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case 6 - introduction to type 2 diabetes Flashcards

1
Q

what is diabetes mellitus

A

metabolic diseases characterised by hyperglycaemia resulting from defects in insulin secretion, insulin action or both

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2
Q

what is type 2 diabetes

A

metabolic disorder caused by insulin resistance and insulin deficiency resulting in hyperglycaemia

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3
Q

what is pre diabetes and how is it diagnosed

A

at high risk of developing type 2 diabetes:
Impaired glucose tolerance - IGT
Above normal glucose blood concentration after fasting (impaired glucose fasting - IFG)
Above normal HbA1c - 42-48 = pre diabetes and 48+ is diabetes

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4
Q

what is the epidemiology of type 2 diabetes

A

in 2015 there were over 415 million people with diabetes worldwide
Type 2 diabetes accounts for around 90% of cases

in the UK, around 3.9 million are diagnosed with diabetes in 2019
Steady increases in diabetes incidence and prevalence

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5
Q

who is type 2 diabetes the most common in

A

more common in men than in women
65+ age group most affected
Increasing numbers diagnosed under 40 years of age
Childhood type 2 diabetes incidence also increasing

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6
Q

what ethnicity is diabetes the most common in

A

3-5 times increased prevalence in ethnic minority groups vs white communities.

south asians

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7
Q

in spite of lower BMI, what do south asians have:

A

more abdominal fat
More insulin resistance + hyperinsulinaemia
Increased inflammatory reponse
Lower adiponectin
More dyslipidaemia

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8
Q

what is the morbidity and mortality causes in type 2 diabetes

A

cardiovascular disease is the cause of death in around 70%
Commonest cause of chronic kidney disease
Commonest cause of lower limb amputation
Commonest cause of blindness in working population
Non-alcoholic fatty liver disease and most common liver disease in the world
10% of the NHS budget

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9
Q

what is the pathophysiology of type 2 diabetes

A
  • there are genetic predisposition and environmental risk factors
  • these risk factors lead to obesity, which leads to insulin resistance
  • this leads to decreased glucose uptake which then leads to hyperglycaemia
  • then hyperglycaemia leads to type 2 diabetes
  • also increased hepatic glucose output, caused by deranged insulin release can also lead to hyperglycaemia
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10
Q

what are the non modifiable risk factors of type 2 diabetes

A

age
Ethnicity
Family history
Low birth weight
History of GDM

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11
Q

what are the modifiable risk factors for type 2 diabetes

A

obesity -approximately 80% of the risk for developing T2DM
Hypertension - 20mmhg increase was associated with 58% increase risk of diabetes
Dyslipidemia - low HDL, high triglycerides
PCOS - elevated androgens and insulin resistance
Poor dietary habit

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12
Q

what is the linear relationship between obesity and type 2 diabetes

A

Visceral and abdominal fat have a much greater associated with type 2 diabetes than cutaneous fat
Variation in distribution of fat with age, ethnicity, and sex
Increased fat mass —> insulin resistance and type 2 diabetes

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13
Q

what are the genetics linked to diabetes

A

polygenic
The risk of developing the condition is as high as 70% if both parents have suffered from the condition
First degree relatives of individuals with type 2 diabetes are about 3 times more likely to develop the disease
Monozygotic twins, there is a 50-90% concordance for developing the condition
Environments —> genetics

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14
Q

what are the steps in the key pathophysiological processes

A
  1. insulin resistance
  2. insulin secretory defect
  3. increased production of glucose by the liver
  4. loss of incretin effect
  5. other mechanisms such as insulin feedback and CNS changes
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15
Q

what processes does insulin lead to

A

Insulin leads to a number of anabolic processes, such as building larger molecules from smaller molecules, which are crucial to cellular survival, the growth of cells and tissues and maintaining normal homeostasis

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16
Q

what is the insulin receptor

A

a modified tyrosine kinase receptor

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17
Q

describe the binding of this receptor and what happens

A

he insulin receptor is a modified tyrosine kinase receptor

when insulin, as the ligand, binds to the insulin receptor, you get the insulin signalling cascade

An important part of the insulin signalling cascade is the exocytosis of GLUT4 channels to the cell membrane and then the facilitated diffusion of glucose, which is in the blood of course, into the cell

Glucose is then used in glycolysis in cellular respiration so that we get energy

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18
Q

in insulin resistance, what else does this increased glucose lead to

A

hyperglycaemia
Increased lipolysis
Increased proteolysis
Increased hepatic gluconeogenesis

