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Palliative care; things to consider
- Current and Past views: is he currently in a state to make an autonomous decision. If not does he have an advanced directive or surrogate family member (power of attorney )? What were his views in the past?
- - dignity and autonomy; right to a good death and not management against his will. May require some education/information of the best course of action
- - difficulties when patient wants curative treatment, and when biomedically it is not likely. Onus on the doctor to reach understanding with the family
- Quality of life (are we prolonging a state of suffering?), treatment risks and costs,
- Need to consider palliative care; define it
- Doctors' POV: easy to be flustered in L/D situations, but with good intentions for patient and good documentation one can be at ease
Palliative care: How do you make the decision?
- Explain what it is and how it differs from curative/disease modifying medicine
- - mention it early, so fresh mind -> informed decision later rather than rushed one; allow time for calm discussion with family
- Acknowledge that patients tend to have high expectations when there is a chance to be cured;
- - but balance of hope and being realistic
- - death/dying is normal and there will be a point where treatment is harmful and futile irrespective of hope
- *ULTIMATELY DECISION IS THE PATIENT'S*, reassure him that
- Describe what a Hospice is, and tell them to check it out
- - constant care and no abandonment, will regular follow-ups
- Team effort; culture and beliefs respected
- Family involved; shared decisions and counseling for all in the face of grief
- Own home; more care than treatment in hospital
- Disease modifying therapies can be used together (e.g. tumour surgery or radiotherapy if affecting functionality)
- Doctor: ask self is death in next 12 months expected?
- - scientific markers and functional status
- - let go of unwillingness of patient death
- Patient barriers: Though of as giving up, and other attitudes
- - denial
- - not prepared to talk about death; cultural or linguistic differences
What should PHARMAC consider when deciding what drugs to fund?
- Same wellbeing vs. suffering argument; and limitations to the process; QALYs is the best objective guess we have but has its limitations
- Nature of treatment;
- - cost; is it worth it? are there better and cheaper alternatives?
- - who it affects; fair chance to life, meaning a drug to help those in developing age more likely than old people morbidities, even if the cost is much greater. *Not fair to leave somebody without a fair chance to life*
- - burden of disorder treated
- - evidence base; how long has the drug been around, quality of supporting evidence, and do we know if the side-effects are well studied via. meta-analytical data? If not, doubt cast over whether it is a safe investment
- Personal factors; usability, recall of inhalers and learning to use new ones is distruptive and affects adherence
- - vs. preventative medicine. Better to pour resources into statins (even if cheap and effective) vs. preventative measures and education?
- Good that there is an independent application process for cases not picked up by blanket policies
What needs to be considered when prioritizing patients for elective surgery?
- As a general framework; aim to maximise wellbeing out of the limited resources. No crystal ball, can't predict exactly who will make the most out of the surgery (+ fall into trap of biasing our decision).
- - With these limitations in mind the best thing we can possibly go by is research and the subsequent probabilities we've come to understand about what's more likely to make an ideal candidate for surgery
- - in some ways this is what the quality-adjusted life-year (QALY) is a generic measure of; considering disease burden, including both the quality and the quantity of life lived post intervention. *although limitations with QALYs such as ageism*
- # At a micro level, broken down into the following;
- - age; important to consider older person, and stage of social development etc.
- - other personal factors; line of work, developmental age, comorbid factors which limit the amount of benefit they could get, lifestyle factors (raging alcoholic?)
- - risk; to patient treatment may be harmful to baby/ other adversities; IVF may not be effective if too old,
- - needs vs. benefit weighed up: if IVF,
- - time waited; if a patient has lived longer (= suffered more) waiting for treatment then can be elevated up the list, but need to consider how much 'suffering' you will prevent
- - money/funding; private healthcare as a sidenote
- Things get tricky: it's never black and white = multifactorial, and for instance, a 30 year old vs. 5 with AIDS. who to pick?
Patient does not want chemotherapy despite the advise of his oncologist. What needs to be considered with respect to (a) the subsequent consultation and (b) the goal of care and potential benefits for Mr Neil and his family?
- OH SMASH QBEC A = acronym of the goals of paliative care
- O: Own Home
- S: Suffering and symptomology; what is the patient's current state? is the person in a place of suffering that is unbearable? And is it likely that the patient can be alieviated from this state?
- M: multidiciplinary approach; should consider other fields out of biomedicine which could help in this situation; e.g. grief councilor
- A: affirm life; inform and change attitude that dying is a normal process, against euthanasia
- S: Support systems; family, financial, spiritual and for friends; council them into a piece about their grief
- H: neither Hasten or postpone death
- Q: quality of life; to improve that in him and family
- B: biopsychosocial factors; is his unwillingness for treatment a symptom of his depression? have a talk and uncover
- E: Early in illness?
