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Year 2 LCRS > Endocrinology 18 - Microvascular Complications > Flashcards

Endocrinology 18 - Microvascular Complications Flashcards

1
Q

List the sites of microvascular complications

A
  • Retinal arteries
  • Glomerular arterioles
  • Vasa nervorum (tiny blood vessels that supply nerves)
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2
Q

List the causes of microvascular complications

A
  • Severity of hyperglycaemia
  • Hypertension
  • Hyperglycaemic memory (better control longer term results in reduced risk of microvascular disease)
  • Tissue damage through originally reversible and later irreversible alterations n proteins
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3
Q

Describe the mechanism of glucose microvascular damage

A
  • High glucose results in high cytokines, inflammation, and nerve damage in the feet eyes and kidneys
  • Polyol pathway
  • AGEs
  • Protein kinase C
  • Hexosamine
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4
Q

What is diabetic retinopathy the cause of?

A
  • Main cause of visual loss in people with diabetes

- Main cause of blindness in people of working age

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5
Q

Describe background diabetic retinopathy

A
  • Hard exudates (cheese colour lipid - protein goes out of the vessels)
  • Microaneurysms (bulging vessles)
  • Blot haemorrhages (bleeding from these vessels)
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6
Q

Describe pre-proliferative diabetic retinopathy

A
  • If you don’t treat background diabetic retinopathy
  • Cotton wool spots also called soft exudates
  • Represent retinal ischaemia
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7
Q

Describe proliferative retinopathy

A
  • Visible new vessles

- On disk of elsewhere in retina

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8
Q

Describe maculopathy

A
  • Hard exudates near the macula
  • Same disease as background, but near the macula
  • Can threaten direct vision
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9
Q

How is background diabetic neuropathy treated?

A
  • Improve blood glucose control

- Warn patient that warning signs are present (screen once a year)

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10
Q

How is pre-proliferative diabetic retinopathy managed?

A
  • Suggests general ischaemia, if left new vessels will grow
  • Pan retinal photocoagulation (small laser beams fired into the back of the retina to prevent new vessels forming and bleeding)
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11
Q

What is needed in management of proliferative diabetic retinopathy?

A

Pan retinal photocoagulation

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12
Q

How is maculopathy managed?

A
  • Only problem around the macula

- Needs a grid of photocoagulation (targeted to the macula)

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13
Q

List the glomerular changes in nephropathy

A
  • Mesangial cell expansion
  • Basement membrane thickening (important)
  • Glomerulosclerosis
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14
Q

Describe the epidemiology in nephropathy

A
  • T1DM 20-40% after 30-40 years (lower risk of cardiovascular disease as usually younger)
  • T2DM - probably equivalent, but depends on age of development, race, age at presentation, and loss due to cardiovascular morbidity
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15
Q

List the clinical features of diabetic nephropathy

A
  • Progressive proteinuria (urine dipstick or microalbumin)
  • Increased BP
  • Deranged renal function
    (- Increased risk of heart disease)
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16
Q

List the strategies for intervention in diabetic nephropathy

A
  • Diabetic control
  • Blood pressure control (ACE inhibitors)
  • Inhibition of activity of the RAS system
  • Stopping smoking
17
Q

How does inhibition of RAS system stop diabetic nephropathy?

A

Angiotensin II has negative effects on the kidney

  • Mediation of glomerular hyperfiltration
  • Increased tubular uptake of proteins
  • Induction of pro fibrotic cytokines
  • Stimulation of glomerular and tubular growth
  • Podocyte effects
  • Induction of pro inflammatory cytokines
  • Stimulates fibroblast proliferation
  • Up regulation of adhesion molecules on endothelial cells
  • Up regulation of lipoprotein receptors
18
Q

What is diabetic neuropathy?

A

When small vessels supplying nerves (vasa nervorum) are blocked

19
Q

List the types of diabetic neuropathy

A
  • Peripheral polyneuropathy (most common - glove and stocking distribution)
  • Mononeuropathy
  • Mononeuritis multiplex
  • Radiculopathy
  • Autonomic neuropathy
  • Diabetic amyotrophy
20
Q

What is peripheral neuropathy?

