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BRS Y1 > Week 4- Introduction to Diabetes Mellitus > Flashcards

Week 4- Introduction to Diabetes Mellitus Flashcards

1
Q

What effects does insulin have on glucose, protein and fat?

A

Glucose- increases muscle uptake and HGO

Protein- decrease proteolysis

Fat- decreases lypolysis and ketogensis

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2
Q

Where is GLUT 4 mainly found?

A

Myocytes (muscle) and adipocytes (fat)

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3
Q

What is GLUT 4?

A

A glucose transporter that is recruited and enhanced by insulin

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4
Q

What is the short term energy store?

A

Carbohydrates

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5
Q

Where are carbohydrate stores found?

A

Liver and muscle

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6
Q

What is used as an energy store after carbs run out?

A

Fat

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7
Q

What enzyme breaks down triglycerides?

A

Lipoprotein lipase

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8
Q

What hormone is needed to breakdown triglycerides?

A

Insulin

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9
Q

What is hepatic portal circulation?

A

Blood goes to gut then liver (smaller circulation route)- insulin can be released into this system

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10
Q

What effect does insulin have on ketone body synthesis?

A

Inhibits conversion of fatty acids to ketone bodies

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11
Q

What can low ketone body levels suggest about blood glucose?

A

Blood glucose is high as insulin is inhibiting ketone body synthesis

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12
Q

What is hepatic glycogenolysis?

A

Generation of glucose from stored glycogen in the liver

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13
Q

What is special about glucose in muscles?

A

It cannot be released only used internally

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14
Q

What are the 4 tests for diagnosing diabetes mellitus and what are their positive results?

A

Fasting glucose- >7.0 mmol/L
Random glucose- >11.1 mmol/L
Oral glucose tolerance test
HbA1c- >48 mmol/mol

Diagnosis requires 2 positive tests or 1 positive test and osmotic symptoms (polydipsia, polyuria, nocturia)

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15
Q

How does type 1 diabetes mellitus present?

A

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

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16
Q

What are useful diagnostic tests for type 1 DM?

A

Antibodies (GAD and IA2)
C-peptide
Presence of ketones

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17
Q

What happens if too much insulin is taken?

A

Reduced glucose output as hepatic gluconeogenesis is switched off and too much glucose uptake by muscles causing hypoglycaemia

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18
Q

What is impaired awareness of hypoglycaemia?

A

When theres reduced ability to recognize symptoms of hypoglycaemia due to loss of counterregulatory response, causes hypoglycaemia to be recurrent

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19
Q

What are autonomic symptoms of hypoglycaemia?

A

Sweating, pallor, palpitations, shaking

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20
Q

What are neuroglycopenic symptoms of hypoglycaemia?

A

Slurred speech, poor vision, confusion, seizures, loss of conciousness

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21
Q

What does a CBG test stand for?

A

Capillary blood glucose

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22
Q

For type 2 diabetes, where is insulin resistance mainly located?

A

Liver, muscle and adipose tissue

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23
Q

How does type 2 DM present?

A 
Hyperglycaemia
Overweight
Dyslipidaemia
Less osmotic symptoms 
Insulin resistance
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24
Q

What are risk factors for type 2 DM?

A 
Age
High BMI
Ethnicity
PCOS
Family history
Inactivity
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25
Q

Whats the medical term for feeling thirsty?

A

Polydipsia

26
Q

Whats the medical term for frequent urination?

A

Polyuria

27
Q

What does Hba1c show?

A

Glucose levels over the past few months

28
Q

What distinguishes a diagnosis of T1DM from T2DM?

A

If they have ketone bodies in their blood this shows it is T1DM as this shows they have no insulin

29
Q

What is the renal threshold for glucose reabsorbtion? What happens once this threshold is surpassed?

A

10 mmol/L- after this point the glucose is excreted leading to large volumes of urine

30
Q

What can C peptide indicate and why?

A

Indicates insulin levels as one mol of c peptide gives rise to one molecule of insulin

31
Q

What are the main differences between T1DM vs T2DM?

