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Metabolism CC > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

Diabetes definition

A

Chronic non-communicable disease characterised by hyperglycaemia
Usually irreversible
Late complications

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2
Q

Diabetes cause

A

Relative insulin deficiency or resistance to both

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3
Q

How many people diagnosed in UK

A

3.7 million

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4
Q

How many deaths 2015

A

1.6 million

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5
Q

Type 1 Diabetes

A

Chronic autoimmune
Immune (T cell) mediated disruption of the pancreatic Beta cells within the islets of Langerhans
Insulin deficiency- constant need for injections

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6
Q

Type 1 as immune-mediated disease

A

Infiltration of pancreas islets by mononuclear cells (insulitis)
90% newly presenting patients possess autoantibodies against islet constituents

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7
Q

Type 1 hereditary

A

Prominent as disease of childhood or young patients <30
Any age
Increased susceptibility may be inherited

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8
Q

Type 2

A 
Most common - 80-95%
Chronic, progressive disease
Abnormal insulin action + secretion
More present in older, but now increasing in young population
Genetic components to disease
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9
Q

Genes that may be responsible for Type 2

A

GKRP

PPARG

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10
Q

RF Type 2

A 
Obesity
Family history
Age
Ethnicity
Environment
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11
Q

Obesity BMI

A

Greater than 31 –> 40x increased risk

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12
Q

Fam history RF

A

1st generation - lean + otherwise healthy relatives often develop skeletal muscle insulin resistance

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13
Q

Monozygotic twins

A

If 1 has diabetes, other has 60-90% increase chance of diabetes

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14
Q

Obesity- Intrinsic effects

A

Mitochondrial dysfunction
Oxidative stress
ER stress

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15
Q

Obesity- Extrinsic effects

A

Accumulation of lipids + their metabolites
Increased conc. of circulating free FAs
Chronic inflammation
Altered adipokine levels

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16
Q

Obesity- hyperinsulinaemia

A

Increases lipid synthesis + exacerbates insulin resistance

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17
Q

Most common alterations that lead to insulin resistance

A

Decrease in no. insulin receptors
Decrease in catalytic activity of receptor
Increased activity Tyr phosphatases
Increased Ser/Thr phosphorylation of receptor or of IRS
Decreased PI3K/Akt activity
Decreased levels + functions GLUT4

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18
Q

Serine/Threonine kinase activation

A

Activated by pro-inflammatory cytokines, saturated FFAs + amino acids
Phosphorylate IRS, reducing its Tyr phosphorylation + increasing its degradation

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19
Q

Insulin resistance in healthy individuals

A

Body can generate new Beta cells in response to insulin resistance associated with obesity or pregnancy

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20
Q

Insulin compensation in insulin resistance

A

Islets increase both in size + number due to beta cell increasing in size and number
Increased Beta cell function

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21
Q

Glucose tolerance can be maintained by…

A

Increased insulin resistance

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22
Q

Impaired islet compensation

A

In Type 2, number of islets decreases

–> significant reduction in number of Beta cells per islet

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23
Q

Reduced pancreatic beta cell mass/increased death

A

Reduced pancreatic Beta cell function

–> reduced insulin synthesis + secretion

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24
Q

Susceptibility genes associated with Type 2 diabetes

A

Most are regulators of cell turnover or regeneration

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25
Q

Glucagon deregulation

A

Excessive circulating glucagon levels reported in all diabetes forms

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26
Q

Beta cell adaptation to insulin resistance

A

Increased glucokinase activity
Increased malonyl-CoA –> inhibition of CPT1 + increase in DAG levels
Fatty acids bind to GPR40
GLP1 binding to its receptor
Release of Ach from parasympathetic nerve terminals

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27
Q

Mechanisms in insulin resistance

A

Impaired islet compensation
Reduced pancreatic Beta cell mass + increased death
Pancreatic Beta cell loss of function

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28
Q

Impaired islet compensation - Type 2

A

Number of islets decrease

Significant reduction in number of Beta cells per islet

29
Q

Type 2- Reduce pancreatic Beta cell mass + increased death

A

Many susceptibility genes associated with type 2 diabetes are regulators of cell turnover or regeneration

30
Q

Type 2- Beta cell loss of function

A

Most risk variants for type 2 diabetes in healthy pop. act through impairing insulin secretion rather than action
Inherited abnormalities of Beta cell function or mass
–> further enhances insulin resistance

31
Q

Mature onset diabetes of young (MODY)

A

Autosomal dominant inheritance
Present at birth, but often detected only later in life
Pancreatic Beta cell dysfunction

32
Q

Gestational diabetes

A

Occurs 2-6% pregnancies European women
Insulin resistance not compensated
Increased complications 2nd half pregnancy
Increased risk subsequent development type 2

33
Q

Latent autoimmune diabetes of adults (LADA)

A

5-10% phenotypic type 2 diabetics have markers of autoimmunity
Progression to insulin dependency faster than normal type 2

34
Q

Diagnosis

A 
One abnormal plasma glucose
Random >11.1mmol/L 
Fasting >7mmol/L
Thirst
Increased pee
Recurrent infections
Weight loss
Drowsiness
Coma
35
Q

