NOTES

NOTES
BLOOD COMPONENTS &
FUNCTION

BLOOD COMPONENTS
osms.it/blood-components
BLOOD COMPONENT SEPARATION BUFFY COAT
▪ Blood components separate by density in ▪ Comprises < 1% of total blood volume
centrifuge ▪ Contains platelets, leukocytes
▫ Heaviest layer: erythrocytes ▪ Platelets clump together → seal damaged
▫ Middle layer: buffy coat blood vessels
▫ Lightest layer: plasma ▪ Leukocytes ward off pathogens, destroy
cancer cells, neutralize toxins
ERYTHROCYTES
▪ Comprise 45% (hematocrit) of total blood PLASMA
volume ▪ Comprises 55% of total blood volume
▪ Carry O2 to tissues; bring CO2 to lungs ▪ No cells: 90% water + proteins,
▪ Biconcave discs (depressed center) electrolytes, gases
▫ Fit through vessels, ↑ surface area (for ▪ Albumin: maintains oncotic pressure, acts
gas exchange) as transport protein
▪ No organelles ▪ Globulins: antibodies, transport proteins
▫ ↑ space for hemoglobins ▪ Fibrinogen: involved in clot formation (helps
platelets attach)
▪ Electrolytes: include sodium, potassium,
calcium, chloride, carbonate

Figure 43.1 Blood components and their relative proportions.

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PLATELET PLUG FORMATION

(PRIMARY HEMOSTASIS)
osms.it/platelet-plug-formation-primary-hemostasis
▪ Hemostasis: blood-loss prevention 3. Adhesion
▪ First two hemostasis steps: platelets ▪ GP1B surface proteins on platelets bind to
clump, form plug around injury site in five Von Willebrand factor
steps
4. Activation
PLATELET PLUG FORMATION ▪ Platelet changes shape (forms arms to
STEPS grab other platelets), releases more von
Willebrand factor, serotonin, calcium, ADP,
1. Endothelial injury
thromboxane A2 (positive feedback loop)
▪ Nerves, smooth muscle cells detect injury
▪ ADP, thromboxane A2 result in GPIIB/IIIA
▪ Trigger reflexive contraction of vessel expression
(vascular spasm) → ↓ blood flow, loss
▪ Secretion of nitric oxide, prostaglandins 5. Aggregation
stop; secretion of endothelin begins → ▪ GPIIB/IIIA binds to fibrinogen, links platelets
further contraction → platelet plug
2. Exposure
▪ Damage to endothelial cells exposes
collagen
▪ Damaged cells release Von Willebrand
factor (binds to collagen)

Figure 43.2 Layers of an arterial wall.

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 Figure 43.3 Platelet plug formation steps.

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COAGULATION (SECONDARY
HEMOSTASIS)
osms.it/coagulation-secondary-hemostasis
▪ Last two hemostasis steps: clotting factors 4. Factor IXa + factor VIIIa (binds to Von
activate fibrin, build fibrin mesh around Willebrand factor) + calcium → enter the
platelet plug common pathway
▪ Begins with either extrinsic/intrinsic
pathway; factor X activation → coagulation COMMON PATHWAY
cascade (common pathway)
1. Factor X is cleaved → factor Xa
2. Factor Xa cleaves factor V → factor Va
EXTRINSIC PATHWAY 3. Factor Xa + factor Va + calcium →
1.Trauma damages blood vessel, exposes prothrombinase complex
cells under endothelial layer ▫ Prothrombin (factor II) → thrombin
▫ Tissue factor (factor III) embedded in (factor IIa)
membrane 4. Thrombin activates platelets, cofactors (V,
2.Factor VII in blood binds to tissue factor, VIII, IX); cleaves fibrinogen, stabilizing factor
calcium → VIIa-TF complex (→ factor XIIIa + calcium → cross-links in
mesh)
INTRINSIC PATHWAY
1.Circulating factor XII contacts negatively COAGULATION TESTS
charged phosphates on platelets/ ▪ Prothrombin time (PT): tests extrinsic
subendothelial collagen → factor XIIa pathway
2.Factor XIIa cleaves factor XI → factor XIa ▪ Activated partial thromboplastin time
3.Factor XIa + calcium cleaves factor IX → (aPTT): tests intrinsic pathway
factor IXa

