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eLCRS - 엔도 > Endo 16: Type II diabetes mellitus > Flashcards

Endo 16: Type II diabetes mellitus Flashcards

1
Q

Define Diabetes Mellitus

A

State of chronic hyperglycemia sufficient to cause long term damage to specific tissues, notably the retina, kidneys, nerves + arteries

note: fasting glucose level >7mmol/L

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2
Q

What are 3 major factors that influence the pathophysiology of T2DM ?

A
  • genetics
  • intrauterine environment (causes epigenetic changes )
  • adult environment
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3
Q

Insulin resistance + insulin secretion defects causes :

A

T2DM

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4
Q

What is MODY?

A
  • maturity onset diabetes of the young
  • autosomal dominant
  • -> involves mutation of transcription factor genes glucokinase genes
  • -> single gene hereditary condition

–> ineffective pancreatic B-cell insulin production

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5
Q

Insulin leads to _______
which stimulates the mitogenic pathway

what is the effect of this?

A

Insulin leads to DYSLIPIDAEMIA
which stimulates the mitogenic pathway

effect:
- causes smooth muscle cell hypertrophy
- -> causes increase in BP
- -> can cause microvascular disease

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6
Q

How is low birth rate linked to diabetes?

A
  • low birth weight increase risk of impaired glucose tolerance + diabetes

–> epigenetic effect

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7
Q

As we age, we secrete more / less insulin

and we become more/ less insulin resistant

A

As we age, we secrete more insulin

because with age we become more insulin resistant

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8
Q

How might T2DM present?

A
  • obesity
  • insulin resistance
  • insulins secretion deficiency
  • hyperglycemia
  • dyslipidaemia
  • acute/chronic complication
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9
Q

How does insulin lower blood glucose level?

A
  • by reducing HGO
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10
Q

what happens to HGO before and after a meal ?

A

before meal = HGO maintains blood glucose level at 4 mmol/L

after meal = insulin stops HGO

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11
Q

IN T2DM:

THERE IS INSUFFICIET INSULIN TO INHIBIT HGO + INSUFFICIENT INSULIN TO MOVE GLUCOSE INTO MUSCLE + FAT

A

-

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12
Q

what is the relationship between insulin sensitivity + insulin secretion in NORMAL individuals?

A

with age insulin sensitivity decreases
–> so insulin secretion increases to maintain normal blood glucose levels

i.e insulin resistance increases with age

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13
Q

what is the relationship between insulin sensitivity + insulin secretion in DIABETIC individuals?

A

with age insulin sensitivity decreases

–> but can’t increase insulin secretion sufficiently

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14
Q

What are major effects of insulin resistance?

A
  • there is an increase HGO

- there is a decrease in glucose uptake into tissues

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15
Q

perturbation in gut microbiota

A

bacteria in gut modulates intermediary metabolism

  • associate with obesity, T2DM
  • involved in host signaling
  • involved in bacterial lipopolysaccharides fermentation to short chain FA
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16
Q

What is a common side effect of diabetes treatments

except:

A
  • weight gain

except metformin

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17
Q

How might T2DM present?

A
  • osmotic symptoms
  • infections
  • screening test

if with complication

  • acute: hyperosmolar coma
  • chronic: Ischaemic heart disease, retinopathy
18
Q

What are some microvascular complications associated with T2DM ?

A
  • retinopathy
  • nephropathy
  • neuropathy
19
Q

What are some macrovascular complications associated with T2DM ?

A
  • ischemic heart disease
  • cerebrovascular
  • renal artery stenosis
20
Q

What are some metabolic complications associated with T2DM ?

A
  • lactic acidosis

- hyperosmolar

21
Q

How would you manage T2DM?

A
  • educate
  • change diet
  • pharmacological treatment
  • complication screening
22
Q

How would you change lifestlyle/diet of patients with T2DM?

A
  • increase exercise
  • reduce refined carb
  • increase complex carb
  • reduce fat
  • increase unsaturated fat proportion
  • increase soluble fibre
  • less salt
23
Q

How does Metformin act as a treatment method for T2DM?

A
  • biguanide
  • acts on LIVER
  • reduced insulin resistance
  • -> reduces HGO
  • -> increases peripheral glucose disposal

note:
avoid if severe liver/heart/ mild renal failure

24
Q

How does Sulphonylurea act as a treatment method for T2DM?

A
  • they block the ATP sensitive K+ channel in Beta cell
  • which causes depolarization
  • activates VGCC
  • causes Ca2+ influx
  • which causes insulin secretion
25
Q

How does Acarbose act as a treatment method for T2DM?

A
  • acarbose = alpha glucosidase inhibitor
  • prolongs absorption of oligosccharides
  • allows insulin secretion to cope after loss of 1st phase insulin response
26
Q

What is a major side effect of acarbose?

A
  • flatus
27
Q

How do Thiazolidinediones act as a treatment method for T2DM?

A

Thiazolidinediones = peroxisome proliferator activated receptor (PPAR-gamma) agonists

  • they are insulin sensitisers
  • increases glucose uptake in muscles

e.g pioglitazone

28
Q

How do GLP-1 act as a treatment method for T2DM?

A
  • it acts to stimulate insulin + suppress glucagon
  • it restores B-cell glucose sensitivity
  • decreases glucagon conc
  • decreases glucose conc

–> GLP-1 = injectable

29
Q

What is the dilemma with GLP-1 and how is this overcome?

A

dilemma:
GLP -1 has short half life
–> due to rapid degradation
by DPP4

overcome by gliptins:

  • gliptins = DPP4 inhibitors
  • -> increases half life of exogenous GLP-1
30
Q

note: other aspects of control
- BP
- diabetic dyslipidaemia

A

-

31
Q

Compare between T1DM vs T2DM

A

T1DM

  • prevalence = lower
  • onset: acute in children/teens
  • often thin
  • uncommon family history
  • ketosis prone
  • HLA association: DR3, DR4
  • Islet Bcell = destroyed

T2DM

  • prevalence = higher
  • onset: gradual in middle age
  • often obese
  • common family history
  • NOT ketosis prone
  • NO HLA association
  • islet Bcell = functioning
32
Q

note:
Fasted glucose level < 6 mmol/L = normal
faster glucose level after 2 hours < 7.8 mmoL = normal

A

-

33
Q

glucose has

A
  • mitogenic pathway
  • metabolic dyslipidaemia

–> both can lead to macrovascular diseases

34
Q

note: 70% of monozygous twins = will have T2D

40% of dizygous twin = will have T2D

A

-

35
Q

In T2DM –> insulin administration is more/less effective in controlling blood glucose levels

A

In T2DM –> insulin administration is LESS effective in controlling blood glucose levels

36
Q

insulin switches off lipolysis
- Tri glycerol(TG) broken down to glycerol –> glucose
- glucose can’t be taken up into the muscle
–> so there is high level of glucose in the blood
then NEFA comes in –> forms VLDL - TG
–> there is increase in small dense VLDL (which is atheromatic)

A

-

37
Q

NOTE:
FAT IS AN ENDOCRINE SYSTEM
—> produces hormones

A

-

38
Q

Central obesity = more/less risky than peripheral obesity

why?

A

Central obesity = more risky than peripheral –> due to effect of metabolism effects of the liver

39
Q

what is orlistat

A
  • GI lipase inhibitor
40
Q

how are SGLT2 inhibitors used to in T2DM

A

acts on kidney
blocks uptake of glucose so glucose in excreted (glycosuria)

– > and they also lower mortality (esp heart failure)

eLCRS - 엔도 (20 decks)

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