Chapter 14 alterations and hemostasis and blood coagulation

Process of hemostasis

Hemostasis is stopping bleeding after vessel injury, bouncing clot formation versus excessive clotting

Stages of hemostasis 5

Vasospasm

Platelet plug formation

Coagulation cascade

(Intrinsic pathway, extrinsic Pathway, common pathway)

Clot retraction

Fibrinolysis

Vasospasm

Immediate vessel restriction after trauma, reduces blood flow

Platelet plug formation

Platelets adhere to exposed collagen via VWF, receptors GPIB.

Platelets release, ADP, thromboxane A2 (TXA2), Serotonin leads to recruit/activate more platelets

GPIIB/ILLA receptors Bind fibrinogen Which leads to platelet aggregation

This process time is 3 to 7 minutes

Coagulation cascade and its pathways

This process leads to fibrin clot stabilizing plug

The intrinsic pathway is triggered by collagen/contact factors

Extrinsic pathway is triggered by tissue factor

Common pathway converts prothrombin 2 to thrombin, which turns to fibrinogen one to fibrin

Calcium and phospholipids are essential

Clot retraction

Platelets contract fiber strands, which tightens clot

Fibrinolysis

Plasminogen turns to Plasminogen which dissolves fibrin clot, present vessel occlusion

Activated platelets secrete…

Factor V, VIII, VWF, ADP, TXA2, fibrinogen, fibronectin, and Thrombosopondin

blood coagulation factors 7

Fibrinogen turns into fibrin, which is scaffold for clot

Prothrombin turns into thrombin, which activates fibrinogen, platelets, V, VIII.

Tissue factor, which is an Extrinsic trigger

Calcium, which is a cofactor in multiple steps

VIII, IX which is deficiencies which leads to hemophilia a which is VIII, and B, which is IX

XIII stabilizes fibrin clot

Vitamin K dependent factors include II, VII, IX, X, protein, C, protein S

Anticoagulant Are antithrombin III, which is inhibited by heparin, PROTEIN C/S WHICH IS INACTIVE V, AND VIII

History and assessment of hemostasis

Family history of bleeding, like hemophilia or VWD

Excessive bruising, mucosal, bleeding, menorrhagia, and bleeding after surgery.

Medications include aspirin and NSAIDS and anticoagulant

Key laboratory tests for hemostasis

Platelet counts show 150 to 400 K/UL

Bleeding time is 3 to 10 minutes, and there is an increase in platelet dysfunction, VWD, aspirin use

PT is extrinsic, 11 to 13 seconds which leads to prolonged in vitamin K deficiency, liver, disease, warfarin

APTT is intrinsic and it is 30 to 45 seconds and it leads to prolonged in hemophilia, DIC, heparin therapy

INR is standardized PT, normal is equivalent to one

Fibrinogen is 200 to 400 MG/DL and it is lower in DIC or liver disease

D-dimer Is higher with clots breakdown, DVT, PE, DIC

Disorders of hemostasis

Vascular disorders like vascular Purpura fragile vessels, which leads to allergic, drug induced, vitamin C deficiency.

Hereditary hemorrhagic telangiectasia: dilated Capillaries/venules→ Recurrent epistaxis, GI Bleeds, Red lesions on lips/face

Thrombocytopenia less than 150 K

Causes lower production like a plastic anemia, chemo, higher destruction, like ITP or DIC, Sequestration or splendomegaly

Clinical: Petechiae, purpura, mucosal bleeding

ITP: autoimmune, platelet destruction

Thrombocytosis which is over 400 K

Causes are bone marrow proliferation, reactive to inflammation

Risk is thrombosis

Qualitative platelet disorder

Normal counts, but defective adhesion/aggregation

Causes: drugs, like aspirin, VWD, genetic syndromes

Coagulation disorders

Hemophilia, von Willebrand disease or VWD, Vitamin K deficiency, disseminated intravascular coagulation or DIC, and hepatic disease