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Michael Mansfield Diabetes Consultant Leeds Teaching Hospitals. New units for HbA1c Diabetes is relevant to in-patient care NHS diabetes resource Gliptins & GLP-1 analogs & SGLT-2 inhibitors End of life Sodium. type 1 diabetes type 2 diabetes gestational diabetes - PowerPoint PPT Presentation
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Michael MansfieldDiabetes ConsultantLeeds Teaching Hospitals
New units for HbA1cDiabetes is relevant to in-patient careNHS diabetes resourceGliptins & GLP-1 analogs & SGLT-2 inhibitorsEnd of lifeSodium
type 1 diabetestype 2 diabetesgestational diabetesdiabetes secondary to pancreatic diseaseunknown / uncleargenetic diabetesother
MODY 3Mutations of the hepatocyte nuclear factor 1α gene Disordered insulin releaseAutosomal dominant pedigree over 2, ideally 3 generationsAge of onset < 25 years in at least one family member No need for insulin (or detectable C-peptide) in first 2-5 years after diagnosisProgressive rise in glucose levels through lifeLow renal threshold for glucoseOften very sensitive to sulphonylurea therapy
Permanent neonatal diabetes mellitusActivating mutations of the KCNJ11 gene, which codes for the Kir6.2 subunit of the beta cell K-ATP channel.Congenital impairment of insulin releaseMostly new mutationsOnset in first 3 (- 6) months of life but no immune markers of type 1 diabetes Often responds well to sulphonylurea therapy
New units for glycated haemoglobin
DCCTHbA1c
%
IFCCHbA1c
mmol/mol
6.0 42
6.5 48
7.0 53
7.5 59
8.0 64
9.0 75
The Think Glucose programme provides a package of tried and tested products, learning and support to improve awareness and remove the obstacles to the treatment of patients with diabetes as a secondary diagnosis.
Implementing a clinical pathway will improve the patient experience and the quality of their care.
Training of staff
Links to and alerting of diabetes team
New and NHS-wide documentation
Importance of careful medicines reconciliation
IV insulin infusion safetycannulaIV fluid
Insulin storage and insulin syringes
National or local guidelines for:DKA, HHS hypoglycaemiasurgery, endoscopyhyperkalaemiaend of lifetube feedinglaboursteroids for fetal lung maturation
Capillary glucose monitoring and recording
Patient self-management/admin of insulin
“Sliding scales” and other insulin prescribing
Increased insulin releaseReduced glucagon release
Slowed gastric emptying
Site of GLP-1 synthesisSecretion increased after meals
Satiety effectreduced food intake
Increased glucose uptake& glycogenesis
Overview of GLP-1 physiology
The problem with…..Metformin is bowel side effects, risk of lactic acidosis when eGFR decreased
Sulphonylureas weight gain and risk of hypoglycaemia
Insulin is weight gain, risk of hypoglycaemia, some driving restrictionsinjections
Glitazones take weeks to start working, expensive, very marked weight gain, fluid retention and heart failure, distal bone fracture risk
Gliptins (DPP4 inhibitors) expensive, no long-term safety recordweak pancreatitis signal
Exenatide expensive, nausea and vomiting in first monthsinjected, no long-term safety record, pancreatitis signal
Liraglutide even more expensive, nausea and vomiting in first monthsinjected, no long-term safety recordpancreatitis signal, v weak thyroid malignancy signal
Dapaglifozin expensive, genital thrush, no long-term safety record
glucose control in diabetes at the end of life
altered nutritionnegative energy balanceweight reductionreduction in physical activity
systemic humoral stress response
pancreatic destructionrenal impairment
liver destructionloss of fat and muscle
steroids
psychological stressmental illness
Aims for glucose levels:
1.No glucose level less than 6 mmol/L2.No glucose level higher than about 15 mmol/L
Breaks down care in to 4 scenarios:
1.End of life but prognosis of more than 1 year2.Prognosis in months3.Prognosis in weeks4.Prognosis in days
A few words on hyponatraemia
Always check for hyperglycaemia:For every 3.5 mmol/L the glucose is high, sodium falls by 1 mmol/L
It’s all about the brain
Always look for timescale of sodium fallBrain tolerates slow changes (up or down) remarkably well
SIADH is not the only cause, dehydration is common too
Assessment of patient’s circulating volume status is key
A cause for appropriate ADH release/activity excludes SIADH
If patient has been on steroids then suppressed HPA axis possible
Low circulating volume (NB intact thirst)acute medical emergency including sepsissurgical abdomenhypoadrenalism (Addisons or suppressed HPA axis)diuretics
ascitesnephrosiscongestive cardiac failure
Normal or increased circulating volumesyndromes of inappropriate ADH activity (secretion or receptor)sick cell syndrome
Redistribution of body waterhyperglycaemia
Management
Usually not urgent unless the cause itself is emergencyTreatment obviously depends on the causeIn practice it often seems to self correct
May need treatment anyway if brain function impaired by sudden and/or severe fall:
ie neurological signs / seizures / reduced GCS
IV saline and in some exceptional circumstances hypertonic saline appropriate. Aim for slow improvement in Na 5mmol/L in 12 hours.Not much improvement needed to reverse brain dysfunction
Read this article: Adrogue 2000 NEJM 342: 1851