Diabetes Flashcards
Approach to unconscious patient with hypoglycaemia
ABCDE
A- guedel
B-O2
C-pulse, BP,IV access
D-GCS
EFG- glucose
specific- IV glucose and then IM glucagon if glucose less than 4mmol/l recheck every 10 mins
Features of ketoacidosis
Hyperglycaemia
ketonuria
acidosis
Clinical features of ketoacidosis
Dehydration (high glucose-osmotic diuresis) tachycardia, hypotension (Acidosis is a negative inotrope)
air hunger- kussmaul respiration - acidosis
smell of ketones
vomiting and abdo pain- hyperkalaemia/ acidosis- paralytic ileus, careful of aspiration pneumonia
signs of precipitating cause
What happens to potassium in DKA?
Osmotic diuresis takes potassium
dehydration activates RAAS —> further loss
total body K+ low
serum occassionally high or normal
Acidosis—> H+ moved into cells, forcing K+ out
no insulin—> no K+ uptake, until insulin given, where sudden fall
pre-Renal kidney failure- oliguria with failure of K+ excretion
Management of DKA in 1st hour
PANICS
Potassium- measure hourly, omit if anuria suspected or >5.5mmol/l
Acidosis- check venous pH and ketones
Normal saline- 500mls over 15 mins if systolic <90mm, otherwise 1 l over 1hr
Insulin- 0.1 units/kg/hr
Catheter and cultures: urine, blood etc
Stomach aspiration if drowsy, ET tube first if no gag reflex
Examining the diabetic foot
Inspect-including heels
palpate- cap refill and pulses
light touch- finger, cotton wool or monofilament
avoid pinprick testing
vibration sense
ankle jerks- usually absent
’loss of Protective sensation’
vibrationa and light touch lost first
Joint position, temperature (ethyl chloride spray) if time
Stages of diabetic retinopathy
Pre proliferative
cotton-wool spots
infarcts of unmyelinated nerve cell layer in front of retina
>3 blot haemorrhages
venous bleeding and looping
intra-retinal microbascular abnormalities
Proliferative
New vessels around the disc
peripheral new vessels
new vessels on iris- rubeosis
End-stage
Vitreous haemorrhage from fragile vessels
scarring
tractional retinal detachment
blindness
Indications for eye referral
Fall in corrected visual acuity
single cotton wool spot
3 blot haemorrhages
anything macula
new vessels - emergency
Implications of microalbuminuria
nephropathy is associated with increased risk of macro vascular disease
increased mortality (macro vascular disease)
‘detected early with screening
usually tested as unremarkable albumin: creatinine ratio
extra attention to risk factory’s is indicated (smoking, lipids, HTN)
ACEi slows progression of impairment
what Are the effects of nephron loss in hyperglycaemia
How does Hyperglycaemia lead to nephron loss?
Plasma glucose ranges
Diabetes symptoms (e.g. polyuria, polydipsia and unexplained weight loss for Type 1) plus:
a random venous plasma glucose concentration ≥ 11.1 mmol/l or
a fasting plasma glucose concentration ≥ 7.0 mmol/l (whole blood ≥ 6.1 mmol/l) or
two hour plasma glucose concentration ≥ 11.1 mmol/l two hours after 75g anhydrous glucose in an oral glucose tolerance test (OGTT).
With no symptoms diagnosis should not be based on a single glucose determination but requires confirmatory plasma venous determination. At least one additional glucose test result on another day with a value in the diabetic range is essential, either fasting, from a random sample or from the two hour post glucose load. If the fasting random values are not diagnostic the two hour value should be used.
HBA1c ranges
Give some presenting symptoms of DM
thirst
polyuria
blurred vision
infections- thrush
weight loss/gain
CVA,CVD
foot ulcers
How do you screen for diabetic renal disease?
