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MBD > Diabetes And Hypoglycaemia > Flashcards

Diabetes And Hypoglycaemia Flashcards

1
Q

What are blood glucose levels maintained by?

A
  • Dietary carbohydrate
  • Glycogenolysis
  • Gluconeogenesis
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2
Q

Name the 4 broad effects of insulin (on the liver and on the periphery)

A
  • Decreased liver glucose production (so less glycogenolysis and gluconeogenesis)
  • Increased movement of glucose into the liver for storage
  • Increased peripheral uptake of glucose
  • Decreased peripheral catabolism
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3
Q

What is the FED state?

A
  • FED = catabolism
  • After eating when your body is digesting food and absorbing nutrients
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4
Q

What happens to metabolism in the fed state?

A
  • Glucose increases → insulin release
  • Increase of liver nutrient uptake
  • Increase in peripheral uptake
  • Decrease in peripheral catabolism
  • Decrease in liver glucose production
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5
Q

In the fasting state, describe the effects of low insulin

A
  • Increased glucose production via gluconeogenesis and glycogenolysis in the liver
  • Increased lipolysis and proteolysis
  • Decreased peripheral glucose uptake
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6
Q

When and where is glucagon secreted?

A
  • Alpha cells of the pancreas secrete glucagon when there is low blood sugar
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7
Q

When and where is insulin secreted?

A
  • Beta cells of the pancreas secrete insulin when there is high blood sugar
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8
Q

What is the effect of insulin on adipose tissue?

A
  • increased glucose uptake
  • increased lipogenesis
  • decreased lipolysis
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9
Q

What is the effect of insulin on Striated muscle?

A
  • increased glucose uptake
  • increase glycogenolysis
  • increased protein synthesis
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10
Q

What is the effect of insulin on the Liver?

A
  • decreased gluconeogenesis
  • increased glycogenolysis
  • increased lipolysis
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11
Q

What are the 4 counter-regulatory hormones to insulin?

A
  • Glucagon - Maintains blood glucose in fasting
  • Adrenaline - Mobilises fuels in acute stress
  • Cortisol - Changing long term
  • Growth hormone - Inhibits insulin action
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12
Q

How does glucagon counter regulate insulin?

A

Glucagon maintains blood glucose in fasting

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13
Q

How does adrenaline counter regulate insulin?

A

Adrenaline mobilises fuels in acute stress

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14
Q

How does cortisol counter regulate insulin?

A

cortisol changes long term?

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15
Q

How does Growth hormone counter regulate insulin?

A

Growth hormone inhibits insulin action

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16
Q

What is the function of insulin?

A

Promotes storage and growth

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17
Q

What are the major metabolic pathways involving insulin?

A
  • Glucose storage in muscle and liver
  • Protein and fatty acid synthesis
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18
Q

What are the major metabolic pathways involving glucagon?

A
  • Activates gluconeogenesis
  • glycogenolysis
  • fatty acid release
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19
Q

What are the major metabolic pathways involving epinephrine (adrenaline)?

A
  • Stimulates glycogenolysis and fatty acid release
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20
Q

What are the major metabolic pathways involving cortisol?

A
  • Amino acid mobilisation
  • gluconeogenesis
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21
Q

What are the major metabolic pathways involving growth hormone?

A

Stimulates lipolysis

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22
Q

Define diabetes mellitus

A

“a metabolic disorder characterised by chronic hyperglycaemia, glycosuria and associated abnormalities of lipid and protein metabolism”

  • increased hepatic glucose production AND decreased cellular (peripheral) glucose uptake
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23
Q

Why does DM cause glycosuria?

A

High blood glucose of excess of 10mmol/l causes glycosuria as this is above the renal threshold

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24
Q

What are the classifications of diabetes mellitus?

A
  • Type 1
  • Type 2
  • Secondary
  • Gestational
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25
Q

What is type 1 diabetes?

