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What is global health?

The health of populations in a global context
It has been defined as "the area of study, research and practice that places a priority on improving health and achieving equity in health for all people worldwide".


What are the 5 metaphors applied to global health? Describe them.

1. AS FOREIGN POLICY – using global health policies to create positive worldwide reputation and exert political influence, forging alliances with countries where they have strategic interests
2. AS SECURITY – health policy seeks to protect ones own population, focusing mainly on communicable diseases that threaten this population. Only diseases of poor countries that pose a potential threat to citizens of rich countries matter
3. AS CHARITY - promotion of health as a key element in the fight against poverty
4. AS INVESTMENT - use of health as a means of maximising economic development
5. AS PUBLIC HEALTH – seeks to decrease the worldwide burden of disease, with priority given to those risk factors and diseases that make the greatest contribution to this burden


Describe and explain global in equity.

Arises from the uneven distribution of power, resources, and status
Inequities are a matter of social injustice:
– can influence patterns of advantage and disadvantage
across the globe
– can have significant and unfair adverse effects on the health of individuals and groups
Inequity can result in the unequal attainment of the human right to health


What is globalisation?

the incorporation of national economies and societies into a world system ‘through movements of goods and services, capital, technology and (to a lesser extent) labour'


What are the (i) challenges (ii) benefits of globalisation?

(i) Population growth fuels resource competition and food price rises.
Already challenged infrastructures struggle to cope.
Tribal and ethnic tensions may increase and violence may result.
Devastating effects on specialist local communities (e.g. coal mining in South Wales) and may lead to exploitation.
(ii) Economic developments lift people out of poverty.
Opportunities for education and participation.
Usually results in improvements in health.
But, the transition can be difficult and the benefits unevenly distributed.


What is the value of the resting membrane potential? What ion is the membrane more permeable to as a result of this? What does the value of the resting potential depend upon?

More permeable to K+ than Na+
Dependent upon the ratio between PNa:PK


If the potassium permeability increased by a factor of 50, how would Em be affected – would the membrane potential depolarize (become more positive) or would it hyperpolarise (become more negative)?

Hyperpolarise (more + charged ions leaving the cell)


If the sodium permeability increased by a factor of 100, how would Em be affected – would the membrane potential depolarize (become more positive) or would it hyperpolarise (become more negative)?

Depolarise (more + charged ions entering the cell)


Would the following make it harder or easier to reach the threshold potential compared to the normal situation (i) An increase in the [K+] concentration of extracellular fluid to 10 mM (ii) A decrease in the [K+] concentration of extracellular fluid to 2 mM ? (HINT: think of the gradient)

(i) EASIER: increasing the extracellular [K+] will cause depolarisation and move the resting membrane potential nearer to the threshold
(ii) HARDER: decreasing the extracellular [K+] will cause hyperpolarisation and move the resting membrane potential away from threshold

(NB: the resting potential is -70mV and the threshold is -50mV) IC = 140 EC = 5


Would the following make it harder or easier to reach the threshold potential compared to the normal situation (i) Increase in the [Na+] concentration of extracellular fluid to 180 mM (ii) Decrease in the [Na+] concentration of extracellular fluid to 110 mM ?

(i) EASIER: increasing the extracellular [K+] will cause depolarisation and move the resting membrane potential nearer to the threshold
(ii) HARDER: decreasing the extracellular [Na+] will cause hyperpolarisation and move the resting membrane potential away from the threshold (fewer + ions entering the cell down the concentration gradient)
(NB: the resting potential is -70mV and the threshold is -50mV) IC = 10 EC = 140


(i) Interpret the graph showing the relationship between the extracellular concentrations of Na+ and K+ the membrane potential
(ii) Explain the ionic basis of an action potential with reference to the initial resting membrane potential and subsequent changes in membrane permeability

(i) Changing the EC potassium concentration has a much greater effect on the membrane potential than changing the extracellular Na concentration confirming that the membrane is more permeable to K+ than it is to Na+ (at rest)
(ii) During the action potential the membrane becomes much more permeable to Na+ than to K+ as a consequence of the opening of Na channels – the membrane potential approaches the Na+ equilibrium potential. Repolarisation occurs as a result of the closing of the Na channels and the delayed opening of K channels – both processes bring about repolarisation as the membrane potential moves closer to the to K+ equilibrium potential


Why does changing the extracellular concentration of K+ have a greater effect on the membrane potential than changing the extracellular Na+ concentration?

