Diabetes Mellitus

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  • Created by: LBCW0502
  • Created on: 07-04-21 15:39
State features of type 1 diabetes
Typically develops as a child or young adult. Autoimmune destruction of pancreatic beta cells. Sudden onset usually associated with rapid weight loss
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State features of type 1.5 diabetes
Latent Autoimmune diabetes in adults. Gradual autoimmune destruction of pancreatic beta cells. Commonly presents with a slower onset in patients >30 yrs old. NOT linked to insulin resistance
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State features of maturity-onset diabetes of the young
Hereditary condition - autosomal gene mutation. Ineffective insulin production. Commonly presents with a slow onset in patients < 45 yrs old
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State features of type 2 diabetes
Typically affects people > 45 yrs old. Insulin resistance and relative insulin deficiency. Slow onset often associated with patients who are overweight
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What is diabetic ketoacidosis?
A serious problem that can happen in people with diabetes if their body starts to run out of insulin. When this happens, harmful substances called ketones build up in the body, which can be life-threatening if it's not found and treated quickly.
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How is diabetic ketoacidosis managed?
Fluid replacement: restore circulatory volume, clearance of ketones, correct electrolyte imbalance. Continuous IV Insulin infusion: inhibit gluconeogenesis and lipolysis, facilitate uptake of glucose into cells. Start SC insulin once out of ketoacidosis
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What are the aims of treatment for T1DM?
Replace body's own insulin. Mirror natural insulin release profile. Prevent acute complications: hyperglycaemia, DKA, hypoglycaemia
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What are the chronic complications of diabetes? (1)
Microvascular. Eyes (retinopathy,cataracts,glaucoma,blindness). Kidneys (nephropathy, CKD, HTN). Nerves (sensory neuropathy - numbness, tingling, neuropathic pain, autonomic neuropathy – ED, GI disturbance (Gastroparesis), postural hypotension
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What are the chronic complications of diabetes? (2)
Macrovascular. CVD (angina, MI, stroke, peripheral artery disease,
heart failure), HTN, PVD. Increased susceptibility to infection, impaired immune response. Diabetic foot (caused by PVD, neuropathy, ­ susceptibility to infection)
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What is the HbA1c target in patients with T1DM?
Support adults with T1DM to aim for a target HbA1c level of 48 mmol/mol (6.5%) or lower, to minimize the risk of long-term vascular complications. Agree an individualised HbA1c target with each adult with T1DM
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What blood glucose concentrations are we aiming for?
T2DM (4-7 before meals, <8.5 90 mins after meals). T1DM (5-7 upon waking, 4-7 before meals, 5-9, 90 mins after meals). Children/young adults with T1DM aged 12-18 years (4-7 upon waking, 4-7 before meals, 5-9, 90 mins after meals)
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What are the different types of insulin available?
Human insulin (Fast e.g. Actrapid, Humulin S, Intermediate e.g. Insulatard, Humulin I). Analogue insulin (Very Fast e.g. Lispro, Aspart, Long acting e.g. Glargine, Detemir, Degludec – very long acting). Continuous subcutaneous insulin infusion
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Describe features of insulin analogues (1)
Structure of insulin is modified to change the pharmacokinetics of the insulin – in which the lysine and proline at positions 28 and 29 of the beta chain are reversed in the case of lispro. In insulin aspart, aspartate is substituted for proline at positi
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Describe features of insulin analogues (2)
More rapid absorption. Less variability in absorption rate. Can be injected immediately before food. Limit the post-prandial glucose increase more effectively. Less risk of nocturnal hypoglycaemia. Long acting insulin analogues – precipitate in physiologi
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What are the insulin types and durations?
Rapid/short (onset 5-15mins/15-60 mins, peak 60 mins/1-2 hours, duration 3-5h/3-8h). Intermediate (onset 1-2h, peak 6-10h, duration 12-18h). Long degludec (onset 1-2h, peak flat profile, duration 18-36h, beyond 42h). Mix, biphasic (onset 15-60mins, peak 1
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Describe features of insulin preparations
Most preparations are 100units/ml. Now have some which are higher strength preparations (200 – 300units/ml). (Tresiba®(degludec), Humalog® (lispro), Toujeo®(glargine). Be very careful when prescribing and dispensing. Biosimilar insulin glargine available
