Diabetes and Sugar Flashcards
(31 cards)
What is the definition of hypoglycaemia?
The definition of hypoglycaemia is quite broad. There are many numerical definitions depending on the context (<3.5 in diabetics, <2.5 in neonates). The definition is now a triad of (Whipple’s triad):
- Low glucose
- Symptoms most of the time (adrenergic and neuroglycopenic)
- Relief of symptoms with glucose administration
What are the clinical features of hypoglycaemia?
There are two main types of symptoms produced by hypoglycaemia:
- Sympathetic overactivity (glucose <3.6 mmol/L) - tachycardia, palpitations, sweating, anxiety, pallor, tremor.
- Neuroglycopenia (glucose <2.6 mmol/L) - confusion, slurred speech, focal neurological deficits mimicking stroke syndromes. Coma occurs when the blood close is <1.5 mmol/L.
Hypoglycaemia can be relatively asymptomatic in certain patients:
- Patients with well-controlled diabetes mellitus have more frequent episodes becoming desensitised to sympathetic activation. These patients may therefore develop neuroglycopenic symptoms before sympathetic ‘warning symptoms’.
- Patients taking beta blockers as they blunt the symptoms of sympathetic activation.
Describe the management of hypoglycaemia
What are the investigations for hypoglycaemia?
The most important investigation is blood glucose concentration. Bedside glucose meter must be confirmed by a lab for a new admission or hypoglycaemic coma. It is important to send off bloods before administration of glucose in patients not known to have diabetes mellitus to check for levels of insulin and C-peptide.
Other routine tests such as FBC, U&Es, LFTs, ABGs. Depending on presentation i.e. confusion.
What are the causes of hypoglycaemia?
Diabetes is the most common cause of hypoglycaemia. Patients with diabetes are more likely to develop hypoglycaemic episodes due to:
- Mismatch between medication and carbohydrate consumption
- Inadequate carbohydrate intake/missed meal
- Impaired awareness and accidental over-dosage of diabetes medicine
- Excessive alcohol
- Strenuous exercise - particularly aerobic exercise
- Co-existing autoimmune conditions
All oral diabetes drugs apart from metformin can cause hypoglycaemia - especially sulphonylureas. Insulin for T1DM is an obvious cause of hypoglycaemia. However, patients may be on other drugs, including beta blockers, salicylates, and alcohol.
IN PATIENTS WITHOUT DIABETES, INSULIN AND C-PEPTIDE MEASUREMENT IS IMPORTANT
- Low insulin and low C-peptide indicates a hypoinsulinaemic hypoglycaemia. This is an appropriate response to low glucose and is caused by starvation, strenuous exercise, critical illness and liver failure.
- High insulin and high C-peptide indicates a hyperinsulinemia (endogenous) hypoglycaemia.
Before considering insulinomas or other causes of endogenous insulin production, a sulphonylurea drug screen must be performed (urine or serum).
- High insulin and suppressed C-peptide indicates exogenous insulin administration.
What is the definition and epidemiology of Diabetic Ketoacidosis (DKA)?
Diabetic ketoacidosis (DKA) is an acute metabolic complication of diabetes that is potentially fatal and requires prompt medical attention for successful treatment. It is characterised by absolute insulin deficiency.
DKA involves a triad of hyperglycaemia, ketosis and acidosis. It is the most common acute complication of diabetes mellitus.
What are the common precipitants of diabetic ketoacidosis (DKA)?
Infection (30%)
Non compliance with treatment (20%)
Newly diagnosed DM (25%)
Surgical abdomen / pancreatitis (10%).
What are the clinical features of Diabetic Ketoacidosis (DKA)?
Symptoms of DKA include:
- Excessive thirst and frequent urination
- Weakness
- Nausea and vomiting
- Abdominal pain
- Confusion
On examination, may notice signs of volume depletion such as poor skin turgor, dry mucous membranes, tachycardiaand hypotension. Also may notice Kussmaul breathing (rapid and deep due to acidosis) as well as fruity breath and altered mental status.
What are the investigations for Diabetic Ketoacidosis (DKA)?
Patients with suspected DKA:
- Plasma glucose usually>13.9mmol/L
- ABG showing metabolic acidosis with high anion gap.
- Urinalysis positive for glucose and ketones.
- U&Es Serum urea and creatinine usually increased from dehydration. Very important to assess K+ concentrationas insulin administration may need to be delayed if the K+ is too low.
- FBC may indicate infection.
- CXR to look for infections
- ECG to look for ischaemic changes.
A diagnosis of DKA requires all three of:
- Blood glucose >11 mmol/L
- Ketonaemia >3 mmol/L (>= 2+ on urinalysis)
- Acidosis (pH <7.30) on arterial or venous blood and/or serum bicarbonate <15 mmol/L.
