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75 Cards in this Set
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- Back
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What is the advice to patient's with a risk of developing hypoglycaemia and why? |
advice to patients is "four's the floor"
- symptoms typically occur at glucose ~3.6mmol/L |
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When do symptoms of hypoglycaemia typically occur? |
Symptoms typically occur at glucose ~3.6 mmol/L - but this may vary between individuals - phenomenon called "false hypoglycaemia" - patients with consistently high glucose levels may experience symptoms of hypoglycaemia at a higher level than someone with good glycaemic control |
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What is false hypoglycaemia? |
false hypoglycaemia" - patients with consistently high glucose levels may experience symptoms of hypoglycaemia at a higher level than someone with good glycaemic control |
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What are causes of hypoglycaemia ? |
- Imbalance between carbohydrate and insulin or sulfonylurea therapy - exercise with too much insulin or not enough carbs - alcohol - can cause hypoglycaemia even in non-diabetic people - vomiting - breastfeeding
remember other medical causes: - liver disease - progressive renal impairment - hypoadrenalism (is associated with type 1 diabetes) - hypothyroidism - hypopituitarism (rare) - insulinoma (rare)
In a person with Type 1 DM, new onset of hypoglycaemia can occur with new diagnosis of hypoadrenalism or adult coeliac disease, which are commoner in patients with type 1 DM |
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What are the signs and symptoms of hypoglycaemia? |
Autonomic symptoms - glucose ~3.6 mmol/L - sweating - shaking or tremor - anxiety - palpitations - hunger - nausea
Neuroglycopenic symptoms - glucose ~2.7 mmol/L - confusion - slurred speech - visual disturbances - drowsiness - aggression |
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What are the problems with hypoglycaemia unawareness? |
- Loss of early warning signs of hypoglycaemia early onset of a hypo - Increased risk of having severe hypo requiring third party assistance bed”) - Increased risk of road traffic accidents, hence implications for driving |
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What are the causes of hypoglycaemia unawareness? |
- increased duration of diabetes - very tight glycaemic control - autonomic neuropathy |
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How do you reverse hypoglycaemic awareness? |
Reversal: - Strict hypoglycaemia avoidance by relaxing glycaemic control |
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How do you treat mild hypoglycaemia? |
Mild (conscious, lucid, able to self treat) - 5-7 glucose tablets, or 3-4 heaped teaspoons of sugar in water |
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How do you treat moderate hypoglycaemia? |
Moderate (conscious, but can’t self administer and needs help) * Glucogel– 1-2 tubes buccally, or jam, honey, treacle massaged into the cheek. * Intramuscular glucagon |
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How do you treat severe hypoglycaemia? |
Severe (unconscious) - Do not put anything in the mouth - Administer 0.5-1mg glucagon IM In hospital, administer IV glucose - 50mls 50% glucose can be given, but take care with veins – extravasation can cause chemical burns |
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If a severely hypoglycaemic patient (unconscious) comes into hospital, how do you treat them? |
In hospital, administer IV glucose - ideally 75 mL of 20% glucose or 150 mL 10% glucose over 15 minutes - 50 mls 50% glucose can be given, but take care with veins - extravasation can cause chemical burns |
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How do you treat the patient after a hypoglycaemic episode? |
Post hypo once glucose above 4.0 mmol/L, must have some longer acting carbs, eg: * Two biscuits * One slice of bread/toast * 200-300ml glass of milk (not soya) * Normal meal if it is due (but must contain carbohydrate) |
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What is the advice you give for hypoglycaemia and driving? |
Use of insulin does not prohibit driving cars nor large vehicles * Advice to all drivers on insulin * Plan driving in advance * Always carry carbs in the car * Check blood glucose before driving * Check blood glucose every 2 hours * At first signs of a hypo stop as soon as it is safe to do so * Leave the drivers seat and remove the key * Do not drive again until fully recovered * All drivers on insulin must inform DVLA and insurance company (if they fail to do so, they will not be covered) * Licence will be revoked if one or more severe hypo requiring third party assistance |
