Diabetic complications Flashcards
(21 cards)
What are the three main long term complications of diabetes?
Retinopathy
Neuropathy
Nephropathy
What is the aim of primary prevention of diabetic complications?
To prevent the earliest clinical manifestation (prevention of metabolic tissue damage)
What is the aim of secondary prevention of diabetic complications?
Preventing early manifestations of tissue damage progressing to the point of treating organ function
What primary prevention is done for retinopathy?
Blood glucose control
BP control
What does secondary prevention involve for retinopathy?
Early detection of sight threatening retinopathy - retinal screening
Prompt and appropriate ALLC (anti-VEGF) - reduce new blood vessel growth or oedema (as you can get vasculopathy in diabetes where new blood vessels start forming)
Glucose & BP control
Why is the role of BP important in kidney damage?
Before anti-hypertensives are given, arterial pressure rises but eGFR goes DOWN linearly and amount of protein (albumin) in blood is rising
When anti-hypertensives are started it reduces the BP and also immediately slows the rate of decline of renal function and amount of albumin in blood also goes down
What primary and secondary prevention is done for nephropathy?
Primary prevention - blood glucose control
Secondary prevention
- Early detection of minimal nephropathy (UACR - urine albumin to creatinine ratio, eGFR)
- Intensive (<120/75) BP control (ACEI, A2RB) - these are most
- Blood glucose and Vascular Risk Factor Control
How can neuropathy present in feet?
Burning, cold, tingling, stabbing, toothache, walking on glass, contact sensitivity, allodynia (pain from non-painful stimuli), numbness, restlessness,
Why do neuropathic foot ulcer?
Loss of protective sensation and abnormal foot function
Normally, we get minor injuries in our foot all the time, but in those with diabetes (loss of foot sensation) they can turn into major injuries - e.g. continuing to put pressure on sore areas
Another sign would be calluses & blisters in the feet
Holes in feet due to damage can allow bacteria to enter, usually staphylococcus aureus & streptococcus pyogenes
- Bacteria can spread through lymphatics -> can cause cellulitis and lymphangitis -> resulting in septicaemia
What is osteomyelitis?
Osteomyelitis can occur secondary to infected diabetic foot ulceration
- It is infection of the bone
What is Charcot arthropathy?
Due to sensory loss in the feet can also lead
Bone weakness in foot due to significant nerve damage > can lead to severe deformity, disability and even amputation
What preventative measures can be done for foot neuropathy?
Primary prevention
- Blood glucose control
- Lifestyle (smoking, exercise, alcohol)
Secondary prevention
- Early identification of ‘at risk’ feet - neurovascular examination
- Foot care protection programme (education, podiatry, footwear)
- Blood glucose & vascular risk factor control
How are diabetic foot ulcers managed?
Offer 1 or more:
- Offloading
- Control of foot infection
- Control of ischaemia
- Wound debridement
- Wound dressings
What antibiotics are used to treat diabetic foot infections?
Flucloxacillin
Co-amoxiclav
Co-trimoxazole
Ceftriaxone
What causes DKA?
hyperglycaemia + hyperketonaemia + acidosis
What are the clinical features of DKA?
Hyperventilation - metabolic acidosis
Vomiting - ketosis + hyperglycaemic gastric stasis
Dehydration - osmotic diuresis + vomiting
Hypotension with warm peripheries - dehydration & vasodilation (due to acidosis)
Decreased conscious level: severe hypotension – CV shock
What metabolic characteristics are seen in DKA?
Water deficiency ~ 5l Na+ deficiency ~ 500 mmol K+ deficiency ~ 300-1000 mmol Hyperglycaemia > 25 mmol/l Metabolic acidosis – low pH, low HCO3
What is the difference between DKA and HHS?
Metabolic characteristics are similar but NO keto-acidosis
How to prevent DKA/HHS?
PREVENTION is always best - NEVER STOP BASAL INSULIN
If DKA or HHS has developed do these:
- Hypovolaemic shock - fluid resuscitation
- Aspiration pneumonitis - airway protection if comatose (GCS <9)
- Cerebral oedema (F) - a complication of giving IV fluids can be cerebral oedema (occurs mainly in females)
- Fatal arrhythmia - monitor/replace K+
- Pulmonary embolism - prophylactic LMWH
Treatment of hypoglycaemia?
◦ Able to cooperate - 30ml Lucozade or equivalent
◦ Unable to cooperate but conscious
‣ Glucose gel (glucogel) – buccal
◦ Comatose, fitting
‣ Glucagon – sc, im, iv
‣ [IV glucose 50%; try to avoid as it’s ventoxic]
How does hypoglycaemia present?
Adrenergic symptoms (e.g. sweating, trembling, hunger) Neuroglycopenia (e.g. paraesthesiae, blurred vision, confusion)
