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Y2 LCRS 1 - Endocrinology > Microvascular complications of diabetes mellitus > Flashcards

Microvascular complications of diabetes mellitus Flashcards

1
Q

What does poor diabetes control increase the risk of?

A

Microvascular AND macrovascular complications

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2
Q

What are some sites of microvascular complications? What do they cause

A
  • Retinal arteries → retinopathy
  • Glomerular arterioles → nephropathy
  • Vasa nervorum → neuropathy
    • Vasa vasorum = small blood vessels which supply the nerves

NOTE: -pathy = damage

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3
Q

What are the risk factors for microvascular complications?

A
  • Severity of hyperglycaemia
  • Hypertension
    • The higher the SBP, the higher the risk of microvascular complications
    • NOTE: There is a link between hypertension and diabetes - they often co-exist
  • Genetic predisposition
  • Hyperglycaemic memory
    • This refers to the phenomenon where prolonged exposure to hyperglycemia can epigenetically modify gene expression
    • This effect is sustained even after hyperglycemic control is therapeutically achieved
    • Therefore, patients who had poorly controlled diabetes at some point, even if their blood sugar levels are controlled now, are at an increased risk of microvascular complications
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4
Q

Describe the mechanism of how hyperglycaemia can lead to microvascular complications.

A
  • Hyperglycaemia and hyperlipidaemia leads to hypoxia and oxidative stress
  • This activate inflammatory signalling cascades, leading to local activation of pro-inflammatory cytokines and hence inflammation
  • Inflammation causes damage to organs

Important pathways to remember

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5
Q

What are some important things to remember about diabetic retinopathy?

A
  • Main cause of visual loss in people with diabetes
  • Main cause of blindness in people of working age
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6
Q

What would a normal retina look like when looking through a fundoscope?

A
  • Optic disc - more medial (nasal)
  • Macula - more lateral (temporal)
    • ​Macula involved in visual acuity (central vision) and colour vision
  • Lots of blood vessels
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7
Q

What are the 4 types of retinopathy?

A
  • Background diabetic retinopathy
  • Pre-proliferative diabetic retinopathy
  • Proliferative retinopathy
  • Maculopathy
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8
Q

What would background diabetic retinopathy look like when looking through a fundoscope?

A
  • Hard exudates
    • Yellow flecks - cheese colour
    • This is due to leakage of lipid contents from the retinal blood vessels
  • Microaneurysms
    • Red dots
    • This is due to localised dilation (bulging) of the micovessel vessel walls
  • Blot haemorrhages
    • The microaneurysms can rupture and leak blood

If untreated, this leads to pre-proliferative diabetic retinopathy

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9
Q

How is background diabetic retinopathy managed?

A
  • Improve control of blood glucose
  • Warn patient that warning signs are present
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10
Q

What would pre-proliferative diabetic retinopathy look like when looking through a fundoscope?

A
  • Cotton wool spots (also called soft exudates)
    • ​These represent retinal ischaemia
    • EXTRA:
      • Ischaemia → hypoxia → blockage of axoplasmic flow (as this requires energy) → deposition of intra-axonal organelles (these are the cotton wool spots that we see)

If untreated, new vessels will grow → proliferative retinopathy

NOTE: Axonal transport = a cellular process responsible for movement of substances (e.g. organelles) to and from the cell body, through the cytoplasm of its axon (i.e. axoplasm)

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11
Q

What would proliferative retinopathy look like when looking through a fundoscope?

A

There are visible new vessels on the optic disc or elsewhere in the retina

  • NOTE: Mechanism
    • Significant amount of retinal BVs already damaged (due to microaneurysms → haemorrhages etc.)
    • This leads to the body releasing a growth hormone which stimulates the formation of new blood vessels to try and restore blood supply to the retina
    • However these blood vessels are weaker, which can cause problems
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12
Q

How is pre-proliferative and proliferative diabetic retinopathy managed?

A

Panretinal photocoagulation

  • Laser therapy
  • Laser beams fired into retina to destroy the ischaemic tissue
  • Reduced area of ischemic tissue reduces the stimulus for new blood vessel formation (neovasacularisation)
  • The point of this is not to improve vision as vision will already be poor due to the ischaemia
  • But you want to prevent the condition from getting even worse
    • ​You want to prevent the formation of new blood vessels as this is what causes problems
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13
Q

What would maculopathy look like when looking through a fundoscope?