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How do we start insulin therapy?
Basal bolus regimen is ideal. 0.5 units/kg/day needed. 30-50% as basal insulin. Rest divided over meals. Honeymoon phase - 0.2-0.5 units/kg. During illness, adolescents in growth phase - 1-1.5 units/kg. T2DM with insulin resistance - 0.7-2.5 units/kg
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How is insulin adjusted?
According to blood glucose levels:
Basal Insulin adjusted by 10-20 % at a time
1 unit of mealtime insulin decreases glucose by 2- 3 mmol/L. But be careful when adjusting doses as we do not know how sensitive the patient is.
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What patient educational points will you raise with the patient? (1)
Type 1 diabetes offered DAFNE (dose-adjustment for normal eating) or DESMOND (Diabetes Education for Self Management in the Ongoing and Newly Diagnosed) programme. 6-12 months after diagnosis
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What patient educational points will you raise with the patient? (2)
Injecting insulin - rotating sites to prevent lipohypertrophy which can affect the absorption of insulin. Abdomen is fastest absorption, arms intermediate absorption, thighs low absorption. Diet, carbohydrate counting. Exercising and insulin requirements.
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What patient educational points will you raise with the patient? (3)
Patients are taught to do carbohydrate counting. 10 grams of carbohydrate = 1 carbohydrate portion. Most people start using 1 unit of insulin for every CP to reduce chances of hyperglycaemia. But can vary from 0.5-4units / 10 gram of carbohydrate
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What patient educational points will you raise with the patient? (4)
Hypoglycaemia, driving, monitoring, employment, weight management, healthy eating, coping with illness, storage and disposal of insulin/needles
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What are the monitoring requirements?
Measure HbA1c levels every 3–6 months in adults with type 1 DM. Advise routine self-monitoring of blood glucose levels for all adults with type 1 DM, testing at least 4x/day, including before each meal and before bed (adjustments, annual check of diabetic
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What are the reasons for sub-optimal control on insulin?
Poor or suboptimal adherence. Poor injection technique (e.g. storage, site selection,
site rotation, injection process). Injection timing. Psychological. Presence of lipohypertrophy. Diet and lifestyle. Intercurrent or concurrent illness. Interacting drug
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Describe features of a continuous subcutaneous insulin pump
Battery-driven syringe pump. Fine plastic cannula terminates in sub.cut. implanted catheter. Short-acting analogues. Continuous basal insulin infusion & patient-activated bolus doses at meal times. Dosage instructions entered into pumps small computer and
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A continuous subcutaneous insulin pump is appropriate for which patients?
Recurrent hypoglycaemia. Marked morning glucose rise despite optimum multi-injection regimen. Repeated/unpredictable hypos despite optimum multi- injection regimen. HbA1c levels have remained high (>69 mmol/mol) despite MDI therapy and a high level of car
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What are the HbA1c targets and intensification levels in T2DM?
<48mmol/mol (< 6.5%) for patients on lifestyle or monotherapy with a medication with a low risk of hypoglycemia e.g. metformin. <53 mmol/mol (<7.0%) for patients on a monotherapy associated with the risk of hypoglycaemia e.g. gliclazide. Recommends intens
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What is the aim of therapy for T2DM?
Appropriate control of hyperglycaemia without hypoglycaemia. No micro/macro-vascular complications. Maintain blood glucose, BP and cholesterol
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Why is it important to maintain maintain blood glucose, BP and cholesterol? (1)
Microvascular complications: Eyes: retinopathy, Nerves: neuropathy – autonomic and peripheral neuropathy, Kidneys: Microalbuminaemia, nephropathy, Macrovascular complications (vascular system, heart, CHD, PVD, stroke, TIA)
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Why is it important to maintain maintain blood glucose, BP and cholesterol? (2)
Maintaining tight control of BP and adding statin in patients who have a high CV risk or those who have high cholesterol, LDL – this will help reduce the macrovascular complications
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Which medicines are used for T2DM?
Biguanides. Sulphonylureas. SGLT-2 (Sodium Glucose Co-transporter 2) inhibitors e.g. canagliflozin. GLP-1 (Glucagon like peptide 1) analogues , exenatide, liraglutide. Thiazolidinediones (glitazones). Dipeptidyl peptidase IV (DPP-4) inhibitor, sitagliptin
