Quiz – Platelets high and low

By William Aird

Abbreviations:

Hb – hemoglobin

Hct – hematocrit

MCH – mean corpuscular hemoglobin

MCHC – mean corpuscular hemoglobin concentration

MCV – mean cell colume

RBC – red blood cell count

RDW – red blood cell distribution width

RDW-CV – RDW coefficient of variation

RDW-SD – RDW standard deviation

Note: The terms MCV, MCH and MCHC are all mean values and by definition apply to populations of red cells. To simplify matters, we use the term more loosely to include descriptions of single cells. For example, we may refer to a large red cell as one with a high MCV, or a cell with increased central pallor as one with a low MCHC.

Question 1

What is the principle growth factor that regulates the platelet count?

a
G-CSF
b
Interleukin-6
c
Thrombopoietin
Thrombopoietin is the physiologically relevant regulator of platelet production. It is a glycoprotein hormone produced mainly by the liver that stimulates the formation of megakaryocytes and production of platelets.
d
Interleukin-11
e
Tumor necrosis factor-alpha

Thrombopoietin is produced primarily by the liver. It stimulates the production and differentiation of megakaryocytes.

Question 3

How is extreme thrombocytosis defined?

a
Platelet count > 750 x 109/L
b
Platelet count > 1000 x 109/L
Correct. Some authors use <1500 x 109/L as a threshold.
c
Platelet count > 2000 x 109/L

Patients with extreme thrombocytosis have been referred to as platelet millionaires! That is because 1000 x 109/L is 1 million/ul.

Question 4

True or false: there is no evidence that secondary (reactive) thrombocytosis is associated with an increased risk of thrombosis.

a
True
b
False

Question 2

How is thrombocytosis defined?

a
Platelet count > 350 x 109/L
b
Platelet count > 450 x 109/L
Some labs use >400 x 109/L as a cutoff.
c
Platelet count > 500 x 109/L
d
< 1000 x 109/L

Source. Reference 2 refers to this paper.

What are treatment goals in heparin-induced thrombocytopenia?

•PMID: 17124091

In primary thrombocytosis:

a
The defect resides in the platelet precursors
b
The defect resides in the environment of the platelet precursor
c
The defect resides in the spleen

In primary thrombocytosis, the defect resides in the stem or progenitor cell, rendering these cells impervious to normal growth control mechanisms.

True of false: patients admitted to the ICU may have thrombocytopenia, but thrombocytosis is virtually unheard of.

a
True
b
False
About 2% of patients admitted to ICU are reported to have platelet counts > 500 × 109/L at time of admission.

True or false: infection-related secondary (reactive) thrombocytosis is only associated with chronic infections.

a
True
b
False
Thrombocytosis may be seen in patients with acute infections, including pneumonia, urinary tract infection and soft tissue infection.

What percentage of patients with newly diagnosed essential thrombocythemia have thrombocytosis?

a
10%
b
20%
c
50%
d
85%
e
100%
Thrombocytosis is a major criterion for diagnosis.

Mean platelet lifespan is about:

a
1 day
b
2 days
c
10 days
Platelets survive for up to 10 days under normal conditions.
d
30 days
e
120 days

This 1966 study used Isotopic labelling techniques to tag autologous platelets and reinfuse them back to normal individuals. See Najean et al.

How are levels of circulating thrombopoietin regulated?

a
By the liver
b
By platelet mass
The amount of circulating thrombopoietin is regulated by the mass of circulating platelets. They bind thrombopoietin, providing a negative feedback mechanism to control thrombopoiesis.
c
By the kidney

What is the frequency of splenomegaly in essential thrombocythemia?

a
5-10%
b
20-30%
c
40-50%
d
60%
e
80%

Splenomegaly is more common in myelofibrosis than in essential thrombocythemia or polycythemia vera

A reminder of the differential diagnosis of splenomegaly:

In a patient with thrombocytosis, the presence of pencil cells on the peripheral smear suggest which etiology for the elevated platelet count:

a
Trauma
b
Tubercolosis
c
Thrombopoietin receptor agonist therapy
d
Iron deficiency anemia
e
Pernicious anemia

Iron deficiency anemia is associated with presence of microcytic hypochromic red cells, pencil cells and increased platelets (blue circles) on peripheral smear.

