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Endocrinolgy > More Diabetes (obesity and diabetic complications) > Flashcards

More Diabetes (obesity and diabetic complications) Flashcards

1
Q

What is obesity?

A

Overweight and obesity are defined as abnormal or excessive fat accumulation that presents a risk to health

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2
Q

How do you measure BMI?

A

BMI = weight / height2 (kg/m2)

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3
Q

What percentage of the UK population is obese?

What as the UK prevalence of obesity in 2005 and what will it be in 2015

A

Common- UK 22.7% UK adults are obese Prevalence is increasing - WHO global projections: 2005 >400 million adults obese By 2015 >700 million obese
Increasing in high, middle and low income countries

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4
Q

What are the mechanical consequences of obesity?

A
  • Osteoarthritis
  • Functional/ADLs
  • Obstructive Sleep Apnoea (OSA)*
  • Oesophageal reflux
  • Obstetric complications
  • Idiopathic Intracranial Hypertension
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5
Q

What are the metabolic consequences of obesity?

A 
•‘Metabolic syndrome' 
•Type 2 diabetes 
•Cardiovascular disease 
•Cancers (breast, colon, endometrial)
•PCOS 
•OSA*
 •Steatohepatosis 
•Gallstones
(It is possible to be obese and metabolically normal)
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6
Q

What are the mental health consequences of obesity?

A
  • Body image dysphoria

* Depression

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7
Q

What are the monetary consequences of obesity?

A

•Employment •Discrimination

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8
Q

What is metabolic syndrome?

A

Clustering of risk factors for cardiovascular disease:
• Visceral adiposity / central obesity
• Impaired glucose metabolism
• Dyslipidaemia (low HDL-cholesterol, high triglycerides)
• Hypertension

  • Visceral / central obesity and insulin resistance are central in the pathogenesis of Metabolic Syndrome
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9
Q

What are the consequences of metabolic syndrome?

A 
Metabolic Syndrome is associated with increased risk of: 
• Diabetes RR > 3 
• Cardiovascular disease
• Steatohepatosis 
• PCOS 
• Gallstones 
• OSA 
• Some cancers
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10
Q

What are the consequences of increased Visceral and subcutaneous adipose tissues?

A

VAT - Metabolic - apple shape

SAT - Mechanical, Mental health, Monetary - pear shape

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11
Q

What are causes of obesity?

A

Susceptability to obesity •?Genes – ‘thrifty gene’ hypothesis
•?Intra-uterine environment •?Psychosocial / cultural •Specific conditions •Cushing’s syndrome, hypothyroidism •Leptin deficiency •Prader-Willi syndrome •Medications •Hypothalamic
•Low requirement for energy expenditure
Fat storage: VAT v SAT

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12
Q

What are the controlling factors of food intake?

A 
Energy stores - eg. Leptin
Food intake - eg. GLP-1
Nutrients in blood
Non homeostatic:
Social eating cues
Cost and availability
Palatability
food reward 
Mood
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13
Q

What are the types of Strategies for management of obesity and MetS?

A
  • Public health – not discussed here
  • Management of co-morbidities/complications
  • eg OSA, diabetes, hypertension
  • Behavioural and dietary
  • Medical
  • Surgical
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14
Q

How effective are dietary behavioural interventions in obesity and MetS?

A
  • Small-moderate weight loss (~5%)

* Valuable metabolically – eg reduces risk of Type 2 diabetes

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15
Q

What is the mechanism of action of oralistat?

A

MECHANISM OF ACTION: ORLISTAT
• Inhibition of lipases by orlistat blocks systemic absorption
of dietary fat
• Unabsorbed fat is excreted into faeces (up to one-third of ingested fat)
Side effects: diarrhoea, faecal incontinance

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16
Q

Is Metformin effective in diabetes prevention?

A

Diabetes Prevention Programme (NEJM 2002)
Reduces risk of Type 2 diabetes
Weight neutral
Not licensed in the UK for diabetes prevention

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17
Q

Is Exenatide effective in obese diabetics?

