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BRS Endocrinology > Introduction to Diabetes > Flashcards

Introduction to Diabetes Flashcards

1
Q

What can the actions of glucose be split into?

A

glucose
protein
fat

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2
Q

What action does insulin take on glucose?

A

Decrease HGO (hepatic glucose output)
Increase muscle uptake of glucose

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3
Q

What action does insulin take on protein?

A

decrease proteolysis

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4
Q

What action does insulin take on fat?

A

decrease lipolysis
decrease ketogenesis

In the fasted and fed state

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5
Q

What is GLUT4?

A

Common in myocytes (muscle) and adipocytes (fat)
Highly insulin-responsive
Lies in vesicles
Recruited and enhanced by insulin
7-fold increase glucose uptake

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6
Q

What does insulin do to AA?

A

Insulin stops oxidation of AA
Because it doesn’t need protein or AA as an alternative fuel source

Insulin promotes AA conversion to protein in fed state for storage

If there are any additional Aa lingering around then they leave the muscle cell and they are gluconeogenic (aka they can be taken up by the liver to be converted into glucose at a later stage= gluconeogenesis)

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7
Q

What is an example of a gluconeogenic amino acid?

A

Alanine

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8
Q

What are the effects of insulin on cell metabolism (myocyte)?

A

Inhibits respiration in mitochondria

Insulin, IGF-1, GH= promote AA-> protein

Insulin inhibits protein-> AA

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9
Q

What does cortisol promote in cell metabolism to do with AA?

A

promote protein to AA

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10
Q

Describe the process of gluconeogenesis.

A
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11
Q

How do AA enter the liver for gluconeogenesis?

A

pyruvate lactate

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12
Q

What promotes pyruvate lactate?

A

glucagon

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13
Q

In the liver what promotes and what inhibits gluconeogenesis?

A

promote=
glucagon
cortisol

inhibit=
insulin

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14
Q

In the liver what promotes which part of protein and AA conversion?

A

protein to AA= glucagon

AA to protein= insulin

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15
Q

What are our fuel stores?

A

carbs
protein
fat

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16
Q

What is the mass (kg), energy (Kj/kg), time of carb stores?

A

0.5kg
16 KJ/kg
16 hours (depletable within a day fast)

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17
Q

What is the mass (kg), energy (Kj/kg), time of protein stores?

A

8-9kg
17KJ/kg
15 days

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18
Q

What is the mass (kg), energy (Kj/kg), time of fat stores?

A

9-10kg
37KJ/kg
30-40 days

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19
Q

How much of our E store is protein?

A

20%

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20
Q

What breaks down triglycerides that would otherwise be unable to leave the circulation?

A

Lipoprotein lipase (LPL)

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21
Q

How do triglycerides leave and enter adipocytes?

A

NEFA= fatty acids (non-esterified)

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22
Q

What does the hepatoportal circulation allow?

A

Allows blood to to go to the digestive tract to pick up any nutrients which is then directly taken to the liver for processing

When insulin is released, it goes straight into the hepatic portal circulation
- that’s why insulin secretion in body acts very rapidly

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23
Q

Why do injections of insulin take longer than endogenous insulin?

A

with injections it takes longer because it has to go through adipose tissue and more before entering circulation

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24
Q

What happens to glycerol for gluconeogenesis?

A

Gly enters liver and turns in Gly-3P

Hepatic gluconeogenesis 25% HGO after 10 hour fast

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25
Q

What can the brain use for energy/ what are the cerebral energy requirements?

A

Glucose (preferred)
Ketones (emergency)

  • the brain’s inability to use fatty acids as a fuel makes it unique among body tissues
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26
Q

Where are ketone bodies produced?

A

in the liver

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27
Q

What happens to ketone bodies, glucose and insulin during fasting?

A

ketone bodies increase
glucose and insulin decrease

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28
Q

What happens during type 1 diabetes to the number of ketone bodies, insulin and glucose?

A

glucose levels are high
insulin levels are low
ketone bodies is high

29
Q

What promotes and what inhibits ketone body formation?

A

glucagon promotes
Insulin inhibits

30
Q

How are ketone bodies formed in the liver?

A

Fatty acyl-CoA–>

Acetyl CoA-> acetoacetate-> acetone + 3 OH-B (Beta-hydroxybutyrate)–>

ketone bodies

31
Q

What is hepatic glycogenolysis?

A

generation of glucose from stored glycogen in the liver

32
Q

Describe the process of hepatic glycogenolysis.

A
33
Q

What hormone(s) increase blood glucose?

A

growth hormone and glucagon

34
Q

What happens once glucose enters a muscle cell?

A

Glucose can be taken up into muscle cells and can be stored as glycogen
But the muscle cells can’t release glucose out of the cells as they lack glucose-6-phosphatase

It is used for respiration

35
Q

What is the glucose transporter to bring glucose into muscle cells?

A

GLUT4

36
Q

What promotes and inhibits GLUT4?

A

insulin= promotes

Glucagon and GH= inhibit

37
Q

Diagram for what happens to glucose inside a myocyte.

A
38
Q

What happens during the fasted state?

A

Low insulin-to-glucagon ratio
[Glucose] 3.0-5.5mmol/l
Increased [NEFA]
Decreased [amino acid] when prolonged

Increased Proteolysis
Increased Lipolysis
Increased HGO from glycogen and gluconeogenesis
Muscle to use lipid
Brain to use glucose, later ketones
Increased Ketogenesis when prolonged

39
Q

What is the body’s response to fasting?