Why would you ever order a von Willebrand disease screen in a patient with thrombocytosis?

a
Because hereditary von Willebrand disease may be associated with thrombocytosis
b
Because von Willebrand factor production is suppressed in essential thrombocythemia
c
Because elevated platelet counts may bind von Willebrand factor, leading to an acquired von Willebrand disease
d
Because von Willebrand factor is an acute phase reactant that may increase in conditions associated with secondary (reactive) thrombocytosis

Severe thrombocytosis may result in acquired von Willebrand disease (aVWD), as characterized by reduced VWF activity and loss of high MW VWF multimers, due to excessive binding of platelet GPIb receptors to circulating VWF

What are recognized complications of essential thrombocythemia?

a
Thrombosis
b
Hemorrhage
c
Gastric cancer
d
Myelofibrosis
e
Acute leukemia

What genetic tests are recommended in patients with suspected essential thrombocythemia (together or sequentially)?

a
JAK2 mutation
b
CALR mutation
c
Thrombopoietin mutation
d
Jak1 mutation
e
MPL mutation

Patients with essential thrombocythemia may carry JAK2 (V617F), an MPL substitution, or a calreticulin gene (CALR) mutation. These are called driver mutations. Each genotype is associated with specific clinical characteristics, including differences in symptomatic burden, hematological values, and risk of thrombosis and bleeding.

Jak2MplCALR
Prevalence60% of patients
with essential thrombocythemia
1-4% of patients
with essential thrombocythemia
25% of patients
with essential thrombocythemia
AgeXXYounger vs JAK2Val617Phe genotype
Platelet countXXHigher vs JAK2Val617Phe genotype, similar to Mpl-mutated genotype
HemoglobinXXLower vs. JAK2Val617Phe genotype
Thrombosis riskXXLower vs. JAK2Val617Phe and MPL-mutated genotypes
Leukemic transformationXXNo difference vs. AK2Val617Phe genotype
Fibrotic transformationHigher vs. JAK2Val617Phe genotype No difference vs. AK2Val617Phe genotype

X

True or false: aspirin is recommended in patients with secondary (extreme) thrombocytosis.

a
True
b
False
Antiplatelet therapy is not recommended, even in patients with extreme thrombosis, due to lack of evidence for thrombotic risk and theoretical risk of paradoxical bleeding.

In the interest of full disclosure, the single guideline that is focused on “investigation and management of adults and children presenting with a thrombocytosis” from 2010 suggests considering the use of aspirin in patients with secondary (reactive) thrombocytosis, but it is doubtful that most clinicians would agree with this:

Learn more here.

In a patient with thrombocytosis, the presence of Howell Jolly bodies on the peripheral smear suggest which etiology for the elevated platelet count:

a
Hypersplenism
b
Trauma
c
Alcohol intoxication
d
Asplenia
e
Essential thrombocythemia

2016 World Health Organization (WHO) Criteria for diagnosis of ET includes major and minor criteria. Which three major criteria are always required?

a
Sustained platelet count > 450 × 109/L
b
Bone marrow biopsy showing proliferation mostly of megakaryocytic lineage with abnormal megakaryocyte morphology
c
Not meeting WHO criteria for BCR-ABL+ CML, PV, PMF, myelodysplastic syndromes, or other myeloid neoplasm
d
Presence of JAK2, CALR, or MPL mutation

Platelets are:

a
Nucleated fragments of megakaryocytes
b
Budded cytoplasmic fragments from red cells
c
Anucleate megakaryocyte fragments
d
Derived from single megakaryocytes (one megakaryocyte gives rise to one platelet)

From D. Saintillan:

The in vivo production of platelets takes place inside bone marrow, where large cells known as megakaryocytes develop long tubular membrane projections, or proplatelets, which continuously break up into small fragments destined to mature into functional platelets and enter the blood stream. The formation and growth of these tubular structures and their subsequent fragmentation are driven by ATP-powered processes involving biopolymers and molecular motors.

