Embed Size (px)
Citation preview
WHY WE DO, WHAT WE DO
DR ANITA S RAINA
STRUCTURE
• AT SCALE• INTEGRATED
MODELS
PEOPLE
• FLEXIBLE
• CAREER
WAYS OF WORKING
• SELF & SHARED CARE
• TECHNOLOGY
EVOLUTION OF GENERAL PRACTICE
A FUTURE GP
A GP IN THE FUTURE WILL BE DEFINED AS THE EXPERT MEDICAL GENERALIST
WHO
IS A CONSULTANT
TO
A WIDER MDT
IN
PRIMARY CARE NETWORKS
IN
INTEGRATED CARE SYSTEMS
WHAT DO THEY HAVE IN COMMON?
IT IS 1890 AND THE PAINTER VINCENT VAN GOGH,
CONVALESCENT FROM SEVERE MENTAL ILLNESS,
ARRIVES IN THE SMALL VILLAGE OF AUVERS-SUR-
OISE, NORTH OF PARIS. THERE HE IS BEFRIENDED BY
THE LOCAL DOCTOR, PAUL GACHET, WHOSE
ATTEMPTS TO HELP THE PAINTER BECOME MORE
AND MORE FRUITLESS AS TIME GOES ON.
OVER A CENTURY LATER ANOTHER DOCTOR,
RICHARD AVERY, COMES ACROSS THE PORTRAIT
THAT VAN GOGH PAINTED OF DOCTOR GACHET.
ITS EFFECT ON THE MODERN DOCTOR IS
OVERWHELMING.
THE TWO NARRATIVES, ONE IN THE NINETEENTH
CENTURY AND ONE STRADDLING THE TURN OF THE
MILLENIUM, TELL SIMILAR STORIES ABOUT THE
NATURE OF DOCTORING, ITS DISINTEGRATING
EFFECT AND THE POSSIBILITIES OF REDEMPTION.
YEAR OF CARE HOUSE
YEAR OF CARE HOUSE
• THE DIAGRAM ILLUSTRATES THE CORE FEATURES OF THE HOUSE SURROUNDED BY THE DETAILS
IMPORTANT IN PRACTICE FOR DIABETES.
• THE HOUSE IS A FLEXIBLE SET OF PRINCIPLES WHICH CAN BE ADAPTED TO DIFFERING CONDITIONS
AND DIFFERENT SITES OF CARE.
• THE HOUSE WITH ITS WALLS, ROOF AND FOUNDATIONS ACTS AS A METAPHOR, AS WELL AS A
CHECKLIST, EMPHASISING THE IMPORTANCE AND INTER-DEPENDENCE OF EACH ELEMENT – IF ONE
ELEMENT IS WEAK OR MISSING THE SERVICE IS NOT FIT FOR PURPOSE.
• THE KEY COMPONENTS ARE THE PERSON WITH A LONG TERM CONDITION (LTC) BEING ENGAGED AND
INFORMED, WORKING WITH HEALTHCARE PROFESSIONALS WHO ARE COMMITTED TO PARTNERSHIP
WORKING. THE FRAMEWORK SHOWS THAT THAT THIS WILL ONLY OCCUR IN PRACTICE IF THERE ARE
SOUND ORGANISATIONAL PROCESSES THAT FACILITATE THEIR INTERACTION, BUILT ON THE
FOUNDATIONS OF ROBUST COMMISSIONING PROCESSES.
SNEAK PEEK AT THE NDA RESULTS
2016/17 2017/18
33.0% of GP practices in East Surrey completed all
of the NICE eight care processes for patients with
type 1.
44.2% of GP practices in East Surrey completed all
of the NICE eight care processes for patients with
type 1.
50.9% of GP practices in East Surrey completed all
of the NICE eight care processes for patients with
type 2.
65.4% of GP practices in East Surrey completed all
of the NICE eight care processes for patients with
type 2.
SNEAK PEEK AT THE NDA RESULTS
INDICATOR 2016/17 2017/18
Achievement of NICE-recommended
(3) treatment targets- TYPE 1
17.6% 18.3%
Achievement of NICE-recommended
(3) treatment targets- TYPE 2
37.6% 41%
0
20
40
60
80
100
% p
atien
ts
% patients with T2DM care process completed
East Surrey CCG
England
National Diabetes Audit 2017-18
http://www.digital.nhs.uk/nda
Review of NDA results
NEW DIABETES LCS
• DELIVERY OF KEY CARE PROCESSES
• HYPOGLYCAEMIA
• NDPP (NATIONAL DIABETES PREVENTION PROGRAMME)
• EDUCATION AND AUDIT
Dr Vidhu NayyarConsultant Endocrinologist/Diabetologist
East Surrey Hospital
Nothing to declare
Overview of Type 2 diabetes (T2DM)
Clinical cases
Summary
It is estimated that more than one in 16 people in the UK has diabetes (diagnosed or undiagnosed)
For all adults and children, it is estimated that:
◦ 10% of people with diabetes have type 1 diabetes
◦ 90% of people with diabetes have Type 2 diabetes
Across the UK in 2015, the prevalence of diabetes in the adult population was as follows
Country Prevalence, % Number of people
England 5.3 2,913,538
Northern Ireland 4.6 84,836
Scotland 5.1 271,312
Wales 5.9 183,348
1. Diabetes UK. Diabetes: Facts and Stats. https://www.diabetes.org.uk/Documents/Position%20statements/DiabetesUK_Facts_Stats_Oct16.pdf [Accessed September 2017]; 2. Prevalence calculated from population data available from: https://www.ons.gov.uk/peoplepopulationandcommunity/populationandmigration/populationestimates/bulletins/annualmidyearpopulationestimates/mid2015 (Accessed September 2017).
