Huh

Blogger is now making me word-verify every single post that I make to make sure that this isn't a spam blog, whatever that is. I'm now under review so that they check I'm not posting spam, however on Earth you do that.

In other news, I haven't typed up any of this term's notes yet, and probably shan't do so now until Easter, so sorry about that.

Oh yes, and I've figured out why I've got so many sets of notes for 1.06: a couple of the plenaries were given before the module started, and a couple of sets of notes I scabbed off people who went to plenaries when I stayed in bed listening to cricket. It all makes sense now.

Library Skills

14.12.05

Sources you should consider using include some:
• Articles published in medical journals.
• Books/chapters.
• Presentations at conferences (especially organised by learned societies).
• Government reports.
• Books, technical reports and working papers issued by individual researchers/organisations.
• Publications on the Internet.

MUST USE JOURNAL ARTICLES IN SSM. CAN'T USE ONLY TEXTBOOKS.

Information from the Internet needs to be:
• Accurate.
• Authoritative.
• Current.

• Biome - internet medical search.
• Google Scholar.
• Medhunt.

How to find journal articles?
• Medline - bibliographical database.
• Must have clear idea of what you're looking for beforehand.
• Carry out background reading if necessary.
• The Cochrane Library.
• Psychinfo.
• AMED.
• Encompass.

Medline:
• Library → electronic library → databases → medicine → Medline (Ovid) → connect.
• Combine searches:
-And.
-Or.
-Not.

Vancouver referencing:
• Use number to indicate reference (subscript).
• In bibliography, list references in numerical order as they appear in text.
• Surname, initial.
• Title.
• Journal/publisher.
• Date.
• Where from eg. web page.

Malnutrition And Stroke

13.12.05

Why are patients at risk of malnutrition?
• Inadequate intake.
• Inability to swallow.
• Disease state.
• Malabsorption.
• Psychological problems.
• Metabolic consequences of disease state.

Nutritional support:
• Oral-fortified food/nutritional supplements if poor intake/appetite.
• Form of enteral tube via variety of routes (short term support):
-Nasogastric.
-Gastrostomy.
-Jejunostomy.
• If gut works, use it.
• Don't want to PEG before 3/4 weeks because swallowing function may return.
• Gastrostomy - artificial opening through abdominal wall to stomach to allow feeding.
• PEG feeding - effective and discreet way of feeding long-term.
• PEG insertion - low mortality (2%), 15% at 30 days - low because it's only high-risk patients.
• Tubes last 3 years.
• Methods of placement - nearly all endoscopically or radiologically guided; surgical to jejunum.
• Advantages: not surgical, so:
-No general anaesthetic.
-Less expensive.
-Quick procedure.
-Fewer complications.
-Easily removed.

Other than stroke patients:
• Neurological disorders.
• Head and neck malignancy.
• Confusional states.
• Supplementary feeding.
• Psychological problems.

Pre-insertion checks:
• No disease in stomach.
• Normal gastric emptying.
• No reflux.
• Consent.
• Clear oral cavity and oesophagus.

Contraindications:
• Ascites (very short life expectancy).
• Peritonitis.
• Inability to place by endoscope.
• Malignancy.
• Gastric ulceration.
• Previous gastric surgery.

Complications:
• Peritonitis.
• Aspiration.
• Wound infection.
• Leakage.
• Ulceration.
• Tube displacement.
• Candida colonisation.
• Blockage of tube.
• Accidental removal.

Assessment criteria:
• Assessed by team.
• Explain procedure to patient, family and carers.
• Is patient stable?
• Is PEG insertion appropriate?
• Is endoscopic incubation possible and safe?
• Is PEG placement possible and safe?
• Is tube placement ethically correct?

Tackling The Risk Of Heart Disease And Stroke - Hypertension

12.12.05

What is hypertension?
• Increased blood volume, which increases risk of cardiovascular disease.
-Blood pressure is a continuous variable - not dichotomous.
-Continuous relationship between level of blood pressure and risk of cardiovascular disease.
-No level with no risk.
-Ie. level of blood pressure selected for treatment is arbitrary.
-Different guidelines use different thresholds.
-Morbidity and mortality concentrated in elderly.
-Should interventions concentrated in that group?
• Risk factors summate.

What harm does it do?
• Shearing forces lead to the development of atherosclerosis.
• Increased risk of coronary events.
• Increased risk of stroke (by up to 4 times).
• Compounds other cardiovascular risk factors.
• Risk of heart failure.
• Risk of renal failure.

What causes it?
• 90% idiopathic (=I DON'T KNOW) - primary.
-Abnormalities of sodium flux across cell membranes?
• 10% secondary.
-Cushing's syndrome - secrete excessive amounts of glucocorticoids.
-Conn's syndrome - secrete aldosterone.
-Phaeochromocytoma - tumour of adrenal gland - secrete adrenaline.
-Renal disease (renal artery stenosis, renal failure etc.)
-Coarctation of the aorta - congenital narrowing.
-Alcohol.

How big a problem is it?
• Cardiovascular atherosclerosis common.
-Major cause of disability and death.
-Thrombotic (70%), haemorrhagic (15%), embolic (atrial fibrillation - 15%).
-But decrease in frequency.
• Increased risk of myocardial infarction.
• Hypertensive renal failure/heart failure unusual today.
• Depending on level defined, maybe 20% of adult population have hypertension.

How do we measure it?
• Sphygmanometer.

Measuring blood pressure
• Badly done, badly recorded.
• Digit preference - 5s and 10s.
• "Rule of halves."
-Of all hypertensive patients…
-…Half have ever had blood pressure measured.
-…Of whom half have been treated.
-…Of whom half are controlled.

British Hypertension Society Guidelines BMJ 2004.

Targets for blood pressure control
• Both systolic and diastolic values should be attained.
• Not diabetic - <140/85.
• Diabetic - <130/80.
• Many argue lower for diabetes sufferers eg. 120/70 if proteinuria - controversial.
• Also in secondary prevention eg. post cardiovascular atherosclerosis - very aggressive blood pressure lowering needed.

Benefits of treating blood pressure
• 5-year decrease of 5-6 mmHg in diastolic blood pressure:
-35-40% relative risk reduction in stroke.
-20-25% relative risk reduction in coronary heart disease.
• 1000 person years of drug treatment in older adults (>60 years old) prevents:
-5 strokes (95% confidence intervals 2-8).
-3 coronary events.
-4 cardiovascular deaths.

How do we lower blood pressure?
• Non-drug interventions.
-Exercise (5/3 mmHg).
-Diet.
-Obesity (3/3 mmHg).
-Salt restriction (2/4 mmHg).
-Food supplements (4/2 mmHg).
• Anti-hypertensive drugs.
-Most evidence-based.
-Single drug usually decreases blood pressure by around 10/6 mmHg.
-Multiple drug therapy common.

Classes of drugs to test hypertension (may have other uses also)
• Thiazide diuretics eg. bendrofluazide (smooth muscle relaxation - reduces pressure on arterioles).
-Cheap, easy to use.
-Best evidence behind it.
-20 or more different drugs in class.
• Beta blockers eg. atenolol.
-Less effective than other therapies.
• Calcium channel blockers eg. nifedipine.
-Cause vasodilation of arterioles.
-15 or more.
• Angiotensin converting enzyme inhibitors eg. enalapril.
-12 or more.
• Others…

Drug treatment to decrease blood pressure - heavily studied, very commercial
• Best evidence for thiazides.
• Other drugs as effective, but evidence not as good.
• Tolebility similar (but differs between patients) - match drug to patient profile.
• To cost-effectiveness.

How are we doing?
• Rule of halves - now rule of around 60%.
• Stroke rate declining.
• Barriers to controlling blood pressure.
-Nonadherence.
-White coat hypertension.
-Ageist prejudice.
-Organisational.

Conclusions
• Tackling risk of cardiovascular disease requires multifaceted approach.
• Risk factors known and can be treated.
• Hypertension major risk factor.

Being Strategic About Population Health

9.12.05

Eg. Choosing Health: Making Healthy Choices Easier

Outline strategic approach to population health.
• What is the prevention strategy for stroke?
• Strategy for multidisciplinary care for stroke? What voluntary groups are there?
• Strategy for reducing burden of stroke on population?
• Strategy for reducing impact of
-hypertension
-back problems
on population?
• Do data/statistics help inform strategy?

Population perspective theme (using seven pointers)
• 2, 4, 5 and 7 relevant to strategy.

Strategy
• Consider one model of health promotion.
• Health promotion: "process of enabling people to increase control over and improve their health. It involves the population as a whole in the context of their everyday lives…" World Health Organisation.

Demonstrate awareness of development of national health strategy in England from 1990s.
• Current strategy: Choosing Health.
• Following on from Our Healthier Nation.
• Following on from The Health Of The Nation.

Key features of The Health Of The Nation Green Paper (1991)
• Emphasise health promotion versus health care.
• Setting clear challenging targets.
• 'Working together' - inter-sectoral collaboration.

White Paper (1992)
• Key areas.
-Coronary heart disease and stroke.
-Cancers (breast, cervical, lunch, skin).
-Mental (illness) health.
-HIV/AIDS and sexual health.
-Accidents.
• Action settings.
-Healthy cities.
-Healthy schools.
-Healthy hospitals.
-Healthy workplaces.
-Healthy homes.
-Healthy prisons.
-Healthy environments.

SET TOO MANY TARGETS!

Other public health white papers…
• 2 related government publications.

The New NHS: Modern, Dependable White Paper (1997)
• Increased collaboration, not competition.
• Decreased management costs.
• Decreased waiting times for 'suspected cancer.'
• Establishing primary care groups (now primary care trusts).
• Plus, Health Improvement Programmes, Health Action Zones, National Institute for Clinical Excellence (NICE), 24-hours nurse-led telephone advice, NHSnet.

The NHS Plan (2000)
• Increased beds, facilities, staff, 'modernisation.'
• Increased patients' influence (views; advocates; surveys and forums; action on cancellations…)
• Decreased waiting times.
• Better services for cancer, ischaemic heart disease, mental health, older people.
• National inequalitites target (primary care; screening; smoking cessation; better diets for children).

