Summary
Summary BBS2001 All cases including consolidation cases
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This is a collection of all cases and consolidation cases, including notes from the lecture!
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--------------------------------------------------------------------------------------------------------------------------------------Case 1
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Types of Leukocytes
Leukocyte is a general term for white blood cells, while lymphocytes are a specific subtype which
includes B cells, T cells, and NK cells. These lymphocytes tend to be more highly concentrated in the
lymphatic system (lymph nodes and vessels) rather than the blood like other circulating cells, and are
characterized microscopically by their darkly-staining nuclei.
There are several types of leukocytes:
● Neutrophils: phagocytizes the pathogens and kills them. Neutrophils can leave the
bloodstream and move into the surrounding tissue. As it arrives within 2 hours, it is the first
defence against bacterial infections. There are two types: Band neutrophils (newly developed
when in sickness) and Segmented neutrophils (remain, even during health).
● Eosinophils: are important in allergic reactions and parasitic infections. They are also capable
of phagocytosis and migration.
● Basophils: they play a role in hypersensitivity reactions. They are also able to leave the
bloodstream and go to the surrounding tissue.
● Monocytes: they actively phagocytize as a component of cell-mediated immunity in acute and
chronic infections. When monocytes leave the bloodstream, they are referred to as
macrophages. They are more effective than neutrophils but arrive only after 12h.
● Lymphocytes: these participate in the cellular and humoral defence against infections. The
lymphocytes can be subcategorized into T-lymphocytes (attack invaders from inside the cells)
and B-lymphocytes (attach invaders from outside the cells).
● Plasma cells: these produce antibodies for defence against an infection
● Granulocytes = Neutrophils, Basophils, and Eosinophils.
● Natural Killer Cells (NK): defence against tumour cells, infected, and stressed cells
● Dendritic cells: respond to microbes by producing cytokines that recruit leukocytes and
initiate adaptive immune responses. AN IMPORTANT BRIDGE BETWEEN THE INNATE AND
ADAPTIVE IMMUNITY.
,Transmigration of leukocytes from the bloodstream to the site of
infection
At sites of infection, macrophages and
dendritic cells that have encountered
microbes produce cytokines that
activate the endothelial cells near
venules to produce:
● Selectins: mediate weak
tethering and rolling of blood
neutrophils on the
endothelium
● Ligands for integrins: mediate
firm adhesion of neutrophils
● Chemokines: activate
neutrophils and stimulate
their migration through the
endothelium to the site of infection.
The purpose of rolling and slow rolling is to bring the leukocyte into contact with the endothelial cell
so that the leukocyte can be further activated by chemokines and other proinflammatory agents
presented on the surface of the endothelial cells. Lymphocytes and monocytes accept an integrin of
the β1 family that binds to VCAM-1 (vascular adhesion molecule 1). Once activated, leukocyte
integrins bind tightly to their ligands on endothelial cells, allowing leukocytes to arrest on the
endothelial surface. Diapedesis is the process whereby the leukocytes squeezes in ameboid fashion
across the endothelial cells, and at this point, there is no return in the inflammatory response. The
other steps, like rolling and adhesion, are reversible
Cytokines are soluble protein secreted by the cells of innate and adaptive immunity and therefore
mediate many of the functions of these cells. Based on their cellular sources:
● monokines (mononuclear phagocytes)
● lymphokines (lymphocytes)
● interleukins (leukocytes) (IL-2, IL-2, etc)
● chemokines
Wound healing
,Hemostasis is the process to keep blood inside a damaged blood vessel
Blood vessels are located in the dermis of the skin and
when you are speaking of bleeding, the rupture of the
epidermis and the dermis has resulted in a damaged
blood vessel.
‘Abrasion’ is when only the epidermis is broken
Major components of Hemostasis includes: 1) Vasoconstriction 2) Platelet activation 3) Secondary
haemostasis is also known as Coagulation 4) Regulation of coagulation 5) Fibrinolysis & Clot
degradation
● Primary hemostasis → platelet plug formation
● The secondary hemostasis → coagulation cascade
Vasoconstriction: damaged endothelial cells will release paracrine vasoconstrictors
● The blood flow and pressure will decreases as the blood vessel is narrowed down.
● This allows the platelet to be formed on the site of damage as the inhibition of the former two
factors would prevent them from flowing away.
● Serotonin is a vasoconstrictor
Platelet activation: when there is vasoconstriction, platelets bind to collagen. The platelet in the blood
vessel adheres to the integrins:
● The von Willebrand factor (vWF, integrin) binds to glycoprotein 1b. These two binds the
platelet to the collagen of the blood vessel, located underneath the endothelial lining.
○ When the platelet and the collagen are bound, platelets release their granules:
Fibrinogen, vWF, serotonin, ADP (platelet aggregation = formation of a cluster of
platelets) and Platelet-Activating Factor (PAF)
■ These factors are stored by granules so they can easily be released and don’t need
to be synthesized when needed
■ PAF: converts platelet membrane phospholipids into thromboxane A2 and
serotonin, which serve as vasoconstrictors, activate more platelets → contributing
to platelet aggregation.
● The healthy endothelial lining is a physical barrier between the blood/platelets and the
collagen, to which platelets rapidly adhere to.
