Week 12 Heam (finally!! Im So Done) Flashcards
Haemostasis
Process of blood clotting
1. Vasoconstriction to reduce blood flow
2. Primary Heamostasis - platelets adherence to injured blood vessel wall, and garage to form a temporary plug
3. Coagulation - formation of a stable blood clot through cascade of biochemical reactions including clotting factors and fibrin
Von williebran factor (vWF)
-sticky protein that allows platelets to ahere to damaged endothelium, extends life of factor VIII
Platelet plug formation steps
1. Adhesion - certain factors bind to certain subendothelial factors
2. Activation - platelet binding to collagen triggers platelet activation, resulting in shape change, granule secretion, and receptor activation
** 3. Aggregation ** 8 GPllb/IIa on platelets binds to fibrinogen irreversibly, fibrinogen acts as a molecular glue
4.Plug formed by degenerated platelets trapped by fibrinogen
ADP
Screwed by activated platelets. Activates its self and platelets in the vincicnty
Thrombaxnae A2
Diffuses out of activated platelets, activates itself and other platelets
Thrombin
Is formed in the coagulation cascade, enables coagulation to occur and activate platelets
Platelet aggravation
Injury to a blood vessel – A blood vessel gets damaged, exposing the underlying collagen.
Platelet activation – Platelets in the blood recognize the injury and become activated, changing shape to stick better.
Release of chemicals – Activated platelets release signaling chemicals (like ADP and thromboxane) that attract more platelets to the site.
Platelet aggregation – New platelets are recruited and stick together, forming a clump (platelet plug) at the injury.
Clot formation – The platelet plug is reinforced with a fibrin mesh, creating a stable blood clot to stop bleeding.
Platelet aggregation
Injury to a blood vessel – A blood vessel gets damaged, exposing the underlying collagen.
Platelet activation – Platelets in the blood recognize the injury and become activated, changing shape to stick better.
Release of chemicals – Activated platelets release signaling chemicals (like ADP and thromboxane) that attract more platelets to the site.
Platelet aggregation – New platelets are recruited and stick together, forming a clump (platelet plug) at the injury.
Clot formation – The platelet plug is reinforced with a fibrin mesh, creating a stable blood clot to stop bleeding.
COX inhibitor mechanis,
Blocks COX anzymes to reduce synthesis of prostaglandins which play a role in inflamation and pain
ADP receptor antagonist
Blocks ADP receptors on platelets preventing activation and aggregation
Phosphodiesterase Inhibitor
Inhibits phosphodiesterase enzymes to increase cyclic AMP levels, leading to vasodilation and reduced platelet aggregation.
GPIIb/GPIIIa Inhibitor
Blocks the GPIIb/IIIa receptors on platelets, preventing fibrinogen binding and inhibiting platelet aggregation
Contradictions of anti-platelet medications
Active bleeding, thrombocytopenia, bleeding disorders.
Tranexamic Acid
Tranexamic acid (TXA) is an antifibrinolytic medication used to inhibit fibrinolysis, the process by which the body breaks down blood clots.