- C: care; can integrate early and transition; be planned and at peace with death
- A: Advanced directive
- He had the right to refuse treatment, but because this conflicts with the doctor's duty to work toward the patient's best interests we need to uncover why;
- - is the pain and suffering the reason? Is it curable?
- - Family and patient's beliefs; if suspicious he is being coerced attempt to empower his autonomy
- - what is the patient's outlook and goal for his decision?
- - dignified death
- Honesty: important to avoid a false sense of hope
- Trust: a great dr px relationship is paramount to getting through the situation without bad blood if compromises need to be made. requires;
- - try not to be don't be clouded by personal biases, and be fully disclosing
Molly’s mother contacts a Trainee Intern (TI) via Facebook and makes a ‘friend request’. The TI is not sure about whether to accept Molly’s mother as a friend or not and asks the House Surgeon her opinion. What recommendations should the House Surgeon offer the TI? Provide justifications for your recommendations.
- Politely decline the request: yes you stand to learn more about your patient, but one must consider (a) whether this is valid information and (b) what the cost is and what they stand to learn about the TI
- - FB pages can be groomed, you can create an online identity which tailors how you want to be perceived (or even falsify somebody's identity); and a user at the end of a monitor is powerless to know
- - loss of face to face; guard of professionalism is let down and no visual clue of sincerity or sarcasm, no visual feedback
- Rejection can = trust lost: understand that the patient puts himself in a vulnerable position in adding FB friend; may be a reaching out for trust and communication, may be non-significant. Could be important to ask why of if anything was wrong. If they thought it would be a good way to help her reach better research articles/information, then suggest email use
- - so need to be very clear and respectful in explaining the reasons for the decline. Best be done over the phone and as soon after the request as possible.
- Strongly consider changing FB privacy settings or even leaving: internet is a permanent storage site, and great caution is required for; how much of our life we document online and who we allow to see it. Made more difficult by the fact that we have no control over what others put up;
- - set it so only you can add, and others can't. Also strongly consider doing without it as an extreme measure; it only takes one tasteless joke to tarnish a professional reputation
- *The days of social media are early, and the culture may change so that it becomes professional to habour social media for clinical practice. But at this early juncture probably save to veer conservatively, as people have lost their jobs
Patient comes in seeking advice on alternative therapies. What factors should be considered and what do you say?
- Transition of role of doctor; from healer to guide. Onus is on the doctor in this situation to guide him to the right information, and assess whether the research is valid/useful
- - do so in a way that does not in any way leave the patient feeling pressured. As though giving him the tools to make an informed decision, and leaving it up to his free will to make it.
- Empower autonomy: It is important to leave the patient feeling that the decision was in the end his own call
- Understanding: unpack why he wants to use alternatives. If out of desperation, may be very therapeutic for patient to feel unrestrained in his decision making
- - BUT consider how destructive and harmful the intervention is. If patient is considering a million dollar faith healing, or suicide, it may be best to be more assertive and pressing within reason. Also find out if it interferes with existing treatments.
- Judgement based on patient: Once you get to know your patients, you can make a read without being patronizing. Some patients may not have the means, some may find articles useful, others may need you to summarize them. Best to get to know the patient first so you know how best to "empower" their autonomy.
- DON'T LIE TO PATIENT: coming from an evidence base, easy to dismiss these therapies. We shouldn't dismiss the inherent therapeutic value of exercising our own autonomy.
Describe what positive predictive value is (if at %85), and false alarm rate. What is meant by sensitivity and specificity?
- Screening tests can fail in two ways; it can show a result positive for a disease in an undiseased patient, or it may show a negative result for a disease in a patient with the disease
- Positive predictive value: is the proportion of people who test positive who actually have the disease
- The false alarm rate: is the proportion of people who don't have the disease out of everybody who tests positive. that is "false positives"
- Sensitivity: proportion of people who tested positive out of everybody who has the disease (i.e. including those who are false negatives)
- - a gauge of how many people are left undetected by the test
- Specificity: proportion of people who test negative out of all the people who don't have the disease (i.e. including those who are false positives)
What do the following mean; (a) Primary prevention (b) population based prevention strategy
- (a) interventions which help prevent the disease by minimising risk factors; e.g. using diet and exercise in the hope that one doesn't develop heart disease
- (b) is primary prevention, but at a population level so the intervention is targeted to affect everybody within the population. E.g. taxation of smokes or chlorination of water
What is a violation and what are the different types?
