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Phase 2 3. Endocrinology > Microvascular complications of diabetes > Flashcards

Microvascular complications of diabetes Flashcards

1
Q

What are acute complications of T1DM?

A

> Ketoacidosis

> Hypoglycaemia

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2
Q

What are chronic microvascular complications of T1DM?

A

Retinopathy
Neuropathy
Nephropathy

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3
Q

What are chronic macrovascular complications of T1DM?

A

Ischaemic heart disease
Peripheral vascular disease
Cerebrovascular disease

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4
Q

Name the two landmark trials comparing conventional with intensive treatment

A

> DCCT

> UKPDS

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5
Q

Describe the intensive treatment used in T1DM

A

Injection of long-acting insulin once a day = basal - prevents ketone formation

Bolus insulin at meal times

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6
Q

What is glycaemic control important for?

A

Can help to prevent microvascular disease

Isn’t important for macrovascular disease

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7
Q

What factors are important in macrovascular disease?

A

General cardiovascular risk factors

  • cholesterol levels
  • HTN
  • smoking
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8
Q

What are the causes of microvascular disease?

A

> Capillary damage

> Metabolic damage

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9
Q

Describe how capillary damage leads to microvascular disease

A

hyperglycaemia -> structural/functional abnormalities in small blood vessels -> increased blood flow -> increased capillary pressure -> thickened/damaged vessel walls -> endothelial damage = exudate (leakage of albumin and other proteins)

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10
Q

Describe how metabolic damage leads to microvascular damage

A

Most tissues require insulin to take up glucose except retina/kidneys/nerves
Glucose flows across cell membranes and is metabolised to sorbitol by aldose reductase

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11
Q

What metabolic changes occur as a result of glucose conc. rising?

A
  • Excessive glucose enters polyol pathway (insulin-independent glucose pathway)
  • sorbitol accumulates
  • Less NADPH is available for cell metabolism
  • Build-up of ROS and oxidative stress
  • Cell damage ensues
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12
Q

What disease is associated with microvascular complications?

A

Diabetes-specific

Only occurs with longstanding hyperglycaemia

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13
Q

Which type of diabetes is microvascular complications more of an issue for?

A

T1DM

T2DM will usually die of CV disease first

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14
Q

What is the common onset of microvascular complications in diabetic patients?

A

T1DM = takes a few years to develop

T2DM = may be present at diagnosis because they may have had the condition for a long time already

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15
Q

What is the treatment for microvascular complications?

A

No cure

Early detection is key

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16
Q

What are the common features of early stage (non-proliferative retinopathy?

A
  • Microaneurysms
  • Dot haemorrhages
  • Hard exudates
  • Cotton wool spots
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17
Q

Describe how microaneurisms occur in early stage retinopathy?

A

Hyperglycaemia causes damage to small vessel wall -> microaneurysms

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18
Q

Describe how dot haemorrhages occur in early stage retinopathy?

A

Occur when the vessel wall is breached

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19
Q

Describe how hard exudates form in early stage retinopathy?

A

From the protein and fluid left behind

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20
Q

Describe how cotton wool spots occur in early stage retinopathy?

A

As a result of micro-infarcts

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21
Q

What are common features of late stage retinopathy?

A
  • Damage to veins
  • Ischaemia
  • Fluid build up
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22
Q

Describe the results of venous damage in late stage retinopathy

A

Causes:

  • venous budding
  • blockage of blood supply
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23
Q

Describe the results of ischaemia in late stage retinopathy

A

-> VEGF and other growth factors

  • neovascularisation occurs but these new blood vessels are very fragile and can easily rupture -> Haemorrhages
  • proliferative retinopathy
  • vitreous haemorrhage
24
Q

Describe the results of fluid build up in late stage retinopathy

A

fluid not cleared from the macular area -> macular oedema

25
Q

How can retinopathy be prevented?

A
  • Good glycaemic control
  • Smoking cessation
  • Good BP control
26
Q

How can retinopathy be treated?

A 
Address risk factors
Opthalmic review:
- laser
- VEGF inhibitors (bevacizumab)
- vitectomy
27
Q

How is retinopathy screened?

A
  • Annual retinal screening from the age of 12 years old
  • camera
  • refer to opthalmology if sight threatening
28
Q

What are the stages of diabetic nephropathy?

A
  • Renal enlargement and hyperfiltration
  • Microalbuminuria
  • Macroalbuminuria
  • End stage renal failure

Process occurs over many years

29
Q

What is microalbuminuria?

A

Tiny traces of albumin
- too small to be detected on dipstick

defined as 30-300 mg albumin/24 hours (normal <20)
ACR > 3.5mg/mmol

Independent CV disease predictor

30
Q

What is the pathophysiology of microalbuminuria

A

> renal hypertrophy
increase in GFR
afferent arteriole vasodilates
- golmerular pressure is increased
- thickened glomerular basement membrane
- capillary damage due to shear stress on endothelial cells

End result = leakage of protein into urine

31
Q

What is the pathophysiology of the later steps of microalbuminuria?

