of excessive bleeding
31
Define thrombus
Blood clot that forms and remains within a blood vessel
32
Define embolus
Dislodged or travelling mass, often a blood clot, that can obstruct a blood vessel in a different location
33
Define thromboembolus
Blood clot that has broken free and is carried through the bloodstream potentially causing blockages in distant blood vessels
34
What is virchow's triad
three factors that contribute to the formation of blood clots
35
what are the 3 components of virchow's triad
endothelial damage blood stasis hypercoagulability
36
describe factor V leiden mutation
genetic alteration causing resistance to inactivation of clotting factor V
37
describe activated C protein resistance
reduced sensitivity to the anticoagulant effects of activated protein C, often due to factor V leiden mutation
38
describe protein C or S deficiency
inherited deficiencies of natural anticoagulant proteins, protein C or S
39
describe antithrombin deficiency
genetic deficiency of antithrombin, a protein that regulates blood clot formation
40
what is an example of an inherited hypercoagulapathy
thrombophillic conditions
41
what are thrombophillic conditions
genetic predisposition to excessive blood clotting due to inherited mutations in clotting factors or regulatory proteins
42
what are 5 examples of acquired hypercoagulapathies
pregnancy - due to changes in hormone levels, blood flow, and clotting factors hormone replacement therapy - oestrogen-based hormone therapies, esp in post menopausal women COVID19 - viral infection > inflammatory and prothrombotic state long-distance travel - immobility > slow blood flow carcinoma - tumour cell interactions w blood components, cytokine release, Rx-related factors
43
what are 6 risk factors for coagulapathies
increased age sex obesity recent surgery malignancy pregnancy
44
describe how deep vein thrombosis can result in a PE
DVT occurs when blood clot forms in a deep vein (typically leg) which can obstruct blood flow in affected vein this can then dislodge from its original location and travel through the bloodstream (embolus) the embolus moves to the heart and then enters the pulmonary circulation when the embolus blocks blood flow in the pulmonary arteries, it results in PE
45
describe prothrombin time (PTT)
this is an investigative process for the diagnosis of coagulapathies it measures the time it takes for the blood to clot, and is used to assess blood clotting ability and monitors the effects of anticoagulant meds, with results often reported as an international normalised ratio (IRN)
46
describe activated partial thromboplastin time (APTT)
this is an investigative process for the diagnosis of coagulapathies it evaluates the clotting function of the intrinsic and common coagulation pathways, helping diagnose bleeding disorders and monitor heparin therapy
47
describe fibrinogen level
this is an investigative process for the diagnosis of coagulapathies measures the concentration of fibrinogen in the blood which is essential for blood clot formation
48
describe thrombin time
this is an investigative process for the diagnosis of coagulapathies assess the ability of blood to form fibrin clots by measuring the time it takes for a clot to form after the addition of thrombin
49
describe antithrombin activity
this is an investigative process for the diagnosis of coagulapathies measures the activity of antithrombin
50
describe protein C activity
this is an investigative process for the diagnosis of coagulapathies evaluates the activity of protein C
51
describe VWD
this is an investigative process for the diagnosis of coagulapathies specialised test to assess the levels and function of von willebrand factor and factor VIII in individuals w a designated risk
52
what are 4 clinical features associated w venous thrombosis
unilateral chest pain peripheral oedema erythema tenderness
53
what are 5 clinical features associated w PE
dyspnea pleuritic chest pain tachycardia haemolysis syncope
54
what is haemophilia
genetic bleeding disorder characterised by a deficiency of clotting factors, leading to a prolonged bleeding and easy bruising
55
what is disseminated intravascular coagulation
a complex and life-threatening condition where the body's coagulation system is excessively activated, causing both excessive clotting and bleeding
56
what is von Willebrand Disease
hereditary bleeding disorder resulting from a deficiency or dysfunction of vWF
57
What are 5 risk factors for bleeding disorders
Family history - e.g haemophilia or vWD Gender - e.g haemophilia more common in males Age - e.g older ppl at risk Medications - e.g NSAIDs and anticoagulants Trauma/surgery - loss of blood components
