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diabetes mellitus Flashcards

1
Q

what is type 1 diabetes?

A

chronic autoimmune disease

insulin deficiency - constant need for insulin injections

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2
Q

what is type 1 diabetes characterised by?

A

immune T-cell mediated disruption of pancreatic B cells in the islets of Langerhans.

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3
Q

who is type 1 diabetes common in?

A

childhood/young patients <30 but can present in any age

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4
Q

what is the genetics of type 1 diabetes?

A

• Not genetically predetermined but increased susceptibility may be inherited
o Genetic basis isn’t fully understood

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5
Q

what is the most common form of diabetes?

A

type 2 diabetes

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6
Q

what % of diabetes cases are type 2?

A

85-90%

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7
Q

what is type 2 diabetes characterised by?

A

abnormal insulin action and secretion (insulin resistance)

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8
Q

what age group is type 2 diabetes common in?

A

Used to be more present in older patients (>30 years) but increasing in younger

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9
Q

what genes are involved in type 2 diabetes?

A

o GKRP: glucokinase receptor protein gene

o PPARG: transcription factor which regulates genes associated with lipid and glucose metabolism

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10
Q

what are the risk factors for type 2 diabetes?

A
  • obesity
  • family history
  • age
  • ethnicity
  • environmental influences
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11
Q

why does age have an effect on risk of getting type 2 diabetes?

A

increased mitochondrial dysfunction, inflammation

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12
Q

what are the intrinsic causes of insulin resistance?

A

Mitochondrial dysfunction, oxidative stress, ER stress

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13
Q

what are the extrinsic causes of insulin resistance?

A

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

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14
Q

what are the causes of insulin resistance?

A

intrinsic
extrinsic
hyperinsulinaemia

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15
Q

what are the most common alterations that can lead to insulin resistance?

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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16
Q

describe how islet compensation occurs

A
  • New β cells can be generated in response to insulin resistance associated with obesity or pregnancy
  • Islets increase in both size and number bc of  cell increase in size and number
    There is also increased β function
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17
Q

explain how impaired islet compensation occurs?

A

• In T2D, number of islets of Langerhans decreases and there’s a significant reduction in the number of B cells per islet
o Reduced pancreatic β cell mass/ increased death, Reduced pancreatic β function

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18
Q

why does hyperglucagonaemia occur in all forms of diabetes?

A

defect of insulin secretion, resistance of a cells to insulin and/or to hyperglycaemia

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19
Q

name other forms of diabetes

A
  • Maturity onset diabetes of the young (MODY)
  • Gestational diabetes
  • Latent autoimmune diabetes of adults
  • Type 3c diabetes
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20
Q

how is MODY inherited?

A

autosomal dominant

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21
Q

when does gestational diabetes occur?

A

Increased complications during the second half of pregnancy

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22
Q

what is type 3c diabetes?

A

Diabetes due to diseases of the exocrine

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23
Q

how do you diagnose diabetes?

A
  • one abnormal plasma glucose in the presence of symptoms
  • two fasting venous plasma glucose samples in asymptomatic people
  • oral glucose tolerance test
  • HbA1c
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24
Q

what should the results be of one abnormal plasma glucose test in symptomatic people?

A

random ≥11.1 mmol/L or fasting ≥7 mmol/L

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25
Q

what should the results be of the two fasting venous plasma glucose samples?

A

≥7 mmol/L

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26
Q

how does the oral glucose tolerance test work?

A

patient is asked to fast for 8 hours then given a sugary drink for 2 hours. Values should be higher than normal in insulin resistance.

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27
Q

what is HbA1c?

A

glycated Hb

28
Q

what are the advantages of the HbA1c test?

A
  • Reliable measure
  • HbA1c levels are relatively stable vs glucose
  • Ease of sample collection
  • Patient convenience – haven’t got to fast for 8 hours
29
Q

what are the limitations of the HbA1c test?

A
  • Costs in some part of the world
  • Influence of Hb traits e.g. HbS, HbF
  • Conditions affecting RBC turnover
30
Q

what is the main aim of treatment of diabetes?

A

low blood glucose levels

31
Q

how do the TZD family of drugs work?

A
  • act at the level of the PPRG transcription factor – regulates GLUT4 transporter expression –> increases glucose uptake in skeletal muscle
    o Also decrease gluconeogenesis in the liver
    o Push towards lipogenesis rather than lipolysis
32
Q

what type of drug is metformin?

A

biguanides

33
Q

what is the first line of treatment for T2D?

A

metformin

34
Q

what effects do metformin have?

A

o Increases glucose transport and function of the insulin receptor – makes cells respond better to the insulin sensitivity
o Inhibits gluconeogenesis
o Stimulates GLP-1 synthesis

35
Q

how does insulin secretion occur in beta cells?

A
  • Glucose enters B cells through glucose transporter  increases ATP:ADP ratio
  • Closes the Katp channels and induces membrane depolarisation
  • Allows opening of the voltage gated Ca2+ channels  insulin secretion
36
Q

how do sulfonylureas work?

