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Metabolic and Endocrine > Diabetes > Flashcards

Diabetes Flashcards

1
Q

what countries have a high prevelance of type 1 diabetes?

A

north america
australia
scandinavia
UK

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2
Q

what is the basic pathophysiology of type 1 diabetes?

A

inability to produce insulin-autoimmune against beta cells.

destruction of beta cells, effecting production and secretion of insulin.

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3
Q

when is the peak age of onset for type 1 diabetes?

A

9-14

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4
Q

what genes are implicated in type 1 diabetes?

A

HLA-DRQ

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5
Q

what are the possible ‘destruction markers’ used in suspected type 1 diabetes?

A

GAD antibodies
islet cell antibodies
peptides

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6
Q

describe normal insulin secretion?

A

over 24 hours a day especially at meal times

50% of requirement as ‘background requirement’ and the rest at meal time

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7
Q

what is the gold standard treatment for patients with type 1 diabetes?

A

4 injections a day

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8
Q

what are the benefits of good glucose control?

A

eye, kidney, nerve damage risk reduction

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9
Q

describe multiple injection therapy in type 1 diabetes?

A

flexible, dose depends on what patient eats

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10
Q

what are the increase risks assoicated with type 1 diabetes?

A

stroke
heart disease
eye, kidney, nerve damage

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11
Q

what is an insulin pump?

A

Pulse insulin which can be set up in appropriate rhythm for patient

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12
Q

what is flash glucose monitoring?

A

Small sensor automatically measures and stores glucose readings during day and night

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13
Q

give examples of transient diabetes mellitus?

A

gestational diabetes, drug induced, pancreatic toxicity

every other cause of diabetes is chronic

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14
Q

describe diabetes mellitus?

A

Chronic, metabolic, defective glucose homeostasis (hyperglycaemia)

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15
Q

what is the role of insulin?

A

facilitate uptake of glucose by cells. Insulin resistance (a lot of insulin but cells are not responsive to it)
Insulin stimulates the receptor which signals to glucose channel to let glucose into the cell

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16
Q

what investigations can be used to aid the diagnosis of diabetes?

A
  • urine dipstick
  • HbA1c
  • oral glucose tolerance test
  • fasting glucose
  • plasma glucose
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17
Q

describe the role of urine dipstick in diagnosing diabetes?

A

old method, now used as guidance not diagnostic. People have didn’t renal thresholds eg in pregnancy it is lower.

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18
Q
  1. what is HbA1c?
  2. when can HbA1c not be used?
  3. what HbA1c levels are indicative of diabetes?
A
  1. Glycated hemoglobin is a form of hemoglobin that is chemically linked to a sugar.
  2. Cannot be used in haemoglobinopathies, anaemia, renal failure (chronic anaemia of disease), children, pregnancy
  3. Borderline 41-47 / Diabetes -48
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19
Q

describe the role of oral glucose testing in diagnosing diabetes?

A

measure of PPG (postprandrial plasma glucose) levels and is better guide to beta cell dysfunction than FPG (fasting plasma glucose)
Normal = <7.8
Diabetes = >11.1
Impaired glucose tolerance = 7.8-11.1

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20
Q

what plasma glucose levels suggest diabetes?

A

<6.1mmol/l = normal

> 7mmol = diabetes

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21
Q

what is the consequence of untreated type 1 diabetes?

A

without insulin
DKA
death

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22
Q

what is the main treatment for type 1 diabetes?

A

insulin

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23
Q

what are the aims of treatment for type 2 diabetes?

A 
Doesn’t need insulin to survive
Lifestyle changes- cannot bring beta cells back but can minimize resistance to insulin
Lower renal threshold
Reduce insulin resistance
Improve beta cell secretion of insulin
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24
Q

what are the consequences if glucose isn’t absorbed?

A

If glucose isn’t absorbed ends up in gut with bacteria and helps growth of bacteria and co2 accumulation and patient will be bloated.

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25
Q

what are the sites of action for medication in type 2 diabetes

A
  • insulin secretion
  • GI
  • glucagon secretion
  • appetite control
  • neurotransmitter dysfunction
  • glucose reabsorption
  • glucose uptake and utilisation
  • lipotoxicity
  • hepatic glucose output
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26
Q

what diabetes medication act on insulin secretion?

A

sulfonyureas
meglitinides
incretins
increase secretion

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27
Q

what diabetes medication act on glucagon secretion?

A

incretins
amylin
decrease secretion

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28
Q

what diabetes medication are appetite controllers?

A

incretins

amylin

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29
Q

what diabetes medication act by neurotransmitter dysfunction?

