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Y3 Medicine > 22 - Diabetic Complications > Flashcards

22 - Diabetic Complications Flashcards

1
Q

What are the acute and chronic complications of diabetes?

A

Acute:

- Hypoglycaemia

  • DKA
  • HHS

Chronic:

Microvascular - retinopathy, nephropathy, neuropathy

Microvascular - cerebrovascular, peripheral vascular, cardiovascular

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2
Q

How do you assess and treat the following diabetic complications:

  • Vascular disease
  • Nephropathy
  • Retinopathy
A

Vascular disease: check plasma lipids, check BP, check smoking status, offer statin and aspirin 75 mg

Nephropathy: microalbuminaemia (negative urine proteins but ACR >3) so give ACEi

Retinopathy: anual retinal screening and refer to ophthalmologist if pre-proliferative changes (cotton wool spots, haemorrhages, venous beading)

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3
Q

What is the definition of hypoglycaemia for diabetic hospital inpatients?

A

Blood glucose less than 4mmol/L

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4
Q

What are some clinical features of hypoglycaemia?

A
  • Coma
  • Seizures
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5
Q

How can hypoglycaemia in diabetics be recognised by hospital staff?

A
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6
Q

What are some risk factors for hypoglycaemia?

A
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7
Q

What are some causes of inpatient hypoglycaemia and what are the most common?

A

EXPLAIN

  • Exogenous drugs e.g insulin, sulfonylureas
  • Pituitary insufficiency
  • Liver failure
  • Addison’s disease
  • Insulinoma
  • Non pancreatic neoplasms
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8
Q

What is the general management of hypoglycaemia?

A
  • Quick acting carbohydrate followed by long acting
  • Consider cause
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9
Q

How should you categorise hypogylcaemic patients to help with their management?

A
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10
Q

How do you treat a conscious and orientated patients with hypoglycaemia?

A

15 - 20g fast acting carbohydrate e.g:

  • 5-7 dextrose tablets
  • Glucojuice
  • 3 to 4 heaped teaspoons of sugar into water
  • 150-200ml fruit juice

followed by long acting carbohydrate once BG>4 e.g toast

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11
Q

After you have given a conscious and orientate hypoglycaemic patient fast acting carbohydrate, how should you follow this up?

A
  • Check CBG after 15 minutes
  • If not improved repeat step
  • If low after 45 minutes then 1mg IM glucagon or 10% 150-200mls glucose over 15 mins
  • Document in notes, review CBG closely for next 24-48 hours, hypo education
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12
Q

Which patients with hypoglycaemia won’t respond to IM glucagon?

A

Cirrhotic liver patients

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13
Q

How do you treat a conscious patient who is able to swallow but uncooperative with hypoglycaemia?

A

Either

  • 1.5 - 2 tubes of glucogel
  • 1mg IM Glucagon

Repeat CBG after 15 minutes. Do not use glucagon more than once!!!! After 3 cycles give 150-200mls 10% glucose IV

Give long acting carbohydrate once BM>4

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14
Q

How do you treat an unconscious patient with hypoglycaemia?

A
  • ABCDE
  • If on IV insulin stop

- Glucagon IM 1mg

  • If not worked after 10 minutes give glucose 10% intravenous infusion 150-200mls
  • If insulin dose due to not omit, if was on IV insulin then check CBG every 15 mins until BM>3.5 then restart insulin
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15
Q

How do you treat a NBM patient with hypoglycaemia?

A

Once BG over 4 then continue on 10% dextrose 100mls/hr until no longer NBM

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16
Q

What is the definition of ketoacidosis including the diagnostic criteria?

A

- Ketonaemia

- Hyperglycaemia (reduced peripheral uptake due to insulin deficiency)

- Acidosis

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17
Q

What is the pathophysiology of ketoacidosis?

A

Lack of insulin causes switch to lipolysis for energy source as cannot use glucose. This leads to free fatty acid metabolism and formation of ketones 3-betahydroxybutate, acetone and acetoacetic acid

In early stages ketones are buffered, when no longer buffered they appear in urine

Induces nausea and vomiting

Hyperglycaemia, osmotic diuresis, serum hyperosmolality and metabolic acidosis lead to electrolyte disturbance

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18
Q

What are the key issues in ketoacidosis?

A

- Hyperglycaemia

- Acidosis

- Dehydration due to vomiting and osmotic diuresis

  • Sodium and Potassium loss due to osmotic diuresis

- Cerebral oedema

  • Electrolyte disturbances, especially hypoK
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19
Q

How do you test for ketoacidosis?

A
  • 3-B- Hydroxybutyric acid using blood ketone meter (more sensitive)
  • Acetoacetic acid using ketostix so urine ketones
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20
Q

How does DKA present?

