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LAMP Week 3 > Platelets > Flashcards

Platelets Flashcards

1
Q

How does a platelet plug form?

A

damage to vascular endothelial cells >
send out factors>
attract plts >
form plugs

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2
Q

What are platelets?

A

disk shaped cells produced in the megakaryocytes of the bone marrow (anucleur!)

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3
Q

What is important to know about the anatomy of a platelet?

A

Important to know there are Ag on surface of plts including blood group Ags.

Factors inside that help not only w/plt adhesion to endothelial surface but also progress clotting cascade and clot lysis cascade both of which have to be in sync or you have bleeding or clotting

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4
Q

Plt lifespan?

A

10 days

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5
Q

where do 1/3 of our platelets pool?

A

spleen 2/3 are in circulation

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6
Q

What is the function of platelts?

A

adhesion>
agggregation>
coagulation > fibrin formation

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7
Q

What tests are used for plts?

A
  • Platelet count
  • Bleeding time (or new alternatives)
  • Blood smear morphology USEFUL
  • Platelet aggregometry
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8
Q

What are artifactual causes of thrombocytopenia?

A

– EDTA induced platelet clumping in PURPLE test tube (pt has normal count but it measures as low as specimen is clumped) –> unexplained thrombocytopenia
– Clotted specimen
– Platelet clumping in Myelodysplastic or Myeloproliferative Disorders

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9
Q

What do you do if you suspect artifactual thrombocytopenia?

A

can redraw pt in light blue top tube (Na citrate tube used for coagulation testing) then you won’t get EDTA-produced clumping. Tricky b/c machines are calibrated for EDTA but still good for identifying drastic differences in counts and recognizing clumping artifact. Otherwise best to have someone look at smear.

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10
Q

What causes decreased numbers of megakaryocytes

A

aplastic anemia
drug induced suppression (common)
**viral suppression

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11
Q

What caues impaired production of plts by megakaryocytes

A

– Myelodysplastic processes (myeloid leukemia or preleukemia)
– Megaloblastic processes (Remember? Things that stop you from making DNA but not from making protein)

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12
Q

megaloblastic…..

A

Any situation where you can synthesize protein (cells can grow) but can t synthesize DNA (cells can t divide).
• Examples
– Vitamin B12 or folate deficiency
– Drugs that block DNA synthesis
– Toxins that block DNA synthesis (like EtOH)

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13
Q

What drug/toxin is the MCC of megakaryocyte suppression?

A

ETHANOL!

valproic acid

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14
Q

How do you diagnose decreased platelet/megakaryocyte productioN?

A

blood smear folllowed by Bone marrow bx

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15
Q

A 50 year old male with multiple medical problems including insulin dependent diabetes is being treated with a combination of antibiotics (including Vancomycin) for staphylococcal osteomyelitis/sepsis. After one week of therapy his platelet count drops from 450 k/ul to 20 k/ul (normal 150- 450)

What steps should you take for this work up?

A
  • Step 1 - Is he getting heplock heparin and has he had previous exposure?
  • Step 2 - Order a blood smear and consider ordering labs to rule out DIC.
  • Step 3 - Go through his list of new medications and see what is associated with thrombocytopenia (and what can be discontinued).
  • Step 4 - Carefully consider what meds can/should be changed/discontinued.
  • Step 5 - Once you ve quickly and carefully gone through steps 1-4 and you still can t figure it out, get a Hematology Consultant to help you request a bone marrow biopsy.
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16
Q

What are immune causes of platelet destruction?

A

– Idiopathic thrombocytopenia purpura (ITP) – Neonatal purpura
– Post-transfusion purpura
– Drug induced immune thrombocytopenia – Heparin Induced Thrombocytopenia
– Autoimmune disorders

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17
Q

what are non immune causes of platelet destruction?

A

– Increased loss (bleeding)
– Increased use (pathologic clotting)
– Sequestration (alcoholic cirrhosis–> complementary splenomegaly)

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18
Q

What is ITP?

A

• Presumed due to anti-platelet antibodies
• Associated with viral infections and
autoimmune disorders

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19
Q

How do you diagnose ITP?

A

Bone marrow biopsy findings and anti- platelet antibody studies help support the clinical diagnosis of immune platelet destruction

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20
Q

What percent of neonates have some degree of thrombocytopenia?

A

1-4% of neonates have some degree of thrombocytopenia and account for 20-40% of NICU admissions.

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21
Q

What is hte MCC of severe neonatal thrombocytopenia?

A

Most common cause of severe neonatal thrombocytopenia is fetomaternal platelet incompatability
• Antibodies directed against Human platelet antigen (HPA) -1a (previously known as Pl-A1) account for 90% of cases in Caucasians

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22
Q

How do you diagnose neonatal purpura?