A

bromocriptine

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30
Q

what diabetes medicatoin act on glucose reabsorption

A

SGLT2 inhiitors

decrease reabsorption

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31
Q

what diabetes medication act to increase glucose uptake and utilisation?

A

thiazolidindiones

metformin

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32
Q

what diabetes medication cause lipotoxicity?

A

thiazolidinediones

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33
Q

what diabetes medications decrease hepatic glucose output?

A

metformin

thiazolidinediones

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34
Q

what diabetes medication act on GI tract

A

incretins
alpha glucosidase inhibitors
amylin
bile acid sequestrant

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35
Q

metformin
1. class
2. action
3 potential for hypo?

A

1 biguanides

  1. reduces amount of glucose released by liver and decreases insulin resistance by muscle cells
  2. not as monotherapy
36
Q

acarbose / miglitol
1. class
2. action
3 potential for hypo?

A
  1. alpha glucosidase inhibitors
  2. slows digestion and absorption of dietary carbhydrates
  3. increased risk when in combination with insulin or sulfonylurea agent
37
Q

pioglitazone / rosiglitazone
1. class
2. action
3 potential for hypo?

A
  1. thiazolidinediones
  2. increase insulin sensitivity, decrease liver glucose output. takes 12 or more weeks to achieve maximal effectiveness
  3. increased risk when used in combination with insulin or insulin secretagogues
38
Q

-liptin
1. class
2. action
3 potential for hypo?

A
  1. DPP-4 inhibitors
  2. shows inactivation of GLP-1 by DPP-4. prolongs action of GLP-1 so increases insulin secretion and decreasing glucagon secretion
  3. may increase risk with insulin secretagogues
39
Q

-agliflozin
1. class
2. action
3 potential for hypo?

A
  1. SGLT-2 inhibitors
  2. inhibits glucose reabsorption in kidneys
  3. low risk when monotherapy
40
Q

glimepiride / glipizide / glyburide
1. class
2. action
3 potential for hypo?

A
  1. sulfonylureas
  2. stimulates beta cells to increase insulin production
  3. yes
41
Q

-glinide
1. class
2. action
3 potential for hypo?

A
  1. meglitinides
  2. stimulates beta cells to increase insulin production. shorter acting than sulfonyureas
  3. yes
42
Q

exenatider / liragluide
1. class
2. action
3 potential for hypo?

A
  1. incretin mimetics
  2. mimics effect of incretin hormones to increase insulin secretion in presence of elevated blood glucose levels, decreases glucagon production, slows gastric emptying and improves first phase insulin response
  3. used with drugs that do
43
Q

prarnlinitidine
1. class
2. action
3 potential for hypo?

A
  1. amylin analogues
  2. slows gastric emptying (so delays glucose entering blood stream), suppresses glucagon
  3. yes
44
Q

insulin

  • mechanism
  • can it cause hypos?
A
  • increases passage of glucose from bloodstream into cells and decreases the production of glucose by liver
  • can cause hypos
45
Q

describe the features of type 1 diabetes?

A

Younger, lean, European
Not generally inherited
Autoimmune
Insulin deficient and always needs insulin

46
Q

what are the features of type 2 diabetes?

A

Older, overweight, all racial groups
Stong familial tendency
No autoimmunity
Partial insulin deficiency, insulin resistance

47
Q

what genetics are associated with type 1 diabetes?

A

HLA-DQ moleculaes
IDDM locus
IDDM 2 locus

48
Q

what antibodies are produced in type 1 diabetes?

A

antibodies to glutamic acid dexarboxylase

49
Q

what environmental factors are important in type 1 diabetes?

A

early exposure to cows milk, enterovirus, vit D deficiency

50
Q

what is the aetiology of type 2 diabetes?

A
  • Insulin resistance and beta cell dysfunction
  • Lifestyle-sedentary lifestyle and excessive food
  • Intrauterine-decresed birth weight, thrifty phenotype
  • Genetic-strong familial tendency, no genes identified
51
Q

describe the epidemiology of type 1 diabetes?

A

Geographical variation (35 fold difference between jaan and finland
UK prevelance is about 0.25%
Usually occurs in children and can present at any age (10% over age 65)

52
Q

what is the consequence of a stressful environment in patients with type 1 diabetes?

A

produce glucagon, cortisol counteract action of insulin, when ill high glucose production in liver, produce more ketones and break down fat for energy as no insulin so can cause high blood glucose, high ketone bodies leading to high urine production, dehydration, acidotic and presents as DKA

53
Q

what is the presentation of type 1 diabetes?

A

Thirst (polydipsia), excessive passing of urine (polyuria), weigh loss and fatigue
May cause life threatening, severe illness with collapse, coma and death

54
Q

what are the potential complications of type 1 diabetes?

