Diabetes Flashcards
(75 cards)
1
Q
what is diabetes?
A
- Diabetes is a lifelong health condition that occurs when the blood glucose level is too high (hyperglycaemia) because the body can’t use it properly
- This is caused by a dysfunction in insulin production or reduced sensitivity
- Untreated hyperglycaemia can cause serious health complications
- Two most common types - type 1 and type 2. They’re different conditions, caused by different things
2
Q
Diabetes pathophysiology
A
- Insulin is a hormone produced by the pancreas that plays a very important role in our bodies
- After we eat, we begin to digest carbohydrates, breaking them down into glucose
- The insulin released by the pancreas moves the glucose into our cells, where it is used as fuel for energy
3
Q
Type 1 vs Type 2
A
- Type 1 diabetes – the body’s immune system attacks and destroys the β-cells in the pancreas that produce insulin
- Type 2 diabetes – the body doesn’t produce enough insulin, or the body’s cells don’t react to it (insulin resistance)
4
Q
What is type 1 diabetes
A
An autoimmune condition where the body attacks and destroys the β-cells of the islets of Langerhans in the pancreas
* This results in an absolute deficiency of insulin
* This causes hyperglycaemia
* Usually occurs in childhood and young adults (but not always!), peak age is 10-14 years old
* About 10% of people with diabetes have type 1
5
Q
Causes of type 1 diabetes
A
genetic predisposition, environmental triggers of immune response (not yet fully known)
6
Q
What is type 2 diabetes
A
- The body doesn’t make enough insulin, or the insulin it makes doesn’t work properly (insulin resistance)
- This causes hyperglycaemia
- Type 2 diabetes is caused by a complex interplay of genetic and environmental factors
- About 90% of people with diabetes have type 2
7
Q
Causes of type 2 diabetes
A
age, obesity, ‘Western’ diet, sedentary lifestyle, metabolic syndrome, genetics (family history & ethnicity), previous gestational diabetes, polycystic ovary syndrome, some medication
8
Q
Medications that cause hyperglycaemia
A
- Beta blockers
- Anti psychotics
- Thiazide like diuretics
- Loop diuretics
- Corticosteroids
- Statins
9
Q
Medications that cause hypoglycaemia
A
- Alcohol
- Aspirin
- Morphine
- Nifedipine
10
Q
Other causes of diabetes
A
- Polycystic Ovary Syndrome (PCOS)
- Pancreatitis or pancreatectomy
- Cushing’s syndrome - increased production of cortisol hormone may increase blood glucose levels
- Steroid induced diabetes - due to prolonged use of glucocorticoid therapy
11
Q
Other types of diabetes
A
- Maturity-onset diabetes of the young (MODY)
- Latent autoimmune diabetes of adults (LADA)
- Gestational diabetes
- Neonatal diabetes
12
Q
signs and symptoms of diabetes
A
- The symptoms occur because of hyperglycaemia & because glucose isn’t used as fuel for energy
- The main symptoms common to both types are:
O urinating more often than usual (polyuria)
O feeling thirsty & drinking more (polydipsia)
O lethargy
O unexplained weight loss
O frequent episodes of thrush or UTIs
O cuts or wounds that heal slowly
O blurred vision
13
Q
type 1 presentation
A
symptoms usually obvious and develop very quickly (over a few weeks)
* Undiagnosed patients are often admitted to hospital with diabetic ketoacidosis (DKA)
14
Q
Type 2 presentation
A
the symptoms aren’t always as obvious; they are often mild and develop gradually over a number of years
* Often diagnosed during a routine check-up
* This means patients may have type 2 diabetes for many years without realising it
15
Q
Type 1 diagnosis
A
presenting with hyperglycaemia, people with type 1 diabetes typically have one or more of:
* ketosis
* rapid weight loss
* age of onset below 50 years
* BMI below 25 kg/m2
* personal and/or family history of autoimmune disease
* Antibodies confirms type 1 diabetes
16
Q
consider type 2 diabetes if
A
obese, strong family history, black or Asian, low insulin requirements, low blood/urine ketones, evidence of insulin resistance
with symptoms:
* Random blood glucose level >11.1mmol/L
* Fasting blood glucose level > 7mmol/L
* Oral glucose tolerance test (2 hours post 75g of carbohydrate) – blood glucose of 11mmol/L or more
