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Y2 - ENDO > T2DM > Flashcards

T2DM Flashcards

1
Q

List some conditions within the group macrovascular disease

A
  • Ischaemic Heart Disease
  • Cerebrovascular Disease (stroke)
  • Renal Artery Stenosis
  • Peripheral Vacular Disease (PVD)
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2
Q

1) When do microvascular complications occur?
2) List some microvascular complications

A

1)

  • Only in diabetes

2)

  • Retinopathy
  • Nephropathy
  • Neuropathy
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3
Q

In what condition will you get diabetic ketoacidosis?

A
  • In T1DM
  • NOT in T2DM
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4
Q

What should a normal fasting sugar be in an oral glucose test?

A

<6 mmol / L

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5
Q

What should a normal 2-hour glucose be in an oral glucose tolerance test?

A

< 7.8 mmol / L

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6
Q

What are the boundaries for blood sugar levels in an oral glucose tolerance test in fasting and in 2-hour glucose to consider someone diabetic, and at what level would you always consider someone to be diabetic?

A
  • If glucose > 7 mmol / L at fasting OR…
  • If glucose > 11.1 mmol / L at 2-hour glucose OR
  • If glucose >11.1 at any point - always considered diabetic
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7
Q

1) Define the intermediate levels in oral glucose tolerance tests at fasting and in 2-hour glucose tolerance tests
2) What risks / indications are indicated by someone having this sugar levels?

A

1)

  • Fasting: 6 - 7 mmol / L
  • 2-hour glucose test: 7.8 - 11 mmol / L

2)

  • Increased risk of developing diabetes
  • Increased macrovascular risk
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8
Q

At what point would microvascular risk occur as suggested by sugar levels in an oral glucose test?

A
  • Once you are deemed diabetic in accordance with the defined boundaries at fasting and in 2-hour glucose tests
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9
Q

Epidemiology of T2DM:

1) What age group is it more common in?
2) What does its prevalence vary based on (i.e. some other factors that affect its prevalence)?
3) Its greatest in particular in people doing what?

A

1) Elderly

2)

  • Ethnicity
  • Other environmental factors

3)

  • People from ethnicities that have great amounts of rural → urban shift
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10
Q

3 Factors that can play a role in the development of MODY?

A
  1. Genes
  2. Intrauterine environment
  3. Adult environment
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11
Q

1) What is the genetic basis of MODY?
2) What does the family history for MODY look like, and why?

A

1)

  • Autosomal dominant
  • There are 8 hereditary forms of MODY

2)

  • Positive family history because of the fact that it is autosomal dominant - if it were recessive, perhaps there may not be immediately positive family history
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12
Q

What is the basic pathophysiological basis for the development of T2DM?

A
  • Genes (unknown) encode…
  • Insulin resistance through adipocytokine action
  • Leading to ß-cell failure too
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13
Q

How does T2DM lead to…

1) Macrovascular complications
2) Microvascular complications

A

1)

  • The insulin resistance through adipocytokine action leads to metabolic dyslipidaemia and mitogenesis which causes macrovascular symptoms

2)

  • ß-cell failure leads to hyperglycaemia and thus microvascular complications
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14
Q

What role does obesity play in the development of T2DM and associated symptoms?

A
  • Obesity contributes to the development of insulin resistance, but genetics is the major causative factor in the development of this resistance
  • Adipocytokines released from adipose tissue to cause insulin resistance as well as genetically encoded adipocytokine release
  • Adipose tissue release NEFAs which eventually lead to metabolic dyslipidaemia and thus macrovascular complications associated with T2DM
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15
Q

What is T2DM associated with in the neonate?

A
  • Low birth weight / small size
  • Due to intra-uterine growth (IUGR) restriction associated with T2DM
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16
Q

Is T2DM monogenic?

A

No

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17
Q

How have studies shown that there is a likely genetic element to T2DM?