Asymptomatic ppl diagnosis

A

Two fasting venous plasma glucose samples in abnormal range

36
Q

Oral glucose tolerance test

A

Normal fasting <6.1

Normal after 2h <7.8

37
Q

HbA1c advantages

A

Reliable measure
HbA1c levels relatively stable vs glucose
Ease of sample collection
No need for 8h fast- convenient

38
Q

HbA1c limitations

A

Cost
Influence of Hb traits
Conditions affecting RBC turnover

39
Q

HbA1c cut off point diagnosis

A

48mmol/mol (6.5%)

40
Q

Treatment aim

A

Lower blood glucose levels

41
Q

Treatment drugs

A

Biguanides (Metformin)
Sulfonylureas
TZDs
others

42
Q

Treatment pathways

A 
Enhance insulin activity
Inhibit gluconeogenesis
Stimulation of insulin secretion
Enhance GLP1 activity
Reduce DDP4 activity
43
Q

Enhancement of insulin sensitivity- drug

A

Biguanides (Metformin)

44
Q

Inhibition of gluconeogenesis- drug

A

Biguanides (Metformin)

45
Q

Stimulation of insulin secretion- drug

A

Sulfonylureas
Meglitinides
–> act on ATP sensitive potassium channel, closing it

46
Q

Enhancement GLP1 action- drug

A

Biguanides (metformin)

47
Q

GLP 1 actions

A

Inhibits glucagon secretion + hepatic glucose production
Augments glucose induced insulin secretion
Slows gastric emptying
Promotes satiety
Restores beta cell function
Increases insulin biosynthesis
Promotes Beta cell differentiation

48
Q

Inhibition of DDP-4 action- drug

A

DDP 4 inhibitors

–> block DDP4 and decrease glucose (DDP4 enzyme inactivates GLP 1)

49
Q

Acute complications of diabetes

A

Ketoacidosis

Hypoglycaemia

50
Q

Ketoacidosis

A

Continual use of FAs for energy –> ketone body production
Blood + urine acid levels rise, dehydration, coma, death
Potentially life threatening
More common type 1

51
Q

Ketoacidosis emergency treatment

A

Fluids
Electrolytes
Insulin

52
Q

Hypoglycaemia

A

<70mg/dL (<3.9mmol/L)

Presence of Whipple triad

53
Q

Whipple triad

A

Low blood glucose
Symptoms + signs associated with low blood glucose
Resolution of symptoms + signs by carbohydrate ingestion

54
Q

Hypoglycaemia causes

A 
Alcohol excess
Insulinoma
Excessive exercise
Reactive hypoglycaemia
Type 1 diabetes
55
Q

Chronic complications of diabetes

A

Hyperglycaemia

Dyslipidaemia

56
Q

Hyperglycaemia- Macrovascular

A

Atherosclerosis

57
Q

Hyperglycaemia- Microvascular

A

Kidney disease
Nerve disease
Blindness
Amputation

58
Q

Dyslipidaemia

A

Ectopic fat deposition in skeletal muscle + liver in exacerbation of insulin resistance
Macrovascular complications

59
Q

Hyperglycaemia Pathophysiology

A

Excess glucose diverted into other pathways

60
Q

Hyperglycaemia- hyperactivation of PKCs

A 
Can damage blood vessels
Increased permeability
Increased occlusion
Increased reactive O2 species levels
Increased inflammation
Mitochondrial dysfunction
61
Q

Diabetic retinopathy- Non-Proliferative

A

Dilation of retina veins + microaneurysms
Can cause internal haemorrhaging + oedema in retina
Oedema in central retina is main cause of vision loss in this case

62
Q

Diabetic retinopathy- Proliferative

A

Fragile, new blood vessels form near optic disk
Grow on vitreous chamber and elsewhere in retina
Can bleed, reduce vision + lead to separation + detachment of areas in retina

63
Q

Diabetic retinopathy occurrence

A

20 years poorly controlled diabetes

64
Q

Diabetic nephropathy

A

Damage to BVs in glomerulus

  • -> proteinuria, glomerular hypertrophy, decreased GFR, renal fibrosis
  • -> 1/3 patients affected
65
Q

Diabetic neuropathy

A

Damage to nerve vessels + blood vessels supplying nerves
Peripheral- pain or loss in hands, arms, feet, legs
Autonomic- changes in digestion, bowel + bladder control, erectile dysfunction, nerves supplying heart
Proximal- pain in thighs + hips, weakness in legs
Focal- any nerve in body

66
Q

Atherosclerosis mechanism

A

AGE modification of oxidised LDL receptor
–> enhanced LDL uptake into atherosclerotic plaques
AGE-LDL induces pro-inflammatory cytokine production
Glycation of apolipoprotein –> impaired cholesterol efflux from atherosclerotic plaques
Glycation of LDLR and LDL –> impaired cholesterol clearance

67
Q

Atherosclerosis effect

A

Tissue nutrient + O2 supply to heart, brain + extremities compromised

68
Q

Most common cause of death for patients with diabetes

A

Atherosclerosis

70%

Metabolism CC (29 decks)

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