* Patients should also be assessed for the presence of proteins in the urine & ketones in the blood (or urine)
* HbA1c (glucose saturation of the haemoglobin) – if this is high it indicates hyperglycaemia for several months
17
Q
The rationale for diabetes treatment
A
Optimise glycaemic control
Treat hyperglycaemia and prevent hypoglycaemia
18
Q
treatment of type 1 diabetes
A
- Insulin is a life-saving treatment for these patients
- Without insulin these individuals would develop severe hyperglycaemia — resulting in ketoacidosis & death
- Management of type 1 diabetes with insulin aims to:
- Control the symptoms of hyperglycaemia
- Prevent diabetic ketoacidosis
- Prevent microvascular complications (retinopathy, nephropathy and neuropathy)
- Avoid the development of macrovascular complications (cardiovascular and peripheral vascular problems) in later life
19
Q
Basal Bolus regimen
A
- The aim is to try to mimic normal physiological insulin release
- These regimens involve injecting a long- or intermediate-acting insulin once or twice a day, plus a bolus injection of a short-acting insulin before each meal
- The bolus insulin injections control post-prandial peaks in glucose levels and the daily insulin injections regulate basal hepatic glucose output
20
Q
Biphasic regimen
A
- A mixture of short and long acting insulin in a fixed dose preparation can be used as an alternative to the basal bolus regimen
- This is known as a biphasic regimen and is usually injected twice a day
- Only if basal bolus does not allow the patient to meet targets, or is not suitable for other reasons
21
Q
Types of insulin
A
- Can be derived from animals (porcine or bovine), humans, or insulin analogues can be synthesised
- Animal insulin is no longer commonly used in the UK
- Human insulins carry a higher risk of hypoglycaemia than analogues (less predictable absorption), but analogues are more expensive and there are concerns over an increased risk of cancer
- The main types of insulin are classified as long-acting, rapid/short-acting, intermediate-acting, and biphasic
- The onset of action, peak activity and duration of action differs and they are all subject to interpatient variability
22
Q
Long acting insulins
A
- In general, the start working 2-3 hours after administering, and last for 16-24 hours or more. * Insulin detemir (Levemir) is first line
- Second line: insulin glargine (Lantus/Abasaglar/Toujeo)
- Ideally administered twice daily but can be once daily
- Insulin degludec (Tresiba) has recently been launched and has a longer duration of action than insulin glargine and levemir – lasts up to 42 hours so doesn’t need to be administered at the same time everyday
- Used as the ‘basal’ insulin in basal-bolus regimens
23
Q
Rapid and short acting insulins
A
- Rapid acting start working 15 mins after administering, lasts 3-5 hrs
- Short acting works within 30-60 mins and lasts up to 8 hours
- Rapid acting insulin analogues and short acting insulin human insulin
- Should be administered before meals to control blood glucose levels during and after eating
- The main advantage of the rapid-acting insulin analogues over shortacting insulins is the reduced risk of severe hypoglycaemia
- Another advantage of rapid-acting insulin analogues is that they can be injected just before a meal
- The ‘bolus’ insulin in basal-bolus regimens
24
Q
Intermediate acting insulins
A
- Isophane or neutral protamine Hagedorn (NPH) insulin
- An intermediate duration of action, given once or twice a day & do not need to be co-ordinated with meals
- If administered at bedtime, then a peak in insulin activity will occur overnight when glucose levels are low — increasing the risk of nocturnal hypoglycaemia
- Concerns about this can prevent patients from achieving optimal glucose control (they tend to use lower doses of insulin at night to prevent hypoglycaemia occurring
25
Biphasic insulins
* Biphasic insulins contain a mixture of a rapid or short-acting insulin and an intermediate-acting insulin
* The rapid or short-acting component covers the post-prandial rise in blood glucose, and the intermediate acting component provides basal glycaemic control
* They are usually injected twice daily
* NICE recommends these regimens be used if keeping the number of daily injections at a minimum is an important factor
