Diabetes Flashcards
What is the epidemiology of diabetes mellitus?
Estimated 5 million ppl with diabetes in UK by 2025.
Estimated 850,000 ppl in UK undiagnosed
12.3 million at risk of type 2 DM
A patient contacts you to update their medication list prior to an appointment for a dental extraction next week. In addition to his usual Metformin, he is now taking Gliclazide. He asks whether or not this will affect his dental treatment.
Does this patient suffer from type 1 or type 2 diabetes mellitus?
Type 2
Identify two differences between diabetes mellitus type 1 and 2.
age of onset: type 1 = younger
prevalence: type 2 more prevalent
aetiology: type 1 = autoimmune type 2 = insulin resistance/B cell dysfunction
Initial presentation: type 1 = loss of weight/polyuria/DKA: type 2 = hyperglycaemia, diabetic complications
association with BMI: usually reduced BMI in T1. Increased BMI in T2
Name two oral complications of diabetes mellitus (5)
- oral infections
- periodontal disease
- poor healing
- xerostomia
- neuropathic changes/changes in sensation.
Identify the main actions of metformin on the liver and muscle.
Decreases hepatic gluconeogenesis
Increases glucose uptake and utilisation in skeletal muscle
Increases sensitivity to insulin
A patient contacts you to update their medication list prior to an appointment for a dental extraction next week. In addition to his usual Metformin, he is now taking Gliclazide. He asks whether or not this will affect his dental treatment.
Can the extraction for this patient still go ahead as originally planned?
Yes
Give two treatment measures that are used in the management of hypoglycaemia in the dental setting.
Glucagon
Lucozade, or any other suitable example of high sugar substance
Hypostop
What is normal blood glucose?
fasting: 4.0-6.0 mmol/L Post prandial (2hrs after meal) <7.8mmol/L
What does each cell type release in the islets of langerhans?
Alpha cells - glucagon
Beta cells - insulin
Delta cells - somatostatin
When is insulin released?
What does insulin cause in 1) liver and muscle cells 2) fat cells 3) liver and kidney cells?
High blood sugars (e.g. after a meal) stimulate insulin release from pancreas.
1) liver and muscle cells
> incr storage of glucose as glycogen
> amino acid production from proteins
2) fat cells
> formation of fats from fatty acids + glycerol
3) liver and kidney cells
> inhibition of making glucose (gluconeogenesis)
overall, insulin increases storage of glucose, fat, amino acids
therefore, reducing concentration in circulating blood stream
When is glucagon released?
What does glucagon cause in 1) liver and muscle 2) liver and kidney cells?
Low blood sugars (e.g. fasting) stimulate glucagon release form the pancreas.
1) LIVER AND MUSCLE CELLS
> breakdown of glycogen to release glucose (glycogenolysis)
2) LIVER AND KINDEY CELLS
> stimulate gluconeogenesis
Overall, glucagon stimulates release of glucose form body stores to increase concentration in bloodstream.
What does insulin deficiency or resistance cause?
> Cells unable to absorb glucose despite high levels in blood.Glucagon release stimulated to try and increase glucose levels.Increased release of glucose from storage + gluconeogenesisIncreases blood sugars further but cells still unable to take up and use.
What does high levels of blood sugar in diabetic pts cause?
> Increased filtration of glucose by kidneysExcess glucose in renal tubules causes loss of water by osmosisResults in excess glucose being excreted in urine, with polyuriaPolydipsia results because of vol loss + due to osmotic effects stimulating thirst receptors.
What is polyuria?
Lots of urine
What is polydipsia?
Very thirsty
What are symptoms of diabetes mellitus? (7)
1) Polyuria
2) Polydipsia
3) Weight loss
4) Sx + signs of diabetic ketoacidosis
5) Lethargy
6) Blurred vision
7) Recurrent infections
How do you diagnose diabetes?
