A Curious Case of Autism Spectrum Disorder

I have read ‘The Curious Incident of the Dog in the Night-time’ and have also seen the play in London. I really enjoyed it and from my experience working with autistic children, in Romania, it made me want to investigate more. I also recently saw an article about the first person to be diagnosed with Autism and that inspired me to write this blog.

curious incident

‘The Curious Incident’ written by Mark Haddon and adapted for the stage by Simon Stephens is about a boy called Christopher who writes about his adventures; solving the mystery of the death of his neighbour’s dog, taking his Maths A-level, looking after his pet rat Toby and talking with people of whom he has never met before. Christopher has autism and the book is cleverly written to show the reader how a young person with autism sees and reacts to the world. It is an excellent book and I would highly recommend reading it.

Romania Project Team

Romania Project Team

From my experience working with children in Romania, a life for children with Autism in that country is very different to in England. Where Christopher, in the Curious Incident had a care-worker and many people looking out for him, I saw that the carers in Romania did not really know how to care for the children in a similar way. Many of them were left alone to do their own thing and the carers had to look after so many children at once, with other learning difficulties, that they were unable to give the boys with autism the extra attention they needed. I spent some time with a boy in Romania and integrated him into the activities we were doing, taking notice of what he liked and disliked. For example, when the children were given a painting activity, I noticed that this boy did not like getting his hands dirty so I sat with him and gave him many different materials to feel and find what he liked to work with- he absolutely loved the fur!

So, after all of this, it made me want to look further into Autism.

Autism Spectrum Disorder

Autism Spectrum Disorder (ASD) is a life-long developmental disability that affects communication, behaviour, social interaction and interest. Children are usually diagnosed before the age of 3.

Around 1 in 100 people suffer from ASD and around 700,000 people in the UK are on the autism spectrum.

Interestingly, the term ‘autism’ was derived from the clinical description of the withdrawal and internalisation demonstrated by schizophrenia patients.

amygdala

The cause of autism is unknown but it is considered that a combination of genetic and environmental factors account for the changes in brain development. Some researchers believe that an abnormality in the area of the brain called the amygdala may play a part in the deficits of ‘social intelligence’ of the disorder (http://www.ncbi.nlm.nih.gov/pubmed/10781695)

ASD covers a range of different disorders, such as:

  • Autistic disorder
  • Asperger syndrome
  • Childhood disintegrative disorder
  • Pervasive developmental disorder

Symptoms:

Children and young people with autism often experience a range of cognitive, learning, emotional and behavioural problems, such as:

Behaviour:

  • Short attention span
  • Is overactive or very passive
  • Has very narrow interests
  • Uses repetitive body movements
  • Shows aggression towards others or themselves

Social Interaction:

  • Does not make friends
  • Do not get involved in interactive play
  • Does not react to eye contact or smiles
  • Shows a lack of empathy
  • Prefers spending time alone

Communication:

  • Cannot start or maintain a social conversation
  • Develops language slowly or not at all
  • Does not refer to self correctly (e.g. Says ‘you want water’ when they mean ‘I want water’)
  • Repeats words or memorised phrases

Many people with ASD suffer from difficulties with their senses:

  • Sight
  • Sound
  • Taste
  • Touch
  • Smell
  • Balance (Vestibular)
  • Body awareness (proprioception)

People with ASD can be hyposensitive or hypersensitive to any of these senses (this is something that I encountered whilst volunteering in Romania).

Many of the children in Romania who were hyposensitive to vestibular movements needed to rock or swing in order to achieve sensory input and we would spin them on a wheeled board around a room, which they really enjoyed. We also bought them a see-saw which many of the children really loved. We also worked with children who were hyper-proprioceptive and had difficulties with fine motor skills. These children found it very different to colour in small pictures and were unable to do up buttons on their clothes.

On the National Autistic Society website (http://www.autism.org.uk/about/behaviour/sensory-world.aspx) it talks about hyposensitivity to touch and how people like to hold others tightly, have a high pain threshold and may also self-harm. At the rehabilitation centre in Romania, I worked closely with a blind boy who, initially, was not allowed to get involved with the project as the Romanian carers did not see how he would benefit. I persisted and they allowed me to work with him; I sang with him but the leader of our project, an occupational therapist, suggested that I try to stimulate his senses in other ways. I used a stretchy piece of material and wrapped it around his body- he really enjoyed the tightness of the material and therefore when I held his hand, I would squeeze it slightly to stimulate these senses. However, despite being happier on the project, I also noticed that he would poke himself in the eyes for long periods of time; I thought it was because he could not see, and I’m sure to an extent it was, but also from reading this, it is suggesting that he could have suffered from ASD.

The first diagnosis of Autism

Donald Grey Triplett was the first person to be diagnosed with autism by the Baltimore psychiatrist Leo Kanner. It was then known as ‘infantile autism’. Triplett visited Kanner in 1938, at age 5, but Kanner was unable to diagnose his symptoms. However, by 1943, Kanner had encountered 10 other, similar cases and had published an article called “Autistic Disturbances of Affective Contact”, with Donald as case number 1.

Donald Grey Triplett

Donald Grey Triplett

Donald Triplett was born in 1933 in forest, Mississippi. He was a very withdraw child who seemed to mimic what other people had said, instead of forming his own conversations. However, he was a very intelligent young boy with an excellent memory, and was able to sing with perfect pitch at age 2.

In 1937, at age 3, Donald was sent to live in an institution, as instructed by his doctor, but in 1938 his parents took him out of the institution to visit Dr Kanner.

Donald is still alive today, at age 82, living in the home he grew up in, surrounded by a supportive community of friends.

For more about his story, follow this link: http://www.bbc.co.uk/news/magazine-35350880

Thanks, Rachel

The Immortal Life of Henrietta Lacks

The Immortal Life of Henrietta Lacks

immortal life of HL‘The Immortal Life of Henrietta Lacks’ was an incredibly entertaining and informative read that I would highly recommend to anyone interested in science. The balance between the science and relationships built between the characters (who are all real people) further strengthens the aim of the book- to inform the world that HeLa cells originated from a real person- Henrietta Lacks.

“Hela cells were one of the most important things that happened to medicine in the last hundred years.”- Donald Defler

Henrietta Lacks

henrietta lacks

Henrietta Lacks

Henrietta Lacks (originally Loretta Pleasant) was born in Roanoke, Virginia on August 18th 1920. Her mother died in 1924 and she then lived with her grandfather, Tommy Lacks. Henrietta married her cousin David (Day) and had five children: Lawrence, Elsie (who spent the majority of her life institutionalised at Crownsville, and died at age 15), David Jr (Sonny), Deborah (Dale) and Joe (Zakariyya), all of whom are mentioned in great detail in the book.