From Machlus and Italiano:

To assemble and release platelets, MKs become polyploid by endomitosis (DNA replication without cell division) and then undergo a maturation process in which the bulk of their cytoplasm is packaged into multiple long processes called proplatelets, and the nucleus is extruded. An MK may extend 10–20 proplatelets, each of which starts as a blunt protrusion that over time elongates, thins, and branches repeatedly. Platelets form selectively at the tips of proplatelets. As platelets develop, they receive their granule and organelle content as streams of individual particles transported from the MK cell body 

How large is a platelet?

a
< 1 micron diameter, 30 fL volume
b
3-5 microns diameter, 30 fL volume
c
1-3 micron diameters, 10 fL volume
Platelets are small anucleate cell fragments that have a characteristic discoid shape and range from 1 to 3 µm in diameter and about 10 fL in volume.

Scanning electron microscope of a typical red blood cell, platelet and... |  Download Scientific Diagram
Scanning electron microscope of a typical red blood cell, platelet and white blood cell (Source: en.wikipedia.org)

Which of the following are causes of primary thrombocytosis?

a
Essential thrombocythemia
b
Multiple myeloma
c
Polycthemia vera
d
Myelodysplasia
Yes, myelodysplastic syndrome with del (5q)
e
Myelodysplastic/myeloproliferative neoplasms (MDS/MPN) overlap syndrome
Yes, especially MDS/MPN with ring sideroblasts and thrombocytosis (MDS/MPN-RS-T)

The following are causes of spurious thrombocytosis:

a
Neoplastic cell cytoplasmic fragments
b
Schistocytes
c
Bacteria
d
Howell-Jolly bodies
e
Dohle bodies

Question 8

Iron deficiency may be associated with:

a
Thrombocytosis
Secondary (reactive) thrombocytosis occurs in about 10% of patients with iron deficiency anemia (PMID: 19658005).
b
Abnormal platelet function
c
Thrombocytopenia
Thrombocytopenia occurs in about 2% of patients with iron deficiency anemia (PMID: 19658005).

Prevalence of thrombocytopenia and thrombocytosis in patents with iron deficiency anemia. At bottom right is a schematic of megakaryopoiesis and platelet production. Though the mechanism of thrombocytosis in iron deficiency has not been clearly worked out, it appears to involve increased differentiation of megakaryocytes from bipotential progenitor cells.

Question 9

In a patient with a platelet count of 1000 x 109/L, what parameter do you need to calculate the plateletcrit?

a
Mean platelet granule content
b
Variation in platelet size
c
Mean platelet volume (MPV)
Correct. By analogy with the Hct, the plateletcrit = MPV x platelet count. Normal range is 0.20-0.36%.
d
RDW/Hct

Question 5

What is the preferred treatment for secondary (reactive) thrombocytosis?

a
Aspirin
b
Plateletpheresis
c
Hydroxyrurea
d
Treatment of the underlying cause
Resolution of underlying cause will lead to normalization of the platelet count.

Outline of secondary (reactive) thrombocytosis shows macrophage-derived IL-6, which induces expression of thrombopoietin. Thrombopoietin then promoters production of platelets from megakaryocytes in the bone marrow. In some cases, macrophage release of IL-6 (and other chemokines/cytokines) is mediated by pathogens, in other cases by non-pathogenic inflammatory triggers, including cancer. Thrombocytosis in iron deficiency anemia is believed to be mediated by increased differentiation of megakaryocytes from bipotential progenitor cells. Treatment of secondary (reactive) thrombocytosis is to treat the underlying cause.

