Therapy and prevention of coagulopathy Flashcards
Is ITP acquired or inherited?
acquired
women of childbearing age, MPV high, hemoglobin normal, thrombocytopenia is the only symptom
Below what level of platelets warrant treatment in ITP?
30-50K/ul (this is because even with only 30-50K platelets, the platelets in ITP are large and the bleeding time will be fairly normal at this level)
only observe if above 30-50K
What is the initial treatment for ITP?
prednisone and dexamethasome (take 3-4 days to work) +-
quick–IV/Ig (if platelets below 10K and bleeding) and anti-D +-
quick– platelets (if bleeding)
What does anti-D do?
hemolyzes RhD+ red cells which are taken up via the RES in the spleen in a way that “competitive inhibits” the spleens uptake of ITP platelets
but this is costly to the body
What does IVIg do?
saturates the Fc receptors in the RES and platelets are salvaged.
but this is costly to the body
How is relapses ITP treated?
prednisone/dexamethasome and
rituximab or anti-D or IVIg or TPO receptor (Mpl) agonist or splenectomy
What bacteria/viruses can cause ITP?
H. pylori, HIV, Hep C
T or F. Splenectomy can be done with only 30-50K platelets and no platelets are needed
T. No infusion necessary usually
this is effective for ITP
What is the differential for thrombotic microangiopathy?
1) TTP
2) HUS
3) HELLP syndrome
4) DIC
5) SLE
6) Malignant hypertension
What lab findings would indicate thrombotic microangiopathy?
- hemolytic anemia
- thrombocytopenia
- microclots
- elevated liver enzymes
- renal dysfunction
What are the symptoms of TTP (Moscovitz’s pentad)?
- MAHA
- Thrombocytopenia
- renal failure/abnormality
- fever (from dead tissue creating cytokines)
- CNS manifestations
What happens in TTP?
Antibody against ADAMTS13 prevent cleaving of vMF which bind platelets and slice red cells (shistocytes)
What binds Hb dimers after intravascular hemolysis?
haptoglobin, and then they are taken up by the liver so haptoglobin is reduced
What happens to unbound Hb dimers?
it oxidizes to methemoglobin and is taken up by the kidneys and some leaks into urine (brown colored)
What is the treatment for TTP?
plasma exchange (not only adds ADAMST13 but also removes the antibodies so its better)
or infusion
Does TTP show abnormalities in PTT or PT?
No, neither. Even though micro thrombi occur, there really isn’t enough consumption of clotting proteins for that
What happens in HUS?
Shiga toxin makes antibodies to Gb3 (acts similarly to ADAMTS13) on weibel-palade bodies that prevent cleaving, and thus activate micro-thrombi mostly in kidneys
and complement is activated against red cells
How does DIC present?
- PT AND PTT prolongation (clotting factors are used up)
- fever
- CNS changes
- high LDH (mostly from anoxic damage- not hemolysis)
- anemia
- hypotension
- rash from micro thrombi
- cyanosis of digits
What happens in DIC?
intravascular deposition of fibrin leading to overactive clotting and micro thrombi formation and eventually and organ failure from anoxia. Eventually, depletion of platelets and coagulation factors may result in bleeding
both PT and PTT prolonged and d-dimer increased
What can trigger DIC?
the main thing is release of TF
- bacterial sepsis
- acidosis, shock, heat stroke
- malignancies
- obstetrical complications
What is a main clinical site of DIC?
bleeding from 3 unrelated sites and platelets aren’t very low
T or F. Schistocytes are seen in DIC
T.
How is DIC treated?
- stop trigger process
- supportive therapy (only if bleeding)
- no specific treatments
if not bleeding, only watch
treat if an invasive procedure is needed
prophylactic therapy has no proven benefit
What is HIT?
Factor 4 (on platelets) IgG antibodies complex them and activate them in the presence of heparin which causes:
1) platelet aggregation and thrombosis (rare)
2) platelet removal by RES and thrombocytopenia (more common)
What is the 4T pretest scoring system for HIT?
1) Thrombocytopenia
2) Timing
3) Thrombosis
4) oTher causes
Describe the thrombocytopenia portion of the 4T system
2 pts- platelets drop 50+%
1pt- drop 30-50%
0 pts- drop less than 30%
everyone on heparin have at least 8% drop in platelets
Describe the timing portion of the 4T system
2 pts- antibody in 5-10 days
1 pt- not clear if 5-10 days
0 pt- less than 4 days
Describe the thrombosis portion of the 4T system
2 pts- new thrombosis; skin necrosis
1 pt- progressive or recurrent thrombosis; no skin necrosis
0 pt- none
Describe the oTher causes portion of the 4T system
2 pts- none apparent
1 pt- possible
0 pt- definite
How is the 4T test interpreted?
0-3- low (don’t test)
4-5 intermediate (testing indicated)
6-8 high
What is the gold standard assay for HIT diagnosis?
Serotonin release assay (SRA) sensitive and specific
antibody test is very nonspecific
What should you do if the 4T comes back intermediate or high?
- discontinue heparin!!
- obtain anti-PF4/heparin ELISA
What is the anti-PF4/heparin ELISA comes back strongly OD 1+) or weakly positive (OD 0.4-0.99)?
obtain functional assay- if +, HIT, if not, probably not HIT
What is the treatment for HIT?
- avoid platelet transfusion unless bleeding
- other anticoag (fondaparinux might not work)
What is the target platelet level for prevention of spontaneous mucocutaneous bleeding?
10-20K+ (menorrhagia, gum bleeding)
What is the target platelet level for insertion of central venous catheters?
20-50+
What is the target platelet level for administration of therapeutic anticoagulation?
30-50K+
What is the target platelet level for minor surgery and invasive procedures (endoscopy, etc.)?
50-80K+
What is the target platelet level for major surgery (neuro, etc.)?
80-100K+
