Bleeding and coagulation Flashcards
Exlplain Platelets
150,000 -400,000 (normal range per microlitre)
we don’t care about thrombocytopenia unless it is less than 50,000
we don’t care about thromocytosis unless its more than 750,000
Megakaryocytes generated in BM= pass through sinusoid sand break not thousand pieces– platelets fromation
platelats are not even cells
Why the Buffy coat (the white part between the plasma and the RBC in the westergen tube consisting of the WBC and platelets) sometimes can appear green?
Due to the myeloperoxidase created by the neutrophils (WBC)
here we take blood and add anticoagulant and then wait for the contents to sediment
plasma 55%
rbc 45%
buffy coat less than 1%
how can we obtain the serum (plasma-clot) from a sample of the blood?
We will not add the anticoagulant to the test tube and wait for the blood to coagulate in presnece of atmospheric pxygen
we will gwt a blood clot (platelets + rbc + coagulation factors)
and the serum
serum have high concentration of serotonin
Why can splenomegaly lead to low platelt count?
1/3 platelets are normally in the spleen
spllen gets big= more platelets go to spleen= platekets no. Decreases int he peripheral blood
so we can also treat thrombocytopenia via splenectomy
Explain the structure of Platelets.
The basic structure contains of the cytoplasm and plasma membrane
The PM is covered by glycoprotien coat receptors (Gp1b and Gp2b /3a)
PM made of lipid and Archidonic acid (the most pro inflammatory thing in body)
cytoplasm have
actin,myosin,thrombosthenin (contraction and release)
residuals of golgi and RER for enzyme syn (COX)
Fibrin Stabilizing Factor (factor 13)
PDGF (help in repair of vessels)
Granules
What inhibits Arachidonic acid?
corticosteroids
What is arachidonic acid
It is a constituent of the phospholipid of the plasma membreane (its a FFA)
its an inflammatory mediator== vasodilation and vaspoconst
It is freed from the phospholipid via PHOSPHOLIPASE A2
corticosteroids inhibits the phospholipase A2 thus inhibiting the AR. ACID relaease
not an essential FA
but linoiec acid (essential) is necessary to make AA
see aa pathay :)
Why do pro cagulation and anti coagulation have the same root?
Arachidonic acid converts to prostaglandin and leukotrines with COX and LOX enxymes respctively
Now Prostaglandins if in platelets become thromboxane A2 that os pro coagulation
If Prostaglandin is in endothelium it becomes Prostacyclin that is anti coagultaion
What is the diffrence between Aspirin Ans NSAIDS in relation to anti thrombosis
Both blocks the COX so no prostaglandins no TXA2 no coagulation
Aspirin is irreversible while NSAIDS is reversible
we still do not know why aspirin doesn’t block the prostacyclin pathway (which is anti coagulation) and coming from the same prostaglansin :/
Why do an old person take aspirin in low doses?
Because aspirin in low doses is anti thrombotic or anti coagulation by blocking TXA2
In high doses aspirin acts as analgesic and antipyretic
by bocking prostaglandin- PGI2 PGE2
Why do we use anti-leukotrines for asthmatics?
Leukorines C4 D4 and E4 are bronchoconstrictors.
That’s why blocker used in asthma
some antileukorines are- Zileton
some that block the leukotrine receptors are - Monteleukast
Where is Thromboxane synthase present?
Platelets are the only cells in the body to have Thromboxane synthase which convert PG into TXA2.
TXA2 is a platelet aggregator, vasoconstrictior and bronchoconstrictor
Explain Thrombocytosis.
Clinically we care only when >750,000
it can be
Primary- (essential) related to one of the myeloproliferative diseases (high In the elderly)
secondary (reactive) (most common) 100 percent of case in infant
80% of cases
Explain Myeloproliferative disorders
There are 6 types of chronic myeloproliferative disorders: chronic myelogenous leukemia (CML), polycythemia vera, primary myelofibrosis (also called chronic idiopathic myelofibrosis), essential thrombocythemia, chronic neutrophilic leukemia, and chronic eosinophilic leukemia
it is the disease of the elderly
All cell lines are affected but ONE is affected mainly like
In Polycythemia vera - RBC
In Essential Thrombocytosis - Platelets
In Chronic Myeloid Leukemia- Neutrophils
All these can lead to acute leukemias
All of them have rapid cell turnover—–> nucleus——-> purine metabolism—–> uric acid high——> precipitate attacks of gout
explain the diffrence between Myelo dysplastic syndrome and Myeloproliferative disorders.
When a hematological malignancy is characterised by normal differentiation of cells of myeloid cell line, it is referred to as myeloproliferative. On the other hand, when there is abnormal differentiation of cells of myeloid cell line, it is referred to as myelodysplastic
. Myeloproliferative neoplasms and myelodysplastic disorders are often confused. They are, in fact, different entities.
a. Myeloproliferative neoplasms (MPNs) are a group of clonal myeloid neoplasms in which a hematopoietic progenitor proliferates, leading to an increase in peripheral blood white blood cells (WBCs), red blood cells (RBCs), platelets, or a combination of these.
b. Myelodysplastic syndrome (MDS) is also a group of clonal myeloid neoplasms that result in ineffective hematopoiesis. This may lead to a hypercellular or hypocellular bone marrow with a decrease in circulating WBCs, RBCs, platelets, or a combination of these. The hallmark of MDS is dysplasia: the unusual appearance of myeloid precursors in the bone marrow.
Types of disorders. There are four primary myeloproliferative neoplasms. They all involve clonal proliferation of a hematopoietic progenitor cell, leading to both qualitative and quantitative changes in all cell lines. While the name of the disorder typifies the predominant cell line that is affected, more than one cell line is affected in most of these disorders.
- Chronic myeloid leukemia (CML) is characterized by a prominent proliferation of myeloid progenitor cells, leading to an expansion of the granulocytic series of cells resulting in a “left shift”—an increase in immature granulocytes of all stages of maturation in the peripheral blood.
- Polycythemia vera (PV) is characterized by prominent proliferation of myeloid progenitor cells, leading to elevated RBC indices (RBC count, hemoglobin, and hematocrit).
- Essential thrombocytosis (ET) is characterized by prominent proliferation of megakaryocytes, leading to an elevated platelet count.
- Primary myelofibrosis (PMF) is characterized by a proliferation of myeloid progenitor cells that leads to a prominent nonclonal proliferation of fibroblasts. The resulting deposition of reticulin and collagen leads to fibrosis (scarring) of the bone marrow. Compared with the other MPNs, patients with PMF often have low blood counts due to the fibrosis.
