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Clinical medicine II

Where do platelets come from megakaryocytes in the bone marrow: called thrombopoiesis
DNA is repeatedly duplicated but nucleus and cytoplasm does not divide Endomitosis
How do cells divide w/ endomitosis the cell get so large, bits of the cytoplasms shed off, and released into blood
How many are produced a day? 2,000-3,000 per cell per day: 200 billion a day produced
Two parts of a platelet membrane: phospholipids and glycoproteins, Granules: Dense and Alpha
What are the three types of glycoproteins and their names/fxn GP Ia/IIa: collagen receptor-platelet adhesion, GP Ib/IX/V: volWildebrand factor receptor : platlet adhesion, GP IIb/IIIa: fibrinogen receptor, platelet aggregation
Which GP’s used for beginning the clotting cascade, and which help adhese to each other GP Ia/IIa and GP Ib/IV/V and then GP IIb/IIIa
Two fxns of platelets binds to site of injury, form a platelet plug, provides phosopholipid surface for which the clotting cascade can occur
Why is the action of the platelet so important many drugs inhibit their action
What does aspirin have on the platelet blocks cyclooxygenase which prevents the production of thromboxane A2 which prevents platelets from sticking to each other.
Difference b/w aspirain and NSAIDS aspirin permanently blocks cyclooxygenase for the life of the platelet, NSAIDs only ~ 3 days, aspirin, rapid, delayed recovery, NSAIDS, drug must be present for enzyme inhibition
Thienopyridines drugs that impaire platelet functions by impairing effects on platelet aggregation, irreversible platelet fxn, lasts up to 10days after drug stopeed, examples: ticlopidine, clopidogrel (Plavix)
Use of GP IIb/IIIa inhibitors block fibrinogen receptor (crucial for platelet aggregation) used for management of ACS and preventing restenosis post angioplasty/stent placement: examples abcimximab, eqtifatide, tirofiban
What drugs impair platelet function SSRIs, Herbal Supplements, Combination meds
What SSRIs impair platelet fxsn Prozac, Zoloft, paxil, celexa, Lexapro
Do these drugs have the same effect as aspirin no, usually ok by themselves, but when drugs are mixed together: problems!
Nl platelet count 100,000-450,000
When will bleed from trauma and some surgical procedures platelets 50,000-100,000
What happens when platelets reach 20-,50,0000 usually minor spontaneous bleeding in skin, mucous membrane
Life threatning bleeding may occure platelets 10,000
3 mechanisms of thrombocytopenia ↓ production, ↑ destruction/consumption, hypersplenism
Causes of ↓ thrombocyte production bone marrow failure: aplastic anemia, MDS, marrow replacement: leukemia, lymphoma, Marrow toxins: drugs, radiation, ethanol, Nutritional deficiency: B12, folate
What causes pseudothrombocytopenia clotting activation within in the test tube, or EDTA abs against the stuff in test tube
How do we r/o pseudothrombocytopenia repeat CBC and look at the blood smear
Diagnostic tests CBC and smear, bone marrow biopsy, adb US
2 mechanisms w/ drug induced thrombocytopenia myelosupression and immunologcy: abs directed against drug/platelet complex
Signs for drug induced thrombocytopenia detailed hx, sever, rapid onset thrombocytopenia, drug-dependent abs may be present
Tx thrombocytopenia stop offending rugs, usually take 10-14 days, transfuse if necessary (can’t take off drugs)
Do steroids help the tx of thrombocytopenia no they don’t shorten the duration of thrombocytopenia
Most important cause of immune mediated, drug induced thrombocytopenia heparin (HIT)
Two causes if increased platelet destruction Immunologic: HIT, ITP, non immune: DIC, and TTP
Why is HIT so crucial can paradoxicall cause life or limb-thretening venous and/or arterial thrombosis
Patho of HIT heparin→platlets produce PF-4→immune response: IgG, which bind to platelet→significantly ↑ platelet activity makes them burst→↓ number but ↑↑↑↑↑ clotting d/t ↑ granuals in blood stream
Dx of HIT more than 50% decrease from BASELINE platelet count (even if still in nl range)