A

Maternal serology; Maternal and Paternal platelet antigen testing (newer approach is to genotype the parents and infant)

Fetomaternal platelet incompatibility is incredibly rare. Auto rec inheritance of absence of this HPA-1A antigen. If mom is HPA-1A negative and baby is positive, mother will form antibodies. Need to be prepared for this and prepared for the birth of this baby. Be prepared to transfuse w/these rare HPA-1A platelets, preferably harvested from mom. Very rare. So not screened for this. When baby born w/mild thrombocytopenia, mom and baby both get tested for HPA-1A antigen and antibody. If mom is negative for antigen, subsequent pregnancies are carefully monitored and planned.

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23
Q

How do you tx neonatal purpura?

A

Prenatal IVIgG/ Transfuse infant with ABO compatible/ (HPA) -1a negative platelets

24
Q

What is post-transfusion purpura?

A
  • Occurs in HPA-1a (Pl-A1) negative individuals

* Usually 1-2 weeks after first blood transfusion exposure, more rapidly after any subsequent exposure.

25
Q

How do you diagnose post transfusion purpura?

A

Diagnosis: Serology for anti-platelet antibodies (ELISA) and/or HPA Genotyping

26
Q

What drugs cause drug induced immune thrombocytopenia?

A
  • Innocent bystander (Quinine/Quinidine)
  • Hapten mechanism (Penicillin)
  • Heparin Induced Thrombocytopenia**
27
Q

What is the pathophys of HIT?

A

we all have circulating Platelet Factor 4 and heparin binds to it.

Bovine heparin has higher amount of high molecular weight heparin fraction, which bind more PF4 and some individuals make antibodies against the combo of heparin and PF4.

These antibodies bind to activated platelets which then get picked out by the spleen, causing thrombocytopenia.

28
Q

what is the incidence of HIT?

A
  • 2-20% of patients who receive unfractionated heparin
  • Higher incidence with bovine than porcine heparin
  • Bovine heparin has greater fraction of high molecular weight heparin
29
Q

How do you diagnose HIT?

A

• Heparin associated Platelet Aggregation
– Only 50% sensitive
– Requires a heparin free specimen

• ELISA for Heparin-PF4 Complex* STANDARD!!
– 100% Specific?; at least 90% sensitive
– DOES NOT require a heparin free specimen
– FDA approved in 1999 is widely available
– False positives?
• Serotonin Release Assay

no longer do aggregation test. Do ELISA instead. It’s Much more specific and sensitive. Not sure about its false positives. ELISA is the standard. It’s not expensive.

30
Q

What are causes of nonimmune platelet destructioN?

A

MAHA (TTP, HUS)
DIC
Congenital plt abnormalities

31
Q

how do you diagnose non immune peripheral platelet destruction?

A
  • Blood smear
  • Coagulation testing
  • Reticulocyte count
  • Lactate dehydrogenase • Haptoglobin
32
Q

what is happening in TTP?

A

There is an enzyme (ADAMTS13) that is responsible for breaking down HMW multimers of von willebrand factor (important in early clotting and lysing clots). If you can’t break down these HMW VW factors, then you get persistent clotting. Microclots form in circulation. Need ADAMTS13. Some infants born genetically deficient and adults who develop (due to infection or pregnancy or drugs or malignancies) antibodies against ADAMTS13. Now have test to measure level of ADAMTS13 and detect antibodies against ADAMTS13.

33
Q

What should you do if you have a child/adult who presents w/ classif featurs of ttp/hus?

A

have someone look at smear and look for fragments. Get labs to confirm microangiopathic process (TTP or HUS). Then order ADAMTS13 antigen and ADAMTS13 antibody. If low antigen w/o antibody, then it’s hereditary deficiency (more typically in infant or child). If low antigen w/antibody, immune-mediated destruction (more common in adults). Managed differently so ordered in both.

34
Q

sxs of ttp/hus

A 
fever
ANEMIA
Thrombocytopenia
Renal dyxfxn
neuro sxs
35
Q

adult cases of TTP are thought to be linked to ….

A

acquired (autoimmune) deficiency of the enzyme ADAMTS 13

36
Q

pediatric cases of ttp may be related to …

A

congenital deficiency of ADAMTS 13

37
Q

what other infections are associated wtih ttp?

A

congenital deficiency of ADAMTS 13

38
Q

what is seen on a blood smear /labs of a pt w/ ttp?

A

anemia with red cell fragments (schistocytes) on blood smear, thrombocytopenia, elevated LDH, low haptoglobin

39
Q

how do you tx ttp?

A

plasma exchange

40
Q

Obese 35 year old African-American female presents to ED on 12/26/2009 with Worst flu of my life. I’m sick every morning

  • CBC shows normocytic anemia.
  • Plt count is super low. Not her baseline. Marked thrombocytopenia.
  • Pregnancy test is negative.
  • LDH is elevated.
  • Haptoglobin is very low.
  • Smear shows fragments. Recommended ADAMTS13.
  • ADAMTS13 activity very low. Antibody was positive.
A

classic TTP

41
Q

thrombocytopenia secondary to platelet sequestration can be caused by…

A

splenomegaly

congenital vascular deformities (cavernous hemangioma)

42
Q

What causes primary thrombocytosis?

