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Yr 2 Endocrine > Diabetes Complications > Flashcards

Diabetes Complications Flashcards

1
Q

List the major complications of Diabetes?

A

Short Term:
Diabetic Ketoacidosis (DKA)
Hyperglycaemic Hyperosmolar State (HHS)
Hypoglycaemia

Long Term:
Macrovascular –> CAD/PAD/Stroke
Microvascular –> Retinopathy, Nephropathy, Neuropathy & PAD

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2
Q

Explain the macrovascular effects of diabetes?

A

DM accelerates Atherosclerosis

The Excess Glc bind to LDL preventing it from being cleared by liver cells –> Hyperlipidaemia

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3
Q

What is the major consequence of DM’s macrovascular effect?

A

Increased risk of athermatous diseases including CAD, MI, PAD & stroke

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4
Q

Explain DM’s microvascular effects?

A

DM triggers the Hyaline Change in areterioles/capillaries by:

  • Glycosylating collagen in the subendothelial space allowing it bind albumin from the plasma
  • Glycosylating basal lamina proteins allowing them to bind and cross-link

These mechanisms cause a build up of proteins in the vessel wall causing narrowing

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5
Q

What are the consequences of DM’s microvascular effects?

A

Neuropathies
Retinopathy
Nephropathy
Peripheral Arterial Disease

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6
Q

What are the forms of Diabetic retinopathy?

A
  • Background Retinopathy
  • Proliferative Retinopathy (occurs after background retinopathy
  • Maculopathy (exudate/haemorrhage specfically at the macula)
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7
Q

What events occur causing diabetic retinopathy?

A

Background (Pre-proliferative):

  • Microaneurysms
  • Hard Exudates
  • Cotton wool spots (damaged nerves)

PRoliferative:

  • VEGF from damaged vessels –> Proliferation
  • Vitreous hemorrhage (potential complication of proliferation)
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8
Q

How do we treat proliferative retinopathy?

A

We can do a vitrectomy if theres a vitreous haemorrhage

Laser photocoagulation destroys ischaemic retina, reducing Endothelial Growth Factors causing the new vessels to regress

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9
Q

How do we treat maculopathy?

A

Grid laser therapy
Glc Control
BP control

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10
Q

How does diabetes affect cataracts?

A

It doubles risk of cataracts due to build up of glucose

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11
Q

What are the main types of diabetic neuropathy?

A

Peripheral Neuropathies (primarily the feet) including acute senory peripheral neuropathy and proximal motor neuropathy.

Mononeuritis

Autonomic Neuropathy

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12
Q

What is the main danger of peripheral neuropathy?

A

Foot ulcers that arn’t noticed -> infection -> Amputation

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13
Q

How would you tell if someone has peripheral neuropathy?

A

Small muscle wasting (e.g. between toes/tendons on foot)

Chronic sensory changes like paraesthesia, burning or numbess

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14
Q

How do we care for a peripheral neuropathy?

A

Pain relief:

  • Capsaisan cream
  • Amitriptyline

Protection of feet from ulceration:

  • Fitted footwear
  • Regular podiatry visits
  • Foot screening and risk assessment
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15
Q

What is Acute Sensory Peripheral Neuropathy?

A

A type of peripheral neuropathy brought on by Diabetes.

Its a rapid onset of neuro symptoms that can be severe followed by a gradual recovery.

Can be caused by rapid tightening of Glc control or acute metabolic upset

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16
Q

What is proximal motor neuropathy?

A

A type of peripheral neuropathy

Causes weight loss, pain and wasting, mainly in the legs of elderly men

17
Q

What are the main nerves affected by diabetic mononeuritis

A 
Motor ocular nerves (III, IV, VI)
Peroneal Nerve (acute foot drop)

They have acute onset and slow recovery

18
Q

What are the main features of autonomic neuropathies?

A 
Erectile Dysfunction
Postural hypotension
Gastric stasis -> Recurrent vomiting
Diarrhoea
Sweating, peripheral oedema & urinary retention
19
Q

Erectile dysfunction is a potential diabetic autonomic neuropathy, how do you treat it?

A

Phosphodiesterase inhibitors e.g. Viagra

20
Q

Postural Hypotension is a potential diabetic autonomic neuropathy, how do you treat it?

A

Tell them to stand up slowly, otherwise:

NSAIDS or Fludrocortisone

21
Q

Gastric stasis and vomiting is a potential diabetic autonomic neuropathy, how do you treat it?

A

Domperidone.

Dopamine antagonist that acts as an antiemetic and progastrokinetic

22
Q

Diarrhoea is a potential diabetic autonomic neuropathy, how do you treat it?

A

Loperamide (i.e. imodium)

23
Q

How does diabetic nephropathy arise?

A

Microvascular damage to glomeruli capillaries causing them to leak proteins into the urine and eventually become unable to filter blood

24
Q

How do we detect Diabetic nephropathy early on?

A

a 1st morning urine sample or timed over night urine collection to test for albumin in the urine

Important as its still reversible early on

25
Q

Whats the progression of Diabetic Nephropathy?

A

Microalbuminuria
Proteinuria
Impaired renal function (+/- nephrotic syndrome)
End stage renal disease

26
Q

How do we manage diabetic nephropathy?

A
  • Glycaemic control
  • BP control
  • ACE inhibitor slows progression & treats BP
  • CVD risk factor control
27
Q

What is Diabetic Ketoacidosis?

A

A large number of Ketone bodies produced from FAs by the liver, turning the blood acidic

28
Q

What causes DKA?

A

Low levels of insulin allow glucagon to rise, causing FAs to be released from adipose and broken down for energy.

Period of extra energy need can trigger DKA such as stress, infection or insulin omission

Its far more common in Type 1

29
Q

How does DKA present?

A
  • N&V
  • Thirst & Dehydration
  • Kussmauls Respiration (Deep, rapid & sighing)
  • Polyuria
  • Tachycardia & Hypotension
  • Weakness, confusion and coma
  • Sweet Ketotic Breath
30
Q

What is the hyper Glycaemic Hyperosmolar state (HHS)?

A

A state of high osmolarity due to blood sugar without significant ketoacidosis.

More likely in Type 2

31
Q

How does HHS present?

A 
Dehydration
Weakness
Leg Cramps
Visual Problems
Altered consciousness
32
Q

DKA itself has complications, what are they?

A 
Hyper/hypokalemia
Cerebral oedema (the cause of confusion, coma and death)
Aspiration & pneumonia
Thromboembolism
ARDS
Hypoglycaemia
33
Q

How do we test for DKA?

A

Inititial Investigations:

  • ABCs
  • Vital Signs
  • IV access
  • Clinical Assessment
  • Glucose fingerprick test

First Investigations:

  • Lab Blood Glucose to confirm
  • ABGs (Low CO2 from hyperventilation & acidosis)
  • Urinalysis and blood ketones
  • U&E + FBC

Other:

  • Blood/urine cultures (rules out infection as a trigger/complication)
  • ECG
  • Consider CXR
34
Q

How do we manage DKA?

A 
o	IV saline
o	IV Insulin -- Drives glucose into cells
o	~Abx
o	~Heparin (prevents thromboembolism)
o	~NG tube

Yr 2 Endocrine (27 decks)

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