Platelets Flashcards by Meghan May

What are the major components of plats

Plasma membrane with lots proteins invaginated canalicular system

microtubles

Granles: alpha and dense are key

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How do plats get around the blood and in what state?

Inactive state

Adhesion to vessel endothelium till find a break in vessel
Secreation of granules
Aggretation to each other

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What tethers Platelts to collagen once plateltes stick to tear in vessel?

Platelet–GPIb–vWF–Collagen

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What happens when a platelet gets activated?

undergoes biochemical and physical changes

You see plates squeeze all granules to center

then podocyte processes reach out to surroundings

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What are inside our Dense or Delta plat granules?

ADP, ATP, Seratonin (key for vasoconstriction) and Calcuim

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What is inside the Alpha granules

Fibrinogen, factor V

Thrombosponsin

*****PDGE, PF4 and TG-B which are all key in atherosclerotis pathogenesis (how clotting contributes to this disease)

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There are receptors on the surface of platelets that once activated will induce activity of phospholipase A inside the platet… what does this result in?

PL-A cleaves phospholipids to arachadonic acid

this is the key precursor to prostaglandins and thromboxanes

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Arachadoinc Acid —-> PGG2 and PGH2

via Cyclooxygenase (inhibted by aspirin and COX inhibitors)

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PGG2 and PGH2—> TXA2 and TXAb

Via thromboxane synthase

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What is the role of thromboxanse and where do they come from

from AA inside plats

fnx to make membranes fuse and dump contnets out of cell

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What two paths does PGG2 or PGH2

thromboxane synthase—> to TxB2 = platelet stimulation

OR
Prostacyclin synthast –> PGI2 = Plate INHIBTION

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How to platelets adhere to one another?

Plat–GPIIIa/GPIIb —–FIBRINOGEN—-GPIIIa/GPIIb—–Plat

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What is characteristic of Quantitative platelet disorders?

Decreased Platelet count

Prolongued bleeding time

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What is characteristic of Qualitative Plat disorders?

Normal plat cound

Prolounged bleed time

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von-Willebrands disease is what type of disorder?

Cofactor abnormality of platelets

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Ehlers Danlos, Scury and Pseudoxanthoma elastiucm are all expamples of

Substrate abnormalities

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What do we see in von Willebrand Disease

(whats missing, what test confirms it, what happens to bleed time)

Decreased vWF acitivty and antigen

Abnormal Ristocetin aggregation

Prolongued beelding time

What do we see in Bernar Soulie syndrome (insufficiency of GPIb)

normal vWF activity

Abnormal Ristocetin aggregation

Prolonged bleed time

What do we see when there are collagen abnormalities

normal vWF activity and antigen

Normal Ristocetin aggregation

Prolongued bleed time

phospholipase, cyclooxygenase and thromboxane synthase disorders are all what types of defects?

Defects of secreation: Prostaglandin defects

If a platet is missing granules, what type of defect is this?

storage pool defect

Membrane changes like Glanzmanns thrombasthenia and Peniccillin/carbenicillin are what type of defects

defects of aggregation

What are two types of defects seen with Increased Destruction of platelets?

Increased utlization: DIC, TTP and abnormal valves

Immunological destruciton: Idiopathic TTP, Lupus, Drugs

4 yo girl comes to the office with purpura on her trunk and legs. She has prominent bleeding from an IV site. She has a viral infection last week and has no prior hx of bleeding

Acute ITP; often proceeded by viral syndrome

How is chronic ITP differnt from acute ITP

chronic: bleeding is less prominent and often discovered incidentally. Plats are usually low and pt has long hx of bruising 3: 1 (F:M)

What are some different characteristics of ITP antibodies

Platelet specific, restricted heterogeneity, Antigenic heterogeneity (GPIb, GPIIb) and site of produciton (spleen or BM)

What do we need to make a dx of ITP

1. Evidence for immune thrombocytolysis - thrombocytopenia---Normal or incresase megakaryocytes---antiplat antibody 2. Absence of other causes of thrombocytopenia (like lupus or DIC) 3. Absence of splenomegaly

What do we tx those dx with ITP with?