A

Deficiency in insulin secretion (autoimmune destruction of Beta cells by T cells)

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26
Q

Explain how in type 1 DM, insulin deficiency leads to ketoacidosis and then diabetic coma

A
  • Insulin deficiency causes increased lipolysis so increased FFAs (free fatty acids) so increased FFA oxidation in the liver which causes ketoacidosis which causes diabetic coma.
  • Also, insulin deficiency causes hyperglycaemia, glycosuria, polyuria, volume depletion and this can cause diabetic coma also.
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27
Q

What is polyphagia?

A

Polyphagia is increased appetite, can be caused by hyperglycaemia

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28
Q

What is Polydipsia?

A

Polydipsia is increased thirst which can be caused by the volume depletion (due to the glycosuria so polyuria so volume depletion)

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29
Q

What is type 2 diabetes?

A

insulin secretion retained but target organ is resistant to its actions

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30
Q

Describe the onset of type 2 DM and if it has a strong familiar incidence or not

A
  • Slow onset (months to years)
  • Middle aged or elderly - prevalence increases with age
  • Strong familiar incidence
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31
Q

Describe the pathophysiology of Type 2 DM

A
  • Genetic predisposition + environmental factors (like obesity) will lead to insulin resistance
  • Beta cell hyperplasia to compensate = normoglycemia
  • Beta cell failure (early) = impaired glucose tolerance
  • Beta cell failure (late) = diabetes
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32
Q

What is the HONK state?

A

Hyperglycaemic, hyperosmolar non-ketotic state

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33
Q

Describe the effects that low insulin levels has on the metabolic processes of the body

A
  • Low insulin causes increased gluconeogenesis and increased glycogenolysis = hyperglycaemia
  • Hyperglycaemia will then cause glycosuria … leading to dehydration, thrombosis and cerebral dehydration
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34
Q

Name the 3 ways (tests) that we can diagnose DM type 2 (in the presence of symptoms)

A
  • Random plasma glucose greater than 11.1 mmol/l
  • Fasting plasma glucose greater than 7.0 mmol/l
  • Oral glucose tolerance test (OGTT) plasma glucose greater than 11.1 mmol/l
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35
Q

How do you diagnose DM in the absence of symptoms?

A

In the absence of symptoms you need to take 2 blood samples on 2 separate days

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36
Q

Explain what is meant by impaired glucose tolerance (IGT)

A

This is a pre-diabetic state, person is at risk of diabetes and CVS disease

  • fasting plasma glucose is greater than 7mmol/l and OGTT is between 7.8 and 11.1
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37
Q

Explain what is meant by impaired fasting glycaemia (IFG)

A

This is a pre-diabetic state, person is at risk of diabetes and CVS disease. Blood glucose levels are raised but not high enough for diabetes yet.

  • fasting plasma glucose 6.1 to 6.9 mmol/l and OGTT value of less than 7.8mmol/L
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38
Q

What is the first step in DM type 2 treatment?

A

Diet and exercise (lifestyle changes)

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39
Q

What is secondary diabetes?

A

chronic pancreatitis, pancreatic surgery → causes secretion of insulin antagonists

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40
Q

What differentiates gestational diabetes?

A

It occurs for the first time in pregnancy

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41
Q

Describe the common ages and onset of DM Type 1

A
  • children and young adults mostly
  • sudden onset (days or weeks), symptoms may be preceded by a prediabetic period
42
Q

Describe the most common cause of DM type 1

A
  • Most common cause is autoimmune destruction of beta cells of pancreas (due to genetic and environmental factors)
43
Q

What genes are strongly linked with type 1 DM?

A
  • There is a strong link in the HLA genes (HLADR and HLADQ) in MHC region of chromosome 6
  • these increase susceptibility to the disease - so people with these genes may be more prone to the environment triggering the autoimmune destruction of the beta cells
44
Q

Describe the pathogenesis of DM type 1 (role of TH1, TH2, autoantibodies …)

A
  • Autoantigens are presented to T lymphocytes (T helper 1 and T helper 2) to initiate an autoimmune response.
  • T helper 1 will secrete IL2 and IF
  • IL2 will activate autoantigens specific to T cytotoxic lymphocytes which destroy the beta islet cells through secretion of toxins
  • T helper 2 will secrete IL4 which stimulates lymphocytes to proliferate and produce autoantibodies
  • These autoantibodies are specific to various beta cell antigens such as glutamic acid decarboxylase, islet auto-antigen and tyrosine-phosphatase-like molecule - most common antibody is is the islet cell antibody
45
Q

What is the most commonly detected antibody associated with type 1 diabetes?

