Type 2 Diabetes Mellitus Flashcards

1
Q

What is type 2 diabetes mellitus?

A

“A condition in which the combination of insulin resistance and beta-cell failure result in hyperglycaemia”
- Body makes insulin but tissues don’t respond to it (reason not fully understood)
- INSULIN RESISTNACE
- obesity and genetic risk factors of T2DM
- Body makes excess insulin to try to move the glucose out of blood
- Eventually puts strain on beta cells (overworked)- beta cell damage
- Insulin starts to go down (depending on time of diagnosis, insulin levels will vary)

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2
Q

What is the fasting glucose level that shows impaired fasting glucose (pre-diabetes)?

A

patient doesn’t eat/ drink for 8 Hrs
6 mmol/L ≤ fasting glucose levels ≤ 7 mmol/L
(6-7 mmol/L is pre-diabetes)
(less than 6 is normal)
(more than 7 is diabetes)

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3
Q

What is the reading of an oral glucose tolerance test for impaired glucose tolerance (pre-diabetes)?

A

Give glucose & take blood samples at time intervals
7.7 mmol/L ≤ 2-hr glucose (OGTT) ≤ 11mmol/L
(7.7-11 is prediabetes)
(less than 7.7 is normal)
(more than 11 is diabetes)

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4
Q

What is the HbA1c level for pre diabetes or non-diabetic hyperglycaemia?

A

glycated hemoglobin (hemoglobin attached glucose)- glucose level for the part 3 months
42 mmol/L ≤ HbA1c ≤ 48mmol/L
(42-48 is prediabetes)
(less than 42 is normal)
(more than 48 is diabetes)

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5
Q

What is needed for the diagnosis of type 2 diabetes?

A

(1 positive test + symptoms or 2 positive tests)
Usually:

First line test for diagnosis is HbA1c.

1x HbA1c >=48mmol/L with symptoms
Or
2x HbA1c >=48 mmol/mol if aysymptomatic

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6
Q

What can occur from a long duration of T2DM?

A

In long-duration type 2 diabetes, beta-cell failure may progress to complete insulin deficiency
=Hyperglycaemia
important not to stop giving insulin as at risk of ketoacidosis

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7
Q

What effect does T2DM have on insulin release?

A
  • Normally we encounter a “first phase insulin release” which is an immediate/ spike release
  • This is lost in T2DM
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8
Q

How does the liver react to the reduced insulin levels seen after T2DM?

A

Hepatic glucose production is increased due to both a reduction in insulin action and increase in glucagon action
“excessive glucagon-mediated glucose output” (but reduced clearance of glucose- still not being removed from circulation”

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9
Q

What is the relationship b/t insulin secretion and insulin sensitivity?

A

As insulin secretion decreases, the insulin sensitivity increases

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10
Q

What is the random glucose (non-fasting glucose) level for diabetes?

A

(Can be done at any time)
levels greater than or equal to 11.1 mmol/L + symptoms

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10
Q

What consequences do other body tissues face from T2DM?

A

Skeletal muscle:
- Reduced glucose uptake
- Impaired glycogen synthesis

Adipocytes:
- Reduced glucose uptake
- Increased lipolysis
- Reduced lipogenesis

Liver:
- Increase in hepatic glucose production
- Increased lipogenesis

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11
Q

Is diabetes monogenic or polygenic?

A

Type I and II (most common types) are polygenic: not born with the diabetes but high risk and may develop later depending on other factors

MODY diabetes is monogenic: you are born with the single gene mutation and it is always going to develop into diabetes

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12
Q

What are other associations seen with T2DM?

A
  • Obesity
  • Perturbations/ abnormalities in gut microbiota (inflammation causes various signaling metabolic pathways)
  • Intra-uterine growth retardation
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13
Q

What are the presentations of T2DM?

A

Hyperglycaemia
Overweight
Dyslipidaemia
Fewer osmotic symptoms
With complications
Insulin resistance
Later insulin deficiency

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14
Q

What are the risk factors of T2DM?

A
  • Age
  • PCOS
  • high BMI
  • Family History
  • Ethnicity
  • Inactivity
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15
Q

What is hyperosmolar hyperglycaemic state?

A

EXTREME DEHYDRATION
Osmotic diuresis leads to severe fluid loss “Hypovolaemic shock” insulin for suppression of lipolysis and ketogenesis.
Symptoms:
- Polyuria
- Dehydration
- (if left untreated): lethargy, seizures, coma, death

treat with intravenous fluids immediately
(CAUTION: rectifying fluids too quickly can cause Central pontine myelinolysis (brain depletion) rapid rise in Na+ conc

16
Q

What is the management for T2DM?

A
  • Diet
  • Oral medication
  • Structured education
  • May need insulin later
  • Remission / reversal
17
Q

What are some possible risks from prevention-diabetes treatments?