Key features of Our Healthier Nation Green Paper (February 1998)
• Key aims:
-Lengthening lives.
-Higher quality of life free from illness.
-Narrowing inequality gap.
• Criteria.
-'Marked inequalities.'
-'Real causes of public concern.'
-'Significant cause of premature death.'
• One target in each of four priority areas:
-Heart disease and stroke.
-Cancers (all).
-Mental health.
-Accidents.
• Three health settings:
-Healthy schools.
-Healthy workplaces.
-Healthy neighbourhoods.
• Strengthen public health function and research.
• Expect all NHS personnel to accept responsibility for public health issues.

White Paper (July 1999)
• As per Green Paper.
• Want to:
-Improve health of everyone.
-Improve health of worst off in particular.

Main features of Choosing Health
• Consultation (early 2004).
-Choosing health.
-Choosing better diet.
-Choosing activity.
• Through by November 2004.
• Overarching priorities.
-Decreased number of smokers.
-Decreased obesity and increased diet/nutrition.
-Increased exercise.
-Decreased alcohol misuse.
-Increased sexual health.
-Increased mental health.
• Plus, underpinning principles.
[-Free healthcare.
-Free at point of delivery.]
-Informed choice.
-Personalisation.
-Working together.
• Action setting still the same.
• Attention focuses on:
-Health in a consumer society.
-Children and young people - starting on the right path.
-Local communities leading for health.
-Health as a way of life.
-A health-promoting NHS.
-Work and health.
-Making it happen - national and local delivery.

Other elements of strategy
• National service frameworks and their standards.
• One for 'older people' (2001).

Epidemiological indicators
• Incidence of outcome in exposed = Relative risk
Incidence of outcome in unexposed
• Incidence = Epidemiological measure of risk. Absolute measure of risk.
• Relative risk = incidence risk ratio.
• RR of 4: 4 times as many new cases occurring per unit population per unit time in those exposed to risk factors versus those not exposed to risk factors ie. more in exposed groups.
• 95% confident that true RR lies between 1.6 times as many and 8.2 times as many in exposed versus unexposed.
• RR only estimate of truth - want to know how precise estimate is.
• Risk from inactivity.
-Incidence rate.
-RR (l¬e/lu).
-Population attributable fraction (percentage disease in population associated with certain risk factor).
• Comparing 'like' with 'like.'
-Standardised mortality ratio versus standardised mortality rate?
• Eg. SMR = 150 - 50% higher mortality than expected - indirect.
• Standardised rate (direct).

How to be strategic?
• Where are we now?
-Describe.
• Where are we trying to get to?
• How are we going to get there?

An Introduction To Critical Appraisal

8.12.05

Five questions to ask when reading a paper:
1. What was the research question (introduction)?
2. What did the authors do (methods)?
3. What did the authors find (results)?
4. How did the authors interpret the findings (discussion)?
Was all this 'reasonable'?

What is the research question?
• Usually in the introduction.
• Why is it important?
-An important problem.
-Summary of previous evidence.
-Further question to ask.

What did the authors do?
• Usually from the methods.
-Study design?
-Cohort (group of people with shared characteristic: lived in defined geographical area).
-Both routine and non-routine sources of data.
Verified cases fit case definition.
-Date on ethnic origin, social class, age, stroke pathology recorded.
• Statistical analysis.
-Incidence rates.
-Age-adjusted rates for sex and ethnic groups (direct adjustment/standardisation).
-Confidence intervals.
-Rate ratios.
-Case fatality rates.
-Regression.
• Potential confounders.
-Age.
-Sex.
-Social class.

What did the authors find?
• Results.
• Crude incidence, age-adjusted incidence.
• Age and sex adjusted relative risk for ethnic group.
• Social class.
• After adjustments, ethnic differences identified and quantified.

How did the authors interpret these findings?
• Conclusion.

Was all this 'reasonable'?
Any study result may be:
• Correct.
• Incorrect, due to chance (random error).
-Type 1 error (identifies difference that doesn't exist).
-Type 2 error (fails to identify true difference).
• Incorrect, due to bias (systematic error) in study process.
-Design, execution, analysis.
-Confounding - third factor related to both exposure and outcome, not accounted for in analysis.

• Bias.
-In selection? (Selection bias).
-In information gathering? (Information bias).
-Stroke occurred outside area?
-Geographical population base incorrect?
• Potential confounders identified.
-Age.
-Sex.
-Social class.
• Other issues that could lead to confounding bias.
-Other risk factors (genetic, behavioural, physiological).
-Diabetes, hypertension.
• Can you think of other potential explanations for results, other than that hypothesised by the authors?
-Authors themselves admit haven't considered other risk factors.
• So, authors provide some evidence, and recognise more evidence required.

Speech And Language Therapy

7.12.05

What does a speech therapist do?
• Work with children and adults who have communication difficulties, and/or problems with eating/drinking/swallowing.
• Work in partnership with range of professionals from variety of agencies.

Knowledge and skills
• 4-year degree course.
• Anatomy and physiology (particular emphasis on head and neck).
• Phonetics and linguistics.
• Psychology.
• Child development.
• Speech pathology and therapeutics.

Where can you find speech and language therapists?
• Community health centres.
• Hospitals - wards and outpatients.
• Mainstream and special schools.
• Day centres and homes.
• Courtrooms, prisons and young offenders' institutes.

Assessing communication impairment.
• Have well-established knowledge of process required to communicate effectively.
• Ability to identify whether impairment at language or speech level.
• Separate problems of understanding and expression.

Communication framework.
• Language.
-Phonology (sounds).
-Syntax (grammar).
-Semantics (meaning).
-Pragmatics (social rules).
• Speech.
-Articulation.
-Voice.
-Fluency.
-Resonance.

Client groups.
Children…
• Feeding and swallowing difficulties.
• Learning difficulties (mild, moderate, severe).
• Language delay.
• Specific language impairment.
• Specific difficulties in producing sounds.
• Hearing impairment.
• Cleft palate and other structural abnormalities.
• Stammering 9stuttering).
• Autism.
• Dyslexia.

Adults…
• Eating, swallowing and communication problems following stroke, head injury.
• Neurological impairment and degenerative conditions.
• Cancer of head, neck and throat, including laryngectomy.
• Voice problems.
• Mental health issues.
• Learning difficulties.
• Physical difficulties.
• Stammering.
• Hearing impairment.

How many have these problems in the UK? 2.5 million or more?
• Improved mortality rates in premature and very sick infants.
• Complex surgery available.
• Health care for long-term disabled improved.
• Improved trauma care for head injury.
• Better recognition.
• Still missing some - youth offenders.

Stroke
• Around 30% stroke patients will experience significant communication difficulties.
• 45% stroke patients admitted into hospital will experience swallowing problems, either transient or long-term.

GLOSSARY
Dysphasia
• Loss of ability to formulate, express or understand meaning of spoken needs.
• May also be difficulty in reading, writing, understanding and using gesture.

Dysarthria
• Occurs at speech level.
• Can be slurred, weak articulation with poor coordination of breathing and voicing.

Dyspraxia
• Inability to perform sequence of movements, despite having normal power, sensation, coordination and understanding.

Broca's dysphasia
• Motor/expressive dysphasia.
• Comprehension good, handwriting poor.
• Speech may be limited to a few repeated words.
• 'Shorthand' speech - conjunctions/articles missing.

Wernicke's dysphasia
• Sensory dysphasia.
• Comprehension and handwriting poor.
• Speech nonsensical, but fluent with seemingly accurate grammar and social phrases.
• Nonsense words/wrong words.
• Patient unaware.
• Sometimes confused with speech of someone with dementia.

Global dysphasia
• Mixed motor and sensory dysphasia.
• Impaired understanding.
• Non-fluent speech.
• If severe, poor prognosis.

Core programmes
• Direct one-to-one/group programmes.
• Training carers both professional and non-professional.
• Dysphasic support (voluntary sector).

NB. Different expectations for communication than for mobility.

Dysphagia (eating, drinking, swallowing)
• 33% in acute care.
• 66% in long-term care.
• 30% of stroke patients.
• Only one-third of sufferes get professional help.
• UK has poor European record.

Loss of communication may result in:
• Affected self-esteem.
• Affected retirement plans.
• Changed relationships with partner, family members - living with stranger.
• Bring about sense of isolation, boredom, depression.

Ethnic And Cultural Diversity In Healthcare

6.12.05

Ethnic minority groups in the UK:
• 7.9% in 2001 (4.6 million in 58.8 million).
• Younger than white population - more than 25%.
• Have fewer older people - less than 20%.
• Concentrated in cities, except Chinese.
• Indian 28%, Pakistani 19%, Black Caribbean 15%, African 13%, Black other 12%, Bangladeshi 7%, Chinese 6 % (2001).

Ethnic minorities and health inequalities:
• Diverse ethnic minority groups include refugees, travellers and Irish people.
• Health issues vary with ethnic group - coronary heart disease, diabetes (Asian), hypertension/stroke (African, Caribbean).
• Poverty leads to poor health in Pakistanis and Bangladeshis (Fourth National Survey of Ethnic Minorities 1997).

Cardiovascular disease and BME (British minority ethnic) groups:
• Bangladeshi and Pakistani men 60-70% higher than general population.
• Pakistani, Bangladeshi and Black Caribbean women 33-45% higher rate.

Factors in South Asian coronary heart disease:
• Smoking - some BME men smoke more than white men, but Sikh men and most Asian women do not smoke.
• Alcohol - low, except Sikh men.
• Blood pressure - same as white.
• Serum cholesterol - same/lower.
• Insulin resistance in South Asians - body needs more insulin to cope with blood sugar, resulting in diabetes and low fibrinolysis.

Diabetes in BME groups 1999:
• Diabetes non-insulin dependent.
-Pakistani and Bangladeshi 5 or more times greater than white rate.
-African/Caribbean 2-4 times greater than white rate.
• Diabetic nephropathy, end-stage renal disease several-fold more.
• Deaths:
-South Asian 3.5 times more than white.

