12.4.1 Chronic Complications Of Diabetes Mellitus Flashcards

1
Q

List chronic complications of DM

A

Vascular
- Microvas (type 1)
➡️ Nerves, retina, glomeruli
➡️ distinct pathogenesis
➡️ thickening of capillary basement membrane
- Macrovas (type 2)
➡️ atherosclerosis

Others
- Diabetic foot
- Infections
- GIT
- Skin
- Connective tissue and joint involvement
- Bone and mineral metabolism

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2
Q

Microvascular disease pathogenesis

A
  • sensitive to injury from sustained hyperglycaemia
  • This, and the body’s responses aimed to repair, accounts for tissue/ organ damage
  • Affects quality and duration of PLWD Type 1/2
  • All types of DM
  • Improved glycemic control decreases incidence and severity of microvascular damage
  • Body’s microvasculature is a diffuse target, properties differ between tissues and organs, and therefore damage/ repair differs
  • Remember all organs are affected simultaneously, to lesser or more degree
  • Interactions between metabolic abnormalities (hyperglycaemia, dyslipidaemia) also genetics and epigenetic modulators

Classic microvascular pathologies
- Retinopathy, nephropathy, neuropathy
- Also: brain, myocardium, skin and other tissue

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3
Q

Relation between A1C and Relative risk

= Glycemia

A

One goes up, other too

Slide 6 + 7 + 8

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4
Q

Risk factors for microvascular disease

A
  • 8Glycaemic control8 - DCCT showed a 60% decrease in diabetic retinopathy, nephropathy and neuropathy in group with HbA1C < 7.2%
  • Blood pressure control- decreased nephropathy and retinopathy
  • Genetic susceptibility/ endogenous differences
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5
Q

3 factors where cells are influenced

A

Slide 11
- Cell signaling dysfunction
- Toxic metabolites
- Altered osmols and redox potential

Hyperglyceamia -> tissue damage -> cell tries to fix it but can’t

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6
Q

NB Microvascular complications classification

A

1. Diabetic retinopathy
Retinopathy
-Non-Proliferative
• Mild/Moderate/Severe
• Mild = microaneurysms ONLY
• Mod/Severe = anything more
- Proliferative
Cataracts (subcapsular {type 1}; sensile)
Glaucoma
{review page 13}

2. Diabetic nephropathy
- End stage diabetic nephropathy accounts for a significant proportion of ESRD pts worldwide
- Key characteristic of diabetic nephropathy = persistent proteinuria
- ~ 30 % of type 1 develop nephropathy after 15-25 years
- ~ 10% of type 2 diabetics already have proteinuria at time of diagnosis
- NB better glycaemic and BP control!
{Pathology page 17}
- microalbuminuria

3. Diabetic neuropathy
- Peripheral symmetrical sensorimotor neuropathy (common)
- Autonomic neuropathy
- Mononeuropathy (spontaneous; nerve entrapment; external pressure paralysis)
- Proximal motor neuropathy
Clinical presentations page 29

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7
Q

Microalbuminuria
Definition
Prognostic value
Reversible

A

Def
- Albumin excretion of 30 - 300 mg per 24 hours
- Not detected on routine dipstix (measures >0.5g proteinuria)
- Expressed as: albumin:creatinine ratio (mg/mmol)
- Posture, infection and exercise can give false positive results (have to repeat test before diagnosis)

Prognostic value
- predictor of developing nephropathy (basement membrane changes)
- Marker of macrovascular disease (General endothelial dysfunction; Other cardiovascular risk factors)

Reversible
- good BP control

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8
Q

Other causes of renal disease to consider if pt don’t have proteinuria?

A
  • haematuria
  • very short history of type 1 diabetes
  • acute renal fail
  • recurrent UTI’s (chronic pyelonephritis)
  • small kidney in renal ultrasound
  • papillary necrosis (rare)
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9
Q

What is the hallmark for diabetic nephropathy?

A

Proteinuria

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10
Q

Sensorimotor neuropathy
Acute vs Chronic

A

Prevalence increases with age and duration of illness

Acute
- Periods of poor control
⬇️
- typical symptoms
⬇️
- reversible with control

Chronic clinical picture
- Predominantly sensory
- Motor component late
- Symmetrical in a stocking-glove distribution
- Affects most distal parts of long nerves first - toes and foot soles
- Hands affected late

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11
Q

Sensorimotor neuropathy
Neuropathic symptoms
Clinical signs

A

Neuropathic symptoms: symptoms come first; clinical signs is only later
- Pain - sharp, burning, especially foot soles and shins
- Skin tender - hyperesthesia
- Paraesthesia - pins and needles or ‘dead’ feeling in feet
- Symptoms may be persistent and severe
- Worse at night and may keep the patient out of sleep

Clinical signs:
Early:
- Decreased vibration sense
- Absent ankle reflexes
- Also: loss of pain and temperature sense
Late:
- Muscle weakness and atrophy

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12
Q

Autonomic neuropathy
General
Major clinical implications

A
  • Involves the small unmyelinised nerve fibres
  • Sympathetic and parasympathetic

Cardiovascular system:
- Tachycardia without arrhythmia
- Postural hypotension (if pt get up; they fall over)
- Painless myocardial infarct (pt don’t get chest pain)

GIT:
- Gastroparesis nausea and vomiting + labile control
- Constipation / nocturnal diarrhoea

Major clinical implications
- Hypoglycaemia unawareness a life threatening complication

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13
Q

Proximal neuropathy

A

Diabetic amyotrophy:
- Severe pain and paraesthesia in thigh, asymmetrical
- Weakness and muscle atrophy - especially quadriceps
- Involves lower motor neuron of lumbo-sacral plexus
- Middle-aged and older patients
- Associated with periods of poor glycemic control

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14
Q

What is the most typical type of diabetic neuropathy?

A

Symmetrical sensory neuropathy

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15
Q

What are the microvascular complications in DM?

A
  • diabetic neuropathy
  • diabetic retinopathy
  • diabetic nephropathy
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16
Q

Macrovascular complications of DM

A
  • Myocardial infarctions
  • Peripheral vascular disease
  • Carotid stenosis / disease
  • Cerebrovascular accidents / stroke
17
Q

Other complications of DM

A

1. Cardiomyopathy
- Microangiopathy - cardiomyopathy in the absence of coronary artery disease
- CAD - far more common (results in ischaemic cardiomyopathy)
- Commonest cause of death in type 2 DM

2. Musculoscletal complications: Charcot joints
- Loss of proprioception and deep sensation leads to recurrent trauma, which ultimately leads to progressive destruction, degeneration, and disorganisation of the joint.

3. Dupuytrens’ contracture

4. Neuropathic ulcers
- Predominantly secondary to neuropathy, but aggravated by PVD (peripheral vascular disease)
- Painless (don’t have sensation)
- Poor healing of lesions
- Infections (more susceptible to fungal infections poor immune response to infection)

5. Necrobiosis lipoidica

6. Infections
- candida
- abscesses
- wounds not healing
- tuberculosis
- covid-19