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7118 - Clinical Therapeutics for Core Conditions > Type 2 diabetes > Flashcards

Type 2 diabetes Flashcards

1
Q

two mechanisms for T2 diabetes

A

Relative insulin deficiency

Insulin resistance

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2
Q

pre diabetes for >10 years without diagnosis

A

may lead to 50% reduction in pancreatic beta-cell function and this may continue to decline even after treatment initiation which often leads the need for insulin therapy

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3
Q

over weight patients

A

free fatty acids leading to insulin resistance in the muscles and the liver

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4
Q

what is insulin resistance also associated with

A

atherosclerosis

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5
Q

MODY

A

maturity onset diabetes of the young

several subsets with different genetic defects

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6
Q

HbA1C is not suitable in some T2DM patients including..

A
  • all children and young people
  • patients with symptoms for < 2 months
  • patients who are acutely unwell
  • patients who are on medicines which are known to raise glucose for example antipyscotics and steroids
  • patients with pancreatic damage
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7
Q

Patients treated with one agent which is not known to cause hypoglycaemia should aim for HbA1c to be….

A

<48mmol

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8
Q

Patients taking two or more agents or one agent that is known to cause hypoglycaemia should aim for HbA1c to be

A

<53mmol

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9
Q

Patients who are symptomatically hyperglycaemic should be offered

A

sulphonylurea

insulin until blood glucose control is achieved.

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10
Q

Treatments for T2DM if metformin is tolerated

A

1) Lifestyle factors
2) Metformin
3) Metformin MR

If HbA1c >58mmol

4) - DPP-4 inhibitor (gliptin)
- sulphonylurea
- pioglitazone
- SGLT-2 inhibitor (flozins)

HbA1C >58 mmol

Consider triple therapy of metformin with one of the following:
sulphonylurea + DPP-4 inhibitor
sulphonylurea + pioglitazone
sulphonylurea + SGLT-2 inhibitor (flozin)
pioglitazole + SGLT-2 inhibitor

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11
Q

Treatment for T2DM is metformin is not tolerated….

A

1) - DPP-4 inhibitor (gliptin)
- sulphonylurea
- pioglitazone
- SGLT-2 inhibitor (florins)

if HbA1c >58mmol then….

  • DPP-4 inhibitor (gliptin) + pioglitazole
  • DPP-4 inhibitor + sulphonylurea
  • pioglitazole + sulphonylura

if HbA1c > 58mmol then consider insulin therapy

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12
Q

How does metformin work?

A
  • inhibits gluconeogenesis and glyconolysis
  • improve peripheral glucose uptake and utilisation in muscle
  • delay gastro intestinal uptake of glucose
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13
Q

metformin

A
  • dose not cause hypo’s
  • does not cause weight gain (actually weight loss)
  • reduction on cardiovascular risk
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14
Q

Metformin is C/I in….

A
  • eGFR <30ml/min
  • acidotic states such as ketoacidosis
  • sudden drop of renal function e.g. sepsis
  • conditions associated with tissue hypoxia - decompensated HF, respiratory daily, recent MI, hepatic insufficiency, acute alcohol intoxication, alcoholism.

Caution in eGFR <45ml;min (max dose 1g)

Max dose 2g eGFR 45-59ml/min

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15
Q

Metformin is associated with

A

GI disturbances
B12 deficiency

Titrate up slowlyMax dose 3gram daily, no benefits beyond this.

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16
Q

Sulfonyureas (gliclazide, glipizide, glibenclamide, tolbutamide)

A

Act on the pancreatic beta cells by stimulating the release of insulin and also decrease the hepatic output of glucose.

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17
Q

sulphonyureas are associated with

A
  • weight gain
  • hypos (may not be suitable for a lorry driver)

Should always be given with meals. Gliclazide is favoured as short half life and part renal, part hepatic clearance. Longer acting ones can accumulate and cause more problematic hypos.

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18
Q

DPP-4 inhibitors (sitagliptin, saxagliptin, linagliptin, vildagliptin, alogliptin)

A

Hormones such as GLP1 and GIP are released by the intestinal cells throughout the day with the levels becoming elevated after a meal.

They act by stimulating insulin synthesis and release from the pancreatic beta cells and in the cause of GLP-1 decrease glucagon secretion.

