(38) diabetes for dentists

8/11/2019 (38) Diabetes for Dentists

1/37

Diabetes for Dentists

Dr Jackie ElliottClinical Lecturer in Diabetes

6 Nov 2012
http://www.google.co.uk/imgres?imgurl=http://www.cryst.bbk.ac.uk/PPS2/press/insulin8.gif&imgrefurl=http://www.cryst.bbk.ac.uk/PPS2/press/biochemist.html&usg=__Yb9G25y0BsbXRNEZoO7EEq2ff6k=&h=576&w=576&sz=47&hl=en&start=6&zoom=1&um=1&itbs=1&tbnid=Uq7rPDDp8AN4eM:&tbnh=134&tbnw=134&prev=/images%3Fq%3Dinsulin%2Bmolecule%2Bmodel%26um%3D1%26hl%3Den%26sa%3DN%26tbs%3Disch:1http://images.google.co.uk/imgres?imgurl=http://www.worlddiabetesday.org/files/images/dka.jpg&imgrefurl=http://www.worlddiabetesday.org/the-campaign&usg=__p3xnV02kxE9lwrAxfN_yCCXH6Ks=&h=105&w=101&sz=5&hl=en&start=81&tbnid=nhcsnJ_NOEAUBM:&tbnh=84&tbnw=81&prev=/images%3Fq%3DDKA%2Bdiabetes%26gbv%3D2%26ndsp%3D20%26hl%3Den%26sa%3DN%26start%3D80


2/37

Objectives

Describe Type 1 and Type 2 diabetes, the differencesbetween them, their effects, management and treatment

Elicit a history of diabetes including polyuria, polydipsia,

recurrent infections and weight loss Demonstrate knowledge of insulin, oral hypoglycaemic

drugs, new injectables and implications for dentaltreatment

Demonstrate knowledge of the complications ofdiabetes, particularly hypo- and hyperglycaemic coma

Demonstrate knowledge of systems for monitoring bloodand urine glucose


3/37


4/37

Diagnosis

Symptoms and random plasma glucose

>11.1 mmol/l

Fasting plasma glucose > 7 mmol/l

No symptoms - OGTT (75g glucose)

fasting > 7 or 2h value > 11.1 mmol/l


5/37

Presenting features of diabetes

Thirst osmotic activation of

hypothalamus

Polyuria

osmotic diuresis

Weight loss and fatigue dehydration

lipid and muscle loss

Pruritis vulvae and balanitis Vaginal candidiasis

Hunger

Blurred vision Altered acuity due to uptake of glucose/water into lens


6/37

Clinical features of newly diagnosed

Type 1 diabetes

Short

history

(weeks) of

severesymptoms

Weightloss

Moderate or large urinary ketones

Any 2 of these three features indicate Type 1

diabetes and are an indication for immediate

insulin treatment at ANY age


7/37

Clinical features of type 1 diabetes

Commonest age at diagnosis, 5-15y , butcan occur at any age

Relatively rare (prevalence of 3/1000among children and adolescents)

250,000 in the UK

An insulin deficiency disease (autoimmunedestruction of the beta cell)

Treatment consists of restoring

appropriate insulin concentrations


8/37

Aims of treatment in Type 1 diabetes?

Initially to achieve this


9/37

Aims of treatment in Type 1 diabetes

Relieve symptoms and prevent ketoacidosis

Prevent microvascular and macrovascularcomplications

Avoid hypoglycaemia


10/37

Microvascular Complications

Around 30% in the UKwill develop diabeticnephropathy CV mortality with

no nephropathy x2, butwith nephropathy x30

Those withnephropathy tend to

develop proliferativeretinopathyandsevere neuropathywith major effect onquality of life


11/37

Treatment of Type 1 diabetes

To restore the physiology of the beta cell Insulin treatment

Twice daily mixture of short/medium actinginsulin

Basal bolus, (once or twice daily medium actinginsulin plus pre meal quick acting insulin)

Ability to judge carbohydrate intake

Awareness of blood glucose lowering effect ofexercise

All combined to keep blood glucose close to normal

(and so prevent diabetic complications)


12/37

SYMPTOMS

SYMPTOMS


13/37


14/37

Benefits and risks of tight glucose control

141312111098765

0

20

40

60

80

100

Severehyp

oglycaemiaper10

0patientyears

Intensive group

Hypoglycaemia

Haemoglobin A1cDCCT Group, Diabetes 1996

0

2

4

6

8

10

12

14

16

Retinopathyper100patienty

ears

Retinopathy


15/37

The dilemma for those with

type 1 diabetes:

Setting higher glucose targets will

reduce the risk of hypoglycaemia butincrease the risk of diabeticcomplications

Setting lower glucose targets will reducethe risk of complications but increase

the risk of hypoglycaemia


16/37

Type 1 diabetes - Conclusions

2/3 of all patients can expect a reasonable

life expectancy with minor complications

Tight glucose control will increase this

proportion but often at the expense of

hypoglycaemia and weight gain The challenge is to engage most patients

in the management of their own disease


17/37


18/37

Type 2 diabetes

Perhaps the greatest non-infective threat toglobal health

7% prevalence in Sheffield

2.7 million in the UK, i.e., ~1 in 20

Medications cost the NHS >700 million / y

Currently affects ~360 million worldwideA disease of western industrialised lifestyle