The membrane is more permeable to K+ than it is to Na+


Why is the graph of extracellular K+ v membrane potential (Em) not linear?

Because the relationship between the concentrations of ions, equilibrium potentials and membrane potential is not linear (LOGARITHMIC).
The deviation from linearity at low [K+]o is due to the increasing contribution of the Na+ at low values of [K+]o


At what concentration of extracellular K+ does Em = 0 mV (approximately)? Why does this concentration of extracellular K+ give an Em = 0?


The intracellular and extracellular K+ concentrations are equal (no gradients therefore no potential!)


At the peak of an action potential, when Em = 30 mV, would you expect changing the extracellular Na+ concentration to have a greater or smaller effect on Em?

GREATER EFFECT – at the peak of the action potential the membrane is more permeable to Na+ than it is to K+. Therefore changing the extracellular Na+ concentrations will have a greater effect.


Which ionic gradient is most important in the generation of the membrane potential?



What are the 4 criteria required for valid consent?

1. Patient must have CAPACITY - a person is able to understand, retain and use the information as well as communicate their decision.
2. Patient must give consent VOLUNTARILY - must be no coercion or undue pressure.
3. Patient must be INFORMED - must be informed of and understand the treatment that is going to take place
4. Consent must be CONTINUING - has the right to withdraw consent at any point


What are the three types of form consent can be?

- fertility treatment
- good practice in surgery
- conduct: seeking and complying with treatment


What are the 2 approaches to capacity?

1. Status
2. Function


What are the 4 criteria for adult capacity?

A person is able to make decisions for themselves if they are able to:
1. UNDERSTAND the information
2. RETAIN the information
3. USE OR WEIHG the information
4. COMMUNICATE their decision


What makes assessing capacity difficult? (NOTE: there's 5 points)

1. It’s not a once and for all judgement
2. Non-cooperation - they don’t want to be there and don’t want to speak to you, this does not mean that they lack capacity
3. Just because the decision is irrational or bizarre, does not mean patient lacks capacity
4. Underlying conditions may cloud your judgment (and may or may not affect patient’s capacity)
5. Communication problems


What are the ways in which decisions can be made on behalf of a patient who lacks capacity?

1. LPA (Lasting Power of Attorney)
2. Advance Directives
3. Best interests test (HCP, relatives, carers)


What are the problems with proxy decision makers? (HINT: there's 2)

1. Proxy and patient do not always agree (~68%
2. Proxy decisions are normally subject to “best interests”...not so our own decisions


What is a Gillick-competent patient?

Used to decide whether a child (16 or younger) is able to consent to his or her own medical treatment, without the need for parental permission or knowledge.
"...it is not enough that she should understand the nature of the advice which is being given: she must also have a sufficient maturity to understand what is involved."
- Respect for mature minor’s autonomy
- Q’s exist around consent, refusal and seriousness of decision


What are the rights of a capacitous patient as regards refusal of, preference for and demanding of treatment?

REFUSAL - within rights, does not have to seem rational
PREFERENCE FOR - within rights. Can inform of other treatments but must give accurate information for each one.
DEMANDING TREATMENT - NOT within a patient’s right.


What are some of the difficulties around the area of informed consent in practice? (HINT: there's 3)

How much is enough (“sufficiently” informed)?
Consent is a process (continuing) not an event. Can be withdrawn at any time.
Do patients understand what consent is all about?


Define Evidence Based Medicine.

Use the best evidence in the scientific literature to provide the best care for an individual patient


What are the 3 principles of evidence based medicine (EBM)?

1. High quality health care rests on objective and clinically relevant information
2. There is a hierarchy of evidence where some types are stronger than others
3. Scientific data alone is not a sufficient basis for making clinical decisions


What are the potential sources of bias in medical research?

Selection bias
Performance bias
Attrition bias
Detection bias
Reporting bias
Publication bias
Time-lag bias
Language bias
Funding bias
Citation bias
Developed country bias
Multiple publication bias


What is a systematic review? What is the strategy used for conducting a systematic review? Why are they viewed as the 'gold standard'?

A systematic review attempts to identify, appraise and synthesise all the empirical evidence that meets pre- specified eligibility criteria to answer a given research question.
Researchers conducting systematic reviews use explicit methods aimed at minimizing bias, in order to produce more reliable findings that can be used to inform
decision making.
Avoidance and/or the minimisation of bias


What is a meta-analysis? Explain the value of a meta-analysis.

