Thrombocytopenia

• Thrombotic thrombocytopenic purpura (TTP) is caused by a deficiency in something known as ADAMTS13, leading to an increase in von Willebrand factor which causes small vessel thrombi and thrombocytopenia.
• Von Willebrand factor is a glycoprotein involved in hemostasis that helps blood clot when needed.
• If a patient with HIT is given heparin, their platelet count can drop significantly within a short period of time.
• Thrombocytopenia is present in the patient, but it is rare to see bleeding in HIT.
• The CBC in a patient with HIT will show thrombocytopenia, which can be unique due to the patient's previous treatment with heparin.
• The diagnosis of HIT is made with a combination of clinical and laboratory findings.
• Willie, the von Willebrand factor, likes to stick all the platelets to himself, which is great when needed but can cause problems if it gets out of control.
• Adam, the antithrombin, snips off excess von Willebrand factor when it gets out of control, keeping things in control.
• In TTP, there is not enough Adam to keep Willie in check, leading to thrombin in the vessels and all the problems associated with it.
• Antibiotics and anti-motility agents should be avoided in patients with hus as they can disrupt the bacterial membrane of the e coli organisms and cause them to dump out more exotoxins.
• Treatment of hus is mainly supportive, including IV fluids, dialysis, red blood cell transfusion, and supportive care.
• Clinical manifestations of hus include gi and renal symptoms such as bloody diarrhea, abdominal pain, vomiting, and hematuria.
• Vascular endothelium damage leads to microthrombi at the site of damage in the vessels and then these microthrombi can lead to hus.
• Diagnosis of hus is done through thrombocytopenia, normal coag panel, negative d-dimers, and elevated serum creatinine.
• E coli O157:H7 is the only bacteria that can cause hus, but other infective organisms can also cause hus.
• The clinical manifestations of TTP, also known as pen tag, consist of fever, renal failure, anemia, thrombocytopenia, and neurologic changes.
• Plasma exchange in TTP is the main stay of treatment until the platelet count normalizes.
• In patients with TTP, platelets are stuck to von Willebrand factor, causing low platelets.
• Diagnosis of TTP is made with low platelets, thrombocytopenia, normal coag panel, schistocytes, and a negative d-dimer.
• Treatment for TTP is plasma exchange or plasmapheresis, which removes the bad plasma from the patient with TTP and replaces it with donor plasma.
• Prior to the introduction of plasma exchange therapy, the mortality rate for patients with TTP was close to 90.
• Neurologic changes in TTP are caused by clots obstructing flow to the distal tissue, decreasing brain perfusion.
• Renal failure in TTP is usually a decline in kidney function rather than failure.
• Microangiopathic hemolytic anemia, also known as MAHA, is a type of hemolytic anemia that results from those red blood cells passing through vessels packed with microthrombin.
• Schistocytes are fragmented red blood cells that indicate microangiopathic hemolytic anemia.
• Infections, usually viral, and systemic conditions that alter the immune homeostasis are two main triggers of ITP.
• Hematuria, oliguria, and gi complaints are common in children under five.
• Clinical manifestations of ITP include asymptomatic patients and symptoms related to thrombocytopenia such as bleeding, petechiae, and purpura.
• Diagnosis of ITP involves isolated thrombocytopenia, normal coagulation factors, and normal red blood cell and leukocyte morphology.
• Immune thrombocytopenic purpura (ITP) is an acquired autoimmune hematologic disorder characterized by isolated thrombocytopenia, more common in females, and auto antibodies against the platelet membrane leading to splenic sequestration and phagocytosis.
• E. coli O157 is likely to be involved in a case where hamburger is undercooked and urinary symptoms are present.
• Treatment of ITP includes IVIG and steroids, which depends on severity levels.
• The increased prothrombin time and partial thromboplastin time (PT and PTT) in DIC are due to the consumption of clotting factors by the clots formed throughout the body.
• Glucocorticoids and Ortiximab are adjunct agents used in severe cases of TTP to improve patient outcomes and decrease the required duration of plasma exchange.
• The main clinical manifestation of DIC is a sick patient who is bleeding, with a history of trauma, sepsis, malignancies, and other underlying conditions.
• Diagnosis of DIC involves a complete blood count (CBC), which shows thrombocytopenia, schizocytes, and microangiopathic hemolytic anemia.
• Platelets are not used in patients with TTP as they feed the beast, creating more clots.
• Disseminated intravascular coagulation (DIC) is an acquired syndrome that leads to activation of the coagulation pathway and has the potential to cause both thrombosis and hemorrhage.
• Exchange the plasma, not the platelets, to fix the problem.
• DIC occurs in patients with underlying conditions that lead to it, such as sepsis, malignancies, trauma, burns, heat stroke, and amphetamine overdose.