South College AVL Lab Med: Hemostasis - Lecture 4

platelets

small, round, nonnucleated cells

<20,000/mm^3 OR >1 million/mm^3

What are CRITICAL VALUES for platelets?

spontaneous bleeding (epistaxis)

What would cause <20,000 platelet values?

Hypercoagulability, "throwing clots" (blood clot breaking free and traveling throughout blood)

What would cause >1 million platelet values?

maintenance of vascular integrity

what is the main role of platelets?

platelets aggregate (platelet plug) then initiate coagulation factor cascade

What is the most important function of platelets?

bloodstream (25% in liver and spleen)

where are most platelets found?

thrombocytosis

too many platelets

iron deficiency anemia - (caused by maximal stimulation of cellular production by marrow. Platelets DO NOT need iron - respond to stimulation)

malignant disorders - (unknown patho)

polycythemia vera - (PV - elevation of ALL blood cells)

post-splenectomy syndrome - (spleen extracts aging platelets - if you don't have spleen - cant remove platelets effectively)

RA - (unknown patho)

What are some causes of thrombocytosis?

Thrombocytopenia

low platelet count

production dysfunction, sequestration (hyperspleenism), accelerated destruction, consumption of platelets (due to disseminated intravascular coagulation - DIC), and hemorrhage

What are the five big causes of thrombocytopenia?

bleeding and clotting at the same time

what is disseminated intravascular coagulation (DIC)?

bone marrow failure, fibrosis (marrow replaced by fibrotic/neoplastic tissue), tumor, pernicious anemia (B12 required for platelet production), chemotherapy (destroys good and bad cells)

What are some reasons for production dysfunction?

antibodies, infections, drugs, prosthetic heart valves, hemolytic anemia

What are some reasons for accelerated destructions?

living in high altitudes (increase), platelets can clump during automatic counting (~10-15% error), strenuous exercise (increase), menstruation (decrease just before), meds (estrogen, OCPs - INCREASED RISK OF BLOOD CLOTS, histamine-2 H2 blockers, thiazide diuretics - DECREASE)

What are some interfering factors of platelets?

hemostasis and coagulation system

What two components aid in the homeostatic balance between factors encouraging clotting and factors encouraging clot dissolution?

vascular spasm, formation of platelet plug, development of clot (coagulation phase)

What are the three steps of the common pathway for a damaged blood vessel?

clotting factors

Injury of the blood vessels triggers the release of what?

platelet plug (sticky)

vasoconstriction limits the blood flow - platelets form this?

fibrin

these strands adhere to the platelet plug to form insoluble clot?

coagulation cascade

What happens after the fibrin clot is formed?

intrinsic and extrinsic pathway

what are the two pathways of the coagulation cascade?

when there is exposed collagen in injured vessels

when is the intrinsic pathway activated?

tissue injury (releases tissue factor - III)

when is the extrinsic pathway activated?

PTT or aPTT (partial thromboplastin time/activated partial thromboplastin time)

How do we measure the adequacy of intrinsic and common pathway?

time it takes for plasma to clot

What does PTT or aPTT measure?

>70 seconds (normal: 30-40 seconds)

What is the critical value for aPTT?

>100 seconds (normal: 60-70 seconds)

What is the critical value for PTT?

evaluate unexplained bleeding, DIC, initiating/monitoring anticoagulation (ex: heparin), liver disease (hepatitis - "bleeding nightmare")

When do we order a PTT or aPTT?

PT/INR (prothrombin time/international normalized ratio)

How do we measure the adequacy of extrinsic and common pathway?

>20 seconds (normal: 11-12.5 seconds)

What is the critical value for PT?

>5 (normal: 0.8-1.1)

What is the critical value for INR?

evaluate unexplained bleeding, DIC, intiating/monitoring anticoagulation (warfarin), liver synthetic function (excess alcohol, cirrhosis), preop testing (want to make sure clotting is okay)

When do we order a PT or INR?

time it takes to clot when exposure to tissue factor

What does PT/INR measure?

XII, XI, IX, VIII...X

What factors are involved in the intrinsic pathway (TENET)?

VII...X

What factor is involved in the extrinsic pathway?

X

Where do both the intrinsic and extrinsic pathway converge (what factor)?

X and V (Ca 2+ lipids) act on - Prothrombin (II) to produce - Thrombin -

Thrombin cuts - soluble fibrinogen (I) to produce - insoluble fibrin clot (XIII)

What factors are involved in the common pathway?

Play Table Tennis Inside (PTT/aPTT - intrinsic pathway)

How can we remember what PTT/aPPT is for?

Play Tennis Outside (PT/INR - extrinsic pathway)

How can we remember what PT/INR is for?

liver

Where are ALL clotting factors made?

I (fibrinogen), II (prothrombin), V, X

What factors does the common pathway consist of? (dollar bills smaller than $20)

indicates a problem with common pathway OR sick liver

What would it mean if both PTT and PT were BOTH prolonged (taking longer to clot)?

VII deficiency

What would it mean if ONLY PT was prolonged and NOT PTT?

XII, XI, IX, VIII deficiency

What would it mean if ONLY PTT was prolonged and NOT PT?

XI, IX, VIII, VII, X, V, prothrombin (II), and fibrinogen (I)

What deficiencies matter clinically (clinically significant)?

hemophilia A

what is a factor VIII deficiency known as?

heparin

what type of med acts on the intrinsic pathway?

warfarin - inhibits Vit K clotting factors

what type of med acts on the extrinsic pathway? why?

prone to bleeding/clotting, anticoagulants

Why are inhibitors of factors XI, IX, VIII, VII, X, V, prothrombin (II), and fibrinogen (I) clinically significant?

acquired/inherited deficiencies in coagulation factors, anticoagulation, biliary obstruction, DIC, liver disease, Vitamin K deficiency, meds (ex: allopurinol)

What are some causes of prolonged aPTT and PT/INR?