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Medicine Block - Endocrinology > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

What is the difference between Type 1 and 2 diabetes mellitus?

A

Type 1 - autoimmine destruction of beta pacreatic islet cells leading to insulin insufficiency Type 2 - insulin resistance and reduced effeciveness of endogenous insulin and beta cell dysfunction. As the disease progresses, a lack of insulin may also develop. Both lead to hyperglycaemia

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2
Q

Other than Type 1 and 1 DM, what is the third main type of diabetes?

A

Gestational diabetes is the third main form, and occurs when pregnant women without a previous history of diabetes develop high blood sugar levels.

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3
Q

What are the causes of T1DM?

A

Autoimmune causes Genetics - HLA D3 and D4 are linked

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4
Q

What are the characteristic presentations of T1DM?

A

Weight loss Ketoacidosis Polyuria Polydipsia

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5
Q

What is the epidemiology of T1DM?

A

Usually before onset of puberty but can occur at any age

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6
Q

What are the causes of T2DM?

A

Obesity Lack of exercise Calorie and alcohol excess Genetic influence appears to be stronger than T1DM

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7
Q

What are some other causes of DM or hyperglycaemia?

A

Steroids Anti-HIV drugs Newer antipsychotics Pancreatic problems: - Pancreatitis - Pancreatic surgery - Trauma - Pancreatic destruction - Pancreatic cancer Cushings disease Hyperthyroidism Glycogen storage diseases Congenital lipodystrophy

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8
Q

What is metabolic syndrome or syndrome X?

A

Metabolic syndrome is a cluster of conditions — increased blood pressure, high blood sugar, excess body fat around the waist, and abnormal cholesterol or triglyceride levels — that occur together, increasing your risk of heart disease, stroke and diabetes.

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9
Q

How is metabolic syndrome or syndrome x treated?

A

Exercise Treat individual components Lose weight

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10
Q

How is diabetes mellitus diagnosed?

A

1) Symptoms of hyperglycaemiam (polyuria, polydipsia, weight loss, visual blurring, genital thrush, lethargy) and Raised venous glucose detected once on fasting (>7mmol/L) or random (>11mmol/L) 2) Raised venous glucose detected on two separate occasions on fasting (>7mmol/L) or random (>11mmol/L) or oral glucose tolerance test (>11mmol/L) 3) HBA1c >48mmol/mol (avoid doing this in pregancy, children T1DM and haemoglobinopathies)

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11
Q

Why is a blood glucose better than a urine test?

A

Urine tests give false negatives

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12
Q

How can you differentiate T1DM and T2DM in diagnosis?

A

Features of T1DM include persistent hyperglycaemia despite diet and medications, weight loss, presence of autoantibodies such as islet cell antibodies and ketonuria T2DM can be asymptomatic but present with complications such as MI

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13
Q

What is the general management of diabetes mellitus?

A

Focus on education and lifestyle advice: - Exercise increases insulin sensitivity - Healthy eating - Targets for HbA1c - Assess global vascular risk - Foot care - Advice for driving if they have hypoglycaemic spells

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14
Q

What is the treatment for T1DM

A

Insulin

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15
Q

What is the treatment for T2DM

A

1) Lifestyle modification 2) Monotherapy - Metformin 3) Dual therapy is HbA1c rises to 58mmol/mol Metformin + DPP4 inhibitor or glitazone or Sulfonylurea or SGLT-2i 4) Triple therapy 5) Insulin and review the need for existing oral treatments

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16
Q

How does metformin work?

A

It is a biguanide and increases insulin sensitivity, decreases hepatic gluconeogenesis, decreases intestinal glucose absorption, increase glucose uptake in fat and muscle

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17
Q

What is the mode of action of sulphonylurea?

A

It antagonises K+ATPase in pancreatic beta cells preventing K+ efflux causing a relative depolarisation which activates VOCC and calcium influx causes insulin vesicle fusion and release

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18
Q

What are the side effects of sulphonylurea?

A

Hypoglycaemia Weight gain GI disturbances

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19
Q

What are the side effects of metformin?

A

ADRs: lactic acidosis (due to lack of gluconeogenesis) B12 deficiency GI disturbances

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20
Q

What are the contraindications of metformin?

A

Renal/respiratory problems Increase lactic acidosis risk

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21
Q

What is the mode of action of Glitazones?