When results of the individual studies are combined to produce an overall statistic.
Data are collected from more than one clinical trial and are combined to generate an average result.
This aims to provide a more precise estimate of the effects of an intervention and to reduce uncertainty.


Explain the importance of a confidence interval.

The point estimate (usually the mean) indicates the magnitude of the effect of the experimental intervention compared to the control intervention (Risk ratio is 0.7 of that in the control group).
The confidence interval describes the uncertainty of this estimate. It describes a range of values within which we can be reasonably sure that the true effect actually lies.
A 95% confidence interval is often interpreted as indicating a range within which we can be 95% certain that the true effect lies. This statement is a loose interpretation of the statistical meaning (but is useful as a rough guide).


What are the boundaries of the vertebral canal?

Vertebral bodies
Intervertebral discs
Posterior longitudinal ligament
Pedicles (forms the borders of intervertebral foraminae)
Intervertebral foramina
Facet (zygapophyseal) joint
Spinous processes
Ligamentum flavum


What are the contents of the vertebral canal?

Spinal cord
Spinal roots that form spinal nerves
Meninges: Pia, arachnoid and dura mater
Extra dural space and fat
Blood vessels


Where does the spinal cord begin and end? What is the name(s) given to the inferior end of the cord?

Begins at the foramen magnum of the skull as the continuation of the brain stem
In adults it ends at L1/L2
Inferior end of cord is conus medullaris which narrows as filum terminale


Between what spinal roots is the (i) cervical enlargement (ii) lumbosacral enlargement?

(i) C4 - T1 (brachial plexus)
(ii) T11 - S1 (lumbosacral plexus)


Describe and explain the development of the spinal cord.

In the embryo (8 wks), the spinal cord and vertebral canal are equivalent lengths (spinal segments = vertebrae)
In neonates, the spinal cord ends at L3 vertebra
BUT In adults, the spinal cord exists in upper 2/3 of vertebral column (foramen magnum to disc between L1/L2)
The vertebral column grows faster than spinal cord


Explain the development of the cauda equina.

The vertebral canal grows faster than the spinal cord and the lumbar nerves must travel down the vertebral canal to find their own intervertebral foramen before they exit.

The lower third of the vertebral canal contains the roots of the spinal nerves and the film terminale.

Cauda equina = horse’s tail


What is the arrangement of the meninges within the spinal cord?

DURA MATER = Outermost; thick protective layer consisting of 2 layers in the cranium
Is attached to the inner surface of the cranium. As it descends through the canal it's called the dural sac
It narrows extensively at lower border of S2 where it fuses with filum terminale at coccyx
Dura covers roots of the spinal nerves as they pass through the intervertebral foramina
ARACHNOID MATER = Delicate, avascular layer which lies deep to dura (lining dural sac); no space between the layers. It connects to pia via arachnoid trabeculae
It encloses the subarachnoid space between arachnoid and pia mater, which isontinuous with space around brain
Ends at lower border of S2
Contains CSF and blood vessels supported by spider-like fibres
Encloses the caudal equina (as lumbar cistern)
PIA MATER = A thin, vascular layer closely adhered to the surface of the spinal cord and brain.
In the vertebral canal, triangular extensions of pia (denticulate ligaments) are attached to the arachnoid mater in the dural space and suspend the cord in the space.
It ends as the film terminale attaches to the sacrum.


What is the extradural space?

A fatty matrix that runs from the foramen magnum to the sacral hiatus.
It is internal to the periosteum and contains internal vertebral venous plexus


What is the arterial supply of the spinal cord?

There are 2 sets of arteries:
- 3 longitudinal arteries that are branches of the subclavian and lie on the surface of the cord. Posterior spinal arteries (2 paired) and Anterior spinal artery (in anterior median fissure); gives off sulcal arteries
Vertebral arteries ascend in the neck via the foramen transversaria of cervical vertebrae. They give branches at the foramen magnum.
- Numerous segmental arteries that are branches of the aorta and enter the vertebral canal via intervertebral foramina. Cervical (arise from vertebral arteries). Thoracic (arise from intercostal arteries). Lumbar (arise from lumbar arteries)


What is the venous drainage of the spinal cord?

Longitudinal channels on surface of cord - no valves, blood flows sluggishly in either direction
Internal vertebral venous plexus - lies in extradural fat of epidural space
External vertebral venous plexus - drains the medullary cavity of the vertebral bodies and connects to segmental veins (e.g. lumbar and azygous veins)

Venous connections allow the metastatic spread of tumours to vertebral bodies e.g. from breast and prostate (bony metastases)


What are the structures through which the needle must pass when performing a lumbar puncture?

