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TCA 5 - Diabetes Mellitus > Diabetic complications > Flashcards

Diabetic complications Flashcards

1
Q

What are the short-term complications

A
  1. Hypoglycaemia

2. Hyperglycaemia

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2
Q

What are the common symptoms of hypoglycaemia?

A

Adrenergic symptoms:

  • Tremor
  • Sweating
  • Irritability
  • Dizziness
  • Pallor
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3
Q

What are the serious symptoms of hypoglycaemia?

A

Neuroglycopenic:

  • Reduced consciousness
  • Coma
  • Death
  • Paraesthesia
  • Blurred vision
  • Seizures
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4
Q

What are the causes of hypoglycaemia?

A 
EXPLAIN
•	E - exogenous drugs
      Insulin, sulphonylurea, Alcohol, ACE-I, Beta-blockers, pentamidine, quinine sulfate, aminoglutethimide, insulin-like GF
•	P - pituitary insufficiency
•	L - liver failure
•	A - addison’s disease
•	I - islet cell tumours
•	N - non-pancreatic neoplasms
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5
Q

How would you treat hypoglycaemia?

A

Able to cooperate
- 30ml Lucozade or equivalent

Unable to cooperate but conscious
- Glucose gel (glucogel) - buccal

Comatose, fitting

  • Glucagon – SC, IM, IV
  • IV glucose 50%; try to avoid
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6
Q

What are the long-term effects of poorly controlled diabetes?

A
  • Chronic exposure to hyperglycaemia causes damage to endothelial cells.
  • This causes leaky malfunctioning vessels that are unable to regenerate
  • Hyperglycaemia suppresses immune system and provides an ideal environment for bacteria
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7
Q

What are the macrovascular consequences of diabetes?

A
  • CAD
  • Peripheral ischemia
  • Stroke
  • HTN
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8
Q

What are the microvascular consequences of diabetes?

A
  • Peripheral neuropathy
  • Retinopathy
  • Nephropathy
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9
Q

What are the infective consequences of diabetes?

A
  • UTIs
  • Pneumonia
  • Skin and soft tissue infections
  • Fungal infections
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10
Q

What is retinopathy associated with?

A
  • Prolonged hyperglycaemia

- Other conditions linked to DM such at HTN

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11
Q

How does retinopathy cause loss of vision?

A
  • Capillary leakage

- Capillary occlusion

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12
Q

What is a cataract?

A

Degenerative opacity of the lens

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13
Q

What is rubeosis iridis?

A
  • New vessels in the iris

- Can cause glaucoma

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14
Q

What are the primary preventions for nephropathy?

A

Control BP and blood glucose

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15
Q

What does diabetes most commonly cause regarding the kidneys?

A

End stage renal disease

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16
Q

What is the pathophysiology of nephropathy?

A

Changes to haemodynamics of glomerulus which leads to increased glomerular capillary pressure

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17
Q

What are the primary preventions for nephropathy?

A

Control BP and blood glucose

18
Q

What T2DM drugs should be avoided in nephropathy?

A

eGFR <30
o Metformin
o 1st gen sulfonylureas (not glipizide and glicazide)
o GLP-1 agonists

eGFR <60
o SGLT2 inhibitors

19
Q

Why does diabetic foot disease occur?

A

o Neuropathy: loss of protective sensation, Charcot’s arthropathy, dry skin
o Peripheral arterial disease: macro- and micro-vascular ischaemia

20
Q

How does diabetic foot disease present?

A

o Neuropathy: loss of sensation
o Ischemia: loss of foot pulses, reduced ankle-brachial pressure index, intermittent claudication
o Complications: calluses, ulceration, Charcot’s arthopathy, cellulitis, osteomyelitis, gangrene

21
Q

What is the primary prevention for diabetic foot disease?

A 
o	Control blood glucose
o	Lifestyle (smoking, exercise and alcohol)
22
Q

What is Cherioarthropathy?

A

Limited joint mobility in the hands

23
Q

How would you treat HTN in DM?

A

1st line: Ace-i

2nd line: ARB

24
Q

What is the primary prevention for CV disease?

A

o Lifestyle (diet, weight, exercise, smoking, alcohol
o Metabolic control (glucose, BP, lipids)
o ACE-I, A2RB, aspirin, statins/fibrates

25
Q

What can DM cause in pregnancy?

