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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
What happens to FFAs
Transported to the liver for gluconeogenesis where they are oxidised to ketone bodies
26
Name three ketone bodies
1. Beta hydroxybutyrate 2. Acetoacetate 3. Acetone
27
Define type II diabetes
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)
28
How is glucose output affected in type II diabetes
Raised
29
How does glucose effect insulin levels in the blood
1. Causes increase in insulin normally 2. No change in insulin in type II diabetes Insulin levels are lower in diabetics
30
How does insulin secretion change over time
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
31
What happens to fasting and postprandial glucose in diabetes type II
Increases exponentially as insulin secretion decreases
32
Effect of decreased insulin secretion in type II diabetes
1. Reduced muscle and fat uptake after eating 2. Suppression of lipolysis is failed -> Free Fatty Acids 3. HIGH glucose output after a meal
33
Overview of type I diabetes
1. Absent insulin secretion 2. Unrestrained glucose + ketone production 3. Hyperglycaemia + plasma ketone increased GLYCOSURIA and KETONURIA
34
Does DKA occur in type 2 diabetes?
No because insulin levels are low but not non-existent so there is suppression in lipolysis -> free fatty acids -> ketone bodies
35
When can DKA occur in type two diabetes
High levels of adrenaline
36
Why does insulin secretion become impaired in type II diabetes
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
37
When is rapid acting insulin given
At meal-time
38
Name some prandial/meal-time insulins
1. Insulin lispro (NPH insulin) 2. Insulin glulisine (Insuline glargine) 3. EDTA/citrate human insulin (Insulin determir) 4. Insulin aspart (insulin degludec)
39
Why does glucose need tone tightly controlled
Risk of retinopathy
40
What is basal bolus therapy
1. Insulin pumps that try mimic the physiology of insulin
41
How is insulin pump delivered into th body
SUBCUTAENOUSLY
42
Why is basal insulin given throughout the day
Control blood glucose between meals particularly at night
43
What is the fasting blood glucose that needs to be achieved by the basal insulin
5-7 mmol/L
44
Describe treatment of type 2 diabetes mellitus
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
45
Name an intermediate-acting insulin
Human basal insulin (NPH)
46
How long does it take for intermediate-acting insulin to act
90 minutes
47
Peak action of intermediate-acting insulin
2-4 hours
48
Duration of intermediate acting insulin
24 hours
49
Name a basal analogue
Deter or Glargine U100
50
Benefit of basal analogues
Keeps insulin secretion at steady state
51
Onset of basal analogues
1-2 days for 24 hours
52
Name three rapid-acting analogues
1. Insulin aspart 2. Insulin lisper 3. Insulin glulisine
53
Onset for rapid-acting analogues
10-20 minutes
54
Peak time for action of rapid-acting analogues
30-90 minutes
55
Duration of rapid-acting analogue actions
2-5 hours
56
Name a premixed insulin
Humulin M3
57
What is a premixed insulin
70% - rapid acting analogue | 30% - normal insulin
58
Onset of Humulin M3
30 minutes
59
Peak action of Humulin M3
2-8 hours
60
Three ways we can treat type II diabetes
1. Once daily basal insulin 2. Twice daily mix-insulin 3. Basal-bolus therapy
61
Advantages of basal insulin in type II diabetes
1. Simple 2. Can carry on with oral therapy 3. Less risk of hypoglycaemia at night
62
Diasvntage of basal insulin in type II diabetes
1. Doesn't cover meals | 2. Has to be used with long-acting insulin analogues which are costly
63
Advantages of pre-mixed insulin
1. Can cover insulin requirements throughout the day as they have basal and prandial components
64
Disadvantage of pre-mixed insulin
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
What is th best treatment therapy for T1DM
1. Intensive basal-bolus insulin therapy
66
At what level do we begin insulin therapy for T2DM
>9%
67
Ideal treatment approach for T2DM
1. Basal insulin + oral therapy to reduce hypoglycaemia
68
Define hypoglycaemia
<3.9mmol/L
69
How is mild hypoglycaemia treated
Self-treated
70
Consequence of hypoglycaemia
BRAIN NEEDS ENERGY - neuroglycopenia
71
What is level 2 hypoglycaemia
1. <3.0 mmol/L Level one is <3.9
72
Autonomic symptoms of hypoglycaemia
1. Trembling 2. Palpitations 3. Sweating 4. Anxiety 5. Hunger
73
Neuroglycopenic symptoms
1. Difficulty concentrating 2. Confusion 3. Weakness 4. Drowsiness 5. Vision Changes 6. Difficulty speaking Headache + Nausea
74
Physiological changes to stop severe hypoglycaemia
1. RELEASE OF ADRENALINE at 3.5mmol/L | 2. Inhibition of insulin secretion at 4.6 mmol/L
75
Risk factors for hypoglycaemia in T1DM
1. History of severe episodes 2. Hb1Ac <48 mmol/mol 3. Long duration of diabetes 4. Renal impairment 5. Extremes of age
76
Risk of hyperglycaemia in T2DM
1. AGE 2. Cognitive impairment 3. Depression 4. Duration of MDI insulin therapy 5. Renal impairment
77
Target HbA1c in elderly people
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
How do we prevent hypoglycaemia
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
What do people on basal-bolus insulin have to ensure
Check BG before each meal every day Adjust insulin in relation to excercise
