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Metabolism 2 > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

what is diabetes mellitus

A
  • This is a chronic non-communicable disease characterised by hyperglycaemia
  • Usually irreversible and its late complications result in reduced life expectancy and major health costs
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2
Q

what causes diabetes mellitus

A
  • Caused by relative insulin deficiency or resistance or both
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3
Q

what is the 7th biggest cause of death

A

diabetes

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4
Q

what is type 1 diabetes

A

this is a chronic autoimmune disease where you have an insulin deficiency therefore you have a need for insulin injections

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5
Q

what causes type 1 diabetes

A
  • Characterised by immune T cell mediated disruption of the pancreatic B cells within the islets of Langerhans
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6
Q

is type 1 diabetes genetic

A
  • Type 1 Diabetes is not genetically predetermined but increased susceptibility to the disease may be inherited
  • Genetic basis of the disease not fully understood Major genetic determinants only account for ~40-50% of the familial clustering of the disorder)
  • Incidence increasing in most populations suggesting that environmental factors are involved in its pathogenesis
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7
Q

what are the types of insulin that are available

A

short acting and long acting

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8
Q

when does type 1 diabetes usually present itself

A

usually in young patients before the age of 30 but it can present at any age

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9
Q

what is the most common type of diabetes

A
  • Most common (85-90% of all diabetes)
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10
Q

what age group is type 2 diabetes in

A
  • It used to be more present in older patients (>30 years of age) but increasing in younger population
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11
Q

is type 2 diabetes genetic

A
  • Concordance rates are significantly higher in identical twins compared to non identical twins
  • Genetic component to the disease but genes responsible for most of the cases are still not known
  • GKRP and PPARG genes are thought to have a role
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12
Q

what are the risk factors for type 2 diabetes

A
  • Obesity
  • Family history – first generation, lean otherwise healthy relatives often develop skeletal muscle insulin resistance
  • Age – increased mitochondrial dysfunction, inflammation
  • Ethnicity
  • Increased in incidence follows the trend of urbanisation and lifestyle changes suggesting environmental influences
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13
Q

what is the major risk factor for type 2 diabetes

A

Obesity

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14
Q

what are the intrinsic and extrinsic factors of obesity that can lead to insulin resistance

A

Intrinsic factors as obesity can increase these
- (mitochondrial dysfunction, oxidative stress, ER stress) – this eventually impairs the reaction of the insulin

Extrinsic

  • Accumulation of lipids and their metabolites or increased concentrations of circulating free fatty acids
  • Chronic inflammation
  • Altered adipokine levels
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15
Q

what does hyperinulinaemia do

A
  • It increases lipid synthesis and exacerbates insulin resistance
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16
Q

name the most common alterations that can lead to insulin resistances

A
  • Decrease in the number of insulin receptor
  • Decrease in the catalytic activity of the receptor
  • Increased activity of Tyr phosphatases
  • Increased Ser/Thr phosphorylation of the receptor or of IRS
  • Decreased PI3K/Akt activity
  • Decreased levels and function of GLUT4
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17
Q

how can pro-inflammatory cytokines, saturated free fatty acids and amino acids cause insulin resistant

A

Pro-inflammatory cytokines, saturated FFAs, amino acids can activate Serine/Threonine kinases that can phosphorylate IRS, reducing its Tyr phosphorylation and also increasing its degradation

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18
Q

Why do not all insulin resistance people have diabetes

A
  • this is because insulin resistance can be overcome by increasing insulin secretion therefore glucose control can be maintained

this happens by

  • new Beta cells being generated in response to insulin resistance associated with obesity or pregnancy
  • islet of langerhans increase in size and number due to beta cell increase in size and number
  • there is an increased beta cell function
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19
Q

what happens in type 2 diabetes which means that they become insulin resistant

A
  • the number of islet cells decrease and there is a reduction in the number of beta cells per islet
  • this is due to reduced pancreatic B cell mass, increased death and reduced pancreatic B cell function
  • this is all widely due to the fact that many of the genes associated with type 2 diabetes are regulatory of cell turnover and regeneration therefore if they are impaired then the beta cells are not regenerated and insulin secretion is reduced
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20
Q

most of the risk factor for type 2 diabetes act by …

A
  • Most risk variants for Type 2 diabetes in healthy populations act by impairing insulin secretion rather than insulin action
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21
Q

what are the 2 critical precursors in type 2 diabetes

A
  • inherited abnormalities of B cell function

- inherited abnormalities of B cell mass

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22
Q

lack of insulin can lead to….