Type 1 diabetes – due to β-cell destruction, usually leading to absolute insulin deficiency
Type 2 diabetes – due to a combination of defective insulin secretion and insulin resistance
Gestational diabetes mellitus – diabetes diagnosed in the second or third trimester of pregnancy that is
not clearly overt diabetes
American Diabetes Association. Diabetes Care 2015;38(Suppl):S8–S16.
Images adapted from Servier Medical ArtAdapted from Defronzo RA. Diabetes 2009;58:773–795.
Insulin Secretion
Lipolysis
Glucose Production
Incretin Effect
Glucose Reabsorption
Glucose Uptake
PancreaticDysfunction
InsulinResistance
Hyperglycaemia
T2D
Structured education and self-management programmes improve outcomes by:
◦ Addressing health beliefs
◦ Optimising metabolic control
◦ Addressing cardiovascular risk factors
◦ Changing behaviour
◦ Improving quality of life
◦ Reducing depression
Patient education programmes in the UK:
◦ Programmes increasingly developed and evaluated scientifically,2
e.g. DESMOND3 and X-PERT diabetes programme4
Initial monotherapy
Two-drug combinations
Three-drug combinations
Combination injectable therapy
Metformin
Metformin + SUMetformin + TZD
Metformin + DPP-4 inhibitorMetformin + SGLT-2 inhibitor
Metformin + GLP-1 receptor agonistMetformin + insulin
Metformin + SU + TZD or DPP-4i or SGLT-2i or GLP-1 or insulinMetformin + TZD + SU or DPP-4i or SGLT-2i or GLP-1 or insulin
Metformin + DPP-4i+ SU or TZD or SGLT-2i or insulinMetformin + SGLT-2i + SU or TZD or DPP-4i or insulin
Metformin + GLP-1 + SU or TZD or insulinMetformin + insulin + TZD or DPP-4i or SGLT-2i or GLP-1
Metformin + basal insulin + mealtime insulin or GLP-1
• Glycaemic targets and therapies must be individualised (HbA1c target <7.0% for most patients)• All treatment decisions should be made in conjunction with the patient (focus on preferences, needs and values)
SU, sulphonylurea; TZD, Thiazolidinediones; DPP-4i, dipeptidyl peptidase 4 inhibitor; SGLT-2, Sodium-glucose co-transporter-2 ; GLP-1, glucagon-like peptide 1Inzucchi SE et al. Diabetes Care 2015;38:140–149.
Oral class Mechanism Advantages Disadvantages
Biguanides •Activates AMP-kinase (? other)
• Hepatic glucose production
• Extensive experience• No hypoglycaemia• Weight neutral
• ? CVD
• Gastrointestinal• Lactic acidosis (rare)• B-12 deficiency• Contraindications
Sulphonylureas • Closes KATP channels
• Insulin secretion
• Extensive experience
• Microvascular risk
• Hypoglycemia
• Weight• Low durability•? Blunts ischemic preconditioning
Meglitinides • Closes KATP channels
• Insulin secretion• Postprandial glucose• Dosing flexibility
• Hypoglycemia
• Weight•? Blunts ischemic preconditioning• Dosing frequency
Thiazolidinediones • PPAR-γ activator
• Insulin sensitivity
• No hypoglycaemia• Durability
• TGs (pio)• HDL-C • ? CVD events (pio)
• Weight • Oedema/ heart failure• Bone fractures
AMP, adenosine monophosphate-activated protein channel; CVD, cardiovascular disease; HDL-C, high-density-lipoprotein cholesterol; KATP, Adenosine Triphosphate -sensitive potassium channel; LDL-C, low-density-lipoprotein cholesterol; MI, myocardial infarction; PPAR-γ, Peroxisome proliferator-activated receptor gamma; pio, pioglitazone; TG, triglycerides;
Adapted from Inzucchi SE et al. Diabetes Care 2015;38:140–149.