Henrietta first went to see her doctor on January 29th, 1951 regarding a pain. Her doctor examined her and found a lump which he assumed was a sore from syphilis. It tested negative for this and her doctor recommended that she visit Johns Hopkins gynaecology clinic. Despite being treated, she died on October 4th 1951.

The book

This book, written by Rebecca Skloot, covers a variety of themes in detail. The first is forgotten identity; the scientists who studied the HeLa cells did not know their origin (other

Rebecca Skloot

Rebecca Skloot

than George Gey, the original researcher). They used the cells for amazing research but it wasn’t until many years later that people began to question whose cells they were using. For decades it was thought that the woman who ‘donated’ the cells was called Helen Lane but this was not true. Not even Henrietta’s family knew about her cells and it wasn’t until many years later that her true name was published in a medical article.

The second theme is the advancement of science. Due to these amazing, cancerous cells, many medical advancements have taken place (some of which are mentioned below).

The third theme focuses on the political argument of ‘informed consent’. Henrietta Lacks did not donate her cells but they were taken from her cervix after some of her radium treatment. Whilst many people profited from the growth of HeLa, Henrietta’s family were not even able to pay for health insurance. Although none of them have actually sued anyone at Johns Hopkins Hospital, it is possible that they would not have had a strong case as it was not illegal to use tissue samples from patients, for research. However, as Henrietta was not supposedly aware of the removal of these cells, it becomes a lot more difficult to state what was ‘okay’ or not, at the time. Nowadays, if doctors wanted to collect samples from a patient for research purposes only, they would require consent. Ironically, HeLa was used as a precedent in another case where a man, John Moore, sued his doctor and the hospital for using his body in research without consent. The judge said that due to no one suing over the growth or ownership of the HeLa cell line, it was obvious that patients did not mind that doctors used their cells and turned them into commercial products. However, the difference was that Henrietta was no longer alive and that her family was still unaware.

What is meant by ‘immortal’?

Before I read the book, I was unsure as to what ‘immortal’ really meant. Learning the mechanism behind it really allowed me to understand why her cells are still alive today.

Scientists had been trying to keep human cells in culture for years previously, without success. Hela cells reproduced an entire generation every 24 hours without stopping. They became the first immortal human cells ever grown in a laboratory.

telomereIn normal cells, the string of DNA at the end of each chromosome is called a telomere and this shortens every time a cell divides. This occurs until the telomere is almost gone and when this happens, the cell stops dividing and begins to die. In the early 1990s, a scientist at Yale used HeLa cells to discover that human cancer cells contain an enzyme called telomerase which rebuilds the telomeres. This meant that cells were able to regenerate their telomeres indefinitely and the cells would not die.

Her cells were part of research into the genes that cause cancer and those that suppress it; they helped develop drugs for treating herpes, leukaemia, influenza, haemophilia, and Parkinson’s disease. They have been used to study lactose digestion, sexually transmitted diseases, appendicitis, human longevity, mosquito mating, and the negative cellular effects of working in sewers.

The Cancer

Henrietta Lacks- after having a biopsy of the tumour in her cervix, Howard Jones (Henrietta’s gynaecologist from Johns Hopkins) diagnosed her with epidermoid carcinoma of the cervix, Stage I. However, a few months after George Gey (researcher of HeLa) died, Howard Jones saw photographs of her biopsy and realised that she had been misdiagnosed and although it was invasive, it was a very aggressive adenocarcinoma of the cervix. This meant that originated from glandular tissue instead of epithelial tissue. Despite the misdiagnosis, this would not have changed the way Henrietta’s cancer was treated.

There are 2 types of cervical carcinomas; invasive carcinomas, which have penetrated the surface of the cervix, and non-invasive carcinomas (carcinoma in situ) which grows in a smooth layered sheet over the surface of the cervix. Carcinoma in situ has only been able to be diagnosed since 1941 when the Greek researcher, George Papanicolaou, developed the ‘Pap smear’ which involved scraping cells from the cervix with a curved glass pipette and examining them under a microscope.

Henrietta’s had an invasive carcinoma and Hopkins treated it with radium, a white radioactive metal that glows blue. When it was discovered in the late 1800s, radium was used on a regular basis but many patients started dying. This is because it causes mutations that can turn into cancer, and in high doses it can burn the skin off a person’s body. Despite this, it is also able to kill cancer cells.

When Henrietta had her first treatment, Dr. Lawrence Wharton Jr (Henrietta’s surgeon) took a sample of her cancerous cervix cells and sent the tissue sample to George Gey (who later died from pancreatic cancer) for his research.

In 1984, a German virologist (Harald zur Hausen) discovered a new strain of STD called Human Papilloma Virus 18 (HPV-18). He believed that this and HPV-16, which he had discovered a year earlier, caused cervical cancer. A sample of Henrietta’s original biopsy was tested and it showed that she had been infected with multiple copies of HPV-18, which turned out to be one of the most severe strains of the virus. HPV inserts its DNA into the DNA of a host cell where it produces proteins that lead to cancer. In Henrietta, HPV inserted its DNA into the long arm of her 11th chromosome and essentially turned off her p53 tumour suppressor gene. It is still unknown why her cells were as virulent as they were due to the fact that cervical cancer cells are some of the hardest to culture. In addition to this, scientist learnt that when they blocked the HPV DNA, cervical cancer cells stopped being cancerous. This led to zur Hausen earning a Nobel Prize.

The beginning of HeLa

George Gey

George Gey

Alexis Carrel- a French surgeon and Nobel Prize recipient claimed to have cultured ‘immortal’ chicken heart cells. Also, he invented the first technique for suturing blood vessels together (for which he won the Nobel Prize) and used it to perform the first coronary bypass and develop methods for transplanting organs. He wrongly believed that light could kill cell cultures. Carrel’s immortal chicken heart was greatly publicized and they had been alive for over 20 years. However, it had never been replicated by any other scientist and other scientists grew suspicious of Carrel. It went against a basic rule of biology- that normal cells can only divide a finite number of times before dying (this is known as the Hayflick Limit, since 1961). It was later discovered that only cells that had been transformed by a virus or a genetic mutation had the ability to become immortal. Apparently, the original chicken-heart cells had actually died soon after he had put them in culture and whether he knew it or not, Carrel had been putting in new cells every time he ‘fed’ the original cells.

In 1951, Henrietta’s cells began growing in Gey’s lab. Gey distributed the cells to many researchers all over the country who were interested in working with them.

What did HeLa do?

