Work Experience-week 17-20

Another common procedure is a total knee replacement.

The most common reason for a knee replacement is again osteoarthritis. This surgery is used only as a last resort though. Therefore all other treatment must have failed in order to resort to this option or maybe the pain is so severe it is impacting on your daily life and the mobility. Again most total knee replacements are carried out on elderly people.   This is an image of what a total knee replacement looks likes.

Work Experience- Week 14-16

A very common operation people will come in for while at work experience was hip replacements. This is a very common operation especially in the older generation.

Some of the common reasons for a hip replacement are:

  • osteoarthritis- the cartilage inside your hip joint gets worn away meaning the bones rub together which can be extremely painful
  • hip fracture- which can be common in the elderly if they fall due to their fragile bones
  • rheumatoid arthritis- when the immune system attacks the joint meaning it can be very painful

The recovery time can vary from two months to a year and the physiotherapy team help you regains full function of your hip.

The purpose of a new hip joint is to:

  • relieve pain in order to increase comfort
  • improve the function of your hip and the ability to move

Work Experience-Week 10-13

While observing a doctor I noticed he was taking a blood test. Upon asking why he was taking a blood test from this particular person he said to observe her potassium levels. She was on blood thinners. This can cause high potassium levels also known as hyperkalaemia therefore I decided to further research these topics. The patient had to be on blood thinners due to a heart valve replacement.

Hyperkalaemia is when you have too much potassium in your blood. The levels of potassium in your body is usually carefully balanced to help your heart and other muscles work properly. Too much potassium in your blood could lead to potentially fatal changes in your heart rhythm. Hyperkalaemia may occur if your kidneys cannot work properly and remove potassium from your body. Certain medication such as blood thinners can make it harder for kidneys to remove potassium as was the case with the patient. However the most common cause of hyperkalaemia is kidney disease. As your kidneys are the ones who carefully balance the potassium in your blood as mentioned previously. If your kidneys don’t work well they cannot filter extra potassium from the blood or remove it from the body. The hormone aldosterone help control the levels of potassium and sodium in the blood by telling the kidneys when to remove potassium and sodium. Therefore disease which affect the production if aldosterone can also lead to hyperkalaemia eg Addison’s disease.

Symptoms of hyperkalaemia include arrhythmia (which can be life threatening), slow heart rate and weakness.

Transplantation

Another interesting talk at Cambridge was made by Dr Menna Clatworthy we discussed a case and what needs to be considered when a kidney is transplanted.

Transplantation is the transfer of cells, tissues or organs from a donor to a recipient. The donor may be animals (pig kidney or hearts). However the cells produce different proteins meaning they are foreign in the human body. The donor may also be human living donors.

Let’s consider a case. Mr X is a 49 year old male who has type 1 diabetes mellitus meaning he does not produce insulin. The diabetes damaged his kidneys. Kidneys are very important for filtering waste products, produces hormone to make red blood cells, makes an active form of Vitamin D and reabsorbs water and minerals. Mr X’s options include dialysis. However this means plastic in the circulation, makes him prone to infection, means a fluid restriction (<750 ml in 24 hours), takes up 3-4 hours 3x week, means a low potassium and low phosphate diet. Right now his best option is a transplant.

Mr X’s wife wants to give him her kidney. Factors to consider include: blood group, tissue type, is the donor fit enough? His wife has to be blood group compatible because blood group A has antibodies against blood group B therefore the transplantation is rejected. It turns out Mr X’s wife is both blood group and tissue type compatible. The kidney is taken out laproscopically (keyhole surgery). Mr X’s transplant takes 3-4 hours and they do not take out his kidney.

What can go wrong?

  • Delayed graft function
  • Plumbing problems
  • Rejection (15-20%) which is tested by biopsy and the presence of immune cells

Immunosuppressants are used by Mr X to reduce risk of rejection which leads to reduced functionality of the immune system which increases the risk of infection. The transplant leads to a huge improvement in quantity and quality of life. 50% of organs survive 15 years.

Finally what does the future hold for transplantations? They are a shortage of organs therefore we could: look at donors never thought of (older donors), help revive organs, lab grown kidney, have people opt out of transplantation than opt in.

Alzheimer’s Disease- What’s the problem and how do we fix it?

There was a very insightful talk by Professor Tim Bussey in the Department of Experimental Psychology at Cambridge.

Here are some facts and statistics about Alzheimer’s. Alzheimer’s disease has 100% mortality (usually within 10 years) as there is no cure or remissions. It is now the 4th leading cause of death in industrialised societies and the annual number of new cases of Alzheimer’s disease is projected to double by 2050. Currently every 68 seconds a person develops Alzheimer’s disease and it is projected to increase to every 33 seconds.