A

GLP-1 analogues eg exenatide
• Licenced in UK for improving glycaemic control in people with T2DM and obesity
• ↓ HbA1c
• ↓weight

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18
Q

4 types of bariatric surgery?

A 
Gastric:
- Vertical Banded Gastroplasty
- Gastric Banding
Combination:
- Roux-en-Y Gastric Bypas
Small bowel:
- Duodenal switch
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19
Q

Summarise what you know about the use of bariatric surgery in obesity and type 2 diabetes

A
  • Effective in reducing weight (15-25%)
  • No randomised controlled trials
  • Improves glycaemic control (may lead to remission of Type 2 diabetes!): • Related to weight loss Related to factors other than weight loss
  • Reduced mortality
  • Sufficient weight loss to impact on non-metabolic complications • Risk of short and long term complications
  • Not an ‘easy’ option
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20
Q

What is diabetic nephropathy and when is the peak onset?

A
  • A specific kidney disorder characterised by changes in the renal microcirculation leading to proteinuria and progressive g p p g decline in renal function
  • Peak onset in patients who have had diabetes for 10 to 20 years
21
Q

Diabetic eye disease?

A

Retinopathy – accounts for 90% of cases of visual impairment in type 1 diabetes

  • In type 2 diabetes, cataracts, macular degeneration and glaucoma account for 50% of cases
  • Incidence of blindness @ 12% in type 1 and 5% in type 2 DM
22
Q

What are the principle abnormalities in diabetic retinopathy?

A

-capillary changes resulting in leaking of protein and capillary closure causing ischaemia.

• The accessibility of the retinal microcirculation to direct observation allows early detection and intervention

23
Q

He is diabetic retinopathy managed?

A

Laser Photocoagulation:
• Effective treatment
• management of proliferative and exudative changes, including maculopathy
• Direct photocoagulation of peripheral new vessels
• Pan-retinal photocoagulation for new vessels near the optic disc/ central retina – leads to regression of new vessel formation

24
Q

What is the first stage of kidney disease?

A

Kidney damage:
Hyperfiltration, or an increase in glomerular filtration rate (GFR) occurs.
Kidneys increase in size.

25
Q

What is the second stage of kidney disease?

A

Kidney damage:

Glomeruli begin to show damage and microalbuminurea damage and microalbuminurea occurs.

26
Q

What occurs in the 3rd stage of kidney disease?

A

Moderate:
Albumin excretion rate (AER) exceeds 200 micrograms/minute, and blood levels of creatinine and urea-nitrogen rise.
Blood pressure may rise during this stage.

27
Q

4th stage of kidney disease?

A

Severe:
GFR decreases to less than 75 ml/min
large amounts of protein pass into the urine
and high blood pressure almost always occurs
Levels of creatinine and urea-nitrogen in the blood rise further.

28
Q

What is the fifth stage of kidney disease?

A

Kidney failure, or end stage renal disease (ESRD).
GFR is less than 10 ml/min.
The average length of time to progress from Stage 1 to Stage 4 kidney disease is 17 years for a person with type 1 diabetes. The average length of time to progress to Stage 5, kidney failure, is 23 years.

29
Q

Hw is kidney disease screened for?

A
  • Testing for urinary protein allows detection of nephropathy
  • Conventional bedside testing detects albumin concentration >200mg/l – indicative of established nephropathy (Stage 4)
  • Earlier detection desirable and can be achieved by more sensitive assays detecting microalbuminuria ( albumin 20 – 200 mg/l)
30
Q

6 ways of reducing risks in diabetes?

A
  • Glycemic control: • New insulins • New oral agents • CBG testing: new sites (forearm), smarter monitors
  • BP control
  • ACE inhibitors
  • Cholesterol control
  • Aspirin
  • Smoking cessation
31
Q

3 area of Generalized symmetric polyneuropathy?

A
  • Acute sensory
  • Chronic sensorimotor
  • Autonomic
32
Q

4 classes of Focal and multifocal neuropathies?

