Diabetes Mellitus Management Flashcards

1
Q

What advice would you give to someone with diabetes?

A
Exercise to increase insulin sensitvity
Health eating low saturated fats, low sugar, high starch, moderate protein
Avoid 'diabetic' foods
Lose weight
Reduced energy intake
Stop smoking
Limit salt intake
Foot care
Attend reviews
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2
Q

What diet would you recommend?

A
Low saturated fat
Low sugar
High starch
High fibre
Low salt
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3
Q

How is T1 DM managed?

A

Monitor HbA1c - target of 48mmol/mol 6.5%
Self monitoring, 4x a day
Offter multiple daily injection basal-bolus insulin regimens
Twice daily insulin
Rapid acting insulin analogues injected before meals for mealtime insulin replacement

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4
Q

How is T1 DM managed?

A

Monitor HbA1c - target of 48mmol/mol 6.5%
Self monitoring, 4x a day
Offer multiple daily injection basal-bolus insulin regimens,
Twice daily insulin,
Rapid acting insulin analogues injected before meals for mealtime insulin replacement

Blood glucose targets:
5-7mmol/l on walking and
4-7mmol/L before meals

Add metformin if BMI>25kg/m2

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5
Q

How is T2DM managed? What are the HbA1c targets for each?

A

Lifestyle 48mmol/mol 6.5%
Lifestyle + metformin 48mmol/mol 6.5%
Any drug which may cause hypoglycaemia (e.g. lifestyle+sulfonylurea) 53mmol/mol 7%

Already on one drug but HbA1c has risen to 58mmol/mol (7.5%) - 53mmol/mol (7%)

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6
Q

What is second line? when do you consider this?

A

If HbA1c > 58mmol/mol (7.5%), dual therapy:

Metformin + DPP4 inhibitor (gliptin)
MEtformin + pioglitazone
Metformin + sulfonylurea
Metformin + SGLT2 inhibitor (glifazon)

Or if intolerant/CI to metformin then
Gliptin (DPP4i) + sulfonyurea
Gliptin (DPP4i) + pioglitazone
Pioglitazone + sulfonylurea

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7
Q

What is third line? when do you consider this?

A
If HbA1c > 58mmol/mol (7.5%) on dual therapy, triple therapy with:
Meformin, DPP4i (gliptin), sulfonylurea
Metformin, pioglitazone, sulfonylrea
Metformin, sulfonylurea, SGLT2i
Metformin, pioglitazone SGLT2i

OR

Insulin based therapy

If metformin not tolerated and HbA1c > 58mmol/mol (7.5%) on dual therapy—> Insulin based therapy

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8
Q

What if triple therapy is not effective, not tolerated or contraindicated and BMI>35

A

Metformin
Sulfonylurea
GLP1 mimetic

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9
Q

What is the MOA, route and SE, CI of metformin?

A

Biguanide
Reduces insulin resistance – increases receptor sensitivity. Inhibits hepatic gluconeogenesis. Stimulated uptake of glucose into muscle and adipose. Decreases absorption of glucose from the GI tract. Also reduces LDLs and VLDLs.

Oral

SE:
GI upset, abdo pain ,nausea, diarrhoea
Lactic acidosis
(weight neutral, no risk of hypos)

CI:
Hepatic, renal or cardiac disease
eGFR <30ml/min due to risk of lactic acidosis

Renal elimination
Half life 4 hours

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10
Q

What is the MOA, route, SE, example of sulfonylurea?

A

Increase insulin secretion from pancreatic beta cells.
Supplement endogenous insulin: bind to and antagonise K+/ATP channels in beta cells which reduces potassium currents, depolarising the cell, increasing calcium entry, increasing exocytosis of insulin

Oral

E.g. Glicazide, glimepride

SE:
Hypoglycaemia
Weight gain
Hyponatraemia
GI disturbance

DDI: Highly bound to plasma proteins

Longer duration but less fine-tuned control

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11
Q

What is the MOA, route, SE, example of thiazolidinediones?

A

AKA glitazone

Pioglitazone

Bind the peroxisome proliferator-activated receptor-γ (PPAR-γ) which is a nuclear hormone receptor. This then binds the retinoid X receptor, and the complex goes on to upregulate genes involved in insulin signalling.
Increase insulin senstivity
Promote adipogenesis and fatty acid uptake

Oral OD

SE
Weight gain
Fluid retention - oedema
Increases LDL/HDL
(no risk of hypoglycaemia)

CI: heart failure

DDI: Heavily bound to plasma proteins – affected by competitive binding

Longer duration but less fine tuned control

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12
Q

What is the MOA, route, SE, example of DPP4 inhibitors? AKA?

A

GLIPTINS (sitgliptin)

Increases incretin levels which inhibit glucagon secretion by blocking DPP4 which destroys incretin. Inhibits DPP-4 which breaks down GLP-1, has the same action as GLP-1 analogues therefore.

Oral

SE
Risk of pancreatitis but well tolerated

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13
Q

What is the MOA, route, SE, example of SLGT2 inhibitors? AKA?

A

Gliflozins e.g. empagliflozin

Block reabsorption of glucose in the proximal convoluted tubule and promotes excretion of excess glucose in the urine

Oral

UTI
Thrush
Weight loss
hypoglycaemia

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14
Q

What is the MOA, route, SE, example of GLP1 agonists, indication?

A

Tides (e.g. exenatide, liraglutide)

Incretin mimetics
Incretins are gut peptides that augment insulin release
Increases insulin levels, decreases glucagon levels, decreases appetite, slows gastric emptying

Patients must have BMI > 35 and psychological or medical problems associated with obesity.
Would benefit from weight loss
OR BMI < 35kg/m2 and insulin is unacceptable because of occupational implications or weight loss would benefit other comorbidities
To continue: 1% reduction in HbA1c and 3% reduction in weight after 6 months

Subcut

Nausea and vomiting (decreased gastric motility)
Pancreatitis
Weight loss

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15
Q

What does incretin do? Which medications work on incretin pathway?