NHS PLAN 2000
Aim: improve health and reduce health inequalities by:
• Primary care trusts knowing health needs of local people.
• Access to information and health services.
• Entitlement to quality care with respect for privacy, dignity, religious and cultural beliefs.
• Little mention of ethnic health.

NHS race equality schemes (RESs):
• RESs required by Race Relations Amendment Act 2000.
• In the NHS, RESs not just to comply with the law.
• To improve services to black and ethnic minority groups.
• Decreased health inequality.

Delivering race equality in mental healthcare January 2005:
• More appropriate and responsive services.
• Community engagement.
• Better information.
• Minister's vision:
-Equality of access.
-Equality of experience.
-Equality of outcome.

General practitioners' views of ethnic minorities:
Issues…
• Mental health: highest priority.
• Frequent visits for minor but multiple problems.
• Substance abuse by young men.
• Problems of deprivation.

Solutions…
• Effective health education for BME patients on chronic disorders and lifestyle (diet, exercise).
• Bilingual workers for users who do not speak fluent English.

Princes Park Liverpool Survey 2000:
• 4581 patients: white 62%, BME 34%.
• Minority ethnic patients needed language interpreters.
• Women wanted female health professionals.
• Cigarette smoking high in Somali and Yemeni.
• Need for health team to know ethnic and cultural issues.

Ethnic healthcare: the way forward:
• Involve local groups in plans, delivery, audit and evaluation.
• Identify health needs and respond within resources.
• Train staff to be aware of ethnic diversity.
• Use ethnic group data in the NHS.
• Quality standards in healthcare.
• Feedback from ethnic users.

Health inequalities and ethnic minorities:
• Trained interpreters needed for some groups to improve access to services.
• NHS needs to be culturally sensitive.
• Today, NHS response patchy - depending on people ("champions") with local knowledge and networks.

Improving Ethnic Health 2004:
• Tackling health inequalities essential for improving ethnic health.
• Ethnic group, first language needs.

Healthcare commission audit 2004 measures for ethnic minority patients:
• Fair access and patient's choice.
• Effective delivery of appropriate healthcare.
• Patient/user experience.
• Health outcomes of NHS care.

The Brain For Beginners

5.12.05

Essential knowledge:
• Basic development of the brain and spinal cord.
• Parts of the central nervous system.
• Blood supply.
• Surface of the brain.
• Circulation of cerebrospinal fluid.
• Structure of the central nervous system and brain.
• Cranial nerves.

• Very complex.
• Anatomy should not be divorced from function.
• Clinical diagnoses based on understanding of anatomy and function.

Components of the human nervous system:
• Central nervous system.
• Peripheral nervous system.
• Autonomic nervous system.

Blood supply:
• Carotid (internal).
• Vertebral.

Thomas Willis (1621 - 1673):
• English physician.
• Father of neurology.
• Co-founder of Royal Society (1652).

Ventricles:
• 4 in total.
• Lateral occupy left and right sides of cortex.

Choroid plexus:
• Specialised capillary network.
• Produces cerebrospinal fluid.
• Located at root of each ventricle.

Practical Approaches To Rehabilitation

2.12.05

Physiotherapy: "The use of physical agents (eg. heat, movement) as a therapeutic intervention."

Rehabilitation:
• Process of physical rehabilitation on concept of neuroplasticity.
• Ability of central nervous system to adapt, rebuild and reorganise itself.

Plasticity of other systems:
• In response to increase/decrease in physical activity, structure of muscles, skeleton, cardiovascular and respiratory systems.

Neuroplasticity after a lesion:
• Reorganisation of blood flow.
• New synaptic connections to surviving neurones.
• New connection refined by practise and repetition of tasks.
-Restructuring of pathways to produce movement.

Neuroplasticity and rehabilitation approaches:
Therapy treatment approaches…
• Seek to guide neuroplastic reorganisation that occurs after lesion of central nervous system.
• Dependent upon understanding of normal movement.
• Use skills of movement analysis and problem solving.

Barriers to movement after stroke:
• Poorly innervated muscles.
• Loss of alignment of joints.
• Loss of normal, efficient patterns of movement.
• Loss of selective graded activity of limbs and trunk.
• Loss of sensory information (tactile, propriceptive, pressure).
• Loss of postural control (balance).
• Secondary musculoskeletal changes.

Rehabilitation approaches:
• Normal movement approach - Bobath.
• Motor relearning - Carr and Shepherd.

Most physiotherapists take an eclectic approach.
Use of knowledge of anatomy and biomechanics.

Aims of treatment in acute phase:
• Chest care - risk of respiratory complications.
• Positioning - to protect vulnerable joints.
• Maintenance of soft tissue length.
• Reduce occurrence of compensatory activity.

MAINTAIN REHABILITATION POTENTIAL.

Early intervention to provide stimulation of sensory pathways, maintain soft tissue length, facilitate muscle activity etc.

Intensive rehabilitation phase:
• May take place in rehab unit/stroke ward.
• Length of stay may be determined by:
-Unit policy.
-Follow-up available.
-Degree of dependence acceptable/manageable on discharge.

Later stroke rehabilitation:
• Refining skills, higher balance functions, more complex activities - return to occupation/leisure.
• May take place in out-patient setting, in patient's home on in leisure setting.
• Should encourage independence and self-management.

Important elements of rehabilitation:
• Patient participation.
-Learning by doing.
-Patient needs opportunities to practise skills.
-Team need to address any issues limiting patient's participation.
• Organised multidisciplinary care.
-Shared learning and skill development.
-Increased opportunities for patient to practise, refine skills - 24 hours.
• Achieving carry-over.
-Skills learnt must be transferable from rehab setting to home environment to be truly functional.
-Skills need to be practised in variety of setting.
• Goal-setting.
-Joint team goals (including patient and carer).
-Should be realistic, measurable, timebound.

Social aspects:
• Home environment.
• Carers.
-Health.
-Ability to adapt, learn new skills.
-What support will the carers get?
• Society - work and leisure opportunities.

Barriers to rehabilitation:
• Unstable medical status.
• Poor nutritional state.
• Depression.
• Pre-morbid personality.
• Co-morbidities.
• Limited pre-morbid level of function.

…Related to stroke damage.
• Communication difficulties.
• Visual field deficit.
• Perceptual problems eg. (L)/(R), poor spatial awareness.
• Reduced concentration.
• Sensory loss/neglect.
• Lack of insight.

Increased awareness of practical aspects of rehabilitation can be gained by observing and discussing therapy assessments and treatments.

Will help to:
• Discuss patient's potential realistically.
• Inform patient/carers accurately about rehabilitation process.
• Refer patients correctly to rehab.

The Effects Of Stroke

22.11.05

Agnosia = no recognition.
Sensory dysphasia = no understanding, speaks nonsense, has no realisation of this.
Motor dysphasia = understanding, telegrammatic/no speech (Brocca's dysphasia).

Functions of other lobes
TEMPORAL LOBE
• Dysphasia; memory. Therefore, lesion in temporal lobe affects memory (ability to register, retain and recall)
• Also, deeper memory eg. Alzheimer's.

PARIETAL LOBE
• Mixed dysphasia - inability to speak in absence of sensory and motor deficit.
• Agnosia.
• Dyspraxia - inability to carry out sequence of voluntary actions in absence of sensory and motor deficit.
• Topographical disorientation - cannot visualise.
• Body image - loss of awareness of body.

LIMBIC AND FRONTAL LOBES
Limbic lobe associated with anger, love, sex, sadness etc. Emotions channelled into frontal lobe.

Frontal lobe captions information from limbic lobe, sifts it out, leading to reasoning:
• Intellectual reasoning.
• Conceptual reasoning.
• Emotional reasoning.
• Speech fluency.
STROKE CAN CHANGE ANY OF THESE FUNCTIONS.

Do not forget: DEPRESSION.
• Despair, blackness etc.
• Physiological changes as well as suicide
• Males three times more likely to die.
• Females two times more likely to die.
• BUT 80% cure rate - TREATABLE.
• Frequently missed and rarely treated.

Module 1.06

A Sudden Onset Of Weakness.
5.12.05 - 16.12.05.

I've got ten sets of notes for this module. Wow. How did I manage that? All I can remember about that side of term was that I was completely knackered.

From Harvey To HARC

1.12.05

• 1537 - Pope Clement VII permitted teaching of anatomy by dissection.
• Dissections became public events in Italy.
• Leonardo Da Vinci - practiced dissections and produced 750 anatomical drawings.

Andreas Vesalius (1514 - 1564):
• Studied in Paris, Louvain and Padua.
• Medical degree in 1537.
• Published De Humani Corporis Fabrica in 1543.
• Challenged Gallenic ideas.
• Deemed unacceptable to dissect females at the time - drawn with exaggerated hips to emphasise reproduction.

[Galen = red bile, yellow bile, phlegm, blood.]

William Harvey (1578 - 1657):
• Studied medicine at Caius College, Cambridge.
• Studied at Padua with Girdamo Fabrizio.
• Set up practice as physician in London.
Etc…
• First person to propose that circulation occurs as results of beating heart.

William Hunter (1718 - 1783):
• Scottish anatomist and obstetrician.
• Anatomy of the Human Gravid Uterus.

Anton van Leeuwenhoek (1632 - 1723):
• Inventor of the microscope.

Herman Boerhaave (1668 - 1738):
• Dutch anatomist.
• Idea of body as pressurised system.
• Importance of physiology.
• Discovered role of electricity in body - manifested in Mary Shelley's Frankenstein.

René Lannec (1781 - 1826):
• French physician.
• Invented the stethoscope.

19th Century:
• As anatomy becomes key to medical education, supply of bodies decreases.
• Only supply: hanged criminals.
• Ressurectionists: West Port Murders - Burke and Hare prosecuted in 1832 - had murdered 16 or more people to supply Robert Knox.
• Grave-robbing eg. in Liverpool - associations between grave diggers and anatomy schools. Imported from Ireland, left in cellars in Seel Street.
• Public fear of dissection - fate worse than death.
• 1832 Anatomy Act tried to solve this, but legalised use of bodies of destitute dying in workhouses - body degraded.