58
Outline primary haemostasis
Initial blood vessel injury response involving platelet adhesion and aggregation to form a temporary plug
59
Outline secondary haemostasis
Cascade of enzymatic reactions leading to the formation of a stable blood clot through the activation of clotting factors
60
What are 2 examples of bleeding disorders of primary haemostasis (platelet disorder)
Thrombocytopaenia vWD
61
What are 3 examples of bleeding disorders of secondary haemostasis (coagulation defect)
Haemophilia Factor V Leiden Disseminated intravascular coagulation
62
Outline the pathogenesis of disseminated intravascular coagulation (DIC)
Underlying cause e.g sepsis Leads to, activation of coagulation cascade Leads to, widespread microthrombi formation Leads to, consumption of coagulation factors Leads to, fibrinolysis and plasmin overactivation Leads to, increased bleeding Leads to, end organ damage
63
How do NSAIDs lead to bleeding disorders a
They interfere w platelet function and can cause GI bleeding by damaging the stomach lining
64
Outline the pathogenesis of thrombocytopenia
Reduced platelet production (e.g bone marrow disorders) / increased platelet destruction (e.g immune thrombocytopenic purpura [ITP]) Leads to, low levels of platelets in the blood
65
Outline the pathogenesis of bleeding disorders resulting from renal failure
Renal failure (e.g CKD) leads to, uraemic toxin build up Leads to, platelet dysfunction due to impairment of the platelet’s ability to aggregate / and leads to increased vWF cleavage Leads to, reduced vWF
66
Outline how the pathogenesis of malignancy leads to bleeding disorders
Myeloma/lymphoma Leads to, anaemia and thrombocytopenia and disseminated intravascular coagulation
67
Outline the pathogenesis of haemophilia A
X-linked genetic mutation Leads to, factor VIII deficiency Leads to, clotting cascade impairment Leads to, increased bleeding risk
68
Outline the pathogenesis of haemophilia B
X-linked genetic mutation Leads to, factor IX deficiency Leads to, clotting cascade impairment Leads to, increased bleeding risk
69
What are 6 clinical features associated with bleeding disorders
Bruising Purpura Post-op bleeding Menorrhagia Haematuria Epistaxis
70
Describe clopidogrel
An antiplatelet drug that blocks platelet activation and aggregation to prevent blood clots
71
Describe ticagrelor
Antiplatelet agent that inhibits platelet activation by binding to P2Y12, reducing the risk of clot formation
72
What are NOACs/DOACs often used for
AF to reduce the risk of of stroke and systemic embolism DVT prophylaxis Rx of venous thromboembolism
73
Describe thrombolytic agents
Drugs used to dissolve blood clots, which it does by activating plasminogen into plasmin which then degrades the fibrin’s network Used in severe situations e.g MI, ischemic strokes and PE While effective in certain conditions, they carry a risk of bleeding so they are administered under careful medical supervision
74
Describe factor replacement therapy
Involves the infusion of specific clotting factors that are deficient or missing in the patients blood It can be administered as prophylactic therapy or as a Rx Therapy is tailored to individual patients needs, considering the type and severity of their bleeding disorder
75
What are 3 indications for the prescription of anti-platelet meds
CVD Cerebrovascular disease PVD
76
What are 3 contraindications for the prescription of anti-platelet meds
Active/recent haemorrhage Upcoming/recent surgery Severe thrombocytopenia
77
What are 5 side effects of anti-platelet meds
Blood loss GI irritation/ulceration Dyspnea (ticagrelor) Bradycardia (ticagrelor) Gout (ticagrelor)
78
What are 2 indications of heparins
Cases of renal impairment (unfractionated hep) Cases where monitoring is difficult (LMWH)
79
What are 2 contraindications for prescribing heparins
Active/recent haemorrhage Severe thrombocytopenia
80
What are 4 side effects of heparin
Heparin-induced thrombotic thrombocytopenia syndrome (HITTS) Liver enzyme elevation Bleeding Alopecia
81
What are 3 indications for the prescription of vitamin K antagonists
Mechanical heart valves Renal disease Arterial thrombi
82
What are 3 contraindications for the prescription of vitamin K antagonists
Active/recent haemorrhage Severe thrombocytopenia Pregnancy
83
What are 4 side effects of vitamin K antagonists
HITTS Liver enzyme elevation Bleeding Alopecia
84
What are 3 indications for the prescription of DOACs
Venous thromboembolism (VTE) Prophylactic VTE Rx AF
85
What are 3 contraindications for the prescription of DOACs
Active/recent haemorrhage Severe thrombocytopenia Severe renal impairment
86
What are 6 side effects of DOACs