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19
Q

what else is this glucose used for in anabolic processes and cellular growth

A

cellular respiration
Proteins and lipid synthesis
Inhibit hepatic gluconeogenesis
Promote hepatic glycogen synthesis

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20
Q

what are the damaging molecules in obese people

A

free fatty acids

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21
Q

what are free fatty acids used as

A

used as a substrate, as an energy by the liver and gluconeogenesis is increased

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22
Q

what is there less of because of this free fatty acid accumulation around the liver

A

there is less insulin feedback

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23
Q

what is there more of because of these free fatty acids

A

there is more gluconeogenesis and more blood glucose

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24
Q

what happens in the muscles

A

the muscles will used more fatty acids instead of glucose, so there is less glucose taken up from the blood and therefore less glycogenesis

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25
what is the relationship between free fatty acids and the beta cell
FFAs are toxic to the beta cell and therefore less insulin is released again leading to problems with hypoglycaemia
26
what mediators are increased with increased lipolysis
inflammatory mediators; released by adipocytes: - TNF alpha and IL-6
27
what kind of activity is increased with lipolysis
greater sympathetic activity
28
what happens to the beta cells as hyperglycaemia develops
beta cells secrete more insulin to deal with increase in glucose
29
what happens when the beta cell mass is depleted
insulin levels fall and there is secretory failure
30
what is shown during autopsy of patients with T2DM
increased deposition of amyloid within islet cells
31
what is toxic to beta cells
hyperglycaemia (glucotoxicity) high lipids (lipotoxicity)
32
what are beta cells damaged by
amyloid deposits Inflammation Glucotoxicity Lipotoxicity
33
describe the mechanism of action of increased hepatic gluconeogenesis
1. Increased availability of gluconeogenic substrates e.g fatty acids leads to increased gluconeogenesis 2. Resistance of the liver to the action of insulin leads to improper suppression of hepatic gluconeogenesis 3. Elevated glucagon due to resistance to feed back suppression from insulin and glucose
34
what are incretins
gut peptide hormones that are secreted after nutrient intake and whose primary role is to stimulate insulin release
35
what is GLP1 secreted by
GLP-1L cells located in the ileum and large intestine
36
what is GIP secreted by
GIP K cells located in the proximal duodenum
37
what are the symptoms and signs of type 2 diabetes
asymptomatic Polyuria and nocturia Lethargy Weight change (weight loss once severe insulin deficiency occurs) Thrush/genetial itching Prolonged healing time Visual disturbance
38
how is type two diabetes diagnosed
diabetes symptoms (e/g polyuria, polydipsia) plus: HbA1c of >48mmol/mol or A random venous plasma glucose concentration of more than 11.1mmol/L or A fasting plasma glucose concentration of more than 7 mmol/L or Two hour plasma glucose concentrations more than 11.1 mmol/L two hours after 75g anhydrous glucose in an oral glucose tolerance test (OGTT)
39
how is diabetes type 2 diagnosed without symptoms
two separate positive results from separate days
40
when do you not use Hb1Ac as diagnoses technique
rapid onset of diabetes - an increase in HbA1c may not be detected until a few weeks later Pregnancy - HbA1c typically lower Conditions with decreased red cell survival, haemolytic anaemia, severe blood loss, splenomegaly, antiretroviral drugs Increased red cell survival may increase Hb1Ac e.g splenectomy Renal dialysis reduced Hb1Ac especially if treated with erythropoietin Iron and B12 deficiency and their treatment
41
for the above (excluding pregnancy) how do we diagnose diabetes then
For the above (except pregnancy) diagnose by fasting glucose more than 7mmol/L twice, or once with symptoms
42
what are the aims of treatment
1. remission 2. improve glycemic control 3. treat co-existing cardiovascular risk factors
43
what are the management factors of type 2 diabetes
lifestyle modification - NHS diabetes prevention programme (DPP) ASSESS cardiovascular risk - e.g QRISK3 Diet and exercise Weight loss - aim 10% reduction Can be enough to put diabetes 2 into remission smoking cessation
44
what are the treatment targets for type 2 diabetes
