TABLE of CONTENTS - StudentVIP

TABLE of CONTENTS

1. Metabolic Syndrome ………..……… 1

2. Stem Cells and Tissue Engineering ……….…..…… 19

3. Respiratory Disease ……… 31

4. Mental Health ………..……….……… 42

5. *** Possible Metabolic Syndrome questions (4) ……….…. 52

6. *** Possible Respiratory disease questions (14) ……….………….……. 53

7. *** Possible Mental health questions (20) ……….……….…. 57

METABOLIC SYNDROME

1&2- Metabolic syndrome as a social and political sickness; a cure?

Metabolic syndrome

- Cluster of risk factors for CVD and T2D which occur together more often than by chance - Risk factors

o Excess abdominal weight (elevated waist circumference) = population/country/ethnicity specific

o Lipid abnormalities/dyslipidaemia = high TG’s, low HDL-C, high LDL-C o Hypertension = elevated BP (over 140/90mmHg)

o Elevated glucose levels = either fasting blood sugar or post-prandial (over 5mmol/L)

Definitions

- Incidence = rate at which new cases occur in population during a specified period

- Prevalence = proportion of a population that are cases at a point in time (percentage); in stable conditions

MetS in developing and developed countries

- Developed countries = MetS marker of poverty

o E.g. in Melbourne, more people overweight in poor suburbs (when thinness used to mark poverty) - Developing countries = MetS is a condition of the affluent

o More adults obese in countries with a more unequal society

o E.g. America- high income inequality and highest percentage of obesity (bad social infrastructure) compared to Japan- rich country but income inequality is low (lowest obesity)

- But obesity has been rising factor compared to inequality → perhaps not enough explain the speed in rise

Epigenetics of obesity

- Biology is shaped by intergenerational epigenetic effects

- Epigenetics = environment changes expression of genes→characteristics passed on to next generation - We are descendants of people who lived on low calories; ethnicity indicates centuries of marginal diet and

famine for multiple people e.g. Chinese, South Asia, West Africa

o E.g. Irish famine middle of 19^th century, survivors went to America, two generations later showed effects of being different compared to poor Italians. People with Irish ancestry had higher death rates for Organic Heart Disease for age bracket (45-65 years) compared to Italians or US whites who were in America and eating well.

- Insufficient explanation→look at environment

Environment- rising inequality

- Obesity increase parallels increase in income inequality

- America – wages flat lined despite increase in cost of living→buy cheaper foods to save money - Australia – wages flat lined in areas that are not unionised (public sector protected)

Environment- social

- Overweight children expend less energy (spend more time indoors) NOT the other way around

- Yet, many overweight people do labour work, burn lots of calories→BUT still putting on weight→FOOD

Neuropeptide Y (NPY)

- 36 AA peptide, highly conserved

- Member of pancreatic polypeptide family (e.g. Peptide YY→reduce appetite; opposite to NPY) - Various actions in CNS & periphery

- Stimulates feeding in satiated rodents (full rodents→administer NPY→more eating) - Chronic administration = obesity

- Hypothalamic action

- Y1, Y2, Y5 receptors implicated - Reduces energy expenditure

- Level changes with feeding status; level regulated by leptin

Leptin

- Secreted predominantly from fat cells - Plasma levels proportional to BMI and fat

o Leptin resistance = high leptin levels downplays the signalling

o Leptin is transported into brain via transporter (saturable process i.e. certain amount of leptin that can get into brain)→produce lots of leptin (due to excess body fat)→system is not going to do anything to turn off meal intake→OBESITY

o Don’t know if this causes obesity or obesity is causing this - Crosses BBB via saturable process

- Leptin receptors located in hypothalamus - Inhibits food intake via CNS mechanism - Obesity = leptin resistance, leptin deficiency

o Only relevant in a very small number of patients = leptin defects causes obesity (Ob mouse) - Regulates energy balance

o WAT→release leptin→binds to leptin receptors in hypothalamus→alter synthesis and release of neuropeptides (which increase food intake again)

