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Met3 > Diabetes: Diabetic complications > Flashcards

Diabetes: Diabetic complications Flashcards

1
Q

Describe why diabetic complications occur [3]

A

Long term exposure to hyperglycaemia:

  • causes mircroaneurysms and venous beading (where the walls of the veins are no longer straight and parallel and look more like a string of beads or sausages)
  • vessel closure: hypoxia & nutrients decreased
  • vessel permeability: damaged vessels dilate and leak
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2
Q

Which is the strongest risk factor for diabetic complications? [1]
Name 3 others [3]

A

1st: Smoking
2nd: HTN
3rd: Dysplidaemia
4th: Hyperglycaemia

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3
Q

Describe the pathophysiology of diabetic retinopathy [3]

A

Chronic hyperglycemia causes:
- basement membrane thickening
- loss of pericytes
- endothelial cell damage in retinal blood vessels (microaneurysms & venous beeding

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4
Q

Describe the three classifications of diabetic retinopathy? [2]

A

non-proliferative diabetic retinopathy (NPDR) marked by:
- microaneurysms
- retinal haemorrhages (dot haemorrhages)
- hard exudates (yellowish deposits of lipid due to vessel leakage)

proliferative diabetic retinopathy (PDR) (more advanced and severe stage), is characterized by:
- the proliferation of new, fragile blood vessels that can bleed into the vitreous, leading to vision loss due to VEGF upregulation
- can be new vessels on disc (NVD) OR new vessels everywhere (NVE)

Diabetic maculopathy:
- Presence of any retinopathy within 1 disc diameter around macula:
Can be:
- Focal
- Diffuse
- Ischaemic

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5
Q

How can you prevent diabetic retinopathy? [3]

A

Good BP control - most important
Good glycaemic control
Annual screening

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6
Q

What are the different types of classification of hard exudates in non-proliferatve retinopathy? [3]

A

Mild
Moderate
Severe: Cotton wool spots (arrow): areas of retinal ischaemia

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7
Q

What does this yellow arrow depict in non-proliferative diabetic retinopathy? [1]

A

Hard exudates

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8
Q

What does the yellow arrow on the image of non-proliferative retinopathy depict? [1]

A

Lipid exudates

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9
Q

Describe what the arrows & circle depict on this image of non proliferative diabetic retinopathy [3]

A

intraretinal microvascular abnormality (IRMA; green arrow)

venous beading and segmentation (blue arrow)

cluster haemorrhage (red circle)

featureless retina suggestive of capillary non-perfusion (white ellipse)

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10
Q

What is the arrow pointing to on this NPDR? [1]

A

Cotton wool spots (severe NPDR

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11
Q

How can PDR lead to blindness? [4]

A
  • New blood vessels are very fragile; easily break and leak
  • Retinal haemorrhage can lead to acute blindness
  • If repeated; leads to fibrosis & scarring
  • Can lead to: tractional retinal detachment: when scar tissue or other tissue grows on your retina and pulls it away from the layer underneath
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12
Q

Which pathology is depicted? [1]

A

Diabetic maculopathy: hard exudates near to the macula

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13
Q

What is depicted in this image? [1]

A

Proliferative diabetic retinopathy:
extensive vitreous haemorrhage obscuring most of fundus (white circle)}

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14
Q

What is the arrow pointing to? [1]

A

Cotton wool spot

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15
Q

What is depicted in this image? [1]

A

Non-proliferative diabetic retinopathy: blot haemorrhage (white circle)}

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16
Q

Describe what is happening in this image [1]

A

Proliferative diabetic retinopathy: NVD new vessels on the optic disc

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17
Q

What is the management of diabetic retinopathy? [5]

A

Laser photocoagulation

Anti-VEGF medications such as ranibizumab, bevacizumab & Aflibercept

Vitreoretinal surgery (keyhole surgery on the eye) may be required in severe disease or a vitrectomy may be necessary to clear severe vitreous hemorrhage or to relieve tractional retinal detachment.

