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BDS2 BAMS > diabetes > Flashcards

diabetes Flashcards

1
Q

diabetes mellitus

A

abnormality of GLUCOSE regulation

  • metabolic disease
  • can die

blood sugar is high, glucose in urine is high

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2
Q

diabetes insipidus

A

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

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3
Q

what does sugar level vary with

A

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
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4
Q

fasting sugar test description

A

fasting sugar sample from overnight before eating

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5
Q

glucose tolerance test description

A

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

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6
Q

random plasma glucose (RPG)

A

> 11.1mmol/L on 2 occasions is diagnostic of DIABETES

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7
Q

glucose tolerance test normal values

A

FPG <6.1

Making enough insulin to move blood sugar into cells

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8
Q

glucose tolerance test impaired fasting glucose values

A

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
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9
Q

glucose tolerance test diabetes values

A

FPG >7.0

Damage from diabetes occurs due to time spent over 7
- Below 7 risk of standard diabetic complication less

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10
Q

FPG <6.1

A

normal reaction after glucose tolerance test

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11
Q

FPG 6.1-7.0

A

impaired fasting glucose after glucose tolerance test

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12
Q

FPG >7.00

A

diabetes result after glucose tolerance test

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13
Q

what does a score <7.8 after 2 hour plasma glucose level indicate

A

normal reaction

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14
Q

what does a score 7.8-11.1 after 2 hour plasma glucose level indicate

A

impaired glucose tolerance

Pre diabetes in impaired group - potential to become fully diabetic

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15
Q

what does a score >11.1 after 2 hour plasma glucose level indicate

A

diabetes

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16
Q

type 1 diabetes mellitus

A

insuline deificient

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17
Q

type 2 diabetes mellitus

A

insuline resistance

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18
Q

what occurs in type 1 diabetes

A

Immune mediated pancreatic B cell destruction

Need to have insulin to stay alive
- Glucose in blood and insulin moves blood sugar into cells

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19
Q

3 circulating antibodies present in Type 1 diabetes

A

GAD glutamic acid decarboxylase
ICA Islet cell antibodies
IAA insulin autoantibodies

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20
Q

what are 2 consequences of type 1 diabetes

A

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

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21
Q

how are pancreatic B cells destroyed in type 1 diabetes

A

Antibodies attacks pancreatic B cells

  • Autoimmune disease
  • Cannot make insulin
  • Normal to diabetic in few months
  • Rapid change
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22
Q

pattern of inheritance for type 1 diabetes

A

Family autoimmune disease

- Genetic predisposition - environmental trigger causes antibody response

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23
Q

factors that contribute to type 1 diabetes

A

genetic and environmental

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24
Q

genetic influences of 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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25
Q

environmental triggers of type 1 diabetes

A

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
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26
Q

adult onset type 1 diabetes

A
  • 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
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27
Q

childhood onset type 1 diabetes

A
  • 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
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28
Q

type 1 diabetes symptoms

A
  • polyuria
  • polydipsia
  • tiredness

Acute Presentation
- Hyperglycaemia with diabetic symptoms
- Ketoacidosis
USUALLY REQUIRE INSULIN from DIAGNOSIS

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29
Q

what do pancreatic B cells produce

A

insulin

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30
Q

role of insulin

A

move blood sugar into cells

Longer to return to normalglycemia if destroyedB cells
- Impaired glucose tolerance
Hit diabetic

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31
Q

how to diagnose type 2 diabetes

A

by excluding type 1

hard to define

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32
Q

what is the most common form of diabetes

A

type 2 diabetes mellitus

  • 90% of all cases - prevalence tripled in 30yrs
  • strongly associated with obesity & inactivity
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33
Q

when does type 2 diabetes usually present

A

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

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34
Q

pattern of inheritance of type 2 diabetes

A

Strong Family history
- 100% concordance in identical twins
- Completely genetic
No environmental trigger – but can decrease risk

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35
Q

4 metabolic disorders that cause type 2 diabetes

A

defect in insulin resistance

defect in insulin secretion

basal hepatic glucose output increased

insulin stimulated muscle glucose uptake is reduced

36
Q

how does reduced insulin stimulated glucose uptake lead to type 2 diabetes

A
  • 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
37
Q

how does a defect in insulin secretion lead to type 2 diabetes

A
  • 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
38
Q

how does a defect in insulin resistance lead to type 2 diabetes

A
  • elevated basal insulin levels

- alike type 1

39
Q

how does increased basal hepatic glucose output lead to type 2 diabetes

A
  • failure of insulin suppression
40
Q

effect of type 2 diabetes

A

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
41
Q

type of onset for type 2 diabetes

A

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
42
Q

what can protect a person from developing type 2 diabetes

A

STRICT DIET AND EXERCISE PROTECTS

43
Q

acute presentation of type 2 diabetes

A
  • polyuria, polydipsia, tiredness (peeing a lot, drinking a lot, being tired) are usually present (noticeable)
  • unusual infections
  • diabetic complications (retinal damage)
  • Cardiovascular
44
Q

age comparison of type 1 and 2 diabetes

A

type 1: younger

type 2: older

45
Q

body comparison of type 1 and 2 diabetes

A

type 1: thin

type 2: obese

46
Q

pattern of inheritance comparison of type 1 and 2 diabetes

A

type 1: questionable family hx

type 2: strong family hx

47
Q

complications and effects comparison of type 1 and 2 diabetes

A

type 1: diabetic symptoms

type 2: present with complications

48
Q

ketosis comparison of type 1 and 2 diabetes

A

type 1: easily get ketosis

type 2: rarely get ketosis (slow progression)