Describe the management of Diabetic Ketoacidosis (DKA)
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Fluid replacement: most patients with DKA are deplete around 5-8 litres (on average dehydrated by around 100mL per kg). Isotonic saline is used initially. Regimens for adults usually start with:
- 1L of 0.9% NaCl over 1 hour
- 1L of 0.9% NaCl over 2 hours (x2)
- 1L of 0.9% NaCl over 4 hours (x2)
- 1L of 0.9% NaCl over 6 hours
Fluid replacement for young adults (18-25 years) and children is often slower to avoid cerebral oedema.
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Administer insulin: an intravenous infusion should be started at 0.1 unit/kg/hour.
- Once blood glucose is < 15 mmol/l an infusion of 5% dextrose should be started
- Correction of hypokalaemia: Potassium concentration falls rapidly with administration of insulin. Add KCL to bags of fluid (more complex criteria).
Fixed-rate insulin is continued until patients are eating and drinking. SC basal insulin should have been continued from administration, however short-acting insulin should be stopped.
What is the definition and aetiology of type 1 diabetes mellitus?
T1DM is a metabolic hyperglycaemic condition caused by absolute insufficiency of insulin production. It is one of the most common chronic diseases in childhood, with a prevalence of 0.25% in the UK. There is considerable Geographic variation in the incidence.
Interactions between genes imparting susceptibility and environmental triggers leads to the autoimmune damage of β-cells. There is a role of T-cells in the pathogenesis of T1DM. Over time, effector cells increases, but regulatory cells decrease - leading to the destruction of β-cells. Although many genes are responsible for the risk of T1DM, the HLA-DR3 and DR4 alleles pose a significant risk, while DR2 is protective.
What are the clinical features of type 1 diabetes mellitus?
Often of juvenile onset (<30 years). Polyuria/nocturia, polydipsia, tiredness and weight loss are key features. Frequent thrush or UTIs may be a sign of DM.
Signs include dehydration, cachexia, hyperventilation due to metabolic acidosis, smelling of ketones, glycosuria and ketonuria.
A patient who has history of other autoimmune conditions, is more likely to suffer from Type 1 DM.
On examination: Perform a fundoscopy to look for diabetic retinopathy, examine the feet for neuropathy, and measure blood pressure.
What are the potential complications of type 1 diabetes mellitus?
- Diabetic Ketoacidosis
- Microvascular complications: retinopathy, neuropathy and nephropathy.
- Macrovascular complications: Peripheral vascular disease, Ischaemic heart disease, Stroke/TIA.
Describe the management of type 1 diabetes mellitus
Aim of management in T1DM patient is glycaemic control. This is achieved by:
- Patient education - involve diabetic nurse specialist and dieticians.
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Basal-bolus insulin: Provide one long-acting insulin (isophane, glargine, detemir) for injection once daily. And provide short-acting insulin (Lispro, aspart, glulisine) for injection three times daily before each meal.
- Insulin pumps may give slightly better glycaemic control. However, they are costly and cumbersome and if malfunctioning can cause DKA.
- Motivated patients can attend DAFNE courses (Dose Adjustment For Normal Eating) to learn how to calculate their carbohydrate intake.
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Monitoring their symptoms and glucose levels with regular finger prick tests by the patient. Also by monitoring their HbA1c levels every 3-6 months aiming for a target of 48 mmol/mol or lower.
- Finger-prick testing recommend at least 4 times a day, including before each meal and before bed. More frequent monitoring is recommended if frequency of hypoglycaemic episodes increases; during periods of illness; before, during and after sport; when planning pregnancy, during pregnancy and while breastfeeding.
- Blood glucose targets:
- 5-7 mmol/l on waking and
- 4-7 mmol/l before meals at other times of the day
What is the definition and epidemiology of type 2 diabetes mellitus?
Diabetes Mellitus Type 2 is a disease characterised by peripheral resistance to insulin with impaired insulin secretion leading to a state of chronic hyperglycaemia.
- It affects 5-10% of the population.
- People of Asian, African and Hispanic descent are at greater risk.
- The incidence has increased over the last 20 years, alongside the incidence of obesity.
What are the clinical features of type 2 diabetes mellitus?
Type 2 Diabetes Mellitus can often be asymptomatic and only detected incidentally.
Patients commonly visit their doctors for candidal infections, skin infections (cellulitis) and urinary tract infections. Diabetes is diagnosed because the patient has strong risk factors (obesity, ethnicity etc.) and a blood test is done.
Patients also commonly present with fatigue, blurred vision and paraesthesias. Uncommonly polyuria and polydipsia, nocturia, polyphagia.
On examination:
- Measure BMI, waist circumference and blood pressure.
- Look for signs of Diabetic foot: Ischaemic and neuropathic signs (Dry skin, reduced subcutaneous tissue, corns and calluses, ulceration, gangrene.
- Look for skin changes (rare) such as Necrobiosis lipoidica diabticorum (well-demarcated plaques on the shins or arms with shiny atrophic surface and red-brown edges) and Acanthosis nigricans.
What are the potential complications of type 2 diabetes mellitus?
- Hyperosmolar Hyperglycaemic State
- Microvascular complications: retinopathy, neuropathy and nephropathy.