Oral class Mechanism Advantages Disadvantages
α-Glucosidaseinhibitors
• Inhibits intestinal α-glucosidase• Slows carbohydrate digestion/ absorption
• No hypoglycaemia• Non-systemic
• Postprandial glucose excursions
• ? CVD events
• Gastrointestinal side effects• Frequent dosing
• Modest HbA1c
DPP-4 inhibitors • Increases incretin (GLP-1, GIP) levels • Increases peripheral glucose uptake
• No hypoglycaemia• Well tolerated
• Acute angioedema/ urticaria• ? Pancreatitis
• ? Heart failure
SGLT-2 inhibitors • Inhibits SGLT-2 in proximal nephron• Increases glucosuria
• Weight• No hypoglycaemia
• BP• Effective at all stages of T2D• CV risk reduction
• GU infections• Volume depletion
• LDL-C• Ketoacidosis
Injectable class Mechanism Advantages Disadvantages
GLP-1 receptoragonists
• Activates GLP-1 receptor
• Insulin, glucagon secretion• Slows gastric emptying
• Satiety
• No hypoglycaemia
• Weight• Postprandial glucose excursions• CV risk reduction found in LEADER
• Gastrointestinal side effects• ? Acute pancreatitis
• Heart rate• Medullary cancer (rodents)• Injectable• Training requirements
Insulin • Activates insulin receptor• Myriad effects
• Nearly universal response• Theoretically unlimited efficacy
• Microvascular risk
• Hypoglycaemia• Weight gain• ? Mitogenicity• Injectable• Patient reluctance• Training requirements
1. If HbA1c levels are not adequately controlled by a single drug and rise to 58 mmol/mol (7.5%) or higher:
◦ Reinforce advice about diet, lifestyle and adherence to drug treatment and
◦ Support the person to aim for an HbA1c level of 53 mmol/mol (7.0%) and
◦ Intensify drug treatment
Adults with Type 2 diabetes HbA1c target
Managed by diet/lifestyle ormonotherapy not associated with hypoglycaemia
48 mmol/mol(6.5%)
Managed by monotherapy with a drug associated with hypoglycaemia53 mmol/mol
(7.0%)
If HbA1c levels are not adequately controlled by a single drug and rise to 58 mmol/mol (7.5%) or higher:
Reinforce advice about diet, lifestyle and adherence to drug treatment and
Support the person to aim for an HbA1c level of 53 mmol/mol (7.0%) and
Intensify drug treatment
National Institute for Health and Care Excellence. Type 2 diabetes in adults: management (NG28). https://www.nice.org.uk/guidance/ng28/resources/type-2-diabetes-in-adults-management-1837338615493 [Accessed August 2017]
68 year male
Type 2 diabetes diagnosed 20 years
Hypertension
Overweight
Previous cardiac event 10 years ago
Metformin 1000 mg bd
Gliclazide 80mg bd
Dapagliflozin 10mg od - 12 months
Aspirin 75mg od
Ramipril 5mg od
Simvastatin 20 mg
Seen by his GP due to abdominal pain and referred to hospital
Temp 37.7 C, HR 130/min Sinus rhythm
BP 160/86mmhg
RR 24
CBG 11.2
Tender abdomen
No guarding
Rest examination unremarkable
Fbc, U&E, LFT,CRP – normal
Urine dipstix – 1+ glucose, 4 + ketones
ECG, CXR - NAD
Lab glucose 11
Noted ‘ ketones on breath’
ABG – Metabolic acidosis
Capillary Ketones 6.3
Capillary Glucose 10.7
Euglycaemic DKA
•First reported in 1973 •Spectrum of DKA •‘Partially treated’ DKA – Decreased CHO intake e.g. starvation, Ramadan, Depression,
Chronic Liver Disease, pregnancy or sick day rules not followed fully
Patients managed to maintain a degree of hydration and insulin intake but glucose levels may be normal but ketone formation continues
Diagnosis of eu-DKA was made
Transferred to ITU
DKA resolved within 2 days
Started on subcutaneous insulin – Twice daily premixed
82yrs, GP referral
History
Productive coughWeight loss Polyuria, polydipsiareduced appetite
COPD PPM Hypertension Eczema Barrett's oesophagus Bullous pemphigoid – treated with steroids 8/52 stopped in
June 2015
No significant family history
Omeprazole 20mg od
Amlodipine 5mg od
Aspirin 75mg od
Adcal D3 bd
Co-codamol PRN
Observations
Afebrile, Pulse: 100/min, BP: 125/75, RR 20, BMI 31
Oxygen saturation: 94% on air
Chest Examination: widespread wheeze, decreased air entry bilaterally
FBC: Normal, CRP 121, U&E normal, amylase normal, Lab glucose 32
ABG – Normal Ph/Hco3, except blood Glucose: 32
Blood ketones <0.3
HbA1c: 109 mmol/mol (12%) (Nv48mmol/mol)
Chest x ray :no focal consolidation
ECG : sinus tachycardia
Breakfast Before lunch Evening
8.9 15 30.1
10.1 17 29.5
11.4 14 20.3
Infective exacerbation of COPD
New onset type 2 diabetes/steroid induced Hyperglycaemia
Rehydration and antibiotics, bronchodilators
Prednisolone 30mg od 5/7
Variable rate insulin Sliding scale
Diabetic Team review
Started Gliclazide 40mg bd
Diabetes education/Dietician/DSN
CBGM still between 15-20
Gliclazide increased to 80mg bd
Added metformin 500mg BD
Discharged with follow with Diabetes specialist nurses
Completed steroid course
Seen in Diabetes clinic – CBGM 4-12
Stopped gliclazide due to hypos
Continued metformin and increased 1gm bd
HbA1C:43mmol/mol (whilst on treatmeant)
Diagnosis – New diagnosis type 2 Diabetes – exacerbated by steroids
Future needs for steroids in the community!