-HbA1c <48mmol/mol if not on medication which cause hypoglycaemia ( otherwise <53mmol/mol) -BP <140/80 (<130/80 if complications present) -Total cholesterol <4.0 mmol/l, LDL<2.0 mmol/l, HDL >1 (men) >1.2 (women)
45
when is there treatment escalation
if Hb1Ac is greater than 58mmol/L
46
what is screened for annually in people with type 2 diabetes
retinopathy - retinal photography Nephropthaty - urine dipstick, albumin creatine ratio, urea and electrolytes Neuropathy - foot inspection , 10g monofilament or 128Hz turning fork tests and pulses
47
what are the different pharmacological treatments in type 2 diabetes
metformin SGLT2 inhibitors Sulphonylurea DPP4 inhibitors Thiazoidendiones GLP-1 analogues Insulin Meglitindes Alpha glucosidase inhibitors
48
what is metformin and what does it do
it reduces insulin resistance and hepatic glucose output it reduces weight and suppresses appetite
49
what are the side effects of metformin
Side effects; diarrhoea, nausea, anorexia, lactic acidosis
50
what are the SGLT2 inhibitors MoA
reduce glucose reabsorption from proximal tubule of nephron
51
what are the additional effects of SGLT2 inhibitors
Additional effects; weight loss, blood pressure lowering, CVD protection, renal protection
52
what are the dosage values of metformin
Dosage:: Dapagliflozin 10mg OD, Canagliflozin 100mg – 300mg, Empagliflozin 10-25mg
53
what are the side effects of SGLT2 inhibitors
increased risk of urinary tract infection, DKA
54
what does sulphonylurea do
increases insulin secretion bind to sulphonyurea receptor 9SUR-1) leading to closure of ATP K+ channel
55
what is the dosage of sulphonylurea
Dosage: *gliclazide 40mg OD, increased to 320mg in divided doses if needed
56
what are the side effects of sulphonylurea
hypoglycaemia, weight gain
57
what are DPP4 inhibitors
dipeptidyl peptidase 4 inhibitors prevent breakdown of incretins, preserving incretin effect
58
what is the combination therapy DPP4 inhibitors are used in
Usually combination therapy with metformin/metformin + sulphonylurea
59
what is the dosage of DPP4 inhibitors
Dosage: alogliptin 25mg OD, saxagliptin 5mg OD
60
what are the side effects of DPP4 inhibitors
GI disturbance, rash, headache, sore throat
61
what are thiazolidinediones
peroxisome proliferator activted receptor gamma agonist
62
PPAR gamma - features
is a nuclear receptor activation decreases insulin resistance
63
what is the dosage of PPAR gamma
*Dosage: pioglitazone 15mg OD, increased to 45mg OD if required
64
what are the side effects
Side effects; increased fracture risk, fluid retention, heart failure, small increased risk of bladder cancer
65
what are the effects of GLP-1 in the pancreas
increased insulin synthesis and secretion Decreased glucagon secretion Increased beta cell survival
66
what are the effects of GLP-1 in the CNS
decreased food intake increased saiety
67
what are the effects of GLP-1 in the stomach and intestine
decreased gastric emptying decreased bowel motility decreased acid secreiton
68
what are the effects of GLP-1 in the liver/fat/muscle
increased glucose uptake Increased glycogen synthesis Increased lipogenesis in fat
69
when does one give GLP-1 analogues
BMI of 35kg/m2 or higher and medical problems associated with obesity OR BMI less than 35kg/m2 and insulin therapy would have significant implications, or weight loss would benefit other significant obesity-related comorbidities
70
what are examples of GLP-1 analogues
*Examples: Liraglutide 0.6mg-1.8mg OD, Semaglutide 1mg once weekly subcutaneous injections
71
what are side effects of GLP-1 analogues
Side effects - vomiting, nausea, diarrhoea, pancreatitis (rare)
72
when should insulin therapy be considered
inadequate control deste dual therapy (metformin plus another oral anti diabetic drug) Oral anti diabetic drugs are contraindicated or not tolerated
73
what would the reasons be for not initiating therapy
obesity physical and mental health - hypoglycaemia anxiety about needles personal preference concerns relating to license to drive group 2 vehicles
74
what is the most common insulin therapy
*Neutral Protamine Hagedorn (NPH) insulin (injected once or twice daily according to need) *NPH plus a short acting insulin should be considered if HbA1c is 75 mmol/mol higher OR *Longer acting insulin analogues e.g. insulin detemir or insulin glargine
75
what is hypoglycaemia
any blood glucose less than 4.0mmol/L
76
what are the symptoms of hypoglycaemia
hunger, paliptations, sweating, tremors
77
what can people with hypoglycaemia not do
drive a group 2 vehicle - bus or lorry

Semester 4 (80 decks)

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