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2.2 Clinical Chemistry > Blood Glucose > Flashcards

Blood Glucose Flashcards

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1
Q

What are the 12 steps of glucose regulation

A

CNS triggers desire to eat
Food consumed and glucose absorbed
Plasma glucose increases
Insulin release stimulated
GLUT externalisation
Glucose uptake by fat and muscle
Glycogen synthesis
Plasma glucose levels fall
Production of glucagon triggered
Triggers breakdown of glycogen
Plasma glucose levels increase
Euglycaemia restored

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2
Q

What two organs play a key role in maintaining blood glucose and how?
(2)

A

Live and kidney

Express glycogen phosphorylase which can supple glucose to bloodstream from glycogen

Liver can also convert many small molecules into glucose via gluconeogenesie

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3
Q

What are the five main GLUT transporters

A

GLUT 1
Glut 2
Glut 3
GLUT 4
GLUT 5

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4
Q

What is the most important GLUT

A

GLUT 4

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5
Q

What does GLUT 4 do?

A

Insulin responsive glucose transporter

For skeletal muscle, cardiac muscle and adipose tissue

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6
Q

What are the hormonal components of glycaemic control?
(3)

A

Oscillation between catabolic and anabolic states

Driven by nutrient supply (post-prandial increase in anabolic processes)

Pituitary also involved (senses low glucose and triggers hormone production)

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7
Q

What are the four catabolic controls for glucose

A

Cortisol
Epinephrine (adrenaline)
Growth hormone (IGF1)
Glucagon

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8
Q

What is the only anabolic control for glucose

A

Insulin

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9
Q

Comment on the type of energy used by most cells
(3)

A

Glucose is the main source of energy during the absorptive (fed state)

Fatty acids are the main source of energy during the long fasting state

Brain is the only exception which uses glucose

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10
Q

What cells secrete insulin

A

Beta cells

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11
Q

What causes insulin to be secreted

A

Rising blood glucose levels

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12
Q

Write about the structure of insulin

A

Polypeptide hormone - 51 amino acids
Synthesised as a precursor (preproinsulin -> proinsulin -> insulin + C-peptide)

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13
Q

Why can’t insulin be taken orally

A

Considered unstable if taken orally

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14
Q

How does insulin act in cells

A

Acts via insulin receptor

Phosphorylation triggers intracellular signalling pathway

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15
Q

What is the function of glucose facilitators and how do they work?
(4)

A

They equalise concentrations across membranes

They transport down concentration gradients

GLUTs are stored in intracellular granules

Insulin signalling promotes externalisation of preformed GLUT

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16
Q

What happens when insulin binds to the insulin receptor

A

This induces a signal transduction cascade which allows the glucose transporter (GLUT 4) to transport glucose into the cell

Results in gene expression and growth regulation and glucose utilisation

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17
Q

Why can the BBB only use glucose

A

The blood-brain barrier excludes fatty acids from the brain

High FFA can act as detergents to the brain

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18
Q

Write about the glucose metabolism in the brain
(5)

A

Brain depends on glucose
Needs a constant supply of about 110g a day
Older brains need more glucose to carry out the same tasks
GLUT1 expressed on the BBB which facilitates blood-brain movement of glucose
GLUT3 expressed on neurons

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19
Q

What happens when blood glucose rises

A

Stimulates the pancreas to release insulin
Insulin stimulates the uptake of glucose and storage as glycogen in the liver and muscles
Insulin also stimulates the conversion of excess glucose into fat for storage
Blood levels begin to decline

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20
Q

What happens when there is low blood glucose

A

This stimulates the pancreas to release glucagon into the bloodstream
Glucagon stimulates liver cells to break down glycogen and release glucose into the blood
Blood glucose begins to rise again

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21
Q

Why is glucose in urine seen in diabetes
(3)

A

If blood glucose is too high some will spill into the urine
Kidney filters glucose into tubules and then reabsorbs it (100% in normal people)

If glucose concentration is too high reabsorption cannot keep up with filtration and some glucose stays in tubule and becomes part of urine

Glucose in the urine will suck more water into the urine via osmosis and cause excess urine production in diabetes -> causes dehydration and thirst

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22
Q

What is the role of the kidney
(4)

A

Its a minor glycogen store
Filtered glucose is reabsorbed by the kidney
For normal concentrations it is 100% effective are reabsorption
If concentration too high it will exceed capacity and will spill over which leads to glucose rich urine (glucosuria)

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23
Q

What is the role of the liver

A

After meals blood glucose comes from carbohydrates in meal

Between meals blood glucose comes from the liver and kidneys

Liver provides 80% of blood glucose supply via
- glycogenolysis
- gluconeogenesis

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24
Q

What is glycogenolysis?