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What would make you consider that a patient was suffering from nocturnal hypoglycaemia? |
- high blood glucose levels (rebound hyperglycaemia) - headaches - feels 'hungover' despite no alcohol - confirm by advising testing blood glucose levels during the night (3 am) or using continuous glucose monitoring sensor (CGMS), which monitors glucose over 5 days subcutaneously |
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How do you manage nocturnal hypoglycaemia? |
- analogue insulins - pre bed snack - change timing of insulin - insulin pump therapy |
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What is diabetic ketoacidosis? |
A state of absolute or relative insulin deficiency resulting in hyperglycaemia and an accumulation of ketoacids in the blood with subsequent metabolic acidosis
- hyperglycaemia - blood glucose >14 mmol/L - acidosis - pH <7.30, bicarbonate <15 mmol/L - ketosis - elevated serum or urine ketones |
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What is the pathogenesis of DKA? |
1. Catecholamines excess (unopposed) - promote triglyceride breakdown to free fatty acids (FFA) and glycerol - stimulates gluconeogenesis
2. Insulin deficiency - inhibits gluconeogenesis
3. Ketosis due to FFA metabolism due to absolute or relative deficiency of insulin - acidosis is caused by ketone body accumulation - 3 hydroxy butyric (3-OH-butyric) acid and acetoacetic acid
4. Ketosis is terminated instantaneously by insulin
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How do you stop DKA? |
Ketosis is terminated instantaneously by insulin |
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What are the clinical features of DKA? |
- often a short history - abdominal pain and vomiting is common - can present as an acute abdomen - Kussmaul’s respiration - deep sighing respirations due to acidosis - Ketones on breath (remember ~40% of people cannot smell these) - drowsiness, confusion
- dehydration and tachycardia |
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What electrolyte losses are seen in DKA? |
Losses in DKA: * Water 6-8 litres
* Sodium 500-1000 mmol
* Chloride 350 mmol
* Potassium 500-1000 mmol
* Calcium 50-100 mmol
* Phosphate 50-100 mmol
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Magnesium 25-50 mmol |
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What are precipitating factors to DKA? |
- insulin omission - infection - pregnancy - myocardial infarction - intoxication/drugs
- unknown in ~40% |
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How do you diagnose DKA? |
- venous blood gases show acidosis (pH <7.35, bicarb <15) - capillary blood glucose (CBG) - usually over 14 mmol/L, but can be lower (euglycaemic ketosis or alcoholic ketosis) - frequently raised urea and creatinine
- urine or plasma ketones - elevated |
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What investigations would you perform for DKA? |
- pregnancy test - ECG/ CXR - MSU/ blood cultures - biochemical profile / lab glucose - FBC
- HbA1c |
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How do you assess the severity of DKA? |
Greater severity of DKA if any of the following: - blood ketones >6 mmol/L - bicarbonate <5 mmol/L - pH <7.1 - potassium <3.5 mmol/L
- GCS<12 |
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What is the supportive management and monitoring of a DKA patient? |
- level 2 bed (high dependency unit) - cardiac monitor - nasogastric tube if impaired conscious level - consider central venous pressure line - especially in elderly - oxygen if PaO2 <10.5 kPa on air - urinary catheter - prophylactic LMW heparin - IV antibiotics as appropriate if suspected infection
- frequent monitoring of conscious level, BP, pulse, temp, glucose, urine output, potassium, acidosis |
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What is urine output like in a DKA patient? |
Excessive urine production is seen; as well as signs of dehydration and tachycardia |
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What is the fluid therapy for a patient with DKA? |
Sodium chloride 0.9% - 1 Litre stat - 1 Litre in 1 hour - 1 Litre over 2 hours (+20 mmol potassium chloride) - 1 Litre over 4 hours (+potassium chloride) - 1 Litre over 4 hours (+potassium chloride)
5% or 10% Glucose
- Start when the CBG is <12 mmol/L and continue at 125ml/hr
- 10 % glucose may be necessary to increase insulin infusion Increase infusion rate if glucose falls below 6.0 mmol/L |