  • Researchers exposed HeLa to different types of viruses- herpes, measles, mumps, fowl pox and equine encephalitis to study how each one entered cells, reproduced and spread.
  • A group of researchers used HeLa to develop methods for freezing cells without harming or changing them and this meant that they could store cells between experiments without worrying about keeping them fed and sterile. This was then used to find out the exact moment when a normal cell growing in culture became malignant, which is known as spontaneous transformation. This was a celebrated prospect for finding a cure for cancer but when it was revealed that HeLa had contaminated the research of other scientists working with other cells, it was probable that instead of normal cells spontaneously becoming cancerous, they were most likely just taken over by HeLa. Many years later, blood was taken from her husband and two of her children which were used to create a map of her DNA which scientists could use to help identify HeLa cells in culture.
  • Harry Eagle (National Institute of Health-NIH) used HeLa to develop the first standardized culture medium.
  • Scientists wanted to grow cellular clones and in Colorado they succeeded using HeLa before Dolly the sheep was cloned, using the DNA from one parent. HeLa cells were taken as a cluster of cells from a section of her tumour and even though they are from the same sample, cells often behave differently, growing faster than others and having unique traits. HeLa then helped develop cloning technology and led to the ability of growing single cells in culture; this included isolating stem cells, IVF and cloning whole animals (like Dolly).
  • HeLa was used to inform researchers that human cells did not contain 48 chromosomes, and when mixedWhat did HeLa do?
    • Researchers exposed HeLa to different types of viruses- herpes, measles, mumps, fowl pox and equine encephalitis to study how each one entered cells, reproduced and spread.
    • A group of researchers used HeLa to develop methods for freezing cells without harming or changing them and this meant that they could store cells between experiments without worrying about keeping them fed and sterile. This was then used to find out the exact moment when a normal cell growing in culture became malignant, which is known as spontaneous transformation. This was a celebrated prospect for finding a cure for cancer but when it was revealed that HeLa had contaminated the research of other scientists working with other cells, it was probable that instead of normal cells spontaneously becoming cancerous, they were most likely just taken over by HeLa. Many years later, blood was taken from her husband and two of her children which were used to create a map of her DNA which scientists could use to help identify HeLa cells in culture.
    • Harry Eagle (National Institute of Health-NIH) used HeLa to develop the first standardized culture medium.
    • Scientists wanted to grow cellular clones and in Colorado they succeeded using HeLa before Dolly the sheep was cloned, using the DNA from one parent. HeLa cells were taken as a cluster of cells from a section of her tumour and even though they are from the same sample, cells often behave differently, growing faster than others and having unique traits. HeLa then helped develop cloning technology and led to the ability of growing single cells in culture; this included isolating stem cells, IVF and cloning whole animals (like Dolly).
    • HeLa was used to inform researchers that human cells did not contain 48 chromosomes, and when mixed accidentally with the wrong liquid, chromosomes were able to be examined and it was realised that there are 46 chromosomes in each human cell. This also then made it possible to diagnose genetic and chromosomal disorders such as Down’s syndrome.
    • People thought that because these cells were immortal they might be able to prevent wrinkles in the neck and throat area. Although this was not possible, cosmetic and pharmaceutical companies throughout the USA and Europe began using HeLa instead of laboratory animals to test whether new products and drugs caused cellular damage.
    • Also, both Russian and American scientists had managed to grow HeLa in space. In 1960, HeLa went up in the second satellite ever in orbit launched by the Russian space programme. Almost immediately, NASA shot several vials of HeLa into space in the Discoverer XVIII satellite. HeLa went with the first humans into orbit so that they could study the effects of space on humans- would it cause cellular changes etc?
    • In 1965, two British scientists, Henry Harris and John Watkins, investigated the consequences of somatic cell fusion (when cells fuse, the genetic material from the two cells combine). They fused HeLa cells with mouse cells and created the first human-animal hybrids (cells that contained equal amounts of DNA from Henrietta and a mouse). Soon after, researchers in NY discovered that the hybrids lost their human chromosomes over time which only left the mouse chromosomes. This allowed scientists to begin mapping human genes to specific chromosomes by tracking the order in which genetic traits vanished. The hybrids were also used to investigate the role of immunity in organ transplantation and realised that DNA from two different individuals were able to survive together inside cells without rejecting one another. This meant that the mechanism for rejecting transplanted organs had to be outside the cells.

    In 2009, storing blood and tissues for research did not legally require informed consent, because the law governing such things doesn’t apply to tissue research. It is possible that the Lacks family might be able to remove HeLa cells from all research worldwide.  Fortunately for medical progress, this is not what they want as they are all very proud of their mother for her involvement in science and the benefit of others. All they wanted was for the world to recognise their mother as a person, as Henrietta Lacks, instead of just ‘HeLa’.

    Overall I have really enjoyed reading this book and looking deeper into the role of one woman as a source of all of the essential parts of Medicine we now have. It is incredible how it took the world so long to find out about Henrietta and her family and the end of the book tugs on your heartstrings as you travel the journey with everyone, in their own way.

    All the information in this post is from the amazing research of Rebecca Skloot- I would like to officially thank her for putting it all together in this amazing book.

    with the wrong liquid, chromosomes were able to be examined and it was realised that there are 46 chromosomes in each human cell. This also then made it possible to diagnose genetic and chromosomal disorders such as Down’s syndrome.

  • People thought that because these cells were immortal they might be able to prevent wrinkles in the neck and throat area. Although this was not possible, cosmetic and pharmaceutical companies throughout the USA and Europe began using HeLa instead of laboratory animals to test whether new products and drugs caused cellular damage.
  • Also, both Russian and American scientists had managed to grow HeLa in space. In 1960, HeLa went up in the second satellite ever in orbit launched by the Russian space programme. Almost immediately, NASA shot several vials of HeLa into space in the Discoverer XVIII satellite. HeLa went with the first humans into orbit so that they could study the effects of space on humans- would it cause cellular changes etc?
  • In 1965, two British scientists, Henry Harris and John Watkins, investigated the consequences of somatic cell fusion (when cells fuse, the genetic material from the two cells combine). They fused HeLa cells with mouse cells and created the first human-animal hybrids (cells that contained equal amounts of DNA from Henrietta and a mouse). Soon after, researchers in NY discovered that the hybrids lost their human chromosomes over time which only left the mouse chromosomes. This allowed scientists to begin mapping human genes to specific chromosomes by tracking the order in which genetic traits vanished. The hybrids were also used to investigate the role of immunity in organ transplantation and realised that DNA from two different individuals were able to survive together inside cells without rejecting one another. This meant that the mechanism for rejecting transplanted organs had to be outside the cells.

In 2009, storing blood and tissues for research did not legally require informed consent, because the law governing such things doesn’t apply to tissue research. It is possible that the Lacks family might be able to remove HeLa cells from all research worldwide.  Fortunately for medical progress, this is not what they want as they are all very proud of their mother for her involvement in science and the benefit of others. All they wanted was for the world to recognise their mother as a person, as Henrietta Lacks, instead of just ‘HeLa’.

