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Clinical Microscopy > Platelet Abnormalities > Flashcards

Platelet Abnormalities Flashcards

1
Q

Thrombosis results from, and in turn causes, three interrelated factors (hypercoaguable state/activation of blood coagulation, vascular endothelial injury/inflam of bv, circulatory stasis/decreased blood flow

A

Virchow’s Triad (1854)

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2
Q

Hypercoagulable states or conditions are usually associated with a?

A

predisposition to venous

thrombosis and/or arterial thrombosis (acquired or inherited)

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3
Q

Hypercoagulable states are secondary to

A 
• Secondary to:
→ Malignancy
→ Pregnancy and pre-partum period
→ Estrogen therapy
→ Trauma or surgery of lower extremities, hips, abdomen, or pelvis
→ Sepsis
→ Thrombophilia
→ Inflammatory bowel disease*
→ Nephrotic syndrome*
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4
Q

Vascular endothelial injury involves abnormalities in?

A

endothelium (ie atherosclerosis, assoc. vascular inflam)

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5
Q

This is secondary to atrial fibirillation, left ventricular dysfunction, immobility or paralysis, venous insufficiency or varicose veins, venous obstruction from tumor, obesity or pregnancy

A

Circulatory Stasis

*Abnormalities of haemorheology and turbulence at vessel
bifurcations and stenotic regions

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6
Q 
This is secondary to:
→ Trauma or surgery
→ Venipuncture
→ Chemical irritation
→ Heart valve disease or replacement
→ Atherosclerosis
→ Indwelling catheters*
A

Vascular endothelial injury

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7
Q

Formation of an abnormal mass within the vascular system which comes from RBCs, WBCs, platelets leading to improper circulation (=necrosis/gangrene)

A

Thrombosis

*Arterial: comp. of platelet aggregates/ white thrombus
Venous: cons. of fibrin and RBC/red thrombus (see table 1: a vs v thrombus)

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8
Q

Acquired predisposing risk factors for venous thrombosis (can be prevented)

A
  • Increasing age
  • Pregnancy (due to hormonal factor; risk:2-6x higher)
  • DIC
  • Elevated levels of microparticle tissue factor (membrane vesicles that can be shed from many cell types)
  • malignant neoplasms
  • surgery/trauma
  • prolonged immobilization
  • smoking
  • obesity
  • arteriosclerotic CVD
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9
Q

venous thrombosis partly due to increasing age is associated with what?

A

increase in procoagulant factors:
→ D-dimer
→ Fibrinogen
→ Factor VIII

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10
Q

What are the risk factors for venous thromboembolism in pregnancy?

A

→ Obstruction of venous return by the gravid uterus
→ Venous astonia caused by hormonal factors
→ Acquired prothrombotic changes in hemostatic proteins (increased plasma levels of VWF, fibrinogen, and factors VII, VIII, and X, essentially unchaged Factors II, V, IX, and XII and declined Factor XIII)

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11
Q

An increase in procoagulant factors due to perturbed endothelial cells and activated mononuclear cells, which may produce proinflammatory cytokines that mediate coagulation activation is associated with which factor for venous t.?

A

DIC
→ Activation of coagulation is initiated by tissue factor expression on activated mononuclear cells and endothelial cells
→ Downregulation of physiologic anticoagulant mechanisms
→ Inhibition of fibrinolysis by endothelial cells
• DIC is an end-complication of infection or sepsis
→ When you have DIC, the resulting event will be death

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12
Q

Elevated levels of microparticle tissue factor can be seen in

A

Atherosclerotic vascular disease, severe infections and

malignancy

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13
Q

refers to a group of conditions where blood clots more easily than normal which may lead to thrombosis

A

thrombophilia or thrombocytosis

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14
Q

[thrombophilia or thrombocytosis] homozygous state can be incompatible with life or present at a very early age

A

Hereditary thrombophilia

*Most common:
• Activated protein C (APC)-resistant factor V Leiden mutation (APC is a natural anticoagulant)
• Elevated prothrombin levels caused by the prothrombin G20210A (or Factor II) polymorphism
• Increased Factor VIII Level
• Homozygous C677T
• Polymorphism in
Methylenetetrahydrofolate
reductase
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15
Q

[thrombophilia or thrombocytosis]
→ Usually become apparent in adulthood
→ Can happen as a result of other medical problems that have developed or problems with the immune system

A

Acquired Thrombophilia

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16
Q

rarely seen in hereditary thrombophilia

A 
Rare:
• Protein C deficiency
• Protein S deficiency
• Antithrombin deficiency
Very Rare:
• Dysfibrogenemia
• Homozygous homocystinuria
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17
Q

Other acquired risk factors for venous thrombosis

A
  • Long flights
  • Myeloproliferative diseases
  • Superficial vein thrombosis
  • Previous venous thrombosis
  • Pregnancy & puerperium
  • Use of female hormones
  • Antiphospholipid antibodies
  • Hyperhomocysteinemia
  • Activated Protein C resistance unrelated to Factor V Leiden
  • Varicose veins
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18
Q

laboratory examination for thrombophilia (screening test NA)