A
  • Monozygotic twin studies show a higher prevalence in identical than non-identical twins (70% and 40% respectively)
18
Q

Describe the presentation of T2DM

A
  • Heterogenous presentation
  • Obesity
  • Insulin resistance and insulin secretion deficiency
  • Hyperglycaemia
  • Dyslipidaemia
  • Acute and chronic complications
19
Q

Describe the pathophysiology for how insulin resistance (as brought on by adipocytokines) leads to hyperglycaemia and metabolic dyslipidaemia (exclude the ketosis aspect)

A
  • Insulin normally directly reduces hepatic glucose ouptut, so resistance increases it, causing hyperglycaemia
  • Insulin normally stimulates glucose uptake into muscle tissue, resistance prevents this, causing hyperglycaemia
  • TGs are broken down normally in the adipose tissue also, insulin normally prevents NEFAs from being released and entering the liver. Resistance means NEFAs enter the liver and here they can form small-dense VLDL-TG which enters the bloodstream to be cleaved into VLDL - this causes metabolic dyslipidaemia
20
Q

What is a simple predictor of ischaemic heart disease and why?

A
  • Waist circumference - higher the omental fat (omental adipose tissue), the higher the waist circumference
  • Omental adipose tissue releases NEFAs which form VLDL-TG in the liver and thus VLDL in the blood which causes metabolic dyslipidaemia and thus macrovascular complications such as ischaemic heart disease
21
Q

How might a failing pancreas cause DM?

A
  • Fails to cleave pro-insulin in order to form mature insulin - so immature insulin is ineffective, essentially causing insulin resistance
22
Q

What metabolic complications can occur in T2DM, and what metabolic complication that occurs in T1DM doesn’t really occur in T2DM?

A
  • Lactic acidosis
  • Hyperosmolar symptoms e.g. hyperosmolar hyperglycaemic coma
  • Metabolic dyslipidaemia
  • Diabetic ketoacidosis does NOT occur
23
Q

What osmotic symptoms occur in T2DM and why?

A
  • ​Hyperglycaemia overwhelms the kidney’s ability to reabsorb all glucose molecules so… Glycosuria
  • The glucose in the urine in the kidneys takes water with it by osmsosis, leading to… Polyuria
  • Hyperglycaemia by osmosis drawing water out of somatic cells and also by causing polyuria leads to… Polydipsia
  • Hyperosmolar hyperglycaemic coma
24
Q

Why can infections be common in someone with T2DM? + What kind of infections might you see?

A
  • Microorganisms thrive in the high glucose conditions
  • Yeast etc
25
Q

What dietary measures should someone with T2DM undertake?

A
  • Reduce calories in (and exercise to increase calorie burning)
  • Reduce refined carbohydrate
  • Increase complex carbohydrate
  • Increase soluble fibre
  • Increase unsaturated fat as proportion of fat
  • Lower salt intake (to lower macrovascular complication risk)
26
Q

What do we monitor during the treatment of T2DM?

A
  • Glycaemic control
  • Weight
  • BP control
  • Dyslipidaemia
27
Q

List some treatments that we use to control hyperglycaemia in T2DM patients

A
  • Meformin + insulin
  • Sulphonylureas + metaglinides
  • Alpha-glucosidase inhibitors
  • Thiazolidinediones
  • GLP-1 and DPP4 inhibitors
  • SGLT-2 inhibitors
28
Q

What is a possible surgical option for T2DM treatment and what is a weakness of this?

A
  • Gastric bypass
  • Adverse effects including nutritional deficiency
29
Q

1) How does metformin work to treat T2DM, and what type of drug is it?
2) What side effects might you experience?
3) In what conditions is metformin use contraindicated?

A

1)

  • Biguanide
  • Increases sensitivity to insulin to counteract insulin resistance

2)

  • GI side-effects

3)

  • Severe cardiac failure
  • Severe liver failure
  • Mild renal failure
30
Q

How does increased glucose stimulate insulin release in the ß-cells of the islet of Langerhans in the pancreas?

