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Diabetes Flashcards

1
Q

What is diabetes?

A

a metabolic disorder in which there is persistent hyperglycaemia in the body

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2
Q

What is the ultimate cause of hyperglycaemia in diabetes?

A

beta cell dysfunction due to decreased insulin secretion

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3
Q

What are symptoms of diabetes?

A
  • increased thirst (polydipsia)
  • increased fatigue
  • increased urination (polyuria)
  • blurred vision
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4
Q

What are the 3 main types of diabetes?

A
  • monogenic
  • type 1
  • type 2
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5
Q

What are the 4 monogenic forms of diabetes?

A
  • MODY
  • neonatal
  • mitochondrial
  • syndromes of insulin resistance
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6
Q

What is MODY?

A

an autosomal dominant disorder that usually occurs before the age of 25

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7
Q

What do most MODY mutations do?

A

affect the pancreatic β cell

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8
Q

What are the effects of the different MODY gene mutations?

A
  • MODY1 – early pancreatic development and insulin secretion defects
  • MODY2 – mild
  • MODY3 – insulin secretion defects; complications occur
  • MODY5 – pancreatic hypoplasia; renal dysfunction
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9
Q

What is mitochondrial diabetes?

A

a maternally inherited disorder caused by a rare genetic defect in the mitochondria that impairs insulin production

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10
Q

What do syndromes of insulin resistance arise from?

A

mutations in the insulin receptor

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11
Q

Give examples of syndromes of insulin resistance

A
  • type A insulin resistance e.g. Donohue syndrome, Leprechaunism, Rabson-Mendenhall syndrome
  • decreased number of insulin receptors
  • impaired insulin binding
  • impaired tyrosine kinase activity
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12
Q

What is T1D?

A

an autoimmune-mediated destruction of pancreatic beta cells

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13
Q

What is a key marker of T1D?

A

autoantibodies that attack the pancreatic beta cells

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14
Q

Give examples of autoantibodies

A
  • islet cell antibodies (ICA)
  • glutamic acid decarboxylase (GAD65)
  • insulin autoantibodies (IAA)
  • protein tyrosine phosphatase IA-2
  • zinc transporter 8 (ZnT8)
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15
Q

What are the 5 main factors that can lead to T1D?

A
  • genetic susceptibility and environmental factors (viruses, bacteria, chemicals) initiate the process
  • immune activation – CD8 T-cells kill β-cells, and inflammation reduces regulatory T-cell function
  • autoantibody production – B cells produce autoantibodies, with CD4 T-cell help
  • epitope spreading – new β-cell antigens are released, amplifying the immune attack
  • clinical diabetes – loss of β-cell mass causes hyperglycaemia, with a temporary “honeymoon phase” of partial β-cell function recovery
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16
Q

What is gestational diabetes?

A

diabetes during pregnancy when the body cannot produce enough insulin to meet the increased demands

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17
Q

What is gestational diabetes usually?

A

asymptomatic and resolved after pregnancy

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18
Q

What is gestational diabetes influenced by?

A
  • genetic factors e.g. TCF7L2, HHEX, CDKN2A
  • modifiable factors e.g. obesity, weight gain, smoking and diet
  • reproductive and medical history
  • foetal factors
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19
Q

What does gestational diabetes increase the risk of?

A

developing type 2 diabetes and related vascular disorders or other comorbidities in later life

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20
Q

What is T2D?

A

a chronic condition that occurs when the body doesn’t produce enough insulin or doesn’t use insulin properly; often coincides with early development of peripheral insulin resistance

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21
Q

When will patients develop impaired glucose tolerance and/or impaired fasting glucose?

A

if pancreatic beta cells fail to compensate for insulin resistance

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22
Q

What can beta cell exhaustion over time lead to?

A

impaired insulin secretion and subsequent hepatic glucose production

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23
Q

What does insulin promote?

A
  • fuel storage and inhibition of breakdown of stored fuel in skeletal muscle, liver and adipose tissue
  • recruitment of glucose transporters to the plasma membrane for glucose transport into skeletal muscle and adipose tissue
24
Q

What does insulin regulate?