Secondary haemostasis - Coagulation: a cascade of enzymatic reactions produce thrombin, which
transforms fibrinogen into fibrin → stabilize the platelet plug. NOTE THAT platelets will not adhere to
intact endothelium, because it releases prostacyclin and nitric oxide (NO) → this prevents platelet
adhesion
● The formation of the plaque occurs in two distinct stages: the Intrinsic Pathway and Extrinsic
Pathway, combined they form the Common Pathway.
, ● Intrinsic Pathway (propagation). The intrinsic pathway begins when damage to the tissue
exposes collagen. This pathway uses proteins that are already present in the plasma. Collagen
activates the first enzyme, factor XII, to begin the cascade.
1. Bacterium/ foreign surfaces are negatively charged. Factor XII is triggered by the negative
charge and converts to Factor XIIa
2. Factor XIIa catalyses for Factor XI to Factor XIa
3. Factor XIa catalyses for Factor IX to Factor IXa
4. Factor IXa can bind to Factor VIIIa to become the “intrinsic tenase complex”
(=phospholipid)
5. This complex can activate Factor X to Factor Xa, resulting in the prothrombinase complex
● Extrinsic Pathway (Initiation). The extrinsic pathway starts when damaged tissue exposes
tissue factors, also called tissue thromboplastin or factor III. The tissue factor activates factors
VII to begin the extrinsic pathway (but also activated monocytes can begin this pathway).
1. Tissue factors exposed at the site of damage is able to combine with Factor VIIa.
2. The Tissue Factor + Factor VIIa → activates Factor X to Factor Xa
3. Factor Xa can pair up with Factor Va, Phospholipids (negative) and Calcium =
Prothrombinase complex, which converts prothrombin into thrombin
● Common Pathway: Factor Xa works together with Factor Va, Phospholipids and Ca2+ to
catalyse the prothrombin into active thrombin → creating the ‘thrombin burst’. The main
function of the thrombin burst is the enhancement from the deactivated Fibrinogen into the
active Fibrin. Under the influence of Factor XIII, the active fibrin mashes together, cross-
linking all fibres and holds together the components of the coagulation clot.
a. Thrombin is soluble which is not bound to a membrane and is localized in free
solutions in the human body
i. Thrombin can:
1. fibrin formation
2. platelet activation
3. feedback loop → e.g. activates Factor V to Va
NOTE: the ‘Factor’ enzymes in coagulation are PRO-enzymes: they are always circulating in an inactive
form, waiting to be activated. ONLY the enzyme Factor VIIa is in traces an active form in our blood.
There are no traces of thrombin etc in the blood at all times, they will be removed.
,Regulation of coagulation:
● Regulation: First of all, the endothelial cells themselves prevent the platelets from adhering
to the underlying collagen → prevents the blood clot from becoming oversized.
● Anticoagulants disrupt the intrinsic and extrinsic pathway by interfering with factors such as
Antithrombin and Heparin:
○ Antithrombin: can bind to thrombin, forming an inactive complex.
■ Produced in the liver and blood plasma
■ Blocks factors IXa, Xa, XI, XII, thrombin
■ The activation of antithrombin is enhanced by heparin, which has no effect
on thrombin
● The thrombin can activate protein C ← anticoagulant function of thrombin.
○ Protein C can cleave factor VIIIa and Va → these factors are no longer functioning co-
factors → the thrombase reaction has delayed → the flow of thrombin activation is
not working anymore + inhibitors like antithrombin make sure that all the thrombin is
captured and then the whole thrombin generation reaction is shut down.
● Thus, there are 2 mechanisms that limit the extent of blood clotting within a vessel:
1. Inhibition of platelet adhesion
2. Inhibition of the coagulation cascade and fibrin production
● If there’s no factor XII, coagulation can still continue, since thrombin has positive feedback to
factor XI
● No Ca2+ = no coagulation
Fibrinolysis & Clot degradation: when the blood vessel has been repaired the temporary blood clot
needs to be removed.
● The endothelial cells start synthesizing and start releasing the NO (nitric oxide) along with
Tissue Plasminogen Activators (tPA)
● tPA can activate plasminogen,
therefore converting it to plasmin.
● Plasmin can degrade fibrin and
cross-links, therefore stabilizing the
blood clot, causing it to dissolve.
Haemostasis in summary:
, What would happen if coagulation cannot be regulated or controlled?
~in case of no coagulation:
● In people with haemophilia, the coagulation factors in the body are malfunctioning and
bleeding “cannot” be stopped. This means that the intrinsic, extrinsic or the common pathway
or a combination of either of the three have malfunctioned, → inhibiting the production of
fibrinogen (and thus fibrin).
● High blood pressure can also prevent platelets from adhering to the endothelial wall, being
washed away → no blood clot can be formed and the bleeding can’t be (easily) stopped.
~in case of extreme coagulation:
● The blood clot (coagulation) doesn’t stop growing. → thrombosis formations
○ One or more blood vessels might be damaged
○ anti-coagulants are absent or malfunctioning.
● It could stop the blood flow in blood vessels and the tissue penetrated by the blocked blood
vessel could die off.
● Potentially, the blood clot shoots loose due to the high blood pressure and up in the heart or
the brain, which can be lethal.
● To prevent this from occurring the fibrin is only found in the inactive state under normal
conditions.
Symptoms of acute inflammation - inflammatory response
● Is a hallmark reaction of the innate immunity.
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