1)Exacerbation of COPD
2)Flare of Pemphigoid
3)Deterioration in glycaemic control
JBD- IP guidelines
October 2014
Oral glucocorticoid use 2.5% population
Short courses of steroids resulting in minimum periods of hyperglycaemia may not warrant intervention
Higher dose of steroids for longer periods may result in osmotic symptoms
Pre-existing type 1 diabetes, type 2 diabetes
People at increased risk of diabetes (obesity, family history, previous gestational diabetes, ethnic minorities, PCOS)
Previously hyperglycaemic with steroid therapy
Target CBG
6-10mmol/l (4-12mmol/mol)
6-15 mmol/l at end of life, elderly frail risk of falling
CBGM od - preferred pre-lunch or pre-evening meal, or 2 hours post lunch or evening meal. If the initial blood glucose is <12mmol continue to test once daily post breakfast or lunch
Subsequent CBGM is found to be greater than 12mmol/l - than frequency of testing increased to fours times daily (pre-meals and before bed)
If the CBGM is found to be consistently greater than 12mmol/l i.eon two occasions during 24 hours than the patient should start treatment
Test four times a day before or after meals and before bed, irrespective of background control
If the CBGM found to be consistently greater than 12 mmol/l i.e. on 2 occasions during 24 hours, then treatment should started/increased
Hba1c prior to commencement of steroids in high risk patient groups and those with known diabetes
Laboratory glucose prior/CBGM prior to steroids (high risk groups)
All those experiencing hyperglycaemia should receive education
Diabetes management
Healthy lifestyles choices
The risk of hypoglycaemia with non insulin and insulin therapies
• Sulphonylurea – Promote insulin release from pancreatic beta cell (short acting)
• Gliclazide 40mg od taken in the morning and 40mg increments, for patients on od steroid therapy, can be titrated to 240mg od, evening dose may also be necessary (max 320mg )
Titration of metformin
No evidence for the use of DPP-IV inhibitors, GLP-1, or SGLT2 inhibitors in the management of steroid induced diabetes/hyperglycaemia
• Pre- mixed - Increase the morning dose
Basal bolus regimen – increase in lunch and evening meal short acting boluses may be appropriate
T1DM - increase doses 2 unit increments every 24-48 hours to achieve targets, significant increase in insulin dose of even 40% may be required to normalise steroid induced hyperglycaemia
DSN/Community DSN involved
May require switch in insulin regimen to basal bolus therapy
After stopping steroid therapy in people without pre-existing diabetes
This should be 6/52 following stopping steroid treatment
Fasting glucose or OGTT – 6/52
Hba1c as screening tool delayed for 3 month following stopping steroid therapy
69 yr female retired sales assistant
Type 2 diabetes 2000
Hypertension
Hyperlipidaemia
PCI – single vessel 2015
Metformin MR 1gm bd
Gliclazide 160 mg bd
Victoza 1.2mg s/c od
Lantus 45 units od on
Previously tried canagliglozin – 12 months ago
Ramipril 10mg od
Atorvastatin 40mg od
Bisoprolol 2.5mg od
Aspirin 75mg od
Exercises minimally, diet tried multiple including orlistat, ETOH – rare BMI 32, BP/lipids – normal, LFT – raised ALT
Urine ACR – raised
HbA1c – 76 mmol/mol (9.1%)
9.2 10 12.9 13.5
6.3 9.5 15 12.7
Background diabetic retinopathy
microvascular and macrovasular complications
Poorly controlled type 2 diabetes
Microvascular and macrovasular complications, raised ALT, overweight, poor glycaemic control
Lifestyle changes – re- visit dietetic changes Exercise
Management 1) BD Insulin, continue rest of medication 2) Restart SGLT2 3) Stop liraglutide, Continue Metfromin & BD insulin 4) Stop liraglutide/gliclazide and start BD insulin 5) Basal bolus regime with liraglutide/gliclazide 6) Metfromin & Basal bolus regime stop liraglutide/glicalzide
Indicated in patients with a BMI above 35
Or in individual BMI above 30 with the presence of at least 1 co-existing morbidity
After 6 months, the drug should be reviewed and only continued if there has been a beneficial metabolic response
A reduction of at least 11 mmol/mol [1.0 %] in HbA1c and a weight loss of at least 3 % of initial body-weight
In 24 February 2017, the European Medicines Agency (EMA) -increased risk of lower limb amputation (mostly affecting the toes) in patients taking the SGLT2 inhibitors canagliflozin, dapagliflozin and empagliflozin used for type 2 diabetes
Patients advised to check their feet regularly
They should also tell their doctor if they notice any wounds or discoloration, or if their feet are tender or painful
The review of SGLT2 inhibitors was prompted by an increase in lower limb amputations (mostly affecting the toes) in patients taking canagliflozin in two clinical trials, CANVAS and CANVAS-R.
