Hemostasis Clinical Lab Test PDF

Clin lab test Hemostasis Q: What is hemostasis?: A: Hemostasis is the process by which the body stops bleeding after a blood vessel is injured, involving vasoconstriction, platelet plug formation, and blood clotting to seal the wound. It ensures vascular integrity while preventing excessive blood lo...

Clin lab test Hemostasis Q: What is hemostasis?: A: Hemostasis is the process by which the body stops bleeding after a blood vessel is injured, involving vasoconstriction, platelet plug formation, and blood clotting to seal the wound. It ensures vascular integrity while preventing excessive blood loss. Q: what is required for normal hemostasis? A:Blood Vessels: The injured vessel constricts (vasoconstriction) to reduce blood flow. Platelets: Platelets adhere to the injury site, activate, and aggregate to form a temporary plug. Clotting Factors: Proteins in the blood plasma (e.g., fibrinogen, thrombin) activate in a cascade to form a fibrin clot. Endothelial Cells: These cells regulate the process by releasing signals that control clotting and prevent unnecessary clot formation. Calcium and Other Cofactors: Essential for the activation of clotting factors and the stability of the clot. Hemostasis is a combo or interaction of 4 events 1.)​ Vasoconstritcon (the response of the blood vessles to injruy) 2.)​ Activation of platlets within the blood (the platelt plug forming) 3.)​ Cogulation cascade 4.)​ Breakdown of the clot A platelet plug is NOT the same thing as a clot a platelet plug is formed in primary hemostasis well a clot is made in secondary hemostais Step 1 Vasoconstricton So the areterys get injured someway and smooth muscle it is made out of constricts these then will DECREASE the rate of blood loss and causes turbalnce which causes platelet attachment the damaged vascular lining/inside of vessels and exposure of compounds within vessels to tissues, stimulates further responses in overall hemostasis process Step 2 platelet response When the vessel gets injured the blood steram gets exposed to “ The subendothelial basement membrane” of vessels and connective tissues this causes the platelets to “activate” These activate platelets will release serval chemicals ex vWF this is the END OF PRIMARY HEMOSTASIS Step 3 Cogluation cascade These clotting factors remain inactive until needed there are a few other things needed such as calciluim and vit K. The whole goal of this cascade is to convert FIBROGEN to FIBRIN this is secondary hemostasis There are two parts to the colgualtion cascade the intrinsic and extrinsic pathway these are also caled PT and PTT to rember which is whic remember you PT play tenis OUTSIDE so its extrinsic and you PTT play tabel tenis INSIDE so its intrinsic Factor 1 is firbriogen (The goal) Factor 2 is prothrobim Factor 3 is tissue factor Etc etc Factor II,VII,IX and X need vit K And most of them need calcium The body has self regulation methods such as each factor activated to stimulate NEXT STEP, it is RAPIDLY DESTROYED by local enzymes so coagulation can be localized to injured area There are 2 ways to start the coagulation cascade Clothing factors are always present in plasma in there inactive forms they are then activated by the precursor being active ex factor 11 needs factor 12 factor 12 needs factor one. That is the interisine pathway And the extrsinve pathway is activated secondary to external trauma and release of tissue factor think of it like the spark Step 4 clot breakdown This is called FIBRINOLYILIS This happens because plasminogen -> plasmin that will break down the fibrin the broken down fibrin produced fibrin degradation products aka FDPs Clincal signs of hemostatic disorders Primary ​ Petchia is very common ​ Hematomas are rare ​ Bleeds at multiple sites ​ Bleeding often involves the mucous membranes ​ Prolonged bleeding time from cuts  Secondary ​ Pethcia is rare ​ Hematomas are common ​ Bleeding is localized ​ Bleeding is common at muscles and joints ​ Recurrent bleeding from the same sites Von willebrand factors It is a large plasma protein produced in endothelial cells and ct it binds to collagen when it is exposed to endothelia cells AND it binds to platelltes the are like BFFS vWF is what allows platelets to become “sticky” so they can adhere to eachtoher and the dmg vessel wall. Factor VIII is bound to vWF when it is inactive tests of Primary hemostais Platelet counts BMBT- Buccal musocall bleeding time VWf Tests of seocndary hemostasis ACT- actaivted clotting time test PT- tests extresinve hemostais PTT- tests intstrive hemostais Fibrogen assays Tests of tertiary hemostasis -​ Fibrogen degradation products determination Aquuired disorders of hemostais -​ May occur at any time and any age of the animal -​ May involve toxictes/drug reactions -​ May be secondary compilations to infections, diease and neoplasia Inhertiend disorders of hemostasis -​ Often presents in young -​ May have affected littermates dam sire etc -​ History important -​ Breed predisotpion  Primary disorders of hemo stasis Accuquried -​ DIC (impairs platelet function) -​ Drug reactions (asprin) -​ Thrombocytopeina -​ Disorders of platelet production Inheitred -​ Von willberantr disease -​ Basst hound thrmobopathy -​ Thromopathias (failure of platelet aggregation0 Secondary disorders of hemostasis Aqquired -​ Toxicts -​ Infections -​ Liver disease -​ DIC MOST