- Violations: a deviation from save operating procedures, standards or rules
- Routine violations: e.g. Doctors who fail to wash their hands due to a feeling they are too busy; common and often tolerated. Other examples include inadequate handovers, not following protocol and not attending on-call requests
- Optimizing violation: when a doctors allows a medical student perform procedures unsupervised because they are with their private patients. This involves being motivated by personal goals such as greed or thrills from risk taking, performing experimental treatments, and performing unnecessary procedures.
- Necessary violation: Nurses and doctors who miss out important steps in medication dispensing because of time constraints and number of patients to be seen. And action- without bad intentions - but deliberately known to be dangerous or harmful, but is through a poor understanding of professional obligations and a weak infrastructure for managing unprofessional behaviour in hospitals.
Why might a drug be prescribed for many days after it is necessary to a point of toxicity?
- A necessary violation has been committed; and due to the restraints of the work conditions.
- - perhaps stretched manpower leading to increased stress, fatigue, forgetfulness, cut corners
- - although no bad intentions in a work environment of this nature, to sidestep the protocol, which is in place for safety measures.
- In a work environment of this nature; general lack of friendliness may cause less communication; nurses and doctors etc. to forget despite best intentions.
- Blame culture not constructive here.
Jane's partner is abusive upon finding out she is pregnant. She gets slapped for wanting to keep the child. This was the first time that there was any violence, but she thought she would tell her GP (10 mins). Where can Jane get help from and what si the role of the GP in this situation??
- Police, Protection orders, women's refuge,
- Doctor's role:
- - assess risk; ask good questions; is she feeling safe? Is there any forced sex?
- - Be supportive, non-judgemental and a warm and welcoming outlet for help
- - assess immediate danger, or any witholding of information in fear, is the partner here now? Safety plan and ensure she is kept from danger
- - sustain relationship and trust by being tactful; can't severe yourself as an outlet of help
- - Provide support groups; e.g. womens refuge or CYFS for kids,
- Think about how you could help the husband
What factors may cause Jane to persist with an abusive partner?
- Fatigue: exhausted and helpless
- Fault: guilty and perceived as deserved punishment
- Fear: repercussions of seeking help. Fear that her story won't be believed
- Family: losing family and mutual friends
- Finances: Scared if partner is provider
- Father: of kids
- False beliefs/forgiveness: Believing that he'll change and that this is an adequate excuse to endure the abuse
- * Normalised behaviour
Define placebo vs. Nocebo
- Nocebo is a negative placebo effect
Research Ethics: What thing should be considered when making the decision whether research should be Approved, Declined, or have minor/major changes done to it.
- Evidence based practice = the basis of what we can do in medicine. Paramount to its advancement
- "Collaborative Partnership": model of research where we are working with study participants to uncover knowledge and truth, not working on people.
- - against this is the fact that much research is done by rich, powerful drug companies (who may have a non-wellness agenda)
- - Non-commercial (academic) research is often academically led, and lacking funding?
- - too idealistic?
- Social value: is it going to benefit health and well-being?
- Scientific Validity: will the data be solid and reliable?
- Fair participant selection: basis of selection of the participants should be scientific rather than e.g. social; think about prisoners
- Favourable risk-benefit ratio: potential risk should ideally be proportional to any potential benefit they may gain
- - Benefits to society may play a part in tipping the balance in favour of research even where the individual’s risk/benefit ratio is bad
- Independent review: reviewer considers relevant scientific and ethical considerations
- Informed consent: Shows respect for the autonomy of the individual
- - THINK there are some groups who are unable to give consent. Should informed consent always be required for research?
- Respect for participants: On going responsibility to the participants in a trial after consent has been obtained
What is conscientious objection?
- Conscientious objection: fundamental tenet of a liberal democracy such as NZ; have a right not to be forced to do things they consider immoral
- - allowed to abort children here; but CO has not been extended to pharmacists who do not provide emergency contraceptives
- Issue for doctors: when personal opinion can make one a CO for giving a certain treatment. But this is unprofessional and is ignorant to patient's best interests = doctor duty
- - and patients are vulnerable and can be misled/coerced/disrespected into bad clinical decisions through this bias
- - should never delay or refuse treatment because you think the patient's at fault for his own condition
- REQUIRES: self-awareness, on-going reflection, and respect for professional boundaries
Give the pathophysiology of diabetic nephropathy
- Formation of advanced glycation end products: several mechanisms;
- - cross linking collagen I and IV to decrease large vessel elasticity and BM thickening/permeability respectively
- - Glycated ECM products trap LDLs which enhance atherosclerosis and albumin in capillaries which further thickens BM
- - AGE-RAGE leads to release of pro-inflammatory cytokines, ROS, and proliferation of tissue you don't want
- Activation of protein kinase C (PKC): Upreg of VEGF → angiogenesis, plus endothelin-1 and vasoconstriction
- Disturbances in Polyol pathways: increase sorbitol and fructose, which ↓ NADPH and glutathione production
For a cardio-renal patient who suffers from congestive heart failure, what is the mechanism of AKI and how is it managed?
