Diabetes Flashcards
What is the normal range for blood glucose
3.5-8 mmol/L
What is the pathology of T1DM
Autoimmune destruction of the B-pancreatic cells leading to decreased insulin release
At what age would you expect someone with T1DM to present with symptoms
<15years - normally before puberty
Is the development of symptoms in T1DM fast or gradual
Acute onset of severe symptoms so fast
What is the presentation of T1DM
Polyuria Polydipsia Decrease weight Increased urinary ketones Diabetic ketoacidosis Ketones on the breath Ketones in the urine
What is T1DM associated with
HLA-D3 and D4
Autoimmune conditions including Addisons, coeliac disease and hypothyroidism
What antibodies might you expect to find in someone with T1DM
Anti-GAD
Anti-islet
What is the pathology of T2DM
Insulin insulin resistance and B cell dysfunction leading to impaired insulin secretion
At what age would you expect someone with T2DM to present with symptoms
Older than 30
Would you expect the onset of symptoms in someone with T2Dm to be fast or gradual
Gradual
What is the presentation of T2DM
Polydipsia
Polyuria
Complications
What is the concordance rate for T2DM in monozygotic twins
80%
What are the associations with T2Dm
Obesity Lack of exercise Calorie Excess EtOH excess Family history Middle East or SE Asian Ethnicity
What is the diabetic diagnostic criteria for someone who is symptomatic
Polyuria, polydipsia, weight loss and lethargy
Increased venous plasma glucose once either
Fasting >7mM
Random >11mM
What is the diabetic diagnostic criteria for someone who is asymptomatic
Increased venous plasma glucose on two different occasions or a 2Hr OGTT >11.1mM
What specific diagnostic criteria might you look for in someone with T1 diabetes
Increased urinary ketones
Decreased arterial pH
Decreased plasma bicarbonate
What are the specific diagnostic criteria you might look for in someone with T2DM
Elevated HbA1c
What are the three categories of potential secondary causes for diabetes mellitus
- Drugs
- Pancreatic
- Endo
What drugs are potential secondary causes of diabetes mellitus
- Steroids
- Anti-HIV
- Atypical neuroleptics
- Thiazides
What pancreatic diseases are potentially secondary causes of diabetes mellitus
CF
Chronic Pancreatitis
What other endocrinological conditions are potential causes of secondary diabetes mellitus
- Phaeochromocytoma
- Cushings
- Acromegaly
What are the lifestyle modifications that can be made by diabetic patients? (Remember DELAYS)
Diet (Reduced calorie intake, refined CHO, Fats and sodium and binge drinking)
Exercise
Lipids (prevent hyperlipidaemia with statins)
ABP (Reduce Na+ and EtOH in order to keep blood pressure <130/80 - Can use ACEi’s)
Yearly/6 monthly check ups
Smoking cessation
What is the first step in the oral hypoglycaemic management approach for diabetics
Life style modifications (DELAYS)
What is the second step in the oral hypoglycaemic management approach for diabetics
Start the patient on metformin (Increases insulin sensitivity and reduces liver glucose production)
500mg after evening meal
What are the Side effects and contraindications for metformin
SE - Nausea, Diarrhoea, Abdominal pain and lactic acidosis
CI - GFR <30, tissue hypoxia (Sepsis) or morning before general anaesthetic
What is the third step in the oral hypoglycaemic management approach for diabetics
Add Sulfonylureas (release insulin from the pancreas) to metformin
Name an example of a sulfonylurea
Gliclazide
What are the Side effects and contraindications of Sulfonylureas
SE - hypoglycaemia and Wt gain
CI - Omit on morning of surgery
What is the third step in the oral hypoglycaemic management approach for diabetics
Additional therapy
1st line is to add insulin to metformin and Sulfonylureas
2nd line DPP4 inhibitor if insulin is unacceptable due to obesity/employment/social issues
3rd line = add subcutaneous exenatide if insulin is unacceptable
4th line = add acarbose
Name a DPP4 inhibitor
Sitagliptin or pioglitazone
How do DPP4 inhibitors work
Incretins are released following a meal which decrease blood glucose by stimulating the release of insulin and inhibiting the release gf glucose