A
  • Most common is loss of sensation in nerves supplying feet
  • More common in taller people
  • Danger is that patients will not sense injury
  • Patients with poor glucose control
21
Q

How is peripheral neuropathy characterised?

A
  • Loss of ankle jerks
  • Loss of vibration sense (using tuning fork)
  • Multiple fractures on x ray (Charcots joint)
22
Q

What is mononeuropathy?

A
  • Sudden motor loss (usually)
  • Wrist drop/ foot drop
  • Cranial nerve palsy
  • Double vision due to third nerve palsy
23
Q

What is pupil sparing third nerve palsy?

A
  • Eye is down and out
  • Pupil responds to light
  • Probably caused by diabetes
24
Q

What are the signs of a space occupying lesion that causes a third nerve palsy?

A

Will press on parasympathetic fibres first, causing a fixed dilated pupil

25
Q

What is mononeuritis multiplex?

A

A random combination of peripheral nerve lesions

26
Q

What is radiculopathy?

A

Pain over spinal nerves, usually affecting a dermatome on the abdomen or chest wall

27
Q

What is autonomic neuropathy?

A

Loss of sympathetic and parasympathetic nerves to GI tract, bladder, cardiovascular system.

28
Q

List the symptoms of autonomic neuropathy

A

GI

  • Difficulty swallowing
  • Delayed gastric emptying
  • Constipation/ nocturnal diarrhoea
  • Bladder dysfunction

Postural hypotension
Cardiac autonomic supply
- Reports of sudden cardiac death

29
Q

How is autonomic neuropathy monitored?

A
  • Measure changes in heart rate in response to Valsalva manoevre (forceful attempted exhalation against a closed airway, usually done by closing one’s mouth, pinching one’s nose shut then exhaling)
  • Normally there is a change in heart rate
  • Look at ECG and compare R-R intervals
30
Q

What is used to test peripheral neuropathy?

A

Monofilament examination - nylon wire bends applying specific amount of force

31
Q

List the predisposing factors for foot disease in diabetes

A
  • Neuropathy (motor, sensory, autonomic)

- Peripheral vascular disease

32
Q

Describe the epidemiology of diabetic food disease

A
  • 2-3% diabetics in England and Wales
  • Past or current foot disease 5-7%
  • Risk of amputation 60 times higher (poor prognosis in diabetics)
  • 10% bed occupancy due to diabetes related problems (half of this diabetic foot disease)
33
Q

What is the pathway to foot ulceration?

A
  • Sensory neuropathy (step on nails/ burns)
  • Motor neuropathy (imbalance between flexors and extensors causes shape of the foot to be lost, clawing of toes causes pressure disturbance)
  • Glycosylated tendons and limited joint mobility (collagen flexibility is lost)
  • Autonomic neuropathy (loss of control of sweat glands causes dry skin)
  • Atherosclerosis (peripheral vascular disease - reduced blood supply)
  • Trauma, reduced resistance to infection, and retinopathy (cant see obstacles in the way)
34
Q

What are the main types of foot disease?

A
  • Neuropathic (numb, warm, dry, palpable pulses and ulcers at points of high pressure loading)
  • Ischaemic foot (cold, pulseless, ulcers at foot margins)
  • Neuroischaemic (both - numb, cold, dry, pulseless, ulcers at points of high pressure loading + at foot margins)
35
Q

How is the foot of a diabetic patient assessed?

A
  • Appearance (deformity)
  • Feel (hot/ dry)
  • Foot pulses (dorsalis pedis and posterior tibial pulse)
  • Neuropathy (vibration, temperature, reflex, fine touch)
36
Q

How is diabetic foot disease prevented?

A
  • Control sugar
  • Dyslipidaemia treated
  • Diet and exercise (weight loss)
  • Inspect feet
  • Stop smoking
  • Hypertension
  • Education
37
Q

How is foot ulceration managed?

A

Relief of pressure

  • Bed rest (risk of DVT, heel ulceration)
  • Redistribution of pressure/total contact cast
  • Antibiotics, possibly long term
  • Debridement (surgery - removal of dead tissue/calluses)

Revascularization

  • Angioplasty
  • Arterial bypass surgery

Eventual amputation of the foot

38
Q

Where do ulcers commonly occur in foot disease?

A

Ball of the great toe

Year 2 LCRS (128 decks)

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