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BDS2 - endocrinology > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

what is diabetes mellitus

A

Abnormality of glucose regulation
Metabolic disease and you are going to die
Glucose problem - blood sugar is high so amount of sugar in urine is high

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2
Q

what is diabetes inspidus

A

Abnormality of renal function (water)
Loss of ability to concentrate urine
Person will remain quite healthy - If they drinks lot they will be okay

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3
Q

what are the tests for diabetes mellitus

A
  • Random sugar?
    § 2 random glucose tests above 11 suggests diabetes
  • Fasting sugar?
    § Have nothing to eat for 8 hours then take a sample
  • Glucose tolerance test?
    § Standardised test - test blood sugar having patient fasted then give a fixed dose of sugar and tested after 2 hours (levels should be in a specific range)

[Ideally want a fasted test sample and a glucose tolerance test]

  • Random plasma glucose (RPG)
    >11.1mmol/L on 2 occasions is diagnostic of diabetes
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4
Q

what is needed in the diagnosis of diabetes

A

Glucose tolerance test (75g load after fasting)
[FPG = fasting plasma glucose - Fasting level shows how well your system is generally working]

○ Before test
§ FPG <6.1 = normal
§ FPG 6.1-7 = impaired fasting glucose = Not yet diabetic but not looking well
§ FPG > 7 = diabetes = Damage from diabetes depends on the time that the patient’s blood glucose levels are above 7

○ 2 hour after plasma glucose
§ <7.8 = normal
§ 7.8-11.1 = impaired glucose tolerance
§ >11.1 = diabetes

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5
Q

what are the types of diabetes mellitus

A

Type 1 = insulin deficiency
Type 2 = insulin resistance [Can progress to insulin deficiency]

Both type 1 and type 2 are related to blood sugar levels but the processes are completely different

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6
Q

what is hyperglycaemua

A

An excess of glucose in the blood

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7
Q

what is ketoacidosis

A

Complication of type 1 diabetes

A life threatening condition resulting from dangerously high levels of ketones and blood sugar

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8
Q

what is type 1 diabetes

A

immune mediated pancreatic b cell destruction

Organ specific autoimmune disease (genetic)

  • Environmental trigger comes along and get antibody response to that
  • Also targets pancreatic B cells and once you start making the antibody you cannot produce any insulin and you will die
  • In some people this will progress very rapidly and in some it will be slow

Type 1 diabetics need insulin or they will die

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9
Q

what circulating antibodies are present in type 1 diabetes

A

○ GAD
§Glutamic acid decarboxylase

○ ICA
§ Islet cell antibodies

○ IAA
§ Insulin autoantibodies

Progress and destruction can take many years if this is produced

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10
Q

what are the genetic influences for type 1 diabetes

A

○ 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

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11
Q

what are environmental triggers for type 1 diabetes

A

Low twin concordance
Change in incidence in migrants
Increasing population incidence with stable genetic pool

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12
Q

when is the peak incidence for type 1 diabetes

A

10-14 years

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13
Q

explain the common ages for onset of type 1 diabetes

A

§Classically in children / adolescents
□ Higher ICA, IAA
□ More severe decompensation
□ Rapid change - go from health to sickness quickly

§ Adult onset
□ LADA - latent autoimmune diabetes in adults (>25 years of age)
□ GAD associated - generally lower AB levels
□ Less weight loss, less ketoacidosis
□ May masquerade as ‘non-obese’ type 2
□ Variable period until insulin required
□ Adult more of an issue
® Slow onset ones
® They had the problem to get diabetes in teens but the antibody killing the pancreatic cells were very slow process
® Eventually if you did nothing they could be the same as type 1 diabetic but would take a long time to get to that stage

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14
Q

what are symptoms of diabetes

A

○ Polyuria
§ Production of abnormally large volumes of dilute urine

○ Polydipsia
§ Abnormally great thirst

○ Tiredness

• Acute presentation
○ Hyperglycaemia with diabetic symptoms
○ Ketoacidosis

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15
Q

how do you diagnose type 2 diabetes

A

excluding type 1 - hard to define, but easiest way is to say it is not type 1

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16
Q

what is the most common form of diabetes

A

type 2

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17
Q

what is type 2 diabetes strongly associated with

A
  • obesity

- inactivity

18
Q

does type2 diabetes run in the family

A

strong family history

completely genetic

19
Q

is type 2 ketoacidosis

A

rarely

Because they are taking so long to go down the line they are likely to die of something else before this