20th Century:
• In 1934, only 3% of bodies were donated.
• By 1960s, most dissection bodies were left in wills.
• Before World War II, living less alienated from dying - died at home.
• Increase in deaths from heart disease and cancer, in hospital death.
• Until final third of 20th Century, public excluded from hospital deaths - rationales challenged in 1970s.
• Importance of witnessing death - big psychological component in grieving.
• First redefining of death - 1968 - Harvard definition.
• 1972 - "persistent vegetative state."
• Still divergence of opinion.
• Reassess how we see the body in death and in life.

Patients' Attitudes To Cardiac Problems

29.11.05

Attitudes to risk of cardiac problems:
• Good lay understanding of risks.
-Coronary candidate: overweight, smoker, little exercise, poor diet etc.
• Beliefs about exceptions.
-Davison et al 1989, 1992.
-"Uncle Norman" and "the last person you'd expect."
• "It's a man's disease."
-Misconception reinforced by medical and scientific research and health promotion campaigns.
• "It's a good way to go."
-Perceived leading cause of death: 41% said heart disease.
-Most important personal health concern: 9% said heart disease (Shepherd, 1998).
• Attitudes about sociological and psychological factors as cause.
-Beliefs about links between stress/strain and cardiac problems are common in patients.
• Highly-stressed executive?
-"Type A" behaviour and coronary heart disease (Rosenman et al 1975).
• Hostility?
-As well as other personality traits.

What are the sociological and psychological risk factors?
• Social class (50% high in manual workers).
• Ethnicity (50% high in South Asians).
• Low status, but demanding occupations with little control.
• Poor social support.
• Depression.

Preventative drug treatment: attitudes about risks and benefits
• Views of doctors, nurses and lay people about minimum benefit needed to justify drug treatment to prevent heart disease (2003).
• Doctors: 5-10 people (out of 100).
• Nurses: 10-25 people.
• General public: 10-99 people.
• Questions included: cost; side-effects; guaranteed effectiveness; lifestyle changes.

Perceiving acute symptoms of cardiac problems:
• Delay in consulting for chest pain associated with:
-Atypical symptoms.
-Not seeing symptoms as cardiac in origin.
-Less knowledge of heart attack symptoms (Rushton et al 1998).

Responding to chronic symptoms
• Reluctance to consult in patients with angina - FEARS, beliefs.
• Socio-economic background important - people from poor areas have:
-Greater perceived vulnerability.
-More exposure to ill health, so normalise symptoms.
-More anxious about seeing doctor.
-Richards et al, 2002.

Ideas about illness
• Illness representations/beliefs (Leventhal et al 1980).
-Identity ie. label/name given to illness (positive? Negative?)
-Causes ie. of illness - beliefs; stress.
-Timeline ie. how long patient expects illness to last.
-Ongoing? Curable?
-Consequences ie. what it will mean to patient's life.
-Cure and controllability ie. can it be kept under control? Lead an ordinary life?
• Impact on how people react to their illness.

Ideas about illness and recovery after myocardial infarction
• Illness perceptions soon after admission for myocardial infarction predicted recovery.
• Perception of myocardial infarction by patients is better predictor of recovery than medical judgements of severity of myocardial infarction.
• Petrie et al, 1996.

Psychological outcomes after myocardial infarction
• After 12 weeks, 30% myocardial infarction patients report quality of life has returned to previous levels.
• 15-30% depressed at 6 months.
• 50% have high anxiety levels.

Social/psychological influences on recovery
• Anxiety/depression.
-Hemingway and Marmot (1999) 6/6 studies found association between depression/anxiety and survival from coronary heart disease.
-Strength of association similar to that of smoking and coronary heart disease.
-Implication: important that depression/anxiety diagnosed and treated.
• Social isolation and lack of social support.
-Hemingway and Marmot (1999) 9/10 studies found association between social support and survival from coronary heart disease.
-Associated with threefold increased risk of poorer outcomes (Bunker et al, 2003).

Cardiac rehab
• Combination of exercise, psychological and educational interventions.
• Can promote recovery, enable patients to maintain health and reduce risk of death.
• Many problems in patients with heart disease due to anxiety and misconceptions about their health.

Psychological influences on recovery: stress
• Stress: process by which we perceive and respond to certain events that we appraise as threatening (Myers, 1998).
• "There is nothing either good or bad, but thinking makes it so." - Hamlet, Shakespeare.
• Patients' beliefs about cardiac problems and stress need to be addressed.
• Stress management training can help.
-Identify challenges.
-Reduce challenges (where appropriate).
-Reappraise challenges.
-Problem-focused coping.
-Relaxation training/techniques.
-Social support.

Tackling The Risk Of Heart Disease And Stroke - Lipids

28.11.05

Cardiovascular risk factors:
• Age }
• Gender (generally males) } irreversible
• Family history }
• Race (SE Asians) }

• Smoking }
• Hyperlipidaemia }
• High blood pressure } reversible
• Diabetes }
• Social class? Stress? }

Complex interplay between factors.
Relative importance of each?
Apply to populations, not always to individual.

Cardiovascular disease
• Ischaemic/coronary heart disease (around 75% of total).
-Sudden death.
-Myocardial infarction.
-Angina.
-Heart failure.
• Cerebrovascular disease (around 25% of total).
-Stroke, haemorrhage, thrombotic (embolic).
• [Peripheral vascular disease.
-Aneurysms, intermittent claudication.]

Levels of prevention:
• Primary - in patients at rish but with no evidence of clinical established disease - individual absolute risk low (5-40% over 10 years).
• Secondary - in patients with established disease (eg. with angina, post myocardial infarction) - individual risk high (30-60% over 10 years).

Clinical signs (hyperlipidaemia)
• Xanthoma - fatty deposit in skin (around elbows).
• Xanthelasma - cholesterol deposits in eyelids - common.

Is this a big problem?
• Major killer.
• Major cost to NHS.
• Extensive government policies.
Rates declining (only partly due to medical intervention.

Cardiovascular Society risk tables
• Can't factor everything in.
• Excludes family history etc.
• Excludes (single gene) family hyperlipidaemias.
• Only for primary prevention.
• Risk calculators available on most general practice computer systems.

http://heart.bmjjoursnals.com/cgi/content/full/80/suppl_2/S1/F1

What can we do about it? Multiple approaches, not single factor!
• Discourage smoking.
-Taxation.
-Smoking bans.
-Stop smoking campaigns.
• Encourage exercise, weight loss.
• Treat diabetes aggressively.
• Treat hyperlipidaemia and hypertension.
• Treat acute episodes/disease aggressively - myocardial infarction.
• Secondary prevention treatments.
-Aspirin.

Treating hyperlipidaemia
• Measure total cholesterol/HDL ratio.
• Almost everyone - advise healthier lifestyle, improve diet.
• Primary prevention: consider pharmacological therapy for any patient with ischaemic heart disease >30% over 10 years and total cholesterol >5.
-Implications: treat older rather than younger; smokers rather than non-smokers.
• Secondary prevention - consider pharmacological treatment in any patient with total cholesterol >5 or LDL cholesterol >4.

Targets for lowering cholesterol?
• Total cholesterol of <5mmol l-1.
OR
• LDL of <3mmol l-1.
OR
• Reduction of 20-25% in total cholesterol/30% in LDL (whichever is lower).
"Fire and forget."

How to reduce cholesterol
• Diet.
• Dietary substitution (fish oils, Benecol and other "nutriceuticals").
• Pharmacologically.
-"Statins"* - hypercholesterolaemia, or mixed.
-Fibrates - hypdertriglyceridaemia, or mixed.
-[Anion exchange resins.]

Statins
• Mode of action - inhibit HMG CoA reductase.
• Reduces formation of cholesterol.
• Can reduce serum cholesterol by ≤50%, depending on dose.
• Adverse effects: mysitis (muscle tissue inflammation - very rare), liver abnormalities (very rare), headaches, GI upsets.
• Safe drugs → "fire and forget."

Eg.
• *Simvastatin - "evidence based."
-Generic available.
• Atavastatin - "evidence based."
• Rosuvastatin - new; most potent, but not clinically proven in trial.
• Do they all have similar effects in reducing serious events?

Benefits of reducing cholesterol
• Decrease of 20% in LDL reduces events by 30% over 5 years.
• 30% = relative risk reduction.
• Absolute risk reduction depends on baseline risk.
• 10% risk over 10 years? Absolute risk reduction = 3% (reduction of 30%).
• 40% risk over 10 years? Absolute risk reduction = 12%.

How are we doing?
• How many possible patients?
-3.4% all between 34-69 for primary prevention.
-4.8% with established disease for secondary prevention.
-Around 2-3% of entire population.
• How many currently treated?
-Around one-third.
• £950million on drugs.

Why not better?
• Capacity.
-To identify patients.
-To treat patients.
• Conflicting priorities.
• Nonadherence.
-50% at 6 months.
-Poor education of patients, no shared decision-making etc.

Conclusions
• Tackling of cardiovascular disease requires a multi-faceted approach.
• The risk factors are known and can be treated for.
• Hyperlipidaemia is a major risk factor, especially for coronary heart disease and cardiovascular attacks.

Cardiac Physiology And The Manifestations Of Cardiac Disease

23.11.05

Myocardial function, dysfunction and heart failure.

Cardiac output affected by:
• Filling - atrial pressure.
• Contractility - strength of contraction.
• Resistance - largely contributed by arterioles.

Definitions:
• CO = cardiac output (5l/min).
• SVR = systemic vascular resistance.
• PVR = pulmonary vascular resistance.
• LAP = left atrial pressure.
• RAP = right atrial pressure.
• BP = blood pressure.
• PAP = pulmonary artery pressure.
• HR = heart rate.
• SV = stroke volume.
• CO = SV x HR.
• MAP (mena-arterial pressure) = CO x SVR.

Autonomic nervous system
Sympathetic response:
• Increases heart rate.
• Increases contractility.
• Increases venous return.
• Redistribution of peripheral flow.
• Adrenergic receptors.
• Adrenaline/noradrenaline (similar, but different effects).

Parasympathetic response:
• Generally opposite effects to sympathetic response.
• Acts via muscarinic receptors.
• Acetylcholine.

