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Clin Med2- Hematology > platelet disorders part 2 > Flashcards

platelet disorders part 2 Flashcards

1
Q

What are thrombocytopenias

A

low platelet count

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2
Q

what is considered sever thrombocytopenia

A

<50,000 platelets
spontaneous bleeding with ‘trauma’
true spontaneous bleeding not until 10-20,000 platelets

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3
Q

what is the presentation of thrombocytopenias

A

excessive/repetitive bleeding
excessive bruising (with minimal trauma)
bleeding at unusual sites (hemarthrosis)
excess mucosal bleeding
petechiae

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4
Q

how is thrombocytopenia worked up

A

CBC with platelet count
peripheral smear

platelet function analysis (PFA)
CMP to assess kidney and liver function
D-dimer to assess for concurrent thromboses (TTP, HUS, DIC, HIT)

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5
Q

what are the causes of thrombocytopendias

A

SPUD
sequestration
production (decreased)
Utilization (increase) - hemorrhage, DIC
Destruction (TTP, ITP, Drugs (HIT), Infection (HUS))

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6
Q

what is DIC

A

disseminated intravascular coagulation
occurs in sick patients: sepsis, trauma, OB emergencies, burns, cirrhosis, malignancies

associated with high rate mortality rate - actual rate difficult to discern due to co-morbid conditions

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7
Q

what happens in DIC

A

coagulation and fibrinolysis pathways in ‘overdrive’
“consumption coagulopathy” - clots everywhere, leads to organ ischemia, uses up platelets and other clotting factors, other areas in body start to bleed from minor injury
both too much and too little blotting at the same time
Kidneys, liver, lungs, brain are most susceptible to organ damage

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8
Q

what are the types of DIC

A

Acute and chronic DIC

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9
Q

what is acute DIC

A

quick, large trigger - sepsis, trauma
platelets cant compensate with production
LIFE THREATENING

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10
Q

What is chronic DIC

A

continuous or intermittent small trigger - malignancy
can compensate - increased production, liver clearance of FDPs

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11
Q

what is the presentation of acute DIC

A

bleeding, oozing, bruising, petechiae
thrombocytopenia
prolonged PT/aPPT
decreased plasma fibrinogen
elevated d-dimer
increased thrombin time
reduced levels of coag factors
evidence of hemolysis on peripheral smear
renal, hepatic, respiratory dysfunction
shock

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12
Q

what is the presentation of chronic DIC

A

most are asymptomatic
venous/arterial clots without other explanation
platelet counts normal or mildly elevated
normal PT/aPTT
normal or mildly elevated plasma fibrinogen
elevated d-dimer
evidence of hemolysis on peripheral smear

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13
Q

what is the workup for DIC

A

high index of suspicious in at risk patients
CBC, peripheral smar and coag panel (PT, aPTT, fibrinogen, D-dimer)
Thrombocytopenia + fibrinogen + D-dimer

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14
Q

what is the treatment for DIC

A

primary - treatment of underlying disorder
hemodyamic stabilization +/- ventilator support
whole blood transfusions - severe bleedings
platelet transfusion
coag factor repletion

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15
Q

what do we not use for treatment for patients in DIC

A

anticoagulants or antifibrinolytics

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16
Q

what is TTP

A

thrombotic thrombocytopenia Purpura
thrombotic microangiopathy
characterized by “small vessel platelet-rich thrombi”
no apparent cause
uncommon before age 20
F>M
EMERGENCY - fatal if not treated properly (stoke, brain damage, MI, renal failure)

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17
Q

what is the cause of TTP

A

deficiency in ADAMTS13 enzyme - hereditary
- procoagulant state
antibody (acquired)&raquo_space; hereditary

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18
Q

what is the presentation of TTP

A

acute or insidious onset - generally episodic, can last days- weeks - months
presents with unusual bleeding/bruising + petechiae/purpura +: fever, weakness, fatigue, dyspnea, dizziness, abd pain, N/V, AMS, HA, visual changes, confusion, lethargy, syncope, seizure, focal deficits, tachycardia, CP, MI, CHF, arrhythmias
often have renal, GI or CNS involvement
often associated with anecedeent URI/ flu-like illness

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19
Q

what is the workup for TTP

A

CBC with diff
SEVERE HEMOLYTIC ANEMIA + THROMBOCYTOPENIA in otherwise healthy person
avg platelet count - 20,000
avg. hematocrit - 21%
avg. hemoglobin - 80 g/L

peripheral smear shows schistocytes (helmet cells), reduced platelets
normal plasma fibrinogen, PT, aPTT
ADAMTS13 assay

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20
Q

what is the plasmic scope for TTP

A

6+ = pressumed dx of TTP - check ADAMTS13

21
Q

what is the treatment of hereditary TTP

A

give plasma infusion to replace

22
Q

what is the treatment of acquired TTP

A

urgent initiation of plasma exchange is mainstay
- TPE- therapeutic plasma exchange AKA plasmapharesis
Ideally start within a few hours
continue until platelet count normalizes (>150,000)

23
Q

what is the treatment of refractory acquired TTP

A

rituximab, vincreistine, cyclophosphonamide

24
Q

what is the generalized treatment options for TTP

A

start immunosuppression with steroids
+/- VTE prophylaxis if needed for clinically significant clots
Splenectomy if TTP acquired and not responding

25
Q

what is the prognosis for TTP

A

usually takes about 11 plasma exchanges to normalize platelet count
25-50% have exacerbation (recurrence within 30 days of treatment)
about 1/3 of pts have a relapse
increase severity of ADAMTS13 deficiency and presence of autoantibodies = higher risk for recurrence
mortality rate still 10-20% even if treated with plasma exchange

