A. ACUTE AND SECONDARY COMPLICATIONS OF DIABETES Flashcards
what are the 3 acute complications of diabetes
- hypoglycaemia (hypo) - T1DM and T2DM
- diabetic ketoacidosis (DKA) - T1DM
- hyperosmolar hyperglycaemia state (HHS) - T2DM
at what blood glucose level does hypoglycaemia occur
<4 mmol/L
(symptoms present at 3 mmol/L)
how might a type 1 diabetic get hypoglycaemia
- insulin overdose
- excessive exercise
- inadequate CHO intake
how might a type 2 diabetic get hypoglycaemia
- sulphonylureas as they stimulate insulin release (elderly)
- hepatic or renal disease (don’t reabsorb glucose well)
- some drugs (beta-blockers, diuretics and steroids)
side effects of hypoglycaemia
palpitations
tremors
sweating
anxiety
dizziness
hunger
irritability
headache
tingly lips
how does the body act to hypoglycaemia
counter-regulatory activity of SNS in order to increase glucose levels
what is neuroglycopenia/neuroglucopenia
glucose deficiency in brain
symptoms of neuroglycopenia
loss of concentration
slurred speech
behaviour mood changes
seizures
loss of consciousness
treatment of hypoglycaemia if conscious
- sugary drink/food which is absorbed quickly
- Glucogel: ie 40% dextrose (D-glucose) gel
- 10-15 minutes for recovery then a snack (biscuit/bread) for sustained carbohydrates
treatment of hypoglycaemia if unconscious
- IV glucose
- IV/IM/SC glucagon but not after alcohol as works on liver
what is diabetic ketoacidosis (DKA)
- diabetic coma
- more likely in poorly-cotrolled T1DM
- medical emergency
- 10-20% mortality rate
what induces diabetic ketoacidosis (DKA)
- hyperglycaemia and metabolic acidosis (ketosis) due to lots of ketones
what is DKA caused by
- omission or reduction in insulin dose (inhibits ketogenesis and lowers blood glucose)
- illness/infection
- emotional upset
- menstruation/pregnancy ketosis
- rare syndromes of insulin resistance
*stress uses insulin more quickly
consequences of loss of insulin action
Liver:
- gluconeogenesis
- glycogen breakdown
Muscle:
- protein breakdown to amino acids
Adipose tissues:
- lipolysis to fatty acids and glycerol
what happens with the breakdown products: fatty acids, glycerol, amino acids
intermediates for gluconeogenesis
- lots of glucose produced
- lots of ketones produced
consequences of the increase in glucose
osmotic diuresis
- frequent passing of urine
- dehydration
- thirst as:
plasma glucose leads to filtered load (water taken with it) > renal absorption for glucose so get glycosuria
consequences of the ketone bodies
metabolic acidosis
- nausea, vomiting (due to change in pH)
- breathlessness (ventilation to change acid-base balance)
- abdominal pain
severe consequences of metabolic acidosis
- CNS depression
- diabetic coma
- death
severe consequences of dehydration (low blood volume)
- decreased peripheral circulatory volume:
- renal failure
- low cerebral blood flow
- death
treatment of DKA
- hospital
- replacement of fluids, electrolytes (NaCl saline, KCl, glucose 10%)
- IV infusion of insulin (suppress ketogenesis, reduce blood glucose, correct electrolyte imbalance)
- treat cause
what is HHS
- severe hyperglycaemia without ketosis (>40mmol/L)
- managed as DKA but less insulin patients can still make insulin
how to monitor blood glucose in primary care
- HbA1c measurements every 3 months
how to self-monitor blood glucose
- capillary blood glucose testing (glucose meter and test strips)
- continuous glucose monitoring:
a) real time - all the Time
b) flash - measures glucose in interstitial fluid
there is a time lag compared to direct blood glucose monitoring due to I.F being measured
long term (chronic) microvascular complications of DM
- retinopathy
- nephropathy
- neuropathy
specific to DM
long term (chronic) macrovascular complications of DM
- CVD (IHD)
- cerebral vascular disease (stroke)
- peripheral vascular disease