Alzheimer’s is a disease of the brain which reduces activity in the brain. Alzheimer’s consists of two abnormal structures:

  1. Beta-amyloid plaques– dense deposits of protein and cellular material which accumulate outside and around nerves. The amyloid precursor protein (APP) is a precursor to the beta-amyloid plaques. The APP sticks through neuron membrane enzymes and cut APP into fragment of proteins (beta-amyloid plaques). The beta-amyloid plaques come together to form plaques.
  2. Neurofibrillary tangles- twisted fibres build up inside nerve cells. The brain cells can’t function when they’re around. Neurons internal support is made of microtubules. Tau is a protein which stabilizes the microtubules. Changes in tau causing the microtubules to collapse and the tau protein clump.

During Alzheimer’s the cells die (affected regions shrink). It starts small and spreads. Alzheimer’s is first noticed in the entorhinal cortex then proceeds to the hippocampus. The cerebral cortex begins to shrink as more and more neurons die. I very severe Alzheimer’s there are even holes in the brain. At this point they are dependent on others for care.

CAUSES (both genetic and environmental)

Environmental:

  • Lower childhood education
  • Age
  • Head injury
  • Cerebrovascular disease
  • Aluminium (still to be confirmed)

Genetic:

  • Mutation in genes (early onset which is rare and genetic)
  • Genes associated to Alzheimer’s contribute to multiple interlinked pathways related to Alzheimer’s.

TREAMENT:

  • Drugs- Aricept (mild effect), Exelon, Reminyl, Wamenda

The solution is to change treatment from symptomatic to preventive such as vaccinations to get rid of plaques and antibodies to destroy plaques. However this is not that simple as people have still died when the plaques are removed. Therefore the plaques may initiate other processes, other invisible plaques? Therefore maybe early detection is key even before the symptoms start because the disease starts 10-15 years before symptoms. However some people may have plaques but not develop the disease.

 

 

The Biology of Appetite- Sadaf Farooqi

Appetite is the desire to eat food in order to maintain energy needs. Sometimes our system (set of behaviour) has to alter to maintain these energy needs e.g. when bears hibernate they need to lower their metabolic rate. Eating is seen as a social activity as well as essential in maintaining energy expenditure (75% of which are for basic needs).

What influences our eating behaviour?

  • Metabolic needs
  • Environment e.g. type of food available, price of food
  • Learning- studies show children have learnt McDonald’s packaging means a reward so they prefer carrot sticks in McDonald’s wrapping

 

Eating behaviour can also be considered as heritable. Twins have similar eating behaviour traits. This helps support how genes strongly influence eating behaviour. There is a certain genotype which means you enjoy food more or less. The heritable of body weight is as heritable as height. Showing body weight runs in families and twins. Studies show that 70% -90% of identical twins have concordant body weights whereas 30-50% of non-identical twins have concordant body weights. However we have seen that genes have a stronger/more potent role in extremes (very thin or very fat). 40-70% of difference in weight is due to genes. Another study showed when identical twins are overfed by 10% they gain a similar amount of weight compared to other people who gain weight in varying proportions. Overall conclusion is that genes influence weight but interact with the environment.

 

We know that rare genetic variants have a bigger impact in weight whereas common genetic variants have a more subtle impact on weight. There is a hormone called leptin which is made by fat. If you are fatter, there is more leptin which goes to the brain and regulate your weight. If there is lepton missing or receptors in the brain which recognise leptin missing you are much heavier. This shows that leptin controls your weight by the leptin going to the brain and triggering a response to control food intake and how we burn calories. The hypothalamus receives signals from the gut. A fall in leptin triggers and increase in food intake and decreases energy expenditure to restore energy stores. When we don’t have leptin the brain would constantly tell us to eats as a survival response and if not we are going to die. Therefore we would become obsessed with food. A defect in the gene means some people don’t make leptin.

Treatment includes taking synthetic leptin as it regulates weight and appetite. It also controls the kind of food we like so without leptin you feel like you have to eat everything that moves. The treatment controls these desires.

The Science of Laughter- Sophie Scott

I went to a very interesting discourse on the science of laughter where the social and neurological implications of laughter was discussed.

Laughter is an action which can overwhelm finely controlled intercostal muscles and the larynx. It also stops you breathing and speaking and only lets you breathe out. Laughter, such a simple and everyday action is also a pain relief. The science behind that is that laughter is a lot of work therefore releasing a lot of endorphins and less adrenalin. Endorphins transmit electric signal within the brain and are found in the pituitary gland. They interact with the opiate receptors to reduce our perception of pain. Laughter is also a highly contagious behaviour.

