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RED - Endocrine Pharmacology & Therapeutics > E4 - Diabetes 2 > Flashcards

E4 - Diabetes 2 Flashcards

1
Q

What is the strategy/NICE guideline for treatment of T2DM?

A

1.) Diet/lifestyle interventions; trialled for 3 months. (w/regular GP meetings/testing)
2.) Monotherapy; anti-diabetic or hypoglycaemic agent.
> First-line: Metformin
> Second-line: SU (sulphonylureas), DDP-4i (DPP-4 inhibitors), pioglitazone.
3.) Dual therapy (after dose titrations tried); metformin + SU/DPP-4i/pioglitazone
4.) Triple therapy OR straight to insulin.
5.) Intensify insulin regime OR add drugs.

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2
Q

What cautions are there for the first-line antidiabetic, Metformin?

A

Caution in renal impairment; may require dose adjustments, but cut off of renal impairment where Metformin not suitable.

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3
Q

What is meant by the first/second intensification in relation to T2DM treatment?

A

First intensification: Dual therapy

Second intensification: Triple therapy

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4
Q

What drug class is metformin and its therapeutic effect/consequences?

A
  • Biguanide
  • Increases glucose utilisation
  • Decreases gluconeogenesis
    (improves action of insulin)
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5
Q

What is known about metformin’s mechanism of action/targets?

A

Not clear; thought to activate AMP kinase.

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6
Q

What do sulphonylureas/prandial glucose regulators do and what is required?

A
  • Stimulates insulin secretion

- Requires some functional β-cells; good for early stage T2DM.

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7
Q

What is the mechanism of action for sulphonylureas/prandial glucose regulators?

A

Blockade of islet β-cell ATP-sensitive K+ channel; respectively bind at different sites within channel.

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8
Q

What are prandial glucose regulators also known as? Give two examples.

A

Meglitinides:

  • Repaglinide
  • Nateglinide
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9
Q

Name 3 sulphonylureas.

A
  • Glicazide
  • Tolbutamide
  • Glibenclamide
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10
Q

How does glucose-induced insulin release share similarities with the action of SUs/PGRs?

A
  • Mimics increase of ATP:ADP ratio which results in K+ channel closing
  • Blocking channel decreases K+ efflux, leads to accumulation of positive charge, membrane depolarisation, opening of VGCCs, exocytosis of insulin.
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11
Q

What class of drugs does pioglitazone belong to and how does it work?

A
  • Thiazolidinedione
  • PPARγ-agonists ‘insulin sensitisers’
    > Improved insulin action of insulin resistant cells etc
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12
Q

What drug class does rosiglitazone belong to and why is it not used any more?

A
  • Thiazolinediones

- License withdrawn as of 21/10/2010

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13
Q

Name an α-glucosidase inhibitor and describe its mechanism of action.

A
  • Acarbose
  • Delays digestion & absorption of starch and sucrose; limiting breakdown hence limits absorption of glucose in the gut, dampening down peaks of glucose from a meal
  • By inhibiting intestinal alpha glucosidases
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14
Q

What is the issue with acarbose?

A
  • Many GI side effects

- Reserved for later therapy

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15
Q

What drug class do exenatide & liraglutide belong to?

A

GLP-1 mimetics/incretin mimetics

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16
Q

What do DDP-4 inhibitors do and what are they also known as?

A
  • Inhibits DPP-4; enzyme which normally degrades GLP1/incretin
  • ‘Incretin enhancers’
  • ‘Gliptins’
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17
Q

What is the principle of incretin-based therapy?

A
  • To push insulin-response curve back to the left

- To have the normal potentiating effect of incretins on insulin secretion

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18
Q

Name 3 DPP-4 inhibitors.

A
  • Sitagliptin
  • Vildagliptin
  • Saxagliptin
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19
Q

What are the therapeutic effects of GLP-1 mimetics/DPP-4 inhibitors?

A
  • Promote insulin secretion
  • Reduce glucagon secretion (thus no increase in blood glucose)
  • Reduce gastric emptying; allows much slower increase in blood glucose with meal absorption
  • Promotes satiety (feeling of fullness; stop eating earlier)
  • Reduces gluconeogenesis (hepatic glucose production, potentially inhibiting glycogen breakdown)
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20
Q

What are the disadvantages with GLP-1 mimetics?

A

Administration via subcutaneous injection instead of PO.

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21
Q

What is Bydureon and why is it preferable?

A
  • Exenatide, a GLP-1 mimetic

- Weekly modified-release formulation (but still S.C. administration)

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22
Q

What drug class do dapagliflozin, canagliflozin and empagliflozin belong to?

A

Sodium-glucose co-transporter 2 (SGLT-2) inhibitors

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23
Q

What is the mechanism of action of sodium-glucose co-transporter 2 (SGLT-2) inhibitors?

A
  • Inhibits renal glucose reabsorption
  • Glucose normally filtered out of blood in the ultrafiltrate and then reabsorbed at PCT; mainly due to SGLT-2
  • Reversibly inhibiting SGLT-2 in PCT reduces glucose reabsorption
  • Glucose excreted in the urine (glycosuria); decrease in blood glucose
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24
Q

What are the side effects with SGLT-2s?