A
  • metabolic enzymes
  • intracellular metabolites
  • gene expression
25
Why is obesity a major contributor to insulin resistance?
increased adipose tissue increases circulating plasma free fatty acid (FFA) levels
26
What does FFA do?
promote hepatic glucose production and inhibit peripheral glucose utilisation
27
What are insulin sensitisers?
medications that help the body use insulin more effectively e.g. TZDs and metformin
28
What are the 3 main functions of pancreatic beta cells?
- make and store insulin - sense glucose - secrete insulin
29
How do pancreatic beta cells make and store insulin?
they package proinsulin into secretory granules which is then processed by proconvertase 1/3 and proconvertase 2 to yield islet amyloid polypeptide (IAPP/amylin), insulin and inert C-peptide
30
What are the 3 steps of glucose sensing?
1. glucose moves into the cell via facilitated diffusion through GLUT1 and/or GLUT2 glucose transporter 2. glucokinase catalyses the first step of glycolysis and glucose phosphorylated 3. metabolism of glucose generates ATP, raising the ATP:ADP ratio
31
What are the 4 steps of insulin secretion from pancreatic beta cells?
1. increase in ATP:ADP ratio causes KATP channels to close 2. K+ ions accumulate in the cell, increasing the potential difference from -70mV 3. voltage-gated Ca2+ channels open, allowing the entry of Ca2+ ions 4. insulin is released by exocytosis
32
What happens in T2D?
lack of first phase glucose-stimulated insulin secretion (GSIS) → reduction in the second phase of GSIS → reduced ability of glucose to potentiate the effects of non-glucose secretagogues on beta cell insulin secretion
33
Where are beta cell changes common?
- individuals with impaired glucose tolerance - relatives of individuals with T2D - elderly individuals - individuals with a history of gestational diabetes - individuals with polycystic ovary syndrome
34
What are common alterations in pancreatic beta cells in T2D?
- IAPP deposits reduce the beta cell mass → altered IAPP processing/secretion - altered/increased proinsulin release → altered beta cell processing and premature release due to increased beta cell secretory demand
35
What is the aetiology of beta cell dysfunction in T2D?
a combination of genes and environment
36
What do diabetes drugs work to do and what can they be?
lower blood glucose levels and can be secretagogues, insulin sensitisers or glycosurics
37
What is the first-line medication for treatment of T2D?
metformin
38
What are adverse effects of metformin?
gastrointestinal irritation and lactic acidosis
39
What is the MOA of metformin?
- decreases hepatic gluconeogenesis (decreased lactate uptake) via activation of AMPK - antagonises the action of glucagon - increases insulin sensitivity in periphery organs
40
What do sulfonylurea (SU) and meglitinide do?
increase insulin secretion from pancreatic β cells but they are ineffective in individuals who cannot produce insulin
41
What are adverse effects of SU and meglitinide?
hypoglycaemia in the presence of excessive insulin secretion which can induce weight gain
42
What is the MOA of SU and meglitinide?
1. binds to and closes KATP channels in the pancreatic beta cells 2. potassium then cannot exit beta cells, and the membrane depolarises 3. voltage-gated Ca2+ channels open 4. increased intracellular calcium leads to increased fusion of insulin granules with cell membrane of beta cells 5. increased secretion of insulin
43
What is the difference between SU and meglitinide?
meglitinide has weaker binding affinity and faster dissociation from the binding site
44
What are adverse effects of TZDs?
- troglitazone was withdrawn due to increased risk of hepatitis - rosiglitazone was linked to an increased risk of heart disease and stroke as well as increased water retention
45
What is the MOA of TZDs?
1. activates PPARusually bound by FFAs and eicosanoids 2 PPARγ complexes with retinoid X receptor (RXR) 3. these heterodimeric nuclear receptors increase their transcriptional activation and repression activity
46
What are the consequences of TZDs?
- increased storage of fatty acids in the adipocytes - increased oxidation of carbohydrates - increased insulin sensitivity
47
What are adverse effects of DPP-4 inhibitors?
joint pain, increased risk of heart failure and acute pancreatitis
48
What is the MOA of DPP-4 inhibitors?
1. dipeptidyl peptidase-4 inhibitors inhibit DPP-4 2. this increases GLP-1 and GIP levels which inhibits the release of glucagon 3. reduced glucagon levels, increased insulin secretion and decreased gastric emptying
49
What is GLP-1 receptor agonist?
an incretin mimetic with a lower risk of hypoglycaemia compared to SU or meglitinides
50
What are adverse effects of GLP-1 receptor agonist?
acute pancreatitis and pancreatic cancer
51
What is the MOA of GLP-1 receptor agonist?
same as DPP-4 inhibitors, but more potent
52
What is gliflozin?
an SGLT2 inhibitor that reduces body weight and blood pressure with a low risk of hypoglycaemia
53
What is SGLT2?
the major cotransporter involved in glucose reabsorption in the kidney
54
What are adverse effects of gliflozin?
ketoacidosis and genital infections
55
How does insulin therapy work?
by mimicking the body’s natural insulin secretion and can be administered via syringe, insulin pen or pump

Topics in Biomedical Science (6 decks)

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