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Year 2 > Diabetes: Part II > Flashcards

Diabetes: Part II Flashcards

1
Q

IN the fasting state where does all glucose come from

A
  1. LIVER (breakdown of glycogen)
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2
Q

Name three carbon precursors used in gluconeogenesis in the fasting state

A
  1. Lactate
  2. Alanine
  3. Glycerol
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3
Q

What is used as an energy source when insulin levels are low and glucose levels have run out

A

Free Fatty Acids are used by muscles for fuel

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4
Q

What is the post-prandial phase

A

Following needing - physiological need to dispose of nutrient load

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5
Q

What happens to rising glucose after eating

A

Increased insulin secretion

Suppresses glucagon

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6
Q

Where is glucose stored in post-prandial phase

A
  1. Liver
  2. Muscles

Used to replenish glycogen stores in the liver and muscle

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7
Q

What surpasses lipolysis and NEFA levels

A

High insulin and glucose

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8
Q

What connects the alpha and beta cells together

A

Paracrine crosstalk

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9
Q

What is glucagon inhibited by

A

Insulin

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10
Q

What cell secretes insulin

A

Beta cell

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11
Q

What cell secretes glucagon

A

Alpha cells

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12
Q

How is insulin secreted by the beta-cell

A
  1. Glucose enters through GLUT2 glucose
  2. Glucokinase breaks down glucose -> Increasing ADP/ATP ratio
  3. Increase in ADP/ATP causes calcium channels to open
  4. Calcium ions cause secretory insulin granules to be moved out by exocytosis
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13
Q

How does insulin cause glucose to enter muscle and fat cells

A
  1. Insulin binds to fat cells
  2. Causes intracellular GLUT4 vesicles to insert into the plasma membrane
  3. Glucose enters into cell via GLUT4
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14
Q

What processes are suppressed by insulin

A
  1. Glycogenolysis
  2. Gluconeogenesis
  3. Lipolysis
  4. Breakdown of muscle
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15
Q

Role of glucagon

A
  1. Increased glycogenolysis/gluconeogenesis
  2. Reduced peripheral glucose uptake
  3. Stimulate release of gluconeogeneic precursors (glycerol, Alanine and Lactate) for lipolysis
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16
Q

Two ways diabetes mellitus causes mortality

A
  1. Acute hyperglycaemia (DKA + Hypersomolar coma)

2. Chronic hyperglycaemia

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17
Q

Describe the pathogenesis of type I diabetes

A
  1. Insulin deficiency disease caused by loss of beta cells due to autoimmune destruction
  2. Beta cells express HLA which activate mediated immune response

INSULITIS

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18
Q

What antibodies of type I diabetes are found in the blood

A
  1. ICA
  2. GAD65
  3. Insulin
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19
Q

What is pre-diabetes

A
  1. Loss of first-phase insulin response

2. Glucose intolerance develops

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20
Q

What percentage of beta cells remain in diabetes

A

10%

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21
Q

What is the consequence of insulin secretion in type I diabetes

A
  1. Continued breakdown of liver glycogen
  2. Unrestrained lipolysis and skeletal muscle breakdown to provide gluconeogenic precursors
  3. Inappropriate increase in hepatic glucose output and suppression of peripheral glucose intake
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22
Q

What is the consequence of rising glucose concentration in type I diabetes

A

Exceeds threshold of 10mM causing urinary glucose

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23
Q

Failure of treating insulin in type I diabetes

A
  1. Increase in circulating glucagon -> increases glucose further
  2. Increased cortisol and adrenaline
  3. Ketoacidosis
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24
Q

How do free fatty acids effect glucose uptake

A

Reduces it

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25
Q

What happens to FFAs

A

Transported to the liver for gluconeogenesis where they are oxidised to ketone bodies

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26
Q

Name three ketone bodies

A
  1. Beta hydroxybutyrate
  2. Acetoacetate
  3. Acetone
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27
Q

Define type II diabetes

A
  1. Increased resistance to insulin by muscle and fat cells as intra-abdominal fat increases (sensitivity to insulin decreases)
  2. Decreased insulin secretion (insulin levels are very low)
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28
Q

How is glucose output affected in type II diabetes

A

Raised

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29
Q

How does glucose effect insulin levels in the blood

A
  1. Causes increase in insulin normally
  2. No change in insulin in type II diabetes

Insulin levels are lower in diabetics

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30
Q

How does insulin secretion change over time

A
  1. During pre-diabetes (impaired glucose tolerance), insulin secretion increases to try bring out the same effect
  2. Body gives up as glucose levels are not going up so insulin secretion decreases in actual diabetes
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31
Q

What happens to fasting and postprandial glucose in diabetes type II

A

Increases exponentially as insulin secretion decreases

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32
Q

Effect of decreased insulin secretion in type II diabetes

A
  1. Reduced muscle and fat uptake after eating
  2. Suppression of lipolysis is failed -> Free Fatty Acids
  3. HIGH glucose output after a meal
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33
Q

Overview of type I diabetes

A
  1. Absent insulin secretion
  2. Unrestrained glucose + ketone production
  3. Hyperglycaemia + plasma ketone increased

GLYCOSURIA and KETONURIA

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34
Q

Does DKA occur in type 2 diabetes?