The mechanism by which canagliflozin may increase the risk of amputation is still unclear.
An increase in lower limb amputations has not been seen in studies with other medicines in the same class, dapagliflozin and empagliflozin. However, data available to date are limited and the risk may also apply to these other medicines.
A warning of the potential increased risk of toe amputation has been included in the prescribing information for these medicines.
Stopped Liraglutide
Stopped gliclazide
Continued metformin
Started BD Novomix 30/70 via flex pen
Repeat Hba1c 8.2% (66mmol/mol) in 4 months
Still requiring insulin titration
Risks - High risk for micro- and macrovascular events
Treatment considerations:
◦ Lifestyle interventions
◦ Metformin is the preferred treatment because of weight loss/ weight neutrality
◦ TZDs are effective in patients with high BMI, but associated with weight gain
◦ GLP-1 receptor agonists and SGLT-2 inhibitors associated with weight loss
◦ Newer agent Saxenda (Liraglutide 3mg/day) not on NICE guidelines
◦ DPP-4 inhibitors are weight neutral
◦ Bariatric surgery in severely obese patients
Type 2 diabetes NICE guidelines
SGLT2 agents cause euglycaemic DKA
Gliclazide in steroid induced hyperglycaemia in type 2 patents
Type 2 diabetes and management – complex patient
CASE STUDIESMRS VIVIEN MCKENNA
DIABETES SPECIALIST NURSE
CASE STUDY 1
• MOLLIE IS A SPRIGHTLY 84 YEAR OLD WIDOW WITH T2 DM AND A SIGNIFICANT VISUAL
IMPAIRMENT. SHE LIVES ALONE WITH GOOD SUPPORT FROM HER FAMILY
• SHE IS CURRENTLY TAKING A COMBINATION OF THREE DIFFERENT ORAL
HYPOGLYCAEMIC AGENTS: GLICLAZIDE 80MG BD, METFORMIN MR 2G OD, SITAGLIPTIN
100MG OD
• ADDITIONAL MEDICATION: RAMIPRIL 5MG OD
• HER RECENT HBA1C RESULT AT ROUTINE DIABETES REVIEW WAS 84 MMOL/MOL.
• ROUTINE RENAL FUNCTION TESTS NORMAL
• CHOLESTEROL: 6.6 MMOL/L, TRIGLYCERIDES 1.5 MMOL/L,HDL1.9MMOL/L,LDL 4 MMOL/L
• BP: 155/85 MMHG
• ON QUESTIONING, SHE IS SYMPTOMATIC WITH THIRST.
WHAT MANAGEMENT OPTIONS COULD BE CONSIDERED AND HOW MIGHT WE TAKE
THINGS FORWARD?
CASE STUDY 2
• KEITH IS A 74 YEAR OLD GENTLEMAN WHO WAS DIAGNOSED WITH T2 DIABETES IN 2009. HE WAS COMMENCED ON
METFORMIN STRAIGHT AWAY AS HIS HBA1C AT THAT TIME WAS 58 MMOL/MOL. AT DIAGNOSIS: WEIGHT 71KG, BMI
25 KG/M2.
• IN 2013 THERE WAS SOME DETERIORATION IN GLYCAEMIC CONTROL AND HE WAS COMMENCED ON SITAGLIPTIN
100MG OD AND IN 2016. DAPAGLIFLOZIN 10MG OD WAS ADDED TO HIS TREATMENT REGIME. OTHER MEDICATION:
RAMIPRIL 5MG OD
• RECENT MEDICAL HISTORY: OVER THE PAST YEAR KEITH HAS BEEN REFERRED TO A GI SPECIALIST AND INVESTIGATED
FOR WEIGHT LOSS. FAMILY AND FRIENDS HAVE BEEN GETTING INCREASINGLY CONCERNED ABOUT HIS APPEARANCE.
