Page 469 - Medicine and Surgery

P1: KOA
BLUK007-12 BLUK007-Kendall May 12, 2005 20:37 Char Count= 0

Chapter 12: Clinical 465

areincreasedinmyeloproliferativedisordersparticularly ulation in disseminated intravascular coagulation (see
chronic myelogenous leukaemia (see page 482). page 494) or thrombotic thrombocytopenic purpura
(see page 258).
Red blood cells
Polycythaemia(increasedredcellcount)mayresultfrom
reducedplasmavolume(diarrhoea,vomiting,diuretics).
Coagulation screening tests
True polycythaemia may be primary (see page 483) or
secondary. Secondary polycythaemia may be due to The basic coagulation cascade (excluding co factors) is
Hypoxia, which may be physiological (neonates, alti- outlined below; the cascade style of reaction allows a

tude), or due to respiratory disease (smoking, COAD) small stimulus of negative charge contact (such as colla-
or cyanotic heart disease. gen) or the release of thromboplastin from the tissues to
Inappropriate erythropoetin production: Renal cell create a large amount of fibrin product (see Fig. 12.1).

carcinoma, renal cysts or following renal transplant. Factors II (prothrombin), VII, IX and X require vita-
Tumour secretion: Hepatoma, cellular haemangioma. minKfortheirsynthesis.Thecoagulationscreenismade

Severe polycythaemia may result in hyperviscosity of the up of a combination of tests:
blood, which prediposes to thrombosis, haemorrhage The thrombin time (TT) is initiated by adding
and cardiac failure. thrombin to a sample and thus assesses deficien-
cies/dysfunctions in fibrinogen. Fibrinogen levels and
Platelets fibrin degradation (D-dimers) products can also be
Thrombocytopenia (reduced platelet count) may be due measured as a measure of intravascular clot break-
to failure of bone marrow production or excess destruc- down, e.g. disseminated intravascular coagulation or
tion of platelets. Bone marrow platelet production may pulmonary embolism.
fail due to aplasia, marrow infiltration or the effects of Theprothrombin(PT)timeisinitiatedbytheaddition
drugs. Peripheral platelet destruction may result from ofthromboplastinandthusmeasurestheextrinsicand
immune mechanisms (see page 495), from excess coag- final common pathway. It is prolonged in deficiencies

INTRINSIC PATHWAY
–ve charge tissue
contact
XII XIIa
FINAL COMMON PATHWAY
XI XIa
IX IXa
Prothrombin
VIII (II)
X Xa V Fibrinogen

Thrombin
(IIa)
VII VIIa
Fibrin

Tissue Throboplastin
(III)
EXTRINSIC PATHWAY
Figure 12.1 The coagulation cascade.