Corticosteroids (triamcinolone, dexamethasone implant) can also be used, particularly in refractory DME.

Pan-retinal photocoagulation (PRP): laser used to make small burns evenly across the peripheral retina - should make blood vessels shrink and dissapear

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18
Q

What are the different types of diabetic neuropathy? [5]

A
  • Periperal sensory neuropathy
  • Autonomic neuropathy
  • Proximal motor neuropathy (amyotrophy; femoral nerve neuropathy - severe pain in anterior thigh & quadricep wasting)
  • Cranial nerve palsies (CN III, VI & VII)
  • Median nerve / Carpal tunnel syndrome
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19
Q

Which cranial nerves are particularly effected by diabetes? [3]

A

Cranial nerve palsies: CN III, VI & VII

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20
Q

Describe the distribution for peripheral sensory neuropathy [1]

A

Glove and stocking distribution

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21
Q

Describe the treatment regime for diabetic peripheral neuropathy [4]

What are two additonal therapies if these don’t work? [2]

A

first-line treatment: amitriptyline, duloxetine, gabapentin or pregabalin

if the first-line drug treatment does not work try one of the other 3 drugs
tramadol may be used as ‘rescue therapy’ for exacerbations of neuropathic pain

topical capsaicin may be used for localised neuropathic pain

pain management clinics may be useful in patients with resistant problem

22
Q

Describe why ulcers commonly occur in diabetic patients [2]

A

Neuropathic ulcers are caused by loss of sensorium, leading to the inability to withdraw the area from painful stimuli such as friction, shear forces, or traumatic processes leading to the opening of the skin and ulceration.

23
Q

Describe the effects of diabetic autonomic neuropathy on genito-urinary [2]; GI [3] & CV [1] systems

A

Genito-urinary
- ED
- Atonic bladder: difficulty voiding / urinary incontinence

Gastrointestinal [3]:
- Gastroparesis: stomach doesn’t empty properly, causing outflow problems: recurrent vomiting & early satiety
- Chronic constipation & diarrhoea
- Gustatory sweating: severe sweating on eating

CV [1]:
- Postural hypotension

24
Q

Risk factors for diabetic nephropathy? [5]

A

Duaration of diabetes
HTN
Poor glycaemic control
Male
Smoking
Ethnicity
Fhx

25
Q

What is the clinical presentation triad of diabetic nephropathy? [3]

A

Hypertension
Albuminuria
Decline renal function

26
Q

What does the green arrows point to? [1]

A

Kimmelstein-Wilson lesion

27
Q

Describe the pathophysiology of diabetic nephropathy [4]

A

Oxidative stress consumes nitric oxide, which prevents flow-mediated dilation of blood vessels (endothelial dysfunction): subjecting the endothelium to injury

Leads to production of cytokines, acceleration of inflammation, worsening of blood vessel rigidity due to atherosclerosis, and further impairment of FMD and susceptibility to oxidative stress.

Platelet-derived growth factor (PDGF) and transforming growth factor-beta (TGF-beta) mediate mesangial expansion and fibrosis via the stimulation of matrix protein (collagen and fibronectin) synthesis and decreased matrix degradation

Angiotensin II (ATII), elevated in DKD, constricts the efferent arteriole in the glomerulus, causing high glomerular capillary pressures, and also stimulates fibrosis and glomerular inflammation

28
Q

What specific things do you screen for with patients of suspected diabetic nephropathy? [1]

A

Microalbuminuria

29
Q

How do you screen for microalbuminuria for suspected diabetic nephropathy patients? [2]

A

Measure urine albumin:creatinine ratio (ACR):
- Normal is < 2.5mg/mmol men; < 3.5 mg/mmol in women
- If evelated repeated x2: 2/3 positive microalbuminuria present
- (can be elevated by meat; running)

30
Q

Describe the treatment regime for nephropathy (have microalbuminuria) [7]