A

No because insulin levels are low but not non-existent so there is suppression in lipolysis -> free fatty acids -> ketone bodies

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35
Q

When can DKA occur in type two diabetes

A

High levels of adrenaline

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36
Q

Why does insulin secretion become impaired in type II diabetes

A
  1. Genetic predisposition
  2. Deposition of amilyn peptides within the beta cell
  3. Glucotoxicity hyperglycaemia inhibits insulin secretion

LIPID DEPOSITION in pancreatic islets prevent normal function

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37
Q

When is rapid acting insulin given

A

At meal-time

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38
Q

Name some prandial/meal-time insulins

A
  1. Insulin lispro (NPH insulin)
  2. Insulin glulisine (Insuline glargine)
  3. EDTA/citrate human insulin (Insulin determir)
  4. Insulin aspart (insulin degludec)
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39
Q

Why does glucose need tone tightly controlled

A

Risk of retinopathy

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40
Q

What is basal bolus therapy

A
  1. Insulin pumps that try mimic the physiology of insulin
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41
Q

How is insulin pump delivered into th body

A

SUBCUTAENOUSLY

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42
Q

Why is basal insulin given throughout the day

A

Control blood glucose between meals particularly at night

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43
Q

What is the fasting blood glucose that needs to be achieved by the basal insulin

A

5-7 mmol/L

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44
Q

Describe treatment of type 2 diabetes mellitus

A
  1. Basal insulin initially introduced before prandial insulin is given (mimics meal-time insulin secretion)
  2. Long-acting basal insulin given
  3. Premix insulins availbale
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45
Q

Name an intermediate-acting insulin

A

Human basal insulin (NPH)

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46
Q

How long does it take for intermediate-acting insulin to act

A

90 minutes

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47
Q

Peak action of intermediate-acting insulin

A

2-4 hours

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48
Q

Duration of intermediate acting insulin

A

24 hours

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49
Q

Name a basal analogue

A

Deter or Glargine U100

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50
Q

Benefit of basal analogues

A

Keeps insulin secretion at steady state

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51
Q

Onset of basal analogues

A

1-2 days for 24 hours

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52
Q

Name three rapid-acting analogues

A
  1. Insulin aspart
  2. Insulin lisper
  3. Insulin glulisine
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53
Q

Onset for rapid-acting analogues

A

10-20 minutes

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54
Q

Peak time for action of rapid-acting analogues

A

30-90 minutes

55
Q

Duration of rapid-acting analogue actions

A

2-5 hours

56
Q

Name a premixed insulin

A

Humulin M3

57
Q

What is a premixed insulin

A

70% - rapid acting analogue

30% - normal insulin

58
Q

Onset of Humulin M3

A

30 minutes

59
Q

Peak action of Humulin M3

A

2-8 hours

60
Q

Three ways we can treat type II diabetes

A
  1. Once daily basal insulin
  2. Twice daily mix-insulin
  3. Basal-bolus therapy
61
Q

Advantages of basal insulin in type II diabetes

A
  1. Simple
  2. Can carry on with oral therapy
  3. Less risk of hypoglycaemia at night
62
Q

Diasvntage of basal insulin in type II diabetes

A
  1. Doesn’t cover meals

2. Has to be used with long-acting insulin analogues which are costly

63
Q

Advantages of pre-mixed insulin

A
  1. Can cover insulin requirements throughout the day as they have basal and prandial components
64
Q

Disadvantage of pre-mixed insulin

A
  1. Requires consistent meals and exercise patterns
  2. Nocturnal hypoglycaemia
  3. Fasting hyperglycaemia
  4. Might have to be fine with a HbA1c goal of <64 mmol/mol
65
Q

