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Part 3 – PM3B COPY T > (PM3B) Diabetes > Flashcards

(PM3B) Diabetes Flashcards

1
Q

What is diabetes mellitus?

A

Metabolic disorder characterised by chronic hyperglycaemia

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2
Q

Name different sources of glucose.

A

(1) Diet
(2) Glycogenolysis
(3) Gluconeogenesis

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3
Q

Which hormones regulate glucose?

A
  • Insulin

- Glucagon

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4
Q

What is the normal glucose range?

A

3-8 mM

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5
Q

Does DM affect life expectancy? If so, by how much?

A

Yes

Approx. 1/3

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6
Q

What is the greatest risk factor for DM?

A

(1) Renal failure - 100x risk

(2) Cardiovascular disease incidence - 3-5x

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7
Q

What co-morbidities does DM increase risk of?

A

(1) Increased risk of blindness

(2) Amputation

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8
Q

What are the major diabetes mellitus complications?

A

(1) Retinopathy
(2) Cerebrovascular disease
(3) Coronary heart disease
(4) Nephropathy
(5) Peripheral vascular disease
(6) Neuropathy
(7) Diabetic foot - ulceration/ amputation

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9
Q

How is low glucose detected? What is the response?

A

(1) Pancreas detects it

(2) Glucagon is secreted:
ø Glucose is freed from muscle, fat + liver
ø Storage of glycogen is stopped

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10
Q

How is high glucose detected? What is the response?

A

(1) Pancreas detects it

(2) Insulin is secreted
ø Removes glucose from the bloodstream
ø Glucose stored in fat and muscle
ø Glucose converted to glycogen in the liver
ø Glucose production by liver is stopped

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11
Q

If someone has DM, and therefore cannot use glucose for energy, what sources do they use? What are these pathways called?

A

(1) Lipids + Proteins

(2) Catabolic pathways

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12
Q

What do effects do catabolic pathways have?

A

(1) Ketotic breath
(2) Acidosis
(3) Increased lipolysis - produces more FFAs (hyperlipidaemia)

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13
Q

What are the types of primary DM?

A

Type 1: Insulin-dependent

Type 2: Non-insulin dependent

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14
Q

Describe Type 1 DM.

A
  • Polygenic autoimmune disorder
  • Specific destruction of pancreatic beta-cells
  • Leads to complete insulin deficiency
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15
Q

Describe Type 2 DM.

A
  • Polygenic disorder
  • Decrease in beta-cell mass
  • Decreased secretion by beta-cells
  • Leads to increased peripheral insulin resistance
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16
Q

What types of risk factors for diabetes mellitus are there?

A

Modifiable and non-modifiable

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17
Q

What are examples of non-modifiable risk factors for DM?

A

(1) Family history
(2) Ethnicity
(3) Age - Type 2
(4) Gestational diabetes/ polycystic ovary syndrome

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18
Q

What are examples of modifiable risk factors for DM?

A

(1) Weight - Type 2
(2) Waist circumference - Type 2
(3) Sedentary lifestyle - Type 2
(4) Social deprivation/ low income
ø 2.5x more likely to develop DM

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19
Q

How could the symptoms of DM Type 1 be described?

A

Acute symptoms

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20
Q

How could the symptoms of DM Type 2 be described?

A

Sub-acute symptoms

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21
Q

What are the common symptoms of Type 1 DM?

A

(1) 2-4 history of thirst
(2) Polyuria
(3) Weight-loss
(4) Lethargy

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22
Q

What are the common symptoms of Type 2 DM?

A

(1) History of thirst
(2) Polyuria
(3) Lethargy
(4) Visual disturbances
(5) Infections

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23
Q

How long is the duration of symptoms for Type 1 DM? How does this compare with Type 2?

A

(1) 2-4 weeks

(2) Several months

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24
Q

What are the clinical signs of DM?

A

(1) Glucosuria - excretion of glucose in urine
(2) Hyperglycaemia
(3) Impaired glucose tolerance
(4) Complications of diabetes
ø Retinopathy
ø Nephropathy
ø Peripheral neuropathy
ø Foot ulceration

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25
Q

How is the symptom of polyuria caused in patients with DM?