A

Chronically raised blood glucose damages tissues
40-50% develop significant complications in their lifetime
Microvascular (small blood vessel – eye, kidney and nerve damage) and macrovascular (disease of larger arteries

55
Q

describe the structure of insulin?

A

51 amino acids arranges as 2 chained molecule connected by 2 disulphide bridges (A chain=21 amino acids / B chain=30 amino acids)

56
Q

describe insulin secretion?

A

Produced in islets of Langerhans In response to glucose
GLUT 2 receptors bind to glucose which is brought into cell and sets in motion stored insulin granules being released
Shouldn’t be released unless glucose presence

57
Q

what are the primary effects of insulin?

A

Released from pancreas and main effect on liver to decrease hepatic glucose production and increases peripheral glucose uptake by muscle
Liver constantly produces glucose unless negative feedback from insulin tells it to stop

58
Q

describe insulin treatment?

A

Mimic insulin secretion in non diabetic indicidual (physiological insulin delivery)
Insulin is secreted at 2 rates
Slow basal secretion over 24 hours
Augmented rate at meal times

59
Q

what are the different insulin injections regimens?

A

4 injections a day (3 short + 1 intermediate acting (basal bolus)
2 injection regime of 30/70 mix per day (70=slow acting)

60
Q

describe insulin absorption?

A

When injected in skin 6 bind together to born which needs to be broken down before absorbing
Fast acting break down quickly and vice versa

61
Q

what are the types of insulin?

A 
Short acting
Intermediate acting
Long acting 
Biphasic 
Analogues-modified
62
Q

what is type 2 diabetes?

A

Genetic predisposition to high blood glucose, sedentary lifestyle cause not utilizing glucose, insulin resistance rises

63
Q

describe insulin resistance?

A

Normal – the body is sensitive to insulin, it unlocks the door and glucose enters the cell
Insulin resistance-the body is insulin resistance, more insulin is necessary to unlock the door and let glucose in so glucose stays in the blood stream

64
Q

describe the features of type 2 diabetes?

A

Closely linked to obesity
No symptoms and condition is detected through routine screening (50%)
Thirst and polyuria
May present as acute or chronic complications
Controlling blood glucose reduces complication rates

65
Q

what is the management of type 2 diabetes?

A

Lifestyle advice (diet, exercise, smoking)
Drug treatment where necessary
Treat risk factors for CVD
Reduce HbA1c and weight loss

66
Q

what are the barriers to type 2 diabetes treatment?

A 
Hypoglycemia
Weight gain from lifestyle or anti-diabetes medication
Natural progression of disease
Poor adherence to therapy
Integrated care
67
Q

what causes blood glucose levels to decrease?

A
  • hepatic IR/glucose output (metformin)
  • SGLT-2
  • carbohydrate digestion (acarbose)
  • beta cell dysfunction (prandial glucose regulations, sulphonylureas, incretins)
  • insulin increased
68
Q

what are the macrovascular complications of type 2 diabetes?

A

heart attack
amputations
strokes
PVD

69
Q

how should a symptomatic patient be diagnosed with diabetes?

A

symptoms of polyuria, polydipsia and unexplained weight loss if type 1 as well as:

  • a random venous plasma glucose concentration ≥ 11.1 mmol/l or
  • a fasting plasma glucose concentration ≥ 7.0 mmol/l (whole blood ≥ 6.1 mmol/l) or
  • two hour plasma glucose concentration ≥11.1 mmol/l two hours after 75g anhydrous glucose in an oral glucose tolerance test (OGTT).
70
Q

how should an asymptomatic patient be diagnosed with diabetes?

A

With no symptoms diagnosis should not be based on a single glucose determination but requires confirmatory plasma venous determination. At least one additional glucose test result on another day with a value in the diabetic range is essential, either fasting, from a random sample or from the two hour post glucose load. If the fasting random values are not diagnostic the two hour value should be used

71
Q

what is the criteria for diagnosing gestational diabetes?

A

a fasting plasma glucose level of 5.6mmol/l or above or

a 2-hour plasma glucose level of 7.8mmol/l or above.

72
Q

what HbA1c is diagnostic for diabetes?

A

An HbA1c of 48mmol/mol (6.5%) is recommended as the cut off point for diagnosing diabetes. A value of less than 48mmol/mol (6.5%) does not exclude diabetes diagnosed using glucose tests.

73
Q

describe the role of finger prick HbA1c?

A

Finger-prick HbA1c should not be used unless the methodology and the healthcare staff and facility using it can demonstrate within the national quality assurance scheme that they match the quality assurance results found in laboratories. Finger prick tests must be confirmed by laboratory venous HbA1c in all patients.

