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JL Endocrinology > Week 2 > Flashcards

Week 2 Flashcards

1
Q

What are the two core defects of type II diabetes?

A

Insulin resistance and beta-cell dysfunction

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2
Q

In type II diabetes: what does ectopic fat accumulation and increase FFA circulation + increase inflammatory mediators (CRP) cause?

A

Inhibition of insulin via serine kinases responsible for phosphorylation of insulin receptor substrate-1 (IRS-1)

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3
Q

What disease of females causes insulin resistance?

A

Polycystic ovarian syndrome

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4
Q

In the initial phase of type II diabetes - what do the beta cells initially compensate for?

A

Increasing insulin resistance

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5
Q

What are glucotoxicity and lipotoxicity a result of?

A

Insulin resistance - and they both lead to declining beta-cell function

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6
Q

Which of the two are more likely to get type II diabetes - apples or pears?

A

Apples

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7
Q

At time of diagnosis of type II diabetes - what four complications are commonly already present?

A
  1. Retinopathy
  2. Erectile dysfunction
  3. Neuropathy
  4. Nephropathy
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8
Q

In what way is family history relevant to type II diabetes?

A

50% genetic

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9
Q

What is the therapy staircase of type 2 diabetes?

A
  1. Diet and exercise
  2. Oral monotherapy - metformin
  3. Oral combination
  4. Injecting insulin
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10
Q

Name a biguanide?

A

Metformin

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11
Q

What class of drugs are glicazide, glibenclamide and glimeparide?

A

Sulphonylureas

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12
Q

Name a thiazolidinedione?

A

Pioglitazone

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13
Q

How does metformin work?

A

Improves sensitivity to insulin

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14
Q

What is the usual starting dose for metformin?

A

500mg twice a day

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15
Q

If a patient is struggling to tolerate metformin what can be done?

A

Moved to slow release tablets (XR) or start low and go slow

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16
Q

Does metformin reduce HbA1c?

A

Yes

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17
Q

Does metformin prevent microvascular complications and macrovascular complications>

A

Yes

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18
Q

Name two other conditions that metformin is good for other than diabetes?

A

PCOS

NAFLD

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19
Q

Give five side effects of metformin

A
  1. GI - anorexia, nausea, vomiting, diarrhoea,ando pain and taste disturbance
  2. Interference with vit B12 and folic acid absorption
  3. Lactic acidosis
  4. Liver failure
  5. Rash
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20
Q

When should metformin be avoided or stopped in relation to renal toxicity?

A

When eGFR is less than thirty ml/min or serum creatinine is greater than 150 umol/l

Half dose if eGFR 30-45 ml/min

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21
Q

When should metformin be discontinued in relation to liver toxicity?

A

When advanced cirrhosis or risk of lactic acidosis e.g. encephalopathy or alcohol excess

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22
Q

What is first line agent for T2DM?

A

Metformin

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23
Q

In what way is the effect of SUs better than metformin in relation to hyperglycaemia management?

A

Results in more rapid reduction in hyperglycaemia than insulin sensitisers

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24
Q

What is the main concern with SUs?

A

Acceleration of beta cell demise

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25
Q

Do SUs prevent microvascular and macrovascular complications?

A

Yes for microvascular but NO for macrovascular

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26
Q

What is there a big risk of with SUs in particular with elderly/frail, alcohol excess and liver disease?

A

Hypoglycaemia

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27
Q

What drug class is used first line in underweight T2DM because of adverse affect weight gain?

A

SUs

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28
Q

What drug class should be considered as the preferred option after metformin or in those intolerant of metformin?

A

SUs

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29
Q

What drugs are PPARgamma agonists?

A

Thiazolidinediones (TZDs)

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30
Q

Give two adverse effects of TZDs?

A
  1. Heart failure - fluid retention

2. Weight gain

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31
Q

What drugs increase the risk of hip fracture by 20% per year of use?

A

Glitazone

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32
Q

What is the incretin effect?

A

If sugar is injected through veins the insulin levels rise less than by mouth.

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33
Q

Name two incretins?

A

GIP from K cells

GLP-1 for L cells

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34
Q

What enzyme breaks down GIP and GLP-1?

A

DPP-IV

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35
Q

What hormones increase satiety and decrease appetitie?