Random glucose >11.1 mmol/L
Fasting glucose >7.0 mmol/L
2 hr postprandial >11.1 mmol/L
HbA1c >4.8 mmol/mol
only pregnant use glucose tolerance test.
normally use HbA1c
What are the types of diabetes? (5)
- Type I DM –> failure to produce insulin
- Type II DM –> resistance to insulin
- Gestational DM –> pregnant women who have never had diabetes before but who have high glucose levels during pregnancy.
- MODY –> genetic defects leading to DM.
5. Secondary diabetes > pancreatic disease e.g. cystic fibrosis, pancreatomy > endocrine e.g. Cushings. Acromegaly > drug induced e.g. steroids > genetic
What are the differences btw type 1 and type 2 DM?
Age of onset: T1DM = younger T2DM = older
UK prevalence T2DM = more prevalent
Aetiology T1DM = autoimmune T2DM = insulin resistance, beta cells destruction + beta cell dysfunction.
Initial presentation: T1DM = polyuria, polydipsia, weight loss, ketoacidosis. T2DM = hyperglycaemic symptoms, diabetic complications.
Appearance; T1DM = low BM1 T2DM = increased BMI
Describe T2DM
Usually insidious onset
Often have developed complications by time of diagnosis
More likely to have additional risk factors e.g. hypertension, hyperlipidaemia.
Lifestyle an important factor
What are the risk factors of T2DM?
> Obesity > Lack of exercise > Ethnicity - south asian, african, african-carribean, middle eastern > History of gestational diabetes > Impaired glucose tolerance > Diabetes > Polycystic ovary syndrome > Family history
What are the goals of treatment of type 2 diabetes?
keep patient feeling well
prevention of hypoglycaemia (low blood sugar)
delay onset + progression of microvascular + macrovascular complications
65% patients with diabetes die from heart disease + stroke.
What are diabetic complications?
stroke heart attack peripheral artery disease diabetic retinopathy cataracts glaucoma diabetic foot diabetic + peripheral neuropathy
What are the treatment options for T1DM and T2DM?
T1DM = only option is insulin T2DM = multiple options
What are the 2 types of insulin regime?
Basal-bolus regime
Basal = long acting background insulin
Bolus = short acting insulin taken with meals
Twice daily insulin
= mixture of shirt and intermediate insulin
- less flexibility
All different types of insulin has similar mechanism of action. How does insulin differ? (3)
- Rate of absorption
- Peak onset of action
- Duration
How is insulin given?
Where on the body?
Subcutaneously
delivered via pen devices
rotate site of injection: \: upper outer arm \: abdomen \: buttocks \: upper outer thigh
What type of diabetes can have insulin delivered via insulin pump therapy?
only type I
unopened supplies of insulin in refrigerator. Insulin in use an be kept at room temp. needles dispose in sharps bin.
What are the different therapies for T2DM? (4)
Metformin, sulphonylureas (e.g. gliclazide), SGLT2 inhibitors (e.g. dapaglifozin), Incretin hormones (GLP)
How does metformin work?
It increases insulin sensitivity
Decreases hepatic gluconeogenesis
Increases glucose uptake and utilisation in skeletal muscle
How does sulphonylureas work?
Increase insulin release, risk of hypoglycaemia
How do SGLT2 inhibitors (e.g. dapaglifozin) work?
Reduce glucose absorption in the kidney
therefore increase glucose excreted in urine
How to incretin hormones work? (GLP)
GLP-1 agonists - act on GLP receptors, s/c injections. DPP4 inhibitors (gliptins) - prevent GLP breakdown
GLP:
: stimulates release of insulin only in presence of glucose
: reduces appetite + promote satiety - feeling fed
: delay gastric emptying
: reduces hepatic glucogenesis
What is hypoglycaemia?
Refers to any episode of low blood glucose <4mmol/L
Occurring in patients taking insulin or sulphonylureas
Symptoms can be divided into two stages.
What are the 2 stage hypoglycaemia can be divided into?