A

(too much blood glucose)
- Retinopathy
- Neuropathy
- Nephropathy
- Cardiovascular

18
Q

What investigations are made during a T2DM consultation?

A

Glycaemia: HbA1c, glucose monitoring if on insulin, medication review
Weight assessment
Blood pressure
Dyslipidaemia: cholesterol profile
Screening for complications: foot check, retinal screening

19
Q

What are the dietary recommendations for T2DM

A

Healthy eating or diet
Total calories control
Reduce calories as fat
Reduce calories as refined carbohydrate
Increase calories as complex carbohydrate
Increase soluble fibre
Decrease sodium

20
Q

What are the drug treatments for T2DM? What do each drug tackle?

A
  1. Metformin (Reduces hepatic glucose production + Improves insulin sensitivity + Increases peripheral glucose disposal)
  2. Thiozolidinediones
  3. Pioglitazone (2/3 Improves insulin sensitivity)
  4. Sulphonylureas
  5. DPP4-inhibitors
  6. GLP-1 Agonists (4-6 boost insulin secretion)
  7. Alpha glucosidase inhibitor
  8. SGLT-2 inhibitor (7/8 Inhibit carbohydrate gut absorption + Inhibit renal glucose reabsorption)

Weight loss help to achieve all of these solutions

21
Q

What are some cons of taking metformin?

A
  • GI side effects
  • Contraindicated in severe liver, severe cardiac or moderate renal failure
22
Q

How does Sulphonyleuras work?

A

“Boosts insulin secretion”
Normal insulin release requires closure of the
ATP-sensitive potassium channel
- Sulphonylureas binds to the ATP-sensitive potasssium channels and closes them (independent of glucose/ ATP)

23
Q

How does Pioglitazone work?

A

“Improves insulin sensitivity”
- Adipocyte differentiation modified
- weight gain but peripheral not central
- Improvement in glycaemia and lipids
- Evidence base on vascular outcomes
- Side effects of older types hepatitis, heart failure

24
Q

What is the role of Glucagon like peptide-1 (GLP-1)

A
  • Gut hormone
  • Secreted in response to nutrients in gut
  • Transcription product of pro-glucagon gene, mostly from L-cell
  • Stimulates insulin, suppresses glucagon
  • ↑ satiety (feeling of ‘fullness’)
  • Short half life due to rapid degradation from enzyme dipeptidyl peptidase-4 (DPP4 inhibitor)
  • Used in treatment of diabetes mellitus
25
Q

What is meant by the gastrointestinal “incretin” effect?

A

A phenomenon by which insulin secretion is increased substantially when glucose is given by the oral or enteral route when compared to an intravenous glucose infusion
- Is attributable to the secretion of the “incretin” hormones, GLP-1 and GIP, from the gut

26
Q

How do GLP-1 Agonists work?

A

“Boost insulin secretion”
- Injectable –daily, weekly
- Decrease [glucagon]
- Decrease [glucose]
- Weight loss
e.g: Liraglutide, Semaglutide

27
Q

How do DPP4-inhibitors work?

A
  • Increase half life of exogenous GLP-1
  • Increase [GLP-1]
  • Decrease [glucagon]
  • Decrease [glucose]
  • Neutral on weight
    e.g: Gliptins
28
Q

How do SGLT-2 inhibitors work?

A

“Inhibit carbohydrate gut absorption + Inhibit renal glucose reabsorption”

  • Inhibits Na-Glu transporter, increases glycosuria
  • HbA1c lower
  • 32% lower all cause mortality
  • 35% lower risk heart failure
  • Improve CKD (chronic kidney disease)
    E.g: Empagliflozin, dapagliflozin, canagliflozin
29
Q

What effect does treatment have on beta cell function?

A

Despite treatment, beta-cell function continues to decline

30
Q

What effect can Gastric bypass surgery have on T2DM?

A

Gastric bypass surgery has the potential to induce remission of type 2 diabetes
(remission= blood sugar levels (also known as blood glucose levels) are below the diabetes range NOT A CURE

31
Q

What effect can a low-calorie diet have on T2DM?

A

low-calorie diet (800 kcal/day) for 3-6 months has the potential to induce remission, which appears to be sustained at 2 years
(remission= blood sugar levels (also known as blood glucose levels) are below the diabetes range NOT A CURE

32
Q

Other than attempting to restore blood glucose levels, what are toher aspects of T2DM management?

A

Blood Pressure management
Hypertension very common in T2DM
Clear benefits for reduction esp with use of ACE-inhibitors

Lipid management
Total cholesterol raised
Triglycerides raised
HDL cholesterol reduced
Clear benefit to lipid-lowering therapy

33
Q

What is the language matters movement?

A

Language matters movement: use language that empowers rather than disengages people with type 1 diabetes