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CSI 2021 term 2 > CSI case 5 - T2 diabetes > Flashcards

CSI case 5 - T2 diabetes Flashcards

1
Q

What is prediabites?

A

when blood sugar > but not high enough to diagnose T2

peoplet at high risk of developing T2 diabities

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2
Q

Other names of prediabetes?

A

borderline diabetes

impaired glucose regulation

non - diabetic hyperglycaemia

impaired fasting glucose AND impaired glucose tolerance

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3
Q

What are symptoms of pre-diabetes?

A

No symptoms

If have symptoms most likely already have it

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4
Q

What are the 2 main types of factors that increase risk of diabetes

A

modifiable and non-modifiable

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5
Q

What are examples of modifable?

A

smoking, high blood pressure, overweight - esp centripetal obesity, sedentary lifestyle (inactivity), alchol

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6
Q

What are examples of non-modifiable risk factors?

A

age,

ethnicity - african/south asian at more risk, person in families with diabetes,

Gestational diabetes ( levels increase during pregenancy)

Polycystic ovary syndrome (associated with insulin resistance)

mental health conditions

antipyschotic medication

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7
Q

What is the NHS prevention programme?

A

joint commitment for NHS england, PHE, and diabities uk to

deliver large scale evidence based behavioural intervetions

for individuals at high risk of T2

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8
Q

Why did they do NHS prevention programme?

A
  1. As T2 diabetes can be prevental
  2. behavourial interventions is evidently effective at reducing risk of T2 through reducing weight, increase activity and improving diet
  3. Diabetes huge implications for NHS and society
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9
Q

What are long term goals of NHS Diabetes Prevention Programme?

A

reducde incidence of T2 diabetes

reduced complications such as micro/macro vascularture problems related to diabets

reduce health unequalities associated with incidence of diabetes

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10
Q

What the interventions of diabetes programme? (3)

A
  1. Achieving healthy weight
  2. achieving dietary requirements
  3. achieve CMO physical activity recommendations
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11
Q

Eligibility of NHS Diabetes Prevention Programme?

A

over 18

have to be non - diabetic hyperglycaemia: - HbA1c 42-47 mmol/mol OR fasting glucose of 5.5 - 6.9

has to be within last 12 months and most recent blood reading

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12
Q

What are referral routes for NHS Diabetes Prevention Programme?

A
  1. Identified of having elevated risk level (by HbA1c or FPG) in past or on register of patients with high levels of them
  2. through NHS health check programmme for ppl 40-74, has a filter to be at high risk and offered blood test to confirm
  3. diagnosed as non-diabetic hyperglaecmia through opportunistic assessment in routine care
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13
Q

What are 2 core defects of T2 diabetes?

A

1. impaired insulin secretion by b cells caused by:

-lipotoxity insulin resistance adipose tissue increase lipolysis and fatty acid in blood

-glucotoxity: increase glucagon and increase glucagon sensitivity in liver leads to increase HGO

-incretin resistance: resistance to GLP-1, dont secrete insulin

  1. insulin resistance in muscle, liver, kidney
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14
Q

By which mechanism does insulin resistance cause hyperglycaemia?

A
  1. increase glucose reabsorption
  2. decrease glucose uptake into cells
  3. increase lipolysis
  4. inflammation
  5. NTs dysfunction
  6. increase glucagon secretions
  7. increase HGO
  8. decreased insulin secretion
  9. vascular insulin resistance
  10. decrase incretin effect
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15
Q

explain each of mechanism that insulin resistance causes hyperglycaemia

A

less insulin produced later stages due to B cell failure

  1. increase renal glucose reabsorption by Na+/gluco co-transporter a
  2. decrease glucose update due to insulin resistance and less of it
  3. inflammation causes expression protiens that supress insulin pathways
  4. resistance of appetite suppressive effects for hormones and low dopamine and high serotonin increases weight
  5. increase glucagon as insulin inhibits its secretion and alpha resistance to insulin when high
  6. adipose resistance increase lipolysis and free acid level in blood. cause resistance muslce and liver and B cell failure
  7. decrease insulin secretion due to GLP-1 resistance and tissue resistance
  8. high insulin increase vasculature resistance
  9. resistance to GLP-1
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16
Q

How is insulin involved in glucose metabolism?