Overall I have really enjoyed reading this book and looking deeper into the role of one woman as a source of all of the essential parts of Medicine we now have. It is incredible how it took the world so long to find out about Henrietta and her family and the end of the book tugs on your heartstrings as you travel the journey with everyone, in their own way.

All the information in this post is from the amazing research of Rebecca Skloot- I would like to officially thank her for putting it all together in this amazing book.

Henrietta and Day

Henrietta and Day

 

 

 

MOOC The science of medicines week 2

I have completed the second week of my MOOC on the science of medicines and I had the opportunity to learn all about diabetes; what it is and how we can treat it. I loved finding out what the mechanism of diabetes actually is- how the taking up of glucose by pancreatic B cells leads to the secretion of insulin.

I have made notes on this weeks topic and have posted them on my ‘MOOC’ blog:

https://rachelruckmooc.wordpress.com/2015/09/16/the-science-of-medicines-week-2/

MOOC The science of medicines week 1

So, along with my A levels, I have decided to do a MOOC (massive open online course) in the very little free time I have. They are amazing if you want to know more about a topic (there is no end to the number of different courses they have!) and I would definitely recommend researching more into what they are and doing one yourself! It takes a few (or more) hours per week and consists of a variety of videos, articles and quizzes. The MOOC I am doing is ‘The Science of Medicines’ and I am finding it fascinating- I like to make notes on paper but I also wanted to share the interesting research I have found, with all of you!

I had to make a separate blog for my MOOC research (due to the size of the files) and I will be updating it each week with all of the research I am doing. Here is a link to week 1:

https://rachelruckmooc.wordpress.com/2015/09/13/the-science-of-medicines-week-1/

 

 

Thomas Addison

Thomas Addison

Because the neurologist I shadowed at Southampton General Hospital told me to research about Thomas Addison, I have decided to write a blog about him.ThomasAddison

Thomas Addison (April 1793- June 29 1860) was an English Physician who studied at Guy’s Hospital, London. During his time at Guy’s, Thomas Bateman, an acclaimed dermatologist, brought about his fascination with skin diseases.   Addison is known for his discovery of Addison’s disease (a degenerative disease of the adrenal glands) and Addisonian anaemia (pernicious anaemia) – a haematological disorder later found to be caused by the failure to absorb vitamin B12.

Addison’s disease

Addison’s disease (primary adrenal insufficiency/ hypoadrenalism) is a rare, chronic condition brought about by the failure of the adrenal glands so that not enough cortisol or aldosterone is produced.

adrenal glands 2The adrenal glands are situated above the kidneys; the inner core (medulla) produces the stress hormone adrenaline whereas the outer shell (cortex) produces the steroid hormones cortisol and aldosterone. Cortisol’s function is to control inflammation, regulate the body’s nutrients, stimulates the liver to produce blood sugar and regulates water content of the body. Aldosterone helps the kidneys to regulate salt and water levels which affect blood volume and blood pressure (your blood pressure drops if your aldosterone levels drop too low).

Adrenal failure is generally brought about as a response to the immune system. When Thomas Addison first discovered the disease in 1855, the main cause was as a complication of TB (this still remains a main cause in developing countries). In third world countries, HIV (AIDS) is becoming an infectious disease that causes adrenal failure. The most common cause of adrenal failure is destructive atrophy- this is where an over-active immune system starts attacking the body’s own organs (including the adrenal glands). This affects more women than men and accounts for 70% of all cases. Rarer causes include adrenal cancer, adrenal haemorrhage (eg. as a result of a car accident) and certain fungal infections.

This disease is not usually apparent until over 90% of the adrenal cortex is destroyed (this can take months to years).

Early stage symptoms:

  • Fatigue
  • Muscle weakness
  • Low mood
  • Loss of appetite and unintentional weight loss
  • Increased thirst

Over time, the symptoms can become more severe and others can also develop

  • Hypoglycaemia
  • Hyperpigmentation- darkened patches of skin, gums or lips
  • Nausea and vomiting
  • Dizziness and fainting
  • Cramps
  • Exhaustion

Addison’s disease is treated with medications to replace the missing hormones which will be needed to be taken for the rest of your life. If left untreated, it can be fatal. With the treatment, symptoms can be mainly controlled so the patient can live an active life but they may experience times of fatigue. There may also be associating health conditions such as diabetes or an underactive thyroid.

Addisonian anaemia (pernicious anaemia)

This disease occurs when a lack of vitamin B-12 affects the body’s ability to produce fully functioning red blood cells. This occurs when the immune system attacks stomach cells that produce a protein vital for the absorption of vitamin B-12.

Gastric parietal cells

Gastric parietal cells

Vitamin B-12 is absorbed into the body through the stomach- gastric parietal cells in the stomach secrete a protein called intrinsic factor. People with pernicious anaemia produce antibodies that attack the parietal cells so that not enough of the protein is produced. As the vitamin B-12 can therefore not be absorbed, the body is unable to produce fully functioning red blood cells. Patients tend to have red blood cells that are underdeveloped or large than normal (megaloblastic anaemia).

Atrophic gastritis- damage to stomach lining

Atrophic gastritis- damage to stomach lining

Pernicious anaemia is the most common cause of B-12 deficiency in the UK and is most likely to occur in women over the age of 60. Having another autoimmune disease (such as Addison’s disease or vitiligo) can increase the risk of developing pernicious anaemia.

The symptoms vary from patient to patient (most probably due to different physiologies) but according to the Pernicious Anaemia Society, the most commonly reported symptoms include:

  • Fatigue
  • Exhaustion
  • Loss of memory
  • Lethargy
  • Weariness

In order to treat this disease, patients are given injections of vitamin B-12 in the form of hydroxocobalamin and they need to be taken every 3 months for the rest of the patient’s life.

Work Experience- Acute Medical Unit

Southampton Hospital: Acute Medical Unit

Monday 8th June 2015

I arrived at Southampton General Hospital to start my week of work experience in the Acute Medical Unit. I was paired up with a Health Care Assistant and I spent the rest of the day with her. Firstly, she taught me how to properly make a bed; folding over the corners, pulling out the sides and wrapping them over like a parcel. It was a simple task to start with and it made me feel useful, being able to use my hands.

