Diabetic Complications

Question 1

At each annual screening of diabetic patients, what is checked?

Answer 1

• eye screening
• kidney function
• foot risk

Question 2

Explain the pathophysiology behind microvascular complications

Answer 2

Increased glucose cannot be processed via TCA cycle in mitochondria due to impaired mitochondrial function

Glucose goes via different pathways -> end products cause

• Increased ROS (reactive O2 species)
• Inflammation

Question 3

The ‘diabetic foot’ is made up of two large groups of complications, name them

Answer 3

PVD

Peripheral neuropathy

Question 4

What is charcot’s foot?

How does it present?

How is it managed?

Answer 4

Destructive inflammation -> destroys bones in foot (this part lasts about 3 mnths)

Hot swollen foot w/ neuropathy - D.D infection

Complete non-weight bearing through cast etc. until healing process is over (4-8mths)

Question 5

Give one very common form of mononeuropathy

Answer 5

Carpal tunnel syndrome

common in diabetics

Question 6

What is the most common form of neuropathy?

Answer 6

Peripheral

Question 7

What type of diabetic is most likely to get neuropathy?

Answer 7

T1 (due to typically having had diabetes for a longer period of time)

Question 8

Proximal neuropathy is rare, how does it present however?

Answer 8

Usually unilateral neurologic symptoms in upper thigh, buttock and hips

• affects walking
• getting up out of a chair

Question 9

Painful neuropathy is v. difficult to manage. How is it managed in clinic?

Answer 9

Atypical painkillers e.g. Duloxetine

Capsicum cream

Question 10

Autonomic neuropathy affects the whole autonomic system. How does it affect each of the following systems:

• GI
• Sweat glands (eccrine glands)
• Cardio

Answer 10

GI - gastroparesis
Eccrine glands - ‘gustatory sweating’ -> sweating when eating
Cardio - orthostatic hypotension, tachycardia

Question 11

What is diabetic nephropathy?

What is a defining feature on histology?

What is the urinalysis like?

Answer 11

Progressive kidney disease caused by damage to the capillaries in glomeruli

Nodular glomerulosclerosis/ Kimmelsteil-Wilson nodules

Proteinuria present

Question 12

How is diabetic nephropathy managed?

Answer 12

ARB/ACEi - help to reduce proteinuria
Strict BP management (aim for 130/70mmHg)

SGLT2i in T2DM

Question 13

What can diabetic nephropathy progress to if not managed correctly?

Answer 13

End stage kidney disease

Kidney failure

Question 14

When should a urine sample be taken?

Answer 14

First thing in morning

Question 15

What causes DKA?

Answer 15

Patient with absolute/relative insulin deficiency -> comes under stress -> uncontrolled lipolysis due to no glucose stores to break down -> increase in FFAs -> ketone body production

Question 16

In regard to each of the following factors comment on how HHS, DKA and alcohol-induced ketoacidosis would present:

• venous pH
• ketone level
• blood sugar levels

Answer 16

DKA

• acidotic
• ketones >3mmol/l
• blood sugar levels >11.1mmol/l

HHS

• normal pH
• ketone level normal (~slightly raised)
• v. v. high blood sugar levels >30mmol/l

Alcohol-induced ketoacidosis

• acidotic
• ketones >3mmol/l
• blood sugar low or normal

Question 17

What is blood osmolality?
How is it calculated?
What diabetic emergency is associated with an increased osmolality?

Answer 17

Measure of how concentrated with ions/thick the blood is

2[Na+] + urea + glucose

HHS
- v high levels of glucose in blood + increased urine output = hyperosmolar

Question 18

How is DKA, HHS and alcohol-induced ketoacidosis managed?

Answer 18

1. LOTS OF FLUID

DKA - give FIXED insulin (IV + if already diagnosed long-acting insulin)

HHS - no insulin (unless guided by specialist)

Alcohol-induced - IV anti-emetics + IV vitamins

Question 19

True or false. HHS is more common than DKA and associated with a higher mortality

Answer 19

False

HHS is rarer but is associated with a higher mortality rate

Question 20

Is HHS more likely to occur in T1DM or T2DM?

Answer 20

T2

Question 21

Describe the symptoms of ketoacidosis and HHS

Answer 21

Osmotic related

• polyuria
• thirst
• dehydrated

Ketone related

• abdo pain and tenderness
• vomiting
• flushed
• PEAR drop/ nail varnish breath
• raised RR

HHS is just osmotic related symptoms w/ potential loss of consciousness

Question 22

Should you wait to take a swab before commensing antiobiotics in a patient who is systemically unwell with open foot sore?

Answer 22

No

Question 23

Paitents with DKA/HHS are at a higher risk of thromboembolism. What are they given on admission as a result?

Answer 23

LMWH

Question 24

For questions on diabetic retinopathy. See opthamology section

Answer 24

Refer elsewhere

Question 25

Why is it important to monitor K+ when administering insulin?

Answer 25

Insulin causes K+ to be driven intercellularly = hypokalaemia

Question 26

Explain how HHS occurs?

What does HHS stand for?

Answer 26

HHS = hyperglycaemic hyperosmolar state

Lack of insulin = increase in counter-regulatory hormones
->
increase in glycogenesis and gluconeogenesis
->
increase in blood sugar
->
increase in glucose in urine
->
increase in urine due to osmotic diuresis
->
decrease in blood volume and increase in blood osmolality