Monday, 17 March 2014

The essential difference between humoral and cellular responses as shown by B cells and T cells. The role of plasma cells and memory cells in producing a secondary response.

Lymphocytes are white blood cells. They are created as stem cells in the bone marrow. They have defences that are specific to the pathogen they are attacking (unlike phagocytes which do the same for everything) which makes response slower, but more effective long term.

B cells
  • mature in the bone marrow
  • respond to antigens in the bodies fluids: tissue fluid; blood (humoral response)
  • produce antibodies
  • produce memory cells
  1. ingest pathogen and present antigens on the surface
  2. these are recognised by helper T cells, which stimulate mitosis
  3. plasma cells and a Memory cells are produced
  4. plasma cells secrete antibodies which attach to antigens on a pathogen to destroy it (primary response)
  5. memory cells stay in the blood stream for many years, if they encounter the same pathogen again, they can divide rapidly and with greater intensity to make plasma cells which will make antibodies (secondary response)
The secondary response provides long term protection as they memory cells stay alive for many years. They produce many more plasma cells and are much faster at doing so than the primary response, this means that the pathogen can be fought before it causes harm to the body.

T cells
  • mature in the thymus glands
  • recognise antigens if presented on the surface of other cells (cell-mediated response)
  • stimulate b cells and phagocytes
  • kill infected cells
  • produce memory cells
  1. Phagocytes, infected cells and cancer cells all display antigens on their surface
  2. A specific helper T cell will have receptors that fit exactly with the antigens- when they meet, the helper T cell stimulates other T cells to form appropriate clones by mitosis
  3. These T cells can: stimulate B cells; stimulate phagocytes; develop into memory cells; kill cells
  4. They kill cells by producing a protein which breaks cell-surface membranes.

Thursday, 13 March 2014

Antibody structure and the formation of an antigen-antibody complex.

Antibodies are often compared to a Y shape because of their one receptor binding site and two pathogen binding sites.

Antibodies are made of two different polypeptide chains, a light chain and a heavy chain. They are attached to each other, but can move in the pathogen binding site to help bind to the pathogen.


The variable region is different on different types of antibody because it needs to be specific to the antigen it is targeting. The constant region is the same in all antibodies.

The variable region has a tertiary structure that is complimentary to (fits with) that of the antigen it is aiming to destroy- this is so that the two can bind and form what is known as an antigen-antibody complex.

wikipedia

Wednesday, 12 March 2014

Definition of antigen and antibody.

An antigen is a 'marker' on a cell that is foreign to the body that identifies it as non-self.

An antibody is a protein produced by the body to destroy pathogens.

Phagocytosis and the role of lysosomes and lysosomal enzymes in the subsequent destruction of ingested pathogens.

Phagocytes are white blood cells. They destroy bacteria by engulfing them and breaking them down- this process is called phagocytosis.

The phagocyte recognises a pathogen because of its chemical products and so moves towards it.

It then binds with the pathogen and begins to engulf (wrap around) it- by doing this it forms a vesicle (sac) with the phagocyte inside it know as a phagosome.

Lysosomes (vesicles with enzymes inside) release digestive enzymes into the phagosome, this means that it can be broken down. Useful products are absorbed by the cell and others are excreted.

Risk factors associated with coronary heart disease: diet, blood cholesterol, cigarette smoking and high blood pressure. Candidates should be able to describe and explain data relating to the relationship between specific risk factors and the incidence of coronary heart disease

A number of factors can increase the risk of coronary heart disease:

Diet

  • Salt raises blood pressure.
  • Saturated fat increases blood cholesterol.

Blood cholesterol

  • Low-density lipoproteins associate with white blood cells to cause atheromas.
  • High-density lipoproteins help lower cholesterol.


Smoking

  • Nicotine stimulates the production of adrenalin, this causes a quicker heart rate and therefore raises the blood pressure.
  • Nicotine makes platelets stick together, so thrombosis is more likely.
  • Carbon monoxide combines with heamaglobin so less oxygen can be carried in the blood. The heart has to pump more quickly to deliver the same amount of oxygen, so blood pressure is raised. The heart muscles may not get enough oxygen leading to a heart attack or angina (chest pain).


High blood pressure

  • Arteries are put under more pressure so will form hard walls to resist the pressure- these thicker walls constrict blood flow.
  • The pressure can burst open the arteries (haemorrhage).

Monday, 10 March 2014

Atheroma as the presence of fatty material within the walls of arteries. The link between atheroma and the increased risk of aneurysm and thrombosis. Myocardial infarction and its cause in terms of an interruption to the blood flow to heart muscle.

Atheroma is the name given to fatty build ups in artery walls: consisting of cholesterol, fibres, dead cells and white blood cells attached to fats.

Aneurysm
This is when an atheroma weakens an artery wall and it swells with blood making an aneurysm. If it bursts (haemorrhage) blood is lost- this can be fatal. In the brain this is what we know as a stroke.

Thrombosis
When an atheroma bursts the lining of an artery (endothelium) and obstructs blood flow. A clot (thrombus) can form here and block the vessel, or be carried around the body and block another vessel. The blocked off area doesn't receive oxygen so will die.

Myocardial infraction
This is a heart attack. A blockage stops blood getting to the heart tissue; the tissue doesn't receive enough oxygen and so gets damaged. The damage prevents the heart from pumping properly.

clickforbiology

The effects of fibrosis, asthma and emphysema on lung function.

Fibrosis
Scars in the lung tissue thicken the alveoli increasing the diffusion distance, decrease the volume in the lungs and reduce elasticity. This means that less air can be taken in, and oxygen diffuses more slowly decreasing the bodies supply.

  • Shortness of breath- attempt to increase oxygen supply
  • Cough- reflex to obstruction of the scars
  • Pain- increased pressure
  • Fatigue- lack of oxygen for respiration so less ATP (energy) is produced
Asthma
An allergic reaction causes white blood cells to release histamine, a chemical which inflames breathing pathways and constricts them (by contracting muscles)  and increases mucus.
  • Difficulty breathing- constriction, inflammation and mucus
  • Wheezing- constriction
  • Tight feeling- lungs can't ventilate because of airway constriction
  • Coughing- reflex to obstruction
Emphysema
Elastic tissue in the lungs looses its elastic properties due to smoking. The lungs can't recoil to push air out effectively, and so old air is not replenished and there is a reduced diffusion gradient. Alveoli break down so surface area and the walls thicken so the diffusion distance is increased. Due to these factors less oxygen can diffuse into the blood.
  • Shortness of breath- attempt to increase oxygen supply
  • Cough- reflex to obstruction of damaged tissue
  • Blueish skin- low oxygen levels in the blood