A

Usually type 1 diabetic

N+V

Abdominal pain

Ketone breath

High respiratory rate

Confusion

Hypotension

Polyuria

Kussmaul breathing

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21
Q

Why may K appear high during DKA, even though there is a total body loss of potassium?

A

Shift of potassium out of the cells due to acidosis and lack of insulin

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22
Q

Why is there dehydration in DKA?

A
  • Vomiting
  • Osmotic diuresis
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23
Q

What are some other types of diabetes that can have DKA apart from type 1?

A
  • Type 2 on SGLT2i
  • LADA (Anti-GAD antibody)
  • Ketosis Prone Diabetes (Non-Caucasian)(Temporary diabetes)
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24
Q

What are some precipitating factors for a DKA?

A
  • Poor compliance to insulin
  • Infection
  • First presentation of type 1
  • MI
  • Wrong prescription of insulin
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25
Q

What investigations should you do if you suspect DKA?

A
  • Blood or urine ketones
  • Capillary blood glucose
  • Venous plasma glucose
  • VBG for lactate
  • U+Es
  • FBC
  • Blood culture
  • ECG and cardiac monitoring
  • CXR
  • Pulse oximetry
  • Urine dip/MSU
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26
Q

How do you assess the severity of DKA and what is the importance of knowing the severity?

A

If one of the following then need treatment on HDU

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27
Q

What are the principles of management in DKA?

A

- Fluid administration to restore circulatory volume

  • Fixed rate IV insulin after fluids to reverse ketosis. Add 10% IV glucose if CBG falls below 14

- Monitor and replace potassium

These are done to clear ketones and correct metabolic disturbances

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28
Q

What are some recent changes in DKA investigations and management that are important to remember?

A

- Measure blood ketones not urinary

- Use fixed rate insulin not variable rate

- Use VBG not ABG to look at pH and lactate

- Continue long acting basal insulin as normal

  • Bolus dose of insulin at presentation

- 10% dextrose when BM<14

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29
Q

What are some factors of poor prognosis in DKA and what causes mortality?

A
  • Age and confusion

- Mortality: precipitating illness, hypoK, aspiration, cerebral oedema

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30
Q

What is a fixed rate insulin infusion and why is it used in DKA?

A

- 0.1 units/kg/hr of Humulin S or Actrapid given IV up to 15 units (150kg)

  • If taking long acting basal insulin normally then continue this too
  • Use large bore cannula
  • This helps to suppress ketoacidosis and hyperglycaemia
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31
Q

What are the metabolic treatment targets once DKA treatment has been started?

A
  • Reduce blood ketones by 0.5/hr
  • Increase venous bicarb by 3/hr
  • Maintain K between 4 and 5.5
  • Give 10% dextrose when blood glucose falls below 14

If any of these targets not achieved then up the fixed rate insulin

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32
Q

How much fluid and potassium replacement is given to a patient with DKA?

A
  • 6L of fluid in 24 hours
  • K depends on blood levels
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33
Q

What are the monitoring parameters in DKA ?

A
  • Bicarbonate
  • Venous pH
  • Blood glucose
  • Blood ketones
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34
Q

Overall what is the management of DKA in the first 60 minutes?

A
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35
Q

When is DKA classified as resolved?

A
  • When ketones <0.6mmol/L
  • pH>7.3
  • Patient ready to eat
  • Start s/c insulin before stopping FRII
36
Q

After a patient has had a DKA, what education should you give them to prevent this happening in the future?

A
  • Discuss early warning symptoms of DKA
  • Review insulin regime
  • Provide blood ketone meter and explain how to use
  • Educate staff, patient and family
37
Q

When should you admit a type 1 patient on a sick day?

A
38
Q

What is the pathophysiology of hyperosmolar hyperglycaemic state (HHS)?

A
  • Relative insulin deficiency but endogenous insulin secretion present.
  • Type 2 diabetics on oral hypoglycaemic
  • Insulin levels inadequate to facilitate glucose use but adequate enough to prevent lipolysis and therefor ketogenesis
  • It results in osmotic diuresis and this leads to a significantly raised serum osmolarity.
39
Q

What are the signs and symptoms of HHS?

A

Confusion

Neurological symptoms

Coma

Renal impairment

40
Q

What are some precipitating factors for HHS?

A
  • Infection
  • MI
  • CVA
  • Acute illness
41
Q

How do you distinguish HHS from DKA?

A
  • Occurs in type 2 DM rather than type 1

- Hypovolemia (more than DKA due to osmotic diuresis)

- Significant hyperglycaemia without significant hyperketonaemia

- Osmolality >320

42
Q

In DKA the most common electrolyte disturbance is HypoK, what is the most common electrolyte disturbance in HHS?