What was also discussed was if laughter was a basic expressing emotion. Basic emotions are: universal, based upon a specific neutral expression, evolutionary ancient and a distinct expression. We considered that laughter was the only positive bi-directionally recognised emotion so is it universal? All animals laugh so we would not be surprised if it was universal.

The origin of laughter in us are when as infants we are tickled. This shows laughter is an interactive behaviour. We use laughter as a basis of social interaction and bonding. Laughter is something we do with others. Laughter is also associated with play. When we see a ‘play-face’ and noise (laughter) we associate this with good intentions and no harm intended.

When asking people what makes them laugh most common answer was humour for example comedy. However 30% of people more likely to laugh with other people. On average people laugh 7 times per 10 minutes of conversation. And we are more likely to laugh if we like/know/agree with the person. Another interesting point is that the person laughing most in a conversation is the person talking showing laughter as a voluntary communicative act. Despite the huge rise in social media we laugh most during face to face interaction.

When thinking about how the brain responds to laughter studies have shown that when we hear disgust our brains respond by activity of auditory areas and facial motor areas. As if the brain is mirroring the person making the sound. When there is a positive sound there is more activity and greater mirroring system. Therefore your brain responds to the sound by activity in the areas which would make these sounds and the activity is so large you actually end up laughing showing why laughter is contagious.

Our brain also treats real and posed laughter differently. There is greater activity in audio area with real laughter as we hear sounds not usually heard. There is also more activity brain trying to work out why they are laughing if the laughter is posed. However the mirror system is the same with real and posed laughter.

Finally laughter is an important social cue especially in relationships. Studies have shown if you respond to stress with laughter relationship lasts longer and laughter closes the distance between people.

 

First Aid Course- Level 2

A few weeks ago I completed my First Aid Course Level 2 which I passed!!! There was a lot of recapping Dr ABC, CPR, recovery position, bleeds etc. However what I did learn was the importance of asking the casualty questions to build up a picture of what has happened and their medical history. This emphasies the fact that communication is key.

Too much of a good thing

All organisms are made up of DNA with genetics being an approach or way of looking at life. A gene is a piece of DNA that codes for a protein. However genes are more complicated than that. There are sequences to code for the protein but also signals to cut of intervening DNA, signals to say go and stop and DNA to say where and when the proteins are needed. All cells contain the same DNA but not all cells look the same because DNA can be turned on and off so only certain proteins are made in different cells. DNA is simple but long made up of four bases meaning DNA stays simple at a chemical level. The simplicity of copying DNA is independent of the complexity of the message is contains therefore duplication a gene is easy

The mechanism of translating the message of genes is simple no matter how complicated the gene is however the complexity of genes comes from evolution, New genes comes from other genes which have been copied but tweaked a little. This is evolution by gene duplication.Duplicated genes in our genome evolve to give slightly different but related functions. For example there are 900 olfactory receptor genes in our genome but all recepting to different smells.

Gene duplication is not usually one by one but a whole genome duplication. This is more powerful in effect ad the whole set works together. This whole genome duplication is the basis of our evolution our genome was doubled then doubled again giving us the raw material for complexity, diversity and evolution. Some gene duplication cause disorders for example Down Syndrome is caused by the copy of a chromosome. Genes are sensitive to quantities. Therefore high concentrations of proteins usually drift away and cause an aggregation leading to a plaque. With too much proteins they cannot combine in the right way so they have to stay in balance.

Overall dosage sensitivity influences the pattern of evolution in characteristic ways disrupting the fine balance in genes.

The Neuroscience of Memory-travels through space and time (Eleanor Maguire)

A few weeks ago I went to a RIGB lecture, even though I missed 20 minutes of it this is what I learnt.

The hippocampus is involved with visually planning and without this part of the brain we cannot use small roads and lacks small detail planning. A taxi driver who had part of his hippocampus removed was asked to make a journey from A to B. He was unable to make this journey as without the full function of this part of the brain he was unable to navigate through the streets of London. What was also noticed was that he only used big main roads and no smaller side roads.

Taxi drivers seem to have a larger back hippocampus due to the amount of navigation which is involved in their jobs. A study helped prove that the bran is not fixed but can change. A group of taxi driver trainees had a picture of their brain taken. After taking the test they examined their brains after also. The people who passed and qualified as a taxi driver their hippocampus grew and those who failed their hippocampus stayed the same size.

The hippocampus is important for recalling the past and navigation/planning/distance. So people with hippocampus damage can’t imagine scenes in general past or future. The hippocampus is needed for scene construction and spatial awareness. When people with hippocampus damage are asked to imagine a beach lets say, they cannot reconstruct such an image in their head.

Boundary extension is something that happens with a scene. It extends a scene so we are aware of the world so we extrapolate beyond the picture. People with hippocampus damage have reduced boundary extension so they are stuck in the present and what is in front of them.