Introduction to diabetes mellitus Flashcards

(37 cards)

1
Q
A
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1
Q

How does insulin act

A

Decreases hepatic glucose output - decreases gluconeogensis

Increase muscle uptake of glucose

Decrease proteolysis

Decreases lipolysis

Decrease ketogenesis

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2
Q

Clinical Relevance of glucose

A

Type 1 diabetes

Hypoglycaemia

Insulin Resistance

Type 2 diabetes

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3
Q

What is the GLUT-4 transporters

A

Common in myocytes (muscle) and adipocytes (Fat)

Highly insulin-responsive

Recruited and enhanced by insulin

Increase glucose uptake

Hydrophilic inside and hydrophobic outside

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4
Q

Effects of insulin on cell metabolism

A

Insulin inhibits protein breakdown

Converts amino acids into protein - GH, IGF-1

Cortisol helps gluconeogenic aminoa cids transfer from myocyte to liver

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5
Q

What happens in gluconeogensis

A

AA taken up by the liver - enhanced by glucagon

Insulin encourages AA to protein

Insulin gluconeogenesis

Glucagon and Cortisol encourages protein to AA and gluconeogensis

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6
Q

How long to the fuel stores last

A

Carbs - 16hrs

Protein - 15 days

Fat - 30 to 40 days

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7
Q

How are triglycerides broken down

A

Lipoprotein lipase break them down

Not esterified fatty acid

Insulin activates this enzyme

Glucose can also be taken up by adipocytes by GLUT-4

Insulin also converts gly and NEFA into triglycerides

Insulin inhibits triglycerides

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8
Q

Where is insulin released

A

Hepatic protal circulation

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9
Q

What does glycerol do in the liver

A

During fed state, it converts to triglycerides

It can be converted to glucose

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10
Q

What is the cerebral energy requirement of the brain

A

Glucose (preferred

Keton bodies

No NEFA

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11
Q

WHat does ketones bodies to in liver

A

NEFA enter the liver

Insulin inhibits conversion of fatty acyl-coA into ketone bodies

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12
Q

What does glucose does in the liver

A

Hepatic glycogenolysis

Generation of glucose from stored glycogen in the liver

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13
Q

What can muslce cells utilise as energy

A

NEFA

Glucose

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14
Q

Can muscle cells release glucose into circulation

A

No

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15
Q

What hormones and pathways happen in fasted state

A

Low insulin-to-glucagon ratio

Glucose is low (normal range 3.0-5.5mmol/l)

Increase in NEFA - breaking down lipids and fats

Increase then decrease in amino acids

Proteolysis

Lipolysis

HGO

Ketogenesis production

Muscles will use lipids and brain will use glucose adn ketons

16
Q

What hormones and pathways happen in the fed state

A

High insulin release flowed by slower insulin release

Increase in glycogen

Stop HGO

Decrease gluconeogensis

Increase protein synthesis

Decrease proteolysis

Lipogenesis

17
Q

How do you diagnose diabetes mellitus

A

Fasting glucose >7.0mmol/L

Randome glucose >11.1mmol/L

Oral glucose tolerance test

HbA1c (>48mmol/mol)

Need 2 positive test or 1 positive test and symptoms

18
Q

What is the pathophysiology in type 1 diabetes

A

Autoimmune condition

Absolute insulin deficiency

Diabetic ketoacidosis

19
Q

What are the presentations of T1DM

A

Weight loss - protein break down

Hyperglycaemia

Glycosuria - polyuria, polydipsia, nocturia

Ketones in blood and urine

20
Q

What is the useful diagnostic test of T1DM

A

Antibodies: GAD, IA2

Low C peptide

Presence of ketones

21
Q

What is insulin induced hypoglycaemia

A

Where you take too much insulin

22
Q

What is the couterregulatory response to hypoglycaemia

A

Increae glucagon, catechoalmines, cortisol and growth hormone

Increase HGO and glycogenolysis, glyconeogensis, lipolysis

23
Q

Why is imparied awareness of hypoglycaemia bad

A

Reduce awareness of hypoglycaemia

Due to threshold of glucose being reset

Recurrent hypoglycaenia

24
Symptoms of hypoglycaemia
Sweating, pallor, palpitations, shaking Slurred speech, Poor vision, confusion, seizures, loss of consciousness
25
What is severe hypoglycaemia
Episode where a person needs third party assistance
26
What is the pathophysiology in type 2 diabetes
Enough insulin to suppress breakdown of protein and ketogenesis
27
What happens during insulin resistance
P13K-Akt pathway because resistance however MAPK apthway still works Increase insulin production results in increase growth and proliferation - growth of arteriols which lead to high blood pressure
28
What are the consequences of insulin resistance
Derangement of lipid Hyeprtension Increase weight Inflammatory states Decrease energy expenditure
29
What is the presentaiton of T2DM
Hyperglycaemia Overweight Less osmotic symptoms Dyslipidaemia Insulin resistance
30
What are the risk factors of T2DM
Age Increase BMI Ethnicity Family Inactivity PCOS
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What are diabetes complications
32
What treatment are there for diabetes
Healthy eating or diet control - Reduce calories in fat and refined carbohydrates, sodium, increase fibre and complex carbs
33
What is the management of type 1 diabetes
Type 1 - exogenous insulin (basal-bolus regime, long acting once or twice a day and quick acting right before meal) Self-monitoring of glucose Technology Education
34
What is the management of type 2 diabetes
Diet Oral medication Education May need insulin later
35
Long term coseuqences of diabetes
Retinopathy Neuropathy Nephropathy Cardiovascular disease
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