Microvascular Complications Flashcards

1
Q

What sites are included in microvascular complications?

A
  1. Renal arteries
    - leads to diabetic retinopathy
  2. Glomerular arterioles - kidneys
    - leads to nephropathy
  3. Vasa nervorum - tiny blood vessels that supply nerves
    - leads to neuropathy
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2
Q

What can microvascular complications come about/ be exacerbated by?

A

o Severity of hyperglycaemia

  • the worse it is, the worse the damage
  • the higher the HbA1C, the worse the microvascular complication

o Hypertension
o Genetic

o Hyperglycaemic memory
- poor diabetes control, even for a brief period, will give an increased of microvascular complication (compared to someone that has had good control throughout)

o Tissue damage
- originally reversible BUT later irreversible alterations in proteins

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3
Q

Possible mechanisms of glucose damage?

A

o Polyol pathway
o AGEs
o Protein Kinase C
o Hexosamine

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4
Q

Diabetic Retinopathy?

A

Damage to renal arteries!

Main cause of visual loss in people with diabetes and the main cause of blindness in people of working age

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5
Q

Normal retina?

A

Optic disc - at the nasal part of eye

Macula - more lateral (i.e. central)

ONENOTE!

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6
Q

What is the function of the macula?

A

Involved in
o colour vision
o acuity (clarity of vision)

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7
Q

4 different types of Diabetic Retinopathy?

A
  1. Background diabetic retinopathy
  2. Pre-proliferative diabetic retinopathy
  3. Proliferative retinopathy
  4. Maculopathy
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8
Q

Background Diabetic Retinopathy?

A

o Hard exudates

  • appear cheesy yellow spaces in retina
  • caused by leakage of lipid content

o Microaneurysms
- small blood vessel bulge

o Blot haemorrhages
- blots of blood that are ruptured microaneurysms

ONENOTE!!

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9
Q

Pre-proliferative diabetic retinopathy?

A

o Cotton wool spots - SOFT EXUDATES
- these show retinal ischaemia

ONENOTE!!

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10
Q

Proliferative retinopathy?

A

o Visible NEW vessels

  • form as a response to the retinal ischaemia
  • generally more FRAGILE so can bleed at any time
  • can form on optical disc or elsewhere

If vessels form in region of macula, can cause problems w. acuity & colour vision

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11
Q

Maculopathy?

A

Same as ‘Background DR’ BUT nearer to macula

o Hard exudates NEAR MACULA
- can threaten DIRECT VISION!

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12
Q

How can Background DR be managed?

A

o Improve control of blood glucose

o Warn patient that warning signs are present

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13
Q

How can Pre-proliferative DR be managed?

A

Suggests general ischaemia SO need to stop it from progressing to proliferative DR! Need:

o Pan-retinal photocoagulation
- laser to retina to stop vessels from bleeding

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14
Q

How can Proliferative DR be managed?

A

ALSO needs pan-retinal photocoagulation

dark spots shows its been used - ONENOTE!!

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15
Q

How can Maculopathy be managed?

A

Only have problem around macula so only need a GRID of photocoagulation!
i.e. grid-retinal photocoagulation

NOT pan-retinal photocoagulation

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16
Q

Diabetic Nephropathy?

A

Glomerular arteries in the kidneys

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17
Q

Features of diabetic nephropathy?

A

o Hypertension
o Progressively increasing proteinuria
o Progressively deteriorating kidney function

o Classical histological features

18
Q

What can diabetes increase the risk of?

A

Having diabetes & CKD can increase risk of CV events occurring

19
Q

You can see classic histological features for diabetic nephropathy - what are they?

A
  1. Glomerular changes
    o mesangial expansion
    o BM thickening
    - both are due to overproduction of matrix

o glomerulosclerosis (hardening of capillaries)

  1. Vascular
  2. Tubulointestinal
20
Q

Relationship between retinopathy, CKD and diabetes?

A

If there is NO retinopathy

ANY CKD can NOT be due to diabetes (they come together)

21
Q

Epidemiology of T1 & T2DM in terms of CKD?

A

T1DM
o 20-40% of patient have CKD after 30-40years

T2DM
 o probably equivalent BUT difficult to determine due to
  - age of development of disease
  - racial factors
  - age at presentation
  - loss due to CV morbidity
22
Q

Clinical features of diabetic nephropathy?

