Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
platelets
Clinical medicine II
| Question | Answer |
|---|---|
| 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
Popular Clinical Skills sets