(accelerated atherosclerosis associated with DM)
how do microvascular complications occur
damage of small vessels (capillaries) by hyperglycaemia (eg - sorbitol) and glycation of proteins - leads to advanced glycated end products
how many patients get retinopathy after 20 years of DM
95%
classification of retinopathy - background
- microaneurysm (tiny areas of swelling in the blood vessels)
- haemorrhages
- exudates
classification of retinopathy - pre-proliferative
- bleeding into the retina
- ‘cotton-wool spots’ indicates regions of ischaemia (blurring of vision)
classification of retinopathy - proliferative
- new blood vessels and scar tissue have formed on retina
- new blood vessels can easily rupture
- which can cause significant bleeding
- can lead to retinal detachment, where the retina pulls away from the back of the eye
- vitreous haemorrhage: reoccurrence common, 30% of eyes are blind within one year of first bleed
- impairment of vision: floaters, clouding or loss of vision
classification of retinopathy - maculopathy (retinal retraction)
- blood vessels in macula (centre of eye involved in sharp vision) become leaky or blocked
- retina can heal but there is severe scarring
- scar tissue can peel away from back of eye
- severe loss of vision
- need annual eye checks
optic disc of eye
where optic nerve and blood vessels exit the eye (near back of eye)
macula of eye
central area of retina
fovea
region of sharpest vision
what is nephropathy
angiopathy of capillaries of glomeruli - narrowing and blocking so filter is damaged and proteins appear in urine
(glomerulosclerosis)
symptoms of early nephropathy (5-10 years after diagnosis)
- microalbuminuria
symptoms of later nephropathy (10 years after diagnosis)
- proteinuria
- increased BP
- decreased eGFR
symptoms of advanced nephropathy (10 years after diagnosis)
- end-stage renal disease
- need dialysis or kidney transplant
what drugs help limit nephropathy (ie - renoprotective)
- ACE inhibitors: even if BP is normal
- Primarily used for hypertension and heart failure but also in CKD to limit proteinuria
what is neuropathy
- family of nerve disorders caused by DM
- affects cranial, autonomic, peripheral NS
effects of neuropathy
erectile dysfunction
sweating
postural hypotension
bladder dysfunction
constipation/diarrhoea
symptoms of neuropathy
loss of sensation
tingling
shooting pains
cramps
causalgia
*mainly in feet, increased risk of foot ulcers
what is the leading cause of death in diabetes
ischaemic heart disease
Ischaemic Heart Disease
- develops prematurely
- narrowed heart (coronary) arteries that supply blood to the heart muscle
- myocardial infarction (heart attack) increases risk of complications like heart failure and rhythm disturbances
- need to manage risk factors in diabetics (hypercholesterolaemia, hypertension, stop smoking)
what is a stroke caused by
- area of brain deprived of blood due to blood clot
- 10-fold increase in younger patients
- TIAs less likely
- need to control hypertension
what is peripheral vascular disease caused by
- reduced circulation of blood to a body part other than the brain or heart
- caused by a narrowed or blocked blood vessel
- main cause is atherosclerosis - the build-up of fatty deposits that narrow a blood vessel, usually an artery
effect of PVD
intermittent claudication (cramping) and ulcerations
risks with PVD
- gangrene/amputation
- DVTs
- pulmonary embolisms
risk factors of DM
- hyperglycaemia
- hypertension
- dyslipidameia
- pro-coagulant state
how to control microvascular effects
- good glycemic control
- control of hypertension with ACE1, AIIRA, CCB
- T1DM recommended: 135/85mmHg
- T2DM recommended:140/90 mmHg (<130/80 mmHg if renal impairment)
how to control macrovascular effects
- good glycaemic control
- control of hypertension
- control of dyslipidaemia (statin)
- use anti-platelet drugs (clopidogrel)