A

Islet cell antibody

46
Q

What does the destruction of pancreatic beta cells cause?

A

Hyperglycaemia

47
Q

Why does the destruction of pancreatic beta cells cause hyperglycaemia?

A

Absolute deficiency of insulin and amylin

48
Q

What is amylin?

A

Glucoregulatory peptide hormone co-secreted with insulin

49
Q

What does amylin do?

A

Lowers blood glucose by slowing down gastric emptying and supressing glucagon output from pancreatic beta cells

50
Q

What does an increased plasma osmolarity lead to?

A

Cerebral dehydration and impaired consciousness

51
Q

What does hyperglycaemia cause?

A

Glycosuria

52
Q

What does glycosuria cause?

A

Osmotic diuresis and loss of water and electrolytes

53
Q

What does loss of water and electrolytes cause?

A
  • Dehydration
  • Increased blood viscosity
  • Thrombosis
54
Q

What are the symptoms that would cause you to test for diabetes?

A
  • Polyuria
  • Polydipsia
  • Weight loss (type 1 only)
55
Q

What does fasting mean when testing for diabetes?

A

No caloric intake for at least 8 hrs

56
Q

When do you do an oral glucose tolerance test?

A

In patients with:

  • impaired fasting glycaemia
  • Unexplained glycosuria
  • Clinical features of diabetes with normal plasma glucose values
57
Q

Why do you carry out an oral glucose tolerance test?

A

To check the bodys ability to metabolise glucose

58
Q

How do you do an oral glucose tolerance test?

A

75g oral glucose tolerance and blood tests at 0 and 120 mins after glucose

59
Q

How do you treat type two diabetes?

A

Diet and exercise → oral monotherapy → combination of drugs → insulin with insulin + combinations of drugs

60
Q

What drug is used in oral monotherapy for type 2 diabetes?

A

Metformin

61
Q

What is the function of metformin?

A

Decreases gluconeogenesis and increases utilisation of glucose in the periphery

62
Q

Name some different drugs used in treatment of DM type 2

A
  • Metformin
  • Suflonylureas
  • Thiazolinediones
  • SGLT2 inhibitors
  • Incretin-targeting drugs (DPP-4 inhibitors and synthetic GLP-1 analogues)
63
Q

How do sulfonylureas work?

A

Depolarise beta cells to release insulin, can cause hypoglycaemia.

64
Q

What are some examples of Sulfonylureas?

A
  • Glipizide
  • Glimepiride
  • Glyburide
65
Q

How do SGLT2 inhibitors work?

A

Prevent glucose reabsorption in the kidney

  • so glucose is excreted
66
Q

What are some examples of SGLT2 inhibitors?

A
  • Canagliflozin
  • Empagliflozin
67
Q

What drug is used in oral combination therapy for type 2 diabetes?

A
  • Sulphonylureas
  • Gliptins
  • GLP-1 analogues
68
Q

What do thiazolidinediones do?

A
  • Reduced insulin resistance
69
Q

What are some examples of DPP-4 inhibitors?

A
  • Sitagliptin
  • Saxagliptin
  • Linagliptin
  • Alogliptin
70
Q

What are some examples of GLP-1 agonists?

A
  • Liraglutide
  • Exenatide
  • Lixisenatide
  • Semaglutide
  • Dulaglutide
71
Q

How do incretin targeting drugs work?

A

Help the body to increase glucose when needed

72
Q

What is the aim of monitoring glycaemic control?

A

To prevent complications or avoid hypoglycaemia

73
Q

How can we monitor glycaemic control?

A
  • Capillary blood measurement
  • urine analysis
  • Blood HbA1c
  • Urinary albumin
74
Q

What does glucose in urine give an indication of?

A

Blood glucose concentration above renal threshold

75
Q

What is blood HbA1c?