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What are the typical fluid deficits in a DKA patient? |
Fluid deficits are typically 100 mL per kg of body weight. |
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What is the electrolyte picture in DKA patients? |
Variable - Na+ could be high due to dehydration, or low due to glucose interference
K+ - could be high due to the intracellular to extracellular shift seen due to the acadaemia (or could be low/normal but overall cellular depletion of K+) |
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How do you replace potassium in DKA? |
- For the first 1-2 bags of fluid, give no potassium as fluid is given too rapidly - for every subsequent bag of NaCL 0.9% or glucose 5% use a bag of fluid containing KCL as follows according to serum K+:
- <3.5 may need addition K+ and delay insulin - 3.5-5.5 20-40 mmol/l of K+
- >5.5 - no K+ |
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What is the protocol for insulin therapy in a patient with DKA? |
- if patient is known to be diabetic, continue their normal long acting insulin on admission - commence insulin infusion by intravenous syringe pump (containing 50 units Actrapid made up to 50 ml in Sodium Chloride 0.9%)
fixed rate IV insulin infusion: - 0.1 u/kg - around 6-8 u/hr for most patients - aiming for bicarb rise of 3 mmol/hr and glucose fall by 3 mmol/hour - if not achieved - increase rate by 1 u/hr
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What is the commonest cause of death from DKA in children and also a very important complication of DKA in general?
How do you treat it? |
- cerebral oedema - treated with dexamethasone or mannitol
- high mortality |
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How do you manage a patient who has just recovered from DKA? |
- return to usual subcutaneous insulin once eating and drinking reliably - until ketones clear, patient is likely to be nauseated and not able to eat normally - persisting ketonuria usually reflects lack of adequate glucose and insulin administration
- education in self-care and sick day rules to help prevent future DKA - usually done by diabetes nurse specialist |
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What is hyperosmolar hyperglycaemic syndrome? |
- Usually type 2 diabetes - longer subacute history - hyperglycaemia over >40 mmol/L - osmolality >340 (275-295) ---> can be estimated by the formula 2x[Na + K] + Ur + Glu ---> patient is often hyernatraemic - they may or may not have ketonuria - frequently +ve if not eating - no (keto) acidosis, but may have lactic acidosis - severe dehydration - 66% previously undiagnosed DM |
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What is the treatment for hyperosmolar hyperglycaemic syndrome (HHS)? |
- IVI (intravenous infusion) as for DKA but consider slower fluids if elderly/heart failure - no insulin bolus - much lower dose insulin - maybe no insulin for 1st 12 hours, then very low doses - perhaps 1 u/hr - rapid shifts in glucose should be avoided due to risk of rapid fluid/sodium shitfts, and risk of central pontine myelinolysis (CPM) - correct blood glucose at maximum 2 mmol/L/hr
- central venous pressure monitoring may be required - subcut low molecular weight heparin may help reduce thrombosis - potassium tends to decline rapidly
- avoid 0.45% N saline - accept that biochemistry will be abnormal for days or risk hypernatraemia, CPM, cerebral oedema |
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What are the sick day rules for diabetics? |
Advice to a patient on insulin who is will
- try to drink fluids (a lot) - if you are unable to eat, drink sugary fluids e.g. fruit juice - monitor glucose levels more regularly - never stop your tablets or insulin - indeed insulin doses may need to be increased as you are 'stressed' - people who normally take oral agents may need to be transferred on to insulin for the duration of illness - if the patient is unable to keep fluids down, tell them to come straight to hospital |
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What are the most important life-saving measures in a patient with DKA or HHS? |
Fluid balance, adequate insulin and potassium supplementation are the most important life-saving measures
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What should anyone admitted unconscious to A & E have tested? |
Anyone admitted unconscious to A&E should have a blood glucose check |
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What is the prevalence of diabetes? |
Diabetes prevalence worldwide: 146 million in year 2000 rising to 450million by 2030 |
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What is the cost to healthcare of diabetes? |