Performed between L3/4 or L4/5
- Skin
- Superficial fascia
- Supraspinous ligament
- Interspinous ligament
- Ligamentum flavum
- Epidural space containing extradural fat
- Dura mater
- Arachnoid mater


Evaluate adherence to health care recommendations. Using an example to explain.

Management of chronic disease represents a substantial cost to health care (e.g. CHD, diabetes, asthma).
Good treatment outcomes depends on good medical care AND on SELF-MANAGEMENT.
Self-management relies on appropriate use of medicines by individual i.e. ADHERENCE.

Using ASTHMA as an example:
Most children/young adults with asthma are treated with inhaled steroids. This is the 1st step in preventative therapy. It is largely safe and effective. Steroid inhaler = SELF MANAGEMENT treatment

BUT ... 50% of patients with chronic disease do not use their medications as recommended.
= Costly to provider and receiver (wasted resources, lack of therapeutic benefit)

Understanding WHY so many pts do not adhere to treatment is critical for health outcome.


Explain the main principles of patient treatment beliefs and how they are incorporated into the CSM.

Beliefs about prescribed medicines can be grouped under two categories:
NECESSITY - personal need for treatment
“my health depends on this medicine
“these medicines protects me from becoming worse”
“without these medicines I would be very ill”
Can involve beliefs about efficacy, but perceives necessity is not a form of efficacy belief (2 separate constructs)
- we may perceive a strong need for a treatment that we believe is only moderately effective because we know it’s the only treatment available… i.e. perceived necessity determines adherence

CONCERNS - about negative effects of treatment
- Treatments concerns can be concrete, abstract, relevant across range of disease states, cultures:
(a) Experience of unpleasant symptoms, 'side effects'
(b) Disruptive effects of medication on daily living
(c) Worries that medication could lead to long-term effects…
NB: May be specific to a particular class of medicine
“regular use of analgesic medication now will make it less effective in the future”


Apply the CSMT to general prescribing and health care interventions.

NECESSITY beliefs and illness representations:
1. Identity: Symptom experiences and expectations influence treatment necessity
- severity of symptoms
- absence of symptoms (e.g. hypertension)
2. Cause:Putative causes of illness may influence need for treatment options
- changing diet vs taking medications
3. Timeline & Consequences: Perceptions of illness duration and consequences may influence treatment necessity
- perception of illness as cyclical vs chronic impacts on adherence to preventative medication (e.g. asthma)
4. Control: Beliefs about treatments necessity beliefs correlate with beliefs how the illness will be controlled
- by treatment vs some other behavioural change

CONCERNS and illness representations

Concerns about treatment also comprise beliefs about illness representations:
- symptoms (“identity”) may stimulate concerns if they are interpreted as evidence that the medication is not working (e.g. ant-depressants)

Concerns also about necessity of treatment
- threat to self-identity


What 4 criteria does a molecule need to satisfy in order to be classed as a NT?

1. SYNTHESIS - the NT must be made in the pre-synaptic neurone (cell body or bouton)
2. STORAGE - the NT must be stored pre-synaptically in vesicles (exception is nitric oxide)
3. RELEASE - NT must be released on demand (in response to a signal/action potential)
4. INACTIVATION - NT must be inactivated


What is a receptor?

A receptor is a protein in either the plasma or inserted into the outer membrane of a cell.
The receptor binds to and is activated by a neurotransmitter, or other agonist, via the Lock and Key hypothesis.
Mostly receptors types are activated by only one neurotransmitter, but there are families of receptors sensitive to a single NT


Classify NTs by structure.

- Glutamate
- Glycine
Catecholamines & Indolamines
- norepinephrine - seratonin
- dopamine
- epinephrine
- encephalin
- endorphin
- dynorphin


Describe the function of Glutamate.

The primary excitatory NT of the CNS.
Like most amino acid NTs it acts at the level of individual neuron signalling
Action at post synapse is predominantly by opening cation (eg Na+) channels (AMPA & Kainate receptors as well as NMDA which are also permeable to calcium ions).
Inactivation is by re-uptake and is recycled to either glutamate or GABA.
Distribution is widespread in the CNS.
- Neurons within or spanning hemispheres (intra and interhemispheric connections)
- Neurons descending to the brainstem (corticobulbar tracts) or spinal cord (corticospinal tracts)


What is glutamate involved in? What does excessive glutamatergic stimulation result in?