A

Incretin hormones

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36
Q

What class of drugs do exenatide, exendin LAR, liraglutide and lixisenatide belong to?

A

GLP-1 receptor agonists

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37
Q

Give four benefits of GLP-1 receptor agonists?

A
  1. promote insulin secretion from pacnreas without hypoglycaemia
  2. Suppress glucagon
  3. Decrease gastric emptying
  4. Reduce appetite - weight loss
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38
Q

What class of drugs do vildagliptin, sitagliptin, saxagliptin and linagliptin belong to?

A

DPP-IV inhibitors

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39
Q

Give two benefits DPP-IV inhibitors?

A
  1. Promote insulin secretion from pancreas without hypoglycaemia
  2. Suppress glucagon
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40
Q

What class of drugs do dapagliflozin, canagliflozin and empagliflozin?

A

SGLT2 inhibitors

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41
Q

What drugs decrease uptake of sugar by about one quarter?

A

260g - SGLT inhibitors

42
Q

Give two adverse effects of SGLT inhibitors?

A
  1. Increase in thrush

2. Urine infections

43
Q

Name three insulin secretagogues?

A
  1. Sulphonylureas
  2. DPP4 inhibitors
  3. GLP-1RA
44
Q

How do sulfonylureas, incretin mimetics, glinides, DPP-4 inhibitors all work?

A

Insulin dependent action - increasing secretion of insulin

45
Q

How do biguanides and TZDs work?

A

Insulin dependent action - decreasing insulin resistance and reducing hepatic glucose output

46
Q

How do alpha-glucosidase inhibitors work?

A

Slowing glucose absorption from the GI tract - insulin independent action

47
Q

How do SGLT2 inhibitors work?

A

Enhancing glucose excretion by the kidney - insulin independent action

48
Q

What does increased ATP:ADP ratio within a cell do?

A

Closes ATP sensitive K+ channels causing membrane depolarisation

49
Q

In relation to the kATP channel what makes up the octomeric complex?

A

4 potassium inward rectifier 6.2 subunits (Kir6.2) and 4 sulphonylurea receptor 1 subunits (SUR1)

50
Q

In relation to the kATP channel what do the tetramer of Kir6.2 subunits form?

A

A potassium selective ion channel

51
Q

In relation to the kATP channel what do SUR1 subunits regulate?

A

Potassium channel activity

52
Q

In relation to the kATP channel - what substance binds to each of the Kir6.2 subunits to close the channel causing depolarisation of the beta cell?

A

ATP

53
Q

In relation to the kATP channel - what binds to the SUR1 subunit to open the channel, maintaining the resting potential and inhibiting insulin secretion?

A

ADP-Mg

54
Q

What drugs appear to act by displacing the binding of ADP-Mg from the SUR1 subunit?

A

Sulfonylureas

55
Q

What drugs act similarly to sulfonylreas and bind to SUR1 at a distinct benzamido site?

A

Glinides

56
Q

When are glinides taken?

A

Before meals

57
Q

Name a GLP-1 analogue?

A

Extenatide

58
Q

How are incretin analogues administered?

A

Subcutaneously

59
Q

What diabetic drugs have adverse effects of flatulence, loose stools, diarrhoea, abdo pain and bloating?

A

Alpha-glucosidase inhibitors such as acarbose

60
Q

How does metformin work?

A

Reduces hepatic gluconeogenesis by stimulating AMP-activated protein kinase (AMPK)

61
Q

What drug increases glucose uptake and utilisation by skeletal muscle, reduces carbohydrate absorption and increases fatty acid oxidation?

A

Metformin

62
Q

What sort of infections can hyperglycaemia cause?

A

Fungal infections

63
Q

How is insulin normally secreted to account for about 50% of insulin produced?

A

At a low basal rate

64
Q

What type of insulin analogue is Levemir?

A

Long acting

65
Q

Name a rapid acting anaolguie?

A

Novorapid

66
Q

In relation to insulin adjustment - what is the target for pre meal?

A

3.9 - 7.2 (4-7) mmol/l

67
Q

In relation to insulin adustment - what is the target for 1-2 hours after the beginning of a meal?

A
68
Q

Name two classes of prandial insulins?

A
  1. Insulin analogues

2. Soluble insulin

69
Q

What is the onset of action, peak action and duration of insulin analogues such as Novorapid, Humalog and Apidra?