26
Q

what is the morbidity of TTP

A

persistent neuro deficits in 5-13%
chronic renal insufficiency about 25%
renal failure requiring HD in 3-8%
persistent ADAMMTS 13 deficiency - increased risk of stroke

27
Q

what are the differences between TTP and DIC

A

TTP: hereditary OR acquired, normal PT and aPTT, normal fibrinogen, normal d-dimer. tx: plasma exchange, FFP, steroids; NO PLATELETS

DIC: acquired, elevated PT and aPTT,reduced fibinogen, elevated d-dimer. tx: primary cause, FFP, or cryoprecipitative; GIVE PLATELETS

28
Q

what is hemolytic-uremic syndrome (HUS)

A

presents similary to TTP except: mostly in kids, primarily related to bacterial infection&raquo_space; hereditary
typically from Shiga-toxin (e.coli): prodrome: bloody diarrhea
antibodies, antidiarrheals increases risk for HUS

29
Q

what is the work up of HUS

A

evidence of hemolytic anemia - low Hgb, schistocytes on periopheral smear
thrombocytopenia (platelets about 40,000)
renal injury - hematuria, proteinuria, AKI, reduced UOP, +/- HTN

+ MUTATION IN GENES ENCODING COMPLETMENT OR
+ STOOL CULTURE

30
Q

what is the treatement of HUS

A

supportive care
hemodialysis if severe renal impairemnt
management of HTN

urgent plasma exchange if complement mediated only - not helpful for shiga-toxin mediated HUS

31
Q

what is Immune Thrombocytopenia purpra (ITP)

A

aka idiopathic thrombocytopenia purpura
low platelet count -can be short term (acute - kids) vs chronic (adults) - 6 months
F>M

32
Q

what is the prognosis for ITP

A

children = better prognosis
adults = often stabilize but rarely go into remission
can impact pregnant women

33
Q

what is the cause of ITP

A

poorly defined - auto-antibodies to platelet antigens
primary or secondary types
primary - no identifiable trigger
secondary - trigger by CA, infection, etc

34
Q

what is the presentation of ITP

A

asymptomatic
fatigue (debilitating)
petechiae/purpura
mucous membrane bleeding
nose bleeds
excessive or prolonged menstrual bleeding
overt hemorrhage or hematomas

35
Q

what is the workup of ITP

A

diagnosis of exclusion - no definitive diagnosis
isolated thrombocytopenia
+/- large platelets on peripheral smear without abnormal morphology
other labs largely normal, except consistent with any trigger
+/- iron deficiency related to any bleeding
consider HCV and HIV screen - may be presenting symptom

36
Q

what is the treatment of ITP

A

no cute
acute ITP (kids) - usually resolves on its own
goals = prevent bleeding and stabilize platelet count
if severe or impending bleeding or platelet count: high dose steroid, IVIG, platelet transfusion

37
Q

what is Heparin-induced thrombocytopenia (HIT)

A

adverse reaction to heparin adminitstation

38
Q

what are the types of HIT

A

type 1 and type 2
type 1: non-immune, day 1+, platelets will normalize spontaneously, can continue heparin (more common)
type 2: immune mediated, antibody preodunction, day 5-14 if heparin naive (more severe)

39
Q

what is the effects of type 2 HIT

A

increasing platelet activation leads to more clotting
total platelet numbers fall
characterized by: UNEXPLAINABLE DROP IN PLATELET COUNT IN PT ON HEPARIN, steady drop, not fluctuation, expect stable hgb/hct - bleeding not the problem

40
Q

How is HIT scored

A

4Ts for HIT score
Thrombocytopenia
Timing of platelet count fall
Thrombosis or other sequelae
oTher cause of thrombocytopenia

41
Q

what is the treatment of HIT

A

discontinue heparin
start alternate anticoagulant
evaluate for HIT with PF4 ELISA
if ELISA (+), confirm with serotonin release assay

42
Q

what should be avoided in patients with HIT

A

Coumadin - depletes vitamin K dependent natural anticoagulants
Platelet transfusion

43
Q

what is thrombocytosis

A

elevated number of platelets greater than 400,000

a myeloproliferative disorder (megakaryocyte)
*underlying malignancy (secondary or reactive)
essential or primary thrombocythemia
associated with JAK2 mutations
F>M ages 50-70

44
Q

what is the presentation of thrombocytosis

A

often asymptomatic
can present with throboses
some present wtih abnormal bleeding
associated splenomegaly
seizures, migraines, TIA
pregnancy complications
more rare is erythromelalgia

45
Q

what is erythromelalgia

A

painful burning of the hands

46
Q

how is thrombocytosis worked up

A

elevated platelet count
mild WBC elevations
normal RBCs
peripheral smear: large platelets otherwise normal morphologies

47
Q

who is at high risk of thrombocytosis

A

age >60
WBC count >11,000
history of thromboses
comorbid malignancy
connective tissue disorders, IBD, TB - inflammation/infection

48
Q

what is the treatment of thrombocytosis

A

goal = platelet count <500,000
first line = oral hydroyurea - causes myelosupression
ASA 81mg daily - prevention of thromboses, tx of erythromelalgia
if emergency platelet lowering required - plateletphoresis

49
Q

what is the prognosis of thrombocytosis

A

lifespan greater than 15 years s/p diagnosis
10-15% progress to bone marrow fibrosis within 15 years
1-5% progress to acute leukemia iwthin 20 years
high risk for splenomegaly - splenic infart

Clin Med2- Hematology (8 decks)

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