5. Complications associated with diabetes Flashcards
Pathophysiology of diabetic ketoacidosis DKA:
what are the 3 main problems associated with DKA
ketoacidosis, dehydration, potassium imbalance
Pathophysiology of diabetic ketoacidosis DKA:
why does ketoacidosis occur
inappropriately burn fats through liipolyiss
initially the kidneys produce bicarbonate to counteract the ketone acids in the blood
over time the ketone acid use up the bicarb and the blood starts to become acidic
Pathophysiology of diabetic ketoacidosis DKA:
why does dehydration occur
hyperglaemia overwhelms the kidneys. and glucose starts being filtered into the uric
glucose in urine draws water out (osmotic diuresis)
causes patient to urinate a lot resulting in dehydration which then leads to thirst eg polydipsia
Pathophysiology of diabetic ketoacidosis DKA:
why does it cause potassium imbalance
insulin normally drives potassium into cells
Serum potassium can be high or normal as the kidney continues to balance blood potassium with potassium excreted in urine
total body potassium however is low as no potassium is stored in cells
note that when insulin treatment starts pt can develop hypokalaemia and this can leaad to arrhythmias
what internal changes does DKA cause
Hyperglycaemia Dehydration Ketosis Metabolic acidosis (with a low bicarbonate) Potassium imbalance
how will a patient with DKA present
Polyuria Polydipsia Nausea and vomiting Acetone smell to their breath Dehydration and subsequent hypotension Altered Consciousness They may have symptoms of an underlying trigger (i.e. sepsis)
how would you diagnose DKA
hyperglycaemia (ie blood glucose greater than 11)
ketosis (ie blood ketones greater than 3)
acidosis (ie Ph less than 7.3)
How would you treat a DKA
hint the mnemonic is FIG-PICK
F- fluids (normal saline first and then 4 litres with added K+ over the next 12 hours)
I- insulin
G- glucose (monitor and add dextrose if below a certain level)
P- potassium
I- infection
C- chart fluid balance
K- ketones (monitor blood ketones or bicarb is ketone monitoring is not available)
when you have treated the DKA what is it important to re establish
the patients normal subcutaneous insulin
Name 3 common complications in relation to diabetes
diabetic retinopathy
kidney disease
diabetes foot
how can capillary leakage of plasma into retina lead to sight loss
intra retinal haemorrhages and odema –> exudates ini the retina
if it is in the peripheral retina then it is non-sight threatening
if it is in the macula area then can lead to loss of central vision
how can capillary occlusion lead to total blindness
retinal ischemia, new vessel formation, haemorrhage, and fibrosis and ultimately retinal detachment leading to glaucoma
As well as retinal screening what can be injected into the vitrous
anti vascular endothelial growth factor (anti VEGF)
in management of kidney disease what things would you want to measure
(leads to micro or macroproteinuria)
eGFR (this would decrease in kidney disease)
UACR (urea, albumin, creatinine ratio)
in diabetic foot, what neuropathic pain sensations could they feel and what relieves their symptoms
a lot of sensations !
worse at night
eased by exercise or counter irritation
in diabetic foot, why do ulcers occur
there is a loss of the protective sensation and so abnormal foot function
what early signs can you see in a diabetic foot before an ulcer appears
areas of callus and retracted toes due to the neuropathy
what other complications are assosicated with diabetic foot
can get infections which lead to septicaemia or impact on circulation so get local thrombosis and gangerinne of the toes
what are the complications of diabetics in pregnancy and how can this be optimised
in 1st trimester can get congenital anomalies
in 2nd and 3rd trimester can get accelerated growth
pre-pregnancy blood glucose control and folate supplement
which kind of diabetics have increased coronary heart disease mortality
T2
Heart failure is more prevalent in which ethnic group
people from South Asian ethnic groups
but less common in black ethnic group
In DKA why do patients present with hyperventilation
due to metabolic acidosis
in DKA why do patients present with vomitting
ketosis + hyperglycaemic gastric statis
why do T2 diabetics not tend to suffer from DKA but more just hyperosmolar hyperglycaemic state compared to type 1
only need a small amount of insulin to suppress lipolysis and ketogensis
T2 still produce some insulin whereas T1 produce next to none
how can stress predicate DKA or HHS
increases the secretion of glucagon, catecholamines and cortisol which all oppose the effects of insulin
What symptoms would you get if the patient is suffering from hypoglycaemia
adrenergic symptoms (sweating, trembling, hunger) neuroglycopenia ie paratyhesia, blurred vision, confusion
what would make someone more likely to have a hypo
alcohol excess very young or very old long duration DM recent severe hypo pregnant autonomic neopathy renal or hepatic impairment
what other things can cause peripheral neuropathy and why
excessive alcohol drinking
vitamin B12 deficiency (due to the demyelination)
Under-active thyroid
presence of proteins in the blood
What can be used in the management of neuropathy
ACEi or AT2I (keeps its microalbuminism in its early phase ie for renal protection)
Duoloxetine or gabapentin
