diabetes Flashcards
diabetes mellitus
abnormality of GLUCOSE regulation
- metabolic disease
- can die
blood sugar is high, glucose in urine is high
diabetes insipidus
abnormality of RENAL FUNCTION (WATER)
lost ability to concentrate urine
- volume of urine secretion increase
ADH decreases – pulls water
Ok if fluid input matches fluid output
what does sugar level vary with
food intake, energy usage and fat storage
Need to define what diabetes is
- Know circumstance in which you take test to establish if normal or not
- Need to test in standardised way
fasting sugar test description
fasting sugar sample from overnight before eating
glucose tolerance test description
Give a fixed amount of sugar after doing a fasting test (75g after fasting)
Take again after 2 hours - should be in a certain level as decrease again
random plasma glucose (RPG)
> 11.1mmol/L on 2 occasions is diagnostic of DIABETES
glucose tolerance test normal values
FPG <6.1
Making enough insulin to move blood sugar into cells
glucose tolerance test impaired fasting glucose values
FPG 6.1-7.0
System not coping well – under stress can be ineffective, take longer to return to normal
- Deals less well with glucose load
- More chance of complications
glucose tolerance test diabetes values
FPG >7.0
Damage from diabetes occurs due to time spent over 7
- Below 7 risk of standard diabetic complication less
FPG <6.1
normal reaction after glucose tolerance test
FPG 6.1-7.0
impaired fasting glucose after glucose tolerance test
FPG >7.00
diabetes result after glucose tolerance test
what does a score <7.8 after 2 hour plasma glucose level indicate
normal reaction
what does a score 7.8-11.1 after 2 hour plasma glucose level indicate
impaired glucose tolerance
Pre diabetes in impaired group - potential to become fully diabetic
what does a score >11.1 after 2 hour plasma glucose level indicate
diabetes
type 1 diabetes mellitus
insuline deificient
type 2 diabetes mellitus
insuline resistance
what occurs in type 1 diabetes
Immune mediated pancreatic B cell destruction
Need to have insulin to stay alive
- Glucose in blood and insulin moves blood sugar into cells
3 circulating antibodies present in Type 1 diabetes
GAD glutamic acid decarboxylase
ICA Islet cell antibodies
IAA insulin autoantibodies
what are 2 consequences of type 1 diabetes
hyperglycaemia
Ketoacidosis
Blood sugar down
- Cells need glucose to metabolise - if not ketones
- Not efficient and by waste products are acidic
- Ketoacidosis can be lethal
how are pancreatic B cells destroyed in type 1 diabetes
Antibodies attacks pancreatic B cells
- Autoimmune disease
- Cannot make insulin
- Normal to diabetic in few months
- Rapid change
pattern of inheritance for type 1 diabetes
Family autoimmune disease
- Genetic predisposition - environmental trigger causes antibody response
factors that contribute to type 1 diabetes
genetic and environmental
genetic influences of type 1 diabetes
Familial Clustering
- type 1 diabetes risk in sibling 6% - 0.4% in population
Monozygotic twins concordance ~40%
- 10% in dizygotic twins
HLA associated
- DR 3 & 4, DQ 2 & 8
environmental triggers of type 1 diabetes
Low twin concordance
change in incidence in migrants
increasing population incidence with stable genetic pool
- same genes in population
- gene pool restricted
- increase in rate of type 1 as environmental cause more significant
adult onset type 1 diabetes
- LADA - latent autoimmune diabetes in Adults (>25 yrs of age)
- — Problem occurs in teens but rate losing islet cells in pancreas low
- — So long time for enough insulin to be lost as needed to maintain blood sugar
- GAD associated - generally lower AB levels
- less weight loss, less ketoacidosis
- may masquerade as ‘non-obese’ type 2
- variable period until insulin required
childhood onset type 1 diabetes
- Peak incidence 10-14yrs - up to 60% cases occur AFTER age 16
- classically in children/adolescents
- –higher ICA, IAA
- –rapid change – well to sick quickly
- —more severe decompensation
type 1 diabetes symptoms
- polyuria
- polydipsia
- tiredness
Acute Presentation
- Hyperglycaemia with diabetic symptoms
- Ketoacidosis
USUALLY REQUIRE INSULIN from DIAGNOSIS
what do pancreatic B cells produce
insulin
role of insulin
move blood sugar into cells
Longer to return to normalglycemia if destroyedB cells
- Impaired glucose tolerance
Hit diabetic
how to diagnose type 2 diabetes
by excluding type 1
hard to define
what is the most common form of diabetes
type 2 diabetes mellitus
- 90% of all cases - prevalence tripled in 30yrs
- strongly associated with obesity & inactivity
when does type 2 diabetes usually present
patients over 40yrs of age
- Maturity Onset Diabetes in the Young (MODY) possible