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State features of metformin
Increase sensitivity to insulin. Increase peripheral utilisation of glucose. Reduce hepatic glucose production
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What are the advantages of metformin?
Weight neutral, may be some weight loss. Hypoglycaemia less likely. Some clinical trial evidence supporting a ↓ incidence of MI, stroke and mortality associated with metformin use
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What are the disadvantages of metformin?
GI side effects – Nausea, diarrhoea, anorexia, abdominal, discomfort, metallic taste. Lactic acidosis – in patients with renal impairment, severe heart failure, liver failure. Takes time to work
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What is the NICE guideline for drug treatment? (1)
Offer standard-release metformin as the initial drug treatment for adults with type 2 diabetes. In adults with type 2 diabetes, if metformin is contraindicated or not tolerated, consider initial drug treatment with: DPP-4 inhibitor or pioglitazone or sulf
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What is the NICE guideline for drug treatment? (2)
Consider relaxing the target HbA1c level on a case-by-case basis (e.g. for people who are older or frail) for adults with T2DM: who are unlikely to achieve longer-term risk-reduction benefits, e.g. have a reduced life expectancy, high risk, significant co
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Describe features of sulphonylureas
Increase insulin secretion from b cells. It is dependent on b cell function. Differences in duration of action and metabolism/excretion. Lowers glucose faster than metformin. Reduces HbA1c by up to 2%. But hypoglycaemia, weight gain, stops working over ti
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Describe features of thiazolidinediones (1)
Reduce gluconeogenesis, increase peripheral utilisation of glucose, reduce free fatty acids, reduce insulin resistance. Pioglitazone (licensed)
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Describe features of thiazolidinediones (2)
Reduces HbA1c by approximately 1%. Takes up to 3 months to have max effect. Disadvantages - weight gain, fluid retention (worsens HF), CV safety, risk of bladder cancer and bone fractures. Review safety and efficacy after 3-6 months of treatment
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Describe features of incretin-based therapy
Major incretin based therapies are: GLP-1 , Exenatide (also available
as once a week preparation), Lixisenatide, Liraglutide, Dulaglutide), DPPE-4 inhibitors prevent degradation of GLP-1 (Sitagliptin, vildagliptin, saxagliptin, linagliptin, alogliptin).
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Describe features of GLP analogues (1)
GLP-1 has a very short t1/2, metabolised by DPP4. GLP-1 analogues enhance GLP-1 effects. Short-acting: exenatide (BD), lixisenatide (OD), liraglutide/reduce CVD (OD), affects postprandial glucose. Long-acting: semaglutide, dulaglutide, exenatide (weekly)
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Describe features of GLP analogues (2)
Very low risk of hypoglycaemia. Nausea is common but resolves within 2 weeks. Appetite suppression, headaches, dizziness. Risk of pancreatitis. Other medicines should be taken 1 hour before or 4 hours after dose or taken before meal (minimise absorption i
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Describe features of GLP analogues (3)
At third intensification, consider combination therapy with metformin, a sulfonylurea and a glucagon-like peptide-1 (GLP-1) mimetic for adults with type 2 diabetes who: BMI >35, specific psychological/medical problems associated with obesity or BMI <35, w
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Describe features of DPP-4 inhibitors
Inhibits DPP-4, increases levels of GLP-1, increase pancreatic insulin production & ̄ release of glucose from liver, inhibits glucagon secretion. Licensed drugs: sitagliptin, saxagliptin, linagliptin,
alogliptin & vildagliptin. Combination therapy
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Describe features of SGLT-2 inhibitors
~ 90% of the glucose reabsorption in the kidney. Blocking this transporter causes blood glucose to be eliminated through the urine. Examples - Dapagliflozin, Empagliflozin. Advantages - no risk of hypoglycaemia, reduce weight, reduces risk of CVD. 2nd lin
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What are the side effects of SGLT-2 inhibitors?
UTI’s and genitourinary fungal infections. Cause osmotic effects that may lead to hypotension and dehydration, particularly in patients taking diuretics. May cause hyperkalaemia (so be careful with ACE inhibitors). Efficacy is dependent on renal function
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What are the adverse effects of SGLT-2 inhibitors?
