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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
What can the brain use for energy/ what are the cerebral energy requirements?
Glucose (preferred) Ketones (emergency) - the brain's inability to use fatty acids as a fuel makes it unique among body tissues
26
Where are ketone bodies produced?
in the liver
27
What happens to ketone bodies, glucose and insulin during fasting?
ketone bodies increase glucose and insulin decrease
28
What happens during type 1 diabetes to the number of ketone bodies, insulin and glucose?
glucose levels are high insulin levels are low ketone bodies is high
29
What promotes and what inhibits ketone body formation?
glucagon promotes Insulin inhibits
30
How are ketone bodies formed in the liver?
Fatty acyl-CoA--> Acetyl CoA-> acetoacetate-> acetone + 3 OH-B (Beta-hydroxybutyrate)--> ketone bodies
31
What is hepatic glycogenolysis?
generation of glucose from stored glycogen in the liver
32
Describe the process of hepatic glycogenolysis.
33
What hormone(s) increase blood glucose?
growth hormone and glucagon
34
What happens once glucose enters a muscle cell?
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
What is the glucose transporter to bring glucose into muscle cells?
GLUT4
36
What promotes and inhibits GLUT4?
insulin= promotes Glucagon and GH= inhibit
37
Diagram for what happens to glucose inside a myocyte.
38
What happens during the fasted state?
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
What is the body's response to fasting?
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
What happens during the fed state?
Stored insulin released then 2nd phase High [insulin] to [glucagon] ratio Stop HGO ↑ Glycogen ↓ gluconeogenesis ↑ protein synthesis ↓ proteolysis ↑ Lipogenesis
41
What are the tests for diabetes?
oral glucose tolerance test fasting glucose random glucose HbA1c A diagnosis requires 2 positive tests or 1 positive test and symptoms
42
What are the levels for... oral glucose tolerance test fasting glucose random glucose HbA1c In a patient with diabetes?
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
What is HbA1c?
average of what your glucose has been over the past 3 months
44
What are osmotic symptoms and which diabetes are they most likely linked to?
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
What is the pathophysiology of type 1 diabetes?
Autoimmune condition - destruction of B cells - leading to absolute insulin deficiency No insulin means... proteinlysis increase HGO lipolysis
46
What happens in diabetic ketoacidosis?
pH <7.3, ketones +3, HCO3- <15, gluc >11 Serious acute complication
47
What is the presentation of T1DM?
Weight loss Hyperglycemia Glycosuria with osmotic symptoms (polyuria, nocturia, polydipsia) Ketones in blood and urine
48
What are useful diagnostic tests for T1DM?
Antibodies: GAD, IA2 (both are specific to T1DM) C-peptide- gives indication if pancreas is still making insulin Presence of ketones
49
What happens during insulin induced hypoglycaemia?
less glucose leaving liver more glucose entering muscle levels in blood drop significantly
50
What is impaired awareness of hypoglycaemia and how does it occur?
Reduced ability to recognise symptoms of hypoglycaemia Due to loss of counterregulatory response Recurrent hypoglycaemia
51
What are counterregulatory responses to hypoglycaemia?
52
What are the 2 types of signs and symptoms of hypoglycaemia?
autonomic and neuroglycopenic
53
What are autonomic signs of hypoglycaemia?
Sweating Pallor Palpitations Shaking
54
What are neuroglycopenic signs and symptoms of hypoglycaemia?
Slurred speech Poor vision Confusion Seizures Loss of consciousness
55
What is severe hypoglycaemia?
Defined as an episode where a person needs third party assistance to treat
56
Why are there not extreme presentation in type 2 like there is in type 1?
There is enough insulin circulating around to suppress ketone production and breakdown of fat (so no extreme presentations)
57
Where does insulin resistance reside?
liver, muscle, adipose tissue All metabolic sites and all arms of intermediary metabolism Glucose Fatty acids
58
In type 2 diabetes there is enough insulin the to suppress what?
ketogenesis proteolysis
59
What are the possible pathways when insulin binds to a receptor?
MAPK pathway - growth, proliferation PI3K-Akt pathway - metabolic actions
60
What pathway is involved in insulin resistance?
PI3k-Akt pathway - metabolic actions
61
What is dyslipidemia and what does it cause?
Abnormal lipid levels in the blood This causes your body to be in an inflammatory state
62
What are the symptoms of insulin resistance?
TG= triglycerides HDL= high density lipoproteins
63
What are the presentations of T2DM?
Hyperglycaemia Overweight Dyslipidaemia Less osmotic symptoms With complications Insulin resistance Later insulin deficiency (destruction of B cells- so may need injections)
64
hat are risk factors of T2DM?
Age PCOS High BMI Family Hx Ethnicity Inactivity
65
What are dietary recommendation for T2DM?
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
What are reading recommendations for diabetes?
DAFNE course workbook Then Meet DESMOND
67
What are some long term diabetes related complication that have to be monitored to prevent?
retinopathy neuropathy nephropathy cardiovascular
68
How do you manage type 1 diabetes?
Exogenous insulin (basal-bolus regime) Self-monitoring of glucose Structured education Technology
69
How do you manage type 2 diabetes?
Diet Oral medication Structured education May need insulin later

BRS Endocrinology (12 decks)

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