Bleeding Indigestion Liver function abnormality Nausea Skin rashes Headache
87
Describe the transfusion of fresh frozen plasma
FFP contains clotting factors and is used to treat bleeding disorders associated with multiple factor deficiencies, such as liver disease or DIC
88
Describe the transfusion of platelets
Administered to individuals who are diagnosed with relatively low platelet counts which can lead to bleeding
89
Describe the transfusion of packed red blood cells
PRBCs are given when anaemia or severe blood loss has occurred, as they can increase oxygen-carrying capacity
90
Describe the administration of antifibrinolytics
(E.g TXA) are used to prevent the breakdown of clots and are effective in treating bleeding disorders like vWD and mild haemophilia
91
Outline the administration of desmopressin
DDAVP is used in certain bleeding disorders, such as mild haemophilia A and vWD It helps release vWF and factor VIII from storage sites in the body, temporarily increasing their levels in the blood
92
What are components of blood
Individual parts of blood separated through a process called blood fractionation E.g RBC, platelets, plasma, cryoprecipitate
93
What are products of blood
Prepared blood derivatives designed for specific therapeutic purposes E.g immunoglobulins, albumin, clotting factors
94
What is apheresis
Medical procedure that involves the separation and selective removal or collection of specific blood components, such as plasma, platelets, or WBCs, for therapeutic purposes while returning the remaining blood components to the donor or patient
95
Outline the process of Australian blood donor selection
Involves the donor filling out a form so that the Australian Red Cross lifeblood can assess eligibility based on criteria outlined in the guidelines for the selection of blood donors
96
What are 6 mandatory tests that must be conducted in the blood donor eligibility process
HIV Hepatitis C Human T-lymphocytes virus type II Syphilis Hepatitis B Human T-lymphocytes virus type I
97
Outline the major blood types (phenotypes)
A, B, AB, O A person’s blood group is determined by a pair of genes Each blood group has its own set of antigens on the surface
98
Describe ABO/rhesus incompatibility
Condition that develops when a pregnant woman has Rh-negative blood and the baby in her womb as Rh-positive During pregnancy RBCs from the unborn baby can cross into the mother’s blood through the placenta, meaning if the mother is Rh-negative and the baby is Rh-positive, the mother’s immune system recognises it as non-self so it makes antibodies against the foetal blood cells These antibodies may cross back through the placenta into the baby and then destroy the baby’s circulating RBCs
99
What are 6 risks/complications associated w blood transfusion
Haemolytic reaction - mismatch b/w donor and recipient > destruction of recipient RBC Allergic reaction - itching, hives, anaphylaxis Febrile non-haemolytic reaction - fever and chills but non life threatening Infection transmission - rare but possible e.g bloodborne infections like HIV Iron overload - frequent transfusions > excess iron > damage organs Volume overload - rapid infusion or large volume > fluid overload > HF and pulmonary oedema
100
How can the risk of haemolytic reactions in blood transfusions be minimised
Stringent blood typing and cross-matching procedures to ensure compatibility b/w donor and recipient blood
101
How can the risk of febrile non-haemolytic reactions from blood transfusions be minimised
Leukoreduction, which removes WBC from donated blood to reduce risk of immune reactions
102
How can the risk of infection transmission from the transfusion of blood be minimised
Rigorous screening of donated blood for infectious diseases
103
How can the risk of iron overload from the transfusion of blood be minimised
Limiting unnecessary blood transfusions and using alternative treatments when possible
104
What are the 3 pillars of patient blood management and provide a description of each
Optimising haemoglobin = proactive strategies to optimise a patients haemoglobin levels before surgery and/or medical procedures (e.g iron supplementation, meds, dietary interventions) Minimising blood loss = implementing measures to reduce blood loss during medical procedures (e.g minimally invasive surgical approaches, careful tissue handling, advanced haemostatic agents) Appropriate transfusion = evidence-based decisions for blood transfusions, considering clinical indications and patient factors (e.g Hb levels, Pt symptoms, risks and benefits of transfusion)

Medical Studies 1 (16 decks)

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