Diabetes and Endocrinology Flashcards
State the normal fasting glucose range for non-diabetics (in mmol/L)
4 to 6 mmol/L
State fasting glucose level for which diabetes is suspected (in mmol/L)
Above 7 mmol/L
State random glucose level for which diabetes is suspected (in mmol/L)
Above 11 mmol/L
State HbA1C level for which diabetes is suspected (in mmol/L and %)
Above 48 mmol/L or 6.5%
Outline the symptoms and average age of onset of T1DM
Triad:
- Polyuria
- Polydipsia
- Weight loss
plus
- Tiredness
- Weakness
May also present in DKA
- Nausea and vomiting
- Pear drop breath
- Hypotension (from dehydration)
- Altered consciousness
Average age of diagnosis of 13 years
Outline the symptoms of T2DM
Triad:
- Polyuria
- Polydipsia
- Weight loss
plus
- Fatigue
- Opportunistic infections
- Slow healing
- Glucosuria
Average age of diagnosis is much later in life compared to T1DM
State the investigations for suspected T1DM (how you many you need to be able to diagnose diabetes)
- HbA1C (> 6.5% or 48 mmol/L)
- Fasting blood glucose (above 7mM)
- Oral glucose tolerance test
Symptomatic + 1 abnormal test
Asymptomatic + 2 abnormal tests
Tests need to be 1 week apart
State the investigations for suspected T2DM
- HbA1C (> 6.5% or 48 mmol/L)
- Fasting blood glucose (above 7mM)
- Random blood glucose (above 11mM)
- Oral glucose tolerance test (above 11mmol/L)
Symptomatic + 1 abnormal test
Asymptomatic + 2 abnormal tests
Tests need to be 1 week apart
State the management for T1DM
- Insulin!! Basal-bolus regimen
- Patient education
- Monitor carbohydrate intake
- Monitor blood sugars 3 times a day
- Monitor development of any complications
State the management for T2DM, including:
- Lifestyle modifications
- Regular monitoring required
- Medication hierarchy
Lifestyle modifications:
- Reduce glucose intake and increase fibre intake
- Potentially low carbohydrate (but not mainstream advice)
- Reduce other lifestyle risks e.g. stop smoking, increase exercise and weight loss
- Control other co-morbidities e.g. hypertension, hyperlipidaemia
Monitor for long term complications:
- Diabetic foot reviews
- Kidney disease checks
- Eye checks for retinopathy
Medications:
- Metformin (1st line)
- Sulphonylurea
- Pioglitazone
- Incretin mimetics
- SGLT-2 inhibitors
- Insulins
List short term and long term (microvascular and macrovascular) complications of T1DM
Also list some infection related complications
Short term:
- Hypoglycaemia
- Hyperglycaemia
Long term - macrovascular:
- Coronary artery disease
- Peripheral ischaemia
- Stroke
- Hypertension
Long term - microvascular:
- Peripheral neuropathy
- Nephropathy
- Retinopathy
Infection related complications:
- UTIs
- Thrush and other fungal infections
- Pneumonia
- Soft tissue / skin infections
List long term complications of T2DM (microvascular and macrovascular)
Macrovascular:
- Coronary artery disease
- Peripheral ischaemia
- Stroke
- Hypertension
Microvascular:
- Peripheral neuropathy
- Nephropathy
- Retinopathy
List risk factors for T2DM
Non-modifiable:
- Increased age
- Ethnicity (black, chinese, south asian)
- Family history
Modifiable:
- Obesity
- Sedentary lifestyle
- HIgh carbohydrate intake
Describe how the Oral Glucose Tolerance Test is performed
Performed first thing before breakfast (fasting plasma glucose)
- Measure fasting plasma glucose
- Give 75g glucose drink
- Measure plasma glucose 2 hours post-drink
Assesses ability of the body to cope with carbohydrate
Explain ways of monitoring T1DM (longer term)
HbA1C - reflects glucose control over the past 3 months
Capillary blood glucose (CBG) or libre devices (flash glucose monitoring of glucose level in interstitial fluid)
Describe some ways in which ensure that insulin is prescribed safely
- Check brand name (some are similar)
- Check device.
- Check dose
- NEVER abbreviate “units” to “u” or “iu” due to risk of 10x overdose.
- Check dose time
- Correctly write on both charts (drug/EPMA and green chart)
Diabetic Ketoacidosis - state the following:
- Pathophysiology
- 3 biochemical disturbances that occur (most consequential effects of DKA)
- Presentation
- How it is diagnosed
Pathophysiology:
- Occurs in T1DM
- When there is insufficient exogenous insulin
- Occurs because the body doesn’t have enough insulin to process glucose
3 biochemical disturbances:
These 3 are the most consequential effects of DKA and can KILL the patient!!