α-melanocyte stimulating hormone (α-MSH) - Endogenous agonist- 13 AA peptide - Released in PVN (paraventricular nucleus)

- Inhibits food intake predominantly via MC4R (α-MSH constantly released, act as agonist at MC4R) o Tonic inhibition of food intake

- Increases energy expenditure

- Level regulated by feeding status & leptin - Mutation in POMC or MC4R genes = obesity

o MC4R - 4% of human obesity (not a lot of gene mutations that result in morbid obesity but these receptors account for most of it)

- MC4R- important for homeostatic adaptations to changes in diet composition o Important in maintaining body weight

o Under unlimited access to higher dietary fat food;

o KO mice = increased body weight much more than WT mice – they weren’t able to modify their response to changes in dietary composition→kept eating→lacked adaptive response/MC4R

→process wasn’t there to tell them enough of eating and turn off meal intake

▪ Also didn’t increase their energy expenditure in response to food intake o WT mice = small increase in body weight

▪ Also used more energy to get rid of body weight

STEM CELLS & TISSUE ENGINEERING

9- An introduction to stem cells

Stem cells

- Ability to self-renew for indefinite periods

- Ability to give rise to many of the differentiated cell types that make up an organism - Other characteristics

o May give rise to transit amplifying cells (TACs) = committed to differentiation and reproduce rapidly o Often lacking in specialised organelles, show high nucleus/cytoplasm ratio

o Long-lived (express telomerase –protect ends of chromosomes, maintain integrity of DNA) o May be restricted spatially to specific zones or niches

o NOT ALWAYS- slowly dividing, low numbers, identifiable by expression of genes

- Determine integrity of stem cell – repopulate tissue, lineage tracing, descendants are functional

Types of stem cells

- Totipotent = give rise to a completely new individual (embryo) - Pluripotent = give rise to all types of adult tissue cells (ICM)

- Multipotent = give rise to several types of mature cells in an organ (HSCs) - Unipotent = give rise to a single cell type (spermatogonia, intestinal crypt cells)

Adult tissue stem cells- tissue repair & homeostasis

- Cell turnover e.g. in intestine and blood system; rate of turnover is different

o Blood system – gold standard for adult SCs → one HSC can repopulate entire system, proven by transplantation after BM ablation

o Intestine – SCs in crypt → small number, rapidly dividing at base of villi, supported by Paneth cells, form TACs, out of crypt (differentiate), eventually lost at top of villus

- Discovery of novel stem cell populations in tissues formerly thought to be static in adult life e.g. brain – in Subventricular zone and hippocampus

o E.g. hippocampal neurogenesis → role in learning and memory - Facultative stem cells = conditionally renewing tissues

o Liver – regenerate by proliferation of hepatocytes or from bipotential SCs in biliary tree (injury) - Plasticity = relaxation of restrictions (powerful molecular restraints) in an altered environment - low

frequency

o Restrictions on the developmental potential of adult SCs is required for proper tissue organisation and response to demands of growth/repair

o As adult SCs move out of the niche → expression of BMP and suppression of Wnt (changing growth factor environment in response to signal) → no longer behave as SCs → become lineage restricted - Applications of adult SCs

o Understanding turnover assist in improving repair, mobilising SCs may allow for their harvest and transplantation (HSCs), isolating SCs to model disease (organoids) and screen for treatments

Mesenchymal stem cells

- Thought to have stromal potential and modulate immune system

- Has been improved transplant outcome; cell therapy NOT stem cell therapy, do not last long after delivery

14- Tissue engineering- novel biomaterials

Tissue engineering (TE)

- FUNCTIONAL SUBSTITUTES = for damaged tissues (disease, genetic defects or trauma)

- Alleviating donor tissue shortages, superior results to medical treatments, customised implants, new treatments where none currently suffice (e.g. spinal cord injury- currently untreatable)