* Can also help people who find adherence to lunchtime insulin injections difficult, or for adults with learning difficulties who may require assistance from others
26
Insulin pumps
* Deliver a varied dose of rapid/short acting insulin continuously at a pre-set rate (basal rate)
* Can be altered in small increments
* When patients eat, they press a button on the pump to deliver an extra bolus dose
* NICE recommends insulin pump therapy for adults and children with type 1 diabetes, provided that attempts to achieve target HbA1c with multiple daily injections have resulted in disabling hypoglycaemia or if HbA1c has remained high with other regimens despite a high level of care
* Hybrid closed loop systems are new technology
27
skin related effects to insulin treatments
* Repeated use of the same injection site increases the risk of lipoatrophy and lipohypertrophy
* Lipohypertrophy is the most common complication
* Areas affected will become relatively pain-free to inject into — causing patients to use these areas more
* However, absorption of insulin from these areas can be erratic leading to difficulties in achieving optimal blood glucose control
* The likelihood of lipoatrophy and lipohypertrophy can be reduced by regular rotation of injection sites
28
insulin choice consideration
* Patient preference
* Age
* Comorbidities
* Agreed targets
* Hypoglycaemia patterns
* Work patterns (e.g. shift working)
* Pre-meal blood glucose readings
* Pre-bed glucose readings
29
Insulin safety
* Incidences of severe harm and death caused by 10-fold dosing errors as a result of abbreviating the word “unit”
* The NPSA sent out a rapid response alert in 2010 to address the main types of error and avoid further incidents
* A second alert recommending that all adult patients on insulin should receive an “insulin passport” to provide accurate identification of the insulin products they are using and ensure this information is shared between healthcare settings
* Issues surrounding ‘high strength’ insulins
30
Carbohydrate counting education
* Structured group education programme: DAFNE
* Ensure that any programme includes the following:
* It is evidence-based, & suits the needs of the person
* It has specific aims and supports the person/carers to self-manage
* It is delivered by trained educators
* It is quality assured and reviewed
* The outcomes are audited regularly
* Patients need to be competent and motivated * Some trial and error is needed to know how many units to give per gram of carbohydrate
31
oral antidiabetics for type 1 diabetes
* Metformin - consider adding metformin to insulin therapy in adults with type 1 diabetes if:
* They have a BMI of ≥25 kg/m2 (or ≥23 kg/m2 for people from South Asian and related minority ethnic groups)
* They want to improve their blood glucose control while minimising their effective insulin dose.
32
other treatment options for type 1 diabetes
* Whole-organ pancreatic transplantation for the treatment of type 1 diabetes has largely been reserved for those undergoing renal transplantation for end-stage diabetic nephropathy
* Although normalisation of glycaemic control is achieved following successful transplantation, this option carries the burden of ongoing immunosuppressive medication and the risk of pancreatic graft rejection
33
Treatment of type 2 diabetes
* Metformin
* Sulphonylureas
* Thiazolidineodiones (‘glitazones’)
* DPP-4 inhibitors (‘gliptins’)
* SGLT-2 inhibitors
* GLP-1 agonists
* Insulin, usually not first-line (but not always)
34
NICE type 2 guidelines
* Ensure that the person has an individualized care plan, taking into account their age, preferences, co-morbidities, and risk of adverse effects from polypharmacy and their likelihood of benefiting from long-term interventions.
* Offer referral to a structured group education programme such as the DESMOND (Diabetes Education for Self-Management for Ongoing and Newly Diagnosed) programme, for the person and their family/carers.
* This should be offered at or around the time of diagnosis, with annual reinforcement and review.
* Ensure that the person and their family/carers know how to contact the specialist diabetes team, if appropriate.
