Lecture 6 - 10 overview Flashcards
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Nuetrophils
- what cell do they originate from?
- what does it mean when there are immature neutrophils in the blood?
what growth factor can you use in clinical practice to increase the maturation of neutrophils?
3 main funcitons
myeloblast
- immature forms of neutrophils will spill out into the blood - meaning there is stress, inflammation or cancers of blood
- can use this in clinical practice - G-CSF - increase maturation of nuetrophill
- chemotaxis, phagocytiosis, killing
What does leucocytosis mean?
-neutrophil leucocytosis - increase in immature forms of neutrophils in blood - can indicate infection and inflammation
Monocytes
What does the cytoplasm look like?
What is the precurosor?
What haemopoetic growth factor stimulates this?
What type of infecitons do these usually combat?
3 Main functions
What molecules can they produce?
- blue, gray cytoplasm with granules (not much cytoplasm)
- same precursor as neutrophil (myeloblast)
- CFU-GM
- parasitic infections
- phagocytic, antigen presnetation, make molecules
- also synthetic funciton 0 make complemetn, interferons, cytokines, growth factors, prostaglandins
what type of nucleous do eosinophils have? and what colour stain?
what is Eosinophilia?
what is this in response to?
bilobed, red
Eosinophilia - an increase in the number of eosinophils in the blood, occurring in response to some allergens, drugs, and parasites, and in some types of leukaemia.
we see eosinophils in these reactions ..
- allergic or hypersenstivity reactions - e.g hayefever, astham, drug reactions
- parasitic infestation e.g if have been overseas
Basophils
- what is their appearance
- what reactions are they involved in?
- what do their granules contain?
- what cell do they have a close relationship to?
not very common
- dense purply blue granules
- hard to see bilobed nucleus
- also involved in allergic reactions
- e.g type 1 sensitivity - binding sites for IgE - release granule
- have a close relationship with mast cells
- granules contain contain histamine, and anaphylaxis
Lymph node enlargement
what are the 2 reasons why? and how are they different from each other?
what is Lymphocytosis?
2 reasons?
Reactive -usually reactive, part of inflammatory or infective process (viral, local bacterial infection)
-Malignant - lymphoid tissue (lymphoma) or metastatic spread - normally firm and hard non tender lymph nodes
Lymphocytosis - increase no. of lymphocytes
- reactive - generlaly after viral infections e.g
- malignant - chronic lymphocytic leukemia
what is Lymphopenia ?
what can cause this?
-reduction in lymphocytes
HIV infection CD4 positive T helper cells (lose these)
- profound T cell deficit
- opportunist infections
- malignancies
what cell does a platelet originate from?
-where are these cells in the bone marrow?
megakaryoblast
- Pro-platelets travel into blood vessels and bud of and spilt into platelets (megakaryocytes sit in BM sinusoidal endothelial cells so can easily release platelets into blood)
Activation pathway 1
Activation of pathway 2 primary haemostasis
- Endothelial damage exposes collagen
- Von willibrand factor binds to collagen
- VWB can bind to platelets via Glycoprotein receptor and pulls it in and platelet becomes activated
- activated platelet has integrin exposed, and this can bind other platelets via fibrinogen molecule
- Platelets release granules with other factors to attract other platelets
This pathway is occurring at same time as other activation pathway
- platelet adheres to collagen
- this activated prostaglandin synthesis which activated Thromboxane A2 to be released
- ADP also released
- TaA2 - triggers release of more granules and initiates aggregation
- ADP and taA2 leads to activation of coagulation and recruitment of other platelets
how does aspirin inhibit platelet aggregation
Aspirin inhibits the cyclooxygenase enzyme which helps form TaA2 enzyme
-however does not completely stop aggregation as there are other pathways of activation
How does 2b3a receptor inhibitor block platelet aggregation and to what extent
Blocks this receptor and has a very potent effect as platelets cannot stick together
What does prostacyclin vs thromboxane a2 ?
- will increase platelet cAMP and inhibit release of granules
- Thromboxane a2 - will decrease platelet camp and result in granule release to go onto platelet aggregation and coagulation
Decreases no. of platelets in blood (thrombocytopenia)
What are factors that can decrease production of platelets?
What factors can increase destruction of platelets
- viral infection
- drugs
- bone marrow failure e.g leukaemia, carcinoma ect.
immune thrombocytopenia
drugs
viral infection
What can increase the production of platelets
Myeloprolferative neoplasms