A

Breakdown of liver glycogen

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25
Q

What is gluconeogenesis?

A

Conversion of small molecules into glucose

Reversal of some reactions of glycolysis

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25
Q

What is gluconeogenesis?

A

Conversion of small molecules into glucose

Reversal of some reactions of glycolysis

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26
Q

Give four examples of small molecules that can be converted to glucose

A

Lactate and pyruvate
Glycerol
AcetylCoA
Amino acids

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27
Q

What three tissues require insulin to transport glucose into the cells

A

Muscle
Fat
Liver tissue

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28
Q

What is the endocrine part of the pancrease

A

Small clumps of cells called islets of Langerhans (consists of alpha cells (glucagon) and beta cells (insulin))

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29
Q

What is the exocrine part of the pancrease

A

This makes digestive enzymes and delivers them to the duodenum through ducts

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30
Q

What four main hormones can increase blood glucose

A

Glucagon
Cortisol
Epinephrine (adrenaline)
Growth hormone

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31
Q

When would all four major hormones to raise blood glucose be seen raised together

A

Vigorous exercise

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32
Q

When does diabetes mellitus result

A

When insulin is deficient or ineffective

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33
Q

What does high levels of glucose in blood stimulate
(4)

A

Increased glycogen production from glucose (glycogenesis)

Increased fatty acid synthesis and triglyceride production from glucose

Decreased production of glucose from glycogen (glycogenolysis)

Decreased glucose production from protein (gluconeogenesis)

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34
Q

What does low levels of insulin stimulate but increased glucagon (starvation)

A

Glycogen depletion
Triglyceride catabolism and ketone formation
Protein breakdown and gluconeogenesis

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35
Q

Define diabetes mellitus

A

The term diabetes mellitus describes a metabolic disorder of multiple aetiology characterised by chronic hyperglycaemia with disturbances of carbohydrate, fat and protein metabolism. Resulting from defects in insulin secretion, insulin action or both.

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36
Q

Write about HbA1c
(4)

A

‘Long term bloods’

Formed by non-enzymatic attachment of glucose to haemoglobin A

Formed slowly and continuously

Normally less than 42 (6%) but in diabetics it can increase 2-3 times

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37
Q

Comment on the measurement of HbA1c
(4)

A

Used to be reported as a % of the total HbA which is glycated

Different methods gave different results

All assays must now be calibrated against the international reference method

Results will be reported as a ratio: mmol of glycated HbA: mol of non-glycated HbA

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38
Q

Is HbA1c diagnostic
(4)

A

Could be used as a diagnostic test provided the assay is standardised and stringent QA in place

A HbA1c value of 6.5% (48mmol/mol) is the diagnostic cut point

HbA1c value less than 6.5% does not exclude diabetes

Assay not available throughout the world

39
Q

What would indicate impaired fasting glycaemia

A

Fasting glucose equal to or between 6.1 and 7

40
Q

What would indicate impaired glucose tolerance

A

OGTT between 7.8 and 11.1

41
Q

What HbA1c would indicate intermediate hyperglycaemia

A

Between 5.7 and 6.5%

Between 39 and 48 mmol/mol

42
Q

What are the four types of diabetes

A

Type 1 (previously IDDM)
Type 2 (previously NIDDM)
Gestational diabetes
“other specific types” e.g. endocrinopathies

43
Q

Define type 1 diabetes mellitus

A

Autoimmune destruction of pancreatic cells, usually occurs early in life
Characterised by low insulin output, high blood glucose, glucose in urine, excess urine flow, switch to fat metabolism
Treated with insulin injections, careful balance of diet and exercise
10% of diabetics

44
Q

Define type 2 diabetes mellitus
(3)