- This diabetic is known to have Ischaemic heart disease; and appears to be going through an acute decompensated period of heart failure
- - acute/chronic heart problems → acute/chronic renal problems
- Mechanism of AKI: unlikely diabetic nephropathy as no protein in urine
- - Poor CO (from left ventricular function) meaning pre-renal AKI as kidneys underperfused
- Compensatory mechanisms; Point of entry into the cascade;
- - baroreceptors which gauge volume and stretch at the carotid sinus and aortic arch sense low pressure; feed back to hypothalamus
- - increase SNS and vasopressin
- - acts to increase angiotensin and renal vasoconstriction etc
- Oedema: increase interstitial fluid from; decrease renal excretion and right sided heart failure?
- Management: Treat CHF first before diabetic management
- - frusemide for acute pulmonary oedema to promote diuresis
- - ACEi to improve cardiac function and reduce afterload, improve contractility, naturesis and diuresis
Pre-renal → renal acute kidney failure: On the basis of your explanation, what drugs are you going to use and how will they help to improve the clinical situation?
Based on studies that have investigated efficacy and patient survival prioritise the drugs you would use.
Clinically he is hypotensive (88/60) tachycardic 100/min, cyanotic and has a raised JVP at 5cm.
- First thing: treat acute CHF first then manage the diabetes
- - If no venous pooling; i.e. if pre-renal failure is through dehydration, put in saline IV and replenish fluids so not hypertensive and tachycardic. Don't know evidence but physiology of it speaks for itself
- - in this case there is raised JVP, so not so much volume loss, rather we need to increase heart function
- ACE inhibitors: used in this case even when patient is hypotensive
- - 26% risk reduction of complication with for CHF
- - improves cardiac function by reducing congestion/afterload (improve cardiac contractility, natriuresis and diuresis)
Frusemide: to promote diuresis and reduce the acute pulmonary oedema
- Simvastatin Scandinavian study: 2223 patients were assigned placebo and 2221 were assigned simvastatin treatment for a mean period of 5.4 years. There was a 30% relative reduction in the risk of death with simvastatin treatment.
- - Plus other diabetes targeted interventions; diet, exercise, other glycemic controlling/anti-diabetic drugs (not metformin which is contraindicated in renal disease)
Evidence base suggests that in general, in diabetics the higher the BP, the higher the mortality rate.
Explain the following blood results of a patient with chronic kidney injury
Discuss how you would manage the underlying problems linked to your explanation
- CKD: loss of nephrons less than 70%, loss of excretory ability and low eGFR
- - tendency to retain Na and K+
- Metabolic acidosis: (low HCO3-) loss of nephrons and ability to make bicarb
- - also increased tubule secretion of H+ (in attempt to correct acidosis) with associated K+ retention (= hyperkalemia)
- Calcium and Phosphate management: loss of nephrons = decreased ability to excrete PO43-, and reduced activation of VitD to its active form
- - Recall that PTH is stimulated by low Ca2+ and high PO43-
- - Increase in PO43- stimulates PTH release to try and increase urinary excretion of PO43- (through down-reg of Na/P symporters on the apical surface)
- Vitamin D: without activation of 1α-hydroxylase, can't get formation of calcitriol (from hydroxylation of calcidiol). Calcitriol is the bioactive Vit D. Low D3 means low Ca2+
- - together with low VitD3, low Ca2+ will cause ↑ PTH
- - ↑PTH causes increased bone turnover (= high ALP + osteomalacia/rickets eventually), and bone helps buffer H+
- Blood: lower erythropoietin production → reduced iron availability and normochromic, normocytic anemia due to relatively low feritin
- - Anemia: iron replacement, or even EPO therapy
- - Metabolic acidosis: sodium bicarbonate therapy
- - CKD: manage other risk factors (e.g. blood pressure or CVD risk)
- Secondary Hyperparathyroidism treatment: restrict dietary phosphate, so less cheese, milk, yoghurts and chocolate.
- - Phosphate binding; commenced on a phosphate binder (e.g. calcium acetate or aluminium hydroxide), preventing its absorption from the gut.
- *Calcium-containing agents should not be used in patients who have hypercalcaemia (due to tertiary hyperparathyroidism) or vascular calcification.*
- - PTH suppression; Give active VitD/calcitriol. Or active vitamin D analogues (e.g. paricalcitol) which are less likely to lead to cause hypercalcaemia. Calcimetics also (blocking Ca sensing receptor). Latter 2 are costly
- - Acidosis; both bone and progression CKD (use of sodium bicarbonate)
- Inadequately treated parathyroid hyperplasia progresses to tertiary hyperparathyroidism, which may require surgical intervention. Chronic hypercalcaemia and hyperphosphataemia associated with tertiary hyperparathyroidism make a significant contribution to the increased risk of vascular disease in patients with CKD, and therefore have a significant effect on overall morbidity and mortality.