A

HyperNa

43
Q

How do you work out serum osmolality?

A

2(Na+K)+ Glucose + Urea

44
Q

Investigations for the diagnosis of HHS are the same as for DKA apart from one additional investigation, what is this?

A

Serum osmolality

45
Q

What are the principles of management for HHS?

A

- IV fluids with electrolytes to normalise osmolality

- Fixed rate IV insulin infusion if blood glucose falling <5mmol/hr

- Monitor and replace K

- LMWH anticoagulation to prevent thrombosis

- Protect heels and daily foot checks to prevent foot ulceration

46
Q

How does fixed rate insulin vary in HHS from DKA?

A
  • Only 0.05units/kg/hr
  • Only give if blood ketones over 1 or BM not falling by at least 5 per hour despite fluids
47
Q

What are the fluid losses and commonest cause of death in HHS?

A
  • Fluid loss around 10 litres

- Death: thromboembolic complications, aspiration, pneumonia, underlying pathology

48
Q

What are the stages of development of CKD in diabetic nephropathy?

A

1. Hyperfiltration: due to hyperglycaemia

2. Latent stage

3. Microalbuminuria: due to increased permeability of basement membrane

4. Overt proteinuria

5. ESRD

49
Q

What are the histological changes in diabetic nephropathy?

A

1. Kimmelsteil-Wilson nodules

2. Glomerulosclerosis so thickened GBM

3. Arteriolar hyalinosis

50
Q

What are some risk factors of diabetics that puts them at risk of diabetic nephropathy progression?

A
  • Poor glucose control
  • Blood pressure
  • Smoking
  • Non caucasian ethnicity
  • Hyperlipidaemia
51
Q

What are the issues with having CKD?

A
  • Risk of progression to ESRD
  • Increased CVD risk
52
Q

How is diabetic nephropathy diagnosed?

A

Screen diabetics annually for microalbuminuria and first urine in morning A:CR >3

Or could be eGFR<60 on 2 occasions, one 3 months after the other

53
Q

How is diabetic nephropathy managed?

A

- Control glucose HbA1c<7% to prevent progression to proteinuria

- Control BP <135/85 in type 1, <140/80 in type 2. If complications or features of metabolic syndrome then <130/80

- ACEi or ARB to prevent proteinuria

- Statin to reduce CVD risk

- Smoking cessation

54
Q

What are some complications that need to be managed in CKD and how are they managed?

A
55
Q

When a diabetic develops CKD, what alterations to their diabetic medication need to be made?

A

- Insulin: reduced clearance so need lower dose

- Metformin: reduced clearance, stop when eGFR<30 to prevent lactic acidosis

- Sulfonylureas: reduce clearance so risk of hypoglycaemia

  • GLP-1 mimmetics: stop when eGFR<15

- DPP4i: fine

- Pioglitazone: causes fluid retention and anaemia, which CKD does to so don’t use

- SGLT2i: can only use when eGFR>30

56
Q

What are some reversible causes of renal failure?

A
57
Q

What are some primary and secondary prevention schemes to prevent strokes/vascular disease in diabetics?

A

Primary: smoking cessation, statin to control lipids, improve diet, control BP

Secondary: Aspirin 75mg daily

58
Q

How is a TIA treated?

A
  • Aspirin 300mg and daily after
  • Do not drive for a month
  • Referral to TIA clinic
59
Q

What scoring system is used in A+E to calculate the likelihood that a patient is having a stroke?

A

ROSIER!!!

If +ve score likely having a stroke, if -ve not likely

60
Q

What is a reversible cause of a stroke like presentation in a diabetic?

A

Hypoglycaemia

61
Q

What is the criteria for thrombolysis in a stroke?

A
  • <4.5 hours since onset
  • Bleeding and tumour ruled out by imaging
  • Persistent neurological deficit
62
Q

Why do diabetics have a higher risk of severe ACS?

A

- Larger infarcts

- Less successful coronary angioplasty results

- FFA metabolism due to insulin deficiency so patient needs more oxygen so makes cardiac ischaemia worse

- Hyperglycaemia associated with worse outcomes

63
Q

Hyperglycaemia is associated with poorer outcomes for ACS patients, regardless of whether they are diabetic or not. When a patient has an ACS, what BM are you aiming for, and how do you control this if it goes outside of this range?

A

Aim for BM of 6-12

If goes outside of this start VRII for 24 hours

64
Q

Patients having an ACS may require insulin as an inpatient to control their blood glucose. Do they need to continue this insulin for life?

A

NO!!!!

