a.       Different types of vaccination

                                                               i.      How do they work?

                                                             ii.      What comprise cautions and contra-indications? 

2.       What is the UK program for childhood vaccination?

a.       What vaccination do you need boosters for and when?

b.       How does it vary regionally?

3.       Compare the statistics between the SW and the GP 

a.       https://fingertips.phe.org.uk/search/MMR

b.       What are Read codes?

                                                               i.      Why are they useful?

                                                             ii.      Examples for different diseases

4.       What makes people reluctant to have vaccination? 

a.       For themselves and their children

5.       What are different types of hypersensitivity reactions?

a.       How do they present?

b.       How are they treated?

c.       What are some common types of HS reactions?

d.       How does that relate to vaccines?

a.       Presentation - **including significance of sero conversion

b.       Transmission

c.       Treatment and management (include access to treatment and inequality) - **including prophylaxis and egs in other diseases of prophylaxis

d.       Prognosis - **impact on pregnancy - established and intention

e.       Diagnosis

f.        Epidemiology 

g.       Risk groups - **some comparison of risky behaviours

h.       Mechanism
i.        Prevention at individual an population level
j.        **Review other common STDs - how to distinguish
k.      **Why do pts feel stigmatised and what can we do about it?
l.      **What are our responsibilities towards Alistair - NOT OUR PT
m. **Differential diagnosis for fever on return from abroad

a.       How does it present?

b.       What is the pathophysiology of the disease?

c.       What’s the treatment and management?

d.       How is it diagnosed?

2.       Give 6-8 DD for acute joint pain.

3.       Outline the anatomy of the immune system.

4.       Common pathology affecting the immune system?

a.       Common sites of lymphadenopathy and lymphedema 

Offer to carry out a blood test for rheumatoid factor in adults with suspected rheumatoid arthritis who are found to have synovitis on clinical examination.

Consider measuring anti-CCP antibodies in adults with suspected rheumatoid arthritis if they are negative for rheumatoid factor.

X-ray the hands and feet in adults with suspected rheumatoid arthritis and persistent synovitis.

Symptoms of seroconversion may include:

The diagnosis of a dystrophinopathy is established in a proband with the characteristic clinical findings and elevated CK concentration and/or by identification of a hemizygous pathogenic variant in DMD on molecular genetic testing in a male and of a heterozygous pathogenic variant in DMD on molecular genetic testing in a female. Females may present with a classic dystrophinopathy or may be asymptomatic carriers.

Management.

Treatment of manifestations: ACE inhibitors are used with or without beta blockers for cardiomyopathy in both DMD and BMD phenotypes. Congestive heart failure is treated with diuretics and oxygen as needed; cardiac transplantation is offered to persons with severe dilated cardiomyopathy and BMD with limited or no clinical evidence of skeletal muscle disease. Scoliosis is treated with bracing and surgery. Corticosteroid therapy improves muscle strength and function for individuals with DMD between ages five and 15 years; the same treatment is used in BMD, although the efficacy is less clear.

A commonly held perception in MS has been that men fair worse than women, at least in terms of their disease progression. Our study showed that this is not necessarily true. We found that on average men and women with MS required a stick to walk at around the same age: 59 years old for men and 60 for women.

Another commonly held belief was that the outcome for those older at MS onset was gloomy. We challenged this and found that it was not always true. We found that those who were older at onset of MS were on average still older when they required a stick to walk compared to their younger counterparts. When you combine this with the fact that these people have enjoyed a longer disease free period, then it seems that an older age at MS onset is not so bad after all.

It has often been thought (or assumed) that relapses drive the long-term irreversible disability progression. So much so that many of the disease modifying 🤬 for MS primarily work by reducing relapses rates with the belief that this will automatically result in a beneficial effect on long-term disability outcomes. However, a number of different studies are showing that relapses might not be the main factor influencing long-term progression in MS.

In our study, we were able to look at over 11,700 relapses that occurred in 2,477 people with relapsing-onset MS (ie relapsing remitting or secondary progressive MS) over a mean follow-up of 20.6 years from onset of MS. It was quite challenging to analyze so much information spanning such a long period of time. However, by teaming up with some talented statisticians, we found that relapses tended to pose a transitory short-term risk rather than having substantial longterm consequences. However we did find that relapses occurring in the first five years from disease onset or in people under 25 seemed to have more of an impact than those occurring ten or more years after onset or in people over 35 years at MS onset.

The change in resting membrane potential causes a depression of the ST segment during the diastolic stage and contributes to the appearance of the ST segment elevation on the ECG. Likewise, in transmural ischemia, a shortened action potential occurs which causes an abnormal current flow during the systolic stage of the cardiac cycle. The ST vector is shifted towards the outer positive epicardial zones, producing ST elevations and tall T waves (see Figure 2).