- Hurdles- technical, commercial, regulatory

- Tissue components to take into account → cells, ECM micro-environment, blood supply - Traditional TE approach

o Fabrication techniques (put growth factors etc, culture and insert back in patient) → works for tiny things but is an over simplification (won’t work in human body)

o Neglected the blood supply aspect → tissues need oxygen, nutrients; otherwise won’t survive - Strategies depend on tissue type

o Design criteria based on specific tissue properties

o In vitro construct development for avascular/small 2D tissues (e.g. cartilage – doesn’t require blood vessels throughout) BUT 3D human scale tissues need blood supply early

o In vivo bioreactors = allow construct development concurrently with vascularisation

▪ Blood vessel loop connected to patient’s blood supply → send out factors once hypoxic → triggers sprouting from blood vessels → fill the healthy tissue (vascularisation)

- Key challenges

o Blood supply for 3D vascularised tissues and infection control o Suitable biomimetic matrix signals that can deliver biological signals - Need tailored design of systems for TE (tailored to tissue targets)

Roles and significance of biomaterials in TE

- Scaffolds, surface and microenvironments for cell growth

- Ideally mimic native tissue ECM – (won’t be able to recreate; complex and high cost) - Provide space and biochemical environment to allow new tissue to grow

- The mechanical forces, chemical/biochemical interactions changes how cells/tissues behave/function

Criteria for biomaterials in TE

- Biocompatibility (don’t want to damage or have adverse host response)

- Mechanical properties for target tissue and implantation site (e.g. fat tissue, look for materials that are soft) - Biodegradability profile (time, strength and by-products)

- Suitable in vivo responses (e.g. inflammation, foreign body reaction- how to predict?) - Ability to be fabricated into desired structures (3D printing)

- Cost-effective, available, regulatory approval (regular and reliable supply – if history of usage, then safe) - Ability to be sterilised safely (ECM- don’t like to be exposed to sterilisation methods)

- Adequate stability and shelf-life (make and store in hospital and use at times of need)

- Promote desired cellular responses (e.g. proliferation, differentiation, gene expression – encourage tissue growth and healing of wounds involved)

Limitations and challenges of using biomaterials in TE

- Foreign body reaction, acid release (e.g. lactic acid), toxicity, supply, cost and reproducibility (naturally derived materials hard to reproduce)

- Lack of knowledge of design criteria (don’t really know what mechanical properties of tissue we want) - Lack of predictability of in vivo behaviour and responses (animal testing – but ethical and cost reasons)

RESPIRATORY DISEASE

16- Obstructive airways disease

The Respiratory System

- Structure – nose, pharynx, larynx, trachea, bronchi, lungs ; Function – brings oxygen in, expel carbon dioxide - Effective filter for air breathed in (nose) → air reaches back of pharynx and humidified to 35 degrees,

particles filtered → goes to larynx (same thing happens)

- Upper respiratory system very exposed/vulnerable to environmental influences

- Inspiration = diaphragm comes down, chest wall goes out as intercostal muscles go out = active process - Expiration = elastic recoil of lungs = passive process

The Bronchial System

- 22 divisions down to terminal bronchiole, leads to alveoli - Breathe in = negative pressure, breathe out = positive pressure

- 2 causes of obstructive airway disease (OAD) = bronchiole tubes blocked, collapse of distal airways

Lung function & ageing

- Spirometry = lung function test for FEV1.0, FVC and PEFR

- Normal FEV1.0 = above 70% ; reduced FEV1.0 = hallmark of OAD (pushing hard but causing terminal airway collapse) & FEV1.0/FVC ratio is reduced below 80%

- Age of maximum lung capacity – 20-25 years old ; with ageing, lose lung function (global phenomena) - Smoke and asthma accelerates decline in for FEV1.0

- Chest wall – stiffness of joints, decreased strength of respiratory muscles to drive good inspiration - Lung – decrease in elastic fibres & recoil, reduction in alveolar number, bronchi nor surfactant affected - Dynamic airway closure – progressive obstruction, terminal bronchioles floppy and closing on expiration