We then visited a man who was going to need help escorting to the bathroom for a shower but he was in too much pain to leave the bed so the health care assistants had to wash him in the bed. I learned that all the patients are washed with HiBi scrub for 5 days after they are admitted in order to reduce the risk of spreading MRSA. All patients are swabbed to test for MRSA upon arrival but it can take days for results to come through. Therefore, HiBi scrub is a good preventative measure. If patients arrive at the hospital presenting with diarrhoea and vomiting, they are immediately placed into a side room.

o-MRSA-facebook

MRSA (meticillin-resistant Staphylococcus aureus) is a type of bacteria that is resistant to a number of widely used antibiotics. They can be more difficult to treat than any other bacterial infections. Staphylococcus aureus (staph) is a common type of bacteria that is held on the skin, inside nostrils and throat. It can cause mild infections such as boils but if it enters a break in the skin, it can cause life threatening infections such as blood poisoning and endocarditis (a rare and potentially fatal infection of the inner lining of the heart).
MRSA bacteria are spread by skin-to-skin contact between people who already have an MRSA infection or have the bacteria living on their skin. It can also spread through contact with contaminated objects and because people are more vulnerable when they are in hospital, they are more at risk of becoming infected with MRSA. Therefore, the HiBi scrub and the swab can be very important in preventing the spread of the bacteria.

mrsa dna

The man suffered from obesity and had sores under his arms, under his belly and around his testicles. It took two people to be able to move him just to be able to wash his back and the whole time he was making jokes and had a smile on his face. As much as he must have felt uncomfortable, he didn’t seem to show it.

Later on that day, I learnt that the AMU was the only area that shared the doctors and nurses notes and I was able to find out that the man was suffering from brain tumours. That was very shocking as he acted as though he was fine. Treating the patients with the nurses before finding out what was wrong from the doctors really showed me just how strong people can be- it gave me a whole new perspective on how I viewed the patients. However, it also showed me that I personally would prefer working in the place of the doctor as I was really curious about what was wrong with them.

Whilst at the hospital I learnt more about patient’s rights to privacy and confidentiality as when I asked to sit in with a patient, he refused as he did not feel comfortable. This did not faze me as I wanted him to be comfortable and instead, I spent some time with another HCA. She spent her time trying to persuade an elderly woman that it was not her lunchtime (at 11am) and that she was not able to leave the ward to go to the dining room. The woman was suffering from dementia and she was increasingly becoming more argumentative and even a little aggressive. I was pulled away to observe something else but later that day I saw her calmly talk about how she was feeling with a young male doctor.

When it was lunchtime, I helped to give a lady her soup in a mug instead of a bowl which made the patient very happy and she seemed very grateful even though I had not done very much for her.

The health care assistant then tried to take me to see an MRI scan but they would not let me in as I am under 18 which was very annoying (understandable, but still annoying as I would have found it very interesting). Just as we were about to escort a lady to CT, the fire alarm went off. Everyone was shocked at first and didn’t seem to move but someone, somehow, managed to find out that it was coming from ‘door 59’. We all looked absolutely everywhere for a door 59 but as we found door 58, any others seemed to vanish. It was very baffling. Somehow it was all sorted and there was no fire- someone thought it could have been the patient that kept wandering off as she was missing from her bed in AMU 1 (which was very worrying) but fortunately someone found her safely in AMU 3. It showed me just how much responsibility they all have for the patients- what would have happened if there was a fire and they couldn’t get everyone out? The fire alarm had been continuous in the area where the fire supposedly was and was intermittent in AMU 1 and AMU 3 (in areas around the area of the fire) – it was a very clever system.

After it had all calmed down, the health care assistant and I finally were able to escort the patient to the CT scan of her head. For this, we had to transport her (with help from a porter) down to neuro radiology. The health care assistant told me it was her least favourite area of the hospital as it was an old wing and people always seem to get forgotten down there. There was quite a long wait and it gave me an opportunity to get to know more about the health care assistant who was planning to go to University to become a nurse instead of a HCA. At that point, I hadn’t been told that she was a HCA and I didn’t know the difference between who was who as they seemed to do very similar jobs.

Light (pale) blue uniform: HCA

Blue: Nurse

Dark blue with white strips: Sister

Dark blue with red strips: Senior Sister

We went into the room with the scanner and it was a lot bigger than I thought. I walked into the small adjacent room and watched as they lay the patient in the scanner. I watched as the scan came on the screen and I remember feeling as though I wanted nothing more than to be able to understand what the CT was showing. We then transported the patient back to the waiting room in neuro to wait for the porter. As we were talking, the lady started to choke up and cry and she kept saying that it was difficult to express herself but she loved everything very deeply. It was a very emotional moment and I felt helpless not being able to do more than grab the lady a tissue. However, the next moment the lady was laughing hysterically and it was clear that she was suffering from some emotional instability.

One thing I noticed from today was just how much everyone else could affect how you worked. If one person was rude then it could affect the whole atmosphere and also could affect the way some people interacted with the patients, even if they didn’t mean it to.

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Tuesday 9th June 2015

Today I worked in the Acute Assessment Unit (AAU) of AMU which everyone seemed to call ‘GP’. It was similar to a mini GP surgery for patients who would be admitted and would later on be transferred to a ward or could go home at the end of the day.

As I walked in, I sat with a nurse and a student nurse in her final year at Uni and on her final placement before she could become a registered nurse. The first patient was an elderly lady who had been brought in from her nursing home. The nurse had to fill out a questionnaire of her important information including next of kin etc… and they also have to ask if they are a British citizen and have lived in the UK for the last 6 months- if not, then the patient has to pay for their care.

We also had to give the patients basic examinations- ‘obs’. We measured the lady’s blood pressure, heart rate, temperature and oxygen saturation. These needed to also be checked later on in the day. This needed to be done with every patient that came into the AAU and we also gave them an ECG as they arrived. As this lady arrived, another pregnant lady came in and she presented with a pain in her chest which worsened upon coughing. Although I spent the day with the nurse and we were checking to see if the patients remained stable, I found myself very curious about what was actually wrong. Therefore, I asked if I would be able to sit in with the doctor as she was talking to the pregnant woman. The doctor was a GP ST1 specialising in elderly care but she treated this patient nonetheless. She told me that they had to make sure that the woman was not suffering from a pulmonary embolism as this could be very dangerous during pregnancy. The doctor asked about her pain and it was worse at night and although there was a history of aneurysms in the family, there was no history of blood clots. The patient thought this was the same thing but the doctor explained that an aneurysm is the widening of the blood vessel.

I was able to sit with the doctor as she was writing up her notes and I was curious to know whether all PEs start in the legs as during the examination, she seemed to pay close attention to the patient’s leg. She explained that this is not always the case, even though it is very common but the reason why it ends in the lungs is because as the veins get closer to the heart, they get wider and the vessels in the lungs are the first places where they get thinner so a blood clot is more likely to block blood flow. As soon as the doctor had written her notes, she seemed to run away which sort of made my heart sink- I had really wanted to spend more time with her, following her around.

I then went back to observing the nurse and student nurse as a couple more patients came in. We had to take blood from some of them and different coloured tubes were testing for different things.

