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Clin Med2- Hematology > platelet disorders part 2 > Flashcards

platelet disorders part 2 Flashcards

(49 cards)

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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

Study These Flashcards
A

6+ = pressumed dx of TTP - check ADAMTS13

21
Q

what is the treatment of hereditary TTP

Study These Flashcards
A

give plasma infusion to replace

22
Q

what is the treatment of acquired TTP

Study These Flashcards
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

Study These Flashcards
A

rituximab, vincreistine, cyclophosphonamide

24
Q

what is the generalized treatment options for TTP

Study These Flashcards
A

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

25
what is the prognosis for TTP
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
what is the morbidity of TTP
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
what are the differences between TTP and DIC
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
what is hemolytic-uremic syndrome (HUS)
presents similary to TTP except: mostly in kids, primarily related to bacterial infection >> hereditary typically from Shiga-toxin (e.coli): prodrome: bloody diarrhea antibodies, antidiarrheals increases risk for HUS
29
what is the work up of HUS
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
what is the treatement of HUS
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
what is Immune Thrombocytopenia purpra (ITP)
aka idiopathic thrombocytopenia purpura low platelet count -can be short term (acute - kids) vs chronic (adults) - 6 months F>M
32
what is the prognosis for ITP
children = better prognosis adults = often stabilize but rarely go into remission can impact pregnant women
33
what is the cause of ITP
poorly defined - auto-antibodies to platelet antigens primary or secondary types primary - no identifiable trigger secondary - trigger by CA, infection, etc
34
what is the presentation of ITP
asymptomatic fatigue (debilitating) petechiae/purpura mucous membrane bleeding nose bleeds excessive or prolonged menstrual bleeding overt hemorrhage or hematomas
35
what is the workup of ITP
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
what is the treatment of ITP
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
what is Heparin-induced thrombocytopenia (HIT)
adverse reaction to heparin adminitstation
38
what are the types of HIT
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
what is the effects of type 2 HIT
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
How is HIT scored
4Ts for HIT score Thrombocytopenia Timing of platelet count fall Thrombosis or other sequelae oTher cause of thrombocytopenia
41
what is the treatment of HIT
discontinue heparin start alternate anticoagulant evaluate for HIT with PF4 ELISA if ELISA (+), confirm with serotonin release assay
42
what should be avoided in patients with HIT
Coumadin - depletes vitamin K dependent natural anticoagulants Platelet transfusion
43
what is thrombocytosis
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
what is the presentation of thrombocytosis
often asymptomatic can present with throboses some present wtih abnormal bleeding associated splenomegaly seizures, migraines, TIA pregnancy complications more rare is erythromelalgia
45
what is erythromelalgia
painful burning of the hands
46
how is thrombocytosis worked up
elevated platelet count mild WBC elevations normal RBCs peripheral smear: large platelets otherwise normal morphologies
47
who is at high risk of thrombocytosis
age >60 WBC count >11,000 history of thromboses comorbid malignancy connective tissue disorders, IBD, TB - inflammation/infection
48
what is the treatment of thrombocytosis
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
what is the prognosis of thrombocytosis
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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