• RECORDS DEMONSTRATE STEADY WEIGHT LOSS SINCE DIAGNOSIS IN SPITE OF A HEALTHY APPETITE AND MINIMAL
CHANGES TO DIET.
• WEIGHT NOW 61KG, BMI 22; RECENT HBA1C 60 MMOL/MOL; CHOLESTEROL AND RENAL FUNCTION WITHIN TARGET;
BP: 145/82 MMHG
• WHAT MIGHT KEITH’S NEXT CARE PLAN LOOK LIKE?
CASE STUDY 3
• JOHN IS A 71 YEAR OLD GENTLEMAN WITH T2 DIABETES. HE IS LEAN AND ACTIVE WITH A BMI OF 23 KG/M2.
HE HAS A PAST MEDICAL HISTORY OF IBS.
• HE CURRENTLY TAKES A MAXIMUM TOLERATED DOSE OF METFORMIN 500MG BD. HE HAS PREVIOUSLY TRIED
SLOW RELEASE METFORMIN WITH NO SIGNIFICANT BENEFIT. HE WAS ALSO UNABLE TO TOLERATE SITAGLIPTIN
DUE TO GI SIDE EFFECTS. ADDITIONAL MEDICATION: RAMIPRIL 1.25 MG OD
• RECENT BLOOD RESULTS PRIOR TO REVIEW REVEAL AN HBA1C OF 72 MMOL/MOL. NORMAL KIDNEY
FUNCTION. CHOLESTEROL: 4.6 MMOL/L, TRIGLYCERIDES 1.9 MMOL/L, HDL 1.02 MMOL/L, LDL 2.7 MMOL/L.
• BP: 138/82 MMHG
THERE ARE A RANGE OF MANAGEMENT OPTIONS TO CONSIDER DURING YOUR CONSULTATION WITH JOHN.
Nothing that I tell you today,you don't already know!
Diabetes, and how I manage it
Dr Ian King
Holmhurst Medical Centre
Current setup
• 10,000 patients – currently stable although had been rising sharply over the past 5 years
• QOF register – 286 patients and rising
• 1 doctor for diabetes – that's me :)
• 1 nurse now trained but not yet taking a part in clinics.
• 2nd doctor completed some basic training
• SystemOne – all inclusive
• 1 very good practice manager to sort out CCG issues and make sure we are paid...on time
My interest and background
• For years hated managing people with diabetes
• Didn't understand it
• Didn't understand insulin (how to dose or prescribe)
• Discovered my colleagues felt the same
• Decided to get to grips with this
• Went to Leicester University to do a Masters Module in Insulin Management
• This really challenged me to thinking about using evidence to base management, thus helping understanding.
• Got distinction!
Next steps
• Became diabetes lead
• Colleagues delighted!
• They can dump all diabetes decisions on me
• Developed the concept that I needed more time than 10 mins for a diabetes review
• Started more widespread use of insulin
• Live in perpetual hope that CCG will recognize the importance of diabetes and fund it appropriately instead of talking about it
Diabetes clinic at Holmhurst
• There isn't one!
• Cases are included in my general clinics
• This adds interest to my daily existence
• And, I enjoy ticking off QOF boxes!
• What I really enjoy is sharing a success with my patients and seeing their delight when they have turned things around
8 care processes reminder
1. HbA1c (blood test for glucose control)
2. Blood Pressure (measurement for cardiovascular risk)
3. Serum Cholesterol (blood test for cardiovascular risk)
4. Serum Creatinine (blood test for kidney function)
5. Urine Albumin/Creatinine Ratio (urine test for risk of kidney disease)
6. Foot Risk Surveillance (examination for foot ulcer risk)
7. Body Mass Index (measurement for cardiovascular risk)
8. Smoking History (question for cardiovascular risk)
Other important care processes
• Lifestyle management and support• Retinopathy screening• Structured diet education (DESMOND)• Medication review• Managing co-morbidities• Special cases
• Learning Disability • Severe Mental Illness• Housebound• Frail Elderly / EOLC
• Influenza vaccination
National Diabetes Audit
• Did quite well in 2017
• Unsure how we are doing for 2018
• On back of this I have been asked to speak about what I do at Holmhurst
3 treatment target outcomes 2017 NDA
Administrative considerations
• Need to get the punters tested and in to see me
• Many are very motivated and come in whether they need to or not
• Sizable minority need intensive nagging / messaging / letters (repeatedly)
• This can be supplemented with restricting medication repeats / amounts prescribed reduced from 56 to 28 days. Need to focus their mind (sometimes)
• I am prepared to do a diabetes review ad hoc when they have come for their 'Only 3 problems today doctor' (which doesn't include diabetes), even if this now means I am running 30 mins late. But I now have the upper hand in managing and following them up
• Use QOF register to target ostriches. Do this at 6/12, 7/12 and 9/12 through year.
