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Medical Studies 1 > Haem Week 12 > Flashcards

Haem Week 12 Flashcards

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USMLE® Step 1 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
Q

Describe the mechanism of action of heparins

A

Enhances the activity of antithrombin, which inhibits multiple coagulation factors, including IIa, IXa, Xa, XIa, XIIa

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26
Q

Describe the mechanism of action of LMWH

A

Low molecular weight heparin acts similarly to heparin, but it has a greater effect on factor Xa and less on factor IIa (thrombin)

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27
Q

Describe the mechanism of action of DOACs

A

Direct-acting oral anticoagulants inhibit specific coagulation factors directly

Include factor Xa inhibitors (e.g apixaban) and direct thrombin inhibitors (e.g dabigatran)

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28
Q

What is fibrinolysis

A

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

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29
Q

Outline the process of fibrinolysis

A

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

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30
Q

Describe the role of tranexamic acid in inhibiting fibrinolysis

A

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

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31
Q

Define thrombus

A

Blood clot that forms and remains within a blood vessel

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32
Q

Define embolus

A

Dislodged or travelling mass, often a blood clot, that can obstruct a blood vessel in a different location

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33
Q

Define thromboembolus

A

Blood clot that has broken free and is carried through the bloodstream potentially causing blockages in distant blood vessels

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34
Q

What is virchow’s triad

A

three factors that contribute to the formation of blood clots

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35
Q

what are the 3 components of virchow’s triad

A

endothelial damage

blood stasis

hypercoagulability

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36
Q

describe factor V leiden mutation

A

genetic alteration causing resistance to inactivation of clotting factor V

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37
Q

describe activated C protein resistance

A

reduced sensitivity to the anticoagulant effects of activated protein C, often due to factor V leiden mutation

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38
Q

describe protein C or S deficiency

A

inherited deficiencies of natural anticoagulant proteins, protein C or S

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39
Q

describe antithrombin deficiency

A

genetic deficiency of antithrombin, a protein that regulates blood clot formation

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40
Q

what is an example of an inherited hypercoagulapathy

A

thrombophillic conditions

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41
Q

what are thrombophillic conditions

A

genetic predisposition to excessive blood clotting due to inherited mutations in clotting factors or regulatory proteins

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42
Q

what are 5 examples of acquired hypercoagulapathies

A

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
Q

what are 6 risk factors for coagulapathies

A

increased age

sex

obesity

recent surgery

malignancy

pregnancy

44
Q

describe how deep vein thrombosis can result in a PE

A

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
Q

describe prothrombin time (PTT)

A

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
Q

describe activated partial thromboplastin time (APTT)

A

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
Q

describe fibrinogen level

A

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
Q

describe thrombin time

A

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
Q

describe antithrombin activity

A

this is an investigative process for the diagnosis of coagulapathies

measures the activity of antithrombin

50
Q

describe protein C activity

A

this is an investigative process for the diagnosis of coagulapathies

evaluates the activity of protein C

51
Q

describe VWD

A

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
Q

what are 4 clinical features associated w venous thrombosis

A

unilateral chest pain

peripheral oedema

erythema

tenderness

53
Q

what are 5 clinical features associated w PE

A

dyspnea

pleuritic chest pain

tachycardia

haemolysis

syncope

54
Q

what is haemophilia

A

genetic bleeding disorder characterised by a deficiency of clotting factors, leading to a prolonged bleeding and easy bruising

55
Q

what is disseminated intravascular coagulation

A

a complex and life-threatening condition where the body’s coagulation system is excessively activated, causing both excessive clotting and bleeding

56
Q

what is von Willebrand Disease

A

hereditary bleeding disorder resulting from a deficiency or dysfunction of vWF

57
Q

What are 5 risk factors for bleeding disorders

A

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
Q

Outline primary haemostasis

A

Initial blood vessel injury response involving platelet adhesion and aggregation to form a temporary plug

59
Q

Outline secondary haemostasis

A

Cascade of enzymatic reactions leading to the formation of a stable blood clot through the activation of clotting factors

60
Q

What are 2 examples of bleeding disorders of primary haemostasis (platelet disorder)

A

Thrombocytopaenia

vWD

61
Q

What are 3 examples of bleeding disorders of secondary haemostasis (coagulation defect)

A

Haemophilia

Factor V Leiden

Disseminated intravascular coagulation

62
Q

Outline the pathogenesis of disseminated intravascular coagulation (DIC)

A

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
Q

How do NSAIDs lead to bleeding disorders a

A

They interfere w platelet function and can cause GI bleeding by damaging the stomach lining

64
Q

Outline the pathogenesis of thrombocytopenia

A

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
Q

Outline the pathogenesis of bleeding disorders resulting from renal failure

A

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
Q

Outline how the pathogenesis of malignancy leads to bleeding disorders

A

Myeloma/lymphoma

Leads to, anaemia and thrombocytopenia and disseminated intravascular coagulation