20
Q

explain type 2 diabetes as a metabolic disorder

A

Whole raft of genetic alterations which make your body metabolism work differently which makes you more prone to developing diabetes (high blood sugar)

○ Defect in insulin resistance
§ Elevated basal insulin levels
□ Cells do not respond to insulin well
□ Cell receptors are not working in the way they should

○ Defect in insulin secretion
§ B cell response to hyperglycaemia is inadequate

○ Basal hepatic glucose output increased
§ Failure of insulin suppression

○ Insulin stimulated muscle glucose uptake is reduced
§ Failure of insulin promotion

21
Q

what are the effects of type 2 diabetes

A

‘Metabolic syndrome’ - metabolic issue not bad in the right circumstances (if you need to store food for a while)

○ Impaired glucose tolerance

○ Hyperinsulinemia
§ Primary issue - all comes back to this
§ Increased level of insulin in the blood
§ a condition in which there are excess levels of insulin circulating in the blood relative to the level of glucose

○ Hypertension

○ Obesity with abdominal distribution

○ Dyslipidaemia
§ High VLDL
§ Low HDL
§ Abnormal amount of lipids (e.g. triglycerides, cholesterol and/or fat phospholipids) in the blood

○ Procoagulant epithelial markers

○ Early and accelerated atherosclerosis

22
Q

describe the onset of type 2 diabetes

A

○ Usually IGT for some time
○ Often retinal damage at diagnosis
§ 7-10 years IGT
○ Ability to secrete insulin falls with time [Becomes worse over many years]

23
Q

how does type 2 present

A

○ Polyuria
§ excessive or an abnormally large production or passage of urine
§ Pee a lot

○ Polydipsia
§ excessive thirst or excess drinking
§ Drink a lot

○ Tiredness

The above are usually present But because it happens over 10-20 years in type 2 diabetes people don’t really notice these as symptoms and just put it down to age

○ Unusual infections

○ Diabetic complications
§ Cardiovascular- Because of accelerated atherosclerosis

24
Q

what protects the patient from developing type 2 diabetes

A

strict diet

exercise

25
Q

give a summary of type 1 diabetes

A
  • Younger
  • Thin
  • ? Family history of type 1
  • ? Family history of autoimmune disease
  • Diabetic symptoms

• Easily get ketosis
Unless treated fairly fast

26
Q

give a summary of type 2 diabetes

A
  • Older
  • Obese
  • Strong family history

• Diabetic symptoms ?
Yes - but usually explained / assumed to be something else

  • Present with complications
  • Rarely get ketosis
27
Q

how is diabetes managed

A 
• Education 
○ About diabetes
○ Managing diabetes
○ Health care issues
○ Complication avoidance

• Targets
○ Preprandial 4-6mmol/L
§ Done or taken before dinner / lunch
○ Bedtime 6-8mmol/L

• Management tools
○ Drugs
○ Insulin - Need to have insulin injections every day, Broadly split into 2 categories depending on the type of insulin used and how often they are injected
§ Basal- bolus control
	□ More injections - better
§ Split - mixed control
	□ Fewer injections - poorer

• Nutrition
○ Less than 10% calories from saturated fat
§ Prone to getting atherosclerosis so cannot cope with fat as well
○ Glycaemic index of foods compared with a standard food
○ Carbohydrate counting
§ Basal-bolus regimes

•Exercise
○ Planned activity
○ Understand individual response

• Monitoring

28
Q

what are insulin regimes

A

Not different types of insulin but the way it is packaged varies
Attach insulin to a protein and it will disperse the insulin in a set time period - can be a quick release or a slow release

29
Q

what is specific for type 1 management

A 
• Insulin subcutaneously (human)
• 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% - Often may accept slightly higher, If take a blood sample can see average of blood glucose over the last 120 days as that is how long blood cells last for
30
Q

what is specific to type 2 management

A

• Weight loss

• Diet restriction
○ Avoid refined CHO
○ Encourage high fibre
○ Reduce fat especially saturated