A

Binds to insulin protien in muscle and adipose cell

allos for glucose uptake through glu4 receptor

Glycolysis to pyruvates

pyruvate oxidation to Acetyl coA

Acetyl CoA to ATP via TCA + oxidative phos

30 ATP

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17
Q

What is difference between GLUT receptors and SGLT receptors?

A

GLUT - facilicated diffusions, found everywhere apart from small intestine, kidney.

SGLT- active transport luminal epithelial cells in kidney and small intestine

18
Q

Where is distribution and function of each Glut transporter?

A

all insulin independent apart from GLUT4

19
Q

What happens then when glucose high but insulin resistance?

A

GLUT4 muscles and adipose not glucose in, so lipolysis and glucagonlysis

GLU1,2,3 - neurones, endothelium, kidney, SI, liver, B cells neurones, placenta, erthyotcyes take in lots of glucose

20
Q

What insulin effects on liver, muscle and adipose?

A
21
Q

Stages of insulin levels in type 2 diabetes?

A

insulin resistance in liver, muscle, fat don’t respond to insulin

causes stages increased insulin due to high glucose. (GLUT2 B cells)

over time B cells worn down so don’t produce as much insulin and not enough to overcome resistance

22
Q

Difference between type 1 and type 2?

A

1 - no insulin produced

2 - insulin resistance and eventually little insulin produced

23
Q

What are glucose thershold (fasting, post prandial, random) for impaired fasting glucose?

impaired glucose tolerance?

diabetes?

A
24
Q

What is post pradnial glucose?

A

patient fast for 8 hours

give 75g oral glucose load

measure blood 2 hours after

25
Q

What is difference between fasting glucose and impaired glucose tolerance?

area affected?

A

fasting is predominantly hepatic resitance so large glucose output

while tolerance is muscle resistance and bad insulin release elads to poor cellular glucose

can occur together

26
Q

What are 3PS for diabetes T2 symptoms?

explain each one

A

polydipsia, increase thirst - blood glucose high so kidneys more urine to remove extra glucose

polyuria, increase urination - filter out more water as more glucose in urine

polyphagia - can’t use glucose for energy in muscles and liver so no energy from glucose so feel very hungry

27
Q

How is T2 diagnosed?

A

Symptoms + 1 red glucose test range

no symptoms and multiple red ranges

28
Q

Why is HbA1c measured?

A

as it is haemoglobin glycosylated, jointed to sugar

proportional to plasma glucose levels

blood cells last 120 days, so indicative for 2-3 months of blood glucose

29
Q

Adantages of HbA1c?

A

takes into account 2-3 months, not dependent on day

easy to measure - no fasting and acure pertubations like exercise affect it

cheap

30
Q

disadvantages of HbA1c?

A

only an approximate measure

not reliable for certain groups: sickle cells, pregnancy (as Hb levels changes), renal failure

31
Q

What is drug action of metoformin?

A

decrease glucogenesis and HGO

increase sensitivity of cells to insulin by increase glucose uptake by GLUT4

32
Q

What is behaviour insight?

A

knowledge of how and why people behave to encourage +ve behaviour

33
Q

Why is behavioural insights effective?

A

considers all aspects of behaviour and acknowledeg importance of fast automatic system in driving behaviour

34
Q

How do you implemenent behavioural change?

A

Make it easy,attractive, social, timely to uptake the activity

Retention it

and cause behaviour change

35
Q

What is the least most important diagnoses it T2 diabetes?

A

Urine dip

36
Q

How does obesity lead to type 2 diabetes?

A

Too much visceral fat; release adipokines, lead to inflammation, toxic on beta cells and which lead to vicious cycle of increasing glucose concentration

37
Q

What are causes of insulin resistance?

A

genetic abnormalities

ectopic lipid accumulation

mitochondrial dysfunction

inflammation

endoplasmic reticulum stress

38
Q

What are the 2 umbrella complications associated with T2 diabetes?

A

microvascular and macrovascular

39
Q

Give examples of microvascular

A

(retinopathy, nephropathy and neuropathy)|

40
Q

Gives examples of macrovascular?

A

(myocardial infarction, peripheral vascular disease and stroke) result from dyslipidaemia, hypertension, hyperglycaemia and inflammation

CSI 2021 term 2 (2 decks)

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