Taking so long to move along the scale
- Likely to die of other cause first
pattern of inheritance of type 2 diabetes
Strong Family history
- 100% concordance in identical twins
- Completely genetic
No environmental trigger – but can decrease risk
4 metabolic disorders that cause type 2 diabetes
defect in insulin resistance
defect in insulin secretion
basal hepatic glucose output increased
insulin stimulated muscle glucose uptake is reduced
how does reduced insulin stimulated glucose uptake lead to type 2 diabetes
- failure of insulin promotion
- Insulin promotes storage of blood glucose (glycogen and triglycerides)
- —Reduce sugar level
- Too much insulin in normal blood glucose level - still make glycogen and fat but don’t move sugar into cells
- —larger proportion stored then used as metabolic
how does a defect in insulin secretion lead to type 2 diabetes
- B cell response to hyperglycaemia is inadequate
- Cells Don’t respond as well to insulin
- Cannot bond to receptor well
- Cell receptor not working well
- Make too much insulin - hyperinsulinemia
how does a defect in insulin resistance lead to type 2 diabetes
- elevated basal insulin levels
- alike type 1
how does increased basal hepatic glucose output lead to type 2 diabetes
- failure of insulin suppression
effect of type 2 diabetes
Impaired glucose tolerance
Hyperinsulinaemia
Hypertension
Obesity with abdominal distribution
Dyslipidaemia (High VLDL, Low HDL)
Procoagulant epithelial markers
Early & accelerated atherosclerosis
- Prone of cardiovascular disease linked to type 2 diabetes
- – All come to primary issue - hyperinsulinemia
- —— regulate and use insulin
type of onset for type 2 diabetes
Gradual onset - over many years
- usually IGT for some time (pre-diabetic)
- often retinal damage at diagnosis (7-10yrs IGT)
- —often complication from consistently raised blood sugar when diagnosed
- ability to secrete insulin falls with time
what can protect a person from developing type 2 diabetes
STRICT DIET AND EXERCISE PROTECTS
acute presentation of type 2 diabetes
- polyuria, polydipsia, tiredness (peeing a lot, drinking a lot, being tired) are usually present (noticeable)
- unusual infections
- diabetic complications (retinal damage)
- Cardiovascular
age comparison of type 1 and 2 diabetes
type 1: younger
type 2: older
body comparison of type 1 and 2 diabetes
type 1: thin
type 2: obese
pattern of inheritance comparison of type 1 and 2 diabetes
type 1: questionable family hx
type 2: strong family hx
complications and effects comparison of type 1 and 2 diabetes
type 1: diabetic symptoms
type 2: present with complications
ketosis comparison of type 1 and 2 diabetes
type 1: easily get ketosis
type 2: rarely get ketosis (slow progression)
4 methods of managing diabetes
education
nutrition
exercise
monitoring
pre-prandial target
4-6mmol/L
bedtime target
6-8mmol/L
drugs to manage diabetes
insulin
2 types of insulin regimes
basal bolus control
split-mixed control
basal bolus insulin control
more injections – better
inject themselves
ketone acidosis if don’t
One injection slowly releasing insulin
And small quick acting insulin with meals
- Pump into storage after meals
Amount depends on what you eat/drink/do
- More flexibility with lifestyle
- Decision at the moment of when and how much
split mixed insulin control
fewer injections - poorer
need to have insulin there to last till next one
- Medium acting insulin
- Short acting
Both keep average blood sugar where it should be
- more time higher, and need to be precise of when to eat
factors to consider when delivering insulin to manage diabetes
Need to be careful of sugar intake
- Eating secondary to having insulin
Depends on type of insulin and how often want to inject
how does insulin differ
packaging is different
- Stick to protein
Release into circulation at a fix rate
- Slowly or rapidly
education management of diabetes
about diabetes, managing diabetes, health care issues, complication avoidance
- keep blood sugar in correct level
remain at normal level
type 1 harder to manage than type 2
nutrition management of diabetes
less than 10% calories from saturated fat
- prone to getting atherosclerosis cannot cope as well with fat
glycaemic index of foods compared with a standard food
Carbohydrate counting
- basal-bolus regimes
`
exercise management of diabetes
planned activity
understand individual response to exercise
monitoring management of diabetes
sliding scale’ approach wrong
previous insulin dose determines plasma glucose
- work out how many insulin units you need
type 1 diabetes drug management
INSULIN subcutaneously (human) from diagnosis for life
different preparations available
- time to act from injection varies
- mixed forms possible