A

Inhibits glucagon secretion and stimulate insulin release
Glucagon is responsible for raising blood sugar by promoting gluconeogenesis, glycogenolysis, break down of fatty acids

DPP4-inhibitors stop DPP4 enzymes inactivating incretins increase incretin levels, inhibiting glucagon secretion

GLP-1 agonists imitate incretin, inhibiting glucagon secretion and increase insulin release

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16
Q

Which diabetic medications result in weight loss?

A

SGLT2-inhibitors (-gliflozins)

GLP-1 agonists (-tides)

17
Q

Which diabetic medications may cause weight gain?

A

Sulfonylureas (glicazide, gliceride)
Thiazolidinedions (pioglitazone)
Insulin

18
Q

Which diabetic medications may cause weight gain?

A

Sulfonylureas (glicazide, gliceride)
Thiazolidinedions (pioglitazone)
Insulin

19
Q

What insulin types are there?

A

Short medium and long acting

Pre-mixed with short acting and long acting

20
Q

What are common insulin regimes?

A

BD - twice daily premixed insulins by pen - good for regular lifestyle

QDS - before meals ultra fast insulin + bedtime long acting analogue - good for flexible lifestyle adjusting doses with meal size or exercise

Once daily before bed long-acting insulin: good initial insulin regimen when switching from tablets in T2DM

21
Q

What is DAFNE?

A

Dose adjusting for Normal Eating

Training in flexible, intensive insulin dosing improves glycemic control and well-being

22
Q

What should you tell diabetics if they become unwell?

A

Continue medication/insulin
Increase frequency of blood glucose monitoring to four hourly or more frequent
Encourage fluid intake - 3L in 24 hours
May need to take sugary drinks to maintain carbohydrate intake if struggling to eat
Sick day supply box
Get help from nurse or GP if concerned and glucose levels are rising
Admit if vomiting, dehydrated, ketotic, child or pregnant

23
Q

What can you consider if attempts to reach HbA1c targets with daily injections have resulted in hypoglycaemia or unable to achieve target?

A

Insulin pumps

24
Q

What are the side effects of insulin therapy? How can these be addressed?

A

Hypoglycaemia:
teach signs of hypoglycaemia - sweating, anxiety, blurred vision, confusion, aggression
take 10-20g of short acting carbohydrates
glucagon kit for emergency

Lipodystrophy:
Atrophy of the subcutaneous fat
Prevented by rotating the injection site

25
Q

What are the classes of oral hypoglycaemics?

A
Biguanide - metformin
Sulfonylureas - Gliclizide
Thiazoledinediones - Pioglitazone
DPP4 inhibitors - sitagliptin
GLP-1 analogues - eventide
SGLT2 inhibitors - dpaagliflozin
26
Q

What are the classes of insulin?

A

Ultra-rapid - novorapid/humalog - 5-15 mins
Short acting - Actrapid/humulin S - 30-60 min
Intermediate acting - isophane 2-4 hours
Long acting - insulin glargine 2-6 hours

27
Q

What are the MOA and ADRs of ultra-rapid insulin?

A

Onset in 5-15 minutes.
Replaces endogenous insulin – stimulates uptake of glucose into liver, muscle and adipose tissue, decreases hepatic glucose output, inhibits glycogenolysis, promotes fat uptake

Hypoglycaemia, possibly leading to diabetic coma
Weight gain
Lipohypertrophy
Injection site Discomfort
Insulin allergy
28
Q

What are the MOA and ADRs of short acting insulin?

A

Start to work in 30-60 minutes.
Replaces endogenous insulin – stimulates uptake of glucose into liver, muscle and adipose tissue, decreases hepatic glucose output, inhibits glycogenolysis, promotes fat uptake

Hypoglycaemia, possibly leading to diabetic coma
Weight gain
Lipohypertrophy
Injection site Discomfort
Insulin allergy
29
Q

What are the MOA and ADRs of intermediate acting insulin?

A

Start to work in 2-4 hours.
Replaces endogenous insulin – stimulates uptake of glucose into liver, muscle and adipose tissue, decreases hepatic glucose output, inhibits glycogenolysis, promotes fat uptake

Hypoglycaemia, possibly leading to diabetic coma
Weight gain
Lipohypertrophy
Injection site Discomfort
Insulin allergy
30
Q

What are the MOA and ADRs of long acting insulin?

A

Start to work in 2-6 hours.
Replaces endogenous insulin – stimulates uptake of glucose into liver, muscle and adipose tissue, decreases hepatic glucose output, inhibits glycogenolysis, promotes fat uptake

Hypoglycaemia, possibly leading to diabetic coma
Weight gain
Lipohypertrophy
Injection site Discomfort
Insulin allergy
31
Q

TReatment streps in T2DM combination therapy

A

• Lifestyle & diet
• If HbA1c is still greater than 6.5%:
o Metformin

• If HbA1c is still greater than 6.5%:
o add Sulphonylurea (glibenclamide)

• If HbA1c is still greater than 7.5%
o add Thiazolidinediones
o Or insulin

• If HbA1c is still greater than 7.5%
o Insulin + metformin + sulphonylurea

32
Q

What do you need to monitor in DM?

A

HbA1c - glycosylated Hb blood glucose over 120 days

Renal, hepatic, CVS and near function to determine signs of vascular damage

33
Q

What medication would you give to someone who would benefit from weight loss?

A

Exenatide (GLP1 agonist)