Increase risk of toe amputation with canagliflozin, but may be a class effect. Monitor patients and stop if foot complications develop. Ketoacidosis has been reported even if plasma glucose are near normal – patients should be educated on how to look for
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Describe features of insulin
Should be considered if HbA1c target is not achieved by second intensification. High doses usually required due to insulin resistance. Usually twice a day regime used but basal bolus regime also used. Disadvantages - weight gain, hypoglycaemia.
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What are the other treatments for T2DM?
Target BP 140/80 mmHg
– 130/80mmHg if kidney, eye or cerebrovascular damage. Complications include: – Renal impairment: Retinal damage, increased CVD risk. ACE-Is first line. ACE-I and ARB (reduced microalbuminaemia, CKD, CV risk)
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Describe features of lipid therapy
For patients with T2DM, add atorvastatin if Q risk Score >10% after lifestyle modification as primary prevention. Retinopathy (very high risk of CVD). Baseline blood test: thyroid, renal/hepatic tests, CK levels, lipid profile. For T1DM: >40 years age, CK
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What are the monitoring requirements for T2DM? (1)
HbA1c levels– 3-6 monthly. BP monitoring, Lipid profile monitoring, renal function. Annual monitoring for complications
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What are the monitoring requirements for T2DM? (2)
Do not routinely offer self-monitoring of blood glucose levels for adults with type 2 diabetes unless: the person is on insulin or there is evidence of hypoglycaemic episodes or, the person is on oral medication that may increase their risk of hypoglycaem
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What are the educational points for T2DM?
New medicines. Exercise. Reduce weight (reduce portion size). Type of diet (glycaemic index, carbohydrate reduction, increase fruit/veg, wholegrains, pulses, low salt/sugar/saturated fats in diet). Not to have diabetic diets (high amount of fat)
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Outline the pathophysiology of prerenal AKI
Response to decrease in renal blood flow by increase in vasodilating PGs (blunted by NSAIDs that inhibit PG production). Response to decrease in renal blood flow by preferred constriction of efferent arteriole by angiotensin II (blunted by ACE-I/ARBs)
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What is a structured education course?
Offer all adults with type 1/2 diabetes a structured education programme of proven benefit, for example the DAFNE (dose-adjustment for normal eating) or DESMOND (Diabetes Education for Self Management in the Ongoing and Newly Diagnosed) programme.
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What are the risk factors for hypoglycaemia?
Increasing age, insulin and sulphonylureas, rigid glycemic control, poor eating habits, impaired renal function, alcohol intake, accelerated absorption (e.g. exercise, injecting into muscle by mistake, changing site of injection. Medication errors, ACE-I,
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Give examples of adrenergic effects
Sweating, tachycardia, palpitations, hunger, restlessness, trembling
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Give examples of neuroglycopenic effects
Confusion, slurred speech, drowsiness, abnormal behaviour (anxiety, agitation, aggression), visual disturbance, loss of consciousness, seizures, coma
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Describe features of hypoglycaemia management
Short-acting carbs. 4-7 glucose tablets. 5 large jelly babies or seven large jelly beans. 150–200ml of pure fruit juice but not orange juice in patients with CKD. Three or four heaped teaspoons of sugar dissolved in water. Glucagon IM or SC 1 mg (long-act
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What is the DVLA advice for patients who have diabetes and are taxi drivers?
Not to drive if impaired awareness of hypoglycaemia. Check BG no more than 2 hours before driving. Check glucose every 2 hrs. BG must be > 5mmol/l. For taxi drivers, lorry and bus drivers need to ensure that the monitors record the readings for the past 3
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Card 2

Front

State features of type 1.5 diabetes

Back

Latent Autoimmune diabetes in adults. Gradual autoimmune destruction of pancreatic beta cells. Commonly presents with a slower onset in patients >30 yrs old. NOT linked to insulin resistance

Card 3

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State features of maturity-onset diabetes of the young

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Preview of the front of card 3

Card 4

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State features of type 2 diabetes

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Card 5

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What is diabetic ketoacidosis?

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