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BRS 4 Endocrinology > 1a Diabetes Mellitus > Flashcards

1a Diabetes Mellitus Flashcards

1
Q

Describe the normal response to feeding?

A
  1. Eat a meal
  2. Glucose levels in the blood are elevated
  3. Pancreas releases insulin
  4. Insulin binds to insulin receptor
  5. This causes GLUT4 receptors to move to the plasma membrane of the cells
  6. Therefore glucose is able to pass into the muscle or fat cell
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2
Q

Where are GLUT 4 receptors found?

A

Muscle or adipose tissue

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3
Q

How does GLUT 4 respond to insulin?

A

It is highly insulin dependent

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4
Q

Where is GLUT 4 found before moving to the ccell membrane?

A

Found in vesicles –moves from vesicles to membrane in the presence of insulin

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5
Q

What happens to gluconeogenesis when insulin levels are high?

A

Gluconeogenesis is turned off

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6
Q

What happens to glycogen levels when insulin is released?

A

Glycogen levels increase as the glucose is stored as glycogen

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7
Q

Why is triglycerides the most useful energy store?

A

It is fully reduced therefore is the most efficient energy store

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8
Q

What are NEFAs?

A

Non-esterified fatty acids

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9
Q

How do triglycerides form?

A

They form through an esterification reaction of three NEFA’s and a glycerol molecule

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10
Q

What is the purpose of adipocytes?

A

To store energy

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11
Q

What does lipoprotein lipase do?

A

Breaks down triglycerides into the glycerol and NEFA molecule so that they can leave circulation and enter into the adipocyte for storage

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12
Q

What affect does insulin have on lipoprotein lipase?

A

Insulin switches on lipoprotein lipase

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13
Q

What happens to the glycerol in adipose cells from the breakdown of he triglyceride?

A

Can be converted into glucose - via gluceoneogenesis by conversion into dihydroxyacetone phosphate and then into GALP

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14
Q

What are the effects of insulin in the fed state?

A

INCREASED:
- Glycogen store
- Glucose uptake
- Lipogenesis
- Protein synthesis

DECREASED:
- Ketogenesis
- Gluconeogenesis

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15
Q

How does insulin affect proteolysis and protein synthesis respectively in myocytes in the fed state?

A

Inhibits proteolysis as proteins are not needed as fuel
Stimulates protein synthesis from amino acids for storage

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16
Q

What effect does GH and IGF-1 have on protein synthesis in myocytes?

A

Stimulates it

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17
Q

What effect does cortisol have on proteolysis in myoctes?

A

Stimulates it

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18
Q

What is the brain’s main energy substrate?

A

Glucose

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19
Q

Can the brain use ketone bodies or fatty acids as a source of energy?

A

Can use ketone bodies as a last resort, but not fatty acids

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20
Q

Why can fatty acids not be used in the brain as a source of fuel?

A

The fatty acids cannot pass the blood brain barrier

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21
Q

What happens to insulin levels during starvation?

A

They fall

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22
Q

What happens to glucose uptake in cells during starvation?

A

It falls

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23
Q

What happens to hepatic glucose output during starvation?

A

It rises

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24
Q

What happens to lipolysis when insulin levels are low?

A

Lipolysis is switched on

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25
Q

What happens in lipolysis?

A

Non esterified fatty acids are released

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26
Q

What happens to the non-esterified fatty acids that are released during lipolysis?

A

They are converted into ketones

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27
Q

What happens to blood pH when ketones are made and why?

A

Blood pH starts to fall - this is because ketones are slightly acidic

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28
Q

What happens to gluconeogenesis when insulin levels are low?

A

The liver turns on guconeogenesis

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29
Q

What is hepatic glycogenolysis?

A

The generation of glucose from stored glycogen in the liver

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30
Q

What effect does low insulin levels have on beta oxidation?

A

Increases beta oxidation

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31
Q

What is produced in beta oxidation?

A

acetyl coa which is then used to produce ketone bodies in the starving state

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32
Q

What are the three ketone bodies?