A
  • Glucose is converted by glucokinase at first and this detects it
  • Metabolism of this glucose occurs and ATP is released
  • ATP sensitive K+ channels are blocked, so there is less K+ efflux
  • Membrane depolarisation which causes voltage-gated Ca2+ channels to open
  • This Ca2+ increase stimulates the release of insulin
31
Q

How does sulphonyureas work to treat T2DM?

A
  • Sulphonyureas (glibenclamide) will block the ATP-sensitive K+ channels without the need of ATP
  • So there is less K+efflux and so more membrane depolarisation
  • So Ca2+ channels open more and so greater Ca2+ influx which stimulates insulin release to a greater degree
32
Q

What side effects might you experience with Sulphonyureas?

A
  • Hypoglycaemia
  • Weight gain
33
Q

1) How does acarbose (an alpha glucosidase inhibitor) work to treat T2DM?
2) Side effects of acarbose?

A

1)

  • Acts within the gut to prolong glucose (oligosaccharide) absorption
  • Allows insulin secretion to cope, following defective first phase insulin
  • As effective as metformin

2)

  • Flatus
34
Q

1) Name the only thiazolidinedione in use
2) How does it work in treatment of thiazolidinediones?
3) What side effects might it cause?

A

1) Pioglitazone

2)

  • Peroxisome proliferator-activated receptor agonists PPAR-γ
  • Insulin sensitiser
  • Improvement in hyperglycaemia and dyslipidaemia

3)

  • Peripheral weight gain
  • Older type hepatitis??
  • Heart failure
35
Q

What is the incretin effect?

A
  • Food stimulates more insulin secretion when given orally than intravenously
36
Q

When is GLP-1 secreted and what is the physiological function of GLP-1?

A
  • Secreted in response to nutrients in the gut
  • Stimulates insulin
  • Suppresses glucagon
  • Increases satiety
  • Restores ß-cell glucose sensitivity
37
Q

1) Where does GLP-1 come from?
2) How is its half life?
3) How quickly and how is it degraded?

A

1)

  • Transcription factor product of the pro-glucagon gene
  • Mostly from L-cells

2)

  • Short half-life

3)

  • Rapid degradation
  • Degraded from enzyme dipeptidyl peptidase-4 (DPPG-4)
38
Q

Why are GLP-1 and DPPG-4 inhibitors co-administered in T2DM treatment?

A
  • DPPG-4 (dipeptidyl peptidase-4) degrades GLP-1 normally
  • So by inhibiting this, you increase [GLP-1]
39
Q

1) Give 2 GLP-1 agonists
2) How are GLP-1 agonists useful in treating T2DM?

A

1)

  1. Exenatide
  2. Liraglutide

2)

  • Decrease [glucagon]
  • Increase [insulin]
  • So decrease [glucose]
40
Q

1) Name a SGLT-1 inhibitor
2) How do SGLT-1 inhibitors work to treat T2DM?
3) What effect do SGLT-1 inhibitors have on HbA1C?
4) What effect on the signs of T2DM might it have?

A

1)

  • Empagliflozin

2)

  • Inhibits the Na+-glucose transporter in the PCT of the kidneys
  • So prevents lots of glucose from re-entering blood so reduces hyperglycaemia

3)

  • Lowers HbA1C

4)

  • Increases polyuria
  • Increases polydipsia
  • Increases glucosuria
41
Q

How might perturbations in microbiota be associated with T2DM?

A

Gut microbiota….

  • Obesity
  • Insulin resistance contribution
  • Host signalling
  • Bacterial LPS fermentation to short chain FA
  • Bacterial modulation of bile acids
  • Inflammation
  • Signalling metabolic pathways

Intrauterine microbiota perturbations too

42
Q

Label this diagram

A

Y2 - ENDO (18 decks)

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