Anatomy & Physiology
Learn the structure and function of the human body systems, from cells to organs.
Blood & Hemostasis
Sign in to track progressBlood is a specialized connective tissue that circulates throughout the body. It transports oxygen, nutrients, hormones, and waste products while helping regulate body temperature, maintain pH, fight infection, and prevent blood loss.
Components of Blood
Blood consists of two major components:
- Plasma (~55%): The liquid portion that transports proteins, nutrients, hormones, electrolytes, gases, and waste products.
- Formed Elements (~45%): Includes red blood cells, white blood cells, and platelets.
Plasma
Plasma is the liquid portion of blood.
Composition
- ~90% water
- Plasma proteins (albumin, globulins, fibrinogen)
- Electrolytes
- Nutrients
- Hormones
- Waste products
- Dissolved gases
Functions
- Transports nutrients and hormones
- Carries waste products
- Maintains blood pressure and osmotic balance
- Helps regulate pH
- Contains clotting proteins
Red Blood Cells (Erythrocytes)
Red blood cells transport oxygen from the lungs to tissues and contribute to carbon dioxide transport from tissues back to the lungs.
- Filled with hemoglobin
- Average lifespan: 120 days
Functions
- Deliver oxygen to tissues
- Help transport CO₂ and maintain acid-base balance
Hemoglobin
Hemoglobin is an iron-containing protein found inside red blood cells that binds and transports oxygen.
Structure
- Four protein chains
- Four heme groups
- Four iron (Fe²⁺) atoms
- Each molecule can bind up to four oxygen molecules
Function
- Picks up oxygen in the lungs
- Releases oxygen in body tissues
- Contributes to carbon dioxide transport and acid-base buffering
White Blood Cells (Leukocytes)
White blood cells are immune cells that protect the body from infection and disease.
Major Types
- Neutrophils
- Lymphocytes
- Monocytes
- Eosinophils
- Basophils
Function
- Protect against pathogens
- Coordinate immune and inflammatory responses
- Remove damaged cells and cellular debris
Platelets (Thrombocytes)
Platelets are small cell fragments that initiate blood clot formation following blood vessel injury.
Functions
- Adhere to sites of vascular injury
- Become activated and aggregate
- Form the platelet plug
- Provide a surface that supports coagulation
Erythropoietin (EPO)
- Low blood oxygen levels stimulate the kidneys to release erythropoietin (EPO), which promotes red blood cell production in the bone marrow.
ABO Blood Groups
ABO blood type is determined by antigens on RBCs. Type A has A antigen, type B has B antigen, type AB has both, and type O has neither. Plasma contains antibodies against the missing antigen(s), which determines transfusion compatibility.
Transfusion Compatibility
- For ABO-compatible RBC transfusions, type AB can receive RBCs from any ABO group.
- Type O RBCs lack A and B antigens and can be given across ABO groups. O-negative RBCs are commonly considered the universal RBC donor type.
- Rh factor — Rh-negative recipients should generally receive Rh-negative blood to prevent sensitization.
Hemostasis
Hemostasis is the process that prevents blood loss following vascular injury while maintaining normal blood flow elsewhere. It occurs in three major steps:
- Step 1: Vasoconstriction
- Step 2: Primary Hemostasis (Platelet Plug Formation)
- Step 3: Secondary Hemostasis (Coagulation Cascade)
Step 1: Vasoconstriction
Purpose
- Reduces blood flow
- Minimizes blood loss
- Buys time for clot formation
Step 2: Primary Hemostasis (Platelet Plug Formation)
Platelets rapidly respond to exposed collagen within the damaged vessel.
Platelet plug sequence:
- Vessel injury → exposed collagen/vWF → platelet adhesion → platelet activation → platelet aggregation → platelet plug
- von Willebrand factor (vWF) helps platelets adhere to exposed subendothelial structures at the site of vascular injury.
This creates a temporary seal over the injury.
Step 3: Secondary Hemostasis (Coagulation Cascade)
Clotting factors circulating in plasma become activated through a cascade of reactions.
Fibrin Formation
Fibrinogen (Factor I) is the inactive soluble protein circulating in the blood. Thrombin (Factor IIa) converts fibrinogen into fibrin (Factor Ia). The fibrin molecules polymerize and form long strands to reinforce the platelet plug.