COMMON INHERITED DISORDER OF HEMOSTASIS :vW DISEASE MOST COMMON ACQUIRED DISORDER OF HEMOSTASIS: THROMBOCYTOPENIA (note these are both disorders of primary hemostasis Von Willebrand’s DISEASE On Willebrand's disease (vWD) is a CONGENITAL/INHERITED defect resulting in PLATELET DYSFUNCTION deficiency of plasma vWF results in vWD -​ it is characterized by a deficiency of von Willebrand factor (vWF), a PLASMA PROTEIN THAT IS INVOLVED IN PLATELET ADHESION TO THE VESSEL WALL DURING FORMATION OF THE PRIMARY HEMOSTATIC PLUG -​ this deficiency results in ABNORMAL PRIMARY HEMOSTASIS (PLATELET PLUG FORMATION) and prolonged bleeding time -​ Most common in corgis,dobermen,german shreapeds -​  -​ in animals with vWD , bleeding episodes commonly involve mucosal surfaces prolonged bleeding may be observed after trauma or surgery -​ clinical signs of vWD may include -​ Epistaxis (nose bleed) -​ Gingiva bleeding -​ Heamturia -​ Excess vagina hermraghe -​ GI bleeding -​ Mutilple small bruises -​ Purpura -​ Spontaues bleeding from muscosal surfaces -​ Exessvie bledding from tooth extractions -​ Prolonged bleeding from wounds -​ Increased cuateons bleeding espcilay after venopuncture PRESUMPTIVE DIAGNOSIS of von Willebrand's disease: -​ platelet count and morphology are generally normal normal PT and PTT -​ prolonged BMBT suggestive of vWD -​ The buccal mucosal bleeding time (BMBT) measures the length of time (minutes) required for the platelets to plug a small laceration in blood vessels -​ the BMBT should not be prolonged with deficiency of coagulation factors -​ In vWD , the BMBT is usually prolonged because platelet function is abnormal DEFINITIVE DIAGNOSIS of von Willebrand's disease -​ may be achieved by antigenic measurement -​ test uses anti vWF antibodies to measure vWF antigen (ELISA based immunological test) -​ sample for the vWF antigen test is citrated plasma RODENTICIDE TOXICITY Coagulopathy caused by reduced vitamin K dependent clotting factors in the circulation after exposure to anticoagulant rodenticides -​ Anticoagulant rodenticides inhibit enzyme responsible for recycling of vitamin K, ultimately reducing production of vitamin K dependent coagulation factors SIGNS/CLINICAL PRESENTATION: -​ owner may observe or be suspicious of exposure to toxin  -​ animal may have had history of roaming -​ may present with lethargy, epistaxis,melena, bruising, blindness, seizures, dyspnea PHYSICAL EXAM FINDINGS MAY INCLUDE: -​ depression, pallor, hematemesis,hematuria , gingival bleeding, prolonged bleeding from wounds/ venipuncture sites, hematomas,hemorrhage into body cavities (smaller bleeds often progressing to larger bleeds) CAUSES/RISK FACTORS: -​ small doses over several days may be more dangerous than single large dose -​ different “generations” of rodenticides : first (warfarin) second (brodifacoum, bromadiolone) and third (indandiones) -​ roughly increasing toxicity with increasing generation DIAGNOSTIC PROCEDURES: -​ evaluation (and continued monitoring) of PCV, TP, CBC, platelets coagulation profile → PROLONGED ACT, PT, PTT -​ biochemistry profile, urinalysis TREATMENT: *find source of exposure if possible* -​ induction of emesis if known, recent ingestion, activated charcoal, gastric lavage -​ vitamin K (ANTIDOTE) (various regimes depending on type ingested) -​ restricted activity, monitoring (depending on ingestion) -​ follow up treatment dependent on severity of condition (hospitalization, transfusion) -​ follow up bloodwork is always recommended DIC (DISSEMINATED INTRAVASCULAR COAGULATION) not a PRIMARY condition but generally occurs SECONDARY (as a Sequelae to another disease or condition) *PATHOGENESIS IS COMPLICATED* INVOLVES the CONCURRENT ACTIVATION OF THE COAGULATION AND FIBRINOLYTIC SYSTEMS - may lead to consumption of the coagulation factors, fibrinogen/fibrin, platelets → resulting in bleeding/hemorrhage -if clot formation exceeds lysis , fibrin may accumulate in microvasculature → resulting in ischemia and organ failure (so king of getting BOTH Hemorrhage AND thrombosis) -​ DIC occurs due to systemic, rather than local, activation of coagulation and fibrinolysis -​ can be triggered by many causes including any disorder that causes vascular stasis or endothelial injury including; generalized/systemic infections, neoplasia , severe tissue damage, shock CONDITIONS that have bee ASSOCIATED WITH development of DIC -​ heat stroke -​ sepsis -​ viremia -​ pancreatitis -​ neoplasia (diffuse and local) -​ parasitic infections (including heartworms) -​ intravascular hemolysis -​ immune-mediated diseases -​ exposure to venom/toxins -​ massive tissue injury (including burns, crush trauma, and surgical procedures) -​ obstetric complications -​ insufficiency of major organs (liver, kidney) -​ diabetes mellitus -​ acidosis -​ polycythemia -​ severe prolonged hypotension (including shock) -​ severe volume depletion -​ impaired blood flow to a major organ (including GDV) HEMATOLOGICAL FINDINGS CONSISTENT WITH DIC: -​ thrombocytopenia -​ prolonged PT, PTT -​ hypofibrinogenemia -​ fragmentation of RBCs ( schistocyte formation) -​ Increased FDPs (fibrin degredation products) AND other diagnostic findings related to underlying condition(s) treatment involves managing underlying conditions, administration of anticoagulants, fluid and transfusion therapy → often not a good prognosis once patient exhibiting signs of DIC