Blue: Coagulation

Orange/gold: kidney function

Lilac: full blood count

bloods

We took the bloods to the ‘pod room’ where we put them in a cylindrical tube and sent them to Chem pathology in a large pod through what looked like a large vacuum cleaner. We then went back and another, younger, patient was there and she gave us a urine sample which we analysed in a room around the corner. We did a pregnancy test which came back negative and a dip which only showed traces of blood which seemed to be normal. We also did a urine test on the pregnant woman and she had traces of protein and ketones present and a very high concentration of glucose in the urine. This seemed to surprise the doctor and we tested her blood-glucose levels which came back normal which seemed even more surprising.

Another reason why a PE can be more common in pregnant women is because the blood of a pregnant woman is thicker than that of a normal adult.

What I noticed from spending time with the nurses after spending 5 minutes with the doctor was that I could not stop thinking about what the doctors were doing and what they thought could be wrong with the patient. I was intrigued by looking over their shoulders at the woman’s chest x-ray and that was when I realised for certain that I wanted to be a doctor.

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Wednesday 10th June 2015

Today I asked if I could work with and shadow a doctor but they all seemed to be busy when I arrived and therefore I observed a nurse to start with. She was sorting out which drugs a patient needed and we started with a lady that was clearly suffering from Parkinson’s disease. She had rather violent tremors and the nurse explained that her drug for Parkinson’s was time sensitive but due to the demands of working on the ward, the lady was receiving her medication an hour later than she should be. The nurse had to rush off to deal with another job and I was left with the drug trolley and the patient who still had not had any of her medication (she must have had at least 15 pills to take). I found it very difficult to understand what the patient was trying to say even though I could tell that she was very aware of her surroundings. I felt awful just smiling at her and only being able to answer the question of ‘whether I was training’ as I knew it must have just been a side effect of the Parkinson’s. The nurse eventually came back and had to place the pills into the lady’s mouth as she did not have complete control over her hands.

We then went around to other patients and finally took the “obs” of the patients. The nursebp let me write them in the patient’s notes as she read them out. She explained how they have a scoring system so that if the patient is not under normal readings, this can clearly be seen by a Junior Doctor. She said that it helps with communication between Jr Doctors and Jr Nurses. I wrote the blood pressure with two arrows and lines going between them. Temperature was recorded as an ‘x’ and heart rate as an ‘o’. There was a separate place to write oxygen saturation and other observable features.

We went to check the “obs” of a patient that came in with leg pain when a doctor and a medical student came in. After we had recorded the readings, the nurse let me stay to listen to what the doctor had to stay. For this, she would never know just how grateful I really am. We spent almost an hour with this patient. The doctor was an ST3 neurologist who thoroughly examined the patient. He asked her why she had come in and she explained that she couldn’t move and felt very dizzy every time she did- even sitting up in bed made her feel lightheaded. She also had a history of pain in her legs and at one stage she had lost all feeling in them for months at a time. I had missed the session before they saw the patient when they were examining her x-rays or CT scans and therefore I was quite confused about what was really wrong with her but the doctor explained everything he was looking at in as much detail as he could.

The doctor examined her neck and saw that the monotonous beat in the carotid artery was clear and the beat in the jugular was lower than it should have been. He then looked at her legs and noticed that she was missing a big toe on one foot as it had to be removed as a complication of a surgery she had on her legs- the patient said that she had thought that she might have had to lose her whole foot. The neurologist noticed that there was darker pigmentation around her scar area on her foot and then examined her palms where he also noticed the same, darker pigmentation (hyperpigmentation) in the lines on her palms. He explained to us that this was a clear symptom of Addison’s disease and told us that if we had not heard of Thomas Addison, then we needed to research him. To further add evidence to his predicted diagnosis, he ‘tickled’ the patient’s feet and her toes moved backwards, towards her body. The doctor explained that if a person did not have Addison’s disease, then their toes would curl over, away from the body.

The doctor also explained to us the difference between spasticity and rigidity; spasticity is affected by the rate of movement and is the increased resistance to passive movement which varies due to speed causing an involuntary muscular contraction. Rigidity is the stiffness or inflexibility of a muscle or joint and is the increased resistance to the passive movement which is constant.

As we left the patient, the neurologist told us that the lady was more sick than he had anticipated and as he looked at her notes, he was surprised that she had only been given antibiotics where she should have been given cortisol as Addison’s disease is a rare disease of the adrenal glands which affects the production of the hormone cortisol.

I then had a chance to talk to the medical student who told me that she was in year 2 of the graduate programme after having studied pharmacology. She said that the hardest part of the course, for her, was immunology as there was so much you had to know and because she did the extra degree beforehand, she couldn’t quite remember the basics that she had been taught at A level.

After that, I asked and was able to continue shadowing the neurologist which I was extremely excited about. I followed him into the Acute Assessment Unit in Ambulatory Care where we talked to a patient who could not seem to control all of her muscles. She was always moving and her legs and arms couldn’t stay still, she was always squinting her eyes and seemed to smack her lips together a lot. This had happened overnight and the patient seemed to suffer a lot of distress. As the doctor was examining her, she asked whether some pain in her neck could be related but the neurologist said that this could not be the case as it was affecting her facial features as well which was able to rule out that it was a spinal problem. After we left the patient, the doctor said that she could possibly be suffering from tardive dyskinesia which could have been brought about by a change in her medications however it could also be something else.

After that, the doctor decided to go for his lunch and I was instantly worried that I wouldn’t be able to shadow him for any more time; I had already learned so much and I was having so much fun that I didn’t want it to end! The medical student said she had a meeting at 13.30 and the doctor said it was going to be very interesting and he was also going to go. I was then very surprised that he also invited me along and told me to meet them at 13.30 in neuro radiology, downstairs. I had to get a porter to help direct me but I eventually found the medical student who took me to the room where the doctor was waiting. The meeting consisted of 3 consultant neurologists and a radiologist who were talking about their different cases from that day or a couple of days previously. They showed the MRI scans of the patients on a large screen for the entire room to see. They showed the lady with suspected Addison’s disease and it was fascinating to see the science and anatomy behind what was wrong with her. The doctors shared their cases and expressed their own opinions to help each other.

After the meeting ended, I headed back to the AMU which was very busy. I found a nurse to shadow and she was very busy and didn’t seem to have very much time to explain what she was doing. She put in a ‘didge’ or ‘dig’ (I didn’t want to disrupt her working and ask what it stood for) in a patient and gave an alcoholic treatment that would make their urine and sweat turn orange.

All in all, it had been my favourite day so far and I had learned so much just by spending a short time with the doctor; it was fascinating to see all aspects of that one patient- including spending time with her when I was shadowing the nurse.

