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Endocrinology > Introduction to diabetes mellitus > Flashcards

Introduction to diabetes mellitus Flashcards

1
Q

Metabolic actions of insulin relating to glucose

A

Decrease hepatic glucose output (HGO)

Increase glucose uptake in muscle

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2
Q

Metabolic actions of insulin relating to proteins

A

Decrease proteolysis

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3
Q

Metabolic actions of insulin relating to lipids

A

Decrease lipolysis

Decrease ketogenesis

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4
Q

What does insulin have mitogenic actions on?

A 
Lipoproteins
Smooth muscle hypertrophy
Ovarian function
Clotting
Energy expenditure
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5
Q

How does insulin drive glucose into muscle?

A

Via GLUT-4

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6
Q

Where is GLUT-4 stored?

A

In vesicles

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7
Q

What does insulin cause for GLUT-4?

A

GLUT-4 incorporated into the membrane on muscle cells
Hydrophilic core allows glucose transport
Hydrophobic exterior means it can sit in membrane

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8
Q

How does glucose uptake change when insulin is released?

A

Insulin causes a 7-fold increase in glucose uptake

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9
Q

How does insulin affect the use of protein in muscle cells?

A

Increase protein synthesis

Decrease proteolysis

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10
Q

Glucose in blood

A

Present all the time

Not only after meals

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11
Q

What is the name of stored glucose in the liver?

A

Glycogen

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12
Q

In the liver, when blood glucose is low, (fasting state) gluconeogenesis occurs

A

Break down protein

Gluconeogenic AAs can be used to make glucose

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13
Q

In the liver, when blood glucose is high and insulin is released

A

Gluconeogenic AAs can enter liver and be used to make protein

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14
Q

Carbohydrate in the form of glycogen in liver and muscle is a

A

short term energy store

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15
Q

Fat has a high energy concentration

A

Takes a long time to break down

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16
Q

Insulins’ effect on adipocytes

A

In blood, Triglyceride broken down by lipoprotein lipase (encouraged by insulin), so
Glycerol and NEFAs can enter adipocyte.
Glucose can enter via GLUT-4 and can be used to make NEFAs and glycerol-3-P.
Insulin within cell encourages formation off triglyceride

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17
Q

Triglyceride can be broken down in fight or flight

A

To make glycerol and NEFA

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18
Q

NEFA

A

Non-esterified fatty acid

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19
Q

How do we store fat?

A

In adipocytes

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20
Q

Omental adipocytes

A

more metabolically and endocrinology active due to anatomical location (Central)

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21
Q

What does more omental fat increase?

A

Risk of heart disease

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22
Q

Glycerol enters liver cells

A

Phosphorylated to make Triacylglyerol (Triglyceride)
Triglyceride can be used to make glycerol and then glucose
= Gluconeogenesis

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23
Q

NEFA in liver cells

A

Can’t be used to make glucose, only the glycerol bit

24
Q

What can the brain use as energy substrates?

A

Glucose

Ketone bodies

25
Q

What can’t the brain use as an energy substrate?

A

Fatty acids

Brain fundamentally different from other parts of body

26
Q

Fatty acids can be used to make ketone bodies

A

Insulin stops this

Glucagon stimulates this

27
Q

How can NEFAs be used to make ketone bodies?

A

NEFA enter liver
NEFA broken into Acetoacetate and 3-Hydroxybutarate
Which leave liver as ketone bodies

28
Q

What does the conversion of NEFAs to ketone bodies allow?

A

Brain function after fasting

29
Q

If someone has ketones present and a high blood glucose

A

They are insulin deficient

As when there is plenty of glucose, it is unnecessary to make ketone bodies

30
Q

What can glycogen in liver be broken down into?

A

Glucose by glucagon

= glycogenolysis

31
Q

2 ways of supporting HGO

A

Glycogenolysis

Gluconeogenesis

32
Q

Why can’t muscle release glucose?

A

Glycogen in muscle is just used by muscle, can’t be used to support plasma glucose

33
Q

Fasted state concentrations

A

Low insulin to glucagon ratio
Glucose conc. 3-5.5 mol/l
Increase conc. NEFA
Decrease conc. AA

34
Q

Fasted state actions

A

Increase proteolysis, lipolysis, glycogenolysis and gluconeogenesis
Increase HGO

35
Q

Fasted state use of energy substrates

A

Muscle uses lipids
Brain uses glucose, later ketones
Increased ketogenesis in brain when prolonged fasting

36
Q

Fed state concentrations

A

Stored insulin released, then 2nd phase
High insulin to glucagon ratio
Increase conc. glycogen

37
Q

Fed state actions

A

Increase protein synthesis and lipogenesis

Decrease proteolysis and gluconeogenesis

38
Q

Presentation of T1DM

A

Absolute insulin deficiency

39
Q

How does weight loss occur in T1DM?

A

Proteolysis and lipolysis continue

40
Q

T1DM Glucose exceeds kidneys ability to reabsorb glucose

A

= Glucose and ketones in urine

Glycosuria and ketonuria with osmotic symptoms

41
Q

Insulin induced hypoglycaemia

A

Increased insulin so Glucose enters muscle
Glucagon increases, triumphs over insulin
Increase HGO with gluconeogenesis and glycogenolysis
Increase in catecholamines, cortisol and growth hormone

42
Q

How to treat insulin induced hypoglycaemia in an emergency

A

Intravenous/ intramuscular glucagon

43
Q

T2DM insulin resistance resides in

A

Liver, muscle and adipose tissue

Affects intermediary metabolism, glucose and fatty acids

44
Q

In T2DM insulin resistance, there is usually enough insulin to suppress

A

Ketogenesis
Proteolysis
So don’t lose weight or produce unnecessary ketones

45
Q

What are the 2 effects insulin has after binding to the insulin receptor?

A

MAP Kinase pathway

Insulin receptor PI3 Kinase pathway

46
Q

What is the Insulin receptor PI3 Kinase pathway?

A

Metabolic actions on glucose, fats and AAs

47
Q

What is the MAP kinase pathway?

A

Causes growth and proliferation

48
Q

Which pathway is affected in T2DM insulin resistance?

A

Insulin resistance PI3 Kinase pathway

49
Q

Compensatory hyperinsulinemia

A

Functional pancreas but
resistance in the PI3 kinase pathway leads to excessive insulin production to reduce blood sugar
Thus increasing MAP kinase pathway - overstimulating growth (mitogenic) pathway

50
Q

What does compensatory hyperinsulinemia cause?

A

Patient does NOT have T2DM

May have high BP, risk of ischaemic heart disease

51
Q

Hyperinsulinaemic effect of mitogenic effects in insulin resistance

A

Low HDL cholesterol
Smooth muscle hypertrophy
Reduced ovarian function
Abnormal effects on clotting and energy expenditure

52
Q

Metabolic effect in insulin resistance

A 
Insulin resistance effect 
Fasting glucose >6mmol
High [TG]
Low [HDL]
High BP 
High waist circumference
53
Q

BP is a major issue in T2DM

A

Causes damage to arteries

54
Q

Presentation of T2DM

A 
Insulin resistance
Majority obese
Dyslipidaemia
Later insulin deficiency
Hyperglycaemia
Less osmotic symptoms
With complications
55
Q

Dyslipidaemia

A

Abnormal carriage of lipids in circulation

56
Q

Why is T2DM often presented with complications?

A

Often not found for years

Subtle

57
Q

Healthy eating for T2DM

A

Total calorie control
Reduce calories from fat and refined carbohydrate
Increase soluble fibre and calories from complex carbohydrate
Decrease sodium

Endocrinology (12 decks)

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