Clotting and Anemia

Anemia

Split into 3 types, iron deficency, sickle cell, and pernicious

Symptoms include light headed, cold hands/feet, fatigue, pale skin, headache, and shortness of breath

Iron deficiency anemia

When the body doesn’t have enough iron for the RBC to carry

Caused by malabsorption, diet, trauma, or period

Sickle cell anemia

Mutation that causes RBC’s to become misshapen (sickle) in low oxygen

Can lead to clumping, which pulls them out of circulation

Pernicious anemia

When the body doesn’t have enough B12

Caused by malabsorption or diet

Thrombocytopenia

Having a low platelet count that leads to issues with clotting

Hemostatsis

Blood clotting

Positive feedback loop

Has 3 phases

Phase 1 of hemostasis

Pain and serotonin from platelets cause vasoconstriction

Vasoconstriction

Constriction of blood vessels

Phase 2 of hemostasis

Broken endothelia exposes collagen → platelets adhere to serotonin → release of thromboxane A → triggers more platelet adherence

Phase 3 of hemostasis

Fibrin net catches more platelets and RBC’s

Clotting mechanisms

Can be intrinsic or extrinsic

Intrinsic clotting mechanisms

All the necessary clotting factors that are located in the bloodstream

Initiated by platelet adherence (phase 2) → platelets activate factor XII

Factor XII → factor XI → factor IX → factor VII

Extrinsic clotting mechanisms

Perivascular tissue gets damaged (trauma) → releases thromboplastin → blood clotting

Clotting factors III and VII

Clotting factors

Specialized proteins in the blood plasma that initiate clotting

Is dependent on the liver, which is dependent on vitamin K

Is inactive in the bloodstream, but becomes active during the cascade

Chosen pathway → factor X → thrombonin → fibrin

Hemophilia

A blood clotting disorder that can lead to major bleeding

Can be A or B

Hemophilia A

Mutation of factor VII

Most common

Hemophilia B

Mutation of factor IX

Fibrinolysis

The removal of clots

1. Factor XII activates kallikrein

2. Activates plasmin by either

   1. Inactive plasminogen is converted into active plasmin

   2. Thrombin activates plasmin

3. Plasmin positively feeds back onto kallikrein

4. Plasmin dissolves fibrin

Thrombosis

Inappropriate clotting

Thrombus

The clot

Often forms in the deep veins of lower leg (DVT)

Embolus

Part of a clot that has broken off

Your patient just had a stroke, can you give them tPA?

Hemoragic stroke - No

Ischemic stroke - Maybe

Anticoagulation

Blood flow disrupts small amounts of thrombin

Antithrombin

Prohibit clot formation

Produced by the liver

Heparin

Blocks thrombin

Made by basophils and mast cells

Asprin

Blocks platelet activation

Warfarin and Coumadin

Blocks synthesis of a few vitamin K dependent clotting factors

Eliquis

Specific blocker of factor Xa

Thrombolytic drugs (tPA)

Tissue plasminogen activator