A

Resulting glycosuria leads to:

  • Polyuria
  • Osmotic diuresis (glucose in urine increasing osmotic pressure and taking water with it)
  • Polydipsia
  • UTIs (prime environment for fungus/bacterial infections)
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25
Q

When is exogenous insulin required and what other drug therapies wouldn’t be suitable at this point?

A

In advanced T2DM where:

  • β-cell failure
  • SUs ineffective as no insulin produced
  • Combine insulin with other antidiabetic drugs
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26
Q

What are the acute complications associated with T2DM?

A

Extremes of glucose levels:

  • Hypoglycaemia
  • Hyperglycaemia; HHS
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27
Q

What is hypoglycaemia and how can it develop in T2DM?

A
  • Low blood glucose;
28
Q

What is hyperosmolar hyperglycaemic state (HHS) in T2DM? How does it present?

A
  • Severe hyperglycaemia; > 40 mmol/L
  • Hyperosmolar: glucose increases osmotic pressure in blood
  • Without ketosis (unlike in DKA in T1DM; T2DM retains some β-cell function)
29
Q

How is HHS treated?

A
  • Managed as DKA
  • Insulin given for hyperglycaemia (but much less insulin required than DKA; still have residual insulin production)
  • Fluid/electrolyte correction for dehydration
30
Q

Why are the long-term complications of T2DM noteworthy?

  • Don’t need to know
A
  • Indicator of poor glycaemic control
  • Major cause of morbidity and mortality
  • Substantially impairs quality of life
  • Cause of frequent hospitalisations
  • Reduces life expectancy by 20 years in T1DM, 10 years in T2DM
  • 80% of DM patients die from CV disease
  • RIsk of stroke/heart attack increased by 2-3 fold
  • Leading cause of blindness
  • 1000 DM patients start dialysis every year in UK
  • NHS spends 14 billion GBP PA on DM and its effects (10% of budget)
31
Q

What is the difference between microvascular and macrovascular?

A

Microvacular; affect the small blood vessels (capiliaries)

Macrovascular; affect the larger blood vessels (medium-large arteries)

32
Q

What are the 3 main microvascular complications of DM?

Hint: well vascularised by capillaries/specific to DM

A
  • Retinopathy (eye disease); high capillary network in the retina/back of the eye
  • Nephropathy (kidney disease)
  • Neuropathy (nerve damage); blood supply to nerves
33
Q

What are the 3 main macrovascular complications of DM and why do they occur??

A
  • Cardiovascular disease
  • Cerebral vascular disease (stroke); large blood vessels affected in the brain
  • Peripheral vascular disease

Accelerated atherosclerosis with DM; lipid deposits cause hardening.

34
Q

What factors influence the development of secondary complications in DM?

A
  • Duration of DM; longer you have the disease, the more likely the complications
  • Glycaemic control
  • Risk factors; smoking (increased CVD risk), genetics
35
Q

What is the mechanism of microvascular complications (retino/nephro/neuropathy) in DM?

A
  • Metabolites from elevated blood glucose e.g. sorbitol affecting protein function
  • Glycation of proteins; attachment of glucose to protein can affect function
36
Q

How prevalent in retinopathy in DM?

A
  • Most common cause of blindness in
37
Q

How can retinopathy be classified?

A
  • Background (simple)
  • Pre-proliferative
  • Proliferative
  • Maculopathy (when macula affected)
38
Q

What does background (simple) retinopathy entail?

A
  • Microaneurysm; tiny bulges in capillary network at the back of the eye (can rupture)
  • Haemorrhages (bleeds)
  • Exudates; leakages of lipoproteins from capillaries, harden to form deposits resulting in blurred/deteriorating vision
39
Q

What does preproliferative retinopathy entail and how does it transition from background?

A
  • Capillary network starts to fail
  • Ischaemia of the retina; build-up of toxic metabolites = blurry vision
  • Growth factors released to try and counter above and build new capillaries
40
Q

What does proliferative retinopathy entail?

A

New capillaries formed from growth factors released during preproliferative stage; new blood vessels are prone to rupture (haemorrage); blindness v. likely.

41
Q

Describe a patient’s vision through the different stages of retinopathy.

A
  • Background; normal
  • Pre-proliferative; blurring of vision
  • Proliferative; ‘floaters’, clouding, loss of vision
  • Maculopathy; blurring/distortion of vision
  • Advanced retinopathy; scarring can peel retina off the back of the eye; severe loss of vision
42
Q

How can retinopathy be classified?

A
  • Background (simple)
  • Pre-proliferative
  • Proliferative
  • Maculopathy (when macula affected)
43
Q

What defines each stage of diabetic nephropathy?

What is the timeline with regards to diagnosis of DM?

A

Early; microalbuminuria (albumin not being kept in blood)
Later; proteinuria, increased BP, decreased eGFR
Advanced; end-stage renal disease

Early; 5 - 10yrs (20 - 30%)
Later; 10 yrs
Advanced; 10 yrs

44
Q

What does preproliferative retinopathy entail and how does it transition from background?