• Remove ghost patients
• Important to have a system that works. Need to be anal about it
QOF / Enhanced Services
• Important to get the management right for patients and the practice• Financial consideration.
• A lot of work for not that much financial return• More CCG support needed to ensure we can properly fund the time needed• Play QOF game for year end by excepting. Needs preparation:
• 3 invitations (letters, texts, reminders on prescriptions)• Ensure most of work done by Dec to give time for targets
• Nurses better at QOF than I am (coding – often done after I haven't done it right)
• Working on a joint clinic with Charlie (my nurse) and this is the aim by year end
• Leadership – who does what and when. Still to be done at Holmhurst
Clinical considerations – New cases
• Increasingly regular occurrence that I see a new case• Mostly fat middle aged poor lifestyle. Not always though• T1 or T2 or something else?• I am aware that if I can be motivational, they will come back• Small improvements really count. Build on this. Give them a good
experience• Simple messages for patients• Empowerment is key
• They need to see they can make a difference• They need to have an understanding. Personal responsibility• Homework. Diabetes UK website etc.
What are my simple messages?
•Glucose is poisonous if too much in blood•It attacks arteries and nerves•This ages arteries and nerves more quickly than time ages them (brain / heart / eyes / kidneys / feet)•Keeping glucose levels down prevents this•This is a shared concern between us. 'I will help as much as you will allow'.
Early engagement
• Collaborative working (patient does lion's share 24/7)• Patient perspective: Do not understate the importance of lifestyle or accept excuses
for poor lifestyle – that is collusion and never helps anyone• Weight management – realistic targets. Slow and steady. Will happen if exercise and diet.
• Phone in weights. Call them back • Exercise – Park Run; exercise on prescription. Get sweaty at least 3 times a week.
• Walking the dog is not enough• Diet – briefly touch on carbs and cut out all snacks. I recommend
• 'The 8 week blood sugar diet' (Michael Mosely) – really good book;• 'The Doctor's Kitchen' (Dr Aujla) good food and recipes.
• Doctor perspective:• Motivation – look at the opportunity this has given you to re-evaluate your health and invest
in your future health. (The doctor/nurse is merely the technician / catalyst) (Balint)• Monitoring• Drugs including restricting repeat scripts• Reviews
Motivation
Early clinical management to support lifestyle
• I set a target of 7.0% A1c
• I view >7.5% as uncontrolled diabetes (apart from certain cases e.g. frail elderly, EOLC etc.)
• Metformin to start (assuming creatinine ok)• Build dose over 4 weeks (mostly works regarding tolerance)
• Atorvastatin if chol up (unless high HDL-C so that chol/HDL ratio < 2.5)
• Manage smoking / alcohol
• Check ACR if not done already
• Weight / BMI
• BP and BP follow up management where necessary. I aim BP< 135/80 (depending on co-morbidities)
• Baseline foot assessment (pulses / Monofilament in 9 places each foot). ? Refer Podiatry
• Refer DESP – explain about taking someone with them
• Refer DESMOND – explain really brilliant but 6/12 wait. Discuss diet issues briefly as above
• Follow up with repeat U&E, Lipids (as needed) and A1c after 3/12
• Record and Read Code all findings
Follow-up management to support lifestyle
• Check exercise arrangements / diet / smoking
• Review A1c / lipids / creatinine
• Check weight / BMI.
• Further and ongoing positive discussion
• Reject / ignore negativism and excuses. Flood them with carrots i.e. health improvement benefits
• Put responsibility onto patient who is struggling. • What do you want?
• How do you plan to get there?
• Constant reassurance you will help them achieve but they have to help themselves.
• Expose and pull down barriers.
• Use of Wellbeing service. Mental coaching – CBT approach
• Ensure other areas important to them are being managed
Follow up Clinical management
• Check DESP outcome (any retinopathy?)• Check DESMOND outcome. What changes are you making?• Review ACR (any nephropathy?)• Review BP• Adjust antidiabetic medication. Present options – pros / cons of each drug
group• If on insulin, check injection sites / technique / awareness hypos / driving /
exercise rules / sick day rules• Follow up 3/12 (if not yet engaged), 6/12 if minor problems, 12/12 if well
controlled. Adjust follow up times ad hoc according to QOF needs to ensure practice doesn't lose out and targets achieved
• Read code everything
Drug options
• DPP4 inhibitors – can be taken incorporating metformin so daily tablet intake decreases tablet numbers. Modest drop A1c about 0.7% (Cochrane)
• GLP-1 – good choice if high BMI. Reduces insulin resistance so I drop insulin dose 25% if on both, and retitrate insulin up to avoid hypos
• SGLT2 inhibitors – personal use suggests these are very effective. Can be used first line if can't take metformin. Can cause thrush. Rarely cause DKA. Canagliflozin ? associated with amputation
• Sulfonylureas – I never prescribe these dreadful drugs. They make you fat and can cause hypos. But cheap
• Pioglitazone – may cause HF in conjunction with insulin. Don't use if h/o CA bladder / undiagnosed haematuria / or occupational risk GU cancer
• Insulin – often started too late. It is NOT a last resort drug. It is easy to use in Type 2 and often makes patients feel hugely better (control / energy). Good if there are complications present. Driving rules. Hypo awareness. Occupation e.g. HGV/PSV
• Start basal dosing (I use ATLANTUS titration).