What are the effects of adiponectin?
- Adiponectin is an anti-hyperglycaemic peptide hormone produced by adipose tissue. Adiponectin (and leptin) improve insulin sensitivity by;
- - directly enhancing the activity of the AMP-activated protein kinase (AMPK), an enzyme that promotes fatty acid oxidation and carbohydrate uptake, in liver and skeletal muscle.
- Adiponectin levels are reduced in obesity, thus contributing to insulin resistance.
- - It circulates in the blood and effects metabolism of fatty acids and carbohydrates in the liver and muscle.
- - Adiponectin increases uptake of FA by myocytes and the rate at which FA undergo B-oxidation in the muscle.
- - It also blocks FA synthesis and gluconeogensis in hepatocytes, and stimulates glucose uptake and catabolism in the muscle and liver.
The effects of adiponectin occur indirectly, through activation of regulatory enzyme AMPK by increasing cytosolic AMP concentrations
(note: AMP also results from ATP consumption during intense muscular activity). AMPK phosphorylates proteins critical to metabolism of FA and carbohydrates.
- Adiponectin gene is located in chromosome 3q27; which is a susceptibility locus for type 2 diabetes (T2DM) and related metabolic syndromes
- - exogenous adiponectin has been shown to decrease atherogenesis and inflammation
- - includes reduction in expression of vascular adhesion molecule & intercellular adhesion molecules. It also suppresses phagocytic activity (all indicative of anti-inflammatory properties)
- - unchanged levels after meals, but increased after significant weight loss (e.g. bariatric surgery)
What the difference between adherence and compliance?
Suggest ways you can improve patient adherence
- - implies a passive role, following demands and acting in accordance with the advice of the prescriber
- - noncompliers are seen as being unable to follow instructions
- - paternalistic attitude towards the patient on the prescriber's part
- - implies an active role, in collaboration with the prescriber
- - self-motivated decision to adhere to the treatment advice
- - self-regulation of illness and treatment
- 1. Present treatment rationale clearly and simply
- 2. Write down information and instructions
- 3. Check patient’s understanding of and expectations about the treatment
- 4. Check patient’s motivation regarding treatment or behaviour change (stages of change)
- 5. Involve patient in decision-making about the treatment plan
- 6. Identify barriers and tailor the treatment plan to the individual patient and their situation
- 7. Use of prompts and reminders
- 8. Use of specific techniques for behaviour change (e.g. motivational interviewing)
- 9. Involve others – multidisciplinary team and family members
Consider the ethical arguments for and against offering bariatric surgery in the public health system
Possible criteria that could be taken into account include Mr Jefferson's: Age, prognosis, ability to pay and desert (i.e. has she paid her dues and does she deserve to be supported)
- There are many emotive factors involved including …
- If the damage continues … health status is likely to deteriorate even further.
- We do not know much about ability to pay but if planned on going through the public system would be required to be placed on a prioritised waiting list.
- Do they deserve to have the health resources spent on gastric bypass surgery that could otherwise be spent on other health needs. This is called the opportunity cost of performing the surgery. Some would also comment that not yet exhausted all of her alternatives as she is yet to adhere to her medications and diets.
- Thus it is useful to look at Quality Adjusted Life Years QALYs
- Using this method, a year of healthy life is worth 1 and a year of unhealthy life is worth less than one. The value therefore is lower the worse the quality of the life of the unhealthy person
- The number of QALYs may look to gain can be used to somewhat objectively measure where the money should be spent i.e. if looks to gain 7 whereas the other people opting for surgery may only look to gain 2, this could be a significant factor
QALYs do however work against the elderly in that they have a lower life expectancy and thus fewer QALYs can be gained for the same treatment. The surgery will also not correct behaviours which have led to her continuing obesity and worsening health status so there is a risk may return to where is now once able to eat normal sized meals again.
- However, QALYs are considered by some to be unethical because;
- a) they are ageist - older people stand to gain less QALYs simply because they have less years to live; hence someone younger would be more likely to get more QALYs and hence have higher priority for the surgery.
- b) the double jeopardy objection - if another pre-existing condition which was not resolved by the surgery then her QALYs would not increase as much as they could if she did not have it; thus she is penalised twice for having this other condition.
When considering if in a scenario about patient rights, what should you consider??