Memory, learning and cell death.
Excessive glutamatergic stimulation of NMDA receptors causes a large influx of Ca ions
Through a variety of processes this can result in cell death known as excitotoxicity


What is synaptic plasticity?

The process by which synapses are strengthened or weakened by feedback mechanisms, and is the basic process for storing long and short term memories.


Explain how Glutamate is connected to (i) Migraines (ii) Epilepsy.

(i) Proposed that the aura is caused by a depression in neural activity caused by massive transient depolarisation through the visual cortex which expands at 3mm/min and is induced and sustained by a massive glutamate efflux.
- Other predisposing factors include elevated K+ ions, changes in external calcium levels, loss of inhibition mechanisms
(ii) Excess excitation can feedback on itself to cause uncontrolled waves of excitation over expanding areas in the brain due to lack of inhibition which normally regulates this.
- These begin as partial complex seizures (partial - not the whole brain, and complex - due to an alteration of consciousness)
- If the waves of depolarisation become more uncontrolled, the patient experiences Grad Mal (french - big bad) seizures which involve the whole brain
- Seizure are treated with benzodiazepines, to increase the action of GABA (inhibitory), and drugs like phenytoin, which increase the inactivation (refractory) period between firings in voltage activated Na+ channels. This is a two pronged attack.


Describe GABA; where is it found? What is its function? What diseases can it cause? Their agonists can be used to treat what? etc etc.

GABA is the principle inhibitory neurotransmitter of the CNS and is made from glutamate
- Found predominantly in the interneurones of the CNS but also neurones of the striatum and globus pallidus, where it modulates descending motor information
- GABA acts at ligand gated chloride channels (not K+ channels) and is inactivated by presynaptic re-uptake

- GABAergic dysfunction as in Huntington’s where GABAergic neurones degenerate, can lead to uncontrolled movement. There is a lack of inhibition needed to make smooth controlled movements.
Treatment: GABA mimetic (agonist)

Alcoholism causes a change in GABA transmission such that withdrawal results in convulsive movements and seizures
Treatment: Benzodiazepines (Diazepam, temazepam) and phenytoin

GABA agonists are sometimes used in the treatment of anxiety or sleeplessness as well as epilepsy and as anaesthetics (e.g. propofol)


Describe Glycine; where is it found? What is its function? What diseases can it cause? etc etc.

Glycine is the second most common inhibitory neurotransmitter of the CNS and is synthesised from serine.
- It's the predominant inhibitory neurotransmitter in the interneurones of the spinal cord and brainstem but is also present in the brain.

Glycinergic dysfunction is thought to be the cause of inherited mammalian myoclonus (uncontrolled movement of the arm). Most are benign, others are late symptoms of more serious diseases.

Tetanus is caused by a toxin from the bacteria Clostridium tetani which inhibits the release of glycine resulting in a shift of the excitation - inhibition balance, leading to an imbalance.
- Mild effects are restricted to muscles innervated by the cranial nerves.
- More serious effects include loss of inhibition on the cerebra, leading to epileptiform fits
TREATMENT = injection of antitoxin which binds the toxin and benzodiazepines which boost GABA pathways.


Describe norepinephrine (noradrenalin); What is it? What's it used for? etc etc.

Sympathetic NT, inhibition used in treatment of Parkinson’s, ADHD, agonists are cocaine and tricyclic antidepressants.

Projects to major centres of the brain.
Adrenoceptors = G-protein linked metabotropic receptors.
In the CNS the brainstem uses norepinephrine to influence:
- Sleep, wakefulness and attention through the reticulum and feeding behaviour via the hypothalamus.

The part of the brainstem whose neurones project norepinephrinergic axons is known as the Locus Coeruleus (top of the pons)


Describe dopamine; What is it? What's it used for? etc etc.

NT and neuromodulator involved with pleasure, addiction and movement.

Dopaminergic axons project to majority of CNS (excluding cerebellum) and act at G-protein linked metabotropic receptors.
Found principally in 3 diff CNS's and is involved in:
1. The control of movement
2. Certain symptoms of psychiatric disease
3. Regulation of the release of certain hormones
Control of hormone release at the anterior pituitary is exerted by dopamine which is released into the portal vessels by hypothalamic neurones.
Other effects include:
- Parkinson’s sufferers who experience tremors, muscle rigidity and bradykinesia (slowness of movement) or akinesia (loss of control of voluntary movement) have depleted dopamine in the motor co-ordination circuits
- Schizophrenia can be causes by an over production of dopamine in the mesolimbic system, treatment is with antipsychotics
- Addiction to drugs of abuse, exercise and certain behaviours such as sexual activity. Works through the pleasure centres of the CNS located in the mesolimbic dopamine system


Describe epinephrine (adrenaline).

