hematology/coagulation (week 7) Flashcards
what is thrombocytopenia
- abnormally low platelet count
- below 150
- mild (100-149)
- moderate (50-99)
- severe (less than 50)
what do platelets do?
- they form plugs and activate coagulation
- help stop bleeding
what are the risks with thrombocytopenia
- bleeding from an injury of spontaneous
what are the three pathways that create low platelet counts
- decreased production
- increased breakdown
- abnormal distribution
- or severe hemorrhage
what are acquired thrombocytopenia and what do they lead to?
- immune thrombocytopenic purpura (ITP)
- heparin-induced thrombocytopenia (HIT)
- both lead to premature destruction of platelets
what needs to be assessed if all levels in the CBC lab results are abnormally low?
check bone marrow
if all CBCs are normal excpet for platelets then what would you expect?
- HIT
- ITP
laboratory results for ITP will show:
- very low platelets
- normal hemoglobin, PT, aPTT, and D-dimer
laboratory results for HIT will show:
- decreased platelets
- increased D-dimer (blood clotting problems)
- normal hemoglobin, PT, and aPTT
what is the pathophysiology of ITP (what causes ITP)?
- autoimmune disorder.
- platelets are coated with antibodies and once they enter the spleen they are broken down by macrophages
what is the order of treatment for ITP
- steriod therapy (prednisone)
- splenectomy
- IV immune anti-D antibody
- platelet transfusion
how does steroid therapy help ITP?
- suppress phagocytic response (response to breakdown) of macrophages in the spleen
- and suppresses antibody formation
what happens if you do a spenectomy to treat ITP?
- decreases the act of macrophages, decrease antibodies, and decrease removal of platelets
How does IV immune anti-D antibody help ITP
- if steroid therapy and splenectomy does not work
- these compete with antiplatelet antibodies for macrphage receptor on spleen - prevents from breaking down platelets
how does platelet transfusion help with ITP
- the last resort
- life threatening situations
- can lead to antibody formation
what is the pathophysiology of HIT (how does it occur)?
a drug induced form of thrombocytopenia
- heparin PF4 bind to antibody making antoibody-heparin PF4
- this causes thrombotic activities (platelets form clots )
risk factors for HIT
- bleeding
- DVT, and PE
- HIT starts 5 days after start of heparin medication
treatment for HIT
- immediate discontinuation of heparin and start using warfarin if anti coagulation is needed (takes vitamin K pathway)
what is DIC?
- it is a bleeding and thrombotic disorder (clotting)
- is always in response to a disease or injury that has gone out of control (septic and cardiogenic shock)
bleeding manifestations in DIC
- consumption and depletion of platelets and coagulation factors (excessive clotting - depleting platelets)
signs and symptoms of bleeding in DIC
- skin white,
- purpura
- blood oozing
- hemorrhage
- respiratory: tachypnea, hemoptysis
- cardio: tachycardic, hypotension
- GI: blood in stool
- UT: blood in urine
- neurological: vision changes, dizziness, headache
- MSK: bone and joint pain
thrombotic manifestation in DIC
- fibrin or platelet deposition in microvasculature
signs ans symptoms of thrombotic in DIC
- skin: cyanois, ischemic, gangrene (low purfusion)
- resp: tachypnea, dyspnea, PE
- cardio: dysrythmias
- GI: abdominal pain, no bowel sounds
- urinary tract: AKI, no urine output
what would be shown on the labs results for DIC?
- decreased platelet count
- no change or low hemoglobin (the difference between HIT and ITP)
- increased: PT, aPTT, and D-dimer (coagulation time very fast)