A

APC resistance where Partial Thromboplastin Time (PPT)

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19
Q

More expensive specific assays

A
  • Factor V Leiden
  • Protein C and S Assay
  • Anti-thrombin assay
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20
Q

abnormal results associated with APC resistance (Decreased ratio) test

A 
Pregnancy, use of oral contraceptives,
stroke, presence of lupus anticoagulant,
increased Factor VIII levels, autoantibodies
against activated protein C, use of
anticoagulants
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21
Q

abnormal results associated with decreased level of protein C

A

Liver disease, use of oral anticoagulants,
Vitamin K deficiency, childhood, DIC,
presence of autoantibodies against protein
C

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22
Q

abnormal results associated with Hyperhomocysteinemia

A

Deficiencies of folate, Vitamin B12, or B6,
old age, renal failure, excessive
consumption of coffee, smoking

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23
Q

abnormal results associated with dysfirbinogenemia

A

neonates, liver disease

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24
Q

abnormal results associated with decreased level of antihtrombin

A

Use of heparin, thrombosis, DIC , liver disease, Nephrotic syndrome

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25
Q

abnormal results associated with Increased Factor VIII levels

A

Pregnancy, use of oral contraceptives,
exercise, stress, older age, Acute phase
response, liver disease, Hyperthyroidism

26
Q

abnormal results associated with Presence of
Lupus Anticoagulant and Increased Titer
of Anticardiolopin
Antibody

A

Systemic lupus erythematosus,
Antiphospholipid syndrome, autoimmune
diseases, liver disease, Hyperthyroidism
(anticardiolipin ab: + infectious diseases)

27
Q

abnormal results associated with increased level of fibrinogen

A

acute phase rxn, pregnancy, old age, atherosclerosis, smoking

28
Q

abnormal results associated with decreased level of protein s

A

Liver disease, use of oral anticoagulants, Vitamin K deficiency, pregnancy, use of oral contraceptives, nephrotic syndrome, childhood, presence of autoantibodies against Protein S, DIC

29
Q

(see trans for treatment of thrombophilia)

A

(see trans for treatment of thrombophilia)

30
Q 
• Most common symptom is bleeding
• Usually caused by
→ Decreased production of platelets
→ Increased destruction of platelets
→ Sequestration
→ Pseudothrombocytopenia
A

Thrombocytopenia

31
Q

may be secondary to marrow failure which is secondary to aplastic anemia, chemotherapy and toxin

A

decreased platelet rpoduction

32
Q

Other conditions which cause decreased platelet prod

A 
• B12, folate or, rarely, iron deficiency
• Viral infection
• Drugs (Alcohol, Estrogens, Thiazides, Chlorpropamide, Interferon)
• Amegakaryocytic thrombocytopenia
→ Myelodysplasia (pre-leukemia)
→ Immune (related to apalastic anemia)
• Cyclic thrombocytopenia (rare)
• Inherited thrombocytopenia
33
Q

• Congenital aplastic anemia (Fanconi’s anemia)
• Congenital amegakaryocytic thrombocytopenia
• Thrombocytopenia with absent radius syndrome (recessive)
• Bernard-Soulier syndrome (recessive, giant platelets, defective function, GPlb defect)
• May-Hegglin anomaly and related disorders (dominant,
leukocyte inclusions, giant platelets, MYH-9 mutation)
• Other autosomal dominant syndromes (platelets may be normal or giant)
• Wiskott-Aldrich syndrome (X-linked, immunodeficiency,
eczema)

A

Inherited Thrombocytopenia

34
Q

accounts for about 75% of thrombocytopenia

A

Benign thrombocytopenia of pregnancy (5% in term pregnancies, Asymptomatic, mild, occurs late in gestation)

35
Q

increases in incidence during pregnancy

A 
Idiopathic thrombocytopenia (increased incidence in
pregnancy

*Microangiopathy (preeclampsia/eclampsia, HELLP) may also lead to thrombocytopenia in pregnancies

36
Q

increased platelet CONSUMPTION in thrombocytopenia are due to

A
  • Immune destruction
  • Intravascular coagulation (DIC or localized)
  • Microangiopathy
  • Damage by bacterial enzymes, etc.
37
Q

Immune platelet DESTRUCTION in thrombocytopenia may result from

A
  • Immunologic destruction of platelets resulting when antibodies coat platelets that are then destroyed by macrophages [LabCE]
  • Autoimmune (ITP) (Childhood/adult)
  • Drug-induced (Heparin, Quinine (anti-malarial drug))
  • Immune complex (infection, etc.)
  • Alloimmune (Post-transfusion purpura, Neonatal purpura) → Possibly due to coating of patient’s platelet by donor platelet microparticles
38
Q

Caused by re-exposure to foreign platelet antigen via blood product transfusion which typically presents as sudden onset of severe thrombocytopenia (<10K) 5-7 days after transfusion

A

Post-transfusion purpura

*Almost all cases in multiparous women
→ HPA-1a antigen most commonly involved (98% of the
population) [diagnosis by anti-hpa-1a alloabs in serum]

39
Q

This is treated by
→ IVIg
→ Avoid giving HPA-1a positive platelets
→ Wash RBC to remove passenger platelets

A

Post-transfusion purpura

40
Q

What is involved in thrombocytopenia during infection?