Cardiac response to decreased cardiac output:
• Acute sympathetic activation.
• Chronic effects of adrenergic stimulation.
-Salt/water retention via renal absorption system.
-Cardiac hypertrophy.

Neurohumoral consequence of reduced cardiac output:
• Reduced tissue perfusion.
• Reduced renal perfusion.
• Renin release.
• Angiotensin generation.
1. Salt and water retention; congestive symptoms.
2. Oxidative stress; inflammation and myocardial impairment.
3. (Possibly) cardiac remodelling; cardiac enlargement; increased wall stress.
4. Vasoconstriction; increased afterload.
• Sympathetic activation.
1. Tachycardia; increased oxygen demand.
2. Peripheral vasocontriction; increased afterload.
3. Increased salt/water retention; oedema.

Inappropriate activation: sympathetic - renin-angiotensin, adrenal.
Body tried to deal with decreased cardiac output as if it is caused by trauma and blood loss - this causes a problem when it is not.
Inappropriate activation of rennin-angiotensin, sympathetic nervous system.

Vascular injury, healing and atherothrombosis
Properties of normal endothelium:
• Anti-thrombotic.
• Anti-proliferative.
• Anti-inflammatory.
• Maintenance of tight junctions between cells.
• Nitric oxide.
• Prostacyclin - CRUCIAL TO HOW MUSCLE LAYER CONTRACTS.

Atherosclerosis/thrombosis:
• When blood vessels are damaged, vessels proliferate so they are blocked.
• Eccentric skew of lumen leads to decreased blood flow.
• More prone to ischaemia.

Normal artery:
• Endothelium releases nitric oxide, prostanoids, prostacyclin etc. - keeping it relaxed.
• Factors like smoke, physical pressure (increased blood pressure) cause endothelium to stop working properly.
• No longer anti-inflammatory.

Atherogenesis:
• Endothelium starts to express new molecule allowing attachment of inflammatory cells.
• Cells migrate into subendothelium.
• Basement membrane broken down.
• Smooth muscle cells migrate to subepithelium - causes more inflammation and more activation of smooth muscle - spirals.
• Chronic inflammatory disease.
• Develops atherosclerotic plaque.
• Less blood gets through.
• Less blood to tissues.
• Accumulation of lipid/cholesterol within plaque.
• Symptoms increase gradually.

CHD - sudden death, sudden severity.

Atherosclerotic plaque
Stable:
• Intact endothelium.
• Thick muscle/connective layer.

Unstable:
• Eroded endothelium.
• Thin muscular cap.
• Far more inflammatory cells.
• Macrophages activated - chemicals dissolve connective tissue.
• Increases fragility of cap
• Plaque ruptures - releases nasty stuff.
• Develops blood clot, which rapidly progresses to acclude artery.
• Therefore, very sudden symptoms.

Module 1.05

Cold Feet.
21.11.05 - 2.12.05.

Slipping towards the end of term...

How Do Proteins Work?

15.11.05

Kinetics:
• More complex relationship with substrate concentration.
• Characteristic hyperbolic shape.
• Michaelis-Menten equation
v0 = vmax [S]/Km [S]
Km = Michaelis constant - concentration at which substrate at 50% velocity.
• By modifying Michaelis-Menten equation, various plots can be obtained which enable Km and vmax to be determined.

Enzyme inhibition:
• Activity decreased by specific inhibitors.
• 1. Irreversible - inactivation eg. binding of DIFP to active site Ser of serine proteases.
2. Reversible.
a) Competitive - usually structurally related to substrate, therefore bind to active site and increase Km but do not affect v max for reaction. Inhibition overcome by addition of more substrate.
b) Non-competitive - bind to site distinct from active site, but close enough to interfere with catalytic process. vmax deceased; Km not affected.
• Enzymes often inhibited by substrate or product of reaction. Usually occurs at second (allosteric) site on enzyme and hence in non-competitive inhibition.
• Allosteric inhibition found between product of pathway and controlling (first committed) enzyme of that pathway.
• Inhibition may also be covalent - via phosphorylation controlled by hormones.

Enzymes as targets for drugs:
• Angiotensin is agonist for patients with high blood pressure.
• Angiotensin II, vasoconstrictor.

Social Inequalities In Health

11.1105

Health divide within countries - compared with affluent counterparts, people experiencing poverty tend to…
• Have shorter lives - 5-year gaps.
• Suffer more years of disability before they die - 13-year gap.
• Higher sickness and disease.

• Differences/variation versus inequalities/inequities.
• Inequality/inequity in health has ethical dimension: implies differences that are both avoidable and unfair/unjust.

How do inequalities rise?
• Main determinants of health - Dahlgren and Whitehead, 1991.
-Many determinants of health.
-Health service very important, but many other factors.
-Interaction between different factors.
• Different groups of population exposed to different things.

Eg. how does unemployment and poverty cause poor health?
• Lack of financial resources.
-Lack resources for food, housing, healing.
-Sub-nutrition.
• Psychosocial stress.
-Stress, stigma, social exclusion.
-Anxiety, depression, suicide, physical effects (chronic heart disease).
• Behavioural change.
-Caused by social isolation/coping in hardship.
-Tobacco/alcohol use, less exercise.

What does this mean for planning and delivery of health services?
• Increased need for health care.
• Because of higher levels of morbidity in certain groups and areas.
• Because deprivation makes access to and uptake of services difficult.
• Because poorer living/working conditions may make recovery more difficult.

Inverse care law = "Medical care is least available where it is most needed." Tudor Hart, 1971.
Applies to: access; uptake; quality of care.

Reflect on implications of observed social inequalities in health in:
• Dealing with individuals and people.
• Planning services for population groups.
• Reforming systems.
• Society's response.

Wheezing

10.11.05

What is a wheeze? (Laennec, 1819)
Four groups of 'rales':
1. Moist.
2. Mucous.
3. Sonorous.
4. Sibilant.

Polyphonic wheezing = widespread narrowing with various pitches.
Monophonic wheeze = fixed obstruction in single airway.
Stridor = narrowing of extra thoracic airway (inspiration).

Types:
• Intermittent/episodic wheeze with wheeze-free intervals = reversible airflow obstruction.
• Constant wheeze with no wheeze-free period = fixed airflow obstruction.

P=ν (8lη/πr4)

Where P = pressure, ν = flow, η = viscosity, l = length, r = radius.

Lung function peaks between 10-20 years of age.

1:3 children attend GPs with a wheezing episode that are less than 3 years of age.

12-15% of children younger than 15 years of age have asthma; 25% wheeze.

13 million children have asthma.
50,000 childhood admissions per annum (5% total asthma admissions).
32 childhood deaths per annum (2% total asthma deaths).
£561 million spent by NHS on treating asthma.

Contributing factors to an episodic wheeze:
• Airway.
• Atopy.
• Viral infection.

Viral infection
• Viruses identified in more than 80% of wheezy episodes.
• RSV and rhinoviruses (para influenza).
• Often associated with reduced lung function beforehand.
• Wheezing with virus can occur without underlying asthma.

Why?
• Genetic small airways/genetic abnormal viral response.
• Premature birth, maternal smoking [between conception and birth].
• Environment, viral infection, maternal smoking [after birth].

Atopy - determines recurrent wheezing
• Family history of atopic illness (especially in mother).
• Other atopic diseases in infant.
• Multiple genes.
• Higher environmental house dust mite load.
• Birth between August and October.
• Maternal smoking during pregnancy.
• Normal lunch function at birth.
• Poverty.

Why is there more asthma?
• Parents
-Maternal smoking.
-Lack of breast-feeding.
-Poverty; ethnic minority.
-Broad spectrum antibiotics with change in maternal gut flora?
• Child
-Diet (vitamin E).
-Lack of exercise.
-Lack of infections.
-No worm infections?
• Home environment
-High house dust mite load.
-Indoor air quality.
-Gas stoves/NO2 level.
-Damp housing.
-Central heating.
-More pets?
• Outside environment
-Move from rural to city environment.
-Outdoor air pollution (So2 and ozone).
-High traffic.

A Question Of Confidence? From Sample To Population

9.11.05

Peak expiratory flow rate
• Measured in litres per minutes.
• Based on greatest flow in 2 milliseconds of forced expiration starting from a full lung of air.
• Used to monitor reversible airflow limitation.
• Best of three attempts.

Why do they vary?
• Random/chance variable
-Between subject/samples
-Biological variation
-Height
-Sex
-Age.
-Within subjects/samples.
• Systematic errors (leading to bias)
-Instrumental error.
-Observer error.

Reliability
• Degree to which results can be repeated to give the same value.
• Precision/reproducibility/stability of measurement.

Accuracy/validity
• Degree to which measurement/estimate based on measurements represents TRUE VALUE of attribute being measured.
• Degree to which value represents truth.

Peak expiratory flow rate used to monitor changes in asthma.
• How do we know that (new) treatment for asthma 'works'?

Estimating population figures from a sample
• Most statistical analysis is based on that fact that the sample was used to estimate the population parameters.
• Usually, the best estimate of the population 'average' is the sample mean.
• However, different samples give difference means eg. student height.
• How do we know what the true population is?

Multiple samples
• Each sample will have different means.
• To improve the estimate, look at the "mean of means" - measure distribution by means of standard error.

Improving the reliability of the estimate
• Increasing the size and number of samples.
• The reliability of the estimate is the STANDARD ERROR OF THE MEAN.
• It is not practical to repeat samples in "real life."
• SEM calculated statistically.
• THIS IS NOT THE STANDARD DEVIATION!
-Measure of dispersal in SINGLE sample.

From sample to population
• Based on sample mean and SE, CONFIDENCE INTERVALS can be constructed.

Confidence interval
• Value within which we can be 95% confident that the true value lies.
• General formula = Population +/- 1.96*SE.
• Can be calculatd about most population estimates
-Population point estimates.
-Because confidence intervals don't overlap.

Applicability
• If we want to know whether treatment is improving peak flow, we can compare mean (and confidence interval) of peak expiratory flow rate in the group that has treatment with the mean (and confidence interval) of the peak expiratory flow rate of the group without treatment.
• Despite sample means being difference, if confidence intervals overlap, we cannot exclude the possibility that the two population means are the same ie. the treatment has had no effect.