Peripheral hormone from adrenal medulla, pharmacological target for cardiac and circulatory problems.


Describe the indolamine, Serotonin. Where do their neurones originate? What type of NT is it? What does it modulate? What is its function(s)?

Serotonin neurones originate principally in the Raphe nuclei in the brain stem, and project to the majority of the brain and brain stem
- It has a large family of both excitatory and inhibitory receptors in the CNS and PNS
- Modulates a range of NTs such as glutamate, GABA and dopamine
- Functions associated with sleep, anxiety, depression and mood swings

Serotonin dysfunction (reduction) is also associated with:
- Depression and obsessive compulsive disorder, both of which can be treated with fluoxetine (Prozac a 5-HT re-uptake inhibitor)

Serotonergic systems are exploited by drug abusers to give an altered perception of reality:
1. Receptor agonists include LSD, psilocybin and mescaline
2. Inhibiting mono amine catabolism generally with MAOI’s or inhibiting serotonin re-uptake also increases 5-HT levels


What are 2 psychostimulants?

Amphetamines and Ecstasy


Describe Endorphins and Encephalins

Are associated with the perception of pain
- They act at opiate receptors in the brain and spinal cord where they are the endogenous ligand

Taking opiates such as morphine, codeine, pethidine, methadone and diamorphine (heroin) leads down regulation of opiate receptors throughout the CNS (reduces pain centrally and peripherally)
- This causes opioid tolerance and increased intake
- Because there are opioid receptors in the limbic system (and the periaqueductal grey), opiates affect emotional perception as well as pain

Emotional element to withdrawal avoidance

Withdrawing heroin addicts may be given nalaxone (an opiate receptor agonist) to reduce symptoms


Describe the ester, acetylcholine.

Principal peripheral excitatory neurotransmitter, found in both the CNS and PNS.
ACh neurones project to:
- The hippocampus and Cortex which are both essential for the formation of new memories and learning
- ACh dysfunction (reduction) is associated with Alzheimer’s disease
- Drugs acting on ACh R’s include nicotine (drug abuse), muscarine (agonist), atropine (antagonist) and Tropicamide (antagonist to dilate the pupils during surgery)

Anticholinesterases prevent breakdown of ACh, include insecticides (DDT), nerve gasses (Sarin) and Alzheimer’s treatments such as Donepezil (aricept).
- This increases ACh levels in the synapse.


What is Korsakoff’s psychosis? Explain this.

The diet of an alcoholic often leads to a thiamine deficiency causing damage to the thalamus and the mammillary bodies

Symptoms = amnesia, confabulation, lack of insight and apathy

These cells are cholinergic and partial recovery can sometimes be achieved by using anticholinesterases


Why is access to the vertebral canal safest in the lumbar region?

The spinal cord ends at L1/L2 and the subarachnoid space extends to S2
Therefore the cauda equina unlikely to be damaged


When should a lumbar puncture NOT be performed?

When a pt has increased intercranial pressure


Define (i) dermatome (ii) myotome.

(i) an area of skin that a single nerve innervates
(ii) the group of muscles that a single spinal nerve root innervates


How does shingles come about?

Shingles is caused by Varicella zoster virus.

After infection with the virus (chicken pox) the virus lies dormant in a dorsal root ganglion.
The virus can be reactivated in later life causing Shingles.

The rash develops in the skin supplied by the spinal nerve affected i.e. within a dermatome


Each segment of the spinal cord gives rise to a pair of spinal nerves that consist of what 3 things?

1. Axons of MOTOR neurons that innervate a group of muscles arising from the same somite (they share a function) (myotome)

2. Axons of SENSORY neurons that innervate a defined area of skin (dermatome)

3. Axons of SYMPATHETIC neurons to structures in the body wall that control body temperature (blood vessels, sweat glands etc.)


Dorsal rami of thoracic spinal nerves are mixed nerves and will carry what 3 things?

1. Motor neurones to erector spinae Muscles (back muscles!)
2. Sensory neurones from the skin of the back(!) and from vertebral joints
3. Sympathetic neurones to blood vessels
and sweat glands of the skin


Ventral rami of thoracic spinal nerves are mixed nerves and will carry what 3 things?

