Diabetes Mellitus Flashcards
(48 cards)
T1DM clinical features
Adolescent onset usually but may occur at any age e.g. latent autoimmune diabetes of adults
Insulin deficiency from beta-cell autoimmune destruction
Associated with other autoimmune disorders
Prone to ketoacidosis + weight loss
T2DM clinical features
Higher prevalence in old, Asian men
Less insulin secretion ± increased insulin resistance
Stronger genetic influence than T1DM
Associated with sedentary, obese, alcohol excess
MODY is a rare autosomal dominant form of T2DM
Impaired glucose tolerance definition
Fasting plasma glucose <7mmol/L and
OGTT 2h glucose ≥7.8mmol/L but <11.1mmol/L
Impaired fasting glucose definition
Fasting plasma glucose ≥6.1 but <7mmol/L
OGTT more normal
Causes of DM
Steroids, anti-HIV drugs, newer antipsychotics
Pancreas damage (including haemochromatosis + CF)
Cushing’s disease, acromegaly, phaeochromocytoma, hyperthydroidism, pregnancy
Congenital lipodystrophy
Glycogen storage disease
Metabolic syndrome definition
Central obesity (BMI>30 or inc waist circumference) and two from:
BP≥130/85
Triglycerides ≥1.7mmol/L
HDL ≤1.03(men)/1.29(women)
Fasting glucose ≥5.6
T2DM
DM diagnosis criteria
Hyperglycaemia symptoms + raised glucose once (fasting ≥7, random ≥11.1)
Raised venous glucose twice (fasting ≥7, random ≥11.1)
OGTT 2h value ≥11.1
HBA1C ≥48
Hyperglycaemia symptoms
Polyuria Polydipsia Unexplained weight loss Visual blurring Genital thrush Lethargy
DM general management
Healthy eating Assess vascular risk + statin Review HBA1C every 6mths Foot/eye care Pt inform DVLA and not drive if hypoglycaemic spells
T2DM pharm management stages
Lifestyle
Metformin monotherapy
HBA1C rises to 58, add DPP-4 inhibitor/ pioglitazone/ sulphonylurea (SU) / SGLT-2I (glifazon)
HBA1C still 58 then add SU to DPP4/pio or SGLT-2I to SU/pio, add insulin at this stage if necessary
Add GLP-1 analogues (exenatide, liraglitide) if still not responding and pt not suitable for insulin (e.g. BMI>35)
Metformin MOA
Increase insulin sensitivity + helps weight
DPP4 inhibitor (gliptins) MOA
Block DPP-4 action which destroys incretin
Glitazone MOA
Increases insulin sensitivity
Metformin CI
eGFR ≤36 due to lactic acidosis risk
Glitazone CI
CCF past or present due to fluid retention SE
Osteoporosis
Stop if increased weight/oedema
Sulphonylurea MOA
Increase insulin secretion
SGLT-2I MOA
E.g. empagliflozin
Selective sodium-glucose co-transporter 2 inhibitor blocks glucose reabsorption in kidneys so excreted in urine
Subcut insulin types
Ultra-fast before meals (humalog, novorapid)
Isophane (peak at 4-12h)
Pre-mixed (e.g. Novomix 30 (30% short, 70% long acting)
Long-acting e.g. glargine before bed, detemir in overweight T2DM
Insulin during illness
Don’t stop taking, illness often increases insulin requirement despite reduced food intake
Complications diabetes
Vascular disease
Nephropathy
Retinopathy
Cataracts
Rubeosis iridis (new vessels on iris, may lead to glaucoma)
Metabolic complications
Diabetic feet
Neuropathy
Diabetic retinopathy types
Background (microaneurysms, haemorrhages and lipid deposits), refer if near macula
Pre-proliferative (infarcts, haemorrhages, venous beading) signs of retinal ischaemia, refer
Proliferative (new vessels form), urgent referral
Maculopathy caused by high retinal blood flow from hyperglycaemia causes vascular leak + hypoxia, can reduce visual acuity
BP targets T1DM
T1DM treat BP if >135/85
130/80 if albuminuria/2+ features of metabolic syndrome
BP targets T2DM
<140/80
130/80 if kidney/ eye/ cerebrovascular damage
Anti-RAS unless African/Caribbean, then add diuretic/CCA
Testing diabetic neuropathy
Glove and stocking loss
Test sensation with 10g monofilament and ankle jerk
