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Flashcards in Diabetes management Deck (46):
1

Describe the difference between type 1 and type 2

type 1= autoimmune, absolute insulin deficiency; type 2= insulin resistance and varying degrees of insulin secretion

2

What are the limits for impaired fasting glucose?

6.1-6.9 mmol/l

3

How is diabetes mellitus diagnosed?

Fasting blood glucose of > 7 mmol/l; HbA1C> 48 mmol/mol2 hr and value > 11.1 mol/l in the OGTT

4

What would you look out for if you suspect type 1 diabetes?

antiGAD and islet cells auto antibodies

5

What are the principles of type 2 diabetes management?

weight loss, exercise, oral hypoglycemic agents, regular health checks (monitor Hb1ac), address other CV risk factors such as lipids, hypertension, smoking etc.

6

What are the benefits of exercise (in terms of glucostasis)?

Increases glucose intake into muscle, improved sensitisation of muscle to exercise can last 2-3 days

7

What is the first line of medical treatment in diabetes type 2?

Metformin (biguanides)--> inhibits hepatic glucose output, no weight gain

8

what can cause weight gain (T2 diabetes medication)

sulfonylureas. It stimulates B cell insulin release

9

What is acarbose?

inhibits breakdown of starches and disarccarides in the gut.

10

what are GLP1 analogues?

exenatide- slow gastric emptying and improve satiety

11

DPP4- inhibitors?

prolong GLP1 action-->improved B cell sensing, increase insulin secretion, decrease glucagon secretion

12

SLGT2 inhibitors?

inhibits SGLT2 main glucose transporter in the renal tubule-->to promote glycosuria thus lowering blood glucose

13

management of DKA?

1. replace fluid (500-1000mls of saline)
2. insulin infusion (make sure potassium is within normal range. if not, delay insulin and start IV potassium first)
3. glucose if hypoglycaemia occurs

14

what is thiazolidinediones?

Thiazolidinediones causes insulin sensitisation.
The drug binds to PPAR’s (peroxisome proliferator-activated receptors). When PPAR’s are activated they cause transcription of a number of genes
These activated genes ultimately result in decreased insulin resistance

15

how do we manage peripheral neuropathy in diabetic patients?

Frequent visits to the podiatrist, neuropathic pain management with gabapentin/pregabalin etc.

16

how do we prevent diabetic complications in diabetics?

frequent visits to podiatrist, GP, optometrist and frequent assessment of BSLs and HBA1C. Medication compliance

17

what would we prescribe in a diabetic patient with hypertensions and microalbuminemia?

Ace inhibitor- to slow progression of nephropathy

18

how do we manage hyperosmolar hyperglycaemia?

1. fluid replacement
2. Insulin, + glucose later
3. Potassium replacement
hence similar to DKA

19

for sick day management- what are the recommendations for how often to check BSL?

ever 2-4 hrs

20

why do we have sick day management protocols?

Acute illness in a person with diabetes is usually associated with increased secretion of stress hormones such as glucagon, cortisol and adrenaline. These changes promote hyperglycaemia and consequent dehydration, and may lead to DKA in type 1 diabetes, or Hyperosmolar hyperglycaemia in type 2 diabetes.

21

what is the target HbA1c levels for a patient with T2 diabetes mellitus?

The general HbA1c % should be less than 7, however the HbA1c target should really be INDIVIDUALISED for the patient

22

how do we manage hypoglycaemia?

administer glucose and glucagon

23

what do we have to consider if a diabetic patient comes in with high BSLs?

whether the diabetic patient has an illness such as infection- as it can throw off blood glucose control a bit

24

a type 2 diabetic patient comes in with high blood sugars- approx 20.6, ketones in the urine, polyuria and polydipsia and glucouria. What are you worried about? What do you do?

hyperosmolar hyperglycaemia which can lead to a coma.

Do a blood gas and at anionic gap

25

why do we worry about diabetic patients on beta blockers?

beta blockers would blunt the sympathetic overdrive associated with hypoglycaemia, and so we might miss signs of hypoglycaemia

26

what are some short acting insulins?

aspart (novorapid), lispro (humalog), glulisine

27

what are some long acting insulins?

glargine (lantus), determir (levemir)

28

which sulfonylurea is recommended?

glicazide

29

is DKA associated with hypokalemia or hyperkalemia?

hyperkalemia

30

what do you need to consider before commencing a patient on sulfonylureas who is already on metformin? If sulfonylureas was contraindicated, what other drug could you suggest?

need to determine their occupation/job as sulfonylureas put you at risk of developing hypoglycaemia. Possibly suggest DPP4 inhibitor or GLP 1 agonist

31

what do we mean by NPH insulin?

medium acting insulin. NPH= neutral protamine hagedoone

32

what are mixed insulins made up of? e.g. novomix,

medium acting NPH insulin and short acting insulins

33

what is the onset of action for short acting insulins?

10-30 mins

34

what is the onset of action for long acting insulins?

2-4 hrs

35

main finding for the DCCT study?

first evidence that intensive glycaemic control reduces complications in T1 diabetes. Random controlled trial. Earlier intervention, better prognosis

36

what is the legacy effect from the DCCT trial?

quite a few years of good glucose control--> leads to reduction in CVD microvascular complications many years later

37

Tell me about the ACCORD trial

Group of long term T2 diabetes patients; split into intensive group and standard group. In the intensive group they tried to bring the HbA1c to 6.4%. 3.5 years later the trial was stopped bc mortality rate in intensive group was high due to severe hypoglycaemic events. So this has shaped our approach these days that we aggressively try to control HbA1c EARLY in the disease whereas we try to relax this in late diabetes.

38

what must the HbA1c target be balanced against?

risk of hypoglycaemia

39

what are some things a dietician can recommend to help with stabilising blood sugar levels

low GI foods

40

what is the basic principle of basal bolus insulin therapy?

what are some problems of this therapy?

mimics normal insulin production and control post prandial hyperglycaemia.

1. Subcutaneous --> systemic circulation --> liver
rather than endogenous insulin going straight into the portal vein and to the liver.

2. glucose levels naturally vary every day

3. onset of action of fast acting insulin is generally 10-30 mins rather than straightaway in endogenously produced insulin

41

aside from metformin, which hypoglycaemic agents help with losing weight?

GLP1 (e.g. exenatide) and DPP4 inhibitors

42

what two drugs increase insulin sensitivity?

metformin and glitazone

43

SE of pioglitazone

weight gain, fluid retention, bone loss. Hence sort of going out of favour despite having good efficacy for reducing HbA1c

44

if a Type 2 diabetes patient who was on metformin and sulfonylureas now requires insulin- what happens to the sulfonylureas?

If the patient is just going on basal insulin- then sulfonylureas is continued

if the patient is also going to have bolus insulin before meal times- sulfonylureas is removed from the treatment protocol

45

when is foxiga (SGLT1 inhibitors) not recommended?

in elderly individuals who are more likely to become dehydrated due to excess glucouria

46

what is the samogyi effect? Give me the pathophysiology.

rare phenomenon of posthypoglycaemic hyperglycaemia in the morning.

This may be seen when too much hypoglycaemia may result in a rebound hyperglycaemia.

Can be caused by too much insulin given, missed meals/snacks

pathophysiology- hypoglycaemia stimulates cortisol, glucagon and adrenaline to increase release of glucose in the blood stream