You are on page 1of 1

‎Laboratory Tests ‎Coagulation Disorders

‎x-linked recessive trait


‎( 25-35 seconds)

‎ bnormal homeostasis due to deficiency in


a
‎ heck the intrinsic system ( factor VIII, IX,
c
‎factor VIII, this factor is bounded to vWF in
‎Partial Thromboplastin Time PTT ‎XI & XII) & common pathway factor (V&X)
‎circulation
‎prothrombin & 4 fibrinogen

‎sever HE cause severe bleeding


r‎ esults in excess of 35 seconds are
‎considered abnormal or prolonged.
‎the dentist must be aware of the normal ‎hemarthrosis
‎ranges
‎Vascular defects ‎ecchymosis

‎(11-15 seconds) ‎soft tissue hematomas

‎ heck the extrinsic pathway (factor VII) &


c ‎autosomal dominant ‎ fter trauma or surgery there will be
a
‎Hemophilia A ‎Clinical findings
‎common pathway (V&X) prothrombin time & ‎severe bleeding which may threaten life.
‎fibrinogen) ‎ feature of telangictasia lesions
a
‎Prothrombin Time PT ‎involving the skin & mucous membrane ‎ pontaneous bleeding from
S
{‎ VII & X and prothrombin) are vitamin k- ‎ ereditary hemorrhagic telangictasia ‫توسع‬
H ‎mouth ,gingivae , tongue ,lips
‎dependent & are depressed by coumarin-like ‎‫( الشعيرات الوراثي النزفي‬osler –weber –rendu ‎ leeding as epistaxis (nose bleeding) due to
b
‎Three phases of homeostasis ‎drugs & should be checked by INR P ‎disease ) ‎inert mechanical fragility (‫ )هشاشة‬of the ‎ emophilic patient greatly affected by
H
‎vessels ‎contamination from blood transfusion by
‎ T is prolonged when any factor is blow 10%
P ‎HIV & hepatitis C virus
‎of its normal value. l‎esion appear by age of 40s & increase in
‎Vasoconstriction in the area of injury ‎number with age ‎ inor spontaneous bleeding 25-30 %
M
‎Vascular phase ‎replacement
‎140,000-400,000 cubic mm ‎normal
‎Immediatly
‎ bnormal vessels wall weakness arterial
a ‎Minor dental surgery 50% replacement.
‎1- primary phase ‎manifest excessive bleeding after severe ‎Ehler –Danlod syndrome ‎aneurysms (‫ & )تمدد االوعية الدموية‬bleeding
‎Platelets and vessel wall become "sticky” ‎50,000 -100,000
‎trauma ‎from spontaneous rupture ‎Replacement of factor VIII include ‎Major surgery 80-100% replacement
‎Platelet count
‎ echanical plug of platelets seals off
M
‎Platelet phase ‎ anifest excessive bleeding after minor
m
‎openings of cut vessels ‎Below 50 000 ‎ he choice of which type of factor
T
‎trauma skin & mucosal purpura ‎ hlers-Danlos disease ,osteogenesis
E
‎imperfecta and marfan syndrome are ‎concentrate should be used is based
‎Begins seconds after Injury ‎hereditary disorder of connective tissues ‎on specific findings from the patient
‎20 000 cubic mm ‎spontaneous bleeding
‎management history & infection
‎disease exposure
‎ lood lost into surrounding area coagulates
B ‎scurvy vit C deficiency ‎capillary fragility & delayed wound healing
‎ sed to screening for disorder platelet
u
‎through extrinsic and common pathways ‎Bleeding time (BT)
‎dysfunction & thrombocytopenia. ‎Aquired connective tissue disorder
‎(Christmas Disease,Factor IX Deficiency)
‎long use of steroid therapy ‎thinning of connective tissue ‎bleeding
i‎nitiated through tissue factor after tissue
‎Normal (9-13 sec) ‎X –linked recessive trait
‎injury
‎fibrin-forming system ‎extrinsic system ‫ة‬‎ ‫ اضاف‬:
i‎t's convert fibrinogen into insoluble fibrin ‎an allergic reaction to an injection of serum, ‎ linical manifestation the same as
C
‎Factor Vll (Vila) (tissue thromboplastin) ‎ oth systems (pathways) use common
B
‎ lood in vessels in area of injury coagulates
B ‎which makes up the essential clot ‎typically mild and characterized by skin ‎hemophilia A
‎2- Secondary phase (Coagulation phase) ‎Coagulation phase ‎pathway to form the end product fibrin
‎through intrinsic and common pathways ‎rashes, joint stiffness, and fever.
‎initiated by surface contact
I‎t by-passes the intrinsic, extrinsic & ‎ creening laboratory tests results are
s
‎9-18 minutes ‎intrinsic system ‎Thrombin time (TT) ‎Hemophilia B
‎common pathway. ‫ة‬‎ ‫ اضاف‬: ‎similar to both A&B
‎factor XII ‎purpura: A rash of purple spots on the skin
‎ hrombin is added to the patient blood
t ‎caused by internal bleeding from small ‎ pecific factor assays for factor IX
s
‎Takes place more slowly than other phases ‎sample as activating agent ‎blood vessels ‎establish the diagnosis
‎Serum sickness ‎lead to purpura