A

MoA: agonist binding to PPAR-γ in nuclei causing gene alteration that increases fatty acid storage in adipocytes so cells become more glucose driven energetically so reducing blood glucose and decreasing insulin resistance

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22
Q

What are the side effects of glitazones?

A

Weight gain Increased heart failure risk Osteoporosis Bladder cancer

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23
Q

What are the contraindications for glitazones?

A

Heart failure Elderly (increased bladder cancer risk)

24
Q

What is the mode of action of Gliptins?

A

MoA: inhibits DPP4 which normally breaks down GLP-1 so allows more GLP-1 after meals which increases insulin release, reduces hepatic gluconeogenesis and conveys sense of satiety to the brain It is weight gain neutral

25
Q

What are the side effects of gliptins?

A

GI disturbance Low risk hypoglycaemia Weight neutral

26
Q

How do Sodium-glucose co-transporter 2 inhibitors work?

A

MoA: block SGLT2 in PCT leading to glucose loss in urine and reduced plasma glucose it blocks the reabsorption of glucose in the kidneys and promotes the excretion of glucose in urine

27
Q

What are the side effects of Sodium-glucose co-transporter 2 inhibitors?

A

Polyuria Hypoglycaemia UTI

28
Q

What are the contraindications of Sodium-glucose co-transporter 2 inhibitors?

A

Recurrent UTIs

29
Q

Give an example of each type of oral hypoglycaemic agent: - Biguanide - Gliptin/DPP4 inhibitor - Glitazone - Sulfonylurea - Sodium glucose co transporter 2 inhibitor - Alpha-glucosidase Inhibitors - Glucagon-like Peptide 1 Analogues

A
  • Metformin - Sitagliptin - Pioglitazone/Rosiglitazone - Glicazide - Empaglifozin - Acarbose - Exenatide
30
Q

How do Glucagon-like Peptide 1 Analogues work?

A

MoA: mimic GLP-1 action which is normally released after meals to increase insulin secretion, reduce hepatic gluconeogenesis and convey sense of satiety to the brain

31
Q

What are the side effects of Glucagon-like Peptide 1 Analogues?

A

Nausea Vomiting Diarrhoea

32
Q

What are the contraindications of Glucagon-like Peptide 1 Analogues?

A

GI disease

33
Q

How do Alpha-glucosidase Inhibitors work?

A

MoA: inhibits alpha glucosidase which breaks down intestinal carbohydrates to glucose, so prevents glucose absorption

34
Q

What are the side effects of Alpha-glucosidase Inhibitors?

A

Flatulence Diarrhoea Abdo pain

35
Q

What are the contraindications of Alpha-glucosidase Inhibitors?

A

IBD Hernia

36
Q

When do insulin user need to adjust insulin doses?

A

Exercise Fingerprick glucose result Calorie intake Carbohydrate counting If they’ve been binge drinking (this can lead to delayed hypoglycaemia)

37
Q

Why is it important to write UNITS in full when prescribing?

A

To avoid misinterpretation of U for zero

38
Q

What are examples of short acting insulins and when are they used?

A

Novorapid Actrapid Humalog Inject at start of meal or just after (unless its a sugar laden meal) - injecting after the meal helps to match what is actually eaten rather than what is planned

39
Q

What are examples of intermediate acting insulins and when are they used?

A

Intermediate acting – isophane insulin (Humulin I)

40
Q

What are examples of long acting insulins and when are they used?

A

Long acting – Insulin Glargine Used at bedtime in T1DM or T2DM. There is no awkward peak, it stays at a steady level so good if nocturnal hypogycaemia is an issue Caution if considering pregancy

41
Q

What are some examples of pre-mixed insulins?

A

NovoMix 30 (30% short acting and 70% long acting)

42
Q

How should patients choose an insulin regimen?

A

Plan a regimen to suit the lifestyle, not vice versa

43
Q

What are the three types of regimes?

A
  • BD Biphasic - twice daily premixed insulins for T1DM and T2DM
  • QDS - Ultra-fast insulin before meals and long acting bedtime insulin for T1DM for flexible lifestyle
  • Once daily long acting insulin before bed - a good initial insulin regimen when switching from tablets in T2DM –> if tight control is needed, consider retaining metformin and pioglitazone and if patient is unable to use BD regimen
44
Q

What is DAFNE?