35
NICE first line type 2
* Assess HbA1C, CVD risk and kidney function
Not a CV risk- metformin
Heart failure or established ASCVD- Dual therapy- metformin and SGLT2i once tolerating metformin
High risk of CVD (QRISK>10%)- metformin and consider SGLT2i once tolerance of metformin confirmed
36
Metformin
* First-line as monotherapy if no CVD Risk
* Mechanism of action:
* Suppresses glucose production by the liver
* Increases insulin sensitivity
* Side-effects:
* GI (commonest is diarrhoea), lactic acidosis (rare)
* In renal impairment:
* Safe if eGFR >45ml/min/1.73m2
* Reduce dose if eGFR 30-45ml/min/1.73m2
* Stop if <30ml/min/1.73m2
37
SGLT2 inhibitors
* CVD/HF – Add in as soon as tolerability of metformin confirmed
* Qrisk >10% consider adding once tolerability of metformin confirmed
* Dapagliflozin, empagliflozin, canagliflozin, ertugliflozin
* Mechanism of action:
* Reduces glucose resorption in the kidney
* Increases urinary glucose secretion
* Side-effects:
* glycosuria (glucose in urine)
* candida genital infections
* Requires a degree of renal function to work
* Mild weight loss
38
SGLT2 caution
Mycotic genital infections
* Fournier's gangrene extremely rare, no definite association
* 'Association not causation'…T2DM is the greatest risk factor
* Estimated 1 in 100,000 cases per year
* Refer if severe pain, erythema, tenderness, swelling with malaise or fever
UTIS
* Initial concerns around this, but recent trials have not demonstrated an increase in UTIs
Lower limb amputations
In CANVAS, the CV outcome trial for canagliflozin there was a significant increase in LLA mainly toes in the treatment group. Absolute increase or 4 cases per 1000 patient-years Evidence base moving away from concerns Real world retrospective study May 2021: 3 million pts with T2DM 170,000 on SGLT2i No increased risk of amputation for pts treated with SGLT2i vs those on GLP1, lower risk than in those treated with DPP4 or other agents * Ensure good foot care advice in place
39
SGLT2 and DKA
Risk of DKA even with only mildly elevated blood glucose levels. Avoid SGLT-2 inhibitors in people with
* Any other diabetes diagnosis apart from T2DM (e.g. avoid in type 1,LADA,type 3c)
* History DKA
* Ketogenic diet
* Acutely unwell Use in caution
* Lower BMI or weight loss
* frail, cognitive concerns
* Risk of hyperglycaemia due to non concordance or very high HbA1c
40
Sulphonylureas
* Gliclazide, glipizide, glibenclamide, glimepiride, tolbutamide
* Mechanism of action:
* stimulates β-cells in pancreas to release insulin
* do NOT stimulate them to produce it
* This continues even if a meal is missed
* Side-effects:
* Hypos, weight gain
* Dose reduction needed in renal impairment
41
Thiazolidineodines
* Pioglitazone
* Mechanism of action:
* increases insulin sensitivity
* Side-effects:
* peripheral oedema
* heart failure
* weight gain
* Pioglitazone contraindicated in heart failure, active or past history of bladder cancer, caution in elderly as increased risk of bone fractures
42
DPP4 inhibitors
* Gliptins: sitagliptin, saxagliptin, linagliptin, alogliptin, vildagliptin
* Mechanism of action:
* stimulate pancreas to produce more β-cells by Inhibiting dipeptidylpeptidase4 enzyme
* this results in more insulin production
* Side-effects:
* abdominal pain- pancreatitis, GORD, headaches
* Renal failure: most need dose reductions, linagliptin does not
43
GLP1 agonists
* Glucagon-like peptide-1 agonists: exenatide, liraglutide, lixisenatide, dulaglutide, semaglutide
* Mechanism of action:
* enhance glucose-dependent insulin secretion * slow gastric emptying
* reduce postprandial glucagon
* Benefits:
* weight loss, low risk of hypos, cardiovascular benefits for liraglutide, dulaglutide and injectable semaglutide
* Side-effects:
* GI symptoms, increased risk of pancreatitis
* See later slide for restrictions on prescribing
* Semaglutide available orally – Rybelsus
44
GLP1 and GIP agonist
* New class of medication- currently only tirzepatide (brand name Mounjaro)
* GIP hormone from duodenum K cells and GLP-1 from ileum L cells stimulate pancreas to secrete insulin. Tirzepatide has similar activity to native GIP hormone on GIP receptors and lower activity than native GLP-1 hormone on GLP-1 receptors.