A

increased levels of glucagon

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23
Q

why is high levels of glucagon called

A

hyperglucagonaemia

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24
Q

why does hyperglucagonaemia arise in type 1 diabetes

A
  • In untreated or poorly controlled Type 1 diabetes this is likely due to the insulin deficiency
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25
Q

why can you have hyperglycaemia at the same time as hyperglucagonaemia in type 2 diabetes

A
  • defect of insulin secretion
  • resistance of alpha cells to insulin
  • resistance of alpha cells to hyperglycaemia
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26
Q

name some other forms of diabetes

A
  • maturity onset diabetes of the young
  • gestational diabetes
  • latent autoimmune diabetes of adults
  • type 3c diabetes
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27
Q

what is maturity onset diabetes of the young

A
  • autosomal dominant inheritance

- causes pancreatic B cell dysfunction

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28
Q

what is gestational diabetes and what is the risk

A
  • Occurs in 2-6% of pregnancies in Europe

- Increased complications during the second half of pregnancy

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29
Q

describe latent autoimmune diabetes of adults

A
  • 5-10 % of phenotypic “Type 2DM” patients have markers of autoimmunity
  • Progression to insulin dependency faster than Type 2 DM
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30
Q

what is a risk of having gestational diabetes

A
  • Increased risk of subsequent development of Type 2 DM
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31
Q

what is type 3c diabetes due to

A
  • Diabetes due to diseases of the exocrine pancreas

- (used to be called “pancreatogenic” or “pancreatogenous” diabetes mellitus)

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32
Q

how do you diagnose diabetes using blood tests

A

One abnormal plasma glucose
(random ≥11.1 mmol/L or fasting ≥7 mmol/L) in the presence of symptoms (thirst, increased urination, recurrent infections, weight loss, drowsiness and coma)

Two fasting venous plasma glucose samples in the abnormal range
(≥7 mmol/L) recommended in asymptomatic people

33
Q

what is the oral glucose tolerance test

A
  • Patient is asked to fast for 8 hours and then they are given a sugary drink, then measure the glucose levels fasting
34
Q

what is the advantages of HbA1c

A
  • reliable measure;
  • HbA1c levels are relatively stable vs glucose;
  • ease of sample collection;
  • patient convenience (no need for 8 h fast)
35
Q

what are the disadvatanges of HbA1c

A
  • cost in some parts of the world;
  • influence of Hb traits (e.g. HbS, HbF);
  • conditions affecting rbc turnover
36
Q

how do you use HbA1c to diagnose diabetes

A

• An HbA1c of 48 mmol/mol (6.5%) is recommended as the cut point for diagnosing diabetes

37
Q

what is the main aim of treatment of diabetes

A
  • the main aim is to lower blood glucose levels
38
Q

List some medication that can be used to treat diabetes

A
  • Biguanides (metformin)
  • Sulfonylureas
  • Meglitinides
  • Thiazolidinediones (TZD)
  • DPP-4 inhibitors

These try to act at the level of other organs to lower the blood glucose

  • SGLT2 Inhibitors
  • Alpha-glucosidase inhibitors
  • Bile Acid Sequestrants
39
Q

How do thiazolidinediones TZD work

A
  • work at the transcription level
  • try to push the PPARgamma transcription factor
  • this causes an increase in glucose uptake in the sketal muscle and adipose muscle
  • also produces genes that are responsible for pushing gluconeogensis - this reduces the amount of gluconeogensis in the liver
40
Q

what are the signs and symptoms of diabetes

A 
Signs and Symptoms:
 Weight loss.
 Polyuria (increased urination).
 Polydipsia (increased thirst).
 Polyphagia (increased hunger).
 Blurred vision.
 Headaches.
 Fatigue.
 Nausea and vomiting.
41
Q

what does HbA1c measure

A

Hb1Ac measures the levels of glycosylated Hb.

