Platelets Info and Disorders Flashcards by Luke Hayek

Where is TPO made? and is it made at a static level or changing level?

made in the liver at a static production rate

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C-Mpl receptor

it is the TPO receptor on the megakaryocytes and platelets

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What happens when platelets are high and TPO is produced?

the C-Mpl on the platelets will bind the TPO and then the TPO is engulfed by the platelets so platelet count will not keep rising

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what is the role of integrins?

they are heterodimeric proteins that cells use to bind ECM and communicate from inside to out and from outside to inside

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alpha2beta1 integrin name for platelet and role

GPIa-IIa

binds collagen

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alpha2bBeta3 integrin name for platelet and role

GPIIb-IIIa binds fibrinogen

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GP Ib-IX-V platelet glycoprotein role

binds von willebrand factor

NOT an integrin

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four steps in the formation of platelet plug

adhesion, activation, aggregation and secretion

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how does platelet adhesion happen?

the GP Ib-X-V binds to VWF

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how does the shape of platelet change and why?

from flat to a disc with spikes to increase SA

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how do platelets aggregate?

once activated the GPIIb-IIIa will allow cross links and binding between fibrinogen

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what are four molecules that are platelet activators?

thrombin, thromboxane, ADP and collagen

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where is ADP released from?

damaged RBCs

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what is unique about thrombin as a platelet agonist?

it bites off its own tail and the tail is then the ligand for a GPCR

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what cells release thromboxane?

platelets

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what is thromboxane derived from?

arachidonic acid…cyclooxygenase (COX inhibitors)

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what 3 molecules inhibit platelets from sticking to normal endothelium?

nitric oxide
ecto-ADPase
prostacyclin

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Ecto-ADPase role in platelet inhibition

chews up ADP from RBCs to prevent platelet activation

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where is Prostacyclin (PGI2) made?

endothelial cells

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what is prostacyclin derived from?

arachidonic acid from cycoloxygenase side

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what provides the phospholipid membranes for the coagulation factors?

the platelets once in scaffolding will turn membranes inside out to show negative charge and allow the coag factors to anchor

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Lab findings for a qualitative platelet disorder

prolonged bleeding time

normal PT, TT, or TCT

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Bernard Soulier disorder mechanism and type of platelet disorder

defect in Ib/IX on platelet surface so no adhesion

qualitative so long bleeding time and normal coag tests

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Glanzmanns thromboaesthenia disorder mechanism and type of platelet disorder

defect in IIb/IIIa so no aggregation

qualitative so long bleeding time and normal coag tests

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four other causes of qualitative platelet disorders

uremia drugs like NSAIDs herbs like garlic and ginkgo myeloproliferative disorders

pseudothrombocytopenia clinical presentation

low number of platelets, but this is artificial due to them clumping together will see a funky looking "white cell" in the smear

at what number of platelets do first symptoms show?

less than 50K...bruising

what number of platelets do you start treatment?

less than 20K

what number of platelets is immediate risk for intracranial hemorrhage and needs immediate treatment

less than 10K

three categories of thrombocytopenia

peripheral destruction underproduction splenic sequestration

three common causes for platelet underproduction

marrow failure marrow infiltration marrow toxins

what are two common marrow toxins that leads to underproduction of platelets?

alcohol and chemo

what are two common marrow failures leading to platelet underproduction

aplastic anemia, vitamin deficiencies

DIC (disseminated intravascular coagulation) mechanism

abnormal activation of coagulation leading to consumption and destruction of platelets and activation of fibrinolysis

What coag test will be elevated with DIC?

the PT test because factor VII which has smallest half life is consumed rapidly

if DIC is advanced what other coag test will be longer?

aPTT

four other signs of DIC

low platelets, low fibrinogen, elevated D dimers, SCHISTOCYTES

5 common causes of DIC

gram negative sepsis, burns, obsetric problems, shock, venoms

treatment of DIC

transfusion of platelets, clotting factors and fibrinogen (cryoprecipitate)

TTP mechanism

abnormal activation of platelets and endothelial cells with VWF and fibrin deposition in the microvasculature and peripheral destruction of RBCs an platelets

what are the two things you must have to diagnose TTP?

MAHA causing schistocytes! | low platelets

three other findings with TTP?

fever, neurological changes, renal issues

lab finding with renal failure in TTP?

increased BUN and creatine

neurological changes in TTP

stroke, coma, headache, dizzy, coma

What is the cause of TTP?

auto antibody against the protease (ADAMTS-13) that cleaves the big VWF...so if not cleaving then VWF still there for platelets to adhere to and activate

what is the protease that breaks down VWF and is associated with TTP?

ADAMTS-13

what drugs can induce TTP? and is this a problem with ADAMTS-13 when it is drug induced TTP?

quinine, cyclosporine, tacrolimus

what is the first line treatment for TTP?

plasma exchange

why no platelet transfusion in TTP?

they fuel the fire

in TTP, if plasma exchange does not work what are other treatment options?

steroids, rituximab, splenectomy

What does HUS stand for?

hemolytic Uremic syndrome

HUS cause

usually from Shiga toxin in E coli.. diarrhea

Shiga Toxin mechanism in HUS

binds endothelium cells in kidney and causes cell death

atypical HUS characteristics

no diarrhea, but have MAH, renal failure, low platelets, and complement activation

atypical HUS treatment

plasma exchnage and eculizimab

atypical HUS cause

inherited disorder of complement regulation with over activity...

triggers of atypical HUS

infection and pregnancy

thrombocytopenia inducing drugs (4)

beta lactams sulfa drugs quinine heparin

Heparin induced thrombocytopenia characteristics

7-10 days after drug started have low platelets...stop heparin immediately

Can heparin lead to thrombosis?

yes in patients with heparin induced thrombocytopenia

how to diagnose immune thrombocytopenic purpura

have to exclude everything else...no test

signs of immune thombocytopenic purpura

isolated thrombocytopenia often provoked by viral illnesses

what is the first line of therapy with immune thrombocytopenic purpura?

first is corticosteroids

what happens in immune thrombocytopenic purpura if the steroids and IVig do not work?

give rituximab or splenectomy

if platelet count super low like less than 10K in immune thrombocytopenic purpura...what should you give and why?

IVIg because it will overwhelm the Fc receptors

Platelets Info and Disorders Flashcards

(65 cards)