Depended on glucose levels so do not cause hypos in the same way sulphonylureas do.

19
Q

DPP-4 inhibitors - GLIPTINS are associated with

A

pancreatitis

20
Q

Which DDP-4 inhibitor does not require a dose reduction based on eGFR?

A

linagliptin.

21
Q

What other anti diabetic drug are DPP-4 inhibitors not licensed to be prescribed along side?

A

GLP1 agonistis (exenatide, liraglutide, dulaglutide)

22
Q

GLP-1 agonists (exentide, liraglutide, dulaglutide)

A

work by mimicking the GLP1 hormone

They also slow gastric emptying reducing the rate at which glucose is absorbed into the circulation.

23
Q

GLP-1 agonists are associated with

A

pancreatitis

additional hypoglycaemic effect with sulphonylureas however they individually do not cause hypos.

rapid weight loss (expensive so reserved with patients with high BMI)

continued if a reaction of 1% HbA1C and 3% body weight in 6 months

24
Q

pioglitazone works by

A

reducing peripheral resistance of insulin and they do not cause hypos

25
Q

piogliazole is C/I in

A

HF

co-morbidities that can cause HF e.g. MI

Bladder cancer

fracture risk

26
Q

if patient on pioglitazole gets weight gain what should we check?

A

LFT’s

not recommended in patients with hepatic dysfunction

27
Q

SGLT-2 inhibitors (Dapagliflozin, canagliflozin, empagaflozin)

A

Removed glucose

28
Q

SGLT-2 inhibitors are associated with

A

diuresis so can lower BP. They should be avoided in patients who are volume depleted or taking loop diuretics.

  • ketoacidosis
  • lower limb amputations primarily big toe.
  • They cannot be initiated in patients with eGFR <60ml/min however canagliflozin and empagliflozin can be continued down to 45ml.min

They promote weight loss

29
Q

if a patient is volume deplete what should we do?

A

Suspend the SGLT-2 inhibitor as risk of UTI and gynae infections can occur including urosepsis.

30
Q

insulin therapy in T2DM

A

OD or BD intermediate acting.

  • neutral porcine hagedorn or isophane insulin.
  • humulin I, insulated, Inhuman Basal,
31
Q

Long acting insulins should be trialled in patient who

A
  • daily to achieve HbA1C target
  • get hypos
  • cannot use divide
  • need assistance injecting
  • need intermediate + oral tabs
32
Q

Should metformin be continued with insulin?

A

Yes

33
Q

What is HHS?

A

uncommon complication of T2 DM

34
Q

HHS is complicated by

A

MI, thrombosis, stroke.

Seizures cerebral oedema and central pontine myelinolysis are less common but well documented complications.

35
Q

what is the basic underlying cause off HHS?

A

circulating insulin deficiency

Precipitants of HHS include vascular events, infections and undiagnosed T2DM.

36
Q

Features that differentiate HHS from DKA are

A
  • hypovolaemia (significant dehydration)
  • Marked hyperglycaemia ( a blood glucose >30mmol) but can be higher without the presence of ketones or acidosis.
  • serum osmolality of 320mosmol/kg or greater
37
Q

Treatment

A

1) FLUID (aim to reduce serum osmolality by maximum 3-8mosmol/kg/hr) to reduce the risk of CPM
2) potassium replacement
3) IV insuline (not all will need). If blood glucose is not dropping despite adequate fluid replacement generally after 8 hours then can start at a rate of 0.05 units/kg/hr

38
Q

Does metformin reduce the risk of CVD in T2DM

A

YEs

39
Q

metformin should be stopped at EGFR

A

30ml/min

40
Q

Medicines which can cause pancreatitis?

A

GLP-1 - Exenatide, liraglutide

DPP-4 - gliptins

41
Q

Facts about pioglitazone

A
  • it should be avoided in combination with insulin
  • it is associated with increased fracture risk
  • it reduced peripheral insulin resistance
  • in those that respond to treatment the benefits outweigh the risk of developing bladder cancer
42
Q

Which T2DM drug is associated with ketoacidosis?

A

FLOZINS

Dapagliflozin.

43
Q

HHS facts

A
  • fluid replacement if more important than IV insulin
  • Patients are at an increased risk of VTE
  • Higer mortality rate than ketoacidosis

7118 - Clinical Therapeutics for Core Conditions (31 decks)

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