1. Motor neurones to intercostal muscles
2. Sensory neurones from thoracic skin and pleura and vertebral joints
3. Sympathetic neurones to blood vessels and sweat glands of the skin


Define (i) reflex (ii) reflex arc (iii) spinal reflex.

(i) rapid, involuntary motor response to a stimulus
(ii) receptor, sensory neuron, integration centre, motor
neuron, and effector
(iii) somatic spinal reflexes provides information on
integrity of the reflex pathway and degree of excitability of the SC


What does nerve compression cause?

muscle weakness
loss of sensation and reflexes


What can nerve irritation cause?

Pins and needles (paraesthesiae)


What is pain?

an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage


What is acute pain.

Intense, but time limited
Is as a result of tissue damage or disease
Typically disappears over time as injury heals


What is chronic pain? What are the 3 sub categories it can be divided into? Describe them.

Often begins as acute pain BUT does not dissipate after a min. 6 months (e.g. lower-back pain, headache, pain associated with arthritis, cancer).
High anxiety, feelings of hopelessness due to lack of medical treatment success.
Interferes with daily life.
Divided into 3 sub-categories:
- caused by benign or harmless condition
- repeated, intense episodes separated by period without pain
- benign but persistent pain
- varying levels of intensity, but never disappears
- pain often originates from a malignant condition
- continuing pain and discomfort
- pain worsens over time, as underlying condition worsens


What are the 3 main theories of pain?

Specificity theory
Pattern theory
Gate-control theory


What does (i) specificity theory (ii) pattern theory propose?

(i) Separate sensory system for perceiving pain.
Specific sensory pain receptors for detecting pain stimuli.
Specific peripheral nerves and pathway to the brain.
Specific area within the brain for processing pain signals.
(ii) No separate system for perceiving pain.
Pain results from the pattern or type of stimulation received by the nerve endings.
Intensity of the stimulation is the key determination of pain.
Strong and mild stimuli of the same sense modality produce different patterns of neural activity.
- > damage > pain


What are the limitations of the specificity and pattern theories?

ST: incorrect - there are no specific receptors cells in body that transmit only information about pain.
PT: requires that stimuli triggering pain must be intense
Pain can be experienced without tissue damage (e.g. phantom-limb pain).
Tissue damage can exist without pain (e.g. athletes)
Both fail to account for the importance of psychology in the perception of pain.


What is the Gate-control theory? What 3 things is it influenced by?

Nerve endings in damaged area(s) transmit impulses to the spinal cord.
A “gate” exist in spinal cord - “neural gate”:
- OPEN to let the pain signal through
- CLOSED to reduce the pain experience
Gating mechanism modulates incoming pain signals before they reach the brain.
Includes the role of psychological factors in the experience of pain.

Gate control is influenced by:
1. Amount of activity in pain fibres (A-delta & C)
- more activity —> gate opens —> more pain
- Aδ: pricking/stabbing (fast impulse transmission)
- C: burning/aching (slow impulse transmission)
2. Amount of activity in other peripheral fibres (A-beta):
- harmless stimuli or mild irritation (touching, rubbing)
- closes the gate —> less pain
3. Messages descending from the brain - effects of anxiety, excitement etc... open or close gate


What 2 factors does the gate control theory consist of? What 2 things does it explain? What does it describe the individual as having?

Psychological factors AND physiological factors.
Explains why the same event can be interpreted by different people as more or less painful.
Explains why sometimes pain is not experienced immediately.
Describes the individual as having some control over the experience of pain.


What are the 3 ways that pain is assessed?

1. Physiological
2. Self-report
3. Behavioural

Using of 2 or more of above techniques is advisable


How are physiological measures used to assess pain?

Assume pain perception is associated with specific physiological responses.
increase in heart rate, BP, respiration, muscle tension…
Relationship between physiological responses and experience of pain not consistent.
Limited use.


How are self report measures used to assess pain?