Obesity

Lack of physical exercise


19/37

Pathogenesis of Type 2 diabetes

increased thrombogenesisearly

hyperinsulinaemia

insulin resistance

Abnormal lipids

(low HDL cholesterol

hypertriglyceridaemia)hypertension

hyperglycaemia

central obesity

Major cardiovascular risk (x3-4)


20/37

Pathogenesis of raised blood

glucose in Type 2 diabetes Insulin resistance (probably inherited) which

demands increased production of insulin to

maintain normal glucose levels before thedevelopment of diabetes

Progressive failure of insulin secretion


21/37

Complications in type 2 diabetes

Macrovascular affect themajority and are often

advanced at diagnosis

Myocardial infarction, stroke,

peripheral vascular disease

Microvascular affect 20-

25% at diagnosis and are

modified by underlying

vascular disease

Life expectancy is

shortened at diagnosis by

about 5-10 years

3%

1%

3%

21% 1%

35% HT

18% ECG

20% ED


22/37

Treatment in Type 2 diabetes

Ideally consists of weight loss and exercise(improve insulin resistance) which if substantialwill reverse hyperglycaemia but most of those with Type 2 diabetes have been

making the wrong lifestyle choices all their lives

At present, management usually consists ofmedication to control BP, blood glucose and lipids

Tight control of BP and lipids has a greater effectin reducing the risk of macrovascular disease(and reduces microvascular complications) and isusually easier to achieve than blood glucose

control


23/37


24/37

Typical treatment pathway in

patients with Type 2 diabetes

diet

Eat less and reduce refined CHO


25/37



diet metformin

a biguanide which reduces blood glucose byimproving glucose uptake without increasing body

weight and also reduces CV disease in the

longterm. Now initial treatment of choice for all

those with Type 2 diabetes.

s/e of abdo pain and diarrhoea limit dose


26/37



diet metformin sulphonylurea

Act by stimulating release of insulin from pancreatic

beta cells so can cause weight gain and

hypoglycaemia, examples gliclazide, glibenclamide


27/37




Insulin secretion declines progressively in Type 2 diabetes,

over 50% will need insulin

insulin

0

20

40

60

80

100

InsulinOral Agents

%

0 5 10

Duration of diabetes (yr)


28/37




Or possibly pioglitazone,Or a DPPIV inhibitor, e.g., sitagliptin

Or a incretin mimetic (injection), e.g., exenatide or

liraglutide


29/37

Type 2 diabetes - Conclusions

The best treatment, weight loss and increased

exercise is rarely achieved

Needs multiple medications, many of which areprobably not taken

The challenge is to engage the patient in the

management of their own condition

This is not mild diabetes - high risk of premature

vascular death and other vascular complications


30/37

Emergencies

Phone 999


31/37

Diabetic Ketoacidosis Definition

Hyperglycaemia (use capillary sample but confirm with lab test) Venous bicarbonate less than 15 mmol/l

Ketones

Causes

infections omission of insulin

new diagnosis

Mortality

1-5% Elderly

associated co-morbidity and late diagnosis

Young

severe DKA recognised late

rare and poorly understood condition of cerebral oedema inchildren


32/37

Hyperosmolar Hyperglycaemic State (HHS)

or

Hyperosmolar Non-Ketotic Coma (HONK)

Definition

Hyperglycaemia (blood glucose usually over 50

mmol/l) Hyperosmolality (osmolality usually over 350

mosmoles/l)

Accompanied by dehydration

Those at risk

Poorly controlled Type 2 diabetes

Newly diagnosed Type 2 diabetes patients, oftenelderly


33/37

Symptoms and signs

of hypoglycaemia

Loss ofconcentration

Drowsiness

Anger / sadness

Confusion

Neuroglycopenic

SweatingTremor

Palpitations

Autonomic


34/37

Hypo Management

Patient conscious Patient unconscious

Oral glucose glucogon 1 mg (IM)

IV glucose (100 mls 10% dextrose)

Check blood glucose after 10 mins (further IV/PO glucose ifneeded)

identify cause

re-educate

adopt measures to avoid hypos
http://www.diabetes.co.uk/images/gluco-carry.jpg


35/37

Monitoring Diabetes

Venous blood glucose

HbA1c

Capilliary blood glucose

Blood ketones

Urinary ketones
http://www.mhra.gov.uk/idcm2/groups/dts-bs/documents/medicaldevicealert/con079037.jpg


36/37

Diabetes & Dentistry

?bidirectional relationship

Increased rates of gingivitis / periodonitis (2-5 fold) /dental caries / candidiasis / endocarditis

Stressboth physical & emotional raises bloodglucose levels

Beware of hypoglycaemic medications

Type 1 diabetes is autoimmune process, thereforeSjorgrens is more likely

Some studies suggest improvements in glycaemiccontrol after periodontal intervention

Dentists can help in the early recognition of T2DM(and rarely T1DM)

UKPDS, Lancet 1998, 352: 837-53Sandber et al, Diab Res Clin Prac 2000, 50; 27-34


37/37

Type 1 or Type 2

If you were to be diagnosed with

diabetes tomorrowwhich type do

you think you would prefer to have?

(38) diabetes for dentists

Documents