A

Acetone
Acetoacetate
3-beta hydroxybutyrate

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33
Q

How are ketone bodies produced?

A

In a fasting state, NEFAs released from adipocytes are taken up by the liver
Glucagon is released, which promotes conversion of fatty acyl CoA into ketone bodies as an alternative energy source

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34
Q

What happens in myocytes when insulin levels are low?

A

No glucose is pumped into muscle cells, so the onboard stores of glycogen are used to make glucose, which then undergoes glycolysis and Krebs cycle to make ATP

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35
Q

What happens to proteolysis when insulin levels are low?

A

It increases - proteins are broken down into amino acids

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36
Q

What happens to hepatic glucose output when insulin levels are low?

A

It increases

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37
Q

What happens to ketogenesis when insulin levels are low?

A

It increases

38
Q

What type of disease is Diabetes Mellitus?

A

An autoimmune condition

39
Q

What is destroyed in T1DM?

A

The ISLET cells

40
Q

What word is used to describe the glucose levels of those with T1DM?

A

Hyperglycemia

41
Q

Why does ketone production occur in T1DM?

A

There is a lack of insulin, therefore your body will behave as if it starving, and will increase ketone body production for energy

42
Q

What is ketoacidosis?

A

When you have very large amounts of ketone bodies so they become acidic

43
Q

If you have the presence of ketone, which type of diabetes do you have?

A

Type 1

44
Q

What is the pH range for patients with ketoacidosis?

A

A pH less than 7.3

45
Q

What are some complications of ketoacidosis?

A

Patients with ketoacidosis experience low pH in the blood as the ketones are acidic - a low pH is associated with decreased brain function, which can make the patient unconscious, and experience a low mood, and can also lead to death

46
Q

What are some osmotic symptoms of T1DM?

A

Polyuria, polydipsia and nocturia

47
Q

What is polyuria?

A

A lot of urine

48
Q

What is polydipsia?

A

Drinking a lot of water as you are thirsty often

49
Q

What is nocturia?

A

Waking up at night because you have to urinate

50
Q

What level does resting glucose have to be in order to be diagnosed with T1DM?

A

> 11.1mmol/L

51
Q

What level does fasting glucose have to be in order for a diagnosis of T1DM to be made?

A

> 7.0mmol/L

52
Q

Above what value is HbA1c considered high?

A

> 48mmol/mol

53
Q

What are the values for the diagnosis of diabeteic ketoacidosis?

A
  • pH < 7.3
  • High levels of ketones
  • HCO3 < 15mmol/L
  • Glucose > 11
54
Q

How many positive tests do you require for the diagnosis of T1DM?

A

2 positive tests or 1 positive test and osmotic symptoms

55
Q

Why is measuring C-peptide a useful diagnostic test?

A

C-peptide is cleaved from pro-insulin along with insulin
Thus low C-peptide indicates low insulin

56
Q

What antibodies can be tested for a T1DM diagnosis?

A

GAD (glutamic acid decarboxylase)
IA2 (islet antigen 2)

57
Q

How do you treat T1DM?

A

Replace insulin through injections at a specific dose relative to the meal you are going to eat

58
Q

What happens if you inject insulin without eating food?

A

Insulin results in more glucose being absorbed, so much so that you become hypoglycaemic

59
Q

What is hypoglycaemia?

A

When blood sugars are very low

60
Q

What happens to the brain during hypoglycaemia?

A

Since insulin is present, ketone production is stopped
This results in no fuel for the brain, affecting its function
Results in confusion and unconsciousness

61
Q

What four things increase to counter act hypoglycaemia?

A

Glucagon, catecholamines, cortisol and growth hormone

62
Q

What happens to the hepatic glucose output when the body induces the counter regulatory response to hypoglycaemia?

A

It increases with glycogenolysis and gluconeogenesis

63
Q

What is impaired awareness of hypoglycaemia?