A
  • Same disease as background diabetic retinopathy
    • BUT this time near the MACULA
  • ​Hard exudates near macula
  • Because the problem is near the macula, it’s more likely to cause damage to the macula than a problem elsewhere in the retina
    • This can threaten direct vision
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14
Q

How is maculopathy managed?

A

Only needs a GRID of photocoagulation

  • NOT panretinal photocoagulation
  • There is only a problem around the macula
  • So you only need treatment (photocoagulation) there - not the whole retina
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15
Q

What are the features of diabetic nephropathy?

A

Presents with:

  • Hypertension
  • Progressively increasing proteinuria
  • Progressively deteriorating kidney function
  • Classic histological features
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16
Q

What is a dangerous consequence of diabetic nephropathy?

A

Presence of diabetes and CKD increases the risk for cardiovascular events

17
Q

What are the 3 types of histological features to look at in diabetic nephropathy?

A
  • Glomerular
  • Vascular
  • Tubulointerstitial
18
Q

What histological glomerular changes will be seen in diabetic nephropathy?

A
  • Mesangial expansion
  • Basement membrane thickening
  • Glomerulosclerosis
    • Scarring of the glomerular capillaries (meaning loss of functional filtration tissue)

Mesangium:

  • Essentially a supporting framework which forms between the glomerular capillaries
  • Made up of:
    • Mesangial cells
    • Extracellular matrix
19
Q

COME BACK Describe the pathophysiology of diabetic nephropathy (online and Laz)

A
20
Q

Describe the epidemiology of diabetic nephropathy in diabetes.

A

Type 1

  • 20-40% after 30-40 years

Type 2

  • Probably equivalent to T1DM but epidemiology affected by certain factors
    • Age at development of disease (i.e. of T2DM)
    • Racial Factors
    • Age at presentation of T2DM
  • Loss (i.e. most deaths) due to cardiovascular morbidity??
21
Q

What are the ranges of proteinuria?

A
  • Normal Range: <30mg/24hrs
  • Microalbuminuric Range: 30 - 300mg/24hrs
  • Assymptomatic Range: 300 - 3000mg/24hrs
  • Nephrotic Range: >3000mg/24hr

These ranges represent the amount of urine found in the urine

22
Q

COME BACK What are the strategies for intervention or management of diabetic nephropathy?

A
  • Diabetes control
  • Blood pressure control
  • Inhibition of the activity of RAS system
    • EXPLAIN THIS
  • Stopping smoking
    • Smoking stimulates oxidative stress because of increased formation of reactive oxidative species
23
Q

What is the most common cause of neuropathy?

A

Diabetes

  • Therefore diabetes is the most common cause of lower limb amputation
24
Q

What does neuropathy result from?

A

Neuropathy results when the vasa nervorum get blocked

  • Vasa nervorum = small blood vessels which supply the nerves
25
Q

What are the different types of diabetic neuropathy?

A
  • Peripheral polyneuropathy
  • Mononeuropathy
  • Mononeuritis multiplex
  • Radiculopathy
  • Autonomic neuropathy
  • Diabetic amyotrophy
    • Also known as proximal diabetic neuropathy
    • Caused by damage to the nerves of the lumbosacral plexus
      • ​Affects thighs, hips, buttocks
      • Motor and sensory symptoms
26
Q

COME BACK Describe the initiation and progression of neuropathy.

A
27
Q

What is peripheral neuropathy?

A

Peripheral neuropathy is damage to the peripheral nerves

  • Longer nerves more likely to be affected
    • Therefore it is more common in tall people
    • Longest nerves supply feet
      • So generally the feet are affected first
  • You present with loss of sensation
    • So the danger is that patients will not sense an injury to the foot
      • e.g. Stepping on a nail**​
  • You also get loss of motor function

NOTE: Peripheral neuropathy is most common type of neuropathy in diabetes patients

28
Q

In which patients is peripheral neuropathy more likely to occur?

A
  • Tall patients
  • Patients with poor glucose control
29
Q

How do you test for peripheral neuropathy?