Asthma

- Prevalence – 1 in 10 Australians, 400 people die per year (death rate has fallen in last 90 years but higher than less better countries e.g. France, Germany, Japan), majority women past puberty and young men - Physiological – variable airflow obstruction; usually reversible with β2 agonist to relax smooth muscles and

bronchi (bronchodilator)

- Inflammation – inflammatory nature (basement membrane thick- HALLMARK) leads to airway remodelling (lots of eosinophils)

- Hyperesponsiveness – increased sensitivity of airways to altered environment (test by giving agonist) - Allergic rhinitis – 3x increase in chance of having asthma

- Non-eosinophilic asthma = normal eosinophil count (<1.9%), harder to treat

o Normal neutrophil count (<61%) = paucigranulocytic; raised neutrophil (>62%) = neutrophilic asthma - Eosinophilic asthma = raised eosinophil count (>2.0%), easier to treat (anti-inflammatory treatment works)

o Raised neutrophil count = mixed granulocytic asthma 21^st November 2016

- Severe storm, grass pollen flew across, temperature high, humidity rose, wind speed changed, barometric pressure dropped → excess respiratory-related ED presentations (3365), salbutamol ran out, 10 people died - Age groups presented – 37 years (men, women) day of storm and 24 hrs later (delayed inflammatory

response)

- RMH patients – all had hay fever, most knew they had asthma, risk factors for presentation – rye grass

20- A population health perspective in responding to tobacco-related illness

Impact of tobacco use

- Worldwide > 5million die annually Projected to kill 1 billion people in 21^st century - Risk factor for 6 of the 8 leading causes of death (IHD, CVD, LRTI, COPD etc)

- Massive uptake in 1950s – advertising, production methods, cost/availability, culture, addictive power - Tobacco control – has saved 500,000 Australians, 8 million Americans (treaty to demand and limit supply) o

Smoking prevalence has decreased since 1990s, particular intervention work

Tobacco control strategies

- Raise real tobacco price or excise – make something unaffordable

o As price increases, sales decrease → works more effectively for poor people

o Taxing has increased in Australia – pro-poor policy (decrease inequality in smoking rates) - Banning advertising and marketing of cigarettes – plain packaging (benefit children)

o Reduce appeal of tobacco product o Increase effectiveness of health warnings

o Reduce ability of retail packaging of tobacco products to mislead consumers about the harms - Mass media campaigns – warn people

o Highly cost effective

o Direct effects on viewers – smoking uptake in youth, quitting in adults o Indirect effects – increasing discussion & setting agenda for policy change - Smoke free policies – protect the people not smoking

o Rely on justification that it is injurious to someone else

o Needs to be fully rolled out to beaches, parks, outdoor eating areas – argument how does it really affect other people

Tobacco endgame

- Reduce consumption and availability of tobacco to minimal levels (2-5%) whereby smoking is denormalised - Remove all opportunities for advertising – plain packaging, E-cigarettes

Possible solutions to push towards endgame - Supply/market

o Smoker license, raising the age limit progressively, smoke free generation (ban if born after 2000) o Massive reduction in retail availability – how many can be purchased?

- Product modification

o Mandated reduced/denicotinised cigarettes → reduce palatability/appeal (remove additives) - Tobacco company liability – make them responsible for it (compensation, criminal/civil liability)

Barriers to progress

- Inherent attraction of smoking

- Political addition to tobacco – bureaucratic and legislative inertia & conservatism - Philosophical objection – individual liberty concerns

- Powerful industry – lobby, political muscle, buy loyalty, dispute science, lawsuits - THEREFORE, WE NEED TO…

o Bring society along, focus on children (sporting events), find champions (families who have been destroyed by smoking), beware of industry engagement

o Find common ground in this multi-stakeholder engagement

MENTAL HEALTH

23- Introduction including social determinants of mental health and mental disorders

Mental health

- Definition = state of well-being in which every individual realises his or her own potential, can cope with the normal stresses of life, can work productively and fruitfully, and is able to make a contribution to his or her community

