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Year 2 Collin > Endo 16 - T2DM > Flashcards

Endo 16 - T2DM Flashcards

1
Q

T2DM is not ketosis prone. What tissues are often damaged long term in T2DM?

A

Retina, kidney, nerves, artery

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2
Q

What is the fasted blood glucose threshold for T2DM

A

> 7mmol (over 6 = “impaired fasting glucose”

2 hr glucose > 11.1 = T2DM

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3
Q

Diabetes is the most common cause of what in the UK?

A

Blindness in working age people, renal replacement therapy and amputation

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4
Q

T2DM gene mutations are associated with?

A

Intrauterine growth restriction

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5
Q

Describe MODY

A

Several hereditary forms of MODY. MODY is autosomal dominant

It causes ineffective pancreatic Beta cell insulin production - and mutations of transcription factor genes, glucokinase gene

Positive Family history, not commonly linked to obesity

Specific treatment depending on type of MODY

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6
Q

Only diabetes causes microvascular complications (as in, macrovascular complications may arise from other things but Diabetes will give microvascular complications)

A

Y

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7
Q

Intrauterine environment is key. Studies have shown what?

A

Infant birth weight and birth weight at a young age predicts diabetes risk

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8
Q

Describe the metabolism and presentation of T2DM

A
  1. Heterogeneous
  2. Obesity
  3. Insulin resistance and insulin secretion deficit (but which came first)
  4. Hyperglycaemia and dyslipidaemia
  5. Acute and chronic complications
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9
Q

Describe insulin secretion in T2DM

A

Insulin secretion is in 2 phases, 1st phase (sharply right after meal) and 2nd phase (after meal)

Insulin secretion deteriorates with T2DM / Impaired Glucose Tolerance (IGT)

Also, T2DM/IGT = impaired glucose uptake by muscle and more HGO (as less inhibition by insulin)

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10
Q

Insulin is meant to switch off lipolysis (no need to breakdown fat after we’ve eaten). But insulin resistance may cause problems - e.g. atheroma formation.. How

A

In adipocyte - lipolysis not switched off due to insulin resistance.

  1. Triglyceride broken down into glycerol and non-esterified FA.
  2. Both glycerol + NEFA travel to liver —> NEFA becomes VLDL-TG and glycerol contributes to glucose production (via gluconeogenesis).
  3. Consequence - increased small dense VLDL in blood - increased risk of atheroma, etc. Also increased HGO (+ gluconeogenesis) = increased plasma glucose. Impaired uptake of glucose to muscle means glucose remains in blood
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11
Q

Central/omental fat is more dangerous than peripheral fat.

A

Yah

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12
Q

Gut microbiota perturbations ARE ASSOCIATED (not causative) with T2DM. How

A

Bacterial lipopolysaccharides ferment to short chain FA, bacteria also may modulate bile acids

Inflammation may arise - which signals metabolic pathways

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13
Q

All diabetics drugs, except Metformin, cause

A

Weight gain (e.g. insulin)

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14
Q

Describe T2DM diabetes presentation

A
  1. Osmotic symptoms
  2. Infections
  3. Screening test
  4. Nearly 50% present with complication - e.g.acute: hyperosmolar coma, chronic: IHD, retinopathy
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15
Q

What are the microvascular complications of T2DM

A
  1. Retinopathy
  2. Nephropathy
  3. Neuropathy
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16
Q

What are the macrovascular complications of T2DM

A
  1. IHD
  2. Cerebrovascular
  3. Renal artery stenosis
  4. PVD
17
Q

What are the metabolic complications of T2DM

A
  1. Lactic acidosis

2. Hyperosmolar

18
Q

What can treatment of T2DM cause

A

Hypoglycaemia

19
Q

What is monitored in the treatment of T2DM

A
  1. Weight
  2. Glycaemia
  3. BP
  4. Dyslipidaemia
20
Q

How is weight managed/treated in T2DM

A

Education, diet control (increase complex carbs, increase unsaturated fat as proportion of fat and increase soluble fibre).

Orlistat (GI lipase inhibitor)

21
Q

How is glycaemia treated/managed in T2DM

A
  1. Metformin/insulin (though insulin may increase weight)
  2. Sulphonylureas / metaglinides (increase insulin secretion from pancreas)
  3. alpha-glucosidase inhibitor (increases time taken to absorb glucose - bypassing the 1st phase insulin secretion problem)
  4. Thiazolidinediones
22
Q

Describe metformin

A

It is a biguanide insulin sensitiser - p much prescribed in anyone

Reduces insulin resistance (reduced HGO, increased peripheral glucose disposal)

GI SEs

Not used if severe liver, cardiac or mild renal failure

23
Q

How do B cells work?

How does Glibenclamide (sulphonylurea) work

A
  1. Glucose enters B cell –> metabolised (by glucokinase) and produces ATP
  2. ATP produced inactivates ATP sensitive K channel, which triggers VGCC to open —> influx of Ca causes insulin secretion
  3. Glibenclamide (sulphonylurea) binds to and blocks the ATP sensitive K channel –> No K efflux so cell depolarises –> activates VGCCs —> Ca influx and insulin release

Used in lean T2DM patients where diet hasn’t worked - will cause weight gain

24
Q

What is acarbose and how does it work

A

It is an alpha-glucosidase inhibitor - prolongs absorption of oligosaccharides

This allows insulin secretion to cope (as defective first phase secretion)

May cause flatus (gas)

25
Q

Describe thiazolidinediones

A

e.g. Pioglitazone

It is a peroxisome proliferator-activated receptor agonist (PPAR-gamma)

It allows insulin to work better (insulin sensitiser) - causes weight gain but PERIPHERAL and NOT OMENTAL

Improved in glycaemia and lipids

26
Q

What does GLP-1 do?

A

Stimulates insulin, suppresses glucagon

Increases satiety

It is secreted in response to nutrients in the gut (from L cells)

Causes weight loss, not gain

27
Q

GLP-1 are often given in conjunction with Gliptins (DPPG-4 inhibitors) in T2DM. What are gliptins

BUT GLP-1 more effective than gliptins/DPPG-4 inhibitors

A

They are DPPG-4 inhibitors - they increase the half life of exogenous GLP-1

28
Q

How do SGLT2 inhibitors work, give an example

A

They work in the PCT of the kidney - decrease glucose reabsorption (by inhibiting Na/Glu cotransporter) –> increased glycosuria/polydipsia

They reduce HbA1c, may also reduce all causes of mortality (including heart failure)

e.g. Empaglifozin

29
Q

Which other aspects are treated in T2DM

A
  1. BP

2. Diabetic dyslipidaemia

Year 2 Collin (114 decks)

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