A

Glycated Hb; covalent linkage of glucose to residue in Hb

76
Q

What are the long term complications of (badly managed) diabetes?

A

Micro and macro vascular disease

77
Q

What are the examples of microvascular disease?

A

Retinopathy, nephropathy, neuropathy

78
Q

What are some examples of macrovascular disease?

A

Atherosclerosis heart attack/ stroke

79
Q

What is hypoglycaemia defined as (in numbers)?

A

Plasma glucose <2.5 mmol/L

80
Q

What are the causes of hypoglycaemia?

A
  • Drugs
  • More common in type 2 diabetes (when taking insulin and inslin secretagogues)
81
Q

What is the treatment for hypoglycaemia?

A

Exogenous insulin and insulin secretagogues

82
Q

Describe what sulfonylureas actually are - name 3

A

They are insulin analogues and insulin secretagogues (mimic insulin or increase secretion of insulin from beta cells)

  • glyburide
  • glipizide
  • glimepiride
83
Q

What is a risk of any type 2 DM drugs when used together with insulin secretagogues?

A

Hypoglycaemia

84
Q

What can cause hypoglycaemia in patients without diabetes?

A
  • Alcohol and pharma drugs (Beta blockers, ACE inhibitors, IGF-1 etc)
  • Endocrine disease
  • Insulinoma
  • Inherited metabolic disorders
  • Sepsis
  • Chronic kidney disease
85
Q

Explain how ethanol (alcohol) can cause hypoglycaemia

A

Ethanol inhibits gluconeogenesis BUT NOT glycogenolysis

  • hypoglycaemia may occur after several days of alcohol binge with limited food intake resulting in hepatic depletion of glycogen
86
Q

What happens if you have a several day long alcohol binge with limited food intake?

A

Hepatic depletion of glycogen

87
Q

Explain how sepsis can cause hypoglycaemia

A
  • Is a common cause of hypoglycaemia.
  • Cytokines can accelerate utilization of glucose and inhibit gluconeogenesis
88
Q

Why does chronic kidney disease cause hypoglycaemia?

A

Involve impaired gluconeogenesis, reduced renal clearance of insulin and reduced renal glucose production

89
Q

What is another name for reactive hypoglycaemia?

A

Postprandial hypoglycaemia

90
Q

What is reactive hypoglycaemia?

A

Drops in blood sugar are usually recurrent and occur within four hours of eating

91
Q

What causes reactive hypoglycaemia?

A
  • Possibly a benign tumour in the pancreas overproducing insulin
  • Too much glucose used up by the tumour itself
  • Deficiencies in the counter-regulatory hormones
92
Q

What are the categories for signs of hypoglycaemia?

A
  • Neurogenic
  • Neuroglycopaenic
93
Q

Describe the counter-regulatory response to hypoglycaemia

A

Brain needs glucose.

  • Inhibition of insulin release is the first defence to hypoglycaemia
  • Second response is stimulation of alpha cells to produce glucagon
  • Also stimulates release of cortisol and Adrenaline
94
Q

In the counter-regulatory response to hypoglycaemia, what is the function of adrenaline?

A
  • Stimulates hepatic glycogenolysis and also gluconeogenesis
  • Also decreases use of glucose in the periphery
95
Q

What are the neurogenic symptoms of hypoglycaemia triggered by?

A

Falling glucose levels

96
Q

What are the neurogenic symptoms of hypoglycaemia activated by?

A

Autonomic nervous system

97
Q

What are the neurogenic symptoms of hypoglycaemia mediated by?

A

Sympathoadrenal release of catecholamines and ACh

98
Q

What are the neurogenic symptoms of hypoglycaemia?

A
  • Mood changes
  • Trembling
  • Paleness
  • Sweating
  • Dizziness
  • Blurred vision
  • Hunger
  • Headaches
  • Extreme tiredness
99
Q

What is neuroglycopaenia caused by?

A
  • Neuronal glucose deprivation
100
Q

What are the symptoms of neuroglycopaenia?

A
  • Confusion
  • Difficulty speaking
  • Ataxia
  • Paresthesia
  • Seizures
  • Coma
  • Death

MBD (23 decks)

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