A

• Immune complex-mediated platelet destruction
→ Childhood ITP, Bacterial sepsis, Hepatitis C, other viral infections
• Activation of coagulation cascade (Sepsis with DIC)
• Vascular/endothelial cell damage
→ Viral hemorrhagic fevers (e.g. Dengue Fever)
→ Rocky Mountain Spotted Fever
• Damage to platelet membrane components by bacterial
enzymes (e.g. S. pneumoniae sialidase)
• Decreased platelet production
→ Viral infections (EBV, measles)
• Mixed production defect/immune consumption
→ HIV infection

41
Q

In Heparin Type drug which induces typically mild to moderate thrombocytopenia, What complex forms on platelet surface?

A

Heparin-platelet factor 4 complex

*antibody binds to this complex

42
Q

In Heparin type drug which is associated with thrombosis in many patients, fc portion of antibody binds to where on platelet?

A

platelet/monocyte Fc receptor

43
Q

In Heparin type drug, what is triggered?

A

Platelet and monocyte activation

44
Q

Type of drug which binds to platelet membrane and causes typically severe thrombocytopenia with bleeding. Some patients develop microangiopathy with renal failure (HUS)

A

Quinine type

*Antibody binds to drug

45
Q

In quinine type drug, what does the exposed fc portion do?

A

Exposed Fc portion targets platelet for destruction

Directly destroys platelets

46
Q

How is ITP diagnosed?

A

by exclusion (no known cause)

47
Q

Forms of ITP?

see epidemiology

A 
Childhood form (may follow viral infxn, vaccination)
Adult form (non-prodromal, chronic, recurrences common, spontaneous remission rate about 5%)
48
Q

What are present in most cases of ITP (often specific for platelet membrane glycoprotein; usually autoimmune)?

(mech still not clear)

A

Platelet-reactive autoantibodies

*coat platelets wc are then cleared by tissue macrophages and destroyed in spleen

49
Q

Some patients wc experience impaired platelet production in ITP undergo?

A
  • Intramedullary destruction

* Enhanced thrombopoietin clearance

50
Q

most common manifestation in ITP?

A

mucosal bleeding

[others: petechiae, purpura, major internal/intracranial bleeding (rare; results in death), no consti symptoms or splenomegaly, normal blood counts and coag parameters]

51
Q

T or F: ITP blood smears exhibit schistocytes and platelet clumps

A

False

52
Q

T or F: Marrow in ITP shows abnormal megakaryocytes

A

normal or increased megakaryocytes (compensation for decreased platelet count)

53
Q

T or F: confirmatory lab testing for itp is necessary

*diagnosis mainly based on clinical history

A

false

(methods: serum antiplatelet antibody assay [poor sensitivity and expensive], test for specific anti-platelet gp abs [more specific])

54
Q

How is ITP managed in children with platelets >20-30K and no bleeding?

A

no treatment

**generally for ITP in children: platelet transfusion (if needed)

55
Q

How is ITP managed in children with platelets <10-20K with bleeding?

A 
intravenous immunoglobulin (IVIg) or corticosteroids
• Prednisone, 1-2mg/kg/day
• Single dose IVIg 0.8-1g/kg as effective as repeated dosing
56
Q

How is ITP managed in children with chronic ITP (>12 mos.) or refractory disease with life-threatening bleeding?

A

Splenectomy
• Pre-immunize with pneumococcal, H. influenza and meningococcal vaccines (vaccines for encapsulated
bacteria) because spleen is responsible for eliminating encapsulated bacteria

57
Q

usual treatment for ITP in Newly-Diagnosed adults

→ Indications:
• Platelets <20-30K (you may do platelet transfusion)
• Active bleeding or high bleeding risk, platelets <50K

A

platelet transfusion or steroids and ig

see first line treatment of ITP

58
Q

When is emergency treatment of ITP (platelet transfusion + high dose steroids/continuous IVIg, rVIIa, antifibrinolytics, emergency splenectomy) done?

A

when the patient is severely bleeding (platelet <10,000)

59
Q

it is not a true condition wherein there is an artificially low platelet count due to in vitro clumping of platelets (involves chemical factors ie chelating agents such as EDTA)

A

Pseudothrombocytopenia

*Seen in healthy individuals and in a variety of disease states

60
Q

→ Marked fluctuations in platelet count without apparent cause
→ Thrombocytopenia disproportionate to symptoms
→ Clumped platelets on blood smear
→ “Platelet satellitism”- platelets stuck to WBC
→ Abnormal platelet/ leukocyte histograms
→ Platelet count varies with different anticoagulants

A

Pseudothrombocytopenia

Clinical Microscopy (10 decks)

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