Which forms of heparine can precipitate HIT all forms, tho less common w/ low MW heparins
What occurs very commonly w/ HIT thrombosis 30-50%
When do we stop heparin with suspect of HIT clinical diagnosis, stop it when you suspect it, dx based on lab and clinical suspecian
What do we do once we stop heparin start another blood thinner
ITP immune thrombocytopenic purpura: make abs against platelet. doesn’t kill you by tomorrow
When does childhood ITP present acute post viral illness, often resolve spontaneously ~2m
When does Adult ITP present insidious onset sxs >2m, rarely resolves spontaneiously
Signs ITP sxs>2m, ecchymosis, petechie in dependent regions, menorrhagia, epistaxis, gingival bleeding
Dx of ITP solo sign is thrombocytopenia (can do a bone marrow bx: ↑megakaroycytes marrow looks fine)
What will lab tests look like for ITP severe thrombocytopenia, CBC nl, smear may show large platelets, nl coag times, ↑ megakaryocytes in bone marrow, platelet ab tests rarely helpful
Tx of ITP steroids, IVIG, winRho, rituxan, splenectomy
Curative tx for ITP spenomeagly (but if platelets are around 30-40,000 range, can live w/ that
Steroids effect on ITP 90% respond w/I 3 weeks, problem?: LT effects don’t stay
How does IVIG tx ITP impairs clearance of IgG coated platelets by competing for binding to pslenic macrophage Fc receptors
What is WinRho and fxn IgG directed against Rh antigen: induces mild hemolytic anemia
What is rituximab monoclonal anti-CD20 ab
Problem w/ chronic ITP does not always need to be treated, platelet counts 20-30,000 are acceptable problem arises when pt’s need surgery
DIC disseminated intravascular coagulation
PAtho of DIC clotting system get really activated, clotting factors are being consumed d/t small clots forming everywhere, cause massive bleeding allover
Signs of DIC bleeding, ↑ clotting times, low fibrinogen, schistocytes on blood smear
Schistocytes RBC that get “closed line” by fibrinogen strands in blood stream, broken RBCs
Causes of DIC infx/sepsis, malignancy, obstetrical catastrophes, placentae, amniotic fluid embolism, retain tissue, severe tissue injury (trauma, burns)
Tx DIC tx underlying cause, transfuse platelets, FFP, cryoprecipitate, consider low dose heparin
What is TTP rare clotting d/o that causes microvasuclar clots all over resulting in thrombocytopenia
Patho of TTP normally ADAMTS-13 cleaves long chunks of vWF, in turn vWF streteches with movement exposed platelet binding sites, causes a clot
Signs of TTP (5) low platelets, microangiopathic hemolytic anemia (schistocytes), nero sxs, renal dysfx, fever
When is it too late when all these 5 sxs show up together. Mortalilty ~90%
When do we want to dx when we see low platelets, and schistocytes
Diff b/w TTP and DIC clotting times are nl, there is not a consumption of clotting factors
TX TTP plasma exchange
Signs for HIT ↓ 50% drop from baseline, heparin exposure, variable INR, PTT, fibrinogen, lifethretning
Signs for ITP healthy, severe thrombocytopenia, CBC otherwise nl, nl INR, PTT, fibrinogen not life threatning
Signs for DIC Sick, falling platelets, prolonged INR, PTT, low fibrinogen, treat underlying cause
Sings for TPP sick, falling platelets, MAHA, nl inr, ptt, fibrinogen, 90% not tx
Pregnancy associated thrombocytopenia :D
Why does hypersplenisms cause thrombocytopenia 1/3 platelets hang there, when bigger, there Is more room, more platelets hang there
Causes of thrombocytosis myeloproliferative: myelogenous leukemia, polycythemia vera and Reactive: iron def, inflammation, malignancy, post
What are the congeneital platelet disorders some type of deficit of the glycoproteins required
Bernard-soulier syndrome defective GP Ib/IV/V, von willebrand factor receptor
Glanzmann’s thrombasthenia defective GP IIb/IIIa fibrinogen receptor
Gray platelet syndrome alpha granule defiency
Acquired types of platelet disorders Drugs: aspirin, Uremia, myeloproliferative d/os
Created by: becker15
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