1. Extrinsic Pathway (Tissue Factor Pathway)
The extrinsic pathway rapidly initiates coagulation after tissue injury and contributes to the initial generation of thrombin. Subsequent coagulation reactions amplify thrombin production.
- Damaged tissues expose Tissue Factor (Factor III), which binds to and activates Factor VII.
- The Tissue Factor–Factor VIIa complex forms and rapidly activates Factor X.
- Activation of Factor X serves as the initiation of the common pathway.
Sequence: Tissue Factor (Factor III) + VII → VIIa → X → Xa
2. Intrinsic Pathway (Contact Activation)
In the traditional coagulation cascade model, contact activation initiates a sequence involving Factors XII, XI, IX, and VIII that ultimately activates Factor X. These reactions contribute to amplification of coagulation.
- Factor XII is activated to XIIa.
- Factor XIIa activates Factor XI.
- Factor XIa activates Factor IX.
- Factor IXa works with Factor VIIIa, calcium, and phospholipids to activate Factor X.
- Factor X activation connects this pathway to the common pathway.
Sequence: XII → XIIa → XI → XIa → IX → IXa + VIIIa → X → Xa
3. Common Pathway
Both pathways converge at Factor X. Once Factor X is activated to Factor Xa, the common pathway takes shape.
- Factor Xa combines with Factor Va, calcium, and phospholipids to convert prothrombin (Factor II) into thrombin (Factor IIa).
- Thrombin converts fibrinogen (Factor I) into fibrin, which polymerizes in order to reinforce the platelet plug.
- Factor XIII is activated to Factor XIIIa, which will cross-link the fibrin strands and produce a stable fibrin clot to seal the damaged blood vessel.
- In addition, thrombin activates Factors V, VII, VIII, XI, and XIII to generate a positive feedback loop to rapidly accelerate and strengthen clot formation.
Sequence 1: X → Xa → II (Prothrombin) → IIa (Thrombin) → I (Fibrinogen) → Ia (Fibrin)
Sequence 2: Factor XIII → XIIIa cross-links fibrin strands to form a stable fibrin clot.
Regulation of Coagulation and Fibrinolysis
- Antithrombin inhibits thrombin (IIa) and Factor Xa, helping limit coagulation.
- Plasmin breaks down fibrin during fibrinolysis.
- Fibrinolysis helps remove the clot as the vessel heals.
Summary of Hemostasis
Blood Vessel Injury → Vasoconstriction → Platelet Plug Formation (Primary Hemostasis) → Coagulation Cascade (Secondary Hemostasis) → Stable Fibrin Clot → Tissue Repair → Clot Dissolution (Fibrinolysis)
Clinical Applications
- Anemia: Reduced red blood cells or hemoglobin decreases oxygen delivery.
- Polycythemia: Abnormally increased RBC mass can increase blood viscosity; some forms, particularly polycythemia vera, are associated with increased thrombosis risk.
- Iron Deficiency: Limits hemoglobin production, leading to anemia.
- Leukemia: Cancer affecting white blood cells.
- Thrombocytopenia: Low platelet count increases bleeding risk.
- Hemophilia: Deficiency of clotting factors impairs secondary hemostasis.
- Von Willebrand Disease: Impaired platelet adhesion leads to prolonged bleeding.
- Deep Vein Thrombosis (DVT): Formation of an abnormal clot within a deep vein.
Key Points
- Blood is about 55% plasma and 45% formed elements (RBCs, WBCs, platelets)
- Plasma transports nutrients, hormones, and waste; maintains blood pressure, pH, and osmotic balance
- Hemoglobin in RBCs carries oxygen; each molecule binds up to four O₂ molecules
- WBCs defend against infection; platelets adhere to sites of vascular injury and help initiate hemostasis
- Hemostasis includes vasoconstriction, primary hemostasis (platelet plug), and secondary hemostasis (coagulation cascade)
- The extrinsic and intrinsic pathways converge on factor X to generate thrombin and fibrin
- EPO from the kidneys stimulates RBC production when oxygen is low
- vWF supports platelet adhesion during primary hemostasis
- Antithrombin limits coagulation, while plasmin breaks down fibrin during fibrinolysis