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BRS 4 Endocrinology > 1a Diabetes Mellitus > Flashcards

1a Diabetes Mellitus Flashcards

(90 cards)

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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
What happens in lipolysis?
Non esterified fatty acids are released
26
What happens to the non-esterified fatty acids that are released during lipolysis?
They are converted into ketones
27
What happens to blood pH when ketones are made and why?
Blood pH starts to fall - this is because ketones are slightly acidic
28
What happens to gluconeogenesis when insulin levels are low?
The liver turns on guconeogenesis
29
What is hepatic glycogenolysis?
The generation of glucose from stored glycogen in the liver
30
What effect does low insulin levels have on beta oxidation?
Increases beta oxidation
31
What is produced in beta oxidation?
acetyl coa which is then used to produce ketone bodies in the starving state
32
What are the three ketone bodies?
Acetone Acetoacetate 3-beta hydroxybutyrate
33
How are ketone bodies produced?
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
34
What happens in myocytes when insulin levels are low?
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
35
What happens to proteolysis when insulin levels are low?
It increases - proteins are broken down into amino acids
36
What happens to hepatic glucose output when insulin levels are low?
It increases
37
What happens to ketogenesis when insulin levels are low?
It increases
38
What type of disease is Diabetes Mellitus?
An autoimmune condition
39
What is destroyed in T1DM?
The ISLET cells
40
What word is used to describe the glucose levels of those with T1DM?
Hyperglycemia
41
Why does ketone production occur in T1DM?
There is a lack of insulin, therefore your body will behave as if it starving, and will increase ketone body production for energy
42
What is ketoacidosis?
When you have very large amounts of ketone bodies so they become acidic
43
If you have the presence of ketone, which type of diabetes do you have?
Type 1
44
What is the pH range for patients with ketoacidosis?
A pH less than 7.3
45
What are some complications of ketoacidosis?
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
What are some osmotic symptoms of T1DM?
Polyuria, polydipsia and nocturia
47
What is polyuria?
A lot of urine
48
What is polydipsia?
Drinking a lot of water as you are thirsty often
49
What is nocturia?
Waking up at night because you have to urinate
50
What level does resting glucose have to be in order to be diagnosed with T1DM?
>11.1mmol/L
51
What level does fasting glucose have to be in order for a diagnosis of T1DM to be made?
>7.0mmol/L
52
Above what value is HbA1c considered high?
>48mmol/mol
53
What are the values for the diagnosis of diabeteic ketoacidosis?
* pH < 7.3 * High levels of ketones * HCO3 < 15mmol/L * Glucose > 11
54
How many positive tests do you require for the diagnosis of T1DM?
2 positive tests or 1 positive test and osmotic symptoms
55
Why is measuring C-peptide a useful diagnostic test?
C-peptide is cleaved from pro-insulin along with insulin Thus low C-peptide indicates low insulin
56
What antibodies can be tested for a T1DM diagnosis?
GAD (glutamic acid decarboxylase) IA2 (islet antigen 2)
57
How do you treat T1DM?
Replace insulin through injections at a specific dose relative to the meal you are going to eat
58
What happens if you inject insulin without eating food?
Insulin results in more glucose being absorbed, so much so that you become hypoglycaemic
59
What is hypoglycaemia?
When blood sugars are very low
60
What happens to the brain during hypoglycaemia?
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
What four things increase to counter act hypoglycaemia?
Glucagon, catecholamines, cortisol and growth hormone
62
What happens to the hepatic glucose output when the body induces the counter regulatory response to hypoglycaemia?
It increases with glycogenolysis and gluconeogenesis
63
What is impaired awareness of hypoglycaemia?
The reduced ability to recognize symptoms of hypoglycaemia due to loss of counter regulatory response which leads to recurrent hypoglycaemia
64
What might someone who is having hypoglycaemia feel?
Confused, aggressive, irrational
65
Autonomic symptoms of hypoglycaemia?
Sweating, pallor, palpitations and shaking
66
What is the definition of severe hypoglycaemia?
An episode in which a person requires third party assistance to treat
67
What are some neuroglycopenic symptoms of hypoglycaemia?
Slurred speech, poor vision, confusion, seizures and loss of consciousness
68
What can you give a patient suffering with unconsciousness due to hypoglycaemia?
1mg glucagon injection
69
What can be given to patients suffering from an acute hypo episode?
Jelly babies, lucozade, glucogel
70
What is T2DM?
Where you have insulin resistance in the liver, muscle and adipose issue, however enough insulin to suppress ketogenesis and proteolysis
71
Will you ever find ketoacidosis in patients with T2DM?
No
72
What are some signs and symptoms of T2DM?
High fasting glucose >7 mmol/L High random glucose >11.1 mmol/L Large waist circumference Hypertension (135/80 mmHg)
73
Which type of diabetes is associated with weight gain and loss respectively?
Gain = T2 Loss = T1
74
Why does T1DM result in polyuria?
The excess glucose ends up in the urine, which draws more water into the urine via osmosis, hence the volume of urine increases
75
What are the risk factors for T2DM?
Age, PCOS, High BMI, family history, ethnicity, inactivity
76
What are the four ways to manage T1DM?
Education Technology Exogenous insulin Self monitoring of insulin
77
What is the basal bolus regime for insulin?
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
What four ways can T2DM be managed?
Education Diet Exercise Oral medication - to stimulate the pancreas to increase insulin production
79
What other microvascular systems can be affected due to diabetes?
Retinopathy Neuropathy Nephropathy
80
What macro vascular systems can be affected by T2DM?
Cardiopathy eg heart attack
81
What is dyslipidemia?
Disturbances in fat metabolism cause changes in the lipid concentration in the blood
82
What is diabetic retinopathy?
High glucose levels in the blood result in damage to the blood vessels which supply the retina
83
How does insulin interact with adipocytes in a fed state?
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
What happens to adipocytes in fasting state (recall the two hormones involved)?
Blood glucose and insulin are low Thus GH and cortisol are secreted and stimulate lipolysis, releasing glycerol and NEFAs
85
In the fasting state what happens to the glycerol taken up by the liver?
Converted to glucose in gluconeogenesis
86
In the fed state what happens to the glycerol taken up by the liver?
Converted into triglycerides
87
In the fed state, what does insulin do once NEFA is uptaken by the liver?
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
In the fed state what happens to glucose in the liver?
Converted to G6P Then to glycogen (stimulated by insulin)
89
In the fasting state what happens to glycogen in the liver?
Broken down to G6P Then to glucose and released from liver
90
What does it mean if there is a high level of ketones and glucose?
There is an issue with insulin secretion

BRS 4 Endocrinology (20 decks)

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