74
Q

describe the role of HbA1c in asymptomatic patients?

A

In patients without symptoms of diabetes the laboratory venous HbA1c should be repeated. If the second sample is <48mmol/mol (6.5%) the person should be treated as at high risk of diabetes and the test should be repeated in 6 months or sooner if symptoms develop.

75
Q

what situations are there where HbA1c is not appropriate for diagnosis of diabetes?

A

-ALL children and young people
-patients of any age suspected of having Type 1 diabetes
-patients with symptoms of diabetes for less than 2 months
-patients at high risk who are acutely ill (e.g. those requiring hospital admission)
-patients taking medication that may cause rapid glucose rise e.g. steroids, antipsychotics
-patients with acute pancreatic damage, including pancreatic surgery
in pregnancy
-presence of genetic, haematologic and illness-related factors that influence HbA1c and its measurement (see annex 1 ofthe WHO reportfor a list of factors which influence HbA1c and its measurement)

76
Q

what are the dietary changes that can be made for managing diabetes?

A 
Eat healthier carbohydrates (whole grains like brown rice, buckwheat and whole oats, Fruit, vegetables, pulses such as chickpeas, beans and lentils, dairy like unsweetened yoghurt and milk.)
Eat less salt (6g/day)
Eat less red and processed meat
Eat more fruit and veg 
Healthier fats (unsalted nuts, seeds, avocados, oily fish, olive oil, rapeseed oil and sunflower oil.)
Cut down on sugar
Choose snacks carefully 
Drink alcohol in moderation
77
Q

what are the issues with flash glucose monitors?

A

flash glucose monitoring doesn’t measure the sugar in your blood. It measures the amount of sugar in the fluid surrounding your cells, called interstitial fluid. This causes a delay with the reading so it’s not completely accurate, so you’ll still need to do a finger-prick test every now and again.

78
Q

what is the initial management points for patients diagnosed with type 2 diabetes?

A
  • diet advice, adherence to drug treatment
  • agree HbA1c target (measure at 3/6 monthly intervals)
  • drug choices based on; effectiveness, safety, tolerance, clinical circumstances, preference
  • don’t routinely offer self monitoring
79
Q

what drugs should be considered to treat type 2 diabetes in symptomatic patients?

A
  • insulin

- sulphonylurea

80
Q

describe the management of a patient with type 2 diabetes who can take metformin with HbA1c rises to 48mmol/mol?

A
  • lifestyle changes

- standard release metformin (if not tolerated consider trial of modified release metformin)

81
Q

describe the management of a patient with type 2 diabetes who can take metformin with HbA1c rises to 58mmol/mol after initial treatment?

A

consider dual therapy with metformin and…

  • DPP-4i or
  • pioglitazone or
  • sulphonylurea or
  • SGLT-2i

aim for 53mmol/mol (7%)

82
Q

describe the management of a patient with type 2 diabetes who can take metformin with HbA1c rises to 58mmol/mol after dual therapy fails?

A

triple therapy with

  • metformin + DPP-4i + sulphonylurea
  • metformin + pioglitazone + sulphonylurea
  • metformin + pioglitazone or sulphonylurea and SGLT-2I

aim for 53mmol (7%)

83
Q

describe the management of a patient with type 2 diabetes who can take metformin if triple therapy is not effective?

A

consider combination therapy with metformin, sulphonylura, GLP-1 mimic

84
Q

what is the initial management for type 2 diabetics in which metformin is contraindicated or not tolerated?

A

either
-DPP-4inhibitor or sulphonylurea
-SGLT-2 inhibitor instead of DPP-4 inhibitor if SU or pioglitazone not appropriate
aim for 48mmol

85
Q

what is the first intensification management for type 2 diabetics in which metformin is contraindicated or not tolerated when initial therapy not working?

A

consider dual therapy
-DPP-4 inhibitor and pioglitazone
-DPP-4inhibitor and SU
aim for 53mmol

86
Q

what is the second intensification management for type 2 diabetics in which metformin is contraindicated or not tolerated when the first intensification of treatment is not working?

A

consider insulin based treatment

aim for 53mmol

87
Q

describe insulin based treatment for patients with type 2 diabetes?

A

-continue metformin
-NPH insulin once/twice daily
-start NPH and short acting insulin either seperately or biphasic human insulin
-alternatic to NPH insulin using insulin detemir or glargine
-pre-mixed preparations include short acting insulin analogues. if inject before a meal hypo is problem
-GLP-1 mimetc with insulin
-monitor
SGLT-2 inhibitor with insulin with or without antidiabetic

Metabolic and Endocrine (12 decks)

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