- Macrovascular complications: Peripheral vascular disease, Ischaemic heart disease, Stroke/TIA.
Describe the diagnosis of type 2 diabetes mellitus
The diagnostic criteria are determined by the WHO.
If the patient is symptomatic they only need one measurement of:
- A fasting blood glucose >7mmol/l or
- A random blood glucose >11.1mmol/l (or after 75g glucose tolerance test) or
- A HbA1c of greater or equal to 6.5% (48 mmol/mol). However a value of less than 6.5% does not exclude diabetes as it is not as sensitive as fasting samples. Note that hameoglobinopathies, haemolytic anaemia, untreated iron deficiency anaemia, HIV and CKD makes HbA1c unsuitable for diagnosis.
If the patient is asymptomatic, the criteria must be demonstrated on two separate occasions.
Describe the diagnosis of impared fasting glucose (IFG)
A fasting glucose from 6.1 but less than 7.0 mmol/l implies impaired fasting glucose (IFG). People with IFG should then be offered an oral glucose tolerance test to rule out diabetes:
- A result below 11.1 mmol/l but above 7.8 mmol/l indicates the person doesn’t have diabetes but does have IGT.
Describe the management approach to type 2 diabetes mellitus, including HbA1c targets.
The principle of managing diabetes mellitus are as follows:
- Drug therapy to normalise blood glucose levels
- Monitoring for and treating any complications related to diabetes
- Modifying any other risk factors for other conditions such as cardiovascular disease. Namely:
- Blood pressure control
- Weight loss
- Lipid control
This is done through education, diet, pharmacy and complication screening.
Target HbA1c levels for the average patient 48mmol/mol (different for patients who are frail or on different antidiabetic drugs).
If the patient is on any drug which may cause hypoglycaemia (e.g. sulfonylurea) or if the patient is already on medication but their HbA1c has risen to 58 mmol/mol then the HbA1c target is 53 mmol/l.
In other words, if a diabetic reaches 58 mmol/mol then you need to consider adding another antidiabetic drug to reach 53 mmol/mol
Describe the glycaemic management in type 2 diabetes mellitus
Target HbA1c levels for the average patient 48mmol/mol (different for patients who are frail or on different antidiabetic drugs). If the patient is on any drug which may cause hypoglycaemia (e.g. sulfonylurea) or if the patient is already on medication but their HbA1c has risen to 58 mmol/mol then the HbA1c target is 53 mmol/l.
- Start with lifestyle measures and put patient on metformin (unless contraindicated by lactic acidosis).
- If HbA1c has risen to 58mmol/mol then add a second drug:
- Add sulphonylurea such as glicazide and glimepride (insulin seragogues which block the ATP sensitive potassium channel on β-cells. This leads to depolarisation of the cell before insulin is released). It is used in lean patients where diet alone has not succeeded. Hypoglycaemia and weight gain are side effects). If HbA1c not at target after three months.
- DPP-4 inhibitors (-gliptins) increases incretin levels which inhibit glucagon secretion. They are generally well tolerated but increases risk of pancreatitis.
- Pioglitazone activates PPAR-y receptor in adipocytes to promote adipogenesis and fatty acid uptake. This causes weight gain and fluid retention.
- SGLT-2 inhibitor (-glifozins) inhibit reabsorption of glucose in the kidney. Typically results in weight loss.
- If despite this, the HbA1c rises to, or remains above 58 mmol/mol then triple therapy can be offered. Alternatively, Insulin therapy should be considered.
If weight loss is a major concern consider GLP-1 agonist such as exanatide. NICE advises we consider triple therapy with metformin, sulphonylurea and a GLP-1 mimetic if the patient is >=35 kg/m2.
Describe blood pressure management in diabetics
Patients with diabetes are 2x as likely to die of stroke or MI than those without.
- Target is <140/80 mmHg (or <130/80 if end-organ damage is present)
- ACE inhibits are the first-line mainly because they have a renoprotective effect in diabetes.
- Afro-Caribbean patients should be offered an ACE inhibitor plus either a thiazides diuretic or calcium channel blocker.
What are the stages of diabetic retinopathy?
The disease progresses to bring different clinical pictures:
- Background retinopathy is the presence of blot haemorrhages, microaneurysm and hard exudates which do not affect the macula. Therefore this has no effect on sight.
- Macular retinopathy involves macular oedema, haemorrhages, and hard exudates. It is difficult to diagnose opthalmoscopically and is suspected from a decrease in visual acuity.
- Pre-proliferative retinopathy has all the features of background retinopathy, but there are areas of ischaemia seen as cotton wool spots.
- Proliferative retinopathy has the features of pre-proliferative retinopathy, but there is also the formation of new vessels. These vessels are fragile, and bleed easily.
Describe the screening and management of diabetic nephropathy
Screening: All diabetic patients require annual screening for albumin:creatinine ratio (ACR) in early morning specimens.
ACE inhibitors are the first-line therapy.
Good glycaemic control, lipid lowering agents and aspirin.