Which is more common:

a
Primary (clonal) thrombocytosis
b
Secondary (reactive) thrombocytosis
Secondary or reactive thrombocytosis accounts for ≥ 85% of case

Question 6

Which of the following are established causes of secondary (reactive) thrombocytosis?

a
Chronic kidney disease
b
Hemolysis
c
Asplenia
d
Hyperthyroidism
e
Surgery

Schematic of causes of both primary and secondary thrombocytosis

What is heparin-induced thrombocytopenia (HIT)?

a
An immune disorder
Correct. HIT is mediated by anti-PF4 platelet-activating antibodies.
b
A non-immune inflammatory disorder
c
A direct drug effect on platelets
d
Heparin-induced splenic sequestration of platelets

When does the platelet count typically begin to drop in heparin-induced thrombocytopenia (following initiation of heparin)?

a
1 day
This would qualify as rapid-onset HIT, seen in patients who already have circulating anti-PF4/heparin antibodies because of recent heparin exposure (usually < 30 days, occasionally < 90-100 days earlier).
b
2 days
c
5-10 days
d
>10 days
This would qualify as delayed-onset HIT, which develops or worsens after heparin has been discontinued. Thrombotic manifestations are delayed for days to weeks after heparin discontinuation and discharge.

Nothing like a visual! Here you will note the platelet count starting to fall on day 5 after initiation of heparin. You will also note the earlier reduction in platelet count, which is typical in patients undergoing surgery. Source

What is spontaneous heparin-induced thrombocytopenia (HIT)?

a
HIT that occurs when heparin is administered spontaneously
b
HIT that occurs spontaneously following discontinuation of heparin
c
HIT that occurs spontaneously in the absence of heparin exposure
Correct. Unexplained thrombocytopenia and/or thrombosis are accompanied by laboratory evidence of high-titer platelet activating anti-PF4/heparin antibodies.
d
Thrombosis in HIT may occur in any vascular bed (arteries, veins and/or capillaries)

The PLASMIC score is used to estimate pretest probability of which condition?

a
HLH
b
Thrombotic thrombocytopenic purpura
c
Disseminated intravascular coagulation
d
Heparin-induced thrombocytopenia

From https://onlinelibrary.wiley.com/doi/epdf/10.1111/ijlh.13557

n a recent publication, high scores of 6- 7 versus low/intermediate scores of 0- 5 predicted severe ADAMTS13 deficiency with a positive predictive value of 72%, negative predictive value of 98%, sensitivity of 90%, and specificity of 92%

Which type(s) of heparin is/are associated with the highest rate of heparin-induced thrombocytopenia?

a
Therapeutic low molecular weight heparin (LMWH)
In contrast to prophylactic doses, in which LMWH is associated with a 10-fold lower rate of HIT compared to UFH, therapeutic doses of LMWH and UFH are associated with similar rates of HIT (around 1.5%).
b
Therapeutic unfractionated heparin
Intravenous > subcutaneous; bovine > porcine
c
Prophylactic LMWH
10-fold lower risk of HIT with use of prophylactic-dose LMWH as compared with UFH.
d
Heparin flushes
e
Prophylactic unfractionated heparin
Lower rate of HIT compared to therapeutic doses.

ACCP guideline

True or false: heparin-induced thrombocytopenia may be associated with a drop in platelet count within the normal platelet count range.

a
True
Thrombocytopenia can manifest either as an absolute drop in platelet count (150 x 109 /L) or a relative decline of 30% to 50% from baseline platelet counts.
b
False

Thrombocytopenia can manifest either as an absolute decrease in platelet count (<150 x 109/L) (B) or a relative decline of 30-50% from baseline (A)

In heparin-induced thrombocytopenia, what is the average lag time between detection of HIT antibodies and the clinical manifestations of thrombocytopenia and/or thrombosis?

a
1 day
b
2 days
c
5 days
d
10 days

In heparin-naïve patients, PGF/heparin antibodies become detectable at a median of 4 days from start of heparin therapy. Thrombocytopenia and thrombosis occur on average 2 days after antibody detection.