- Raping Freshers doesn't seem extreme/evil for inexperienced sexy/simple teenaged rascal cunts
- Right to be treated with respect
- Right to freedom from discrimination, coercion, harassment and exploitation
- Right to dignity and independence
- Right to services of an appropriate standard
- Right to effective communication
- Right to be fully informed
- Right to make an informed choice and give informed consent
- Right to support
- Rights in respect of teaching or research
- Right to complain
How should you approach a bioethics question?
- State and define all the priniciples relevant to the scenario;
- - Beneficence:
- - Non-maleficence:
- - Autonomy:
- - Justice (distributive):
- - Patient dignity:
- - Honesty and truth-telling:
- - Informed consent: especially patient comprehension of the issues at hand
Be sure to unpack the tensions which arise in these values, and say what you would do if you couldn't come away with a morally ideal outcome
Define and describe what primary healthcare is
- Primary health care includes general practitioners, dentists, opticians, pharmacists and midwives, amongst others.
- According to the Alma Ata Declaration the goal of Primary Health Care is to protect and promote the health of all people.
- Characteristics of primary health care as defined by Alma Mater declaration
- *Acronym = AA Cover Chronic Carrot Eating*
- -accessibility - all new diseases first seen in primary care setting, with no boundaries (eg transport, hours).
- -Availability of health care - it is available to all members of a community regardless of SES or background-may need govt subsidies for those who cannot easily get care. This means healthcare is more equitable and gives better health across the whole population
- -continuity of care - providing care over long time by focusing on the person not their disease. this may account for the apparent poorer quality of disease as the person is the focus. This also improves the quality of care as the patient feels like they are included not excluded and that they are a part of the health care
- -coordination of care - primary care is centre of care delivery but there is good coordination between care providers
- -comprehensiveness of care - all health problems cared for in primary setting if poss. this is much cheaper than in secondary settings.
- -enrolment - get everyone in a community enrolled with a PHO so know the demographics and know the underlying health problems/ drivers of health. If drivers of health (or poor health) are understood, public health techniques can be used to analyse these and develop campaigns to reduce their impact eg if high rates of chlamydia - safe sex campaigns, free/cheap condoms etc.
- This also targets whole populations not just individual persons
Discuss specific characteristics of primary health care systems that explain this apparent paradox.
Excessive specialization in rich countries mean that a vast proportion of resources are spent on curative, specialty care rather than prevention and health promotion that are the core of primary health care.
Primary care is probably seen to be associated with poorer quality care for individual disease than specialty care because its aims are different. Primary care aims to prevent the very diseases every occurring that would have resulted in the patient ever needing to seek out specialty care. Therefore the statement is somewhat misleading.
Primary care is traditionally cheaper to implement as it does not require specialist facilities or skills and can be administered to larger number of people. For example good primary care nurses can vaccinate children against diseases so they will never have encounter the health system again with regard to that disease. That's a whole lot more effective and cheaper than allowing a child or adult to fall ill with a communicable disease and become a huge burden on secondary care when they require hospitalisation. Polio is a good example of a disease that was eradicated through primary health care which was extremely expensive to treat in specialty care. In this case loss of quality of care for the individual disease is unimportant because it has been eradicated.
Specialty care is not only expensive but also very individualistic. A specialist may only see a handful of patients a day, while a GP will see tens of patients every day with all manner of problems.
There will still always be a need for specialty care, however with effective primary care in place that need should be reduced to only the cases which cannot be helped in the primary care context.
Use Te Pae Mahutonga to assess X's heath and wellbeing (6)
- Mauriora - cultural identity - does Anna have access to whatever culture she belongs to? e.g if she is Maori does she have access to the Maori language, an institution such as a Marae, social services in a whanau
- Waiora - physical environment - she has opportunity to experience the natural environment, water is free from pollutants, air is fresh and free or irritants, earth is abundant with vegetation, noise levels are appropriate and harmonious
- Toiora - healthy lifestyles - is she minimizing harm to herself through regular exercise and maintaining a healthy diet, does she look upon her progress in a positive way, does she relate it back to her culture, is she fully aware of the risks her weight is causing her and how is she managing these risks
- Te Oranga - participation in society - does she contribute to the economy, does she contribute in employment and decision making
- Nga Manukura - leadership - does she have a community leadership position? Does she take leadership over her own health?
- Te Mana Whakahaere - Autonomy - Control, recognition of aspirations, self-governance
Describe each of the FOUR components of the Te Whare Tapa Wha model of health (Durie, 1984, 1994).