‎ aused by excessive plasmin & or fibrin-


c i‎mmune complex deposits in the ‎ urified factor IX product are recommended
p
‎➢ Release of antithrombotic agents ‎(16-18 sec) consider prolonged ‎vessel walls ‎for treatment of minor
‎split product
‎3- Tertiary phase (Fibrinolytic phase) ‎& major bleeding recombinant factor IX is

‎ Spleen and liver destroy antithrombotic ‎ encillin , sulfonamide thiazide diuretics &
p ‎now available for clinical
‎agents ‎INR(international normalized ratio) ‎0.8 to1.1 ‎hepatitis ‎use

‎Bleeding Disorders
‎Jaundice ‫اليرقان‬, Spider angiomas ‫االورام‬ ‎ cquired deficiency because of vit K
a ‎most common
‎‫ الوعائية العنكبوتية‬, Ecchymosis ‫الكدمات‬, ‎deficiency or liver diseases
‎Petechiae ‫ النمشات‬on the skin or mucosa due ‎autosomal dominant traits
‎Liver disease
‎to a reduction in platelets which occurs
‎because of hypersplenism that results from ‎ ongenital deficiency of factor V&X,
C
‎defect in platelet adhesion
‎the effects of portal hypertension ‎prothrombin & fibrinogen are rare

‎mild to moderate bleeding


‎ cchymosis, hemarthrosis ‫& تدمي المفصل‬
E ‎ prolonged a PTT & PT indicates a
A
‎dissecting hematomas ‫ ورم دموي متحلل‬: ( ‎common pathway factor deficiency ‎carry factor VIII
‎describes a loss of function ‎made from a group of glycoprotiens ‎needed to
‎Genetic coagulation disorders ‎allow platelet to adhere to the tissue
‎that eventually results in a breakdown of
‎the protective mechanisms of human ‎vWB factor
‎skin) ‎Disorder of common pathway ‎ he complex of factor VIII & vWB factor
t
i‎t's from this location that the vWB factor
‎attaches to the surface of circulating
‎contribute to hemostasis
‎platelets
‎ lceration of oral mucosa
u
‎hyperplasia of gingiva ‎mild form ‎–ve family history
‎Chronic leukemia ‎Von Willebrand disease (VWD)
‎petechiae
‎ecchymosis ‎severe form ‎+ve family history
‎Clinical finding
‎ evere bleeding
s
‎after trauma or surgery it manifested as
‎Signs ‎cutaneous & mucosal bleeding because of
‎platelet adhesion lacking ,hemarthrosis and
‎or epistaxis.

‎ T& TT are normal


P
‎PFA-100
‎aPTT prolonged
‎laboratory investigation
‎platelet count normal
‎another investigation immunoassay of vWF &
‎specific assays for factor VIII

‎TREATMENT ‎cryoprecipitate

‎Platelet disorders

You might also like