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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
How is the symptom of polyuria caused in patients with DM?
(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
26
How is the symptom of increased thirst caused in patients with DM?
(1) Loss of fluids + electrolytes | (2) Stimulation of thirst
27
How is weight loss caused in patients with DM?
(1) Loss of fluids (dehydration) | (2) Breakdown of fat + muscle energy stores
28
What happens when fats are broken down for energy supply?
(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
29
When are 2 tests to confirm DM required?
When the patient is asymptomatic
30
What are the tests used to diagnose diabetes mellitus?
(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
31
When is the oral glucose tolerance test used?
(1) Testing for Type 1 DM (2) Testing for Type 2 DM (3) Screening for gestational diabetes
32
What is the middle ground between 'normal' and 'diabetes' called?
Impaired fasting glycaemia
33
What is the oral glucose tolerance test?
The gold standard test for diagnosing diabetes
34
What is the normal venous plasma glucose for fasting and 2 hour post-prandial range ?
(1) <6mmol/L | (2) <7.8mmol/L
35
What is the diabetic venous plasma glucose for fasting and 2 hour post-prandial range?
(1) ≥7mmol/L | (2) ≥11.1mmol/L
36
What is the impaired glucose tolerance venous plasma glucose for fasting and 2 hour post-prandial range?
(1) <7mmol/L | (2) 7.8-11mmol/L
37
What is the impaired fasting glycaemia venous plasma glucose range?
6-6.9mmol/L
38
What happens when haemoglobin (RBCs) is exposed to glucose?
They become irreversibly glycated
39
What is the acronym for glycated haemoglobin?
HbA1c
40
What is HbA1c?
Glycated haemoglobin
41
What can the amount of HbA1c be used for?
Determining the average glucose levels that RBCs have been exposed to for last 1-3 months
42
What does FPG stand for?
Fasting plasma glucose
43
What is Type 1 diabetes mellitus?
Auto-immune destruction of pancreatic beta cells Meaning no insulin can be produced
44
Where is insulin produced in the body?
Pancreatic beta cells
45
What are the main risk factors for Type 1 diabetes?
(1) Family history | (2) Ethnicity - Northern European descent
46
What initiates the autoimmune beta cell destruction?
Not fully understood But TRIGGERED by something
47
Define 'iatrogenic'.
Illness following treatment or medical intervention
48
What is the first line treatment for T1DM?
Injected insulin replacement - lifelong
49
What dietary modification is required for management of T1DM?
(1) Low fat (2) High fibre (3) Healthy diet - to spread nutrients across the day
50
What monitoring requirements are there for T1DM?
(1) Insulin dose adjustment (2) Glycaemic control (3) Complications - retinopathy, diabetic foot, CVD risk
51
What management options are there for T1DM?
(1) Injected insulin replacement (2) Diet modification (3) Monitoring (4) Exercise (5) Education on the importance of adherence
52
What is the purpose of insulin replacement therapy?
To be administered in a way that mimics the normal insulin secretion pattern
53
Describe the concentration of insulin secretion in a healthy patient.
(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
Why would it be beneficial to genetically modify a human insulin?
To achieve rapid/ short/ intermediate/ long lasting onset/ duration of effect
55
Name example(s) of rapid onset insulin.
- Lispro - Aspart - Glulisine
56
Name example(s) of short onset insulin.
- Normal insulin
57
Name example(s) of intermediate insulin.
- NPH
58
Name example(s) of long-acting insulin.
- Detemir | - Glargine
59
What is commonly experienced by newly diagnosed T1DM patients when starting treatment?
Patients can experience a partial remission phase Only low levels of insulin are required to maintain good glycaemic control
60
What is hypoglycaemia, and how is it caused?
(1) Abnormally low blood sugar | (2) Most common side effect of insulin therapy
61
What is lipohypertrophy? Where does it occur and what causes it?
Accumulation of fat at injection sites Due to local effects of insulin
62
What is the purpose of rotating injection sites?
To avoid lipohypertrophy
63
How can lipohypertrophy be avoided?
Rotation of injection sites
64
Is insulin allergy common?
No, insulin is highly purified
65
If a patient were allergic to injected insulin, what would be the anticipated effect?
- Atrophy of fat | - Altered effect of insulin
66
Why is monitoring glucose levels important in T1DM?
Allows insulin doses to be adjusted accordingly
67
What is retinopathy?
Disease of the retina, impairs/ loses vision
68
How prevalent is T2DM?
90% of all DM cases
69
How is T2DM characterised?
(1) Reduced insulin secretion | (2) Increased insulin resistance
70
What change is present in patients with T2DM, that affects their insulin secretion?
A 50% reduction in pancreatic beta-cell mass
71
How is hypoglycaemia caused in patients with T2DM?
Impaired insulin secretion in early phase (first meal) Increased second phase response Exaggerated second phase can lead to hypoglycaemia after 3-4 hours
72
What are the common symptoms of T2DM?