A

Control BP:
- ACE inhibitor: captopril; elanapril; lisinopril; ramipril
- ARB if ACE inhibitor not tolerated; losartan; valsartan
- Add calcium-channel blocker amlodopine; felopdipine; nifedipine and/or thiazide-like diuretic: hydrochlorothiazide; and/or beta-blocker carvedilol; metaprolol

Optomise blood glucose control

Manage CV risk factors aggressivey

Manage lipid levels: atorvostatin

Stop metformin when eGFR < 30 mls/min

Refer to specialist if eGFR < 45 mls/min

Renal transplant if giving pancreatic transplant

31
Q

When should you stop prescribing metformin a patient suffering from diabetic nephropathy? [1]

A

Stop metformin when eGFR < 30 mls/min

Refer to specialist if eGFR < 45 mls/min

32
Q

Why is treating CV risks with diabetes a priority? [1]

A

Diabetes increases the risk of cardiac disease (e.g. MI) massively - have 3/10 year reduced life expectancy

33
Q

Why may MIs be ‘silent’ in patients with diabetes? [1]

A

Suffering from autonomic neuropathy

34
Q

What are common skin presentations of diabetes? [6]

A
  • Oral / genital candidiasis
  • Skin abcesses
  • Rhinocerebral mucormycosis infection
  • Fungal nail infections
  • Aconthosis nigricans (sign of insulin resistance)
  • Bullosis Diabeticorum (blisterng)
  • Granuloma annulare
  • Necrobiosis Lipoidica Diabeticorum (pink skin lesion on lower legs)
35
Q

What is this skin condition associated with diabetes? [1]

A

Necrobiosis Lipoidica Diabeticorum

36
Q

What is the name of this skin complication of diabetes? [1]

A

Granuloma annulare

37
Q

What is the name for this diabetic skin complication? [1]

A

Bullosis Diabeticorum

38
Q

Which two rheumatological manifestations of diabetes need to know?

A

Charcot neuroarthopathy: chronic, devastating, and destructive disease of the bone structure and joints in patients with neuropathy; it is characterized by painful or painless bone and joint destruction in limbs that have lost sensory innervation

Diabetic cheiroarthropathy: limited mobility of the joints of the hands

39
Q

Name this complication of diabetes

A

Charcot neuroarthropathy

40
Q

Name this sign [1] and disease [1] that is a complication of diabetes

A

Prayer sign; diabetic cheiroarthropathy

41
Q

The following term describes which sign of diabetic retinopathy

Damaged vessels may rupture and leak blood.

Venous beading
Cotton wool spots
Hard exudates
Dot and blot haemorrhages
Microaneurysms

A

The following term describes which sign of diabetic retinopathy

Damaged vessels may rupture and leak blood.

Venous beading
Cotton wool spots
Hard exudates
Dot and blot haemorrhages
Microaneurysms

42
Q

The following term describes which sign of diabetic retinopathy

transient, small, whitish opacities with feathery edges located within the superficial retina and represent microinfarctions of small retinal arteriole

Venous beading
Cotton wool spots
Hard exudates
Dot and blot haemorrhages
Microaneurysms

A

The following term describes which sign of diabetic retinopathy

transient, small, whitish opacities with feathery edges located within the superficial retina and represent microinfarctions of small retinal arteriole

Venous beading
Cotton wool spots
Hard exudates
Dot and blot haemorrhages
Microaneurysms

43
Q

The following term describes which sign of diabetic retinopathy

Deposits of lipids that have leaked onto the retina through damaged vessels.

Venous beading
Cotton wool spots
Hard exudates
Dot and blot haemorrhages
Microaneurysms

A

The following term describes which sign of diabetic retinopathy

Deposits of lipids that have leaked onto the retina through damaged vessels.

Venous beading
Cotton wool spots
Hard exudates
Dot and blot haemorrhages
Microaneurysms

44
Q

The following term describes which sign of diabetic retinopathy

“Out-pouching” results from weakened capillary walls. The earliest visible clinical sign of diabetic retinopathy.