A
  • Accelerated growth
  • IUGR
  • Congenital abnormalities
26
Q

What is the primary prevention in a woman who is pregnant and has diabetes?

A

o Pre-pregnancy blood glucose control / folate (5mg/day high dose)
o Intensive pregnancy blood glucose control and monitoring (low HbA1c)
o Within 1 week of confirmation of pregnancy -> seen by joint diabetes and antenatal care team

27
Q

What are classed as diabetic emergencies?

A
  • Diabetic ketoacidosis (DKA)
  • Hyperglycaemic hyperosmolar state (HHS)
  • Severe hypoglycaemia
28
Q

What is DKA?

A

Hyperglycaemia + Hyperketonaemia + Acidosis

29
Q

What is the normal physiology of ketogenesis?

A
  1. Ketogenesis occurs when there is insufficient glucose supply and glycogen stores are exhausted
  2. Liver takes fatty acids and converts them into ketones -> water-soluble fatty acids that can be used as fuel
  3. Normally ketones are buffered by HCO3 released by the kidneys to prevent metabolic acidosis
30
Q

What is the pathophysiology of DKA?

A
  1. Severe insulin deficiency + increased catabolic hormones (glucagon, catecholamines, cortisol, HG)
  2. This gives rise to excess glucose, through glycogenolysis and gluconeogenesis, and ketones through lipolysis
  3. Hyperglycaemia and hyperketonaemia are enhanced as the tissues that normally absorb glucose and ketones become saturated, so they stop up taking them
  4. Over time, the high ketone levels use up the HCO3 released by the kidneys, causing metabolic acidosis
31
Q

What are the clinical features of DKA?

A
  • Hyperventilation
  • Nausea and vomiting
  • Dehydration
  • Hypotension and warm peripheries
  • Decreased conscious level
  • Acetone smelling breath
  • Tachycardia
32
Q

Why is dehydration and polyuria a clinical feature in DKA?

A

o Hyperglycaemia overwhelms the kidneys and glucose starts to be filtered into urine.
o The glucose draws water into the urine through osmotic diuresis causing polyuria and dehydration

33
Q

Why is hyperventilation a clinical feature in DKA?

A

Metabolic acidosis

34
Q

What are the metabolic characteristics of DKA?

A
  1. Water deficiency ~ 5l
  2. Na+ deficiency ~ 500mmol
  3. K+ deficiency ~ 300-1000mmol
  4. Hyperglycaemia > 25mmol/l
  5. Metabolic acidosis – low pH, low HCO3
35
Q

Why does potassium decrease in DKA?

A
  • Sodium-potassium ATPase is dependent on insulin, so potassium leaks out of cells when you have insufficient insulin
  • Loss of K+ through urine
36
Q

What are the typical test results in DKA?

A

• Hyperglycaemia, glycosuria
• Ketonaemia, ketonuria
• Na+ = 125-160mmol/l
Can be low or high
Low - glucose in blood is diluting Na+
High - osmotic diuresis means more water than Na+ is being lost from kidneys
• K+ = 3-7 mmol/l
• Urea, creatinine raised (muscle breakdown as well as hypotensive AKI)
• Lipids raised
• Leucocytosis (neutrophils)

37
Q

How do you diagnose DKA?

A 
- Hyperglycaemia
o	Blood glucose ≥11mmol/L
- Ketosis
o	Blood ketones ≥3mmol/L
- Acidosis 
o	pH <7.35
38
Q

What tests would you order for DKA?

A
  • venous blood: U+Es, glucose, ABG or VBG
  • Urine and blood analysis: ketones
  • ECG
  • Infection screen
39
Q

How do you treat DKA?

A

FIG-PICK

- F - Fluids
      Normal saline 
      Be careful due to cerebral oedema
- G - Glucose
      Add dextrose infusion if <14mmol/L
- P - Potassium
      Give if serum K+ <5.5mmol/L
- I - Infection
- C - Chart
- K - Ketones
      Monitor
40
Q

What is Hyperglycaemic Hyperosmolar State?

A

Same as DKA, but without the metabolic acidosis:

  1. Water deficiency ~ 5l
  2. Na+ deficiency ~ 500mmol
  3. K+ deficiency ~ 300-1000mmol
  4. Hyperglycaemia > 25mmol/l

TCA 5 - Diabetes Mellitus (3 decks)

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