A
  • Capillary network starts to fail
  • Ischaemia of the retina; build-up of toxic metabolites = blurry vision
  • Growth factors released to try and counter above and build new capillaries
45
Q

What does proliferative retinopathy entail?

A

New capillaries formed from growth factors released during preproliferative stage; new blood vessels are prone to rupture (haemorrage) bleeding into the vitreous humor (viscous liquid that fills eyeball); blindness v. likely

46
Q

Describe a patient’s vision through the different stages of retinopathy.

A
  • Background; normal
  • Pre-proliferative; blurring of vision
  • Proliferative; ‘floaters’, clouding, loss of vision
  • Maculopathy; blurring/distortion of vision
  • Advanced retinopathy; scarring can peel retina off the back of the eye; severe loss of vision
47
Q

How are ACEis used in DM?

A
  • Help limit diabetic nephropathy (renoprotective) even if BP is normal
48
Q

What defines each stage of diabetic nephropathy?

What is the timeline with regards to diagnosis of DM?

A

Early; microalbuminuria (albumin not being kept in blood)
Later; proteinuria, increased BP, decreased eGFR
Advanced; end-stage renal disease

Early; 5 - 10yrs (20 - 30%)
Later; 10 yrs
Advanced; 10 yrs

49
Q

What nerves can neuropathy affect?

A
  • Cranial NS
  • Autonomic NS
  • Peripheral NS
50
Q

What effects may arise from neuropathy?

A
  • Erectile dysfunction
  • Sweating
  • Postural hypertension
  • Bladder dysfunction
  • Constipation
  • Diarrhoea
51
Q

Where does neuropathy most commonly effect?

A

Feet; increased risk of foot ulcers.

52
Q

What are the symptoms of diabetic neuropathy?

A
  • Loss of sensation
  • Tingling
  • Shooting pains
  • Cramps
  • Causalgia (burning sensation on touch w/o actual heat stimuli)
53
Q

What is the aetiology (causation) of macrovascular complications in T1DM?

A

Glycaemic control

54
Q

What is the aetiology of macrovascular complications in T2DM?

A
  • Glycaemic control
  • Genetic predisposition
  • Metabolic syndrome
55
Q

What is metabolic syndrome?

A

Cluster of risk factors associated with DM and vascular disease; much more common in overweight/obese:

  • Glucose intolerance/DM
  • Dyslipidaemia (high LDL, low HDL, high triglycerides)
  • Hypertension
  • Abdominal obesity
  • Coagulation abnormalities
56
Q

What is ischaemic heart disease and how does it relate to DM?

A
  • Blockage (partial/full) of coronary artery with fatty depostits supplying the heart
  • Can lead to MIs; carries increased risk of complications (heart failure, arrhythmias)
  • Develops prematurely in DM, leading cause of death in DM.
57
Q

How can the risk of ischaemic heart diseaes be mitigated in DM patients?

A

Management of risk factors:

  • hypercholesterolaemia
  • hypertension
  • smoking cessation
58
Q

How does stroke relate to DM?

A
  • 10-fold increase in younger patients
  • More likely to be fatal
  • Less likely for TIAs; warnings of major stroke
  • Hypertension control important
59
Q

What characterises peripheral vascular disease?

A
  • Intermittent claudication (cramping; ischaemia in muscles from blockage of larger vessels)
  • Intermittent ulceration; poor blood supply = poor healing = poor supply of WBCs
  • Hence risk of gangrene/amputation
  • Risk of other vascular events; e.g. DVTs > pulmonary embolism
  • Diabetic foot ulcers
60
Q

What HCPs are involved in the hospital care DM team?

A
  • Consultant/diabetologist
  • Diabetes specialist nurse
  • Ophthalmologist (eye doctor)
  • Psychologist
  • Medical specialists
61
Q

What risk factors are important in preventing microvascular complications?

A
  • Good glycaemic control
  • Control of hypertension (ACEi - limit nephropathy even in normotensive (renoprotective), ATRA, CCB; different to A/C rule)
    > Target: SYS
62
Q

What risk factors are important in the management of macrovascular complications?

A
  • Good glycaemic control
  • Control of hypertension
  • Control of dyslipidaemia (NICE guidelines = statins for all DM > 40 yrs)
  • Use antiplatelet drugs (low dose aspirin, clopidogrel; lower CVD risk)
63
Q

What does the annual assessment for DM complication risk involve?

A
  • Blood tests; HbA1c, glucose, BP, lipids (higher risk of CVD in DM)
  • Eye examination (retinopathy)
  • Kidney function (nephropathy)
  • Footcare (inc. podiatrist; foot consultant) DO NOT SELF-MEDICATE
  • Review of care plan, other info, education, specialists
64
Q

What HCPs are involved in the primary care DM team?

A
  • GP & practice nurse
  • Dietitian
  • Optometrist
  • Podiatrist/chiropodist
  • Pharmacist
65
Q

What HCPs are involved in the hospital care DM team?

A
  • Consultant/diabetologist
  • Diabetes specialist nurse
  • Ophthalmologist (eye doctor)
  • Psychologist
  • Medical specialists

RED - Endocrine Pharmacology & Therapeutics (7 decks)

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