Venous beading
Cotton wool spots
Hard exudates
Dot and blot haemorrhages
Microaneurysms

A

The following term describes which sign of diabetic retinopathy

“Out-pouching” results from weakened capillary walls. The earliest visible clinical sign of diabetic retinopathy.

Venous beading
Cotton wool spots
Hard exudates
Dot and blot haemorrhages
Microaneurysms

45
Q

What is the most common cause of visual loss in patients with diabetes? [1]

Describe this [1]

A

Diabetic macular oedema (DMO)

DMO is the commonest cause of visual loss in patients with diabetes

DMO is characterised by oedematous changes in or around the macula. As the macula is responsible for central vision, affected patients tend to complain of blurred vision when reading or difficulty recognising faces in front of them. DMO is the commonest cause of visual loss in patients with diabetes.9

46
Q

DMO can be subcategorised into three categories. Describe them [3]

A

Focal/diffuse macular oedema:
* the fluid that escapes from damaged vessels can be well-circumscribed (focal) or more widespread and poorly demarcated in nature (diffuse).

Ischaemic maculopathy:
- patients will be symptomatic with defects in visual acuity due to ischaemia at the site of the macula. These areas are best visualised with fluorescein angiography.

Clinically significant macular oedema (CSMO):
- CSMO describes significant changes associated with retinopathy, such as hard exudates and retinal thickening, found within a certain distance to the fovea or greater than a certain size.

47
Q

What is the name of this treatment for diabetic retinopathy? [1]

A

Pan-retinal photocoagulation (PRP)

48
Q

Name a complication of diabetic retinopathy [1]

A

Diabetic retinopathy is one of several causes of neovascular glaucoma: a type of secondary glaucoma.

Neovascularization can occur within the iris and its trabecular meshwork (rubeosis) causing a narrowing and closure of the drainage angle and therefore increased intraocular pressure.

49
Q

Diabetic ketoacidosis: once blood glucose is < 14 mmol/l due to NaCl and fixed rate insulin has been given. What is the next appropriate step? [1]

A

Diabetic ketoacidosis: once blood glucose is < 14 mmol/l an infusion of 10% dextrose should be started at 125 mls/hr in addition to the saline regime

50
Q

When are SGLT-2 inhibitors indicated in diabetes patients? [4]

A

the patient has ahigh risk of developing cardiovascular disease (CVD, e.g. QRISK ≥ 10%)
the patient has established CVD
the patient has chronic heart failure
SGLT-2 inhibitors should also be started at any point if a patient develops CVD (e.g. is diagnosed with ischaemic heart disease), a QRISK ≥ 10% or chronic heart failure

metformin should be established before introducing the SGLT-2 inhibitor

51
Q

If metformin is contraindicated in a diabetic patient, what should a patient be prescribed if:
- the patient has a risk of CVD, established CVD or chronic heart failure [1]
- if the patient doesn’t have a risk of CVD, established CVD or chronic heart failure [2]

A

if the patient has a risk of CVD, established CVD or chronic heart failure:
* SGLT-2 monotherapy
if the patient doesn’t have a risk of CVD, established CVD or chronic heart failure:
* DPP‑4 inhibitor or pioglitazone or a sulfonylurea
* SGLT-2 may be used if certain NICE criteria are met

52
Q

If a patient is presenting with Diabetic ketoacidosis: [] should be used initially, even if the patient is severely acidotic [1]

What is the following treatment? [3]

A

Diabetic ketoacidosis: isotonic saline should be used initially, even if the patient is severely acidotic

an intravenous insulin infusion should be started at 0.1 unit/kg/hour
once blood glucose is < 14 mmol/l an infusion of 10% dextrose should be started at 125 mls/hr in addition to the 0.9% sodium chloride regime

potassium may therefore need to be added to the replacement fluids

Met3 (52 decks)

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