• Consider adding Basal Plus or Basal Bolus as needed
Care Plan
• Try to limit the information presented to simple targets
• Write down the important areas discussed
• Don't overwhelm with information
• Offer time to call back if unsure
• Ensure follow up arrangements and prior testing is understood
• For insulin, ensure they have a BM monitoring diary and tick the columns that are likely to provide the information you need
Reality check
• (Some) Patients frequently screw the system up by forgetting to go to things and needing chasing up
• (Most) Patients usually want to talk about something else (often more than one something else) as well as diabetes. I accept this and go along with it. Can always bring them back again. Keep them onside.
• Each case is individual and management is equally individual
• NICE is just a guide and has its own biases
• In truth there are relatively few rules – as long as it is working!
• Meds management generally don't mind the cost as long as the outcomes are ok....
...But they do pressure (ask) you to do audits
Questions
Preventing and Managing T2DM with Lifestyle
Dr Gillian Orrow
Smallfield Surgery
Type 2 diabetes: a disease of lifestyle
Globally
• 2012: 382 million adults have T2DM
• 2035: 592 million
UK
• 2013: 3.2 million (approx 6% of UK population)
• 2025: 5 million
Diabetes Prevention Program Research Group . New England J Med 2002;346:393-403
Diabetes & Lifestyle
Part I
Things we know about and could do better
Part 2
Ideas with an emerging evidence base
Part 1: We can do this!
Physical Activity
Physical Activity: Suggestions
1. Try to get up between patients
2. Try giving an exercise prescription to patients
Orrow G et al. Effectiveness of physical activity promotion advice based in primary care: systematic review and meta-analysis of RCTs. BMJ 2012;344:e1389
Diet
• Insulin resistance
• Weight loss
What is the Mediterranean diet?
Monteiro et al. Household availability of ultra-processed foods and obesity in 19 European countries. Public Health Nutrition 2018 (21):p18-26
The Mediterranean diet
Rosato V et al. Mediterranean diet and CVD:a systematic review and meta-analysis of observational studies. Eur J Nutr 2017:1582Bonaccio M. Mediterranean diet and mortality in the elderly: a prospective cohort study and a meta-analysis. Br J Nutr 2018;120(8(:841-854
Diet: Suggestions
1. Try to reduce processed foods
2. Try to increase your intake of fresh foods, especially vegetables
3. Enjoy good quality olive oil
Then recommend these changes to your patients
Part 2: the Pursuit of Harmony
Circadian Rhythms
• All aspects of our bodies are controlled by circardian rhythms
• Eating as well as sleep
Time Restricted Eating (TRE)
• Time restricted eating confines eating to a 8-12 hour window
• Human studies have found:
– Weight loss w/o calorie restriction
– Increases insulin sensitivity & improves beta cell function
– Reduced BP
– Reduces oxidative stress
Sutton E et al. Early Time-restricted feeding improves insulin sensitivity, blood pressure and oxidative stress even without weight loss in men with pre-diabetes. Cell Metabolism 2018;27(6):1159-1160
Mattson M et al. Impact of intermittent fasting on health and disease processes. Ageing Research reviews 2017;39:46-58
The Microbiome
• Humans are complex ecosystems
• 99% of our genes are microbial!
Andrew H. Moeller et al. Rapid changes in microbiome during evolution. PNAS 2014;111:46:16431-16435
What can we do to support the microbiome?
• Healthy diet
• Physical activity
• Prioritise sleep
• Prioritise social engagement – social prescribing
Disability, dementia and frailty in later life – mid-life approaches to prevention. NICE 2015
Evidence for Low Carb Med Diet
• Anecdotal• Hard, long term evidence is lacking
• Weight loss: low carb OR low fat diets work*• Diabetes control**:
– Short term HbA1c 1.38% lower in low carb vs low fat– At 1 year -0.36% difference– At 2 years no significant difference
*Johnston BC et al. Comparison of weight loss among named diet programs in overweight and obese adults:a meta-analysis JAMA 2014:312(9):859-73
**Van Zuuren et al. Effects of low carbohydrate compared wth low-fat diet interventions on metabolic control In people with type 2 diabetes: a systematic review. American Journal of Clinical Nutrition 2018(108):300-331
