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Year 2 LCRS Endocrinology > T2DM > Flashcards

T2DM Flashcards

1
Q

What is the definition if Diabetis?

A

A state of chronic hyperglycamia suficcient to cause micorvascular and macrovascular complications

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2
Q

What does ketones in blood/urine show in T1/T2DM?

A

Normally present in T1DM, not in T2DM, but can be present in T2DM

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3
Q

What are the associated conditions of someone with T2DM?

A

•T2DM often involves weight, lipids and blood pressure

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4
Q

What are the diagnostic measurement of blood glucose for Diabetis and imparied glucose tolerance/impaired fasting glucose?

  1. Fasting
  2. 2h after meal
  3. Random time
A

Diabetis?

  1. Fasting glucose > 7mmol
  2. 2h after meal > 11.1 mmol
  3. At any time > 11.1 mmol

Impaired tolerance

  1. Fasting glucose > 6mmol
  2. 2h after meal > 7.6mmol
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5
Q

Explain the epidemiology of T2DM

A
  • Diabetes is prevalent (10% at 60yr) Mostly T2DM
  • Age is a risk factor but also caused by
  • Prevalence of T2DM varies enormously
  • Increasing prevalence
  • Occurring and being diagnosed younger
  • Greatest in ethnic groups that move from rural to urban lifestyle
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6
Q

What is the main characterisitic of T2DM?

A

It is a combination of insulin resistance and a relative insulin production (enough to swith down ketone production, not to reduce hepatic glucose output)

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7
Q

What is MODY?

A

Matuity onset of diabetis in the yound

–> ineffective ß-cell insulin production

–> single gene defect causing diabetis (Family history but no diabetis)

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8
Q

What is the role of genetic in T2DM?

A
  1. There is a genetic component, different in everyone
  2. Some might require very little outside influence to develop T2DM, some mith require more environmental influence
    • Is made worse by obesity and some particular fatty acids
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9
Q

What is IUGR? What is its influence in T2DM?

A

Intra-uterine-growth restriction –>(lack of calories in utero) might modulate gene expression for rest of life and make people more predisponed to diabetis

(due to protein restrictions that are required in pancreatic development)

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10
Q

When does the insulin resistance in people with T2DM develop?

A

Normally already early, but only late detected

–> already causes dyslipidaemia and macorvascular complications early on

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11
Q

When does someone in T2DM required insulin?

A

When the ß-cells can’t keep up with the demand–> ß-cell failure

  • leading to
    • worseining of dyslipidaemia –> macrovascular complications
    • hyperglycaemia –> microvascular complications
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12
Q

What happens naturally to insulin resistance and insulin secretion when you age?

A
  1. Insulin Resistance increases
  2. Insulin production decreases
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13
Q

How does T2DM present?

A
  • Very different in everyone
  • obesity
  • hyperglycaemia
  • dyslipidaemia
  • present with aculte and chronic complications of diabetis
  • might present with osmotic symptoms
  • or infections –> high sugar attracts bacteria
    *
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14
Q

Explain the origin of dyslipidaemia in diabetis

A

Becaue of insulin resistance –> Fat cells break down Triglycerides (normally downregulated by insulin)

The NEFAs are turned into Small Dende VLDL –> dislipidaemia

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15
Q

Why does fasting glucose levels increase in someone with T2DM?

A

Because Hepatic glucose output is not supressed by insulin, due to insulin resistance

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16
Q

What is the prevalence of obesity in T2DM individuals?

A

80%

17
Q

Through which factors does omental obesity influences the development of T2DM?

A

Through special Fatty acids and adipocstokines

18
Q

What is the role of our micorbium in T2DM?

A

There is an associaton in

  • Obesity, insulin resistance T2DM
  • Microbiome modulates Host signaling via
    • Bacterial lipopolysaccharides fermentation to short chain FA
    • bacterial modulation bile acids
      • Leading to antered siganling in Inflammation, and metabolic pathways
19
Q

Which factors influence insulin resistance development?

A
  1. Intra-uterine environmen
  2. Adipocytokines
  3. Microbioata
  4. Diet, exercise
  5. Medication
20
Q

What is the overall management of T2DM?

A

Aim: To treat symptoms and prevent complications to develop

  • Education
  • Diet
  • Pharmacology
  • complication screening
21
Q

What is the recommended Diet in someone with T2DM?

A
  1. Control total calories –> weight
  2. increase complex Carbohydrates
  3. reduce total amount of fat
    • if fat: encourage unsaturated
  4. increase soluble fibre
  5. Low salt –> Lower BP
22
Q

Which factors need to be monitored and treated in T2DM?

A
  • Weight
  • Glycaemia
  • Blood pressure
  • Dyslidiaemia
23
Q

What are possible pharmacological/surgical treatments of weith loss in T2DM?

A
  • Orlistat
    • decreases FA absorbtion
    • GI lipase inhibitor
  • Gastric bypass
24
Q

Explain the physoiology of insulin secretion

A
  • Glucose increases intracellulr ATP
  • ATP blocks ATP regulated K+ channels –> less K+ outflow
  • That causes an inflow of Ca2+ via change of membrane potential
  • Ca2+ stimmulated insulin secretion
25
Q

What is a treatment option for lean individuals with T2DM?

Why only for lean individuals?

Explain the molecular MOA

A

Sulfonylureas (Glibenclamide)

It stimmulates insulin secretion by directly altering the ATP dependant K+ channels

BUT–> the insulin secreted causes weight gain so only in lean patients/more effective in lean patients

26
Q

What is THE DRUG in T2DM? How does it work?

A

Metformin

It makes cells more sensitive to insulin –> reduces Hepatic GO,

  • Mainly for overweight patients where diet has not succeeded
27
Q

What are the side effects and contra-indications for use of Metformin?

A
  • GI side effects
  • Not used in severe liver disease or cardiac failusre or mild renal failure
28
Q

What is acarbose?

When is is used?

What is the MOA?

A

It is a •Alpha glucosidase inhibitor used in the treatment of T2DM

  • prolonges absorbation of oligosaccarides therefore does not increase initial blood glucose as significantly –> slower absorbtion
  • Allows insulin secretion to cope to overcome defective first phase insulin
29
Q

What are Thiazolidinediones?

What is their MOA?

A

Used in treatment of T2DM –> make insulin work better (mainly in peripheral regions)

–> causes redistribution of fat from central to peripheral body parts

  • Improvement in glycaemia and lipids
  • Reduces vascular complications
30
Q

What is the physiological role of Glucagon-like peptide 1?

A

Normally secreted by L-cells with every meal

It:

  • Stimulates insulin, suppresses glucagon
  • Increases satiety
31
Q

Explain the use of GLP1 in diabetis

A

Is effective because it

  1. Increases Insuin
  2. Decreases Glucose output
  3. As injection : decreases weight
32
Q

What are the two ways you could treat someone with GLP1 in T2DM?

A
  1. GLP1 agonist (injections)
    • Long acting GLP-1 agonist
    • Decrease [glucagon]
    • Decrease [glucose]
    • Weight loss
  2. Gliptins (DPPG-4 inhibitors)
    • Increase half life of exogenous GLP-1
    • Increase [GLP-1]
    • Decrease [glucagon]
    • Decrease [glucose]
    • Neutral on weight
33
Q

Explain the use of SGLT2-inhibitors in the treatment of diabetis

What is a brand name?

A

Empaglifozin

  • Inhibits Na-Glu transporter, increases glycosuria –> more sugar peed out, not in circulation
34
Q

What is the prevalence of Type 1 DM

A

0.25%

Year 2 LCRS Endocrinology (15 decks)

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