Inherited abuses of hypercoagubilty
Factor v Leiden mutation
Activated protein c resistance
protein C or S deficiency
Antithrombin deficiency
Primary haemostasis
Initial blood vessel response
Platelet adhesion and aggregation to form a temporary plug
Secondary haemostasis
Cascade of enzymatic reactions leading to the formation of a stable blood clot via clotting factors
Metastatic carcinoma
Cancer that has spread from one part of body to another
Metastatic carcinoma formation
- Tumour development
2.Cancer cells invade nearby tissues/ vasculature - Intravasattion of lymph and blood
- Extravasation of lymph and blood
- Secondary tumour formation
Disseminated intravascular coagulation (DIC)
Cody makes wayyy to many clots
Disseminated intravascular coagulation (DIC) formation
- Underlying cause eg sepsis or trauma
- Activation of coagulation cascade
- Widespread microthrombi formation
- Consumption of coagulation factors
- Fibrinolysis and plasmid overactition
- Increased bleeding
- End organ damage
How can bleeding disorders be caused by renal failure
Renal failure leads to buildup or ureamic toxins, leading to platelet dysfunctions
Also reduces levels of vWF
vWF
Protein needed for blood clot
Haemophilia pattern of inheritance
X linked
Clinical features of bleeding disorders
Bruising
Purpura
Post op bleeding
Menorrhagia
Heamaturia
Epistaxis
Purpura
Widespread small or red or purple skin spots caused by bleeding underskin
Aspirin mechanism
Anti- platelet
Inhibits COX-1, reducing TXA2 production, impairing platelet aggregation
Clopidogrel mech
In anti-platelet
Blockers ADP receptor on platelets, preventing activation and aggregation
Heparin mechanism
Anti- coag
Binds to antithrombin III, inhibiting thrombin and Factor Xa, which reduces platelet activation and aggregation, and can also directly impair platelet function.
Warfarin
Inhibits vitamin K-dependent clotting factors (II, VII, IX, X).
Direct oral anticoagulants (DOACs)/New orally active anticoagulants
Apixiban = inhibits Xa
Dabigatran= inhibits thrombin, preventing thrombosis formation
Tissues Plasminogen Activators (tPA)
Thrombolytic Agents
Enzymes that promote conversion of plasminogen into plasmin, dissolving blood clots
Indications and Contradictions for anti-platelet medications
Indications: Cardiovascular disease, Cerebrovascular disease, PVD
Contradictions: active/recent haemorrhage, Upcoming/recent surgery, serve thrombocytopenia
Side effects of Anti-platelet medications
Blood loss, GI ulceration or irritation
+ for Ticagrelor specifically:
Dyspnoea, Gout and Bradycardia
Side effects of DOACs
Bleeding, indigestion, nausea, skin rashes, liver function abnormality, headache
Mandatory testing for Blood transfusion
HIV, Hepatitis C and B, Syphilis, Human T-lymphotropic virus type I and II
Rhesus incompatibility
Rh incompatibility is a condition that develops when a pregnant woman has Rh-negative blood and the baby in her womb has Rh-positive blood.
Risks and complications of blood transfusions
Haemolytic reaction, Allergic reaction, Febrile, Non-haemolytic reaction, infection, iron overload, volume overload.
Three Pillars of patient blood management
Optimise Hb levels, minimise blood loss, appropriate transfusion
Stages of Change
- Pre-contemplation
- Contemplation
- Preparation-Action
- Maintenance
- Relapse
Impacts of assumptions on patients
- damages doc patient relation
- reinforces feelings of helplessness
- Creats/perpetuates stigma
- hypocritical
- doesn’t minimise harm
Members of interdisciplinary genetic teams
Clinical geneticist - type of doctor
Genetic counsellor - non directive counselling
Phycologist
SMART Goals
Specific
Measurable
Achievable
Relevant
Time based
Branches of law
Parliament, executive, courts/judical
Key considerations of Negligence Law
Duty of Care
Breach of duty
Causation
Damage or loss
Foreseeability
Parameters of consent
Informed
Capacity
Revocable
Cultural factors affecting smoking
- Family Norms
- Occupation
- Peer Pressure
- Media/advertising
- Cultural beliefs
Challenges in Telehealth
Tech issues
Privacy/confidentiality
Limited physical exam
Communication barrier
Legal/regulatory
Steps to help in Telehealth
Confirm audio and video quality
Assess confidentiality
Summarise key points
Heamophilla A vs B
A= Factor VII deficeincy
B= Factor IX deficiency
Disseminated Intravascular Coagulation
Systemic activation of coagulation pathways generating fibrin clots throughout the body, with the resulting consumption of platelets & coagulation factors also resulting in bleeding