* Also slows gastric emptying and increases satiety, reduces postprandial glucagon, increases insulin sensitivity
* Awaiting cardiovascular outcome trial results * Benefits:
* weight loss, low risk of hypos
* Side-effects:
* GI symptoms, increased risk of pancreatitis
45
first intensification of therapy
Intensification for patients who can take metformin
* If initial treatment with metformin has not continued to control HbA1c, consider dual therapy with:
* metformin and SGLT2i where this the QRISK >10% or already have established HF or ASCVD
* metformin and a DPP-4 inhibitor or
* metformin and pioglitazone or
* metformin and a sulfonylurea
46
patients who can't tolerate metformin
* If metformin is contraindicated or not tolerated and initial drug treatment has not continued to control HbA1c, consider dual therapy with:
* SGLT2i if they have HF or ASCVD
* a DPP-4 inhibitor and pioglitazone or
* a DPP-4 inhibitor and a sulfonylurea or
* Pioglitazone and a sulfonylurea
* If dual therapy is not adequate, consider either:
* triple therapy with:
* metformin, SGLT2i, a DPP-4 inhibitor and a sulfonylurea or
* metformin, a DPP-4 inhibitor and a sulfonylurea or
* metformin, pioglitazone and a sulfonylurea or * Start insulin-based treatment
47
second intensification of therapy
* Or, if the above is not tolerated or contraindicated, consider combination therapy with a GLP-1 mimetic OR a GLP-1/ GIP agonist for patients who: have a BMI of ≥35 kg/m2 and specific medical problems associated with obesity or have a BMI
48
Insulin treatment in type 2 diabetes
* Continue metformin if appropriate - review the continued need for other blood glucose lowering drugs
* Used as rescue treatment at any stage in type 2 diabetes for symptomatic hyperglycaemia (or a sulphonylurea) – review when target blood glucose achieved
* Other regimens, such as basal-only, or basal-plus (injecting daily basal insulin plus one single injection with a main meal), can be useful in type 2 diabetes
* These regimens are not routinely used for patients with type 1 diabetes because they do not deliver sufficient glycaemic control
* First-line: NPH insulin once or twice daily
* Second-line: add in short-acting insulin to NPH * Third-line: basal only with long-acting insulin
* Fourth-line: twice daily pre-mixed (biphasic) preparations that include short-acting insulin analogues
* Consider adding short-acing insulin before meals to these regimens if needed
* A GLP-1 mimetic in combination with insulin - specialist initiation only
* SGLT-2 inhibitors in combination with insulin with or without other antidiabetic drugs are also an option
49
monitoring
* HbA1c: long-term blood glucose control – indication of average blood glucose over 2-3 months
* Aim for below 48 mmol/mol (should be below 59mmol/mol), but the target can be adjusted based on patient specific factors
* Ensure that aiming for an HbA1c target is not accompanied by problematic hypoglycaemia in adults with type 1 diabetes
* NICE recommends that patients should have their HbA1c checked every 3-6 months
* Keeping this value within range can help prevent the long-term microvascular and macrovascular complications of diabetes
50
Type 1 monitoring
* Blood glucose: frequency of monitoring will be different for each patient (at least 4 times a day)
* Factors that determine the frequency of blood glucose monitoring: target HbA1c, driving status, the level of control required, physical activity level, during pregnancy and breast feeding, patient preference, risk of hypoglycaemia and illness (during times of illness a period of more frequent monitoring may be needed)
* Optimal targets for blood glucose levels:
* pre-prandial blood glucose level of 4-7mmol/L * post-prandial blood glucose level of 5-9mmol/L
* Ketones: patients should also be taught how to test themselves for urinary or blood ketones to help avoid diabetic ketoacidosis, eg, during times of illness.