A

– Myeloid neoplasms

43
Q

What causes secondary thrombocytosis?

A

..they can be additive

– Asplenia and functional asplenia – Iron deficiency
– Acute and chronic inflammation – Malignancies
– Hemorrhage

44
Q

how do you diagnose primary vs secondary thrombocytosis?

A
  • Suspect primary when platelet count is greater than 600,000/ul or when there is also basophilia (Basophils greater than 200/ul)
  • A BLOOD SMEAR review (by a competent pathologist or hematologist) is a good first step.
  • If clinical history and blood morphology are suspicious for a primary (neoplastic) thrombocytosis then a BONE MARROW biopsy WITH cytogenetic analysis is indicated
45
Q

A 70 year old male with a history of celiac sprue diagnosed by endoscopic biopsy but with no other history of abdominal surgery presents with complaints of weakness and gastrointestinal discomfort.

  • Microcytic anemia (new for him).
  • Iron deficient.
  • Smear showed signs of asplenia.
A

Combo of IDA and functional asplenia –> elevated plts

  • This is a real case
  • The indices are suspicious for iron deficiency (which can produce secondary thrombocytosis and, incidentally, slight basophilia)
  • When platelets are greater than 600 k/ul and there is basophilia, you order a blood smear morphology to look for evidence of a primary myeloproliferative disorder
46
Q

What are congenital causes of plt dysfunction?

A

Rare - the most common is von Willebrand Disease which is really a deficiency of von Willebrand factor; others are things like giant platelet syndromes, etc

47
Q

What are acquired cuases of plt dysfunction?

A

aspirin! - MC
NSAIDS!

– Uremia
– Post cardiac bypass pump (depletes alpha granules)
– Acquired von Willebrands (seen with some chronic myeloproliferative disorders like polycythemia vera)

48
Q

What is bleeding time? Is it a good test?

A

NOT a good test.

  • Lab tech makes a measured incision on clean volar skin at a specific cuff pressure and measures the time to clotting.
  • Rough measure of the interaction between platelets, tissue and clotting factors invalid at platelet counts less than 90K/ul.
  • There are some coagulopathies (e.g. von Willebrand s subtypes) and functional platelet problems (e.g. aspirin) that are only detected by a prolonged bleeding time.
49
Q

When should you order a BT?

A

helpful in diagnosing von willebrands

50
Q

When should you NOT order a BT?

A

when plts are < 90K

51
Q

A 6 year old girl is having a tonsillectomy.
• There is no history of bleeding or bruising.
• CBC and INR are normal.
• APTT = 38 seconds (normal range 21-31 sec). APTT corrects with 1:1 mixing study.
• Bleeding Time = 20 minutes (normal < 10minutes).

A
  • This is an example of von Willebrand s disease which, although rare, is the most common inherited bleeding disorder.
  • This is the one-in-a-thousand situation when an ENT surgeon is glad that they did pre-op screening. Even if they only did the APTT this could have been picked up (don t forget, though, APTT is normal in some von Willebrand patients).
52
Q

what are drawbacks of BT?

A
  • poorly reproducible
  • operator dependent (and labor intensive) • unpleasant, especially for children
  • potential scar formation
  • unsuited to serial or repeated testing
  • questionable sensitivity to platelet defects
  • poor correlation to bleeding tendency
53
Q

What is hte most used alternative to bleeding time?

A

platlet closure time

DO NOT USE if plts are less than 90K

54
Q

what is platelet aggregometry?

A

Measures platelet function by measuring platelet aggregation in response to platelet agonists (ADP, collagen, ristocetin).

55
Q

What are downsides of platelet aggregometry?

A
  • Expensive
  • Labor intensive
  • Requires pathologist interpretation
  • Order this when you have an unexplained increase in the bleeding time (or platelet closure time), however, by this point in the workup you’ve gotten a Clinical Hematology or Coagulation Consultation and they are ordering the tests!
56
Q

should we use MPV?

A

Mean platelet volume

MPV is useless. Everybody’s plts swell in EDTA but all to different degrees and at different rates. Only recently realized and published. Previously marketing people for automated CBC machines were trying to promote this MPV value. Turns out it’s not interpretable.

57
Q

A previously healthy 40 year old African- American female medical records clerk presents to the ER with mouth pain. Her gums appear swollen and while she is talking to you her nose starts bleeding.

WBC 22.5
Hgb 7.4
Plt 10k

A

Leukocytosis, anemia and thrombocytopenia

Dx ended up being Acute promyelogenous? leukemia w/evidence of diffuse coagulation. Life threatening leukemia. Pt was treated w/tretinoic acid and IV vitamin A and never relapsed.

LAMP Week 3 (11 decks)

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