42
Q

what are the signs and symptoms of type 1 diabetes

A

 Glycosuria.
 Polyuria and dehydrations (due to osmotic diuresis).
- Osmotic diuresis occurs when glucose is present in the kidney tubules and is not
reabsorbed.
- This pulls water back into the tubules and it is excreted.
 Weight loss.
- Weight loss occurs due to loss of glucose in the urine.
 Fatigue.
 Diabetic ketoacidosis.

43
Q

what does metformin do

A
  • Increases insulin sensitivity
  • Improved insulin receptor function
  • Improved glucose transport
  • Reduced fatty acid synthesis
  • It inhibits gluconeogenesis
44
Q

name the drugs that act as agonists of GLP-1 receptor

A
  • GLP1 is normally inactivated by DDP-4

- Sitagliptin inhibits DDP-4

45
Q

what does GLP-1 do

A
  • Increase the glucose induced insulin secretion
  • Inhibits glucagon secretion and hepatic glucose production
  • Slows gastric emptying
  • Promotes satiety
  • In the context of obesity, it slows gastric emptying and gives a longer sense of satiety
  • There are some drugs that act as agonist of the GLP-1 receptor
46
Q

what drugs can cause more insulin secretion

A

sulfaonylureas and meglitindes

47
Q

name an example of sulfaonylureas

A

Glicazide is an example.

48
Q

How do sulfaonylureas and meglitindes work

A

 Cause increased secretion of insulin.
 Sulfonylureas inhibit K+ channels in Beta cells to prevent their efflux.
 A build-up of K+ leads to depolarisation in the cell membrane.
 Voltage-sensitive Ca2+ channels open, influx of Ca2+.
 Ca2+ influx triggers exocytosis release of insulin.

49
Q

name the side effect son sulfaonylureas

A

hypoglycaemia and weight gain.

50
Q

what does DPP-4 usually do

A

 DPP4 is an enzyme which breaks down and inhibits incretins.
 If DPP4 is inhibited the levels of incretins can rise.
 Sitagliptin is an DPP4 inhibitor.

51
Q

name a DPP4 inhibitor

A

Sitagliptin

52
Q

what do alpha glucosidase inhibitors do

A

 Block disaccharide breakdown.
 Reduces intestinal glucose absorption.
 Decreases postprandial hyperglycaemia.

53
Q

what ar ether side effects of alpha glucosidase

A
  • Diarrhoea.
  • Flatulence.
  • Abdominal pain.
54
Q

what lifestyle advice can you give someone with type 2 diabetes

A 
 Reduce dietary:
- Fat.
- Sugar.
- Salt.
 Increase dietary fruit and veg content, raises fibre levels.
 Weight loss.
 Increased physical activity.
55
Q

list 2 acute diabetes complications

A

(acute because they are rapid)

  • ketoacidosis
  • Hypoglycaemia
56
Q

how does ketoacidosis occur

A

– Continual use of fatty acids for energy leads to production of ketone bodies (acetoacetate and -hydroxybutarate)
– Blood and urine acid levels rise, dehydration, coma, death

57
Q

what is the treatment of ketoacidosis

A
  • fluids(isotonic) and potassium first

- then insulin

58
Q

name 2 ketone bodies that are produced in keotacidosis

A

acetoacetate and -hydroxybutarate

59
Q

describe how hypoglycaemia can occur

A
  • In Type 1 Diabetes this can occur because of high insulin doses (e.g. insulin injection but missed meal).
  • Recurrent severe hypoglycaemia affects 1-3% of Type 1 diabetes patients, mostly adults having diabetes for > 10 years
60
Q

Name the chronic complications of diabetes

A

Hyperglycaemia

macrovascualr

  • atherosclerosis - cardiovascular events
  • dyslipidaemia

microvascuarl

  • kidney disease (Nephropathy)
  • nerve disease (Neuropathy)
  • blindness (retinopathy)
  • amputations
61
Q

What harm can hyperglycaemia do

A

 Hyperglycaemia is responsible for tissue damage.
 The mechanism of which cause tissue damage are brought about by the formation of reactive oxygen species in the mitochondria; superoxide.

