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Y2 Endocrine Block > PBL 2: T2DM and Microvascular complications > Flashcards

PBL 2: T2DM and Microvascular complications Flashcards

1
Q

what are the risk factors of T2DM

A

obesity (abdominal/truncal obesity)
increasing age
sedentary lifestyle
use of drugs- especially glucocorticoids and Thiazides
genetics
ethnicity- more common in south asian, caribbean and african people

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2
Q

what are the clinical features of T2DM

A
  • polyuria
  • polydipsia
  • polyphagia
  • overweight patients (BMI >30)
  • presents with a longer history, with slowly progressing symptoms
  • islet cell antibodies not present
  • hyperglycaemia less marked than T1DM
  • infections
  • fatigue
  • blurred vision
  • parasthesia (abnormal dermal sensation)
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3
Q

describe the pathological mechanism underlying T2DM

A
  • Increased BG levels, Beta cells secrete insulin.
  • Insulin binds to its receptors on adipose tissue and skeletal muscle to promote glucose transport from blood to cells
  • In Diabetes- insulin receptors don’t respond well to insulin- Insulin resistance = increased BG levels
  • In response, Beta cells try secrete more insulin to lower BG levels.
  • -> Beta cells hyperplasia + hypertrophy to secrete more insulin
  • Beta cell compensation isn’t sustainable
  • -> Beta cells undergo hypoplasia and hypotrophy- Beta cells die
  • -> Insulin levels decrease and BG levels increase
  • -> Hyperglycaemia
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4
Q

Describe the mechanism, example and side-effect of BIGUANIDES

A

Mechanism:

  • Not fully understood but improves insulin sensitivity so causes suppression of hepatic glucose output and enhances insulin-stimulated glucose uptake into muscle
  • 1st line therapy in T2DM

Example:
- Metformin

Side-Effects:

  • GI upset (20%)
  • Lactic acidosis (rare)
  • does not cause weight gain or hypoglycaemia
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5
Q

Describe the mechanism, example and side-effect of SULFONYLUREAS

A

Mechanism:

  • Inhibits ATP sensitive Potassium channels in the beta cell membrane
  • influx of calcium –> insulin release

Example:

  • Glibenclamide
  • Gliclazide
  • Glimepiride
  • Glipizide
  • Tolbutamide

Side-effects:

  • weight gain
  • hypoglycaemia
  • rash
  • nausea
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6
Q

Describe the mechanism, example and side-effect of GLITAZONES/ THIAZOLINEDIONE

A

Mechanism:
- Binds to nuclear receptors in adipocytes to increase transcription of insulin sensitive genes

Example:

  • Rosiglitazone
  • Pioglitazone
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7
Q

Describe the mechanism, example and side-effect of SGLT2 inhibitors

A

Mechanism:

  • inhibits the reuptake of glucose by blocking action of SGLT2 transporters in kidney PCT
  • decreased hyperglycaemia

Example:
- Dapagliflozin

Side-effects;
- glycosuria

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8
Q

What are incretins and give examples

A

Peptide hormones that are released in the GI tract in response to food and potentiates insulin secretion:

  • Glucagon like peptide (GLP-1)
  • Gastro intestinal peptide (GIP)
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9
Q

what normally breaks down incretins

A

rapidly broken down by DPP-4

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10
Q

Describe the mechanism, example and side-effect of DDP-4 inhibitors

A

Mechanism:

  • Inhibits DDP-4 and so prevents the breakdown of incretins
  • Enhances action of GIP and GLP-1

Example:

  • Exanatide
  • Sitagliptin
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11
Q

what are the MICROvascular complications of diabetes

A

Retinopathy
Neuropathy
Nephropathy

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12
Q

what are the MACROvascular complications of diabetes

A

Ischaemic heart disease
Peripheral Vascular disease
Cerebrovascular disease

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13
Q

Does reversal/ improving hyperglycaemia prevent microvascular disease

A

YES

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14
Q

Does reversal/ improving hyperglycaemia prevent macrovascular disease

A

TO AN EXTENT

- preventing macrovascular disease- control of BP, cholesterol and smoking is more important