YOU CAN BE 95% CONFIDENT THAT THE TRUE POPULATION VALUE LIES BETWEEN THE LOWER AND UPPER CONFIDENCE INTERVAL.

Is the estimate valid?
• Recall validity (accuracy) is the degree to which the value represents the truth.

Bias
• Systematic error in the study.
• May relate to sample selection (selection bias) ie. the sample is not representative of the population.
• May relate to systematic measurement errors (measurement bias) eg. systematic error in the measurement tool or its use.

Confounding
• The third factor related to both independent (exposure) and dependent (outcome) variable.
• Eg. age
-Older people may be less likely to try new treatment and may have les severe illness, so they may have a difference response wrt peak expiratory flow rate.
• There are techniques available to allow for this IF YOU KNOW ABOUT IT!

So…
• Opportunities for bias can exist in
-selection
-measurement
-analysis stages of study.

Inferential statistics
• Means, proportion, percentages or any other summary measure.

Assumptions
• Sample REPRESENTATIVE.
• Measure in samples is BEST ESTIMATE.

Another way of expressing association:
• Population of asthma prevalence in 16-24 year olds.
-Male = 70.7 per 1000.
-Female = 81.7 per 1000.
• RELATIVE RISK of asthma in females of 16-24 years compare with males is [ratio]
1.08 (95% confidence interval 1.06-1.10)

Relative risk
• Ratio of risk of death/disease among those exposed to risk to those among unexposed.
Relative risk of 1 means no excess risk.

Signal Transduction: Getting The Message Across

8.11.05

Signal transduction
Plasma membrane = information barrier.

First messenger (outside) ⇒ Binds to receptor ⇒ Second messenger (inside) ⇒ Change in biochemical activity.

Excitation-contraction coupling - excitable cells (eg. nerves, muscles); action potential.
Stimulus-secretion coupling - non-excitable cells (eg. saliva).

The nature of the biological response depends on the cell type.
-NOT the second messenger.
-NOT the cell surface receptor.

Sympathetic response - noradrenaline ⇒ cAMP ⇒ protein.
Parasympathetic response - acetylcholine ⇒ Ca2+ ⇒ fluid.

Summary
• Signal transduction = process that enables cells to respond to changes in their environment.
• Second messenger pathways
-flexibility
-amplification
filtering.

Treating Asthma: Underlying Mechanisms

25.10.05

What is asthma?
• Reversible airways obstruction.
• Characterised by
-wheeze
-expiration greater than inspiration
-younger patient
-small to medium airways
-triggers.

Causes:
• Genes (runs in families).
• Triggers
-infection
-animal dander
-house dust
-coldβ
-exercise
-pollen
-food, drugs etc.
• Inflammation
-mast cell
-lymphocyte
-eosinophil.
• Bronchospasm.
-Sympathetic response [fight of flight - stress-related] = dilate airways - β2 receptors opposite.
-Parasympathetic response [relaxed] = constrict airway - cholinergic receptors.

Clinical features:
• Breathlessness.
• Expiratory wheeze.
• Cough (dry or productive).
• Early morning waking.
• Hyper-expanded chest.
• Low peak flow.

Treatment:
• Acute asthmatic attack.
• Long-term.

Severity of acute asthmatic attack:
• Peak flow.
• Clinical symptoms.
• Chest signs ('silent' chest).
• Arterial blood gases.
NOTE: A 'normal' of high pCO2 may be a danger sign.

Treatment of acute asthma:
• Remove/avoid triggers.
• Treat infection.
• Reverse bronchospasm.
• Reduce inflammation.

Reverse bronchospasm - relievers:
• Immediate relief.
• Treats symptoms.
• Does not prevent attack.

Reduce inflammation - preventers:
• No immediate benefit.
• Treats underlying disease.
• Prevents attacks.

Long-term management
• May not need treatment.
• May need only β2 agonist.
• May need regular inhaled steroid + as-required β2 agonist.
• May need home nebulisers.
• May need long-term oral steroids.
• May need immunosuppressants.

Module 1.04

A Wheezy Adolescent.
7.11.05 - 18.11.05.

Halfway through, and I must've decided that I'd better start going to some more plenaries...

Anyway, I'm back from a weekend partying in Nottingham now, so I'll finish off last term.

Controlling Blood Glucose

3.11.05

Physiological control
• Postprandial increased insulin - glycogen/amino acid/fatty acid synthesis.
• Between meals - glycogenolysis, gluconeogenesis, fatty acid breakdown etc.

Insulin
• Peptide.
• Secreted from β cells of pancreas in response to rise in blood glucose.
• Drive glucose into cells (with K+) - lowers blood glucose.
• Promotes glycogenesis, fatty acid formation, amino acid synthesis - anabolic effects.
• Acts at specific receptors.

Diabetes mellitus
Type I
• Destruction of islets of Langerhans (why? Infection? Autoimmunity?)
• Lack of insulin.
• No glucose entring cells - hyperglycaemia, polyuria, polydipsia, dehydration.
• Fat breakdown increased - weight loss - incomplete, so free fatty acids.
• Ketoacidosis.
• Death.
• Onset occurs at less than 40 years of age.
• Normal/wasted appearance.
• Low/absent insuling.
• Abrupt onset symptoms.

Type II
• Peripheral insulin resistance.
• Less peripheral glucose absorption.
• Insulin levels often high.
• Pulyuria, polydipsia (dehydration).
• Fatigue, infections.
• No ketoacidosis.
• FHx.
• Onset occurs at more than 40 years of age.
• Obesity.
• Normal/increased insulin.
• Gradual onset symptoms.
• Hyper-osmolar coma in elderly sufferers.

Epidemiology
• Type I
-Younger patients.
-Less common.
-Often no family history.
-0.1-0.5%.
• Type II - older patients; very common and becoming more so - 1-4% adults.

Treatment - Type I
• Acutely.
• Rehydrate.
• Insulin.
• Correct acidosis?
• Chronically - insulin, diet.

Treatment - Type II
• Diet.
• Oral agents.
• Insulin.
• Often progressive disease.

Complications of diabetes mellitus:
• Glysylation of proteins (and other problems) leads to complications.
-Angiopathy - macrovascular, microvascular.
-Neuropathy.
-Nephropathy.
-Retinopathy.
• Occur in both forms (no such thing as "mild diabetes").
• Needs prophylaxis and treatment.

Insulin
• Stimulates β2 adrenoreceptors in pancreatic β cells - stimulates conversion of PRO-INSULIN to INSULIN (a and b chain) and C-PEPTIDE.
• Inactive if given orally.
• Given parenterally - subcutaneous, inter-muscular, intravenous.
• Wide variety of preparations.
• Source: bovine (3 amino acids' difference), porcine (1 amino acid).
• Human (90%).
-Chemically modified porcine or genetically engineered.

Duration of action:
• Soluble insulin - short, 0.5-1 hours.
• Insulin complexes - isophane/proteamine.
-Slow relase of insulin over several hours.
• Insulin analogues.
-Short-acting insulin lispro.
-Long-acting - insulin glargine.

Adverse effects of insulin (affect both Types I and II):
• Hypoglycaemia
-Sympathetic over-activity leads to tachycardia, sweats, tremor, palpitations.
-Neuroglycopenia leads to visual disturbance, drowsiness, aggression, coma.
-30% diabetics lose adrenergic symptoms of hypoglycaemia during 15-20 years of insulin therapy.
• Allergy?
-Antibodies - resistance.
• Local problems - lipodystrophy.

Oral hypoglycaemics (Type II):
• Sulphonylureas
-Gliclazide and many others.
-Stimulate insulin release from pancreas.
-Increase insulin sensitivity.
-Hypoglaycaemia.

An Introduction To Medical Sociology

28.10.05

• Medical sociology explores how society shapes occurrence and experience of health and illness.
• IGS in medical education
-how do social class, ethnicity, gender, and age/life cycle affect occurrence/incidence and experience of health and illness?

Social class
• Social stratification is the fact that within society, there is usually a hierarchy of social groups.
• Social class is a form of stratification based upon economic differences.
• The concept is central to much of medical sociology research.

The relationship between health and social class
• Since the 1900s, there have been great improvements in health in the UK.
• However, despite improvements in medicine, social class differences persist and are getting worse.
• The upper social classes are getting healthier, living longer and experiencing less illness.
• The lower social classes are sicker and dying younger.

How do you measure a social class?
• The general measure is obtained by combining occupational groups with roughly equivalent skill and status.

Why?
1. Cultural/behavioural.
2. Materialist.
3. Social selection.
4. Artefactual.

Ethnicity
• Race
-Refers to a person's physical characteristics.
-Little meaning in terms of health - can have greater genetic variation within racial groups than between them.
• Ethnicity
-Denotes how groups of people who share similar histories behave etc.

Measuring ethnicity
• Most research on the health of minority ethnic populations relies on place of birth.
• Other approaches ask people to assign themselves.
• We need to think about the way that ethnicity is defined in studies reporting on the variable.

Variations in mortality
• Coronary heart disease
-Increased in people born in the Subcontinent.
-Increased in men born in the African Commonwealth.
• Death rates for cerebrovascular disease
-Increased in people born in Ireland

Teamwork And Diabetes Mellitus

26.10.05

Goal: "In the successful treatment of diabetes, the patient, the nurse, the practitioner and the specialist are often partners working together to establish the patient's health." RD Lawrence, 1932.

Historical development of diabetes education
• 1920s - insulin discovered.
• 1970s-80s - education recognised.
• 1990s - health promotion movement
-DCCT (1993)
-UKPDS (1998)
-global epidemic, leading to increasing expenditure.
• NOW - holistic strategy - Diabetes Care Model - "expert patients."

Today
• New health and social care policies.
• Evidence-based practice.
• Patient-centred care.
• 'Seamless' service delivery.
• Teamwork and collaborative practice.
• Overlapping of skills and competency.

DIABETES NSF: STANDARD (December 2001)
1. Empowering people with diabetes.
2. Inequalities in care.
3. Inpatient management.
4. Management of type I.
5. Prevention and management.