different regimes for each individual
AIM - ideal sugar 4<7 (HbA1C - 6<10%)
- balance between bringing sugar down to good level and too far to be unconscious
often may accept slightly higher
glycosylated haemoglobin
HbA1C (6<10%)
amount of sugar residue on Hb average value of what bolus sugar has been for last 120 days
want past as well as present
the higher the blood sugar the more
complications of diabetes (e.g. retinopahty)
hypoglycaemia
insulin without enough glucose
type 2 diabetes management
Weight loss
Diet restriction
patient controlled – not always effective
- by managing can prevent progression
‘Diet pills’
- Orlistat, Sibutramine
Surgery
- “Gastric bypass”, gastric vertical banding
Oral Hypoglycaemic agents
- Insulin secretagogues
- –sulphonylureas
- —–gliclazide, glibenclamide, tolbutamide, Chlorpropamide
- Insulin sensitisers
- –Biguanides
- —–metformin
- –Thiazolidinediones
- —–rosiglitazone
diet restriction to manage type 2
- avoid refined CHO
- encourage high fibre food
- reduce fat, esp. saturated
2 types of oral hypoglycaemic agents for type 2 diabetes management
Insulin secretagogues
- sulphonylureas
- —–gliclazide, glibenclamide, tolbutamide, Chlorpropamide
Insulin sensitisers
- Biguanides
- —–metformin
- Thiazolidinediones
- —–rosiglitazone
sulphonylureas
insulin secretagogues oral hypoglycaemic agent
INCREASE pancreatic insulin secretion
- Make too much insulin – low risk
can cause hypoglycaemia!
biguanides
insulin sensitiser oral hypoglycaemic agent
enhance cell insulin sensitivity
reduce hepatic gluconeogenesis
preferred in the obese
- safer starting point
when would insulin be given to manage type 2 diabetes
Patients unable to maintain glycaemic control with
- behavioural changes
- body weight reduction
- oral hypoglycaemic agents
Many regimes available
- Often combined with metformin
- prandial or basal cover
- insulin is to supplement with what they can make
DIGAMI study
- benefits in insulin treatment after MI in type 2 diabetics
acute diabetes complications
hypoglycaemia
hypoglycaemia occurs when
insulin/drug without food!
in:
- Type 1
- Type 2 on sulphonylurea (pills) or insulin
3 chronic complications of diabetes
Cardiovascular risk
infection risk
neuropathy
- Nerves supply body die off, Because have no blood supply
- —-Cardiovascular disease of blood vessels - nerves die off
- —-Lead to complications
symptoms of hypoglycaemia
sweating, tremors, agitates
coma seizure when reach blood sugar 1
what is the effect of neuropathy on blood sugar management
ability to know when going hypo decreases with neuropathy
large vessel diabetic complications
atheroma
angina & MI, claudication, anneurysm
- atherosclerosis increased risk
small vessel diabetic complications
poor wound healing (foot ulcers from blisters)
easy wound infections
RENAL DISEASE
EYE disease
neuropathy (nerve damage, neuropathic pain)
—numb hand, feet and legs
diabetic eye disease
Cateracts
- Fixed by surgery
Maculopathy
Proliferative retinopathy
- Blood vessels grow and cause bleeding in eye
- laser treatment
what increases the chance of success of diabetic retinopathy
more likely success retinopathy if blood sugar well controlled
Retinopathy screening – photos of back of eye, sent to ophthalmologists to assess
general sensation of diabetic neuropathy
glove & stocking’
- Numbness, pain
effect of motor diabetic neuropathy
weakness and wasting of muscles
effect of autonomic dysregulation of diabetic neuropathy
awareness of hypoglycaemia lost
postural reflexes
- cannot work the nerve which works the muscle
bladder & bowel dysfunction
3 issues for diabetics in surgery
Fasting a problem in TYPE 1 DIABTEICS
Metabolic changes associated with surgery
- Increased insulin requirements in type 1
- Type 2 may require insulin cover pre-operatively
how is fasting an issue for diabetes in surgery
need insulin to prevent ketosis
-but no sugar in blood due to fasting – risk of becoming hypo
need carbohydrate to prevent hypoglycaemia
-IV sugar and insulin to prevent
- Increased insulin requirements in type 1
- Type 2 may require insulin cover pre-operatively
how do metabolic changes impact on diabetes in surgery
hormone changes aggravate diabetes (sugar is managed by insulin and hormones)
- epinephrine, cortisol, growth hormone
more glucose production and less muscle - uptake
- metabolic acidosis more likely
6 dental aspects for care of diabetes
Be aware of effect of dental treatment
- food intake may be disrupted
Be aware of acute emergencies
Be aware of diabetic complications
- IHD, dehydration, neuropathy, eyes
Be aware of INFECTION RISK
be aware of POOR WOUND HEALING
appointment times should fit around their insulin regime to prevent hypoglycaemia