62
Q

what tissues does hyperglycaemia effect

A

 Tissues which are independent of insulin are affected, these include:

  • Neurons.
  • Glomeruli.
  • Retina.
63
Q

describe how hyperglycaemia can activate the protein kinase C pathway

A

 Increased glycolysis generates diacylglycerol (DAG).
 DAG activates PKC.
 PKC alters expression of peptides and growth factors to modify blood vessels:

64
Q

How does protein kinase C pathway alter blood vessels

A
  • Increased permeability
  • Increased occlusion
  • Increased reactive oxygen species levels
  • Increased inflammation
  • Mitochondrial dysfunction
65
Q

what are the two ways in which diabetic retinopathy are caused

A
  • non proliferative

- proliferative

66
Q

describe the two ways in which diabetic retinopathy are caused

A

Non proliferative

  • dilation of the retina veins
  • microanuerysms
  • these can cause internal haemorrhages and oedema in the retina
  • oedema in the central retina is the main cause of blindness in this cause

proliferative

  • Damaged capillaries occlude and more VEGF is released.
  • fragile new blood vessels form near the optic disk
  • these grow on the vitreous chamber and elsewhere in the retina
  • they can bleed, reduce vision and lead to separation and detachment of areas in the retina
67
Q

when is diabetic retinopathy caused

A
  • occurs in most people after 20 years of poorly controlled diabetes
  • leading new cause of new blindness or partial vision loss in people aged 20-74
68
Q

what is more common proliferative retinopathy or non-proliferative reitnopathy

A

non proliferative is very common and has mild severity whereas proliferative is very rare and has more severe severity

69
Q

what is diabetes nephropathy and what are its characteristics

A
  • Disease of the kidney involving damage to the blood vessels in the glomerulus, which is critical for blood filtration, kidney glomeruli become thickened

It is characterised by:

  • proteinuria,
  • glomerular hypertrophy,
  • decreased glomerular filtration
  • renal fibrosis
70
Q

what is a leading cause of end stage kidney disease

A

diabetic nephorpahty

71
Q

what is the clinical presentation of diabetic nephorpathy

A

 Clinical presentation:

  • Hypertension.
  • Proteinuria.
  • Decreased renal function.
72
Q

what is diabetic neuropathy

A
  • this is when there is damage to the nerve fibres and blood vessels supplying the nerves
73
Q

what are the 4 types of diabetic neuropathy

A
  • peripheral
  • autonomic
  • focal
  • proximal
74
Q

describe the 4 types of diabetic neuropathy

A

Peripheral neuropathy:

  • More common, affects the peripheries such as hands and feet.
  • Symptoms are: numbness, tingling and loss of balance.
  • Blisters/sores occur on feet as injuries are not detected due to loss of sensation.

 Autonomic neuropathy:

  • Leads to multi-system problems.
  • Genito-urinary dysfunction may cause erectile problems or urinary incontinence.
  • GI issues may cause vomiting and diarrhoea.
  • Cardiovascular problems may cause postural hypotension.

Focal
- It can affect any nerve in the body and it causes pain or weakness

Proximal
- It causes pain in thighs and hips and weakness in legs

75
Q

what are macrovascular complications of diabetes

A
  • Metabolic injury to large blood vessels (arteries and veins)
76
Q

describe how microvascular complications of diabetes arise

A
  • AGE modification of oxidised low-density lipoprotein receptor (LDLR) leads to increased LDL uptake into atherosclerotic plaques
  • AGE-LDL produces more pro-inflammatory cytokine to be released
  • increased Glycation of apolipoprotein impairs cholesterol efflux from atherosclerotic plaques
  • Glycation of LDLR and LDL leads to impaired cholesterol clearance
77
Q

what is the most common cause of death for patients with diabetes

A

macrovascualr complications

78
Q

name the macrovascualr complications

A

The impact of macrovascular complications is reduced nutrient and oxygen supply to
the heart and brain:
- Brain = Stroke.
- Heart = MI, heart failure.
- Extremities = Ulceration or gangrene, peripheral vascular disease.

Metabolism 2 (40 decks)

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