A
  • DAFNE stands for Dose Adjustment For Normal Eating
  • It is a way of managing Type 1 diabetes for adults and provides the skills necessary to estimate the carbohydrate in each meal and to inject the right dose of insulin.
  • The aim of DAFNE is to help you lead as normal a life as possible, while controlling your blood glucose levels, hence reducing the risk of long-term diabetes complications.
  • DAFNE involves attending a 5-day training course (9am to 5pmMonday to Friday) plus a follow-up session around 8 weeks after the course.
  • The DAFNEcourse is about learning from experience. During the week you practice the skills of carbohydrate estimation and insulin adjustment
45
Q

How should insulin be managed during intercurrent illness?

A
  • Continue using insulin when ill
  • Maintain calorific intake eg. drink milk
  • Check blood glucose 4 times a day and look for ketonuria
  • Seek help from diabetic nurse specialist or GP if concerned
  • Admit patient into hospital if they vomit, are dehydrated, ketotic, a child or pregnant
46
Q

When should an insulin pump be considered?

A
  • When attempts to reach HbA1c with mulitple daily injections have failed and resulted in disabling hypoglycaemia
  • A person that has not managed to reach their target HbA1c despite careful management
47
Q

What are the criteria for prescribing Glucagon-like peptide to a patient?

A
  • BMI >35
  • Psychological or medical problem related with obesity
  • Insulin therapy would have significant occupational implications
  • If weight loss would benefit other significant obesity related comorbidities
48
Q

Why should a glucagon like peptide be continued?

A
  • If a person has a beneficial metabolic response which is a reduction of HbA1c by at least 11mmol/mol
  • And a weight loss of at least 3% of initial body weight in 6 months
49
Q

How do glucagon like peptide analogues work?

A
  • As incretin mimetics
  • Incretins are gut peptides that work by augmenting insulin release
  • Given by subcutaneous injection
50
Q

What are the main complications of diabetes?

A
  • Vascular disease - increased risk of MI and stroke (rasied BP)
  • Nephropathy
  • Diabetic retinopathy
  • Cataracts - osmotic changes in the lens induced in acute hyperglycaemia and can be reversed with normoglycaemia (so wait before buying glasses)
  • Rubeosis iridis
  • Metabolic complications
  • Diabetic feet
  • Neuropathy
51
Q

How can a diabetic prevent vascular disease?

A
  • Address other risk factors such as diet, smoking, hypertension
  • Suggest a statin
  • Aspirin can reduce vascular events
  • Treat hypertension in T1DM if BP is >135/85mmHg or >130/80mmHg if here are two or more features of metabolic syndrome
  • Treat hypertension in T2DM if BP >140/80mmHg or >130/80mmHg if kidney, eye or cerebrovascular damage
    • ACEi or CCA if over 55 years or black
    • Offer CCA to pregnant women
    • Do not combine ACEi with ARB
  • Do not offer aspirin for the primary prevention of CVD to adults with T1DM
52
Q

How is nephropathy prevented in diabetes?

A
  • If urine albumin:creatinine ratio is greater than 3mg/mmol inhibiting the RAAS with an ACEi or ARB even if the BP is normal, protects the kidneys.
  • Spironalactone may also help
53
Q

How is diabetic retinopathy prevented and managed?

A
  • Annual retinal screening is mandatory for all patients
  • Refer to opthalmologist if pre-proloferative changes or if there are any uncertainties near or at the macula
54
Q

What are the signs of background, pre-proliferative and proliferative retinopathy?

A
  • Background retinopathy - microaneurysms, haemorrhages and hard exudates
  • Pre-proliferative retinopathy - Cotton wool spots, haemorrhages and venous bleeding (signs of retinal ischaemia)
  • Proliferative retinopathy - New vessels form, needs urgent referral
55
Q

Maculopathy is hard to see in the early stages. How is it suspected and treated?

A
  • Suspected if visual acuity decreases
  • Treatment:
    • Prompt laser
    • Steroids
    • Anti-angiogenic agents for macular oedema
56
Q

What is the pathogenesis of maculopathy?

A
  • High retinal blood flow caused by hyperglycaemia, high BP and pregnancy triggers capillary endothelial change
  • this leads to vascular leak
  • then microaneuryms
  • capillary occlusions
  • local hypoxia and ischaemia
  • new vessel formation

Medicine Block - Endocrinology (22 decks)

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