A

close the K+ channel - help to fix the beta cell function by inducing insulin secretion

37
Q

what are the functions of GLP-1?

A
  • Can increase the glucose induced insulin secretion
  • Can increase beta cell function
  • Reduce glucagon production
  • Reduce glucose production from the liver
  • Slow gastric emptying  Promotes satiety
38
Q

what normally degrades GLP-1

A

DDP-4

39
Q

what drugs inhibit DDP-4?

A

Sitagliptin

GLP-1 receptor agonists

40
Q

what are additional characteristics of GLP-1 based therapies?

A

o Restores B-cell function
o Increases insulin biosynthesis
o Promotes B cell differentiation

41
Q

what are the main acute complications of diabetes?

A

ketoacidosis

hyperglycaemia

42
Q

how do ketoacidosis occur in diabetics?

A

• Continuous use of fatty acids for energy leads to production of ketone bodies (acetoacetate and B-hydroxybutarate)
o Occurs during fasting
o Acidosis bc ketone bodies dissociate into anions and H+ - H+ depletes HCO3-

43
Q

what are long term complications of ketoacidosis?

A

dehydration
coma
death

44
Q

what emergency treatment is given for ketoacidosis and why?

A

o Emergency treatment: fluids, electrolytes (especially K+), insulin
o K+ given especially bc insulin induces a shift of K+ from the blood intracellularly

45
Q

why can hyperglycaemia occur in diabetes?

A

Can occur in T1D bc of high insulin doses e.g. insulin injection but missed meal

46
Q

what are the chronic complications of diabetes?

A

Hyperglycaemia
• Macrovascular: atherosclerosis - cardiovascular events
• Microvascular: Kidney disease (Nephropathy), Nerve disease (Neuropathy), Blindness (Retinopathy), Amputation

Dyslipidaemia

47
Q

what is dyslipidaemia?

A

Ectopic fat deposition in skeletal muscle and liver and exacerbation of insulin resistance, macrovascular complications

48
Q

when there is excess glucose, what other pathways can it be diverted into?

A

protein kinase C

49
Q

what effect can hyperactivation of PKCs have on blood vessels?

A 
o	Increased permeability
o	Increased occlusion
o	Increased reactive oxygen species levels
o	Increased inflammation
o	Mitochondrial dysfunction
50
Q

what structural modifications of proteins can happen?

A

basement membrane thickness, reduced vascular elasticity etc

51
Q

what is diabetic retinopathy?

A

Disease of the retina involving damage to the blood vessels in the back of the eye

52
Q

what are the 2 types of diabetic retinopathy?

A

non-proliferative

proliferative

53
Q

what causes non-proliferative diabetic retinopathy?

A

Dilation of retina veins + microaneurysms –> internal hemorrhaging and oedema in the retina.

54
Q

what is the main cause of vision loss in non-proliferative diabetic retinopathy?

A

oedema in the retina

55
Q

what causes proliferative diabetic retinopathy?

A
  • Fragile, new blood vessels form near the optic disk and grow on the vitreous chamber and elsewhere in the retina.
  • Can bleed, reduce vision and lead to separation and detachment of areas of the retina
56
Q

who does diabetic diabetic retinopathy occur in usually?

A

Occurs in most people after 20 years of poorly controlled diabetes

57
Q

what is diabetic nephropathy?

A

Kidney disease involving glomerulus blood vessel damage – imp for blood filtration

58
Q

what is diabetic nephropathy characterised by?

A

proteinuria, glomerular hypertrophy, decreased glomerular filtration and renal fibrosis

59
Q

what damage can occur in diabetic neuropathy?

A
  • Peripheral; causes pain/loss of feeling in the hands, arms, feet and legs
  • Proximal; causes pain in thighs, hips and weakness in the legs
  • Autonomic; causes changes in digestion, bowel and bladder control problems and erectile dysfunction. Can also affect nerves supplying the heart
  • Focal; can affect any nerve in the body + causes pain and weakness
60
Q

what % of people with diabetes develop some form of nerve damage?

A

60-70%

61
Q

what does AGE formation promote?

A

macrovascular disease (atherosclerosis)

62
Q

what does AGE modification of LDL receptors lead to?

A

enhanced LDL uptake into atherosclerotic plaques

63
Q

what does glycation of apolipoproteins lead to?

A

impairs cholesterol efflux from atherosclerotic plaques

64
Q

what does glycation of LDLR and LDL lead to?

A

impaired cholesterol clearance

65
Q

what other macrovascular complications occur in diabetes?

A
  • Tissue nutrient and oxygen supply to heart and brain and extremities is compromised
  • Cerebrovascular disease (stroke)
  • Heart Disease (Myocardial infarction, congestive heart failure)
  • Peripheral vascular disease (ulceration, gangrene and amputation)

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