- Absence of mental disorder does not necessarily mean presence of good mental health = not opposites - Mental illness = e.g. depression and anxiety (common or high prevalence mental disorders)

o Schizophrenia and bipolar disorder (severe mental illness and low prevalence disorders)

- People with mental disorder can achieve good levels of wellbeing within constraints of distressing symptoms

Social determinants of mental health

- Population subgroups that have greater exposure and vulnerability to unfavourable social circumstances e.g.

gender, poverty/deprivation, lack of education, disease, cultural influences, discrimination

- Social inequalities = greater the inequality, the higher the inequality in risk of mental disorder (middle also) - Mental health conditions emerge later in life but originate in early life (traced back)

- Actions to prevent mental disorders and promote mental health – at all stages of development

o Improve conditions of everyday life (before birth, into early childhood, adolescence, family building, working ages and older age)

- Social adversity = risk of poor mental health; having mental health condition risk of poor social situations - Evidence = policy making at all levels of governance/sectors → positive difference to mental health outcome

Mental disorders

- Anxiety, depression, schizophrenia, alcohol & drug dependency

- Common mental disorders can result from stressful experience, but also in absence of such experiences - Sub-threshold mental disorders – poor mental health, does not reach threshold to diagnose as mental disorder - Impact – societal construction of what is abnormal behaviour and who has disorder

- A disorder is NOT an expected, culturally accepted response to particular events (e.g. grieving) or socially deviant behaviour (political, religious, sexual) or conflict between individual and society (homosexuality) - Disorder – when your behaviour is so inconsistent with your goals e.g. as biomed kid – getting close to disorder

Diagnoses

- Why? – descriptive value, consider treatments, predictive value, public health planning & monitoring, information retrieval (from literature), aids communications, think about whole syndrome (+/- symptoms) - No definitive biological test for any psychiatric disorder; many disorders overlap

- DSM-5 = diagnostic and statistical manual of mental disorders

o Classification of mental disorders in adult and children for worldwide use, divided in categories of disorders e.g. neurodevelopment, anxiety, dissociative disorder etc – diagnose with caution

- Clinical diagnosis not enough – need to consider culture, knowledge of contexts, course of disorder (change) o Behaviour normal in one culture, considered abnormal in another

o Some disorders culturally-specific e.g. eating disorders in Western countries

o Variation in human behaviour – socially and environmentally determined, gene-environment match - Consequence of diagnosis – stigma, unwanted label, reduced to their diagnosis (e.g. schizophrenic)

o Individuals also – take their strengths, have strategies to deal with issues

possible respiratory disease questions- module 3 (14 questions)

what are the causes of COPD and the changes in lung structure which contribute to emphysema? (6 marks) - causes

o

smoking, air pollution, occupational dust and fumes, chronic asthma, impaired lung growth (from small

age), α-1 antiprotease deficiency

- emphysema

o

elastin breaks down progressively (weak, shear/tear)→airway collapses more easily leading to air/gas being trapped = causes lungs to get bigger→makes it difficult to expire

o

there is also microcirculation death (no VEGF/IL-6/gp130)- no blood circulation in small vessels

o

not sure whether some patients have autoimmunity to soft tissue damage

list the main drugs used to treat COPD and explain the mechanism of action- making reference to disease induced pathology (4 marks)

- bronchodilators

o

relax smooth muscle surrounding ducts→help air get released, open up the airways (useful to reduce gas trapping & lung volume ; features of emphysema)

o

help FEV1 get closer to FVC

o

alleviate bronchial obstruction & airflow limitation, reduce hyperinflation, improve emptying of lung &

exercise performance

o

LABA- long acting β agonist= formoterol (rapid onset), salmeterol (slow onset)

o

LAMA- long acting muscarinic antagonist= ipratropium, tiotropium (blocks cholinergic receptors which contract smooth muscle)

•

better to use anticholinergics e.g. LAMA in COPD more than asthma since it has two sources of ACh release (from cholinergic nerves & intrinsic production due to nature of inflammation)