A
  • Loss of sensation - monofilament examination
    • This is when you touch the patient with a single filament to see if they can feel it
      • ​You apply a bit of pressure - not light touch
    • Touch them at various points on their foot (mostly sole)
  • Loss of vibration sense - use a tuning fork
  • Loss of ankle jerk
    • This is the reflex you get when you hit the Achilles tendon
  • Multiple fractures on foot - detect using x-ray
    • This is part of Charcot’s joint
      • Charcot’s joint = progressive degeneration of a weight bearing joint
      • This is due to the fact that you have a loss of sensation, so you can’t detect any trauma
      • Therefore you get repetitive microtraumas
      • This triggers the inflammatory response as a repair process but this ends up making the bones weaker and susceptible to further trauma → vicious cycle
      • Problems with motor control can also generate unnatural pressure on certain joints, leading to additional microtrauma.
30
Q

What is mononeuropathy?

A

Mononeuropathy is damage to a single nerve

  • Usually sudden motor loss
  • You can get a wrist drop or a foot drop
  • Cranial nerve palsy (i.e. nerve damage)
    • Double vision due to 3rd nerve palsy
      • CN 3 = oculomotor nerve
        • Responsible for eye movement
      • Double vision becuase you get damage to one nerve (i.e. on one side) so both your eyes are not properly aligned so cannot both focus on one image
31
Q

What are the two types of 3rd nerve palsies? Which one do you get in diabetes?

A
  • Pupil sparing
    • You get this one in diabetes
  • Aneurysm causing

Explanation:

  • Essentially the parasympathetic fibres which control pupil constriction run on the outside of the nerve
  • And the somatic motor fibres which supply the extrinsic eye muscles run on the inside
  • So if you have nerve compression, then the parasympathetic fibres on the outside will be affected
    • Compression by intracranial aneurysm
      • Aneurysm = weakening in a blood vessel wall, leading to outward bulging (usually arterial)
    • ​So you get a fixed dilated pupil
  • However, if you have ischaemia, it means you have reduced blood supply to the nerves
    • This is what happens in diabetes due to blockage of the vasa nervorum
  • Therefore, you get enough blood flow to the periphery so the parasympathetic nerve fibres are fine
  • BUT there is not enough blood supply to the somatic motor fibres on the inside so they get damaged
32
Q

How does pupil sparing 3rd nerve palsy present?

A

Eye is usually ‘down and out’

  • 4th nerve pulls eye down (trochlear)
  • 6th nerve pulls eye out (abducens)

Pupil DOES respond to light

33
Q

What is mononeuritis multipex?

A

Mononeuritis multiplex is a random combination of peripheral nerve lesions

  • Isolated damage to at least two separate nerves
  • Can affect both sensory and motor function, depending on the nerves affected
34
Q

What is radiculopathy?

A

Radiculopathy is compression (pinching) of a spinal nerve root

  • So essentially you get pain in the dermatome of the pinched spinal nerve
  • Usually affects a dermatome on the abdomen or chest wall
35
Q

What is autonomic neuropathy?

A

Autonomic neuropathy is damage to the sympathetic and parasympathetic nerves

  • i.e. Form of polyneuropathy which affects the autonomic nervous system

So you get loss of sympathetic and parasympathetic nerve function to GI tract, bladder, cardiovascular system

36
Q

What are the features of autonomic neuropathy?

A

GI tract problems

  • Difficulty swallowing
  • Delayed gastric emptying
  • Constipation OR nocturnal diarrhoea
    • Depending on which branch of the ANS is damaged
      • ​PNS - increased gut motility → constipation if damaged
      • ​SNS - decreased gut motility → diarrhoea if damaged

Bladder dysfunction

Cardiovascular problems

  • Postural hypotension
    • Collapsing on standing → can be disabling
  • Cardiac autonomic supply affected
    • Can have lots of different clinical manifestations
      • ​e.g. resting tachycardia, exercise intolerance
    • Case reports of sudden cardiac death
      • ANS dysregulation → arrythmias → cardiac arrest → sudden cardiac death

NOTES - definitions:

  • Exercise intolerance
    • Response to the challenges of exercise fail to achieve levels considered normal for the individual’s age and gender
  • Arrythmia
    • Abnormal heart rhythm due to abnormal electrical activity in the heart
  • Cardiac arrest
    • Sudden loss of blood flow due to the heart failing to pump blood around the body
      • This is the result of an electrical problem

Y2 LCRS 1 - Endocrinology (20 decks)

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