1. Ketoacidosis - ketogenesis is used in order to generate alternative fuel source
2. Dehydration
3. Potassium imbalance
Presentation:
- Nausea and vomiting
- Acetone (pear drop) breath
- Polydipsia (hyperglycaemia)
- Polyuria (hyperglycaemia)
- Hypotension and dehydration
- Altered consciousness
- History / evidence of reduced insulin or illness
How it is diagnosed (HKA):
1. Hyperglycaemia - blood glucose >11mmol/L
2. Ketosis - blood ketones > 3mmol/L
3. Acidosis - pH < 7.3
Hyperosmolar hyperglycaemia syndrome - state the following:
- Pathophysiology
- Presentation
- Are there normally ketones in the urine?
- Diagnosis
- Management
Pathophysiology:
- Occurs in T2DM
- Results from prolonged high blood glucose levels (over weeks)
- High glucose levels usually caused by acute illness (e.g. infection)
- Glucose can rise as a result of hormones the body produces during illness e.g. cortisol
- High glucose causes osmotic diuretics and dehydration
- Can be the first presentation of T2DM
Presentation:
- Polyuria
- Polydipsia
- Nausea
- Hypotension
- Tachycardia
- Dry skin
- Disorientation, drowsiness and altered consciousness
Ketones in the urine?
- No, ketones develop in DKA due to lack of insulin (no glucose into cells)
- T2DM may still be producing some insulin, ketones may not be created
- However it is still possible to get DKA with T2DM (just less common)
Diagnosis:
- Blood glucose (often very high)
- Blood pH and ketones (often low)
Management:
- Transfer to acute care bay or ICU if required
- Fluid resuscitation
- Potassium infusion if required
- Only start insulin infusion if there are raised ketones (otherwise don’t start)
Explain why ketoacidosis occurs in DKA
- Lack of insulin results in lack of glucose WITHIN cells
- Body uses ketogenesis to produce ketone bodies as fuel for brain
- Ketone levels increase which raises the blood pH
- Bicarbonate is produced at the kidneys to reduce acidity
- At point at which there can no longer be compensation then ketoacidosis occurs
Explain why dehydration occurs in DKA
Dehydration occurs because of the hyperglycaemia
- Hyperglycaemia overwhelms kidneys so glucose is filtered into urine (osmotic diuresis)
- Polyuria occurs leading to dehydration
Patient will also have polydipsia as a compensatory mechanism
Explain why potassium imbalance occurs in DKA
- Insulin usually causes potassium to be taken up into the cells
- Without normal insulin levels, serum potassium can be normal (kidney compensation) or rise
- HOWEVER body’s cellular potassium levels are low
- Therefore caution when starting insulin treatment as severe hypokalaemia can ensue
Outline the acute management steps for DKA (acronym)
FIG PICK
Fluids!! - 1L stat of 0.9% saline, then 4L with potassium over next 12 hrs
Insulin - IV Actrapid infusion
Glucose - closely monitor and use Dextrose fluid infusion if low glucose
Potassium - closely monitor and correct as required
Infection - check/treat any underlying infection
Chart - fluid balance
Ketones - monitor ketones closely
Once stable, resume patient on normal subcutaneous insulin regimen
Explain how the following chronic DM complications are managed:
- Diabetic foot ulcer
- Retinopathy
- Nephropathy
- Peripheral neuropathy (painful)
For all complications, control of glucose levels are mainstay of management
Diabetic foot ulcer:
- Offloading (non-weight bearing)
- Debridement
- Wound dressing / negative pressure therapy
- Regular monitoring
Retinopathy:
- Eye test at time of diagnosis
- Regular eyesight/screening tests thereafter
Nephropathy:
- Aim to reduce blood pressure <140/90 mmHg
- Antihypertensives e.g. ACE inhibitor, can reduce proteinuria or preservation GFR, or both
- Cholesterol lowering drugs e.g. statins
- Regular monitoring of UandEs e.g. eGFR, Albumin:Creatinine
Peripheral neuropathy (painful):
- Initial neuropathic drugs: Amitriptyline, Duloxetine, Gabapentin or Pregabalin
Outline some medications used to treat peripheral neuropathy (painful)
Gabapentin or Pregabalin
Amitriptyline
Duloxetine
- Consider additional topical capsaicin cream
How does chronic hyperglycaemia in DM cause retinopathy? What are the 3 main stages?
Retina supplied by small blood vessels which can be damaged by hypergylcaemia over time
3 main stages:
- Bulges in blood vessels - may bleed slightly but don’t usually affect your vision (background retinopathy)
- More significant changes - significant bleeding into the eye (pre-proliferative retinopathy)
- Scar tissue and angiogensis (bleed easily), develop on the retina (proliferative retinopathy) - can result in some loss of vision