A

Associated with obesity, usually starts later in life.
Insulin may be normal, but is ineffective (insulin resistance)
Many of symptoms the same, but less severe

45
Q

What is gestational diabetes

A

Diabetes that lasts for the duration of pregnancy
4% of all pregnancies
Increased risk of type 2

46
Q

What is type 4 diabetes, give some examples

A

Genetic defects of beta-cell function
Genetic defects in insulin action
Diseases of the exocrine pancreas (endocrinopathies)
Drug-or chemical induced
Infections
Uncommon forms of immune-mediated diabetes
Other genetic syndromes sometimes associated with diabetes

47
Q

How does type 1 present
(3)

A

Acute with symptoms of polyuria, polydipsia, lethargy, weight loss, nausea, vomiting, abdominal cramps, blurred vision and superficial infection

This presentation is the end point of recent and continuing beta cell function resulting in near total loss of insulin production

Hyperglycaemia itself begets further beta cell destruction as treatment with insulin often results in a “honeymoon” period

48
Q

Describe the pathogenesis of type 2

A

A group of metabolic diseases characterised by hyperglycaemia resulting from defects in insulin secretion, insulin action or both

The chronic hyperglycaemia of diabetes is associated with long-term damage, dysfunction and failure of various organs, especially the eyes, kidneys, nerves, heart and blood vessels

49
Q

How does type 2 present?
(4)

A

Insidious presentation with symptoms of polyuria, polydipsia, lethargy, weight loss, nausea, vomiting, abdominal cramps, blurred vision and superficial infection

Often discovered at routine medical

This presentation is the end point of the gradual loss of beta cell function in the setting of insulin resistance

90-100% concordance in Twins

50
Q

What are the three macrovascular complications of diabetes

A

Coronary artery disease (MI)
Cerebrovascular disease (stroke)
Peripheral vascular disease

51
Q

What are the three microvascular complications of diabetes

A

Retinopathy
Nephropathy
Neuropathy

52
Q

What can hyperglycaemia cause?
(2)

A

Glucose in urine (weight loss and genital thrush)

Osmotic diuresis, water follows (increased urine volume -> thirst and tiredness)

53
Q

Write about the onset of type 1 diabetes
(8)

A

typical onset less than 30 but can start at any age
Sudden onset
Sever symptoms
Recent weight loss
Usually thin
Spontaneous ketosis
Absent C-peptide
Markers of autoimmunity

54
Q

Write about the onset of type 2 diabetes
(8)

A

Typical onset greater than 20 years but can start at any age
Gradual onset
May be no symptoms
Often no weight loss
Usually obese
Not ketotic
Detectable C-peptide
No autoimmune markers

55
Q

what five laboratory test are carried out for diabetes

A

Blood glucose
Fasting glucose
Postprandial glucose
Glycosylated haemoglobin (HbA1c)
Glycosylated albumin

56
Q

How is diabetes managed

A

diet
Exercise
Oral anti-diabetes medications
Insulin therapy

57
Q

How do oral anti-diabetes medications work

A

Stimulates beta cells to release more insulin

Sensitises the body to the insulin already present

Helps insulin work better in muscle and fat: lowers insulin resistance

Slows or blocks the breakdown of starches and certain sugars: action slows the rise in blood sugar levels following a meal

58
Q

Write about the burden of diabetes

A

Affects 3% of the population
Estimated that 5 million people will have diabetes by 2025 (most will be type 2 due to rapidly rising numbers of overweight and obese people)
The cost of diabetes to the NHS is over 1.5million pounds an hour or 10% of NHS budget, 25, 000 pounds are spent on diabetes every minute
people with diabetes account for 5.4% of all completed hospital episodes, 6.4% of outpatient episodes and 9.4$ of impatient stay

59
Q

Why is diabetes sometimes called starvation in the midst of plenty?
(3)

A

A diabetic has plenty of glucose in their blood but many of their tissues cannot use it because it can’t get into the cells

Glucose is water soluble and cannot cross cell membranes by simple diffusion

A series of facilitated transport molecules move glucose across membranes

60
Q

What is a by product of lipid metabolism

A

Build up of ketoacids

61
Q

How can you tell someone is experiencing ketoacidosis

A

Ketoacids can be smelled on breath: odour similar to acetone

62
Q

Why are ketoacids dangerous

A

They disturb mental functions and lower blood pH

63
Q

What are five consequences of poor glycaemic control

A

Neuropathy (nerve damage) -> impotence is commonly a presenting symptom

Cataracts

Kidney damage (nephropathy)

Arthritis -> damage to collagen in joints

Capillary damage -> circulatory defects and damage to retina

Abnormal plasma lipoprotein metabolism -> increased risk of cardiovascular disease

64
Q

How can poor glycaemic control cause cataracts?