Urinary albumin to creatinine ratio
microalbuminuria- earliest indicator of diabetic nephropathy
ACR>2.5 or 3.5 in men
treatment:
glycaemic controlBP
ACEi/ AngII receptor blocker (renoprotective)
Preventative foot care
washa nd inspect feet daily
use creams/lotions to prevent dry skin/callus formation
feet measured when buying shoes
avoid walking barefoot
medical treatment when foot injury
avoid thermal injury e.g. hot water bottle
avoid self treatment of corns etc
Biochemical diagnosis of DKA
Causes of DKA
Presentation
interruption of insulin therapy
infection
surgery/trauma
MI
Anion gap calculation
Causes of acidosis with increased anion gap
Causes (LTKR)
Lactate
Toxins
Ketones
Renal
Causes (CATMUDPILES)
CO, CN
Alcoholic ketoacidosis and starvation ketoacidosis
Toluene
Metformin, Methanol
Uremia
DKA
Pyroglutamic acidosis, paracetamol, phenformin, propylene glycol, paraladehyde
Iron, Isoniazid
Lactic acidosis
Ethylene glycol
Salicylates
Management of DKA
Insulin
Insulin dose should be based on weight. Sliding scales should not be used, as they can be inaccurate in overweight and pregnant patients
The type of insulin regimen is often referred to as a Fixed rate Intravenous Insulin Infusion, or FRIII
Check the effectivesness of the FRIII using blood ketones and revise the dose if it is not effective
If bedside blood ketone testing is not available, venous blood gasses can be used to asses bicarbonate level, but only for the first 6 hours, as this becomes inaccurate after infusion of large amount of normal saline.
Fluids
Use IV 0.9% sodium chloride (normal saline)
If hypotensive (systolic BP <90mmHg) give a bolus of 500mls normal saline. If still hypotensive, seek senior help. Consider discussion with ICU, and think about other possible causes of hypotension.
Once hypotension is resolved, or if it is not present at presentation, patient will still require large amounts of IV fluid. A typical regimen might be 1L normal saline in the first hour, then 1L over 2 hours, then 1L over 4 hours etc, but be wary of a ‘one size fits all’ regimen
Monitor electrolytes, particularly potassium closely. You will likely need to replace potassium, which can be done by adding KCl to the bags of normal saline. Be careful not to infuse potassium too quickly.
Potassium
DKA patients are at risk of both hypokalaemia, and hyperkalaemia. Initially they are often hyperkalaemic, but their total body potassium is low. This is because potassium is taken up into cells with insulin, so with a lack of insulin, extra cellular potassium rises, and the intracellular level falls.
Titrate potassium replacement to the potassium level, as measured on hourly venous blood gasses.
K+ >5.5mmol/L – dont replace
K+ 3.5 – 5.5 mmol/L – replace by using 40mmol/L in infused solution
K+ <3.5 – seek senior help – additional potassium replacement may be require
blood gasses can be used to asses bicarbonate level, but only for the first 6 hours, as this becomes inaccurate after infusion of large amount of normal saline.
Fluids
Use IV 0.9% sodium chloride (normal saline)
If hypotensive (systolic BP <90mmHg) give a bolus of 500mls normal saline. If still hypotensive, seek senior help. Consider discussion with ICU, and think about other possible causes of hypotension.
Once hypotension is resolved, or if it is not present at presentation, patient will still require large amounts of IV fluid. A typical regimen might be 1L normal saline in the first hour, then 1L over 2 hours, then 1L over 4 hours etc, but be wary of a ‘one size fits all’ regimen
Monitor electrolytes, particularly potassium closely. You will likely need to replace potassium, which can be done by adding KCl to the bags of normal saline. Be careful not to infuse potassium too quickly.
Potassium
DKA patients are at risk of both hypokalaemia, and hyperkalaemia. Initially they are often hyperkalaemic, but their total body potassium is low. This is because potassium is taken up into cells with insulin, so with a lack of insulin, extra cellular potassium rises, and the intracellular level falls.
Titrate potassium replacement to the potassium level, as measured on hourly venous blood gasses.
K+ >5.5mmol/L – dont replace
K+ 3.5 – 5.5 mmol/L – replace by using 40mmol/L in infused solution
K+ <3.5 – seek senior help – additional potassium replacement may be require
Complications of DKA treatment
Fluid overload
hypoglycaemia
hypokalaemia
Warning signs of hypoglycaemia
Autonomic: sweating, palpitations, shaking, hunger
neurological: confusion, drowsiness, slurred speech
What conditions do T1DM sufferers need regular screening for?
hypo/hyperthyroidism
coeliac
commonly associated, make glycaemic control difficult
Causes of peripheral neuropathy
A- alcohol
B- B12 deficiency (+SADC)
C- CKD (+carcinoma)
D- diabetes and drugs
E- every vasculitis (RA, Polyarteritis)
Fibres and what they transmit, and what knocks them out
