Lecture notes
NERVOUS SYSTEM SUMMARY
- Module
- Anatomy (TNA4001)
- Institution
- Birmingham City University (BCU)
Summary lecture notes on the physiology of the nervous system
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Immune system lecture summaryWe are under constant attack of microorganisms, like bacteria, fungi and viruses. Most
microorganisms are perfectly harmless and live on the outside of our body (e.g. skin, inside gut).
However, amongst this commensal flora are pathogens that want to take advantage of the nice
environment of our tissues, and, when they manage to get in, can destroy it and make you ill. These
opportunistic pathogens lie in wait for an opportunity to enter the body and proliferate (increase in
numbers) and take over the place. Good workplace hygiene reduces that chance of spreading
infection.
The first layer of defence are physical surface barriers between inside and outside world.
Mechanical barriers are formed by fast growing epithelium tissue consisting of (layers of) tightly-
coupled cells. Antimicrobial chemicals, like enzymes and acids for additional chemical barriers. In
addition commensal flora competes for resources forms a biological barrier that keeps pathogens at
bay.
The second layer of defence is formed by the innate immunity, a system that recognises pathogen-
associated molecular patterns on common patogens, or damage-associated molecular patterns on
your own damaged cells. Leukocytes like phagocytes, natural killer cells and dendritic cells
recognise these patterns and destroy the cells expressing them. In this process, called inflammation,
histamine released from mast cells increases blood flow to the attacked/damaged area (red, hot)
and makes capillaries permeable (swelling) so that leukocytes can devour the intruders and/or
damaged cells and clear the area ready for reconstruction.
If the pathogen can outnumber or dodge the innate immune system the adaptive or required
immunity kicks in. Antigen is protein specific to a pathogen or foreign body or own cells that are
faulty by which they are recognised by macrophages that swallow the pathogen and then present
the specific antigen of that pathogen to helper T lymphocytes (TH-cells). They present the antigen to
B Lymphocytes that then activate, multiply and start making antibodies selective to that particular
antigen. Antibodies are immunoglobulins, like IgE and IgG, with two binding sites for their specific
antigen. The antibodies locked onto antigens, form markers for cytotoxic T lymphocytes (TC-cells)
and other phagocytes, to destroy the antibody-marked cells. After dealing with a first exposure, a
small number of lymphocytes for a particular antigen remain as memory cells. Upon second
exposure to the pathogen, these specific lymphocytes can quickly proliferate and effectively deal
with the revisiting pathogen, normally even before any symptoms appear. Over time we acquire
immunity (memory cells) for a wide range of pathogens.
As a temporary measure a baby receives passive immunity in the form of antibodies from the
mother through placenta and breast milk, but the child needs to build up its own acquired immunity
through exposure. Vaccination or immunisation introduces antigens in the form of ‘disarmed’
pathogens or harmless parts of toxins, as a controlled first exposure, so that on next accidental
exposure, the memory cells for that particular antigen can mount an effective counter attack and
prevent illness. In this way mayor killer diseases have been eradicated or are brought under control.
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