A

Cant produce insulin vs produce to little/dont respond to it
Sudden onset of symptoms vs gradual onset of symptoms
Must take insulin daily vs can be managed by exercise/diet/oral medication (can be treated by insulin if progresses)

32
Q

What is the basal bolus regimen?

A

A long term insulin dose (taken by those with T1DM) to maintain long term background insulin during the day (as insulin levels in normal people are never 0)

33
Q

How do patients who take insulin measure their blood glucose?

A

Via capillary blood glucose monitoring (NOTE: not used for diagnosis only monitoring, usually venous blood glucose is used in diagnosis)

34
Q

What are capillary blood glucose readings for fasting, before meals and hypoglycaemia?

A

Fasting: 5-7
Before meals: 4-7
Hypoglycaemia: <4

All have units of mmol/L

35
Q

What is neuroglucopenia?

A

When blood sugar is so low there isnt enough glucose for the brain

36
Q

Why do symptoms of hypoglycaemia arise?

A

Due to activation of the sympathetic system

37
Q

What are the effects of insulin on cell metabolism?

A

Promotes the breakdown of protein into gluconeogenic amino acids

Reduces the usage of oxygen

38
Q

Aside from insulin, what molecules promote protein breakdown into gluconeogenic amino acids in myocytes?

A

Growth hormone
IGF 1
Cortisol

39
Q

What effect does glucagon have on gluconeogenic amino acids?

A

It promotes their uptake into cells via transporters and the synthesis of proteins from them

40
Q

What 2 hormones promote gluconeogensis?

A

Cortisol and glucagon

41
Q

What hormone inhibits gluconeogenesis?

A

Insulin

42
Q

What happens to triglyceride levels after eating?

A

They rise

43
Q

What is the enzyme that breaks down triglycerides?

A

Lipoprotein lipase

44
Q

What effect does insulin have on lipoprotein lipase?

A

It promotes its action, resulting in more non esterified fatty acids which can be carried to the liver for storage

45
Q

What effect does insulin have on triglyceride synthesis? How are triglycerides synthesised?

A

They are synthesised from glycerol and non esterfied fatty acids, insulin promotes triglyceride synthesis

46
Q

What hormones encourage breakdown of triglycerides?

A

Growth hormone and cortisol

47
Q

What does hepatic glucose output indicate?

A

Levels of production of new glucose

48
Q

Describe overall what happens in gluconeogensis

A

Glycerol is converted to glucose- it is taken into the liver via transporter and converted to gly-3P before being converted to glucose

49
Q

What effect does insulin have on ketone body synthesis?

A

It inhibits synthesis of ketone bodies

50
Q

How are ketone bodies synthesised in the liver?

A

Fatty acids and acyl coA are converted to acetoacetane/acetyl coA/ acetone which give rise to ketone bodies

51
Q

What is hepatic glycogenolysis?

A

The generation of glucose from glycogen stores in the liver (NOT the synthesis of new glucose)

52
Q

What is special about muscle cells glucose release?

A

Muscle cells cant release glucose only use it internally (so when blood glucose is low muscles stop this uptake)

53
Q

What happens to glucose levels, NEFA and amino acid levels during fasting?

A

Glucose levels fall (3-5.5 mmol/L)
NEFA levels rise
Amino acid levels fall when fasting is prolonged

54
Q

What happens to proteinolysis, lipolysis and HGO in the fasting state?

A

All 3 increase, HGO increases from glycogen and gluconeogensis

55
Q

What happens to proteinolysis, lipolysis and HGO in the fed state?

A

Proteinolysis and lipolysis falls,HGO stops

56
Q

What device is used to measure capillary blood glucose?

A

Glucose meter

57
Q

What 5 hormones are released during hypoglycaemia?

A 
Glucagon
Epinephrine (adrenaline) 
Norepinephrine
Cortisol
Growth hormone
58
Q

What effect does the parasympathetic nervous system have on insulin secretion?

A

Promotes it

59
Q

What effect does the sympathetic nervous system have on insulin secretion?

A

Inhibits it (to increase glucose availability for fight or flight)

60
Q

What is ketoacidosis?

A

Metabolic acidosis due to too many ketone acids in the bloodstream

BRS Y1 (52 decks)

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