A
  • Progressive glomerulosclerosis
  • Glomeruli destroyed
  • Progressive proteinuria - nephrotic range
  • Renal failure
32
Q

How is nephropathy screened?

A

Microalbuminuria is screened every year from diagnosis

33
Q

How is microalbuminuria treated?

A

If present, start with ACEi/angiotensin receptor blocker
(helps to prevent progression to macroalbuminuria)

Aggressive CV risk reduction

  • BP <125/75
  • Statin
  • Smokin cessation

Improve glycaemic control
Refer to renal clinic once patients develop CKD (eGFR <30)

34
Q

What are the different types of neuropathy?

A

Peripheral (sensory) neuropathy -> most common )glove and stoking distribution)

Autonomic neuropathy

Mononeuritis multiplex = peripheral neuropathy with damage to 2+ areas

Diabetic amyotrophy = proximal diabetic neuropathy

35
Q

What tissue changes are noted in diabetic neuropathy?

A

capillary damage, including occlusion in the vasa nervorum

reduced blood supply to the neural tissue results in impairments in nerve signalling that affect both sensory and motor function

36
Q

How does diabetic neuropathy occur?

A

Glucose leads to inability to transmit signals through nerves

Diabetic neuropathy:

  • metabolic changes = sorbitol accumulation
  • vascular changes = capillary damage
  • structural changes
37
Q

What are the signs of diabetic neuropathy?

A
  • Numbness or loss of feeling (asleep or ‘bunched up sock under toes’ sensation)
  • Prickling/tingling
  • Aching pain
  • Burning pain
  • Lancinating pain (sudden, sharp, severe burst of pain)
  • Unusual sensitivity or tenderness when feet are touched (allodynia)
38
Q

What are the symptoms of diabetic neuropathy?

A
  • Diminished vibratory perception
  • Decreased knee and ankle reflexes
  • Reduced protective sensation such as pressure, hot and cold, pain
  • Diminished ability to sense position of toes and feet
39
Q

What are the treatment options for diabetic neuropathy?

A

Duloxetine (or amitriptyline) - SSRI
Amitriptyline (or pregabalin) - TCA

Refer to pain clinic:

  • Try tramadol (opiod)
  • Try topical lidocaine (anaesthetic)
40
Q

What is diabetic foot?

A

Combination of neuropathy (damaged nerve supply) and peripheral vascular disease

  • infection
  • ulcers
  • ischaemia -> reduced blood flow impairs healing
41
Q

What does NICE classify as low risk features for diabetic foot and what recommendations are given?

A

Normal sensation and pulses

Annual review

42
Q

What does NICE classify as medium risk features for diabetic foot and what recommendations are given?

A

Neuropathy OR absent pulses

Review by podiatrist ever 3-6/12

43
Q

What does NICE classify as high risk features for diabetic foot and what recommendations are given?

A

Deformities OR ulceration

Review by podiatrist every 1-3/12

44
Q

What is Charcot foot?

A

Progressive degeneration of weight-bearing joint

45
Q

How does Charcot foot occur?

A

Numb foot - no sensations

  • repetitive microtrauma results and goes unnoticed
  • stress fractures

Increase in dysregulated blood flow to the foot due to vascular disease

  • increased bone turnover
  • fragile bone
46
Q

How does Charcot foot present?

A

With a hot, red, flat foot

47
Q

How is Charcot foot treated?

A

Needs to be completely immobilised in a plaster cast

48
Q

What are the effects of autonomic neuropathy on different systems?

A 
CV = postural hypotension
GU = erectile dysfunction
GI = gustatory sweating (sweating after ingesting food), gastroparesis (delayed gastric emptying
49
Q

What are the different autonomic neuropathies?

A

Diabetic amyotrophy

  • painful proximal neuropathy
  • usually affects thigh/buttock
  • msucle wasting or weakness, pain, or changes in sensation/numbness of the leg

Mononeuritis multiplex

  • painful, asymmetrical motor and sensory neuropathy
  • 2 or more nerves
50
Q

What does the annual review of a diabetic patient comprise of?

A 
HbA1c
Cholesterol, HDL, TG
Creatinine
Microalbuminuria
Lifestyle (exercise, diet, smoking)
Drug therapy
Mental well-being
Visual acuity
Retinal screening
Pedal pulses
Foot sensation
BMI
BP
Erectile dysfunction
Contraception
51
Q

What needs to be considered in pregnancy for a diabetic patient?

A

HbA1c at time of conception (key to reducing risk of congenital malformations)

Glycaemic control during pregnancy helps to prevent macrosomia

Measure baby’s abdominal circumference weekly until birth

52
Q

How do insulin pumps work?

A

deliver insulin in a more physiological way - basal rate then bolus around meals

53
Q

What are the disadvantages of insulin pumps?

A

no background insulin in system if pump fails

training and self management

54
Q

What is continuous glucose monitoring

A

monitor sits in interstitial fluid and gives a reading every 5 minutes

  • insulin can be adjusted according to pattern
55
Q

What is a closed loop system

A

artificial pancreas

aim is to remove patient management from equation creating a closed loop between pump and monitor

Phase 2 3. Endocrinology (25 decks)

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