- Taha Wairua: Focus: Spiritual
- - Key aspects: The capacity for faith, spiritual awareness; spiritual significance; mauri (life essence)
- Taha Hinengaro: Focus: Mental/emotional
- - Key aspects: The capacity to communicate, to think and to feel; including knowledge and awareness
- Taha Tinana: Focus: Physical
- - Key aspects: The capacity for physical growth and development; physical wellbeing
- Taha Whānau: Focus: Family/extended family
- - Key aspects: The capacity to belong, to share, to care; interdependence, collectivity; identity
Mrs Brown's son had an interest in genetics and paid for her to have her DNA tested by 23andMe. Her results showed that she was 0.9 times less likely to get type 2 diabetes than other people of the same ethnicity.
How does this fit in with her diagnosis of type 2 diabetes?
What would you tell her?
Personal genomics and biotechnology company "Order your saliva-based DNA kit today for only $99"
- Things you should remember; Type 2 diabetes has a heritability of around 50% with several common genetic variants, however,
- - genome-wide studies have found 30 - 40 genes that only explain about 10% of the heritability of type 2 diabetes.
- - gene-environment interactions
- What would I say:
- - Check their understanding first, and clarify where they are unsure
- - explain the several complex ideas; SNPs, how they get the data, polygenetic and very complex (give her examples of other GWAS applications e.g. folate and diet)
- - emphasise interplay of environment, and empower her to focus on the things she can change
- - The truth; that the interplay of these genes and their effects still not perfectly understood
- So although she may have a single gene which does make her slightly less susceptible to the disease, she must have several other genes which put her at higher risk of developing type 2 diabetes.
That slightly higher risk coupled with environmental factors and lifestyle, have in her case
produced the disease.
How is insulin released from beta-cells in the pancreas? Name the drug class that acts here directly
- These cells have GLUT-2 receptors which are insulin independent; and allow phosphorylated glucose to diffuse freely into the cell if present in the plasma
- - however glucokinase at the pancreas only creates G-6-P when plasma levels are > 5.5mmol/L
- - Metabolism causes rise in ATP, which activates the ATP-dependent potassium channel
- - The resultant depolarisation allows Ca influx, which binds SNARE and releases insulin
- Sulfonylurea agents: block the opening of the potassium pumps to inhibit insulin release
- - Gut incretins potentiate insulin secretion; i.e. amino acids and other GI hormones release postprandially ;
- - hence why IV glucose = (faster but) small insulin response
When does ketoacidosis occur?
- This is due to the low insulin / glucagon ratio;
- - occurs mostly in T1DM but can happen in T2 if under lots of stress
- Due to increased relative glucagon action -> lipolysis and excess fatty acids to the liver
- Due to lack of oxalloacetate, they can't all be used in gluconeogenesis, and instead enter beta oxidation
- - excess acetyl CoA accumulates which is channeled into ketogenesis of ketone bodies
WRT diabetes; Describe metabolism changes in the liver, muscle and adipose
- Liver: lack of insulin's dephosphorylation of certain enzymes leaves;
- - glycogen synthase inhibitted, and glycogen phosphorylase upregulated
- - causing glycogen breakdown and
- Gluconeogenesis (and de novo lipogenesis) upregulated causing it to release heaps of glucose (and FFAs)
- - VLDLs and ketone bodies increased in production
- Muscle: Decreased GLUT-4 expression -> less uptake
- - Glycogenolysis > glycogen synthesis for fuel
- - Increased FA oxidation
- Adipose: Lack of insulin causes;
- - decreased GLUT-4 and glucose uptake
- - lipoprotein lipase not activated, so VLDLs produced by liver are not endocytosed; remains elevated in blood = hyperlipidemia
- Hormone sensitive lipase is not inhibited; increased lipolysis and increased plasma FFAs
Metabolic changes in cancer
- Cancers are very energy inefficient tissues; many futile cycles etc.
- High energy demands = flux of glycolysis pathway and proteolysis (muscle wasting) (and adipose tissue loss)
- TNFα: cachexic factors are upregulated. This one is a pro-inflammatory cytokine; attracting macrophages to adipose and causing FA spillover
- - At adipose: it stimulates lipolysis and inhibits lipoprotein lipase -> hyperlipidemia
- - At liver: induces PEPCK which stimulates gluconeogenesis -> hyperglycemia
- - Insulin: inhibits secretion and causes insulin resistance
- MOA: stimulates transcription factor NFκB which activates an inflammatory response
Describe metabolic changes in a high carbohydrate diet
How this leads to fatty liver
Explain how this relates to ketoacidosis in T1DM
- If carb-loading exceeds the body's ability to store glycogen, acetyl-CoA and glycerol-3-phophate accumulate
- - they divert to de novo lipogenesis (in liver), where FAs are created and packaged into VLDLs to be stored in adipose tissue
- In this high carb + high insulin environment, the liver upregulates 2 processes; glycolysis (as glycogen has reached capacity), and de novo lipogenesis
- - i.e. glucokinase, pyruvate kinase and pyruvate dehydrogenase all lead to increase acetyl CoA
- - Acetyl CoA carboxylase: activated by insulin and citrate (marker for high ACoA), converts this excess acetyl CoA to malonyl CoA.
