Complications of Diabetes Flashcards

1
Q

Name some acute complications of T1DM?

A

Ketoacidosis

Hypoglycaemia.

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2
Q

List some chronic microvasuclar complications of T1DM?

A

Reinopathy
Neuropathy
Nephropathy.

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3
Q

List some chronic macrovascular complications of T1DM?

A

Ischaemic heart disease
Peripheral vascular disease
Cerebrovascular disease.

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4
Q

What did the UKPDS and DCCT trails prove?

A

That intensive glycaemic control can help prevent microvascular disease.

Glycaemic control isnt as important for macrovascular disease - BP, cholesterol and smoking are more important factors.

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5
Q

What 2 factors cause microvascular disease?

A

Capillary damage.

Metabolic damage.

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6
Q

What can cause capillary damage?

A

Hyperglycaemia (small vessels will be structually and functionally abnormal).
Increased blood flow.
Increased capillary pressure.
Thickened and damaged vessel walls.
Endothelial damage (leakage of albumin and other proteins).

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7
Q

What causes metabolic damage?

A

Most tissues need insulin to take up glucose - except retina, kidney and nerves.
Glucose goes across these cell membranes and is metabolised to sorbitol by aldose reductase.
Excessive glucose enters the polyol pathway and sorbitol accumulates, there is less NADPH for cell metabolism and build up of reactive oxygen species and oxidative stress leads to cell damage.

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8
Q

Why is microvascular disease not so much of an issue in T2DM?

A

As patients with T2DM usually die of CV first.

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9
Q

Describe the stages of diabetic retinopathy?

A
  1. Hyperglycaemia: damage to small vessel wall and microaneurysms.
  2. Dot haemorrhages: When vessel wall is breached.
  3. Hard exudates: When protein and fluid is left behind after blood drain away.
  4. Cotton wool spots: Micro-infarcts.

LATER STAGES
Damage to veins: Venous budding and blockage of blood supply.

Ischaemia - VEGF and other growth factors cause neovascularisation, proliferative retinopathy and these vessels are weak so prone to bursting causing vitreous haemorrhage. This happens as vessels try to pass blockage.

Fluid not cleared from macular area - macular oedema.

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10
Q

How is retinopathy prevented?

A

Good glycaemic control.
Stop smoking.
Good BP control.
Retinal screening for diabetic patients aged 12+. Taking pictures of the eye.

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11
Q

How is retinopathy treated?

A
Addressing risk factors.
Ophthalmic review;
- Laser new blood vessels.
- VEGF inhibitors to stop new vessels forming.
- Vitrecotomy
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12
Q

List the stages of diabetic nephropathy?

A
  1. Renal enlargement and hyperfiltration: so GFR increases. The afferent arteriole vasodilates and there is an increase in glomerular pressure, thickened BM, capillary damage and shear stress on endothelial cells.
  2. Microalbuminuria: Tiny traces of albumin that cant be detected on the dipstick. It can be used as an independent CV disease predictor.
  3. Macroalbuminuria.
  4. End stage renal failure: As there is glomerularsclerosis and destruction.
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13
Q

How can nephropathy be prevented/treated?

A

Screening for microalbuminuria every year from diagnosis.
ACEi/ARB if microabuminuria present to slow progression.
Improve glycaemic control.
CV prevention with statins, smoking reduction.
Refer to renal clinic if eveloped CKD (eGFR <30)

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14
Q

List types of diabetic neuropathy?

A

Peripheral (sensory) neuropathy.
Autonomic neuropathy.
Mononeuritis multiplex.
Diabetic amyotrophy.

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15
Q

What causes neuropathy?

A

Capillary damage occurs to vessels that supply nerves.
Sorbitol can build up and there is often occlusion in the vasa nervorum.
This impairs nervous signalling and impairs both sensory and motor function.

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16
Q

What clinical signs are seen in neuropathy?

A

Decreased vibratory sensation.
Decreased pressure sensation.
Decreased reflexes in knee and ankle.
Loss of proprioception.
Cant sense hot/cold.
Unusual sensitivity when feet are touched.
Decreased proprioception (ability to sense position of feet).
Symptoms such as numbness, prickling and pain.

Can have tissue damage, clawing toes, callus, ulceration.

17
Q

What is the diabetic foot?

A

Combination of neuropathy and peripheral vascular disease.

Often causes infection, ulcers and ischaemia.

18
Q

How is diabetic foot symptoms prevented?

A
If low risk (normal sensation and pulses): Annual review. 
Medium risk (neuropathy or absent pulses): Review by podiatrist every 3-6 month. 
High risk (deformities or ulceration): Podiatrist review every 1-3 months.
19
Q

What is Charcot foot?

A

Numbness (repeated microtrauma and stress fractures) and dysregulated blood flow (bone turnover and fragile bone).

20
Q

Describe features of autonomic neuropathy in different systems?

A

CV: Postural hypotension.
GU: Erectile dysfunction.
GI: Gustatory sweating or gastroparesis.
MSK: Diabetic myotrophy (proximal neuropathy - thigh/buttock).
Mononeuritis Multiplex: Painful assymetrcal motor and sensory neuropathy (2+ nerves).

21
Q

What would be involved in the annual review for DM?

A

HbA1c
Cholesterol, HDL and TG
Creatinine
Microalbuminuria

Lifestyle - exercise, diet, smoking.
Drug therapy.
Mental well-being.

Visual acuity.
Retinal screening.
Pedal pulses.
Foot sensations.
BMI.
BP.
Erectile function. 
Contraception.
22
Q

What test should be done in mothers with DM during pregnant?

A

HbA1c to reduce risk of congenital malformations.

23
Q

What does good glycaemic control during pregnancy help prevent?

A

Macrosomnia.

24
Q

What is HbA1C?

A

Glycosylated Hb.
This develops when Hb joins with glucose.
Takes 3 months to change so when measuring its usually 3 month checks.