A

Pancreas decreases insulin

Leading to…

Proteinolysis (forming AA) in muscles

Hepatic glucose output increases in liver

Lipolysis to form glycerol and NEFA in adipose cells

40
Q

What happens during the fed state?

A

Stored insulin released then 2nd phase
High [insulin] to [glucagon] ratio

Stop HGO
↑ Glycogen
↓ gluconeogenesis
↑ protein synthesis
↓ proteolysis
↑ Lipogenesis

41
Q

What are the tests for diabetes?

A

oral glucose tolerance test
fasting glucose
random glucose
HbA1c

A diagnosis requires 2 positive tests or 1 positive test and symptoms

42
Q

What are the levels for…
oral glucose tolerance test
fasting glucose
random glucose
HbA1c
In a patient with diabetes?

A

Fasting glucose >7.0 mmol/L

Random glucose >11.1 mmol/L

Oral glucose tolerance test
Fasting glucose
75g glucose load
2-hour glucose

HbA1c (>48mmol/mol)

43
Q

What is HbA1c?

A

average of what your glucose has been over the past 3 months

44
Q

What are osmotic symptoms and which diabetes are they most likely linked to?

A

Typical symptoms such as thirst or polyuria are classed as ‘osmotic’ based but these are not always present. Atypical symptoms might include a fall, a change in vision, or a change in memory.

Type 1 diabetes

45
Q

What is the pathophysiology of type 1 diabetes?

A

Autoimmune condition
- destruction of B cells
- leading to absolute insulin deficiency

No insulin means…
proteinlysis
increase HGO
lipolysis

46
Q

What happens in diabetic ketoacidosis?

A

pH <7.3, ketones +3, HCO3- <15, gluc >11
Serious acute complication

47
Q

What is the presentation of T1DM?

A

Weight loss
Hyperglycemia
Glycosuria with osmotic symptoms (polyuria, nocturia, polydipsia)
Ketones in blood and urine

48
Q

What are useful diagnostic tests for T1DM?

A

Antibodies: GAD, IA2 (both are specific to T1DM)
C-peptide- gives indication if pancreas is still making insulin
Presence of ketones

49
Q

What happens during insulin induced hypoglycaemia?

A

less glucose leaving liver
more glucose entering muscle

levels in blood drop significantly

50
Q

What is impaired awareness of hypoglycaemia and how does it occur?

A

Reduced ability to recognise symptoms of hypoglycaemia

Due to loss of counterregulatory response
Recurrent hypoglycaemia

51
Q

What are counterregulatory responses to hypoglycaemia?

A
52
Q

What are the 2 types of signs and symptoms of hypoglycaemia?

A

autonomic and neuroglycopenic

53
Q

What are autonomic signs of hypoglycaemia?

A

Sweating
Pallor
Palpitations
Shaking

54
Q

What are neuroglycopenic signs and symptoms of hypoglycaemia?

A

Slurred speech
Poor vision
Confusion
Seizures
Loss of consciousness

55
Q

What is severe hypoglycaemia?

A

Defined as an episode where a person needs third party assistance to treat

56
Q

Why are there not extreme presentation in type 2 like there is in type 1?

A

There is enough insulin circulating around to suppress ketone production and breakdown of fat (so no extreme presentations)

57
Q

Where does insulin resistance reside?

A

liver, muscle, adipose tissue

All metabolic sites and all arms of intermediary metabolism
Glucose
Fatty acids

58
Q

In type 2 diabetes there is enough insulin the to suppress what?

A

ketogenesis
proteolysis

59
Q

What are the possible pathways when insulin binds to a receptor?

A

MAPK pathway
- growth, proliferation

PI3K-Akt pathway
- metabolic actions

60
Q

What pathway is involved in insulin resistance?

A

PI3k-Akt pathway
- metabolic actions

61
Q

What is dyslipidemia and what does it cause?

A

Abnormal lipid levels in the blood
This causes your body to be in an inflammatory state

62
Q

What are the symptoms of insulin resistance?

A

TG= triglycerides
HDL= high density lipoproteins

63
Q

What are the presentations of T2DM?

A

Hyperglycaemia
Overweight
Dyslipidaemia
Less osmotic symptoms
With complications
Insulin resistance
Later insulin deficiency (destruction of B cells- so may need injections)

64
Q

hat are risk factors of T2DM?

A

Age
PCOS
High BMI
Family Hx
Ethnicity
Inactivity

65
Q

What are dietary recommendation for T2DM?

A

Healthy eating or diet
Total calories control
Reduce calories as fat
Reduce calories as refined carbohydrate
Increase calories as complex carbohydrate
Increase soluble fibre
Decrease sodium

66
Q

What are reading recommendations for diabetes?

A

DAFNE course workbook
Then Meet DESMOND

67
Q

What are some long term diabetes related complication that have to be monitored to prevent?

A

retinopathy
neuropathy
nephropathy
cardiovascular

68
Q

How do you manage type 1 diabetes?

A

Exogenous insulin (basal-bolus regime)
Self-monitoring of glucose
Structured education
Technology

69
Q

How do you manage type 2 diabetes?

A

Diet
Oral medication
Structured education
May need insulin later

BRS Endocrinology (12 decks)

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