What is th best treatment therapy for T1DM

A
  1. Intensive basal-bolus insulin therapy
66
Q

At what level do we begin insulin therapy for T2DM

A

> 9%

67
Q

Ideal treatment approach for T2DM

A
  1. Basal insulin + oral therapy to reduce hypoglycaemia
68
Q

Define hypoglycaemia

A

<3.9mmol/L

69
Q

How is mild hypoglycaemia treated

A

Self-treated

70
Q

Consequence of hypoglycaemia

A

BRAIN NEEDS ENERGY - neuroglycopenia

71
Q

What is level 2 hypoglycaemia

A
  1. <3.0 mmol/L

Level one is <3.9

72
Q

Autonomic symptoms of hypoglycaemia

A
  1. Trembling
  2. Palpitations
  3. Sweating
  4. Anxiety
  5. Hunger
73
Q

Neuroglycopenic symptoms

A
  1. Difficulty concentrating
  2. Confusion
  3. Weakness
  4. Drowsiness
  5. Vision Changes
  6. Difficulty speaking

Headache + Nausea

74
Q

Physiological changes to stop severe hypoglycaemia

A
  1. RELEASE OF ADRENALINE at 3.5mmol/L

2. Inhibition of insulin secretion at 4.6 mmol/L

75
Q

Risk factors for hypoglycaemia in T1DM

A
  1. History of severe episodes
  2. Hb1Ac <48 mmol/mol
  3. Long duration of diabetes
  4. Renal impairment
  5. Extremes of age
76
Q

Risk of hyperglycaemia in T2DM

A
  1. AGE
  2. Cognitive impairment
  3. Depression
  4. Duration of MDI insulin therapy
  5. Renal impairment
77
Q

Target HbA1c in elderly people

A
  1. 58 mmol/mol in healthy elderly
  2. 64 mmol/mol in many chronic illnesses and current hypoglycaemia
  3. 69mmol/mol in end-stage chronic illness
78
Q

How do we prevent hypoglycaemia

A
  1. Educate patients and caregivers on how to recognise and treat hypoglycaemia
  2. Instruct patients to report hypo episode stop doctor of history
  3. Blood glucose awareness training programme
79
Q

What do people on basal-bolus insulin have to ensure

A

Check BG before each meal every day

Adjust insulin in relation to excercise

80
Q

Treatment of hypoglycaemia

A
  1. Check for <3.9 mmol/L
  2. Treat with 15g fast acting carbohydrates
  3. Retest in 15 minutes to ensure glucose >4.0 and retreat
  4. Eat long-acting carbohydrate
  5. MDT support
  6. Change glucose targets
81
Q

Why is hypoglycaemia a side-erect of insulin therapy

A

Insulin analogues can’t fully replicate/mimic the physiological actions of insulin itself

82
Q

What is hyperosmolar hyperglycaemic state

A

COMPLICATION OF TYPE II DIABETES MELLITUS

Where high blood sugar causes high osmolarity without any ketoacidosis

83
Q

What causes hyperosmolar hyperglycaemic state

A
  1. Lack of insulin
  2. Poor kidney function
  3. Old age
  4. Poor fluid intake

USUALLY PRECIPITATED BY INFECTION

84
Q

Clinical presentation of hyperosmolar hyperglycaemic state

A
  1. Altered level of consciousness
  2. Blured vision, headaches, seizures, myoclonic jerking
  3. Hyperviscoity (clot formations)
  4. Dehydration
  5. Weight loss
  6. Nausea
  7. Weakness
    POSTURAL HYPOTENSION
85
Q

Differential diagnosis of hyperosmolar hyperdyclaemic state

A

DKA

However, in HHS glucose level are extremely high and ketone bodies are low (have fruity breath)

86
Q

How is hyperosmolar hyperglycaemic state managed

A
  1. IV fluid 1L/h
  2. K+ replacement
  3. Insulin
87
Q

Mechanism of pramlinitide

A
  1. Delays gastric emptying

2. Inhbitis glucagon release

88
Q

Mechanism of alpha-glucosidase inhibitors

A
  1. Inhibits glucose absorption

2. Stimulation of GLP-1 release

89
Q

Mechanism of Sulfonylureas

A
  1. Acute stimulation of insulin release
90
Q

Mechanism of meglitinides

A
  1. Acute stimulation of insulin release
91
Q

Mechanism of GLP1/DPP-IV inhibitors

A
  1. Stimulates insulin biosynthesis
  2. Inhibits B-cell apoptosis
  3. Stimulates B-cell differentiation
92
Q

Mechanism of metformin

A
  1. Inhibits hepatic glucose production

2. Increases hepatic insulin sensitivity

93
Q

Mechanism of thiazolidinediones

A
  1. Suppreses NEFA release
  2. Fat redistribution
  3. Modulates adipokine release
94
Q

First line treatment for Type II diabetes

A

Metformin

95
Q

If Metformin become ineffective what is done

A

Dual therapy with metformin and sulfonylureas/thiazolidinedione/DPP-4 inhibitor/SGLT-2 inhibitor/GLP-1 agonist etc