(1) Increased thirst/ hunger (2) Polyuria - increased urination - especially at night (3) Fatigue (4) Blurred vision (5) Infection
73
What is HHS?
Hyperosmolar Hyperglycaemic State Hyperglycaemia, dehydrated, uraemia
74
What is uraemia?
Raised level of urea and other nitrogenous waste in the blood - which would normally be eliminated by the kidneys
75
What condition is characterised by a raised level of urea and other nitrogenous waste in the blood?
Uraemia
76
How can incidence of T2DM be reduced?
Lifestyle interventions (1) Reduce weight (2) Reduce fat intake (3) Increase dietary fibre (4) Exercise
77
How long can T2DM be asymptomatic for?
Up to 10 years
78
Why are diabetes screening programmes used?
To prevent T2DM To detect T2DM in asymptomatic patients
79
Universal screening tests are not practical. Who is target by the screening programs?
Patients at risk
80
What tests do diabetes screening programs include?
(1) Oral glucose tolerance test - random glucose levels (2) Fasting blood glucose tests (3) HbA1c levels - glycated haemoglobin
81
What is the first line treatment for T2DM?
Lifestyle interventions, e.g. diet + weight loss + exercise
82
What drug treatment options are there for T2DM?
(1) Hypoglycaemic agents | (2) Insulins
83
What categories of oral hypoglycaemic agents are there?
(1) Insulin sensitisers (2) Insulin secretagogues (3) Inhibitor of glucose absorption from GIT (4) Inhibitor renal glucose reuptake
84
What is an 'insulin sensitiser'?
- Enhances the effect of endogenous insulin - Increases target cell sensitivity to insulin - Decreases glucose production in liver
85
What does metformin do?
- First line treatment for T2DM - Suppresses appetite - Cardio-protective effect
86
When can metformin not be given? Why?
When the patient has renal impairment, cardiac failure, or liver failure Because metformin is associated with lactic acidosis
87
What comorbidity are the glitazones linked to?
Cardiovascular disease
88
What comorbidities does pioglitazone increase risk of?
(1) Heart failure | (2) Bladder cancer
89
What does an insulin secretagogue do?
Stimulates insulin release from the pancreas
90
What is the purpose of an insulin secretagogue?
- To restore early phase insulin release | - To return plasma levels to pre-prandial levels
91
What does post-prandial mean?
Following dinner/ lunch/ a meal
92
What does pre-prandial mean?
Prior to dinner/ lunch/ a meal
93
What are 2 types of insulin secretagogues?
(1) Sulphonylureas | (2) Meglitinides
94
How do sulphonylureas affect a patient's weight?
Cause patients to gain weight Not first choice for overweight patients
95
What is the mechanism of action of sulphonylureas and meglitinides? How does it differ?
Bind to receptors that close a K+ ATP channel Causes a rise in intracellular calcium and insulin release
96
How do the side effects of meglitinides compare to other insulin secretagogues?
Fewer side-effects/ shorter duration Because it is shorter acting
97
Which insulin secretagogue has reduced side-effects? Why?
(1) Meglitinides | (2) Because they are short-acting
98
Give an example of an inhibitor of glucose absorption in the GIT.
Acarbose
99
What is the mechanism of action of an inhibitor of glucose absorption in the GIT?
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
What is more effective in reducing HbA1c plasma concentration, metformin or inhibitors of glucose absorption in the GIT?
Metformin is more effective
101
What side-effects are associated with inhibitors of glucose absorption in the GIT, such as acarbose?
(1) Flatuence (2) Bloating (3) Diarrhoea
102
What is GLP-1?
Glucagon-like peptide-1 - Stimulates insulin release from pancreatic beta-cells - Suppresses glucagon release from pancreatic alpha-cells - Decreases gastric emptying
103
What are incretins? Give 2 examples
- Molecules which reduce glucagon production and increase insulin - GLP-1 or GIP
104
How are GLP-1 analogues (mimetics) delivered?
Subcutaneous injection
105
What is SGLT2? Where is it located?
(1) Responsible for 90% of glucose reabsorption | (2) Proximal tubule of nephron
106
What is gestational diabetes?
Diabetes occurring for the first time during pregnancy
107
What are the side effects of gestational diabetes?
(1) Increases risk of miscarriage (2) Congenital malformations (3) Increased risk of still birth (4) Premature baby death (first year of life)
108
How can the side-effects of gestational diabetes be reduced/ managed?
Effective glycaemic control
109
What are the risk factors for gestational diabetes?
Same as Type 2 diabetes mellitus - Family history - Age - Weight - Ethnicity
110
When are pregnant women screened for gestational diabetes?
If they are at risk
111
What is the treatment for gestational diabetes?
(1) Lifestyle modification | (2) Insulin therapy if lifestyle modification is insufficient

Part 3 – PM3B COPY T (33 decks)

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