- * Malonyl CoA inhibits carnitine transferase which shuttles FAs into the mitochondria for oxidation.
- * during insulin resistance, acetyl CoA carboxylase is not sensitive to decreased insulin, and continues de novo lipogenesis -> fatty liver disease
- Hence; high carb diet, and insulin resistance can cause ADIPOSE in leaving VLDLs to be returned to the liver, + factors which cause cause liver de novo lipogenesis
- - diet, exercise and decrease alcohol (which can cause insulin resistance)
- Ketoacidosis: due to relative insulin insensitivities from enzyme ACoA carboxylase, a T2DM with insulin present can divert the excess acetyl CoA into de novo lipogenesis (rather than ketogenesis)
- - glucagon in its higher proportions in T1DM inactivates ACoA carboxylase, so the excess acetyl CoA is used to produce ketone bodies
Effects of Adiponectin
- Produced by adipose in postprandial state; satiety signal. Increased release with less adipose tissue and exercise
- Effects: high concentrations cause increase insulin sensitivity. MOA includes activation of;
- - AMPkinase; stimulates glucose utilisation in muscle
- - PPARα which in turn regulates FA metabolism in muscle and liver
- Also decreases gluconeogenesis and downregulates proinflammatory cytokines
Neural modulation of appetite; roles of orlistat and glucocorticoids. Changes after bariatric surgery?
- Orlistat: pancreatic lipase inhibitor; causes less fat absorption but rancid stools
- Glucocorticoids: can stimulate hypothalamic production of NPY which is orexogenic; overriding leptin and insulin signals
- - can result in overfeeding
- Surgery: instant raise in PYY and GLP-1 after eating; not present in sham surgeries
Management of gout
- Lifestyle: diet, exercise, moderation of alcohol and sugary drinks
- Acute symptoms: Decrease pain and inflammation through;
- - corticosteroids and NSAIDs
- - anti-inflamatories; e.g. microtubule inhibitors (low therapeutic range)
- - monoclonal IL-1β antibodies
- Urate lowering drugs: can cause acute flares, but useful for reduction of tophi, anaphylaxis and prevent long term complications. Can be uristatic or urisuric
- - allopurinol: xanthine oxidase inhibitor; reduce UA production as precursor is better excreted by kidneys; also decreases de novo synthesis
- - probinecid: increases excretion of uric acid through inhibition of anion exchange via URAT-1
Symptoms of Hypo vs Hypercalcemia
- - Tetany
- - numbness and paraesthesia
- - Stridor = harsh high pitched respiratory sound
- - cateracts
- - Psychological disturbances
- - Weakness: decreased neuromuscular excitability
- - Constipation: decreased activity of GI SM
- - Polyuria and dehydration
- - Renal calculi
- - Hypertension
- - Cardiac arrythmias: e.g. asystole
- - Psychological behaviour; psychotic disturbances
- - Peptic ulceration
Blood Transfusions: What are the important blood groups and considerations?
- Blood groups: the most important are;
- ABO: sugar molecules which the body creates antibodies for. A, B or O groups
- - Anti-A is produced if you lack A, and Anti-B if you lack B. O is universal donor, but somebody with O-type blood has antibodies for both
- - passed on in mendelian fashion
- - special as the antibody is present in high titres, whereas other blood groups not until there is exposure
- Rh Blood group: concerning the blood protein "D"
- - 15% of caucasians lack D, and so can produce anti-bodies against it.
- - antibody causes haemolysis, and can cross placenta to lyse baby blood (can be supressed with 90% efficacy)
When is a blood transfusion indicated?
- i.e. for the different sub-components of blood
What issues exist with Transfusion?
- For Red cell transusion;
- - Depends on Hb levels: if < 70g/L - with the exception of vitamin deficient megoblastic anemia - transfusion is indicated in all patients
- Plasma transfusion: when patient needs coaggulation factors
- - i.e. with INR or APTT are abnormally high; i.e. with severe bleeding or liver disease which depletes the factors
- Cryoprecipitate transfusions: to replace fibrinogen or if bleeding is present
- - Antibodies and transfusion transmitted infections (TTI)
- - viruses like HIV and Hep C
- - Prion disease
Side-effects of Chemotherapy drugs
- Affects fast turnover cells
- - bone marrow supression (megaloblastic anemia + immune suppression)
- - hair loss and skin affects (dermatitis)
- Acute renal failure in methotrexate: metabolites precipitate in tubules
- Secondary cancers: e.g. malignant lymphomas
Diabetes prevention programme/GOAL