A

Onset of action - 10-15 minutes
Peak action - 60-90 minutes
Duration - 4-5 hours

70
Q

What is the onset of action, peak and duration of soluble insulins such as Actrapid and humulin S?

A

Onset - 30-60 minutes
Peak 2-4 hours
Duration - 5-8 hours

71
Q

What should most patients with type I diabetes be on?

A

Analogue based insulin

72
Q

What types of insulin are Insulatard and Humulin I?

A

Isophane ‘basal’ insulins - peak of activity is 4-6 hours after administration

73
Q

Name two analogue based insulins?

A

Lantus

Levemir

74
Q

Who is advanced carbohydrate counting for?

A
  1. Those on MDI

2. Those on SCII pumps

75
Q

What are the two components of advanced carbohydrate counting?

A
  1. Insulin to carbohydrate ration (ICR)

2. Insulin sensitivity factor (ISF) also known as correction factor (CF)

76
Q

What is the ratio of insulin: CHO?

A

1 unit of insulin per 10g CHO

77
Q

What type of insulin do insulin pumps administer?

A

Short acting

78
Q

What is the background insulin dictated by with insulin pumps?

A

Basal rate

79
Q

What is a measure of average blood glucose over a prolonger period of time such as 6-8 weeks?

A

HbA1c

80
Q

What is the HbA1c target?

A

48 mmol/mmol

81
Q

Give four factors that affect insulin absorption/action?

A
  1. Temperature
  2. Injection site
  3. Injection depth
  4. Exercise
82
Q

In what two conditions is IV insulin indicated?

A

DKA and HHS

83
Q

What inheritance does MODY have?

A

Autosomal dominant

84
Q

What are the two distinct types of MODY?

A
  1. Transcription factor (HNF-1alpha)

2. Glucokinase

85
Q

What type of MODY: onset at birth, stable hyperglycaemia, diet treatment and complications are rare?

A

Glucokinase mutations

86
Q

What type of MODY: onset as young adult, progressive hyperglycaemia, 1/3 diet, 1/3 OHA, 1.3 insulin and ocmplications are frequent?

A

Transcription factor mutations

87
Q

When is insulin required in neonatal diabetes?

A

Within the first 3 months of life

88
Q

What are MODY HNF1alpha sensetivie to?

A

SU treatment - GCK does not need treatment

89
Q

What do these symptoms suggest - shaking, sweating, anxious, dizzin ess, hunger, tachycardia, impaired vision, weakness, headache and irritable?

A

Symptoms of hypoglycaemia

90
Q

What is the immediate treatment of hypoglycaemia?

A

Consume 15-20 grams of glucose or simple carbohydrates and recheck BG after 15 minutes

91
Q

If injection is present - what is the treatment of immediate, severe hypoglycaemia?

A

Glucagon 1 mg injected into buttock, arm or thigh

92
Q

What is the term for a disordered metabolic state that usually occurs in the context of an absolute or relative insulin deficiency accompanied by an increase in the counter-regulatory hormones i.e. glucagon, adrenaline, cortisol and growth hormone.

A

Diabetic ketoacidosis

93
Q

In relation to DKA pathophysiology - what four effects occur as a result of insulin deficiency and stress hormone activation?

A
  1. Lipolysis increase
  2. Glucose utilisation decrease
  3. Proteolysis increase
  4. Glycogenolysis increase
94
Q

What is the ketonaemia for DKA diagnosis?

A

> 3mmol/L or significant ketonuria >2+ on standard urine stick

95
Q

What is the BG for DKA diagnosis?

A

> 11 mmol/L or known diabetes

96
Q

What is the bicarbonate for DKA diagnosis?

A
97
Q

Give four common precipitants of DKA?

A
  1. Non-adherence with treatment
  2. Newly diagnosed
  3. Infection
  4. Illicit drugs or alcohol
98
Q

Give two osmotic related symptoms of DKA?

A
  1. Thirst and polyuria

2. Dehydration

99
Q

Give four ketone body related symptoms of DKA?

A
  1. Flushed
  2. Vomiting
  3. Abdo pain
  4. Kussmaul’s respiration
100
Q

Is amylase raised in DKA?

A

Very frequently

JL Endocrinology (12 decks)

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