51
type 2 monitoring
* Blood glucose: do not routinely offer self-monitoring of blood glucose levels in 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 hypoglycaemia while driving or operating machinery or
* the person is pregnant, or is planning to become pregnant
* Consider short-term self-monitoring of blood glucose levels (and review treatment as necessary) to confirm suspected hypoglycaemia
52
Complications
* Diabetic ketoacidosis (DKA)
* Hyperosmolar hyperglycaemic state (HHS)
* Management of hypoglycaemia
* Treatment of diabetes is a balance between managing hyperglycaemia and preventing hypoglycaemia
* Maintaining a low HbA1c is associated with less micro and macrovascular complications, but a higher incidence of hypoglycaemia
* Long-term complications
53
DKA
* Left untreated, hyperglycaemia can lead to diabetic ketoacidosis (DKA)
* Because glucose cannot be used by the body, fat & muscle are used as an alternative source of energy:
* Insulin suppresses lipolysis; in its absence, fat is broken down
* The resulting free fatty acids are converted into ketones in the liver
* Ketones are acidic, and their accumulation results in acidosis
* Clinical features:
* dehydration, nausea, vomiting, abdominal pain, irritability, drowsiness and, in extreme cases, coma & death
* Fruit-smelling breath indicates the presence of excess ketones
* Diagnosis:
* symptoms, a history of diabetes, blood glucose of greater than 11mmol/L, blood ketones of greater than 3 or urine greater than 2, bicarbonate less than 15 or pH less than 7.3
54
Treatment of DKA
* Fluids including potassium replacement (NaCl 0.9% and KCl), insulin
* Fixed rate insulin infusion (FRII):
* IV insulin - 50 units of Novorapid in 50ml NS
* Rate - 0.1 units/kg/hour
* Hourly blood glucose and ketones, 2 hourly potassium and blood pH
* Increase rate by 1 units/hour if not responding to max. 50 units/hour
* Long-acting insulin should continue (if known diabetic)
* Insulin causes potassium to enter cells so replacement is needed to avoid hypokalaemia (low potassium)
* Once blood glucose has fallen to 10–15 mmol/L, give glucose containing fluids to allow continued infusion of insulin at a sufficient rate to clear ketones
* Discontinue FRII when ketones less than 0.6 and pH greater than 7.3
* If E&D - normal S/C insulin, if not E&D - variable rate insulin infusion
55
Hyperosmolar hyperglycaemic state
* Untreated hyperglycaemia in people with type 2 diabetes causes HHS more commonly than DKA
* This causes hyperglycaemia and dehydration (hyperosmolarity) but not ketoacidosis
* Similar symptoms to DKA (but no ketoacidosis)
* Develops more slowly than DKA
* Treatment aims to correct dehydration before correcting hyperglycaemia
* Treatment:
* IV fluids (NaCl 0.9%) first (before insulin)
* If not improving, start IV insulin
* Aim for a low rate of decreasing blood glucose
56
Hypoglycaemia
* Hypoglycaemia: a blood glucose level of <4mmol/L
* A common side-effect of some antidiabetic treatments
* Can cause considerable anxiety for patients
* Warning signs vary between individuals; can include:
* Feeling hungry
* Trembling or shakiness
* Anxiety or irritability
* Sweating and going pale
* Fast pulse (tachycardia) or palpitations
* Tingling of the lips & cold extremities
* Blurred vision
* Signs of a more severe episode: confusion, irrational behaviour, seizures and coma
57
Hypoglycaemia Treatment
* If able to eat or drink:
* 15–20g of a short-acting carbohydrate (Lucozade; Glucojuice; 4 or more Dextrose tabs; Hypostop gel; 120ml glass of non-diet soft drink; five sweets such as jelly babies; 150–200ml glass or carton of fruit juice
* Then give a starchy carbohydrate
* If not able to swallow:
IV glucose
Recheck blood glucose in 15 minutes
Consider what insulin is still in the body as it may still be absorbed over the next few hours
* Glucagon
58
Implication of hypoglycaemia
* Loss of hypoglycaemia awareness
* Fear of hypos may result in deliberate aiming of high blood glucose to avoid
* Hospital admissions
* Implications for driving and employability
59
Long term complications
* 80% of the financial impact of diabetes on the NHS is spent on the complications of diabetes
* Microvascular: nephropathy, peripheral neuropathy, autonomic neuropathy and retinopathy
* Macrovascular: premature cardiovascular, cerebrovascular and peripheral vascular disease * A combination of micro- and macrovascular disease may give rise to diabetic foot disease, which can result in limb amputation
* Poor glycaemic control will hasten the progression of these long-term complications
60
microvascular complications
* Nephropathy management: control blood pressure (ACE inhibitors, ARBs), manage hyperglycaemia, treat hyperlipidaemia
* Peripheral neuropathy management: optimise glycaemic control, treatment of neuropathic pain (duloxetine, amitriptyline, pregabalin, gabapentin)
* Autonomic neuropathy: causes postural hypotension, gastroparesis, erectile dysfunction