ROLE OF VITAMIN K IN
COAGULATION
osms.it/vitamin-k-in-coagulation
▪ Vitamin K regulates blood coagulation non-functional forms of II, VII, IX, X into
▫ Converts coagulation factors into functional forms
mature forms ▫ Adds chemical group made of one
▪ 12 coagulation factors: (I–XIII, no factor VI); carbon, two hydrogens, one oxygen to
factors II, VII, IX, X require vitamin K glutamic acid residues on proteins
▪ Quinone reductase reduces vitamin K ▪ After carboxylation step, vitamin K (as
quinone (dietary form) into vitamin K vitamin K epoxide) is converted back into
hydroquinone vitamin K quinone via epoxide reductase
▪ Vitamin K hydroquinone donates electrons ▪ Coagulation factors appear in all
to γ-glutamyl carboxylase, converting coagulation pathways

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 Figure 43.4 Coagulation steps, including the intrinsic, extrinsic, and common pathways.

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Figure 43.5 Vitamin K cycle. A single molecule of Vitamin K can be reused many times.

ANTICOAGULATION, CLOT
RETRACTION & FIBRINOLYSIS
osms.it/clot-retraction-and-fibrinolysis
ANTICOAGULATION
▪ Occurs during primary, secondary
hemostasis; regulates clot formation
▪ Prevents clots from growing too large →
block blood flow, form emboli
▪ Regulation starts with thrombin (factor II)
▫ Multiple pro-coagulative functions
▫ Proteins C, S bind thrombomodulin-
thrombin → cleaves, inactivates factors
V, VIII
▫ Antithrombin III binds thrombin/factor X
→ inactivates both (plus factors VII, IX,
XI, XII with lower affinity)
▪ Other factors prevent platelets adhering
during primary hemostasis
▫ Nitric oxide, prostacyclin → ↓
thromboxane A2

Figure 43.6 Proteins involved in

anticoagulation. Thrombomodulin is found
on the surface of intact epithelial cells lining
blood vessels.

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 CLOT RETRACTION FIBRINOLYSIS
▪ Occurs one hour after primary, secondary ▪ Occurs two days after primary, secondary
hemostasis hemostasis; degrades clot
▫ Contracts clot ▪ Plasminogen → plasmin (via tissue
▪ Platelets in clot express integrin αIIBβ3 → plasminogen activator)
binds to fibrin expressing actin, myosin → ▪ Plasmin proteases fibrin → clot dissolves
lamellipodia contract, fibrin mesh tightens
closing wood

BLOOD GROUPS & TRANSFUSIONS

osms.it/blood-groups-and-transfusions
BLOOD TRANSFUSIONS ▪ Immune system produces antibodies
▪ Blood transfusion: person receives blood/ against absent glycoproteins
elements of blood (usually through ▪ Type AB: no antibodies → universal
intravenous infusion) recipients
▫ Homologous transfusion: anonymous ▪ Type O: no antigens → universal donors
donor
▫ Autologous transfusion: self-donor (e.g. Rh system
in planned surgery) ▪ Determined by presence of Rh protein
▪ Blood is mixed with calcium oxalate to ▫ Rh positive; Rh negative
prevent coagulation, refrigerated/frozen for ▪ Rh+ can receive blood from either group
storage ▪ Rh- can only receive Rh- blood

BLOOD TYPING CROSS MATCHING

▪ Transfusion blood types not compatible → ▪ Test to confirm donor’s blood is safe for
autoimmune reaction (hemolytic transfusion recipient
reaction) ▪ Recipient serum is mixed with donor blood
▪ Two classification systems (based on ▫ Agglutination reaction: cannot receive
presence/absence of proteins)
▫ ABO system
▫ Rh system

ABO system
▪ Determined by type of glycoproteins found
on red blood cells (RBCs)
▫ Type A; type B; type A & B; type O
(neither)

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Figure 43.7 Blood types are reported as ABO group and Rh + or -. When both classification
systems are combined, there are eight possible blood types: A+, A-, B+, B-, AB+, AB-, O+, O-.

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