49
Q

4 methods of managing diabetes

A

education

nutrition

exercise

monitoring

50
Q

pre-prandial target

A

4-6mmol/L

51
Q

bedtime target

A

6-8mmol/L

52
Q

drugs to manage diabetes

A

insulin

53
Q

2 types of insulin regimes

A

basal bolus control

split-mixed control

54
Q

basal bolus insulin control

A

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

55
Q

split mixed insulin control

A

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

56
Q

factors to consider when delivering insulin to manage diabetes

A

Need to be careful of sugar intake
- Eating secondary to having insulin

Depends on type of insulin and how often want to inject

57
Q

how does insulin differ

A

packaging is different
- Stick to protein

Release into circulation at a fix rate
- Slowly or rapidly

58
Q

education management of diabetes

A

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

59
Q

nutrition management of diabetes

A

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
`

60
Q

exercise management of diabetes

A

planned activity

understand individual response to exercise

61
Q

monitoring management of diabetes

A

sliding scale’ approach wrong

previous insulin dose determines plasma glucose
- work out how many insulin units you need

62
Q

type 1 diabetes drug management

A

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

63
Q

glycosylated haemoglobin

A

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

64
Q

the higher the blood sugar the more

A

complications of diabetes (e.g. retinopahty)

65
Q

hypoglycaemia

A

insulin without enough glucose

66
Q

type 2 diabetes management

A

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
67
Q

diet restriction to manage type 2

A
  • avoid refined CHO
  • encourage high fibre food
  • reduce fat, esp. saturated
68
Q

2 types of oral hypoglycaemic agents for type 2 diabetes management

A

Insulin secretagogues

  • sulphonylureas
  • —–gliclazide, glibenclamide, tolbutamide, Chlorpropamide

Insulin sensitisers

  • Biguanides
  • —–metformin
  • Thiazolidinediones
  • —–rosiglitazone
69
Q

sulphonylureas

A

insulin secretagogues oral hypoglycaemic agent

INCREASE pancreatic insulin secretion
- Make too much insulin – low risk

can cause hypoglycaemia!

70
Q

biguanides

A

insulin sensitiser oral hypoglycaemic agent

enhance cell insulin sensitivity

reduce hepatic gluconeogenesis

preferred in the obese
- safer starting point

71
Q

when would insulin be given to manage 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
  • insulin is to supplement with what they can make

DIGAMI study
- benefits in insulin treatment after MI in type 2 diabetics

72
Q

acute diabetes complications

A

hypoglycaemia

73
Q

hypoglycaemia occurs when

A

insulin/drug without food!

in:

  • Type 1
  • Type 2 on sulphonylurea (pills) or insulin
74
Q

3 chronic complications of diabetes

A

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
75
Q

symptoms of hypoglycaemia

A

sweating, tremors, agitates

coma seizure when reach blood sugar 1

76
Q

what is the effect of neuropathy on blood sugar management

A

ability to know when going hypo decreases with neuropathy

77
Q

large vessel diabetic complications

A

atheroma

angina & MI, claudication, anneurysm
- atherosclerosis increased risk

78
Q

small vessel diabetic complications

A

poor wound healing (foot ulcers from blisters)

easy wound infections

RENAL DISEASE

EYE disease

neuropathy (nerve damage, neuropathic pain)
—numb hand, feet and legs

79
Q

diabetic eye disease

A

Cateracts
- Fixed by surgery

Maculopathy

Proliferative retinopathy

  • Blood vessels grow and cause bleeding in eye
  • laser treatment
80
Q

what increases the chance of success of diabetic retinopathy

A

more likely success retinopathy if blood sugar well controlled

Retinopathy screening – photos of back of eye, sent to ophthalmologists to assess

81
Q

general sensation of diabetic neuropathy

A

glove & stocking’

- Numbness, pain

82
Q

effect of motor diabetic neuropathy

A

weakness and wasting of muscles

83
Q

effect of autonomic dysregulation of diabetic neuropathy

A

awareness of hypoglycaemia lost

postural reflexes
- cannot work the nerve which works the muscle

bladder & bowel dysfunction

84
Q

3 issues for diabetics in surgery

A

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
85
Q

how is fasting an issue for diabetes in surgery

A

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
86
Q

how do metabolic changes impact on diabetes in surgery

A

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

87
Q

6 dental aspects for care of diabetes

A

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

BDS2 BAMS (54 decks)

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