- steroids

o

overall work poorly- suppress inflammation/immune system→can worsen lung function, get infections

o

work best in patients with eosinophilic inflammation (lots of eosinophils)

o

inhaled glucocorticosteroids= beclomethasone, budesonide

o

can add to LAMA/LABA→triple therapy

- xanthines, PDE4 blockers

o

xanthines- prevent wheezing & shortness of breath = theophylline

o

PDE4 blockers- bronchodilator = roflumilast

o

poor efficacy - vaccination

o attenuated responses; don’t really work

explain the pathophysiology of cigarettes/tobacco on the respiratory system (4 marks)

- 1. irritates epithelium→activates macrophages→oxidative stress; if chronic →inflammatory mediators are recruited (IL-8, IP-10)

- 2. amplify process

→

further oxidants, proteases, growth factors (change structure of lung), endothelium &

epithelium die

- 3. persistence leads to→mucous gland hypertrophy, fibrosis & septal detachment, emphysema

what public health measures are in place to combat smoking and what are some barriers to them? (6 marks)

- public health

o

raise tobacco price or excise/tax- sales will decrease, pro-poor policy, decrease inequality in smoking rates

o

banning advertising/marketing of cigs- plain packaging, reduce appeal, health warnings

o

mass media campaigns- warn people, cost effective, direct effect on viewers, indirect discussions

o

smoke free policies- protect others, roll out to all public places - endgame

o reduce consumption & availability of tobacco, remove all advertising opportunities, denormalised smoking

- solutions to push towards endgame

o

supply/market- increase age limit progressively, reduce retail availability (max purchases)

o

product modification- denicotinised cigs, reduce palatability and appeal

o

tobacco company liability- compensation, civil liability, make them less likely to harm - barriers

o

political addiction to tobacco & powerful industry- bureaucratic conservatism, buying loyalty

o

inherent attraction & philosophical objection- individual liberty prevails

- solution

o

bring in society, focus on children, find champions

what pharmacological support is in place to combat nicotine addiction? (6 marks) - 1

^st

line therapy- NRT, varenicline

o

NRT- spray, gum, patches; maintain plasma levels of nicotine, need bolus of nicotine

•

use in combination with nicotine patches & start NRT before quitting smoking

•

no CV risks, cost effective

o

varenicline- α4β2 nicotinic ACh receptor

•

partial agonist- stimulates DA release

•

partial antagonist- prevents binding of nicotine

•

good oral bioavailability, not metabolised by hepatic CYP, minimal pharmacokinetic drug interactions

•

adverse effects- nausea, headache, insomnia - 2

^nd

line therapy- bupoprion

o

primary mechanism- blocks reuptake of DA

o

secondary mechanism- non-competitive inhibition of nicotine receptors

o

reduces urge to smoke & symptoms of nicotine withdrawal

o

in combination with NRT increases efficacy modestly - 3

^rd

line therapy- cytisine & E-cigs

o

cytisine- alkaloid with high affinity for α4β2 nicotinic ACh receptor

•

partial agonist like varenicline but cheaper and less efficacious, used in developing countries

o

E-cigs- launched in 2004, popular in UK

•

can facilitate quitting BUT potential for harm (vapour causes lung injury)

•

normalises smoking for adolescents

•

some people transgress from E-cigs to actual tobacco smoking

describe the pharmacogenetics, pharmacokinetics and pharmacodynamics we need to be aware of with cannabis treatment (4 marks)

- pharmacogenetics- certain genes val > met found in family history of mental illness o make them susceptible to psychotic episodes when using cannabis

o

mental symptoms will be obvious in early life- marker to strongly avoid cannabis use - pharmacokinetics- e.g. clozapine (anti-depressant medication for mental health symptoms)

o

quitting smoking reduces the metabolism of this medication→levels of drug rises→leads to toxicity - pharmacodynamics- a detoxification drug

o

when used at high doses, less sedation required at peak blood levels→reduces nicotine withdrawal

awareness

possible mental health questions- module 4 (20 questions)

describe Australia’s policy response to mental health and strategies they have implemented to treat

mental illnesses (6 marks)

