Managing Diabetes/Diabetic Drugs Flashcards

1
Q

What is the first line drug in T2 diabetes?

A

Metoformin

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2
Q

What is the MoA of metoformin?

A

Decreases hepatic glucose production

Increases insulin sensitivity

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3
Q

What diabetic drugs are weight neutral/loss?

What diabetic drugs cause weight gain?

A

Weight loss/neutral

  • metformin
  • SGLT2 inhibitors
  • Incretin drugs (in part. GLP-1 receptor agonist)

Weight gain

  • TZDs (pioglitazone)
  • SUs
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4
Q

What drug class is associated with hypoglycaemia?

A

SUs

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5
Q

Both incretin drugs and SUs are insulin secretagogues, why do incretin drugs not carry the same risk of hypoglycaemia?

A

Incretin drugs use the amplifying pathway so are glucose dependant

SUs bind to the SUR1 of the ATP dependant K+ channels - glucose independent

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6
Q

What side effect is associated with DPP4 inhibitors?

A

Pancreatitis

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7
Q

How do DPP4 inhibitors work?

A

They inhibit DPP4 which breakdown GIP and GLP-1 (incretins) so with more of them in blood - amplified insulin secretion

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8
Q

Describe the incretin effect.
Where are the incretins released?
How is this affected in T2 diabetes?

A

Oral consumption of glucose leads to a greater increase of insulin due to incretins produced in the gut that amplify insulin secretion as they bind to their receptors on the pancreatic beta cell

GLP-1 - ileum
GIP - duodenum
(I before L, I released first in intestine)

In T2 diabetes this effect is greatly reduced

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9
Q

Match the following drug suffixes/prefixes/ drug names to their drug class

  • flozin
  • gliptin
  • tide
  • gliptin
  • gli-…-ide
Empagliflozin
semaglutide 
Alogliptin
 gliclazide
Pioglitazone
A
  • flozin (Empagliflozin) - SGLT2 inhibitors (think floz = flow = increase sugar in urine)
  • gliptin (Alogliptin) = DPP4 inhibitors (P = dPP4)
  • tide (semaglutide) = GLP-1 receptor agonist
  • gli-…-ide (gliclazide) = SUs (glide into coma into coma = hypoglycaemia = worrying side effect)

Pioglitazone = TZD (zone = movement of fat from visceral to subcutaneous = move zone)

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10
Q

What drug is contradicted in older patients but allowed in young obese female in particular?

A

Pioglitazone

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11
Q

How many times a day should metformin be taken?

A

BD

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12
Q

What is the very common side effect of metformin?

Why is it contradicted in kidney disease?

A

GI upset

Can cause MALA (metformin assoc. lactic acidosis)
- important to test for eGFR and U&Es as a result

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13
Q

How do thiazolidinediones (TZDs) work?
(link to increase weight side effect)

Name the TZD used in the UK?

A
Bind and activate PRAR-gamma
->
increase subcutaneous fat mass
-> 
decreases visceral fat
->
increase adiponectin
-> 
increase insulin sensitivity

pioglitazone

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14
Q

What are the two classes of incretin drugs?

A

DPP4 inhibitors

GLP-1 receptor agonists

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15
Q

What drug is given via 1x weekly injection as opposed to tablets?

A

Semaglutide

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16
Q

How do SGLT2 inhibitors work?

A

Partially block SGLT2 in kidneys -> increase in blood sugar urine secretion -> decrease in blood glucose and kcals

17
Q

Side effects of SGLT2 inhibitors?

A

Thrush
Polyuria and thirst
Fournier Gangrene - v rare but buzzword I feel

18
Q

What drugs are protective for the heart post coronary syndrome?

A
  • GLP-1Ra

- SLGT2i

19
Q

What oral drug requires blood glucose monitoring?

A

SUs due to risk of hypo

20
Q

What should all >50 T2 diabetic patients be started on for CV protection?

A

Statin

21
Q

If there is proteinuria present on dipstick what does this mean?

A

Impaired renal function -> changes what drug might decide to use

22
Q

What is the most important factor in diet when encouraging a patient to lose weight?

What specific components of the diet should be reduced/increased?

A

Maintenance to the diet

Increase fibre
Decrease fat

23
Q

What categories of people should be assessed for their diabetic risk when in clinic using computer scoring methods?

A
  • individuals >40
  • ethnic minority groups 25-39
  • individuals with conditions that raise risk of T2
24
Q

T1 diabetics can undergo carbohydrate counting to adapt their insulin treatment to best suit them.
What are the 3 steps involved?
What is the name of the education programme which teaches how to do this?

A
  1. Identify carbohydrates (CHO)
  2. How much CHO is in each meal?
  3. What is my insulin:CHO ratio and apply this

DAFNE = dose adjustment for normal eating

25
Q

Why are low GI diets no longer recommend for T1 diabetics?

A

There positive effect is so easily impacted by many variables e.g. how the food is cooked, what it is served alongside etc.

26
Q

How are the following monogenic diabetic conditions managed?

  • Neonatal
  • MODY caused by defect in glucokinase
  • MODY caused by defect in HNF-1alpha (transcription factor)
A

Neonatal - high dose SUs
MODY caused by glucokinase - no treatment at all
MODY caused by HNF-1alpha - low dose SUs

27
Q

How do T1DM use insulin on a daily basis?

A

Long acting insulin - to maintain basal levels

Short acting insulin - taken 15 mins prior to each meal

28
Q

How often should glucose levels be checked on IV insulin?

Once trasnferred from IV insulin back to SC, how many times should blood glucose be checked in the first 24hrs?

A

Hourly

4x

29
Q

How is a patient transferred from IV insulin back to SC?

A

SC must be given at a suitable mealtime and IV is stopped an hour after this

30
Q

When should SUs be taken?

A

20 mins before meal due to risk of hypo

31
Q

What is the MoA of SUs?

A

Close K+/ATP channels on beta cells -> continual depolarisation