80
Treatment of hypoglycaemia
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
Why is hypoglycaemia a side-erect of insulin therapy
Insulin analogues can't fully replicate/mimic the physiological actions of insulin itself
82
What is hyperosmolar hyperglycaemic state
COMPLICATION OF TYPE II DIABETES MELLITUS Where high blood sugar causes high osmolarity without any ketoacidosis
83
What causes hyperosmolar hyperglycaemic state
1. Lack of insulin 2. Poor kidney function 3. Old age 4. Poor fluid intake USUALLY PRECIPITATED BY INFECTION
84
Clinical presentation of hyperosmolar hyperglycaemic state
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
Differential diagnosis of hyperosmolar hyperdyclaemic state
DKA However, in HHS glucose level are extremely high and ketone bodies are low (have fruity breath)
86
How is hyperosmolar hyperglycaemic state managed
1. IV fluid 1L/h 2. K+ replacement 3. Insulin
87
Mechanism of pramlinitide
1. Delays gastric emptying | 2. Inhbitis glucagon release
88
Mechanism of alpha-glucosidase inhibitors
1. Inhibits glucose absorption | 2. Stimulation of GLP-1 release
89
Mechanism of Sulfonylureas
1. Acute stimulation of insulin release
90
Mechanism of meglitinides
1. Acute stimulation of insulin release
91
Mechanism of GLP1/DPP-IV inhibitors
1. Stimulates insulin biosynthesis 2. Inhibits B-cell apoptosis 3. Stimulates B-cell differentiation
92
Mechanism of metformin
1. Inhibits hepatic glucose production | 2. Increases hepatic insulin sensitivity
93
Mechanism of thiazolidinediones
1. Suppreses NEFA release 2. Fat redistribution 6. Modulates adipokine release
94
First line treatment for Type II diabetes
Metformin
95
If Metformin become ineffective what is done
Dual therapy with metformin and sulfonylureas/thiazolidinedione/DPP-4 inhibitor/SGLT-2 inhibitor/GLP-1 agonist etc And then triple therapy
96
Lifestyle interventions for diabetes
1. Compliance to treatment 2. Lifestyle an patient education 3. 30 min exercise a day 4. Dietitian 5. Local education programmes
97
Cons of using metformin
Difficult to maintain over long-term and costly SIDE-EFFECTS
98
What consists of the combined injectable therapy
DONE WHEN TRIPLE THERAPY is not working: 1. Basal insulin + Mealtime insulin or GLP-1-RA 2. Metformin
99
What is the recommended HbA1c target in treatment
<7.0%
100
What patients are given sulfonylureas
1. Not overweight 2. Require rapid response to hyperglycaemic symptoms 3. Cannot tolerate metformin
101
What are incretins
Hormones secreted by intestinal endothelial cells in response to nutrient intake
102
How do incretins work
1. Glucose-dependnat insulin secretions 2. Postprandial glucagon suppression 3. Slowing of gastric emptying
103
Name an incretin
GLP-1
104
What cell secretes GLP-1
enteroendocrine L cells
105
Effect of GLP-1 in the body
1. SATIETY 2. Decreased postprandial glucagon secretion 3. Decreased glucagon causes decreased hepatic glucose output 4. Enhances beta-cell insulin secretion
106
What GLP-1 analogue is given in diabetes
SC LIRAGLUTIDE | SC EXENATIDE
107
What agent prolongs activity of normal GLP-1
DPP-IV inhibitors (ORAL)
108
What is DPP-4
Dipeptidyl-peptidase 4 enzyme in vascular endothelial lining that inactivates GIP and GLP-1
109
Name a DPP-4 inhibitor
ORAL SITAGLIPTIN
110
How does SITAGLIPTIN effect weight
NO effect
111
Pros of DPP-4 inhibitors
1. No effect on gastric emptying | 2. Does not cause nausea + vomiting
112
Side-Effects of GLP-1 analogues
1. Delay in gastric emptying 2. Nausea and vomiting 3. Weight loss
113
Name some thiazolidinediones
1. PIOGLITAZONE
114
Benefits of TZDs
1. Low risk of hypoglycaemia
115
Cons of TZDs
Increased CV risk, weight gain and lipid abnormalities
116
Benefits of SU
1. Reduces CV risk
117
Cons of SU
1. Hypoglycaemia 2. Increased risk of CV events 3. WEIGHT GAIN
118
Benefits of Metformin
1. BP reduction | 2. CV risk reduced
119
Cons of Metformin
Lactic acidosis | No weight change
120
Contraindications of TZD
1. CCF 2. High risk fractures 3. Macula oedema
121
Name some SGLT-2 inhibtors
EMPAGLIFOZIN
122
Where are SLGT-2 receptors found
PCT
123
Role of SLGT-2 receptors
Co-tranpsort glucose and Na into renal cells for re-absorption
124
What channel causes movement of glucose out of renal epithelial cells back in to the blood
GLUT2
125
Pros of EMPAGLIFLOZIN
1. Decreased CV death
126
Patient A wants to lose weight, what drugs would she NOT be given
1. Pioglitazone (TZD) 2. Insulin 3. SU 4. DPP-4I
127
What drugs can be given for patient A
1. GLP1a | 2. SGLT2i
128
Patient A does not want injectable treatment so what treatment should she be given
SGLT-2i (orally)
129
Side-effect of SLGT-2i
Causes thrush in women (mycotic) Keep treatment going and manage thrush Causes intravascular volume depletion so hypotension can occur in elderly monitor BP
130
What factor reduces efficacy of SGLT-2i
Increasing renal impairment (they do not worsen it themselves)
131
At what eGFR should SGLT-2i be avoided
1. <30 ml/min/1.73m^2
132
At what eGFR limit is empglifosin and canaglifosin given
>45ml/min/1.73
133
At what eGFR limit is dapaglifosin given
> 60 ml/min/1.73
134
Genetic inheritance of type II diabtes
1. Positive family history | 2. Monozygotic twins!!

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