* Retinopathy management: optimise blood glucose control, regular eye examinations needed
61
macrovascular complications
* Target blood pressure
* Antihypertensives: ACE inhibitors, ARBs, calcium channel blokers (amlodipine), doxazosin, diuretics
* Cholesterol lowering agents: use QRISK assessment tool - if 10 year risk >10% offer primary prevention; statins, ezetimibe, fibrates, bile acid binders
* Aspirin is no longer recommended for primary prevention in patients with diabetes
62
Diabetic foot disease
* Foot ulceration is responsible for more hospital days than all other diabetes complications combined
* Diabetes is the most common cause of non-traumatic limb amputations, with 80% of cases being preceded by foot ulcers
* Mortality rates are high, with 50% of patients dying within five years of developing a diabetic foot ulcer, which rises to 70% if the patient has an amputation because this is believed to be associated with cardiovascular disease
* Charcot neuroarthropathy ‘Charcot foot’
63
Diabetes in pregnancy
* Establish good glycaemic control before conception
* High risk of hypos especially in the first trimester
* High risk of miscarriages, congenital malformations, still birth, neonatal death
* Give folic acid 5mg/day, stop ACE inhibitors & statins
* Labour: hourly blood glucose (aim 4-7mmolL); IV glucose and insulin
* Risk of neonatal hypoglycaemia
* Also high risk of hypos for the mother after birth
64
Diabetes in children
* Usually type 1 but increasing incident of type 2 (& MODY)
* Consider other types if:
* Obese, strong family history of type 2/MODY, black or Asian background, low insulin requirements, low blood or urine ketones, evidence of insulin resistance
* Optimal target ranges for blood glucose control are:
* 4–7 mmol/L pre-prandial; 5–9 mmol/L post-prandial
* A HbA1c target level of 48 mmol/mol or lower is ideal but should be personalised to the patient and a balance between target without frequent disabling hypos
* Education and access to support systems is essential
65
Patient education
* Important because patients need to be motivated to optimise glycaemic control
* Physical activity: can reduce their enhanced cardiovascular risk in the medium and longer term
* Dietary advice
* Sick day rules
* DVLA advice
66
Dietary advice
* No special diet is advised
* The NHS provides the following diet advice:
* Eat plenty of starchy carbohydrates (low GI)
* Increase the amount of fibre
* Eat plenty of fruit and vegetables
* Cut down on fat and saturated fat in particular * Cut down on sugar
* Cut down on alcohol
* Keep hydrated
* Carbohydrate counting for type 1
* Discourage the use of foods marketed for people with diabetes
67
sick day rules
* Usually causes hyperglycaemia but may cause hypos if not eating and continuing usual treatment
* Type 1 and 2 if having insulin: do NOT stop taking insulin; monitor blood glucose more regularly – adjust insulin dose accordingly
* Type 2 with other anti-diabetic drugs: continue taking tablets, but hold metformin and SGLT-2 inhibitors if vomiting or have diarrhoea; hold GLP-1 agonists and seek medical advice if acute onset abdominal pain, nausea and vomiting; monitor blood glucose if have a meter;
* If not eating have carbohydrate containing food or drinks
* Treat hypos if necessary
* SADMAN rules: There are several classes of drugs that should be temporarily stopped in conditions that could lead to complications
* Once the person is feeling better and able to eat and drink for 24– 48 hours, these medications should be restarted.
68
DVLA advice
* Must inform the DVLA if advised by clinician
* Insulin treatment – must always inform the DVLA
* Oral antidiabetics or other injectables that are not insulin – do not need to inform the DVLA if: * no more than 1 episode of severe hypoglycaemia in the last 12 months
* if needed, detection of hypoglycaemia is by appropriate blood glucose monitoring at times relevant to driving and clinical factors, including frequency of driving
* under regular review
69
What antiglycaemic is used to quickly treat symptomatic diabetes
Gliclazide
70
what does ACR test for
kidney function- ratio of 3 or above is classed as proteinuria and kidney dysfunction
71
key test results that indicate DKA
Blood ketones >3
Blood glucose >11
pH <7.3
72
What is HHS
Hyperosmolar hyperglycaemic state (HHS) can happen when people with type 2 diabetes – or undiagnosed type 2 diabetes – have very high blood glucose levels, also called blood sugar levels. By the time HHS is diagnosed your blood sugar levels can often be over 40mmol/l.
73
what is the general definition of hypoglycaemia
- Blood sugar below 4mmol/L
74
what oral antiglycaemics are the least effective
DPP4 inhibitors- gliptins
75
what 2 antidiabetic drugs should NOT be used in combination
gliptins and GLP1 inhibitors- because they provide little additional benefit and have increased costs and side effects