Healthcare costs for diabetes, account for around 9% of totalhealthcare expenditure Around 65% of this cost is for in-patient care – ie care ofcomplications |
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What complications can diabetics present with? |
Around 50% of newly presenting people with type 2 DM have one or more complications at diagnosis. In order of likelihood - retinopathy - erectile dysfunction - abnormal ECG - ischaemic changes to feet - intermittent claudication - plasma creatinine >120 - stroke or TIA |
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Why do complications occur? |
Long term exposure to hyperglycaemia leads to: - Vessel closure (full or partial) – supply of oxygen and nutrients are decreased - Vessel permeability – damaged vessels dilate and leak unwanted substances Risk factors that increase risk of complications: 1. Smoking – the most potent risk factor 2. Hypertension 3. Dyslipidaemia 4. Hyperglycaemia – the least potent risk factor |
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What are the chronic complications of diabetes? |
Complications of diabetes updated Microvascular Retinopathy Nephropathy Neuropathy ▪ Peripheral sensorimotor▪ Autonomic Macrovascular Coronary Heart Disease Cerebrovascular Disease Peripheral Vascular Disease Other Skin Rheumatological Liver |
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How can diabetic retinopathy be prevented? |
Diabetic retinopathy is: Common - ~ 50% of people with diabetes longer than 10 years have some form of retinopathy - Is the commonest cause of blindness in people of working age Can be prevented by: - Good blood pressure control - Good glycaemic control - Regular eye screening |
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How does tight glucose control affect microvascular and macrovascular complications? |
Microvascular complications reduced by 25-40% Macrovascular complications not significantly reduced |
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What are the features of non-proliferative diabetic retinopathy? |
Non-proliferative retinopathy (also called Background retinopathy)- retinopathy not involving the macula, characterised by presence of: • microaneurysms • dot haemorrhages • hard exudates (lipid deposits) Differentiated into: Mild Moderate Severe – where there may also be cotton wool spots (also called softexudates) – which are areas of retinal ischaemia |
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What are the features of proliferative diabetic retinopathy? |
Proliferative retinopathy Ischaemic retina leads to production of growth factors and to new vessel formation (neovascularisation) - new vessels on disc (NVD) - new vessels elsewhere (NVE) |
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What are the features of diabetic maculopathy? |
Maculopathy - is the presence of any retinopathy within 1 disc diameteraround macula. Can be: - Focal or exudative maculopathy – hard exudates around macula which leads to macular oedema and visual loss - Diffuse - Ischaemic – due to retinal vessel closure |
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How do you prevent diabetic retinopathy? |
- Every person with diabetes inthe UK should undergo a yearlydigital retinal screen - Aim to achieve tight glycaemiccontrol (HbA1c < 53 mmol/mol) - Aim to achieve good BP andcholesterol control - Laser photocoagulation can besight preserving for proliferativeretinopathy or maculopathy |
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What are the types of diabetic neuropathy? |
- Peripheral sensory neuropathy - Autonomic neuropathy - Proximal motor neuropathy (Amyotrophy) - Mononeuropathy Cranial nerve palsies Median nerve (Carpal Tunnel syndrome) |
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What are the symptoms of peripheral sensory neuropathy? |
“Glove and stocking” distribution - High risk of ulceration and amputation - Symptoms: ▪ Numbness ▪ Pins and needles ▪ Burning ▪ Shooting |
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How do you screen for high risk of ulceration? |
Look for reduced: - Vibration sense - Fine touch sense (using a Semmes Weinstein Monofilament – see photo) - Ankle reflexes - Evidence of muscle wasting |
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What is the commonest cause of non-traumatic amputation? |
Diabetic neuropathic ulceration |
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What are some of the manifestations of diabetic autonomic neuropathy? |