A

(1) Blood glucose levels are increased
(2) Blood osmolarity is decreased - Water is drawn into blood from interstitial spaces
(3) Blood volume is increased
(4) Increased urination frequency reduces blood volume

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26
Q

How is the symptom of increased thirst caused in patients with DM?

A

(1) Loss of fluids + electrolytes

(2) Stimulation of thirst

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27
Q

How is weight loss caused in patients with DM?

A

(1) Loss of fluids (dehydration)

(2) Breakdown of fat + muscle energy stores

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28
Q

What happens when fats are broken down for energy supply?

A

(1) Leads to production of ketone bodies
(2) Ketone bodies increase the acidity of the blood (ketoacidosis)
(3) Ketoacidosis leads to a hyperglycaemic coma if untreated

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29
Q

When are 2 tests to confirm DM required?

A

When the patient is asymptomatic

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30
Q

What are the tests used to diagnose diabetes mellitus?

A

(1) Detection of glucose in urine (glucosuria)
(2) Random venous plasma glucose test
(3) Fasting venous plasma glucose test
(4) Oral glucose tolerance test
(5) Glycated haemoglobulin levels

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31
Q

When is the oral glucose tolerance test used?

A

(1) Testing for Type 1 DM
(2) Testing for Type 2 DM
(3) Screening for gestational diabetes

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32
Q

What is the middle ground between ‘normal’ and ‘diabetes’ called?

A

Impaired fasting glycaemia

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33
Q

What is the oral glucose tolerance test?

A

The gold standard test for diagnosing diabetes

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34
Q

What is the normal venous plasma glucose for fasting and 2 hour post-prandial range ?

A

(1) <6mmol/L

(2) <7.8mmol/L

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35
Q

What is the diabetic venous plasma glucose for fasting and 2 hour post-prandial range?

A

(1) ≥7mmol/L

(2) ≥11.1mmol/L

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36
Q

What is the impaired glucose tolerance venous plasma glucose for fasting and 2 hour post-prandial range?

A

(1) <7mmol/L

(2) 7.8-11mmol/L

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37
Q

What is the impaired fasting glycaemia venous plasma glucose range?

A

6-6.9mmol/L

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38
Q

What happens when haemoglobin (RBCs) is exposed to glucose?

A

They become irreversibly glycated

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39
Q

What is the acronym for glycated haemoglobin?

A

HbA1c

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40
Q

What is HbA1c?

A

Glycated haemoglobin

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41
Q

What can the amount of HbA1c be used for?

A

Determining the average glucose levels that RBCs have been exposed to for last 1-3 months

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42
Q

What does FPG stand for?

A

Fasting plasma glucose

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43
Q

What is Type 1 diabetes mellitus?

A

Auto-immune destruction of pancreatic beta cells

Meaning no insulin can be produced

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44
Q

Where is insulin produced in the body?

A

Pancreatic beta cells

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45
Q

What are the main risk factors for Type 1 diabetes?

A

(1) Family history

(2) Ethnicity - Northern European descent

46
Q

What initiates the autoimmune beta cell destruction?

A

Not fully understood

But TRIGGERED by something

47
Q

Define ‘iatrogenic’.

A

Illness following treatment or medical intervention

48
Q

What is the first line treatment for T1DM?

A

Injected insulin replacement - lifelong

49
Q

What dietary modification is required for management of T1DM?

A

(1) Low fat
(2) High fibre
(3) Healthy diet - to spread nutrients across the day

50
Q

What monitoring requirements are there for T1DM?

A

(1) Insulin dose adjustment
(2) Glycaemic control
(3) Complications - retinopathy, diabetic foot, CVD risk

51
Q

What management options are there for T1DM?

A

(1) Injected insulin replacement
(2) Diet modification
(3) Monitoring
(4) Exercise
(5) Education on the importance of adherence

52
Q

What is the purpose of insulin replacement therapy?