-

Australia’s policy towards mental health has seen considerable reform in the past 50 years in terms of

organisation, delivery of services and the strategies implemented to treat mental illnesses

- there has been a shift from institutional care (where people were locked up) to community rehabilitation/non-government services in an effort to support person centred recovery as opposed to clinical recovery

o

person centred recovery -patient being to live a contributing life even with a mental health problem - there has been an understanding of mental health and illness across a continuum from prevention, early

intervention, treatment and continuing care as opposed to diagnosing a patient, prescribing them medication and having no appropriate follow-up

- there has been more coordination and integration of care from professionals from various sectors e.g.

psychiatrists, counsellors, GPs (inter sectoral collaborative care)

- organisations such as beyondblue has reduced the stigma around mental illness resulting in more consumer and carer participation to helping loved ones deal with illnesses and not be excluded from society

- the national mental health strategy 1992 includes

o

national mental health policy 2008

o

national mental health plan 2009

o

mental health statement of rights and responsibilities 2012- common course of action by governments, ensure collaboration on policy and service development

o

fifth national mental health and suicide prevention plan- 2017

▪

achieving integrated regional planning and service delivery

▪

improving aboriginal and Torres strait islander mental health and suicide prevention

▪

reducing stigma and discrimination

▪

improving the physical health of those living with mental illness and reducing early mortality

▪

make sure mental health service delivery is of quality and safe

▪

ensure that the system is effective and improves along the way

describe mental health services that have been implemented including the stepped care model approach and their potential benefits (6 marks)

- ATAPs (allied psychological services) 2011

o

has become part of the flexible primary mental health care funding pool

o

uses K10 psychological distress scale and DASS (depression, anxiety, stress) to diagnose patients

o

results- statistically significant clinical improvements

- Better access 2006

o

better access to psychiatrists, psychologists, GPs through Medicare benefits schedule initiative

o

reaching new consumers e.g. rural areas (not had mental health care before)

o

90% of consumers received cognitive behavioural therapy

o

results- consumers experience statistically significant improvements - ATAPs vs Better access

o

ATAPs better able to meet need of at-risk groups since they diagnosed based on scales

o

Better access had a higher overall reach- due to new consumers

- stepped care model

o

delivery of evidence-based services according to need

o starting with treatment of low intensity diagnoses e.g. mild depression- normally online, systematic monitoring of progress (how?), if not responding to treatment, step up to higher intensity e.g. visiting clinic

and getting consultation face to face

o

aim- retarget services to high risk patients, reduce reliance on face to face delivery and matched care

▪

make more efficient use of workforce and technology e.g. sometimes rural people cannot visit clinics but have access to internet

▪

emphasise early intervention and care- by doing questionnaires online about mental health condition

o

benefits- less time from patient and professional, lower cost

▪

lots of evidence for effectiveness for depression/anxiety

why has the prevalence of mental health disorders not decreased despite programs such as beyondblue, headspace being implemented? (4 marks)

- masked by changes in risk factors e.g. a new risk factor points towards a mental health disorder - masked by increased awareness or reporting of symptoms

- poor quality treatment- e.g. not enough sessions at headspace

why is there a need for prevention rather than cure of mental health disorders? (6 marks) - prevention is better than cure

- there is a help seeking gap

o

35% of people with a common mental health disorder get help in a 12 month period whilst it takes some people up to 14 years

- there is a treatment gap

o

50% people are untreated in high income countries, 85% untreated in low and middle income countries

- economic, social and health costs

o

non health expenditure e.g. disability support, insurance payment, social housing for those with mental illnesses amounts to $14.8 billion (2010)

o

spending on mental health services 2015- $9 billion (significantly lower)

o

cost of inaction- increased the worldwide burden by 37.6% between 1990 and 2010 (furthered by population growth and ageing)

o

better for the individual and for government if there was prevention rather than cure

costs born