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Thursday 11th June

Today I worked with the coordinator’s assistant in the discharge lounge. Obviously, at the very beginning of the day, no one was ready to go home so the CA explained to me how people had always thought that working in the discharge lounge was slacking off so she came up with a system that encouraged you to record most of what you did during the day, in a folder. We then walked up to the ward with a wheelchair to collect a patient that was going home. When we arrived on the ward, the occupational therapist was leaving the patient’s room so I carried her bag back down to the discharge lounge.

Most of the day was spent talking to the patients and I spent a surprising amount of time helping them to work their phones so they could call family members.

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Friday 12th June

From my work experience at SGH, I can certainly say that I saved the best ‘til last! Today was amazing.

Because it was my last day, I thought I had nothing to lose by asking to spend time with a doctor. Because they seemed really busy to start with, I walked around with the sister coordinator who seemed really nice. She explained how the system worked and how they can lose thousands of pounds if they make patients wait too long without a bed- they have a green, amber, red system that lets them know how they are doing.

The sister then took me into the doctor’s meeting where she said she would pair me up with a doctor. They also seemed really busy and she didn’t think it was very appropriate at that time. We looked around the wards to see if we could find a free doctor but there didn’t seem to be anyone so we went back to the office. One doctor, who said she was a registrar, said that she wouldn’t mind me shadowing her but because of her position she has a lot of referrals and would therefore be spending quite a bit of time on the phone. I sat with her anyway and she explained that she had just seen a patient and was now writing up her notes. She showed me the chest x-ray which seemed to look quite normal but because the patient’s speech was ‘bubbly’, the patient was supposedly aspirating. This was all very interesting but the doctor said that she didn’t have very much else to show me so she paired me up with another doctor who came in the office.

This doctor was a first year Junior Doctor and I learnt more from her in 5 minutes than I felt I had in the entire week. She was incredible but she was also an excellent teacher. She asked me what I wanted from the experience and she quizzed me as we went along- it was so much fun. She was about to see a patient who had fast AF and she gave me the patient’s notes to read; she then asked me what I thought might be strange and I asked whether the oedema in her legs was caused by the fast atrial fibrillation. This was correct and she explained to me why that was the case by drawing a little sketch of the two circulations (systemic and pulmonary). Because AF reduces the heart’s pumping capacity, fluid can build up in the legs.

We then went to go and see the patient and the doctor examined her thoroughly. She asked the patient if she wouldn’t mind me listening to her heart and the patient said it was fine so I was able to listen to her fast AF using the stethoscope; it was amazing!

We then went back to the office so the doctor could write up her notes and because it took her quite a while, she gave me the BNF and told me to read up about warfarin. I read that it is an anticoagulant that prevents the blood from clotting and is commonly prescribed to those who suffer from DVT, PE and AF. I also read that patients with a mechanical prosthetic heart valve are also given warfarin. Later in the day, the doctor tested me on what I had read and I asked her why it was that they were given the anticoagulant. She explained that because it is essentially a foreign object in the body, the patients are at an increased risk of an emboli and the warfarin therefore works to prevent this from occurring.

warfarin

We then visited another patient who needed an ABG (arterial blood gas). The doctor asked me why I thought these were done instead of just taking blood from the cannula and I suggested that it was because there was a higher concentration of oxygen in the blood in the arteries. This was correct and she explained that it tests the concentration before the oxygen enters the body tissues- it is a more accurate indication. After it was taken, I had to hold the patient’s artery with pressure and the results showed she had low oxygen levels so we increased the concentration of her oxygen mask.

Afterwards, we went to lunch and for the first time I was able to sit in the doctor’s mess. Everyone else in there was a Junior Doctor and they spoke to me about what I wanted to do in terms of University and what I had done as work experience. There was such a variety as one doctor went to Cambridge, another to Nottingham and another to Peninsula. It just showed me that the University doesn’t matter as much as the person and their interest in the course; if they are willing to work hard and become a great doctor, then nothing can get in the way. One doctor did tell me that she went to Nottingham and found that the BMedSci course (which I did not know a lot about) was useful for her when acquiring an FY1 placement. It was really interesting and I still stand by my view that for an aspiring medical student, Junior Doctors are the best people to shadow!

As we were walking out of the mess, the doctor was speaking to me about how she found medicine as a career and she said that every single little thing that they do as doctors, no matter how insignificant it is to them, can affect the patient in a massive way. She said this as, in the mess, one doctor said that she sometimes fed her patients when it looked like they needed it and the doctor I was shadowing agreed with her whereas others thought that was strange. Personally, I would like to think that I would be the kind of doctor to feed my patients when they needed it or even talk to them if it looked like they needed someone to talk to.

After lunch, the last thing I did on my placement was attend a Mortality and Morbidity meeting. This was a meeting of a few of the doctors and senior sister who were involved with the AMU and they were discussing why some of the patients had died in the last month or so and what they thought, if anything, they could do or could have done to prevent this. It was very interesting and the whole team worked efficiently together to try and find any faults in their system to see if they could improve it in any way.

The entire week was an amazing experience and I am so glad that I applied for work experience there; it gave me an insight into many of the different areas of the hospital and confirmed to me that I am certain that I want a career in medicine.

EPQ

Okay, so I have just finished my exams and we have been back in Sixth Form for two days for ‘Planning for your Future’ conferences where they promoted the idea of doing an EPQ. I have always had in mind that I wanted to do one but I just didn’t know what to do it on.

I have also just spent a week in the Acute Medical Unit at Southampton General Hospital (which I will be blogging about soon) and thinking back, I have an idea for my project. I was thinking of doing my EPQ based on Parkinson’s disease as when I was doing a drug round with one of the nurses, I was astonished at how fast the Parkinson’s drug worked in relaxing the patient and stopping the tremors. This disease is also very personal to me and therefore I think that it will be very interesting to research it in a lot more depth.

See you soon,

Rachel 🙂

Infectious VS Contagious

I have always been slightly confused over the differences between the words ‘infectious’ and ‘contagious’. I have heard them being used interchangeably but I wasn’t certain as to whether this was correct.

In short, it depends on the disease; an infectious disease is one that is transferred by micro-organisms in the air or in water and contagious diseases are transmitted by physical contact.

contagious vs infectious

Infectious diseases are caused by pathogenic microbes (bacteria, viruses, parasites or fungi) which enter the body and cause problems. Many diseases fall under the category of being infectious and contagious- this is when the bacteria of the infectious disease is spread from person to person.

Examples:

Infectious Diseases:

  • Malaria
  • Ebola
  • Cholera
  • AIDS

Contagious Diseases:

  • Influenza
  • Cold
  • Flu

Contagion is considered to be measured on a scale with different diseases being highly contagious or not very contagious (eg. the flu is highly contagious as the virus can pass simply by touching or sharing objects. Ebola is said to be much less contagious).

