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Year 2 - Endocrinology > Microvascular Complications > Flashcards

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
Q

How can drugs target the RAS?

A

ACE is found in the lungs!

Drugs can target:
o Block renin activity
o ACE inhibitors
o AT1 antagonists (AT1 is a receptor)

26
Q

Example of ANGII Receptor Antagonist?

A

Irbesartan

27
Q

Diabetic Neuropathy?

A

Vaso nervum are blocked!

MOST COMMON cause of neuropathy
Leads to lower limb amputation

28
Q

6 types of diabetic neuropathy?

A
  1. Peripheral polyneuropathy
  2. Mononeuropathy
  3. Mononeuritis multiplex
  4. Radiculopathy
  5. Autonomic neuropathy
  6. Diabetic amyotrophy

@ Parties, Marilyn Manroe Regularly Abuses Drugs

29
Q

How can diabetic neuropathy occur?

A

Interply between
o genetics
AND
o inflammation cascade

causes diabetic neuropathy to occur

30
Q

Peripheral neuropathy?

A

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
Q

How can peripheral neuropathy be investigated?

A

Monofilament examination

tracks loss of sensation

32
Q

When investigating peripheral neuropathy, what characteristics can be seen?

A

o loss of ankle jerks
o loss of vibration sense (using tuning fork)

o Charcot’s joint - multiple fractures on foot X-ray

33
Q

Mononeuropathy?

A

Only ONE NERVE blocked

o usually SUDDEN MOTOR LOSS
- results in wrist & foot drop

o Cranial nerve palsy

34
Q

Explain cranial nerve palsy in relation to mononeuropathy and the eye movement

A

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
Q

Do the pupils respond to light in mononeuropathy?

A

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
Q

Mononeuritis multiplex?

A

MANY NERVES affected!

A random combination of PERIPHERAL nerve lesions

37
Q

Radiculopathy?

A

Dematomes affected!

Pain OVER spinal nerves
o normally dermatomes on the abdomen or chest wall

38
Q

Autonomic neuropathy?

A

Loss of SNS & PNS nerves to:
o GI tract
o bladder
o CVS

39
Q

What can autonomic neuropathy go on to cause due to its characteristic?

A 
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
Q

How can you check for autonomic neuropathy?

A

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
Q

Diabetic amyotrophy?

A

Inflammation & loss of pain

Diabetic foot?

Year 2 - Endocrinology (19 decks)

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