Diabetes care
1. Health promotion for populations to prevent diabetes.
2. Screening.
3. Ongoing management.
4. Regular examinations.
5. Ongoing treatment.
6. Treatment and management.

Chronic disease model
• Continuous, not episodic.
• Proactive, not reactive.
• Planned, not sporadic.
• Patients centred, not provider centred.
• Population based, as well as individual based.

Team members in treatment of diabetes

THE PATIENT

Community partners:
• Family/friends.
• Diabetes support groups.
• OHN/employers.
• Minority organisations.

Primary care team:
• Practice nurse/nurse practitioner/general practitioner.
• Dietician.
• Chiropodist.
• Orthoptist.
• Dentist.
• Pharmacist.

Secondary care team:
• Diabetes specialist nurse.
• Diabetologist/endocrinologist.
• Dietician.
• Chiropodist.

Other team members:
• Ophthalmologist.
• Cardiologist.
• Vascular surgeon.
• Nephrologist.
• Accident and emergency staff.
• Neurologist.
• Midwife/obstetrician.
• Psychologist.
• Physiotherapist.
• Occupational therapist.

Aims of care
• To achieve optimal glycaemic/lipid/blood pressure control.
• To delay onset and progression of diabetic complication.
• Quality of life acceptable to individual.

Major complication of diabetes
• Ketoacidosis in type I.
• HONC in type II.
• Nephropathy (kidney disease).
• Impotence (nervous system - sexual function).
• Diabetic retinopathy.
• Hypertension.
• Coronary heart disease.
• Stroke.
• Neuropathy (nervous system).

Living with diabetes
• Psychological impact: 'coming to terms' with having diabetes [nurse practitioner/practice nurse/diabetes specialist nurse + internet/magazines/books/other patients].
• Monitoring daily diet [dietician].
• Daily measurements of blood glucose levels [nurse practitioner/practice nurse/diabetes specialist nurse].
• Regular visits to hospital/GP [diabetologist, GP, diabetes specialist nurse/practice nurse, chiropodist, orthoptist].
• Regular activity/exercise [exercise physiologist/physiotherapist].
• Daily tablets and/or injections [pharmacist].
• Work, rest, play.
• Worry about future - complications.

Functioning teams
• Same goals.
• Communicate well.
• Co-operate.
• Help each other.
• Want achievement for team and patient.

Success rests on
• Quality of leadership.
• Clarity of goals.
• Effective communication.
• Motivation.
• Conflict resolution.

What do I need to know?
• Specialist knowledge/skills.
• Roles and responsibilities of others.
• Inter-disciplinary working.
• Audit.

Module 1.03

A Raging Thirst.
24.10.05 - 5.11.05.

You know, if anybody's got any of the notes that aren't up here and fancy sending them to me to put up, that'd be nice.

Dyspepsia

17.10.05

Symptoms:
• Epigastric discomfort.
• Anorexia.
• Retrosternal pain.
• Nausea.
• Vomiting.
• Fullness.
• Early satiety.
• Heartburn.

Aetiology:
• GORD - 15-25%.
• Ulcers - 15-25%.
• Stomach cancer - 2%.
• NUD - 60%.

Alarm signs:
• Anorexia.
• Loss of weight.
• Anaemia.
• Rapid progression.
• Malaena.
• Dysphagia/odynophagia.

Treating dyspepsia
Antacids:
• Weak alkalis.
• Relieve symptoms.
• Increase gastric emptying (short action).
• Heal ulcers at high doses.

Histamine H2 antagonists: block action of histamine.

H+ pump inhibitors:
• Inhibit H+/K+ ATPase H+ pump.
• Decrease acid secretion (blocks H+ transport)
• Irreversible inhibition of enzyme.
• Promotes ulcer healing (including refractory - Zollinger Ellison).

Antibiotics:
• Chronic H. pylori gastritis.
• Increased gastrin release.
• Strongly associated with peptic ulcer disease (especially duodenal ulcers).
• Recurs despite treatment if not eradicated.

Mucosal protection:
• Coats base of ulcer craters.
• Must be given on empty stomach.
• Bismuth, sucralfate.
• Only administered to unconscious

Introduction To Healthcare Ethics

13.10.05

Ethics = how you SHOULD behave.

In medical practice, ethical and professional issues arise on a regular basis.

Aims of ethics:
• To reflect on what it is to be an ethical/professional health care practitioner.
• To reflect on the types of ethical and professional principles, values and consideration that help guide our behaviour.
• To be able to identify relevant ethical and professional issues raised by particular health care scenarios.
• To be aware of relevant sources of ethical, professional and legal guidance etc.

Principles and values - four principles (Beauchamp and Childress):
• Respect for autonomy - we should respect the patient's right to make informed and voluntary choices about how we act on them. This clearly ties in with issues of valid consent - ensure you're familiar with what valid consent involves.
• Non-maleficence - we should not act in ways that are likely to harm the patient. Negative obligation - tells us to refrain from behaving in ways like to harm others. Think: what constitutes a harm? Who should decide what constitutes a harm?
• Beneficence - we should act in ways likely to benefit a patient. Positive obligation - tells us to positively act (and not simply refrain from acting) in a way that will benefit others. Think: what constitutes a benefit? Who is in the best position to decide whether the treatment is beneficial to the patient?
• Justice - we should treat all our patients fairly and equitably. Think: what might be suggested to constitute a fair and equitable way of distributing resources?

Beauchamp and Childress argue that the above pose prima facie, not absolute obligations. DISTINGUISH!

Other values or moral considerations:
• Obligations of confidentiality/privacy: What do these entail? How do privacy and confidentiality differ? Why is it important to respect these? Are there circumstances where privacy and confidentiality shouldn't be respected? What are the professional guidelines on the above?
• Obligations of truth-telling: What is involved? Why should we normally tell the truth? How should we go about telling patients the truth? Are there circumstances in which it is better not to tell patients truthful information? What are professional truth-telling/disclosure guidelines.
• Rights (and Human Rights Act): What are rights? Are there any 'absolute' rights? Why are rights important? Which articles of the Human Rights Act are particularly relevant/important for health care professionals?
• Appropriate/non-judgemental attitudes: What are attitudes? What are examples of good and bad attitudes? Why do you think attitudes are often thought to be morally significant?
• Good inter-professional and intra-professional relations: Why do you think good relations between different professionals is important for providing health care?

The Rise And Fall (And Rise?) Of Epidemic Diseases

12.10.05

19th Century urbanisation:
• Stimulated by industrialisation.
• Unplanned, rapid building.
• Primitive sanitary services - privies, cesspits, private water suppliers.

Demographic crisis:
• Crude death rates over 40/1000 in 1840s.
• State forced to provide basic welfare.
• REACTIVE NOT PROACTIVE.

Cholera:
• Symptoms - severe diarrhoea etc.
• Miasmatic theory of disease.
• All social classes at risk - no effective treatment.
• 1832 - 21,882 deaths.
• 1848-9 - 55,201 deaths.

Public fear of disease:
• Liverpool was one of the unhealthiest places in Britain.
• Liverpool - 8 cholera riots in 1832 - anti-medical profession (1832 = Burke and Hare and Anatomy Act = supply of bodies for anatomy classes).
• 1847 - typhus fever epidemic in Liverpool.

Sanitary response to cholera:
• Short-term responses - temporary Boards of Health.
• Temporary public cleansing.
• Edwin Chadwick - sanitarian.
• Liverpool Sanatory Act 1846.
• Public Health Staff - Medical Officers of Health - Dr Duncan first (Liverpool) 1847.

Bacteriology:
• Robert Koch.
• Louis Pasteur.
• Joseph Lister.
• Tuberculosis bacillus identified in 1882.
• Discovery of cholera vibrio in 1884.

Supremacy of science over sanitarianism:
• Miasmatic, contagious, anti-contagious theories replaced by germ theory.
• COMPULSORY public health.
• By 1880s, most urban areas had sanitary infrastructure - public piper water supply, sewer system etc.

'Personal prevention':
• Decline in epidemic diseases.
• New focus on chronic health problems.
• Tuberculosis, STDs, cancer, heart disease.
• Concern with national deterioration - 'degeneration' - eugenics.
• Development of an individual 'moralising' framework for disease.

1918-19 Influenza pandemic:
• Killed 30 million worldwide in less than 6 months.
• No effective vaccine or treatment.

Inter-war health crises:
• Who is responsible for disease surveillance?
• Conflict between Ministries of Health and wider medical profession.
• Worldwide economic depression.
• Lack of resources.
• Diphtheria scandal.

Post World War II disease regime:
• Culmination of transition from epidemic infectious diseases to chronic health problems.
• NHS 1948 - political priority for curative MEDICAL services.

1970s - the New Public Health
• Low public health status.
• Who has the communicable disease skills?

Conclusion?
• How do we define 'epidemic'?
• Does it matter?
• Are epidemics useful?
• Put pressure on systems.
• Generate demands for change.

Module 1.02

Indigestion.
10.10.05 - 21.10.05

I've only three sets of notes for this module. Two weeks in and I was getting sloppy already...

Handling Data

7.10.05

Data = facts given from which others can be inferred.

Own sources of data:
• Text books etc.
• Own research, including research papers and web pages.
• Also use data in clinical practice
-drug dosages
-quality assurance
-clinical audit
etc.

Resources and support materials:
• Virtual resources
-text-based presentations
-virtual presentations.

Assessment:
• Year 1
-Paper 1
-Paper 2.
• Year 2 and Year 4
-Paper 1
-Paper 3.
• Year 3
-Paper
-Critical thinking module.
• Year 5 - SAMP
• Will not be asked to calculate statistical test in exams.
• Expected to understand and use proper terminology.

Data summary measures
What sort of data?
• The type of data.
• Categorical data (qualitative).
• Continuous data (numerical, quantitative)
-can take any value within a range.
• NOIR
-nominal
-ordinal
-interval
-ratio.

Categorical data summarised as percentage. Percentages ARE NOT continuous data.

Measures of location - summary measures used to describe data include:
• Median.
• Mean.
• Mode.

Measures of spread - summarises scatter or dispersion of data:
• Range.
• Percentiles/quartiles.
• Inter-quartile range.
• Variance.
• Standard deviation.