A

To be administered in a way that mimics the normal insulin secretion pattern

53
Q

Describe the concentration of insulin secretion in a healthy patient.

A

(1) Secreted at a slow basal rate
(2) Secreted rapidly in response to a meal
(3) Secretion returns to basal rate after 2 hours following meal

54
Q

Why would it be beneficial to genetically modify a human insulin?

A

To achieve rapid/ short/ intermediate/ long lasting onset/ duration of effect

55
Q

Name example(s) of rapid onset insulin.

A
  • Lispro
  • Aspart
  • Glulisine
56
Q

Name example(s) of short onset insulin.

A
  • Normal insulin
57
Q

Name example(s) of intermediate insulin.

A
  • NPH
58
Q

Name example(s) of long-acting insulin.

A
  • Detemir

- Glargine

59
Q

What is commonly experienced by newly diagnosed T1DM patients when starting treatment?

A

Patients can experience a partial remission phase

Only low levels of insulin are required to maintain good glycaemic control

60
Q

What is hypoglycaemia, and how is it caused?

A

(1) Abnormally low blood sugar

(2) Most common side effect of insulin therapy

61
Q

What is lipohypertrophy? Where does it occur and what causes it?

A

Accumulation of fat at injection sites

Due to local effects of insulin

62
Q

What is the purpose of rotating injection sites?

A

To avoid lipohypertrophy

63
Q

How can lipohypertrophy be avoided?

A

Rotation of injection sites

64
Q

Is insulin allergy common?

A

No, insulin is highly purified

65
Q

If a patient were allergic to injected insulin, what would be the anticipated effect?

A
  • Atrophy of fat

- Altered effect of insulin

66
Q

Why is monitoring glucose levels important in T1DM?

A

Allows insulin doses to be adjusted accordingly

67
Q

What is retinopathy?

A

Disease of the retina, impairs/ loses vision

68
Q

How prevalent is T2DM?

A

90% of all DM cases

69
Q

How is T2DM characterised?

A

(1) Reduced insulin secretion

(2) Increased insulin resistance

70
Q

What change is present in patients with T2DM, that affects their insulin secretion?

A

A 50% reduction in pancreatic beta-cell mass

71
Q

How is hypoglycaemia caused in patients with T2DM?

A

Impaired insulin secretion in early phase (first meal)

Increased second phase response

Exaggerated second phase can lead to hypoglycaemia after 3-4 hours

72
Q

What are the common symptoms of T2DM?

A

(1) Increased thirst/ hunger
(2) Polyuria - increased urination - especially at night
(3) Fatigue
(4) Blurred vision
(5) Infection

73
Q

What is HHS?

A

Hyperosmolar Hyperglycaemic State

Hyperglycaemia, dehydrated, uraemia

74
Q

What is uraemia?

A

Raised level of urea and other nitrogenous waste in the blood - which would normally be eliminated by the kidneys

75
Q

What condition is characterised by a raised level of urea and other nitrogenous waste in the blood?

A

Uraemia

76
Q

How can incidence of T2DM be reduced?

A

Lifestyle interventions

(1) Reduce weight
(2) Reduce fat intake
(3) Increase dietary fibre
(4) Exercise

77
Q

How long can T2DM be asymptomatic for?

A

Up to 10 years

78
Q

Why are diabetes screening programmes used?

A

To prevent T2DM

To detect T2DM in asymptomatic patients

79
Q

Universal screening tests are not practical. Who is target by the screening programs?

A

Patients at risk

80
Q

What tests do diabetes screening programs include?

A

(1) Oral glucose tolerance test - random glucose levels
(2) Fasting blood glucose tests
(3) HbA1c levels - glycated haemoglobin

81
Q

What is the first line treatment for T2DM?

A

Lifestyle interventions, e.g. diet + weight loss + exercise

82
Q

What drug treatment options are there for T2DM?

A

(1) Hypoglycaemic agents

(2) Insulins

83
Q

What categories of oral hypoglycaemic agents are there?