A

Damage to the protein a-crystallin in the lens

65
Q

What are the mechanisms of damage in hyperglycaemia
(3)

A

Glucose is converted to sorbitol by aldose reductase - Sorbitol accumulates in tissues

Glucose is converted into ketones

Glycation of collagen

66
Q

What happens when sorbitol accumulates in tissues

A

This disturbs control of intracellular osmotic pressure

67
Q

Why is glycation of collagen dangerous

A

Results in stiffening of the collagen in the blood vessel walls, leading to high blood pressure

68
Q

why might diabetics have poor circulation

A

Excess glucose makes the blood syrupy (more viscous) this makes it harder for the heart to pump

Excessive urine flow dehydrates body, reduces blood volume

Both effects reduce the circulation

69
Q

How is diabetic ketoacidosis considered a medical emergency

A

If a diabetic lets their blood glucose get too high he may develop ketoacidosis, a life-threatening emergency
Most of the problems in ketoacidosis are due to:
- Dehydration (due to excessive urine production)
- Low pH (due to excessive lipid metabolism)
- Large amounts of ketoacids in the blood (also due to excessive lipid metabolism)

70
Q

What is Pre-diabetes
(3)

A

WHO and ADA use this new term to describe those with impaired fasting glucose and impaired glucose tolerance

16 million people have pre-diabetes

Most will develop diabetes within 10 years

71
Q

How is pre-diabetes prevented
(3)

A

Screening at risk populations (45+, obese)

Lose 5-10% of weight

Modest exercise 30 minutes a day

72
Q

Comment on using blood versus plasma
(4)

A

Glucose is dissolved in water

Plasma has a higher concentration of water compared to red blood cells

Therefore plasma has a higher glucose concentration that that of whole blood

The difference in glucose concentration will also vary with the haematocrit, the lower the haematocrit the smaller the difference, and the higher the haematocrit the larger the difference between the two sample types

73
Q

How do we compared serum and plasma result(4)

A

International Federation of Clinical Chemistry (IFCC report 2006)

States that a constant factor of 1.11 is used to convert concentration in whole blood to the equivalent concentration in the pertinent plasma

This factor is based on the relationship between plasma and whole blood glucose at normal haematocrit

The conversion will provide harmonized results, facilitating the classification and care of patients and leading to fewer therapeutic misjudgments

74
Q

How are most diabetes patients diagnosed?

A

On the basis of symptoms, examination and random or fasting plasma glucose

75
Q

What is the oral glucose tolerance test

A

75g oral glucose taken
Blood samples takes at 0 and 2 hours for blood glucose
Test is only done if the random or fasting glucose result was equivocal or there was still a high index of suspicion

76
Q

How is the OGTT interpreted
(2)

A

Patient has diabetes if OGTT 2h greater than 11.0 and or a fasting glucose of greater than/equal to 7.0 mmol/L

Patient has IGT if OGTT 2h between 7.8 and 11.1 and a fasting glucose less than 7.0 mmol/L

77
Q

Write about blood glucose testing
(3)

A

Performed mainly on venous plasma

Enzymatic (hexokinase, glucokinase)

Performed mainly on automated analysers

78
Q

Write about Bedside or self monitoring blood glucose tests
(4)

A

BM sticks, glucose meters or urine glucose

Performed on whole blood

Can be enzymatic, chemical or photoelectric

Manual techniques

79
Q

Comment on the monitoring of diabetes

A

Daily
- Self monitoring of blood glucose

Fortnightly
- Fructosamine (glycated albumin)

