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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
what should the results be of the two fasting venous plasma glucose samples?
≥7 mmol/L
26
how does the oral glucose tolerance test work?
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.
27
what is HbA1c?
glycated Hb
28
what are the advantages of the HbA1c test?
* Reliable measure * HbA1c levels are relatively stable vs glucose * Ease of sample collection * Patient convenience – haven’t got to fast for 8 hours
29
what are the limitations of the HbA1c test?
* Costs in some part of the world * Influence of Hb traits e.g. HbS, HbF * Conditions affecting RBC turnover
30
what is the main aim of treatment of diabetes?
low blood glucose levels
31
how do the TZD family of drugs work?
- 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
what type of drug is metformin?
biguanides
33
what is the first line of treatment for T2D?
metformin
34
what effects do metformin have?
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
how does insulin secretion occur in beta cells?
* 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
how do sulfonylureas work?
close the K+ channel - help to fix the beta cell function by inducing insulin secretion
37
what are the functions of GLP-1?
* 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
what normally degrades GLP-1
DDP-4
39
what drugs inhibit DDP-4?
Sitagliptin | GLP-1 receptor agonists
40
what are additional characteristics of GLP-1 based therapies?
o Restores B-cell function o Increases insulin biosynthesis o Promotes B cell differentiation
41
what are the main acute complications of diabetes?
ketoacidosis | hyperglycaemia
42
how do ketoacidosis occur in diabetics?
• 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
what are long term complications of ketoacidosis?
dehydration coma death
44
what emergency treatment is given for ketoacidosis and why?
o Emergency treatment: fluids, electrolytes (especially K+), insulin o K+ given especially bc insulin induces a shift of K+ from the blood intracellularly
45
why can hyperglycaemia occur in diabetes?
Can occur in T1D bc of high insulin doses e.g. insulin injection but missed meal
46
what are the chronic complications of diabetes?
Hyperglycaemia • Macrovascular: atherosclerosis - cardiovascular events • Microvascular: Kidney disease (Nephropathy), Nerve disease (Neuropathy), Blindness (Retinopathy), Amputation Dyslipidaemia
47
what is dyslipidaemia?
Ectopic fat deposition in skeletal muscle and liver and exacerbation of insulin resistance, macrovascular complications
48
when there is excess glucose, what other pathways can it be diverted into?
protein kinase C
49
what effect can hyperactivation of PKCs have on blood vessels?
``` o Increased permeability o Increased occlusion o Increased reactive oxygen species levels o Increased inflammation o Mitochondrial dysfunction ```
50
what structural modifications of proteins can happen?
basement membrane thickness, reduced vascular elasticity etc
51
what is diabetic retinopathy?
Disease of the retina involving damage to the blood vessels in the back of the eye
52
what are the 2 types of diabetic retinopathy?
non-proliferative | proliferative
53
what causes non-proliferative diabetic retinopathy?
Dilation of retina veins + microaneurysms --> internal hemorrhaging and oedema in the retina.
54
what is the main cause of vision loss in non-proliferative diabetic retinopathy?
oedema in the retina
55
what causes proliferative diabetic retinopathy?
- 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
who does diabetic diabetic retinopathy occur in usually?
Occurs in most people after 20 years of poorly controlled diabetes
57
what is diabetic nephropathy?
Kidney disease involving glomerulus blood vessel damage – imp for blood filtration
58
what is diabetic nephropathy characterised by?
proteinuria, glomerular hypertrophy, decreased glomerular filtration and renal fibrosis
59
what damage can occur in diabetic neuropathy?
* 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
what % of people with diabetes develop some form of nerve damage?
60-70%
61
what does AGE formation promote?
macrovascular disease (atherosclerosis)
62
what does AGE modification of LDL receptors lead to?
enhanced LDL uptake into atherosclerotic plaques
63
what does glycation of apolipoproteins lead to?
impairs cholesterol efflux from atherosclerotic plaques
64
what does glycation of LDLR and LDL lead to?
impaired cholesterol clearance
65
what other macrovascular complications occur in diabetes?
* 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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