Patients asked to describe their pain
where, what, when…
Questions often incorporated within a clinical interview (for chronic pain patients)
- Useful for treating chronic pain patients
- Pt, family member, co-workers
Focus on:
- history of pain problem
- pts emotional adjustment and lifestyle before pain began
- impact on pts current lifestyle
- social context of pain episodes
- factors that trigger pain
- how pt copes with pain
- Direct, simple, quick, widely used.
- Useful for measuring how strong the pain is (intensity).
- Repeated ratings
E.g. visual analogue scale, box scale, verbal rating scale
Nature of pain is multi-dimensional (3 dimensions)
- affective: (emotional-motivational) “terrifying”
- sensory: “scalding”
- evaluative: “unbearable”
The McGill Pain Questionnaire (MPQ)


What are the limitations to self report measures? (NB: there's 3 points)

1. Often require fairly high levels of verbal skills.
2. Less useful for children; not fluent in english.
3. Misrepresentation of pain can occur:
- exaggeration
- downplay experience of pain


How is behavioural assessment used to assess pain?

Observing behaviour:
- physical symptoms (limping…)
- verbal expressions (sighing…)
- facial expressions (grimacing, frowning…)
Procedures for assessing pain in 2 types of situations:
- everyday activities
- structured clinical sessions
Useful, but again open to misrepresentation.


What are the (i) physical and (ii) psychological methods of pain management? (HINT: there's 4 physical and 5 psychological)

(i) 1. medical treatments (analgesic drugs)
2. surgical
3. physical stimulation therapies
4. physical therapy / exercise
(ii) 1. biofeedback
2. relaxation and distraction
3. cognitive methods
4. behaviour therapy (operant approach)
5. hypnosis


Explain the 5/6 psychological methods of pain management.

1. BIOFEEDBACK: Monitor and change selected physiological functions (heart rate, muscle activity).
Pts asked to engage in different thoughts/ behaviours to influence physiological response.
Over time, pt learns how to selectively “let go” of tension (e.g. in muscle) by change in behaviour.
Useful for headache, chronic back pain (but drawbacks).
2. RELAXATION: Systematic and methodical approach to re-learning deep muscle relaxation.
Relaxation is a skill that has to be learned (or re-learned).
3. DISTRACTION: Focus taken away from the pain.
Imaginative distraction/guided imagery.
Useful for chronic pain pts.
Effective in reducing a variety of types of pain:
- chemotherapy, migraine headaches, dental procedures, low-back pain, medical procedures (injections, lumbar punctures...)
4. COGNITIVE METHODS: Understanding how thoughts and feelings influence the experience of pain.
Helps people change perceptions of, reactions to, pain.
Information, increased perceived control over pain (e.g. childbirth programs).
Cognitive re-definition - re-label the pain (e.g. childbirth).
Effective in decreased variety types pain (headache, back-pain).
5. BEHAVIOUR THERAPY (operant conditioning): Changing pts pain behaviour.
Eliminate the ‘perks’ of the pain.
Reinforcement for appropriate positive behaviour (activity).
Ignore negative behaviours (complaints of pain).
Enhance social reinforcement.
Aim to decrease pain and disability, reduce reliance on medication.
Effective in reducing a variety of types of chronic pain.
Relieves pain only in individuals who can successfully undergo deeply hypnosis.
Provides a high degree of analgesia (minority of patients).
Cognitive and behavioural techniques are generally more effective.


Why is confidentiality important in medicine? (HINT: there's 4 points/reasons)

1. RESPECT FOR PT AUTONOMY - the pt should have control over information about their own life.
2. IMPLIED PROMISE - idea that confidentiality is assumed between dr and pt.
3. VIRTUE ETHICS - trusting that a dr is practicing with a good ethical background.
4. CONSEQUENTIALISM - consequences associated with breaking/maintaining confidentiality.


What are the circumstances under which confidential information can be disclosed under common law & by statutory requirement? Explain the justifications for doing so in each case. (HINT: there's 3 circumstances)

1. With the patient’s consent (explicit)
2. Unable to seek patients consent but in the patient’s best interests
3. In the public interest


What are the 4 criteria that define "the public interest" in terms of justifying disclosure of confidential information?

1. Risk must be REAL and SERIOUS
2. Risk must be of PHYSICAL HARM
3. IDENTIFIABLE individual(s)
4. Disclosure must only be on NEED-TO-KNOW basis


What is the role of GMC guidance with regards to confidentiality, in particular as it relates to the "duty to warn" (or otherwise) in HIV infection & psychiatry? (HINT: there's 5 points)

1. Public interest
2. Risk of harm to patients or others
3. Driving against medical advice
4. Crime
5. HIV/AIDS - GP & Partner


What are some of the difficulties that arise around genetics & confidentiality (genetic testing & genetic privacy)? (HINT: there's 2 points)

1. An individual’s test result can reveal information about a family member i.e. Huntington’s chorea; BRCA1
2. Genetic privacy: employers or insurers?