A

(1) Insulin sensitisers
(2) Insulin secretagogues
(3) Inhibitor of glucose absorption from GIT
(4) Inhibitor renal glucose reuptake

84
Q

What is an ‘insulin sensitiser’?

A
  • Enhances the effect of endogenous insulin
  • Increases target cell sensitivity to insulin
  • Decreases glucose production in liver
85
Q

What does metformin do?

A
  • First line treatment for T2DM
  • Suppresses appetite
  • Cardio-protective effect
86
Q

When can metformin not be given? Why?

A

When the patient has renal impairment, cardiac failure, or liver failure

Because metformin is associated with lactic acidosis

87
Q

What comorbidity are the glitazones linked to?

A

Cardiovascular disease

88
Q

What comorbidities does pioglitazone increase risk of?

A

(1) Heart failure

(2) Bladder cancer

89
Q

What does an insulin secretagogue do?

A

Stimulates insulin release from the pancreas

90
Q

What is the purpose of an insulin secretagogue?

A
  • To restore early phase insulin release

- To return plasma levels to pre-prandial levels

91
Q

What does post-prandial mean?

A

Following dinner/ lunch/ a meal

92
Q

What does pre-prandial mean?

A

Prior to dinner/ lunch/ a meal

93
Q

What are 2 types of insulin secretagogues?

A

(1) Sulphonylureas

(2) Meglitinides

94
Q

How do sulphonylureas affect a patient’s weight?

A

Cause patients to gain weight

Not first choice for overweight patients

95
Q

What is the mechanism of action of sulphonylureas and meglitinides? How does it differ?

A

Bind to receptors that close a K+ ATP channel

Causes a rise in intracellular calcium and insulin release

96
Q

How do the side effects of meglitinides compare to other insulin secretagogues?

A

Fewer side-effects/ shorter duration

Because it is shorter acting

97
Q

Which insulin secretagogue has reduced side-effects? Why?

A

(1) Meglitinides

(2) Because they are short-acting

98
Q

Give an example of an inhibitor of glucose absorption in the GIT.

A

Acarbose

99
Q

What is the mechanism of action of an inhibitor of glucose absorption in the GIT?

A

It binds to alpha-glucosidase with higher affinity than dietary carbohydrates

Reduces post-prandial peak in blood glucose by slowing the digestion and absorption of glucose

100
Q

What is more effective in reducing HbA1c plasma concentration, metformin or inhibitors of glucose absorption in the GIT?

A

Metformin is more effective

101
Q

What side-effects are associated with inhibitors of glucose absorption in the GIT, such as acarbose?

A

(1) Flatuence
(2) Bloating
(3) Diarrhoea

102
Q

What is GLP-1?

A

Glucagon-like peptide-1

  • Stimulates insulin release from pancreatic beta-cells
  • Suppresses glucagon release from pancreatic alpha-cells
  • Decreases gastric emptying
103
Q

What are incretins? Give 2 examples

A
  • Molecules which reduce glucagon production and increase insulin
  • GLP-1 or GIP
104
Q

How are GLP-1 analogues (mimetics) delivered?

A

Subcutaneous injection

105
Q

What is SGLT2? Where is it located?

A

(1) Responsible for 90% of glucose reabsorption

(2) Proximal tubule of nephron

106
Q

What is gestational diabetes?

A

Diabetes occurring for the first time during pregnancy

107
Q

What are the side effects of gestational diabetes?

A

(1) Increases risk of miscarriage
(2) Congenital malformations
(3) Increased risk of still birth
(4) Premature baby death (first year of life)

108
Q

How can the side-effects of gestational diabetes be reduced/ managed?

A

Effective glycaemic control

109
Q

What are the risk factors for gestational diabetes?

A

Same as Type 2 diabetes mellitus

  • Family history
  • Age
  • Weight
  • Ethnicity
110
Q

When are pregnant women screened for gestational diabetes?

A

If they are at risk

111
Q

What is the treatment for gestational diabetes?

A

(1) Lifestyle modification

(2) Insulin therapy if lifestyle modification is insufficient

Part 3 – PM3B COPY T (33 decks)

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