Which the following statement(s) is/are true:

a
Heparin-induced thrombocytopenia is typically associated with moderate drop in platelet count (around 50-70 x 109/L)
b
Heparin-induced thrombocytopenia is often associated with bleeding complications
c
Heparin-induced thrombocytopenia may be associated with/complicated by disseminated intravascular coagulation.
d
Patients with isolated heparin-induced thrombocytopenia (thrombocytopenia without thrombosis) remain at high risk for subsequent thrombosis (20% to 50%) from circulating antibodies capable of binding endogenous PF4/GAG complexes

True of false: heparin-induced thrombocytopenia does not occur with prophylactic low dose unfractionated heparin.

a
True
b
False

Which 2 patient populatiokns ahve the highesst risk of developing heparin-induced thrombocytpoeani?

a
Medical patients
b
Obstetrical patients
c
Pediatric patients
d
Surgical patients

What is the median platelet count (109/L) in heparin-induced thrombocytopenia?

a
10
b
20
c
40
d
60
e
80

PMID: 17124091

The 4T score is best for:

a
Excluding the diagnosis of heparin-induced thrombocytopenia
A low 4Ts score (< or =3) carries a high negative predictive value (0.998; 95% confidence interval, 0.970-1.000).
b
Confirming the diagnosis of heparin-induced thrombocytopenia

What is Argatroban?

a
A small, synthetic reversible inhibitor of thrombin
b
An antibody that targets HIT antibodies
c
An anti-factor X agent
d
A fibrinolytic agent

True or false: a diagnosis of heparin-induced thrombocytopenia can be made without laboratory evidence of antiPF4/heparin antibodies

a
True
b
False

Question 10

What is the typically timing for the onset of thrombocytosis after major surgery?

a
Postop day 1
b
Postop day 3
c
Postop day 5
d
Postop day 7
e
Postop day 14

What is the frequency of thrombosis in patients with heparin-induced thrombocytopenia?

a
10%
b
20%
c
30%
d
40%
e
>50%

4Ts score estimates pretest probability of heparin-induced thrombocytopenia. Which of the following are included in the 4Ts score?

a
Timing
b
Temperature
c
Other causes of thrombocytopenia
d
Severity of thrombocytopenia

Journal of Thrombosis and Haemostasis, 4: 759–765

ACCP guideline

True of false: Some patients with heparin-induced thrombocytopenia and positive immunoassay never develop thrombosis.

a
True
It is not known why some seropositive patients remain asymptomatic while others progress to severe disease.
b
False

If a patient is taking coumadin at the time heparin-induced thrombocytopenia is diagnosed, in addition to stopping heparin what would you recommend?

a
Stop coumadin
b
Stop coumadin and reverse with vitamin K, no need for additional anticoagulation
c
Stop coumadin and reverse with vitamin K, and treat with alternative anticoagulant
d
Stop coumadin and treat with alternative anticoagulant

Heparin-induced thrombocytopenia has been termed a model “clinico-pathological” disorder. What is/are the pathological feature(s) referred to by this term?

a
Thrombosis of small vessels on biopsy of skin or other organ
b
Demonstration of platelet sequestration along the blood vessel wall in biopsies of skin or other organ
c
Detectability of heparin-dependent, platelet-activating antibodies reactive against platelet factor 4/heparin (PF4/H) complexes
d
Flow cytometry showing platelet activation

True or false: heparin exposure often triggers an anti-PF4/H immune response that does not result in HIT.

a
True
b
False

Iceberg model of HIT
https://www.practical-haemostasis.com/Miscellaneous/hit_assays.html

What’s more a more common complication in heparin-induced thrombocytopenia?

a
Venous thromboembolism
b
Arterial thrombosis

True of false: Not all anti-PF4/heparin antibodies are pathogenic; some do not result in HIT?

a
True
b
False

True or false: some patients with thrombotic thrombocytopenic purpura are not critically ill and have only thrombocytopenia and microangiopathic hemolytic anemia (without evidence of end organ damage).

a
True
b
False

In patients with heparin-induced thrombocytopenia, how long does it take for the antibodies to disappear as measured by immunoassay?

a
1 day
b
10 days
c
30 days
d
90 days
e
One year
Immunoassays may remain positive in >35% of patients for up to 1 year.