A
  • Cranial
  • Truncal
  • Focal limb
  • Proximal motor (amyotrophy)
33
Q

What are the consequences of painful Generalised Sensory Neuropathies?

A
  • Distal, burning pain- particulalry at night

* Parasthesia / hyperasthesia

34
Q

What are the consequences of painless Generalised Sensory Neuropathies?

A

• Asymptomatic sensory loss • Impaired light touch/ vibration/ temperature • Absent reflexes • Autonomic dysregulation – warm skin, bounding pulses

35
Q

Focal / multifocal neuropathies?

A
  • Diabetic Amyotrophy - painful wasting of the proximal leg muscles ( particularly quadriceps)
  • Median and ulnar nerves are commonly affected
  • Cranial nerves rarer – but may present with unilateral III, IV, or VI nerve palsy
36
Q

What are the mechanisms of diabetic foot disease?

A
  • Loss of pain sensation
  • Unrecognized trauma
  • Loss of joint position sense
  • Abnormal foot posture
  • Wasting of small intrinsic muscles
  • Foot deformity
37
Q

What are the consequences do cardiovascular autonomic neuropathy?

A

– Resting tachycardia
– Postural hypotension
– Risk of cardiac arrhythymias / sudden death

38
Q

What are the consequences of gastrointestinal autonomic neuropathy?

A

– Gastroparesis

– Autonomic diarrhoea

39
Q

What are the consequences of genitoirinary autonomic neuropathy?

A

– Bladder dysfunction

– Erectile dysfunction

40
Q

7 areas/mechanisms/causes of diabetic microvascular complications?

A
  • Enzymatic and non-enzymatic glycosylation
  • Accumulation of polyol pathway products
  • Oxidative stress (increase in H2O2)
  • Diacylglycerol and Protein Kinase C activation
  • Hypoxia and growth factors (VEGF, FGF, TGF1)
  • Haemodynamic insult
  • Genetics
41
Q

What are AGES and why are they important in microvascular pathology?

A

Advance glycation end products - AGES - glycation of long living proteins eg. Collagen, fibronectin - makes it harder to refresh/turnover proteins - they become thicker - accumulation
- focal point for areas of the immune system
- contribute directly to oxidative stress.
Glucose and lysine - non enzymatic glycation - forms a tough bond.

42
Q

What is advanced glycation?

A
  • Glucose binds non-enzymatically to free amino acid residues
  • Complex rearrangement to form Advanced p g Glycation end-products (AGEs)
  • AGEs accumulate in proportion to hyperglycaemia and time
  • Leads to tissue dysfunction
43
Q

How is sorbitol generated and how does this contribute to diabetic microvasular complications?

A

Aldose reductase

Aldose reductase catalyses Glucose into Sorbitol
via Polyol pathway
• Unfavourably affects cellular redox potential
• increases generation of reactive oxygen species

44
Q

What happens in oxidative stress?

A
  • Increased free radicals
  • Endothelial damage
  • Decreased NO bioavailability
  • Vasoconstriction
  • Link between vascular and biochemical theories
45
Q

Metabolic Mechanisms Protein Kinase CBeta?

A

• Member of a family of protein serine-threonine kinases • Expressed in retina
• Glucose causes Diacylglycerol which causes increased PKCBeta
- growth and proliferation effects

46
Q

What is the role of TGFBeta in diabetic microvascular complications?

A

• TGFBeta – increased by AGE and PKCBeta –

  • decreases ECM breakdown causi Basement membrane thickening
  • increased vitreous TGFBetaj in Diabetic retinopathy
  • Scarring in the kidney and the eye
  • thickening of the BM of the glomerulus
47
Q

What is the role of VEGF in diabetic microvascular complications?

A

• VEGF – Hypoxia is a potent stimulus to VEGF production by retina – increased by AGE and PKCBeta
– Stimulates angiogenesis causing neovascularisation
– increases vascular permeability causing Macular oedema

48
Q

See notes on complications of diabetes mechanisms for rest as it is hard to make into questions

Endocrinolgy (8 decks)

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