Incretins are inhabited by DPP4 so DPP4 inhibitors can be used to prevent this
What are the 3 most common regimes for insulin administration
- Biphasic Regime
- Basal Bolus regime
- Long acting before bed
Describe the principles of the biphasic insulin administration regime and which diabetic individuals is this suitable for
Insulin administered 30mins before breakfast and dinner
- Rapid acting (Actrapid)
- Intermediate (Insulatard)
Suitable for T2 or T1 with regular lifestyles (Children and older pTs)
Describe the principles of the basal-bolus regime and which diabetics is it suitable for
Bedtime long acting (Glargine) and short acting before each meal (Lispro)
Need to adjust dose according to meal size
Best for T1Dm to enable a flexible lifestyle
What are the three main side effects seen in patients on insulin regimes
- Hypoglycaemia
- Lipohypertrophy (need to rotate injection site)
- Wt gain in T2DM
Describe the pathogenesis of diabetic ketoacidosis
- Decreased insulin
- Increased glucagon
- Decreased glucose utilisation
- Increase fat oxidation in liver
- Increased fatty acid production
- Increased generation of ketone bodies
What are the three major signs of diabetic ketoacidosis
- Ketoacidosis
- Dehydration
- K+ imbalance
Describe why you get dehydration in patient with DKA
Decreased insulin leads to severe hyperglycaemia. This leads to glycosuria which causes an osmotic diuresis, drawing water into the urine thus leading to dehydration
Describe why you get K+ imbalance in patients with DKA
insulin normally drives the storage of K+ into cells however in diabetes insulin is deficient so K+ is not stored leading to hyperkalaemia
What are the common presentation of DKA
Abdominal Pain hypotension tachycardia Vomiting breath smells of ketones Gradual drowsiness Sighing Kussmaul hyperventilation Dehydration Ketotic breath
What is the diagnostic criteria for DKA
Arterial pH <7.3 (HCO3- <15mM)
Hyperglycaemia (>11.1mM)
Ketonaemia (>3mM)
What investigations would you carry out to determine if an individual has DKA
Urine (Ketones and glucose)
Capillaries (Glucose and ketones)
VBG (Acidosis and increased K+)
Bloods (U and E, FBC and glucose)
What are the common complications of diabetic ketoacidosis
Cerebral oedema due to exces fluid accumulation
Aspiration pneumonia
Hypokalaemia
What is the management approach for DKA
FIGPICK
Fluid resuscitation (normal saline, 1L stat then 4L with K+ over 12hr
Insulin - Actrapid 0.1u/kg/hr IVI
Glucose - monitor blood glucose and add dextrose
Potassium - Monitor serum K+
Infection - treat the underlying causes
Chart - fluid balance
Ketones - monitor blood ketones
What criteria is used to determine that DKA has been resolved?
Ketones <0.3mM
Venous pH >7.3
HCO3- >18mM
What is Whipple’s triad for hypoglycaemia
Low plasma glucose <3mM
Symptoms consistent with hypoglycaemia
Symptoms relieved by administration of glucose
At what point do autonomic hypoglycaemic symptoms develop
Blood glucose between 2.5-3
At what point do neuroglycopenic hypoglycaemic symptoms develop
Blood glucose <2.5
What are the autonomic symptoms of hypoglycaemia
Sweating Anxiety Tremor Palpitations Hunger
What are the neuroglycopenic symptoms of hypoglycaemia
Confusion Dizziness Personality changes Seizures Coma (<2.2) Visual changes
What are the causes of hypoglycaemia (Remember EXPLAIN)
Exogenous drugs (Insulin, oral hypoglycaemics, alcohol)
Pituitary insufficiency
Liver failure
Addison’s disease
Insulinoma (Islet cell tumour)/Immune (Insulin receptor Abs: Hodgkins)
Non-pancreatic neoplasms (Fibrosarcomas)
What investigations would you carry out in someone with hypoglycaemia
72hr fasting monitoring
Describe the treatment for T1DM.
- EDUCATION - make sure the patient understands the benefits of good glycaemic control.
- Healthy diet - low in sugar, high in carbohydrates.
- Regular activity, healthy BMI.
- BP and hyperlipidaemia control.
- Insulin.
Give 4 potential complications of insulin therapy.
- Hypoglycaemia.
- Lipohypertrophy at ejection site.
- Insulin resistance.
- Weight gain.
- Interference with life style.
Why do you rarely see diabetic ketoacidosis in T2DM?
