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Summary BBS2001 - Threats and defence mechanisms
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A good summary of all cases of this block. Notes from the lectures are integrated in this summary.
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By: semfeenstra7221 • 1 year ago
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Course BBS2001Case 1
- Histamine increases permeability and causes vasodilation
- Coagulation and inflammation happen at the same time
- Primary Hemostasis (platelets)
- Secondary Hemostasis (coagulation)
- Extrinsic and Intrinsic Coagulation cascades (Tissue Factor, Damaged collagen, cleaving of
coagulation factors, Factor X, Factor II (thrombin), fibrin formation and stabilization)
- Fibrinolysis (plasmin)
- Inhibition of coagulation
- Leukocytes: myeloid (monocytes, macrophages, dendritic cells, granulocytes) and
lymphoid (T- and B-cells, NK cells)
- Inflammation (≠ infection)
- Leukocyte transmigration (selectins - rolling, chemokines - affinity maturation, integrins –
firm adhesion, junctional molecules – diapedesis)
Learning goals:
1. What are the different blood cells and their function? (coagulation): grouping (no
details)
2. How does the coagulation cascade work?
3. And how is the coagulation cascade regulated?
4. What are the different immune cells? grouping
5. The signs of inflammation: how are these caused? (histamine etc.)
6. Chemoattract: how is the chemoattraction recruited and how they pass the
endothelial layer?
https://www.youtube.com/watch?v=cy3a__OOa2M&feature=youtu.be
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,Used source: Silverthorne (basic principles)
Learning goal 1.1 - What are the different blood cells and their functions?
Blood consists of plasma and cellular elements. The cellular elements can be divided into
red blood cells (RBCs), also called erythrocytes; white blood cells (WBCs), also called
leukocytes and platelets or thrombocytes.
White blood cells are the only fully functional cells in the circulation. Red blood cells have
lost their nuclei by the time they enter the bloodstream, and platelets, which also lack a
nucleus, are cell fragments that have split off a relatively large parent cell known as a
megakaryocyte
- Red blood cells play a key role in transporting oxygen from lungs to tissues, and
carbon dioxide from tissues to lungs.
- Platelets are instrumental in coagulation, the process by which blood clots prevent
blood loss in damaged vessels.
- White blood cells play a key role in the body’s immune responses, defending the
body against foreign invaders, such as parasites, bacteria, and viruses.
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,3
, Learning goal 1.2 – How does coagulation work?
If there is a break in the “piping” of the system, blood will be lost unless steps are taken.
One of the challenges for the body is to plug holes in damaged blood vessels while still
maintaining blood flow through the vessel.
It would be simple to block off a damaged blood vessel completely. However, cells
downstream from the point of injury die from lack of oxygen and nutrients if the vessel is
completely blocked.
The body’s task is to allow blood flow through the vessel while simultaneously repairing the
damaged wall. This challenge is complicated since the blood in the system is under pressure.
If the repair “patch” is too weak, it is blown out by the blood pressure. For this reason,
stopping blood loss involves several steps:
1. First, the pressure in the vessel must be decreased long enough to create a secure
mechanical seal in the form of a blood clot.
2. Once the clot is in place and blood loss has been stopped, the body’s repair
mechanisms can take over.
3. Then, as the wound heals, enzymes gradually dissolve the clot while scavenger
leukocytes ingest and destroy the debris.
Hemostasis is the process of keeping blood within a damaged blood vessel and can be
divided into three major steps: vasoconstriction, platelet plug and coagulation.
1- Vasoconstriction
The first step in hemostasis is immediate constriction of damaged vessels to decrease blood
flow and pressure within the vessel temporarily. Vasoconstriction normally is caused by
paracrine molecules released from the endothelium.
2- Temporary blockage of a break by a platelet plug: Primary Hemostasis (platelet
adhesion and aggregation)
Vasoconstriction is rapidly followed by the second step, mechanical blockage of the hole by
a loose platelet plug. Plug formation begins with platelet adhesion, when platelets adhere
or stick to exposed collagen in the damaged area.
In general, platelets are cell fragments in the bone marrow from megakaryocytes. Platelets
are smaller than red blood cells, are colourless and have no nucleus. Their cytoplasm
contains mitochondria, smooth ER and many granules filled with clotting proteins and
cytokines.
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