Which is more specific for the diagnosis of heparin-induced thrombocytopenia?

a
Anti-PF4/heparin antibody assay
b
Serotonin release assay

What is the cause of acquired thrombotic thrombocytopenia purpura?

a
Antibodies against PF4
b
Decreased production of ADAMTS13
c
Autoantibodies against von Willebrand factor
d
Autoantibodies against ADAMTS13

What is the normal function of ADAMTS13?

a
Promotes platelet production
b
Inhibits production of anti-platelet antibodies
c
Reduces expression of von Willebrand factor
d
Cleaves ultra-large von Willebrand factor multimers

Which of the following are part of the classic trial in thrombotic thrombocytopenic purpura?

a
Fever
b
Liver dysfunction
c
Microangiopathic hemolytic anemia
d
Thrombocytopenia
e
Elevated C-reactive protein

What is the mortality associated with untreated thrombotic thrombocytopenic purpura?

a
10%
b
30%
c
50%
d
70%
e
90%

In addition to thrombocytopenia and anemia, what serum lab abnormalities might you see in a patient with thrombotic thrombocytopenic purpura?

a
Low haptoglobin
b
Elevated LDH
c
Elevated AST
Don’t forget that AST is a marker of hemolysis.
d
Elevated ALT
e
Elevated direct bilirubin
Elevated indirect, not direct, bilirubin may be elevated.

Can heparin-induced thrombocytopenia occur when platelet activation assays are repeatedly negative (SRA-negative HIT)?

a
Yes
“We believe this HIT patient category—if it truly exists—must be uncommon. However, it remains problematic regarding how to define and detect this disorder” (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7581458/)
b
No

True of false: the number of schistocytes on peripheral smear are generally higher in thrombotic thrombocytopenic purpura compared to disseminated intravascular coagulation

a
True
b
False

What is the sensitivity of the serotonin release assay in heparin-induced thrombocytopenia?

a
10%
b
20%
c
50%
d
80%
e
>95%

Which condition is associated with massive systemic activation of secondary hemostasis with generation of fibrin thrombi?

a
Thrombotic thrombocytopenic purpura
b
Disseminated intravascular coagulation
c
Hemolytic uremic syndrome
d
Valve hemolysis

True or false: HLH may be associated with thrombocytopenia?

a
True
b
False

What is the definition of severe ADAMTS13 deficiency?

a
<10% activity
b
<15% activity
c
<20% activity

The ADAMTS13 activity assay is usually sent out to specialized lab and it takes several days for the results to come back. True or false: treatment for suspected thrombocytopenic purpura should be withheld while waiting for the result.

a
True
b
False
TTP treatment should be initiated on initial suspicion of the disorder (MAHA, thrombocytopenia, and pretest probability score), rather than at the confirmation of severe ADAMTS13 deficiency.

Diagnostic samples for ADAMTS13 from a patient with suspected thrombotic thrombocytopenic purpura should be obtained:

a
Prior to initiation of treatment
Yes, because plasmapheresis may confound the results.
b
After treatment has been initiated

How common is the classic pentad in patients with thrombotic thrombocytopenic purpura?

a
1%
b
5%
The classic pentad of TTP (anemia, thrombocytopenia, fever, acute renal failure, and severe neurologic symptom) is rare (<5%) at diagnosis and today, its use for diagnostic purposes has become obsolete.
c
10%
d
20%
e
>30%

