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Exam 1 PNP > Type 2 Diabetes > Flashcards

Type 2 Diabetes Flashcards

1
Q

what is the pathophysiology of T2DM

A

genetic disposition + obesity lifestyle factors

insulin resistance
=
compensatoy beta cell hyperplasia (normoglycemia)
=
early beta cell failure (impaired glucose tolerance- pre diabetes)
=
beta cell failure late (diabetes)

can also be caused by primary beta cell failure (rare)

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2
Q

what are the components of the ominous octet that contribute to hyperglycaemia in T2DM

A 
decreased insulin secretion (pancreas)
increased glucagon secretion (pancreas)
decreased incretin effect (gut peptide)
increased hepatic glucose production (liver)
neurotransmitter dysfunction
increased lipolysis
increased glucose reabsorption (kidneys)
decreased glucose uptake (muscles)
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3
Q

why is the prevalence of T2DM increasing more than the incidence

A

as people are living longer

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4
Q

what ethnic group has a higher risk of diabetes

A

eastern Asian

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5
Q

insulin resistance is more assocaited with micro/macro vascular disease

A

macro

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6
Q

hyperglycaemia is more associated with micro/macro vascular disease

A

micro

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7
Q

how is CVD risk most effectively treated

A

statins/ anti-hypertensives

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8
Q

when is one blood test diagnostic for diabetes

A

when its over diagnostic limit and patient is symptomatic

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9
Q

what is the treatment areas for T2DM

A

lifestyle changes
glycaemic management- metformin (most), insulin (last line)
blood pressure management
lipid management- statin
antiplatelet therapy- aspirin, clopidogrel

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10
Q

what is the treatment for acute T2DM

A

basal bolus insulin

metformin

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11
Q

what is the first line treatment give to most people for glycaemic control

A

metformin

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12
Q

what is the mechanism of metformin

A

decreases hepatic gluconeogenesis

increased peripheral glucose uptake

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13
Q

what outcomes does metformin usually have

A

decreases HbA1c
weight neutral
no hypoglycaemia control when used as monotherapy
decreased Cancer and CHD risk

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14
Q

what are some adverse effects of metformin

A

GI, lactic acidosis

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15
Q

what can metformin be combined with as a second step

A 
SGLT2
glitazone
gliptin 
GLP-1R
SU
basal insulin
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16
Q

what is the mechanism of sulphonylurea

A

blocks beta cell KATP channels , increased 1st and 2nd phase insulin secretion

17
Q

what are the outcomes seen when using sulphonylurea

A

decrease in HbA1c
weight gain
hypoglycaemia

18
Q

what are adverse effects of sulphonylurea

A

abnormal LFTs

increased CHD

19
Q

name a sulphonylurea

A

gliclazide

20
Q

what is the maximum effective dose of gliclazide

A

80-120mg

21
Q

what happens as the dose of sulphonylureas is increased

A

efficacy is reduced

22
Q

what are gliptins

A

e.g. GLP-1 receptor agonist and DPP4 inhibitors

23
Q

how do DPP 4 inhibitors work

A

blocks action of DDP- an enzyme that destroys the hormone incretin

24
Q

how does GLP-1 receptor work

A

is an incretin- increases secretion insulin and somatostatin, reduces secretion of glucagon

25
Q

what are the outcomes of GLP-1 receptor agonists

A

lower HbA1c

increase in weight

26
Q

can GLP-1 help with hypoglycaemia

A

when used in combination with metformin and/or a sulphonylurea

27
Q

what is the outcome of DPP4 inhibitors

A

decrease HbA1c

weight neutral or decreased

28
Q

what do SGLT-2 inhibitors do

A

reduce the amount of glucose being absorbed in the kidneys, passed out in the urine instead of being reabsorbed into the blood

29
Q

how does glitazone work

A

lower insulin resistance, increasing peripheral glucose uptake via PPAYgamma activator

30
Q

what are the outcomes of glitazone

A

decrease HbA1c

increase weight

31
Q

what are the adverse affectes of glitazone

A

fracture risk increase
hepatoxicity
fluid retention

32
Q

what should you consider if drugs not working

A

adding on another instead of titrating up the dosage

33
Q

what is the max dosage or metformin

A

1000mg bid

34
Q

what is given if there is a history of cardiovascular disease

A

metformin + SGLT2

Exam 1 PNP (21 decks)

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