A

o Progressive proteinuria

  • hallmark for CKD
  • Normal range = <30mg/24hrs
  • Nephrotic range = >3000mg/24hrs

o Increased BP

  • glomerulus becomes less flexible & harder
  • absorption of nutrients can change - more pressure going through kidneys
  • changes BP control

o Deranged renal function
- GFR decreases

23
Q

Intervention strategies for diabetic nephropathy?

A
  1. Diabetic control
    o the lower the HbA1C, the lower the microvascular complications
  2. BP control
    o will slow down the deterioration of kidnet function
  3. Inhibition of RAS
    o ACE inhibitors reduce rate of decline of creatinine and thus kidney function
    o ANGII involved in many growth & inflammatory pathways so inhibiting it is good
  4. STOP SMOKING
24
Q

Why can ANGII be detrimental in diabetic nephropathy?

A

o Stimulates pathways resulting in overproduction of matrix

o Cause constriction of efferent arterioles
- increasing transglomerular capillary pressure

o Lead to increasing rigidity of endothelial cells (onenote!!)

25
How can drugs target the RAS?
ACE is found in the lungs! Drugs can target: o Block renin activity o ACE inhibitors o AT1 antagonists (AT1 is a receptor)
26
Example of ANGII Receptor Antagonist?
Irbesartan
27
Diabetic Neuropathy?
Vaso nervum are blocked! MOST COMMON cause of neuropathy Leads to lower limb amputation
28
6 types of diabetic neuropathy?
1. Peripheral polyneuropathy 2. Mononeuropathy 3. Mononeuritis multiplex 4. Radiculopathy 5. Autonomic neuropathy 6. Diabetic amyotrophy @ Parties, Marilyn Manroe Regularly Abuses Drugs
29
How can diabetic neuropathy occur?
Interply between o genetics AND o inflammation cascade causes diabetic neuropathy to occur
30
Peripheral neuropathy?
Affects peripheral nerves! o affects longest nerves that supply the feet - causes loss of sensation (dangerous as will not sense injury to foot) - more common in tall people - more common in patients w. poor glucose control
31
How can peripheral neuropathy be investigated?
Monofilament examination tracks loss of sensation
32
When investigating peripheral neuropathy, what characteristics can be seen?
o loss of ankle jerks o loss of vibration sense (using tuning fork) o Charcot's joint - multiple fractures on foot X-ray
33
Mononeuropathy?
Only ONE NERVE blocked o usually SUDDEN MOTOR LOSS - results in wrist & foot drop o Cranial nerve palsy
34
Explain cranial nerve palsy in relation to mononeuropathy and the eye movement
Double vision due to 3rd nerve palsy ('down and out') o Lateral rectus - abducent nerve (CNXI) - pulls eye OUT o Superior oblique - trochlear nerve (CNIX) - pulls eye DOWN
35
Do the pupils respond to light in mononeuropathy?
YES! Pupil-sparing as PNS fibres on the outside - so these do NOT lose blood supply in diabetes Aneurysms can cause 3rd nerve palsy o will press on the PNS fibres o causes a FIXED DILATED PUPIL o this is NOT due to diabetes!!
36
Mononeuritis multiplex?
MANY NERVES affected! A random combination of PERIPHERAL nerve lesions
37
Radiculopathy?
Dematomes affected! Pain OVER spinal nerves o normally dermatomes on the abdomen or chest wall
38
Autonomic neuropathy?
Loss of SNS & PNS nerves to: o GI tract o bladder o CVS
39
What can autonomic neuropathy go on to cause due to its characteristic?
``` GI tract o Dysphagia o delayed gastric emptying o constipation/nocturnal diarrhoea o bladder dysfunction ``` Postural hypotension o can be disabling - collapsing on standing Cardiac autonomic supply o can have sudden cardiac death
40
How can you check for autonomic neuropathy?
Measure changes in HR is response to VALSALVA MANUOUEVRE o make them blow into a tube and this normally causes a change in HR o look at ECG and compare the R-R intervals
41
Diabetic amyotrophy?
Inflammation & loss of pain Diabetic foot?