• ‘Diet pills’
○ Orlistat
○ Subutramine

• Surgery
○ “gastric bypass”
○ Gastric vertical banding

• Oral hypoglycaemic agents
○ Insulin secretagogues - when still making a bit of insulin, will make you produce more insulin or make the cells better at accepting the insulin
	§ Sulphonylureas
		□ Glicazide
		□ Glibenclamide 
		□ Tolbuatmide 
		□ Chlorpropamide 
○ Insulin sensitizers
	§ Biguanides
		□ Metformin 
	§ Thiazolidinediones 
		□ Rosiglitazone
31
Q

what are common oral hypoglycaemics

A

• Sulphonylureas - in theory can make too much insulin and go hypo but it is not that big of a risk
○ Increase pancreatic insulin secretion
○ Can cause hypoglycaemia

• Biguanides
○ Enhance cell insulin sensitivity
○ Reduce hepatic gluconeogenesis
○ Preferred in the obese

32
Q

explain insulin in type 2 diabetes

A

• 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

• DIGAMI study
○ Benefits in insulin treatment after MI in type 2 diabetics

33
Q

what are the complications of diabetes

A

Acute - hypoglycaemia
○ Type 1
○ Type 2 on sulphonylurea or insulin
○ Insulin / drug without food

Chronic
○ Cardiovascular risk
○ Infection risk
○ Neuropathy
§ When the nerves supplying your body die off
□ Nerves have a blood supply to keep them alive
□The CVD affecting the blood vessels causes the nerves to die off

this says continued complications in the lecture so im not sure if they are acute or chronic but im assuming it is chronic xox

• Large vessel - atheroma (all because of risk of athersclerosis)
○ Angina & MI
○ Claudication
○ Aneurysm

• Small vessel disease - the nutrient supply to the nerves gets cut off and this causes the nerve to die off
○ Poor wound healing
○ Easy wound infections
○ Renal disease
○ Eye disease
○ Neuropathy
§ Numb hands, feet and legs, Can also be painful - neuropathic pain

34
Q

how does a patient with diabetes know when they are going hypo

A

get symptoms

ability to know when they are going hypo gets less over time due to neuropathy

35
Q

what is included in diabetic eye disease

A
  • cataracts
  • maculopathy
  • proliferative retinopathy
  • laser treatment
36
Q

explain cataracts

A
  • a normal lens allows light to pass into the eye, images are clear
  • a clouded lens allows less light to pass into the eye, images are blurry

cataracts = opacities in the lens, lens in the eye has coagulated and you cannot see properly

cataract surgery is removing the lens and putting a new lens in

37
Q

what does disease of the retina result in

A

impairment or loss of vision

38
Q

what is laser ablation

A

a process in which a laser bean is focused on a sample surface to remove material from the irradiated zone

39
Q

what is diabetic neuropathy

A

• General sensation
○ ‘glove & stocking’

• Motor neuropathy
○ Weakness and wasting of muscles

• Autonomic regulation
○ Awareness of hypoglycaemia lost
○ Postural reflexes
○ Bladder and bowel dysfunction

40
Q

what are the problems that patients with diabetes face when having surgery

A

• Fasting is a problem for type 1 diabetics
○ Need insulin to prevent ketosis
○ Need carbohydrate to prevent hypoglycaemia
○ If going to have an operation you have to fast
○ But this patient needs insulin and if you don’t have sugar with the insulin the patient will go hypo
○ So the type 1 diabetes patient needs to come in early and be put on glucose IV and insulin

• Metabolic changes associated with surgery
○ Hormone changes aggravate diabetes
§ Epinephrine changes aggravate diabetes
○ More glucose production and less muscle uptake
○ Metabolic acidosis more likely
§ A condition in which there is excess in the bodily fluids

  • Increase insulin requirements in type 2
  • Type 2 may require insulin cover perioperatively
41
Q

what are the dental aspects associated with diabetes

A

• Be aware of effect of dental treatment
○ Food intake may be disrupted
§ Ideal to see patient first thing in the morning or first thing in the afternoon as soon as they have had something to eat so that they won’t go hypo during the appointment

• 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
○ Big issue if doing perio treatment or a wisdom tooth extraction
○ Healing is going to be less effective in a diabetic patient

BDS2 - endocrinology (3 decks)

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