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15
Q

Describe the pathogenesis of microvascular disease

A
  • Capillary damage

- Metabolic damage

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16
Q

Describe capillary damage in the pathogenesis of microvascular disease

A
  • Prolonged Hyperglycaemia
  • Increased blood flow
  • Increased Capillary pressure
  • Thickened and damaged blood vessels
  • Endothelial damage (leakage of albumin and other proteins)
17
Q

what tissues need insulin to take up glucose

A

retina
kidney

nerves do not

18
Q

Glucose is metabolised to sorbitol by ___________

A

aldose reductase

19
Q

In diabetes, glucose levels rises. What happens when excessive glucose enter polyol pathway

A
  • sorbitol accumulates
  • less NADPH available for cell metabolism
  • build up of ROS and oxidative stress
  • cell damage
20
Q

what is the leading cause of impaired vision in ages 20-74

A

diabetic retinopathy

21
Q

what are the early stages (non-proliferative) of diabetic retinopathy

A

Hyperglycaemia

  • damage to small vessel wall
  • micoraneurysms

When vessel wall is breached
- Dot haemorrhages

Protein and fluid left behind
- Hard exudates

Micro-infarcts
- cotton wool spots

look at pics

22
Q

what are the later stages (non-proliferative) of diabetic retinopathy

A

Damage to veins

  • Venous budding
  • Blockage of blood supply

Ischaemia –> VEGF and other growth factors

  • neovascularisation
  • proliferative retinopathy
  • vitreous haemorrhage

Fluid not cleared from macular area
- Macular oedema

23
Q

what is the prevention of diabetic retinopathy

A

Good glycaemic control
Stop smoking
good blood pressure control

24
Q

what is the treatment of diabetic retinopathy

A 
Address risk factors 
Opthalmic review (retinal screening of diabetics aged >12)
- laser 
- VEGF inhibitors (bevacizumab)
- vitrectomy
25
Q

Why is retinopathy screening important

A

as no symptoms until too late

early detection is key

26
Q

what are the stages of diabetic nephropathy

A

Renal enlargement and Hyperfiltration

  • -> microalbuminuria
  • -> macroalbuminuria
  • -> end stage renal failure
27
Q

what is the normal albumin levels in urea and what are the abnormal levels in microalbuminuria

A

<20 mg

abnormal: 30-300mg albumin/24 hrs

28
Q

what is the pathophysiology of diabetic nephropathy (early stages)

A
  • Renal hypertrophy
  • Increase in GFR

Afferent arteriole vasodilates

  • glomerular pressure
  • thickened GBM
  • capillary damage
  • shear stress on endothelial cells

End result- leakage of protein into urine

29
Q

what is the pathophysiology of diabetic nephropathy (later stages)

A

Progressive glomerulosclerosis
Glomeruli destroyed (protein filtered into urine)
Progressive proteinuria
Renal failure

30
Q

what is the prevention of microalbuminuria

A

Screen for microalbuminuria

IF microalbuminuria present- help prevent progression to macroalbuminuria

31
Q

IF microalbuminuria present, what to do to help prevent progression to macroalbuminuria

A

ACE inhibitors
ARB (angiotensin receptor blocker)

Agressive CV risk reduction (statin, stop smoking)

Improve glycaemic control

32
Q

Describe the pathophysiology of diabetic neuropathy

A

Glucose leads to inability to transmit signals through nerves

  • Metabolic changes (sorbitol accumulation)
  • Vascular changes (Capillary damage)
  • Structural changes
33
Q

what are some of the signs and symptoms of diabetic neuropathy

A 
Tingling
Aching pain
Burning pain
Lancinating pain
Numbness 
Unusual sensitivity or tenderness when feet are touched

symptoms progress from distal to proximal over time

34
Q

what is the treatment of diabetic neuropathy

A

Duloxetine
Amitriptyline

refer to pain clinic (Try Tramadol or topical lidocaine)

35
Q

What is the diabetic foot a combination of?

A

Neuropathy and Peripheral vascular disease (PVD)

36
Q

give example of conditions of diabetic foot?

A

Infection
Ulcers
Ischaemia

37
Q

What is charcot foot

A

Numb foot

  • repetitive microtrauma
  • stress fractures

Dysregulated blood flow

  • increased bone turnover
  • fragile bone
38
Q

Give example of autonomic neuropathy affecting cardiovascular, GU and GI

A

CV: postural hypotension
GU: erectile dysfunction
GI: Gustatory sweating and gastroparesis

Y2 Endocrine Block (21 decks)

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