Only if poor control HbA1c >9% then use s/c insulin. Otherwise give SGLT2i

65
Q

What are the blood pressure targets for different diabetics?

A

Type 1: <135/85

Type 2 without kidney, eye, cerebrovascular damage: <140/80

Type 2 with kidney, eye, cerebrovascular damage: <130/80

66
Q

What are the stages of diabetic retinopathy and what do you see in each?

A

1. Background Retinopathy: micro-aneurysms and hard exudates

2. Pre-proliferative Retinopathy (Refer at this point): cotton wool spots and haemorraghes

3. Proliferative Retinopathy (Urgent referral): new vessel formation and haemorraghes

67
Q

Apart from retinopathy, what are some other eye disorders that can occur in diabetes?

A
  • Macular degeneration
  • Cataracts
  • Glaucoma
  • Retinal detachment
68
Q

What do diabetic foot ulcers typically look like?

A

Painless punched out ulcer in an area of thick callus

69
Q

When assessing a diabetic foot ulcer what are some things you need to assess?

A

Degree of:

- Neuropathy: use 10g monofilament, absent ankle jerks, loss of transverse arch

- Ischaemia: check pulses, if cannot be felt use doppler

- Bony deformity: look for Charcot’s both clinically and on X-ray

- Infection: swabs, blood culture, x-ray, probe ulcer to reveal depth

70
Q

What is the pathophysiology of diabetic foot?

A
  • Neuropathy and vascular damage.

-Neuropathy reduces sensation, leading to unnoticed injuries, while vascular issues slow down wound healing and increase the risk of infections. Combined, these factors can escalate minor foot problems into severe complications, including ulcers, gangrene, and even amputation if not properly managed.

71
Q

What patients with diabetic foot are considered high risk?

A
72
Q

In hospital, which diabetics are at risk of pressure ulcers on their feet?

A

Need to check their feet everyday!!!!

73
Q

How are diabetic foot ulcers prevented in hospital?

A
74
Q

How are diabetic foot ulcers prevented outside of hospital?

A
  • Good glycaemic control
  • Regular chiropody
  • Therapeutic shoes
75
Q

How is Charcot’s foot managed?

A
  • Immobilise in cast and either bed rest or crutches for 8 weeks
  • If serious involve surgical team
76
Q

What does autonomic neuropathy in diabetics cause?

A

Autonomic neuropathy is a type of nerve damage that affects the autonomic nervous system, which controls involuntary functions like heart rate, blood pressure, digestion, and bladder function. In diabetes, high blood sugar levels can damage the nerves controlling these functions, leading to various symptoms such as dizziness upon standing, urinary problems, digestive issues, and sexual dysfunction. Proper management of diabetes is crucial in preventing and managing autonomic neuropathy.

  • Postural hypotension
  • Arrhythmias
  • Gastroparesis
  • ED
77
Q

What is type 3c diabetes and what are some symptoms of this?

A

An illness or condition stopping the pancreas from producing insulin e.g pancreatitis, pancreatic cancer, CF, haemochromatosis

Will have symptoms related to not being able to digest food

78
Q

How is type 3c diabetes diagnosed?

A

Difficult as not widely recognised but consider if:

  • Previous pancreatic issues
  • Pancreatic damage on CT
  • Lack of autoimmune markers in blood
79
Q

How is type 3c diabetes managed?

A
  • Start on metformin

- Then straight to insulin. These diabetics progress to insulin much quicker than type 2

- Treat underlying pancreatic disease

80
Q

What should you always prescribe VRII and FRII with?

A

VRII: always have dextrose solution running

FRII: give 10% dextrose once BM<14, if >14 0.9% NaCl 1L

81
Q

What factors contribute to perioperative hyperglycaemia?

A
82
Q

What do you need to do when you have a diabetic patient on a surgical list?

A
  • Put them top of the list to avoid prolonged starvation
  • Consider if they need VRII
  • Stabilise BMs for a few days before surgery
83
Q

How is a diabetic foot ulcer managed?

A
  • Offloading
  • Pressure redistributing devices
  • Control infection
  • Control ischaemia
  • Wound debridement
  • Wound dressings
84
Q

What is the most common organisms in a diabetic foot ulcer and what are the antibiotics used?

A
  • S.Aureus
  • P.Aeruginosa
  • Use flucloxacillin or vancomycin
  • If penicillin allergy use clarithromycin
85
Q

What are some complications of HHS?

A

Seizures

Coma

Cerebral oedema

Organ failure

86
Q

What is a target HbA1c for a type 2 diabetic on metformin and SU?

A

Lifestyle and Diet: <6.5% or <48mmol/L

One or more drugs: <7.0% or <53mmol/L

Y3 Medicine (24 decks)

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