Derived data - based on data, certain information can be derived:
• Rate.
• Incidence.
• Severity of condition.

Rates
• Measures frequency of occurrence.
• Important when making comparisons.

Probability - summarises chance.

Approaches to calculating probability:
• Subjective - personal belief.
• Frequentist - based on observation.
• A priori - theoretical model ie. calculate from theoretical model.
• Frequentist and theoretical used most in data handling.

Vaccination And Immunology

5.10.05

Features of the immune response:
• Specificity.
• Memory.
• Self-nonself discrimination.
• 'Redundancy.'

Types of immune response:
• Innate response
-rapid, relatively non-specific, no memory, first line of defence.
• Adaptive response
-slower, highly specific, long-lasting memory, ultimately more effective, second line of defence.

Innate response 1: soluble mediators
• Bind to pathogens or their products.
• Opsomise pathogens for phagocytosis.
• Recognise mainly bacterial carbohydrates.
• Eg. complement (alternate pathway), collectins, LPS binding protein.

Innate response 2: phagocytic cells
• Eg. neutrophils, macrophages.
• Bind and engulf (phagocytose) pathogens.
• Use pattern recognition receptors (PRRs) that recognise bacterial, viral and fungal molecules eg. scavenger and toll-like receptors.
• Binding triggers adaptive immune response.

Adaptive immune response 1: soluble mediators - antibodies
• IgM (primary response); pentamer.
• IgG (secondary response); monomer.
• IgA (mucosal surfaces); dimer.
• IgE (parasites/allergy); monomer.
• Made by plasma cells (derived from B cells).
• Bind and neutralise pathogens.
• Stimulate removal by phagocytes and compement.

Antibody responses:
• In primary response, IgM produced.
• Later in response, antibody class switches to IgG, IgA or IgE of same specificity.
• Antibody affinity then further refined to give more efficient response.
• Memory B cells produced; switched on more quickly and produce higher affinity antibodies.

Adaptive reponse 2: cellular mediators - CD4 and T cells
• 'Helper' T cells.
• Recognise exogenous bacterial or viral peptide antigens presented by dendritic cells or macrophages in association with class II HLA.
• Generate help for antibody production and stimulate cell-mediated immunity.

Adaptive response 3: CD8 and T cells
• 'Cytotoxic' T cells.
• Recognise endogenous viral peptide antigens presented in association with class I HLA.
• Generate 'killer' cells that directly kill virus-infected cells.

Antigen presentation
• Dendritic cells and macrophages take up antigen, process it and present it in the form of short peptides to T cells in association with HLA.
• Exogenous antigen processed and presented in association with class II HLA, but can also associate with class I HLA.

Vaccination: designed to mimic natural infection and stimulate immunological memory.

Gut Secretion And Absorption

4.10.05

Fluid and electrolyte transport are important functions of the gastrointestinal tract (even in the absorption of food).

Epithelial cells may
• secrete water and electrolytes ie. transport from blood to gut lumen
• absorb water and electrolytes.

Diarrhoea = malabsorption of water.

Movement of water and solutes
• Water moves down osmotic gradients.
• Electrolytes move down electrochemical gradients.
• To move solutes against their concentration gradients, energy is required.
• Energy is supplied by Na+ gradients (generated by Na+ pump) and by H+ gradients.

Water molecules: Paracellular route = between cells.
Ions: Transcellular route = through cells (active or passive transport)

Diarrhoea
• Hypermotility - transport too fast for absorption.
• Osmotic - non-solute absorption.
• Defective transport - Na+ or Cl- transporters absent.
• Secretory
-inflammatory, blood hormones, tumours.
-enterotoxins, viruses/parasites.

Oral rehydration therapy: water, electrolytes, glucose.

Barriers, Pores, Pumps and Gates

3.10.05

Cell membranes
Channels and pores
• Membrane-spanning proteins.
• Hydrophilic domain allows water molecules and ions to cross membranes.
• Selective.
• Gated-channels.

Selectivity
• Main cations: Na+, K+, H+, Ca2+ + non-selective cation channels.
• Main anion channels: Cl-, HCO3-.

Ion movement through a channel or pore is always DOWN the electrochemical potential gradient of the ion.

Nernst equation: membrane potential.

Movement of an ion or any other substance against its EPG requires active transport.

Active transport
Involves an ENERGY INPUT into the transport process.

Primary active transport makes direct use of metabolic energy in the form of ATP.
Sodium pump = sodium/potassium ATPase. 3 Na+s out, 2 K+s in.

• Na+ pump.
• Ca2+ pump.
• H+ pump.
• No ANION pumps.
• No sugar or amino acid pumps.
• No water molecule pumps.

Secondary active transport: Utilises energy stored in EPG of one substance to drive the movement of another.

Cotransport: Na+ +
• Glucose (epithelial cells) }
• Amino acids } symports
• Also antiports - Na+ in, something else (eg. H+) out.

• Glucose, amino acids, bicarbonate, ions etc.
• Most commonly utilised driving force - inwardly directed Na+ gradient.
• Na+ gradient created by primary active transport (Na+ pump).

Transepithelial water movement
Na+ outside much much greater than Na+ inside.
K+ inside much much greater than K+ outside

IGS Theme And Communications Skills

29.9.05

IGS
• The inter-relationships of social, cultural (groups) and psychological (individual) factors in health and disease.
• Important theme in curriculum - reflecting this, students are examined on IGS throughout the whole course.
• Health behaviour.
-Risky lifestyles: can they be changed?
• Coping with chronic illness.
• Adherence.
-Why do half of all patients not take their medicines as prescribed?

Communication skills - vital!
• Trust, care, respect.
• Patient satisfaction is a key NHS priority.
• Adherence to treatment.
• Ethical duty to do the best for your patients.
• Complaints and litigation: 90% = poor communication.
• Your own quality of life as a practitioner.

Can they be taught?
• We all have communication skills.
• Communicating is complex and there is always more to learn.
• Good communication involves:
-being flexible
-being aware of the impact you are having
-finding your own style.
• BUT there are some key skills you can learn and develop.
• EVERYBODY can improve.

Challenging situations:
• Breaking bad news.
• Talking with patients with shome it may be difficult to communicate:
-emotionally-charged situations
-patients with mental health difficulties
-communicating via an interpreter
-children and their parents
-sensitive and difficult topics.

The consultation: key questions:
• Do I know significantly more about this patient than when I started the consultation?
• Did I really listen?
• Did I find out what really matters to the patient?
• Did I share treatment options?
• Did I attempt to make sure they understood?
• Was I approachable, caring and respectful?
• Did I go all I could to win this patient's trust?

Who's who?
Ms Janine Carroll - j.l.carroll@liv.ac.uk
Dr Bridget Young - bridget.young@liv.ac.uk

Medical Science In The Clinical Context (How Drugs Work)

28.9.05

"Pharmacodynamics" - how drugs work.
"Pharmacokinetics" - how drugs get about and where they go.

Therapeutics:
• Concept of benefit versus risk.
• The disease
-Causation.
-Natural history and prognosis.
-The aims of treatment.
• The evidence base for 'therapeutic strategy' (which drug do I choose first?)
• How to monitor progress.

What is a drug?
• Any molecule used to alter a disease process.
-Smallest = ions.
-Largest = polypeptides.
• All drugs are also poisons - it's just a matter of dose - also idiosyncratically eg. allergy.

Where do drugs come from?
• Origins:
-synthetic
-biological
-semisynthetic.
• Discovery:
-serendipity
-systematic search of vast numbers of molecules
-by design (human/pathogen genomes will help)

• How do drugs work?
Receptors 1
• Regulatory molecules for endogeneous ligands.
• Proteins or glycoproteins.
• Drug-receptor bonds are usually reversible.
• Activation [leads to] structural alteration.
• Activation changes cellular activity [leads to] response.
• Speed of response varies from milliseconds to hours.
• Receptor numbers may increase or decrease.

Receptors 2
• Transmembrane ion channels eg. Na+, lignocaine.
• Transmembrane protein linked to G-protein eg. adrenaline, salbutamol.
• Transmembrane pro-enzymes eg. insulin.
• Intracellular receptor eg. steroids.

Other macromolecule targets
• Enzymes: competition for active site eg. methotrexate (cancer therapy) inhibits enzyme of folate pathway.
• Membrane-bound ion pumps.
• Transport proteins.
• Structural proteins.
• Ribosomes.

Physiochemical activity
• pH: antacids.
• Osmolality: mannitol.
• Resins: cholestyramine.

Stimulates receptor = agonist.
• Agonists
-bind to a receptor and stimulate it
-full agonists
-partial agonists.
• Antagonists
-bind to a receptor without stimulating it
-competitive antagonists: can be overcome by increasing agonist concentration
-non-competitive antagonists: cannot be overcome.

Therapeutic window
• Terms 'therapeutic' and 'toxic' are arbitrary - are simply two ends of a continuity.
• Inter-subject variability in:
-dose needed for benefit
-dose needed for harm.
• Drugs differ in 'gap' between benefit and harm

Population Perspective Theme

Population Perspective Theme
27.9.05

A framework of seven questions for taking a ‘public health view’:

1. What public health issues are raised by this problem?
Is the problem present for the public's health?
What 'case' definitions are being used?
The Acheson definition of Public Health: "The science and art of preventing disease, and prolonging and promoting health through the organised effort of society.

2. How does this problem affect the population?
Who? When? Where? By how much? Why?
Epidemiology: distribution and determinants of disease in human populations.
What data? What data handling?

3. What are the health needs of the population in relation to this problem?
Epidemiological profile; comparative; corporate.
With people, want and demand are not the same thing.

4. How can the burden of the problem be reduced?
Health education.
Health protection - using legal and fiscal measures.
Disease prevention
-Primary (before)
-Secondary (early stages)
-Tertiary (eradication/rehabilitation)

5. How should health (and other) services be organised and delivered to address this problem?
NHS: "Our Healthier Nation," "The NHS Plan."

6. What are the main research and development issues raised by the problem?
What works?
How do we know?
How robust?
Evidence used in practise?
What gaps?

7. What are the main public health implications of this problem?