Autonomic neuropathy leads to multi-system problems: Genito-urinary: ▪ Erectile dysfunction ▪ Atonic bladder – leading to difficulty voiding or urinary incontinence Gastrointestinal: ▪ Gastroparesis – recurrent vomiting and early satiety due to gastric outflow problems ▪ Chronic constipation or diarrhoea ▪ Gustatory sweating – severe sweating on eating Cardiovascular ▪ Postural hypotension |
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What are some of the stats of diabetic nephropathy? |
Commonest cause of end stage renal failure in the UK ▪ One third of all people starting renal replacement therapy have diabetes - 25-30% of people with type 2 diabetes have some degree ofnephropathy - South Asians / Afro-Caribbeans have higher risk - Nephropathy is associated with a greatly increasedincidence of atherosclerotic vascular disease |
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What are the risk factors that contribute to the development and progression of nephropathy? |
Factors that contribute to development and progression ofnephropathy include: - Duration of diabetes - Hypertension - Poor glycaemic control - Smoking - Gender – male preponderance - Ethnicity – South Asian / Afro-Caribbean - Having a relative with hypertension |
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What are the clinical features of diabetic nephropathy? |
A clinical triad of: - hypertension - albuminuria (preceded by microalbuminuria) - declining renal function On renal biopsy, the pathological lesion is the “Kimmelstein -Wilson lesion” |
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What is the pathological lesion seen in diabetic nephropathy? |
On renal biopsy, the pathological lesion is the “Kimmelstein -Wilson lesion” |
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What do you screen for in diabetic nephropathy? |
Microalbuminuria - meausure urine albumin: creatinine ratio (ACR) - normal is <2.5 mg/mmol in men or <3.5 mg/mmol in women - if elevated, repeat x2 - if 2 out of 3 positive - microalbuminuria present |
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How do you treat diabetic nephropathy? |
1) Most important to maintain blood pressure <130/80 mmHg - ACEI first line (ACEI is given if BP normal) - consider angiotensin receptor blocker if ACEI not tolerated - often more than one anti-hypertensive is needed to achieve this BP 2) Optimise blood glucose control (HbA1c <53 mmol/mol) 3) Manage cardiovascular risk factors aggressively 4) Stop metformin when eGFR <30 mls/min 5) Refer to specialist if eGFR below 45 mls/min and falling 6) Renal replacement therapy may be needed e.g. peritoneal dialysis/haemodialysis/transplant - in type 1 diabetes consider simultaneous pancreas and kidney (SPK) transplant |
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What is the risk of developing an MI in a non-diabetic and a diabetic? |
Diabetic patients without previous MI have as high a risk of MI as non-diabetic patients with previous MI |
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What is the life expectancy of diabetics? |
Adults with diabetes have an annual mortality of about 5.4 % , double the rate for non-diabetic adults. Life expectancy is decreased by around 5-10 years. |
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What is the treatment to prevent complications in diabetics? |
Smoking Cessation–“1cigarette in a diabetic=5 cigarettesin a non-diabetic” Blood pressure - NICE guidelines suggest optimal BP<140/80mmHg (<130/80 if known CVD or microalbuminuria) - Often needs more than one treatment, in this order: - ACEI - Calcium channel blocker - Thiazide - Alpha Blocker or Beta Blocker Cholesterol - NICE guidelines states all diabetic>40yrs, or diabetic <40years+ 1 other risk factor should be on a statin - Aiming for total cholesterol <4.0mmol/l Improve HbA1c < 53 mmol/mol (7.0%), but individualised to the patient |
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What should be the aim for glycaemic control in diabetics? |
Recent evidence from large controlled trials suggests that tighterglucose control may not necessarily be better. Risk of very tightglucose control is hypoglycaemia (especially in the elderly) Therefore, : - Glycaemic control early in type 2 diabetes is probably important (aim for < 53 mmol/mol [7.0%] in first 10 years) - Later (>10 years) – less important and more risky (perhaps aim for < 58 mmol/mol [7.5%] or higher) NICE suggests individualised glycaemic target: ▪ Eg The target for an 80 y/o lady with type 2 diabetes and dementia might be very different to that of a 40 y/oman with type 2 diabetes and a family history of CHD ▪ “Target level for an individual may be above the general target of 48 mmol/mol 6.5% and should benegotiated with the patient” |
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What is the presentation of an acute MI in diabetics? |