MAHA; microangiopathic hemolytic anemia; prevalence figures from J Clin Apher 2014;29:148

If ADAMTS13 activity levels are less than 10%, what is the next step?

a
No further testing
b
Mutational analysis of the ADAMTS13 gene
c
Assay for the presence of antibodies against ADAMTS13
The presence of antibodies will determine the diagnosis of acquired (also called idiopathic) TTP and will rule out in principle the existence of congenital TTP.
d
Tissue biopsy to stain for presence of ADAMTS13

https://www-tandfonline-com.ezp-prod1.hul.harvard.edu/doi/pdf/10.1080/17474086.2021.1956898?needAccess=true

What are treatment goals in thrombotic thrombocytopenic purpura?

a
Prevent thrombi formation to avoid organ damage
b
Eradicate the inhibitory antibody in acquired TTP to restore ADAMTS13 activity
c
Replace ADAMTS13 in congenital TTP
d
Boost liver production of ADAMTS13

Typical sites of bleeding in ITP include:

a
Hematuria
b
menorrhagia
c
Epistaixs
d
Muscle hematoma

In a patient with thrombotic thrombocytopenic purpura in whom plasma exchange is delayed, what would you recommend?

a
Platelet transfusion
b
Plateletpheresis
c
Plasma infusion
Correct. Typical dose is 15-30 ml/kg.
d
von Willebrand factor concentrate

What is Caplacizumab?

a
Antibody that blocks von Willebrand factor-platelet interactions
Yes. It is a bivalent humanized nanobody (i.e. variable domain-only immunoglobulin fragment) that targets the GpIb-binding site of VWF (A1 domain), blocking the interaction between platelets and VWF.
b
Antibody that targets ADAMTS13
c
Antibody that targets autoantibodies against ADAMTS13
d
Antibody that targets ultra large von Willebrand factor multimers

Which of the following immunosuppressant(s) should be used up front in the treatment of thrombotic thrombocytopenic purpura?

a
Rituximab
b
Corticosteroids
c
Cyclosporine
d
Cyclophosphamide
e
Bortezomib

True of false: red cell transfusions are relatively contraindicated in thrombotic thrombocytopenic purpura.

a
True
b
False

True of false: prophylactic platelet transfusions are relatively contraindicated in thrombotic thrombocytopenic purpura?

a
True
Some reports have associated platelet transfusion with worsening of the thrombotic disease.
b
False

Which therapies may be instituted in patients with thrombotic thrombocytopenic purpura once the platelet count > 50×109/L

a
Low dose aspirin
b
Prophylactic heparin
c
Tranexamic acid

It is generally safe to carry out invasive procedures on patients with platelet counts (x 109/L):

a
>10
b
>20
c
>50
d
>75
e
>100

Which of the following are important to ask about in a patient with newly diagnosed thrombocytopenia?

a
Do you drink alcohol?
b
Do you have any nausea, vomiting and/or diarrhea?
c
Have you had any recent immunizations?
d
What medications are you taking?
e
Do you have a family history of thrombocytopenia?

True or false:

A diagnosis of DIC can only be made if there is a primary condition known to be associated with DIC and clinical signs and symptoms are
compatible with this underlying disease.

a
True
b
False

True of false: A single laboratory assay exists that can reliably confirm or reject a diagnosis of DIC.

a
True
b
False

PMID: 29999440

True of false: disseminated intravascular coagulation is an independent (‘standalone’) clinical disorder.

a
True
b
False
DIC is always a complication of another condition/disease that leads to hemostatic activation.