1. corticosteroids (see 70% respond w/ high relapse rate) 2. Splenectomy (50% response and low relapse, remove source of antiB prodcution) 3. Immunosuppresive agents

18 yo girl, bilateral rash on ankles for 3 days, petichae and has progressively increased feels fine, no recent illness on birth control, active and in high school LMP: 3 weeks ago w/ moderate bleeds for 5 days changed out every 6 hrs neg for lymphadenopathy, normal vitals normal coagulation times and CBC below – WBC =7.0 (normal 4-10) with normal differential – Hemoglobin = 11.9 (normal 11.2-15.4) – Platelet count = 6 (normal 150-350) next step?

Peripheral blood smear

Get peripheral blood smear for girl with petichae and CBC of ## Footnote – WBC =7.0 (normal 4-10) with normal differential – Hemoglobin = 11.9 (normal 11.2-15.4) – Platelet count = 6 (normal 150-350) What are some differentials you should include in workup

IMmune thrombocytopenia: autoimmune syndormes, drugs, infections DIC: unlikley bc no prolongued bleeds TTP: no hemotonizing, so prbly not Hematologic malignancy: not likley bc nothing going on with WBC and no lymphadenopathy

Your pt is dx with ITP, what do you treat her with

prednisone and IVIg

Pt has hx of ITP managed for 10 yrs with prednisone and IVIg. Decreased tolerance to running (marathon runner) and gtes tired. Uses aspirin 4-5x week for ankle pain and ibuprofen for mentral pain prn. Vegetarian but eats fish and has increased menorrhagia over past two months PE: slight tachy, thin conjunctival pallor, no rash but bruising. – WBC = 5.2 (normal 4-10) with normal differential – Hemoglobin = **8.1** (normal 11.2- 15.4) – Platelet count = 216 (normal 150- 350) – MCV = **70** (normal 80-100) Normal coag times

Microcytic hemochromatic Iron deficiency anemia

What studies could you use to confirm a dx of iron deficency anemia?

– Ferritin – Iron (transferrin) saturation – Total iron binding capacity – Reticulocyte count

MCV Decreased RDW: incresed Iron sat% Decreased Ferritin: **Decreased** BM irone: **Decreased**

Fe defiency anemia

MCV: low or normal RDW: normal IRon Sat%: Decreased/normal Ferritin: Increased/normal BM Iron: increased

Anemia of Chronic Disease

MCV: decreased RDW: increased/normal IRon Sat%: increased Ferritin: BIG increase BM Iron: Big increase

Thalassemias

MCV: decreased RDW: increased IRon Sat%: increased/normal Ferritin: increase BM Iron: increase

Sideroblastic anemia

Further evaluation of the patient’s bleeding includes: – Von Willebrand’s antigen = 90% (nml 60-130) – Von Willebrand’s activity = 110% (nml 60-130) – Factor VIII activity =95% (nml 65-140) – Von Willebrand multimers = normal distribution – Thrombin time = 13 seconds (nml 12-14 sec) – Platelet function assay**- prolongation on collagen/epinephrine cartridge \>300 sec (nml \<180); normal on collagen/ADP cartridg**e what caused this?

d. decreased platelet aggregation due to reduce formation of thromboxane A2 : from aspirin use

Mechanism of aspirin

Decreaes plat aggregatiob via COX-1 inhibiton see decreased thromboxane formation which is responsible for platelet aggregation via mediation of GPIIB/IIIA

cause mucocutaneous bleeding including petechiae and mucosal bleeding (epistaxis, gingival bleeding, menorrhagia)

Defects of primary hemostasis (formation of platelet plug)

Disorders that affect primary hemostasis include

qualitative and quantitative platelet defects, vW disease, and disorders of the endothelium

is a diagnosis of exclusion, requiring lab testing to evaluate for other causes of bleeding

ITP