Immediate and later mortality rates following MI are high in peoplewith Type 2 diabetes MI maybe“silent”(i.e. nochestpain) inpeoplewithdiabetesorsymptoms may be atypical (e.g. epigastric pain) |
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What is the treatment of an acute MI in diabetics? |
Treatment: - Aspirin - Primary angioplasty or thrombolysis - Glucose-insulin infusion Secondary prevention - ACE Inhibitors, β-blockers, statins, aspirin, improve glycaemic control Cardiac rehabilitation |
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How do you treat cerebrovascular events in diabetics? |
If within 3 hours–consider thrombolysis - General consensus is to treat all vascular riskfactors aggressively - ACEi - Statins - Aspirin ? - Glucose / insulin infusion during acute phase |
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What are the symptoms of peripheral vascular disease? |
Approx.20% of people with PVD will die within 2yrs of symptoms Most deaths are from MIs Symptoms include: - Intermittent claudication - Rest pain - Buttock pain |
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What is the management of peripheral vascular disease? |
- aspirin - vasodilating agents - reconstructive surgery - angioplasty - amputation & rehabilitation & foot care |
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What are the skin manifestations of diabetes? |
- oral/genital candidiasis - common presenting symptom - skin abcesses - especially perianal/axillary - diabetic dermopathy - necrobiosis lipoidica diabeticorum - seen in type 1 diabetes - bullosis diabeticorum - granuloma annulare - acanthosis nigricans - a sign of insulin resistance - fungal nail infections |
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What are the rheumatological manifestations of diabetes? |
- Charcot neuroarthropathy - a “neuropathic” joint leads to severe deformity and high risk of ulcers - Diabetic cheiroarthropathy - due to limited joint mobility - Adhesive Capsulitis - “frozen shoulder” much more common amongst people with diabetes - Diffuse idiopathic skeletal hyperostosis - Flexor tendinopathy - Diabetic osteoarthropathy |
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Why does neuropathy occur in diabetes? |
Neuropathy is a term used to describe problems with the nervous system. In diabetics this is called peripheral neuropathy and affects the sensory nervous system to the peripheral, or farther, points of the body (i.e. feet and hands) causing loss of feeling or numbness. Diabetic neuropathy also involves the autonomic (involuntary) nervous system which controls regulation of blood vessels and skin moisture, and may result in increased blood flow to the limb, contributing to swelling and osteoporosis of the bones as the Charcot process occurs. Arthropathy is a term used to describe a problem with a joint. Therefore, neuropathic arthropathy is used to describe problems with joints related to lack of nerve system input. It is believed that as the peripheral neuropathy progresses in long-standing diabetes, the joints are unable to recognize the forces put across them and the relative positions of the various joints, sustaining microtrauma or microfractures because the body does not adjust to these forces and positions. It would therefore be reasonable to assume that most cases of neuropathic arthropathy would occur in the lower extremities, with their weight-bearing function. This is indeed the case, although on occasion other joints can be involved. |
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What liver problems are related to diabetes? |
Non-alcoholic fatty liver disease is very common amongst people with diabetes - Can progress to non-alcoholic steato-hepatitis (NASH)/fibrosis/cirrhosis raised ALT and AST>2x upper limit of normal needs investigation - hepatitis serology - Ultrasound scan - ferritin (to exclude haemochromatosis which can cause diabetes) - needs vigorous treatment of diabetes and risk factors - possibly a specific role for pioglitazone in reducing progression to cirrhosis |
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What is Charcot’s foot? |
Neuropathic arthropathy (or neuropathic osteoarthropathy), also known as Charcot joint (often "Charcot foot"), refers to progressive degeneration of a weight bearing joint, a process marked by bony destruction, bone resorption, and eventual deformity. Onset is usually insidious.If this pathological process continues unchecked, it could result in joint deformity, ulceration and/or superinfection, loss of function, and in the worst-case scenario, amputation or death. Early identification of joint changes is the best way to limit morbidity. |