In patients taking corticosteroids for immune thrombocytopenia, what should they be monitored for?

a
Hypertension
b
Hyperglycemia
c
Sleep and mood disturbances
d
Gastric irritation
e
Osteoporosis

Recommended initial therapy for immune thrombocytopenia includes:

a
Dexamethasone 40 mg PO daily x 4
b
Prednisone 0.5-2 mg/kg per day
c
Dexamethasone 100 mg single dose
d
Cyclosporine 5 mp PO daily
e
Rituximab 375 mg/m2 weekly x 4

Patients with presumed immune thrombocytopenia should be tested for:

a
Cytomegalovirus
b
Hepatitis C virus
c
HIV
d
Epstein Barr virus
e
Zika virus

Newly diagnosed immune thrombocytopenia is ITP diagnosed within:

a
Last 6 months
b
Last 2 weeks
c
Last one week
d
Last 3 months

True of false: with the availability of the occurrence of thrombotic thrombocytopenic purpura, there is no longer a need to obtain ADMATS13 activity levels?

a
True
b
False

Thrombocytopenia and peripheral smear showing target cells and macrocytosis suggest:

a
Hypothyroidism
b
Pernicious anemia
c
Liver disease
d
Alcohol toxicity

What is the estimated prevalence of thrombocytopenia (platelet count <100) in patients with myelodysplastic syndrome?

a
10%
b
20%
c
30-40%
d
40-65%
e
> 65%

What percentage of patients with myelodysplastic syndrome present with isolated thrombocytopenia?

a
1%
b
5-10%
c
10-20%
d
>20%

What is the prevalence of thrombocytopenia in alcohol-dependent patients requiring hospitalization?

a
1%
b
5%
c
10%
d
>15%

In immune thrombocytopenia, at what platelet level (x 109/L) should you normally think about initiating therapy?

a
<5
b
<10
c
<30
d
<50

Chronic immune thrombocytopenia is ITP lasting:

a
> 1 month
b
> 2 months
c
> 3 months
d
> 6 months
e
> 12 months

True of false: alcohol-induced thrombocytopenia resolves with abstinence.

a
True
b
False

True of false: thrombocytopenia related to alcohol use can occur independently of liver damage.

a
True
b
False

Mechanisms of thrombocytopenia include:

a
EDTA-dependent antibodies
b
Antibody-mediated destruction
c
Consumption in platelet or fibrin clots
d
Reduced production in bone marrow
e
Sequestration in spleen

Your patient with thrombocytopenia has an elevated AST and normal ALT. What are the possible explanations?

a
The patient is having a stroke
b
The patient has alcoholic cirrhosis
c
The patient is a heavy drinker
d
The patient has Evans syndrome
e
The patient has inflammatory bowel disease

What is the prevalence of thrombocytopenia in cirrhosis?

a
10%
b
30%
c
50%
d
70%
e
90%

Thrombocytopenia and peripheral smear showing schistocytes is consistent with:

a
Disseminated intravascular coagulation (DIC)
b
Thrombotic thrombocytopenic purpura (TTP)
c
Liver disease
d
Immune thrombocytopenia (ITP)
e
Babesiosis

How long does it take for the platelet count to recover following abstinence in a patient with alcohol-induced thrombocytopenia?

a
1 day
b
3-5 days
c
1 week
d
2 weeks
e
1 month

Thrombocytopenia and concomitant anemia are consistent with:

a
Babesiosis
b
Evans sydnrome
c
Liver disease
d
Rheumatoid arthritis
e
Sickle cell disease

What is the prevalence of pseudothrombocytopenia in the general population?

a
1:100
b
1:1000
c
1:10,000

What is the most common cause of thrombocytopenia in pregnancy?

a
Preeclampsia
b
Gestational thrombocytopenia
c
Immune thrombocytopenia
d
HELLP syndrome

Which statement is true:

a
Gestational thrombocytopenia is a benign condition
b
Gestational thrombocytopenia is associated with increased maternal and neonatal morbidity and mortality

True or false: gestational thrombocytopenia can be distinguished from immune thrombocytopenia by ordering anti-platelet antibodies.

a
True
b
False

What are the 2 main mechanisms underlying cirrhosis-associated thrombocytopenia?

a
Splenic sequestration
b
Reduced production of thrombopoietin
c
Immune-mediated destruction
d
Suppression of megakarypoieis