And then triple therapy

96
Q

Lifestyle interventions for diabetes

A
  1. Compliance to treatment
  2. Lifestyle an patient education
  3. 30 min exercise a day
  4. Dietitian
  5. Local education programmes
97
Q

Cons of using metformin

A

Difficult to maintain over long-term and costly

SIDE-EFFECTS

98
Q

What consists of the combined injectable therapy

A

DONE WHEN TRIPLE THERAPY is not working:
1. Basal insulin + Mealtime insulin or GLP-1-RA

  1. Metformin
99
Q

What is the recommended HbA1c target in treatment

A

<7.0%

100
Q

What patients are given sulfonylureas

A
  1. Not overweight
  2. Require rapid response to hyperglycaemic symptoms
  3. Cannot tolerate metformin
101
Q

What are incretins

A

Hormones secreted by intestinal endothelial cells in response to nutrient intake

102
Q

How do incretins work

A
  1. Glucose-dependnat insulin secretions
  2. Postprandial glucagon suppression
  3. Slowing of gastric emptying
103
Q

Name an incretin

A

GLP-1

104
Q

What cell secretes GLP-1

A

enteroendocrine L cells

105
Q

Effect of GLP-1 in the body

A
  1. SATIETY
  2. Decreased postprandial glucagon secretion
  3. Decreased glucagon causes decreased hepatic glucose output
  4. Enhances beta-cell insulin secretion
106
Q

What GLP-1 analogue is given in diabetes

A

SC LIRAGLUTIDE

SC EXENATIDE

107
Q

What agent prolongs activity of normal GLP-1

A

DPP-IV inhibitors (ORAL)

108
Q

What is DPP-4

A

Dipeptidyl-peptidase 4 enzyme in vascular endothelial lining that inactivates GIP and GLP-1

109
Q

Name a DPP-4 inhibitor

A

ORAL SITAGLIPTIN

110
Q

How does SITAGLIPTIN effect weight

A

NO effect

111
Q

Pros of DPP-4 inhibitors

A
  1. No effect on gastric emptying

2. Does not cause nausea + vomiting

112
Q

Side-Effects of GLP-1 analogues

A
  1. Delay in gastric emptying
  2. Nausea and vomiting
  3. Weight loss
113
Q

Name some thiazolidinediones

A
  1. PIOGLITAZONE
114
Q

Benefits of TZDs

A
  1. Low risk of hypoglycaemia
115
Q

Cons of TZDs

A

Increased CV risk, weight gain and lipid abnormalities

116
Q

Benefits of SU

A
  1. Reduces CV risk
117
Q

Cons of SU

A
  1. Hypoglycaemia
  2. Increased risk of CV events
  3. WEIGHT GAIN
118
Q

Benefits of Metformin

A
  1. BP reduction

2. CV risk reduced

119
Q

Cons of Metformin

A

Lactic acidosis

No weight change

120
Q

Contraindications of TZD

A
  1. CCF
  2. High risk fractures
  3. Macula oedema
121
Q

Name some SGLT-2 inhibtors

A

EMPAGLIFOZIN

122
Q

Where are SLGT-2 receptors found

A

PCT

123
Q

Role of SLGT-2 receptors

A

Co-tranpsort glucose and Na into renal cells for re-absorption

124
Q

What channel causes movement of glucose out of renal epithelial cells back in to the blood

A

GLUT2

125
Q

Pros of EMPAGLIFLOZIN

A
  1. Decreased CV death
126
Q

Patient A wants to lose weight, what drugs would she NOT be given

A
  1. Pioglitazone (TZD)
  2. Insulin
  3. SU
  4. DPP-4I
127
Q

What drugs can be given for patient A

A
  1. GLP1a

2. SGLT2i

128
Q

Patient A does not want injectable treatment so what treatment should she be given

A

SGLT-2i (orally)

129
Q

Side-effect of SLGT-2i

A

Causes thrush in women (mycotic)

Keep treatment going and manage thrush

Causes intravascular volume depletion so hypotension can occur in elderly

monitor BP

130
Q

What factor reduces efficacy of SGLT-2i

A

Increasing renal impairment (they do not worsen it themselves)

131
Q

At what eGFR should SGLT-2i be avoided

A
  1. <30 ml/min/1.73m^2
132
Q

At what eGFR limit is empglifosin and canaglifosin given

A

> 45ml/min/1.73

133
Q

At what eGFR limit is dapaglifosin given

A

> 60 ml/min/1.73

134
Q

Genetic inheritance of type II diabtes

A
  1. Positive family history

2. Monozygotic twins!!

Year 2 (155 decks)

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