67
Q

Outline the pathogenesis of haemophilia A

A

X-linked genetic mutation

Leads to, factor VIII deficiency

Leads to, clotting cascade impairment

Leads to, increased bleeding risk

68
Q

Outline the pathogenesis of haemophilia B

A

X-linked genetic mutation

Leads to, factor IX deficiency

Leads to, clotting cascade impairment

Leads to, increased bleeding risk

69
Q

What are 6 clinical features associated with bleeding disorders

A

Bruising

Purpura

Post-op bleeding

Menorrhagia

Haematuria

Epistaxis

70
Q

Describe clopidogrel

A

An antiplatelet drug that blocks platelet activation and aggregation to prevent blood clots

71
Q

Describe ticagrelor

A

Antiplatelet agent that inhibits platelet activation by binding to P2Y12, reducing the risk of clot formation

72
Q

What are NOACs/DOACs often used for

A

AF to reduce the risk of of stroke and systemic embolism

DVT prophylaxis

Rx of venous thromboembolism

73
Q

Describe thrombolytic agents

A

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
Q

Describe factor replacement therapy

A

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
Q

What are 3 indications for the prescription of anti-platelet meds

A

CVD

Cerebrovascular disease

PVD

76
Q

What are 3 contraindications for the prescription of anti-platelet meds

A

Active/recent haemorrhage

Upcoming/recent surgery

Severe thrombocytopenia

77
Q

What are 5 side effects of anti-platelet meds

A

Blood loss

GI irritation/ulceration

Dyspnea (ticagrelor)

Bradycardia (ticagrelor)

Gout (ticagrelor)

78
Q

What are 2 indications of heparins

A

Cases of renal impairment (unfractionated hep)

Cases where monitoring is difficult (LMWH)

79
Q

What are 2 contraindications for prescribing heparins

A

Active/recent haemorrhage

Severe thrombocytopenia

80
Q

What are 4 side effects of heparin

A

Heparin-induced thrombotic thrombocytopenia syndrome (HITTS)

Liver enzyme elevation

Bleeding

Alopecia

81
Q

What are 3 indications for the prescription of vitamin K antagonists

A

Mechanical heart valves

Renal disease

Arterial thrombi

82
Q

What are 3 contraindications for the prescription of vitamin K antagonists

A

Active/recent haemorrhage

Severe thrombocytopenia

Pregnancy

83
Q

What are 4 side effects of vitamin K antagonists

A

HITTS

Liver enzyme elevation

Bleeding

Alopecia

84
Q

What are 3 indications for the prescription of DOACs

A

Venous thromboembolism (VTE)

Prophylactic VTE Rx

AF

85
Q

What are 3 contraindications for the prescription of DOACs

A

Active/recent haemorrhage

Severe thrombocytopenia

Severe renal impairment

86
Q

What are 6 side effects of DOACs

A

Bleeding

Indigestion

Liver function abnormality

Nausea

Skin rashes

Headache

87
Q

Describe the transfusion of fresh frozen plasma

A

FFP contains clotting factors and is used to treat bleeding disorders associated with multiple factor deficiencies, such as liver disease or DIC

88
Q

Describe the transfusion of platelets

A

Administered to individuals who are diagnosed with relatively low platelet counts which can lead to bleeding

89
Q

Describe the transfusion of packed red blood cells

A

PRBCs are given when anaemia or severe blood loss has occurred, as they can increase oxygen-carrying capacity

90
Q

Describe the administration of antifibrinolytics

A

(E.g TXA) are used to prevent the breakdown of clots and are effective in treating bleeding disorders like vWD and mild haemophilia

91
Q

Outline the administration of desmopressin

A

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
Q

What are components of blood

A

Individual parts of blood separated through a process called blood fractionation

E.g RBC, platelets, plasma, cryoprecipitate

93
Q

What are products of blood

A

Prepared blood derivatives designed for specific therapeutic purposes

E.g immunoglobulins, albumin, clotting factors

94
Q

What is apheresis

A

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
Q

Outline the process of Australian blood donor selection

A

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
Q

What are 6 mandatory tests that must be conducted in the blood donor eligibility process

A

HIV

Hepatitis C

Human T-lymphocytes virus type II

Syphilis

Hepatitis B

Human T-lymphocytes virus type I

97
Q

Outline the major blood types (phenotypes)

A

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
Q

Describe ABO/rhesus incompatibility

A

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
Q

What are 6 risks/complications associated w blood transfusion

A

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
Q

How can the risk of haemolytic reactions in blood transfusions be minimised

A

Stringent blood typing and cross-matching procedures to ensure compatibility b/w donor and recipient blood

101
Q

How can the risk of febrile non-haemolytic reactions from blood transfusions be minimised

A

Leukoreduction, which removes WBC from donated blood to reduce risk of immune reactions

102
Q

How can the risk of infection transmission from the transfusion of blood be minimised

A

Rigorous screening of donated blood for infectious diseases

103
Q

How can the risk of iron overload from the transfusion of blood be minimised

A

Limiting unnecessary blood transfusions and using alternative treatments when possible

104
Q

What are the 3 pillars of patient blood management and provide a description of each

A

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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