A

The reduced ability to recognize symptoms of hypoglycaemia due to loss of counter regulatory response which leads to recurrent hypoglycaemia

64
Q

What might someone who is having hypoglycaemia feel?

A

Confused, aggressive, irrational

65
Q

Autonomic symptoms of hypoglycaemia?

A

Sweating, pallor, palpitations and shaking

66
Q

What is the definition of severe hypoglycaemia?

A

An episode in which a person requires third party assistance to treat

67
Q

What are some neuroglycopenic symptoms of hypoglycaemia?

A

Slurred speech, poor vision, confusion, seizures and loss of consciousness

68
Q

What can you give a patient suffering with unconsciousness due to hypoglycaemia?

A

1mg glucagon injection

69
Q

What can be given to patients suffering from an acute hypo episode?

A

Jelly babies, lucozade, glucogel

70
Q

What is T2DM?

A

Where you have insulin resistance in the liver, muscle and adipose issue, however enough insulin to suppress ketogenesis and proteolysis

71
Q

Will you ever find ketoacidosis in patients with T2DM?

A

No

72
Q

What are some signs and symptoms of T2DM?

A

High fasting glucose >7 mmol/L
High random glucose >11.1 mmol/L
Large waist circumference
Hypertension (135/80 mmHg)

73
Q

Which type of diabetes is associated with weight gain and loss respectively?

A

Gain = T2
Loss = T1

74
Q

Why does T1DM result in polyuria?

A

The excess glucose ends up in the urine, which draws more water into the urine via osmosis, hence the volume of urine increases

75
Q

What are the risk factors for T2DM?

A

Age, PCOS, High BMI, family history, ethnicity, inactivity

76
Q

What are the four ways to manage T1DM?

A

Education
Technology
Exogenous insulin
Self monitoring of insulin

77
Q

What is the basal bolus regime for insulin?

A

Basal (long acting) insulin is given once
Bolus is given throughout day before meals in order to manage the rises in glucose after meals

78
Q

What four ways can T2DM be managed?

A

Education
Diet
Exercise
Oral medication - to stimulate the pancreas to increase insulin production

79
Q

What other microvascular systems can be affected due to diabetes?

A

Retinopathy
Neuropathy
Nephropathy

80
Q

What macro vascular systems can be affected by T2DM?

A

Cardiopathy eg heart attack

81
Q

What is dyslipidemia?

A

Disturbances in fat metabolism cause changes in the lipid concentration in the blood

82
Q

What is diabetic retinopathy?

A

High glucose levels in the blood result in damage to the blood vessels which supply the retina

83
Q

How does insulin interact with adipocytes in a fed state?

A
  1. Increases glucose uptake via GLUT-4
  2. Carrys out lipogenesis by converting glycerol and non-esterified fatty acids into triglycerides again for later use
  3. Inhibits triglyceride breakdown in adipocytes as no alternative energy source is needed
84
Q

What happens to adipocytes in fasting state (recall the two hormones involved)?

A

Blood glucose and insulin are low
Thus GH and cortisol are secreted and stimulate lipolysis, releasing glycerol and NEFAs

85
Q

In the fasting state what happens to the glycerol taken up by the liver?

A

Converted to glucose in gluconeogenesis

86
Q

In the fed state what happens to the glycerol taken up by the liver?

A

Converted into triglycerides

87
Q

In the fed state, what does insulin do once NEFA is uptaken by the liver?

A

NEFAs are converted into Fatty Acyl-CoA
Insulin inhibits the conversion of Fatty Acyl-CoA into ketone bodies
This prevents it from being used as an alternative metabolic substrate to glucose

88
Q

In the fed state what happens to glucose in the liver?

A

Converted to G6P
Then to glycogen (stimulated by insulin)

89
Q

In the fasting state what happens to glycogen in the liver?

A

Broken down to G6P
Then to glucose and released from liver

90
Q

What does it mean if there is a high level of ketones and glucose?

A

There is an issue with insulin secretion

BRS 4 Endocrinology (20 decks)

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