Introduction to diabetes mellitus Flashcards

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
Q

Symptoms of hypoglycaemia

A

Sweating, pallor, palpitations, shaking

Slurred speech, Poor vision, confusion, seizures, loss of consciousness

25
Q

What is severe hypoglycaemia

A

Episode where a person needs third party assistance

26
Q

What is the pathophysiology in type 2 diabetes

A

Enough insulin to suppress breakdown of protein and ketogenesis

27
Q

What happens during insulin resistance

A

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
Q

What are the consequences of insulin resistance

A

Derangement of lipid

Hyeprtension

Increase weight

Inflammatory states

Decrease energy expenditure

29
Q

What is the presentaiton of T2DM

A

Hyperglycaemia

Overweight

Less osmotic symptoms

Dyslipidaemia

Insulin resistance

30
Q

What are the risk factors of T2DM

A

Age

Increase BMI

Ethnicity

Family

Inactivity

PCOS

31
Q

What are diabetes complications

A
32
Q

What treatment are there for diabetes

A

Healthy eating or diet control - Reduce calories in fat and refined carbohydrates, sodium, increase fibre and complex carbs

33
Q

What is the management of type 1 diabetes

A

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
Q

What is the management of type 2 diabetes

A

Diet

Oral medication

Education

May need insulin later

35
Q

Long term coseuqences of diabetes

A

Retinopathy

Neuropathy

Nephropathy

Cardiovascular disease

36
Q
A