Diabetic Complications Flashcards
At each annual screening of diabetic patients, what is checked?
- eye screening
- kidney function
- foot risk
Explain the pathophysiology behind microvascular complications
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
The ‘diabetic foot’ is made up of two large groups of complications, name them
PVD
Peripheral neuropathy
What is charcot’s foot?
How does it present?
How is it managed?
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)
Give one very common form of mononeuropathy
Carpal tunnel syndrome
common in diabetics
What is the most common form of neuropathy?
Peripheral
What type of diabetic is most likely to get neuropathy?
T1 (due to typically having had diabetes for a longer period of time)
Proximal neuropathy is rare, how does it present however?
Usually unilateral neurologic symptoms in upper thigh, buttock and hips
- affects walking
- getting up out of a chair
Painful neuropathy is v. difficult to manage. How is it managed in clinic?
Atypical painkillers e.g. Duloxetine
Capsicum cream
Autonomic neuropathy affects the whole autonomic system. How does it affect each of the following systems:
- GI
- Sweat glands (eccrine glands)
- Cardio
GI - gastroparesis
Eccrine glands - ‘gustatory sweating’ -> sweating when eating
Cardio - orthostatic hypotension, tachycardia
What is diabetic nephropathy?
What is a defining feature on histology?
What is the urinalysis like?
Progressive kidney disease caused by damage to the capillaries in glomeruli
Nodular glomerulosclerosis/ Kimmelsteil-Wilson nodules
Proteinuria present
How is diabetic nephropathy managed?
ARB/ACEi - help to reduce proteinuria
Strict BP management (aim for 130/70mmHg)
SGLT2i in T2DM
What can diabetic nephropathy progress to if not managed correctly?
End stage kidney disease
Kidney failure
When should a urine sample be taken?
First thing in morning
What causes DKA?
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
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
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
What is blood osmolality?
How is it calculated?
What diabetic emergency is associated with an increased osmolality?
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
How is DKA, HHS and alcohol-induced ketoacidosis managed?
- 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
True or false. HHS is more common than DKA and associated with a higher mortality
False
HHS is rarer but is associated with a higher mortality rate
Is HHS more likely to occur in T1DM or T2DM?
T2
Describe the symptoms of ketoacidosis and HHS
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
Should you wait to take a swab before commensing antiobiotics in a patient who is systemically unwell with open foot sore?
No
Paitents with DKA/HHS are at a higher risk of thromboembolism. What are they given on admission as a result?
LMWH
For questions on diabetic retinopathy. See opthamology section
Refer elsewhere
Why is it important to monitor K+ when administering insulin?
Insulin causes K+ to be driven intercellularly = hypokalaemia
Explain how HHS occurs?
What does HHS stand for?
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