Insulin secretion is impaired but there are still low levels of plasma insulin. Even low levels of insulin can prevent muscle catabolism and ketogenesis.
Describe the treatment pathway for T2DM.
- Lifestyle changes: lose weight, exercise, healthy diet.
- Metformin.
- Metformin + sulfonylurea.
- Metformin + sulfonylurea + insulin.
- Increase insulin dose as required.
How does metformin work in treating T2DM?
Metformin increases insulin sensitivity and inhibits glucose production.
How does sulfonylurea work in treating T2DM?
Sulfonylurea stimulates insulin release.
Give a potential consequence of taking Sulfonylurea for the treatment of T2DM
Hypoglycaemia.
Wt gain
Give 3 microvascular complications of diabetes mellitus.
- Diabetic retinopathy.
- Diabetic nephropathy.
- Diabetic peripheral neuropathy.
Give a macrovascular complication of diabetes mellitus.
CV disease and stroke.
What is the main risk factor for diabetic complications?
Poor glycaemic control!
Give a potential consequence of acute hyperglycaemia?
Diabetic ketoacidosis and hyperosmolar coma.
Give a potential consequence of chronic hyperglycaemia?
Micro/macrovascular tissue complications e.g. diabetic reinopathy, nephropathy, neuropathy, CV disease etc.§§
What is the commonest form of diabetic neuropathy?
Distal symmetrical polyneuropathy
Give 3 major clinical consequences of diabetic neuropathy.
- Pain.
- Autonomic neuropathy.
- Insensitivity.
Describe the pain associated with diabetic neuropathy.
- Burning.
- Paraesthesia.
- Nocturnal exacerbation.
Diabetic neuropathy clinical consequences: what is autonomic neuropathy?
damage to the nerves that supply body structures that regulate functions such as BP, HR, bowel/bladder emptying.
give 5 signs of autonomic neuropathy
- Hypotension.
- HR affected.
- Diarrhoea/constipation.
- Incontinence.
- Erectile dysfunction.
- Dry skin.
What are the consequences of insensitivity as a result of diabetic neuropathy?
Insensitivity -> foot ulceration -> infection -> amputation.
Describe the distribution of insensitivity as a result of diabetic neuropathy?
Insensitivity starts in the toes and moves proximally. Glove and stocking distribution.
Give 5 risk factors for diabetic neuropathy.
- POOR GLYCAEMIC CONTROL.
- Hypertension.
- Smoking.
- HbA1c.
- Overweight.
- Long duration of DM.
Describe the treatments for diabetic neuropathy
- Improve glycaemic control.
- Antidepressants.
- Pain relief.
PVD is a potential complication of Diabetes. Give 6 signs of acute ischaemia.
- Pulseless.
- Pale.
- Perishing cold.
- Pain.
- Paralysis.
- Paraesthesia.
Give 5 ways in which amputation can be prevented in someone with diabetic neuropathy.
- Screening for insensitivity.
- Education.
- MDT foot clinics.
- Pressure relieving footwear.
- Podiatry.
- Revascularisation and abx.
Would there be increased or decreased pulses in a diabetic neuropathic foot?
There would be increased foot pulses.
Give 5 risk factors for diabetic retinopathy.
- Long duration DM.
- Poor glycaemic control.
- Hypertension.
- Insulin treatment.
- Pregnancy.
- High HbA1c.
Describe the pathophysiology of diabetic retinopathy
Micro-aneurysms -> pericyte loss and protein leakage -> occlusion -> ischaemia
How can diabetic retinopathy be sub-divided?
- Proliferative - evidence of neovascularisation in retina.
- Non-proliferative.
What is the treatment for diabetic retinopathy?
People with diabetes are offered regular screening to assess visual acuity.
- Laser therapy treats neovascularisation
What is the hallmark of diabetic nephropathy?
Development of proteinuria and progressive decline in renal function
What happens to the glomerular basement membrane in someone with diabetic nephropathy?
On microscopy there is thickening of the glomerular basement membrane.
Give one way in which the presentation of diabetic nephropathy differs between T1 and T2DM.
T1 DM: microalbuminuria develops 5-10 years after diagnosis.
T2 DM: microalbuminuria is often present at diagnosis.
Describe the treatment for diabetic nephropathy.
- Glycaemic and BP control.
- ARB/ACEi.
- Proteinuria and cholesterol control.