Statins: a clinical controversy

I have been attending my local GP Surgery for work experience, since September, and last week was the first week I was able to shadow a nurse and see something clinical. I sat in during the ‘Red Clinic’ which is an outpatient clinic for chronic diseases. Many of the patients had high cholesterol and some were taking a certain medication called ‘Statins’.

I was not completely aware of what these were but when I read this month’s issue of the Student BMJ, I read that one of the clinical controversies of 2015 was ‘should most people over 50 take statins?’

It was very interesting to see the connections between the information in the journal and the practices they were carrying out at the Surgery; it seemed to make it a lot more real. It mentions about a risk calculator and how the National Institute for Health and Care Excellence (NICE) has reduced the risk threshold from 20% to 10% of any future problems relating to developing a cardiovascular disease. I was aware of this as they were using a similar calculator as the GP’s; it takes into account your age, weight, previous medical history and attempts to give you a reading of how likely you are to develop any more diseases in the next 10 years.

Statin pills

Statins are a group of medicines that can help lower the level of low-density lipoprotein (LDL) cholesterol in the blood.

LDL cholesterol is most commonly known as ‘bad cholesterol’ and statins reduce the production of this in the liver. High levels of ‘bad cholesterol’ in the blood can lead to fatty deposits building up in your arteries. This can be very dangerous as it can reduce the flow of blood and cause diseases such as atherosclerosis.

Statins inhibit an enzyme called HMG-CoA reductase, which controls cholesterol production in the liver. The medicines act to replace the HMG-CoA that exists in the liver, thus slowing down the cholesterol production process.

pharmaceuticals-03-03186-g002-1024

Additional enzymes in the liver cell sense that cholesterol production has decreased and respond by creating a protein that leads to an increase in the production of LDL (low density lipoprotein) receptors. These receptors relocate to the liver cell membranes and bind to passing LDL and VLDL (very low density lipoprotein). The LDL and VLDL then enter the liver and are digested.

hobbs_380

Although statins aim to reduce the level of cholesterol by 30% and are successful (researchers discovered that the pills, taken by around seven million people in Britain, save around 750 lives a years by preventing fatal heart attacks and strokes), other, less drastic measures, have also been successful. Other health interventions aimed at lowering cholesterol and blood pressure, such as reductions in salt and fat consumption and upping activity levels prevent 4,600 deaths a year.

Furthermore, Prof Sir Michael Marmot, Director of the Institute of Health Equity, UCL, said it was important to address the causes of heart disease rather than use drugs to treat the consequences.

Despite this, statins have made a real difference and therefore it is a very controversial debate as to whether GPs should prescribe these. It is possible that they may be good as a preventative medicine but it might be better if they should only be prescribed when it is necessary to be taken.

I am looking forward to learning more about the different cases of hypertension and high cholesterol and understanding which different treatments are appropriate in each case.

Arrhythmias

How the heart works:

An electrical impulse is produced by your sinus node (SA node) which consists of a cluster of cells found in the upper part of the wall of the right atrium of your heart. The impulse is conducted to your atria, causing them to contract and push blood into the ventricles. The electrical signals pass to the atrioventricular node which is a cluster of cells found in between the atria and ventricles. After passing the AV node and after blood has passed into the ventricles, the electrical impulses are transmitted to the ventricles through special fibres embedded in the wall of the lower part of the heart, causing them to contract. This then pushes the blood around the body, out of the heart.

Normal Cardiac Conduction

Normal Cardiac Conduction

An arrhythmia is a disturbance of your heart’s usual electrical rhythm. It can be detected using an echocardiogram (ECG).

 Normal ECG Reading

Normal ECG Reading

Types of Arrhythmia:

Atrial Fibrillation

This is the most common form of arrhythmia and occurs when the electrical signals in your atria become disorganized, overriding your normal heart rate. This causes your atria to contract randomly and can cause an irregularly fast heart rate. A normal rate can be between 60 and 100 bpm (beats per minute) whereas in atrial fibrillation, it can be over 140 bpm. However, this is not always the case; your heart rate can be any speed. Attacks such as these can last from a few seconds up to a week.

ECG of Atrial Fibrillation showing tiny waves in between heartbeats.

ECG of Atrial Fibrillation showing tiny waves in between heartbeats.

 

Symptoms can include:

  • Palpitations
  • Breathlessness
  • Tiredness
  • Dizziness
  • Chest pain

Atrial Fibrillation can lead to a blood clot due to the irregular heartbeat which can potentially travel to the brain and cause a stroke.

Supraventricular Tachycardia

Also known as SVT, supraventricular tachycardia is caused by an extra electrical pathway in the heart, in between the atria and ventricles. This means that the impulses are able to re-enter the atria without passing through the ventricles, resulting in them travelling around your heart in a circle, producing a fast heart rate. This can be up to 250 bpm.

SVT ECG

SVT ECG

A vagal manoeuvre can sometimes be used to stop these attacks. Although these techniques work in less than 1 in 3 cases, they are simple ways in trying to stop it before more serious measures need to be taken. They stimulate the vagus nerve which can slow down the speed of the electrical impulses.

Ventricular Tachycardia

Electrical impulses are fired too quickly from your ventricles, resulting blood to be pumped out faster than usual. This could result in your ventricles not filling up with blood meaning that your heart could stop pumping blood around the body, resulting in cardiac arrest. This can lead to ventricular fibrillation.

Ventricular Tachycardia ECG

Ventricular Tachycardia ECG

Ventricular Fibrillation

Electrical impulses start firing from multiple sites in your ventricles, rapidly and in an irregular rhythm. Your heart is unable to beat properly and little to no blood is pumped around the body. This is a type of cardiac arrest which needs to be immediately treated with CPR (cardiopulmonary resuscitation) as it is fatal. Early defibrillation can reduce long-term disabilities.

Ventricular Fibrillation ECG

Ventricular Fibrillation ECG

It can be due to acute myocardial infarction.

Heart Block

This means that there is a problem with the electrical signal being transferred from the atria to the ventricles. This can occur in the Atrioventricular node; there are three different types of heart block (first, second and third degree).

Heart block can be congenital but it can also be caused by a number of different things:

  • Heart attacks
  • Infections such as diphtheria
  • Certain medicines
  • Open heart surgery
Heart Block Third Degree

Heart Block Third Degree

 

Arrhythmias can be caused by a number of things:

  • heart failure
  • heart valve disease
  • inflammation of your heart (myocarditis)
  • thyroid disease
  • diabetes
  • high blood pressure
  • heart attacks
  • coronary heart disease
  • chronic obstructive pulmonary disease (COPD)
  • Wolff-Parkinson-White syndrome (an electrical abnormality in the heart that can cause SVT and atrial fibrillation)

You are more at risk of developing an arrhythmia as you get older, if you are pregnant or if you have recently had heart surgery.