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PM3B > (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 are two risks DM can incr?
R C

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
eye
(2) Cerebrovascular disease
e.g. stroke
(3) Coronary heart disease
due to atherosclerosis
(4) Nephropathy
deterioration of kidney function
(5) Peripheral vascular disease
slow and progressive circulation disorder
(6) Neuropathy
nerve damage
(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 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 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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17
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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18
Q

How could the symptoms of DM Type 1 be described?

A

Acute symptoms

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19
Q

How could the symptoms of DM Type 2 be described?

A

Sub-acute symptoms

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20
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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21
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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22
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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23
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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24
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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25
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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26
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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27
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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28
Q

When are 2 tests to confirm DM required?

A

When the patient is asymptomatic

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29
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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30
Q

What does the oral glucose tolerance test positive for?

A

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

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31
Q

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

A

Impaired fasting glycaemia

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32
Q

What is the oral glucose tolerance test?

A

The gold standard test for diagnosing diabetes

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33
Q

What is the normal venous plasma glucose for fasting and 2 hour after eating range ?

A

(1) <6mmol/L
(2) <7.8mmol/L

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34
Q

What is the diabetic venous plasma glucose for fasting and 2 hour after eating range?

A

(1) ≥7mmol/L
(2) ≥11.1mmol/L

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35
Q

What is the impaired glucose tolerance venous plasma glucose for fasting and 2 hour after eating range?

A

(1) <7mmol/L
(2) 7.8-11mmol/L

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36
Q

What is the impaired fasting glycaemia venous plasma glucose range?

A

6-6.9mmol/L

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37
Q

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

A

They become irreversibly glycated

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38
Q

What is the acronym for glycated haemoglobin?

A

HbA1c

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39
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

40
Q

What does FPG stand for?

A

Fasting plasma glucose

41
Q

What is the first line treatment for T1DM?

A

Injected insulin replacement - lifelong

42
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

43
Q

What monitoring requirements are there for T1DM?

A

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

44
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

45
Q

What is the purpose of insulin replacement therapy?

A

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

46
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

47
Q

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

A

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

48
Q

Name example(s) of rapid onset insulin. LAG

A
  • Lispro
  • Aspart
  • Glulisine
49
Q

Name example(s) of short onset insulin.

A
  • Normal insulin
50
Q

Name example(s) of intermediate insulin.

A
  • NPH
51
Q

Name example(s) of long-acting insulin. DG

A
  • Detemir
  • Glargine
52
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

53
Q

What is hypoglycaemia, and how is it caused?

A

(1) Abnormally low blood sugar

(2) Most common side effect of insulin therapy

54
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

55
Q

What is the purpose of rotating injection sites?

A

To avoid lipohypertrophy

56
Q

Is insulin allergy common?

A

No, insulin is highly purified

57
Q

If a patient were allergic to injected insulin, what would be the anticipated effect? name 2

A
  • Atrophy of fat
  • Altered effect of insulin
58
Q

How prevalent is T2DM?

A

90% of all DM cases

59
Q

How is T2DM characterised?

A

(1) Reduced insulin secretion
(2) Increased insulin resistance

60
Q

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

A

A 50% reduction in pancreatic beta-cell mass

61
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

62
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

63
Q

What is HHS?

A

Hyperosmolar Hyperglycaemic State

Hyperglycaemia, dehydrated, uraemia

64
Q

What is uraemia?

A

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

65
Q

How can incidence of T2DM be reduced?

A

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

66
Q

How long can T2DM be asymptomatic for?

A

Up to 10 years

67
Q

Why are diabetes screening programmes used?

A

To prevent T2DM

To detect T2DM in asymptomatic patients

68
Q

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

A

Patients at risk

69
Q

What tests do diabetes screening programs include? 3 tests

A

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

70
Q

What is the first line treatment for T2DM?

A

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

71
Q

What drug treatment options are there for T2DM?

A

(1) Hypoglycaemic agents
(2) Insulins

72
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

73
Q

What is an ‘insulin sensitiser’?

A
  • Enhances the effect of endogenous insulin
  • Increases target cell sensitivity to insulin
  • Decreases glucose production in liver
74
Q

What does metformin do?

A
  • First line treatment for T2DM
  • Suppresses appetite
  • Cardio-protective effect
75
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

76
Q

What comorbidity are the glitazones linked to?

A

Cardiovascular disease

77
Q

What comorbidities does pioglitazone increase risk of?

A

(1) Heart failure
(2) Bladder cancer

78
Q

What does an insulin secretagogue do?

A

Stimulates insulin release from the pancreas

79
Q

What is the purpose of an insulin secretagogue?

A
  • To restore early phase insulin release
  • To return plasma levels to pre-prandial levels
80
Q

What are 2 types of insulin secretagogues?

A

(1) Sulphonylureas
(2) Meglitinides

81
Q

How do sulphonylureas affect a patient’s weight?

A

Cause patients to gain weight

Not first choice for overweight patients

82
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

83
Q

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

A

Fewer side-effects/ shorter duration

Because it is shorter acting

84
Q

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

A

Acarbose

85
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

86
Q

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

A

Metformin is more effective

87
Q

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

A

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

88
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
89
Q

What is SGLT2? Where is it located?

A

(1) Responsible for 90% of glucose reabsorption

(2) Proximal tubule of nephron

90
Q

What is gestational diabetes?

A

Diabetes occurring for the first time during pregnancy

91
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)

92
Q

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

A

Effective glycaemic control

93
Q

What are the risk factors for gestational diabetes?

A

Same as Type 2 diabetes mellitus
- Family history
- Age
- Weight
- Ethnicity

94
Q

When are pregnant women screened for gestational diabetes?

A

If they are at risk

95
Q

What is the treatment for gestational diabetes?

A

(1) Lifestyle modification
(2) Insulin therapy if lifestyle modification is insufficient

PM3B (33 decks)

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