- AUTONOMIC:
- due to activation of autonomic nervous systems (sweating, tremor, anxiety, palpitations, etc) WARNING SYMPTOMS) - NEUROGLYCOPAENIC
- due to reduced glucose delivery to the brain (poor concentration, odd behaviour, dizziness, blurred vision etc.)
if left untreated, leading to coma + death
What causes hypoglycaemia?
missing or delaying a meal not having carbohydrate at last meal exercise taking more insulin than you need drinking alcohol on an empty stomach unknown
How do you treat hypoglycaemia?
if able to have oral intake:
- 3 glucose or dextrose tables
- 5 jelly babies
- small glass of a sugary drink
- small carton of pure fruit juice
- tube of glucose gel
If unable to swallow
- IM glucagon
- IV glucose
Recheck BM 10-15 mins after treating
Then have 15-20 g of a slower acting CHO: - sandwich, fruit, cereal, milk
What is diabetic ketoacidosis (DKA)? MEDICAL EMERGENCY
only type II
Due to insulin deficiency
Cells unable to use glucose so breakdown
Fatty acids instead
Leads to ketone formation. Acidosis develop. Sever dehydration.
What are common risk factors diabetes?
obesity, physical activity, diet
influence both oral health and diabetes risk
What are the oral manifestations of diabetes?
- Increased prevalence, extent + severity of periodontitis
- Periodontal abscesses
- Poor healing
- Recurrent infections
- Medication side effects e.g. gingival overgrowth from calcium channel blockers.
- Dry mouth - increased risk of caries, candida injection + chronic mouth ulcers.
How are diabetes and periodontitis linked?
Diabetics are 2-4x more susceptible to gum disease due to poor blood glucose control
>
Gum infection further decreases blood glucose control and increases insulin resistance and hyperglycaemia (an excess of glucose in the bloodstream)
>
High blood glucose levels make fighting infections more difficult and causes more severe gum disease
>
Severe gum disease can then increase blood glucose levels further, contributing to increased periods of time with high blood sugar
>
cycle round
What is the link btw gum disease & diabetes? (4)
- Diabetic control: gum disease is linked to blood glucose control. People with poor blood sugar control get gum disease more often, more severely and they lose more teeth.
- Blood vessel changes: blood vessel deliver oxygen and nourishment to body tissues, including mouth, and carry away the tissues’ waste products. Diabetes causes blood vessels to thicken, which slows the flow of nutrients and the removal of harmful wastes, increasing the risk of gum injection.
- Bacteria: many kinds of bacteria thrive on sugars, including glucose - the sugar linked to diabetes. when diabetes is poorly controlled, high glucose level in saliva enable gums to grow and set the stage for gum disease
- Smoking: a smoker with diabetes, age 45 or older, is 20x more likely to get severe gum disease.
What links periodontitis to diabetes? (slides)
3-4x increased prevalence of severe periodontitis
Severity of perio is associated with poor glycaemic control
Adverse outcomes in diabetes are more likely in the of periodontitis.
Successful treatment of periodontitis can lead to improvements in glycaemic control.
Studies have shown consistently a 0.4 reduction in HbA1c with treatment of periodontitis.
Every 1% reduction in HbA1c is associated with a reduced risk of diabetes complications.
What considerations do you need to make with a diabetic patient undergoing a procedure?
For procedures with LA and no requirement to be NBM (nil by mouth), then generally no changes will be needed.
However if a pt has had (or will) reduced oral intake due to procedure, then may have to make alterations to meds to avoid hypoglycaemia (insulin, gliclazide)
Alterations to meds depend on likely starvation period + what meds taking.
Ideally planned procedure.
Seek advice from diabetes team if unsure.
Infection + stress cause hyperglycaemia
Hypoglycaemia may occur if reduced oral intake.
What are the implications of diabetes for dental practice?
a) risk of hypoglycaemia whilst attending the dental surgery
b) higher risk of oral disease, particularly if diabetes is poorly controlled
c) undiagnosed diabetes may be present at the dental surgery
d) pts with diabetes may experience some improvement in their glycaemic control following successful periodontal treatment.