Bi-Monthly - Quarterly
- Total glycosylated haemoglobins
- HbA1c

80
Q

What is fructosamine and why is it measured

A

Fructosamine is a glycation product that forms when glucose binds to proteins1. It measures average blood glucose levels over the past two to three weeks and is used to help manage diabetes

It is an earlier indicator of diabetes control compared to haemoglobin A1c (HbA1c), which measures average blood sugar over the previous two to four months

81
Q

Write about HbA1c measurements
(4)

A

Formed by non-enzymatic attachment of glucose to haemoglobin A

Formed slowly and continuously

Normally less than 42 mmol/mol (6%) but in diabetics can be 2 to 3 times higher

Provides an index to average plasma glucose over the last 2 to 3 months

82
Q

Write about microalbuminuria
(4)

A

The excretion of a small amount of albumin in urine

Diabetic nephropathy is a major complication in 35-45% of IDDM which may progress to end stage renal failure

Microalbuminuria is the excretion of 50-200mg albumin in 24 hours

Its detected by sensitive immunoassays (using antibodies directed against human albumin)

83
Q

How can we use detection of microalbumin to predict future complications?
(2)

A

Early detection can allow reversal of nephropathy through good glycaemic control, hypotensives and a low protein diet

However once proteinuria has developed then improving glycaemic control may transiently slow down progression but will not reverse it

84
Q

What are four acute metabolic complications of diabetes mellitus

A

Diabetic ketoacidosis (DKA)
Hyperosmolar non-ketotic coma (HNC)
Lactic acidosis (LA)
Hypoglycaemia

85
Q

How does diabetic ketoacidosis develop
(3)

A

Altered lipid metabolism
Increased concentrations of total lipids, cholesterol, triglycerides and free fatty acids

Free fatty acids are shunted into ketone body formation due to lack of insulin

The rate of formation of these ketone bodies exceeds the capacity for their peripheral utilisation and renal excretion leading to accumulation of ketoacids and therefore metabolic acidosis

86
Q

What are symptoms of DKA

A

Dehydration
Acidosis
Hyperosmolality
Diminished cerebral oxygen utilisation
Consciousness becomes impaired
Ultimately patient becomes comatose

87
Q

What are the laboratory findings of DKA

A

Hyperglycaemia
Glucosuria
Ketonaemia
Ketonuria
Metabolic acidosis

88
Q

What might cause DKA in diabetics

A

Not enough insulin
Skipping insulin
Stress, trauma
Insulin resistance

89
Q

Why is ketoacidosis considered so important

A

Ketoacidosis is responsible for the initial presentation of up to 25% of children

90
Q

How does someone usually present if they have ketoacidosis
(4)

A

Early manifestations are mild and include vomiting, polyuria and dehydration

More severe cases include Kussmaul respirations (acetone breath)

Abdominal pain or rigidity may be present and mimic acute appendicitis or pancreatitis

Cerebral dehydration and coma ultimately ensure

91
Q

What is a hyperosmolar non-ketotic coma (HNC)
(2)

A

Presence of relative insulin deficiency and hyperglycaemia with associated elevated serum osmolality, dehydration and stupor progressing to coma if uncorrected without the presence of ketosis or acidosis

These patients have sufficient circulating insulin to prevent lipolysis and ketosis

92
Q

What might cause a hyperosmolar non-ketotic coma?
(5)

A

Dehydration
Medications such as steroids and thiazides
Acute illness
Cerebral vascular disease
Advanced age

93
Q

What is lactic acidosis

A

Elevated lactic acid with acidosis and without ketoacidosis

There may be low levels of ketones present

Half of the reported cases of LA have been in diabetics

Rarely seen in diabetic patients particularly since the withdrawal of phenformin from the market

94
Q

What causes lactic acidosis

A

Hypoxia
Medications such as phenoformin

95
Q

What is hypoglycaemia?
(4)

A

Common in insulin-treated diabetics and occasionally seen in those treated with oral hypoglycemic sulfonylurea agents

Can range from very mild (3.3 to 3.9) with minimal or no symptoms

To severe (<2.2 mmol/L) where there is neurologic impairment

Associated with insulin therapy, may be related to errors in dosage, delayed or skipped meals, exercise and/or intensity of glycaemic control

2.2 Clinical Chemistry (28 decks)

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