Metabolic L2: Metabolic syndrome and diabetes Flashcards

1
Q

What is metabolic syndrome?

A

highly complex and multifactorial disorder, which shares several common underlying mechanisms

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2
Q

What are the 3 common underlying mechanisms of metabolic syndrome (Met-S)?

A
  1. Fat accumulation (ectopic fat e.g. visceral/intra-abdominal fat)
  2. Impaired insulin sensitivity (i.e. insulin resistance), and
  3. Low-grade chronic systemic inflammation (the pro-inflammatory state).
    • Anabolic and catabolic reactions irrgulated (normally –> more catabolic than anabolic)
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3
Q

What are the 3 pathophysiological effects (clinical diseases) of metabolic syndrome?

A
  1. Type 2 diabetes (T2d)
  2. Non-alcoholic Fatty Liver Diseases (NAFLD)
  3. Cardiovascular diseases (CVD)
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4
Q

Met-S is rapidly increasing in prevalence worldwide as a consequence of the continued ______‘‘epidemic’’

A

obesity

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5
Q

What are the 6 clinical features of Met-S?

A
  1. Impaired Glucose Regulation/Insulin Resistance
  2. Abdominal/Central Obesity
  3. Hypertriglycemia
  4. Low Levels of HDL Cholesterol
  5. Raised Blood Pressure
  6. Microalbuminuria
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6
Q

Once one part of metabolism is compromised, will have ____ impacts

A

secondary

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7
Q

What are characteristics of Impaired Glucose Regulation/Insulin Resistance?

DO NOT NEED TO KNOW SPECIFICS

A

Type 2 DM or impaired fasting glycaemia [≥6.1 mmol/L (110 mg/dl) or impaired glucose tolerance or glucose uptake below lowest quartile under hyperinsulinemia

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8
Q

What are characteristics of Abdominal/Central Obesity?

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A

Waist/hip ratio 0.90 in. in men, 0.85 in. women or BMI > 30 kg/m2

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9
Q

What are characteristics of Hypertriglycemia?

DO NOT NEED TO KNOW SPECIFICS

A

≥ 1.7 mmol/L (150 mg/dl)

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10
Q

What are characteristics of Low Levels of HDL Cholesterol?

DO NOT NEED TO KNOW SPECIFICS

A

< 0.9 mmol/L (35 mg/dl) in men, <1.0 mmol/L (39 mg/dl) in women

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11
Q

What are characteristics of Raised Blood Pressure?

DO NOT NEED TO KNOW SPECIFICS

A

≥ 140/90 mm Hg

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12
Q

What are characteristics of Microalbuminuria?

DO NOT NEED TO KNOW SPECIFICS

A

≥ 20μg/min or albumin: creatinine ratio ≥ 30 mg/g

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13
Q

What is white fat?

A
  • Under skin
  • Easy to get rid of
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14
Q

What is brown fat?

A
  • Visceral fat (sits around organs)
  • Dangerous Very difficult to get rid of
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15
Q

________ the largest endocrine organ

A

Adipose tissue

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16
Q

_____ are the primary cell type of adipose tissue

A

Adipocytes

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17
Q

________ is a highly active metabolic and endocrine organ.

A

Adipose tissue

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18
Q

Adipose tissue is the primary site of storage for excess ______.

A

energy

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19
Q

An endocrine organ - synthesizing a number of _________ that regulate metabolic homeostasis.

A

biologically active compounds

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20
Q

What is the problem of extreme obesity in the long term?

A
  • Dysregulation in tissue (fat stores)
  • Releasing proinflammatory factors
  • Affect other parts of the body
    • Constantly alert and activated
  • The body will try to re-balance this dysfunction
    • Might have chances in insulin pathways = diabetes
    • Cells in pancreas affected= stop producing insulin = diabetes
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21
Q

Insulin signaling regulates _____, _____ and _____homeostasis.

A

glucose, lipid; energy

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22
Q

Insulin has 3 major target tissues: _______, ______ and ______.

A

skeletal muscle, liver and adipose tissue

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23
Q

________ are overexpressed in the cells of these tissues,

A

Insulin receptors (IR)

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24
Q

Insulin resistance is defined where insulin levels are normal or elevated but target cells become less sensitive to insulin. What is the consequence?

A

Consequences:

  • After a meal – hyperglycemia & compensatory hyperinsulinaemia
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25
Q

When the balance between glucose and insulin is disrupted (insulin resistance), what happens

A
  • Increase glucose levels
  • Receptors for insulin are not functioning anymore
  • Glucose sits there
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26
Q

Why are skeletal muscles, liver and adipose tissue most affected by insulin?

A
  • Liver is important for metabolism
  • Skeletal muscles need lots of energy for day to day activities
  • Adipose tissue is where we store excess energy (stored as fat)
  • Since they are overexpressed –> insulin has the highest impact
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27
Q

Why is glucose “sitting” there without insulin a bad thing/problem since glucose helps produce ATP?

A
  • There are other ways to store glucose
  • Liver starts to overwork
  • If insulin receptors are not working, when there are high level of glucose (short term) –> pancreas still produces insulin –> too much insulin (hormone) –> impact on the system
    • People can go into a coma due to high levels of either insulin or glucose
    • Good to produce energy but has to be within a reasonable range
  • Over a certain range –> no longer beneficial –> can be dangerous
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28
Q

A _______ appears to be a central mechanism underlying the pathophysiology of MetS

A

chronic state of inflammation

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29
Q

Low grade chronic state of systemic inflammation drives the release of many _______ –> impact on the organs

A

pro-inflammatory factors

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30
Q

_______ factors actually drive the production of other factors from the white blood cells in the immune system –> impact and affect the organs

A

Pro-inflammatory

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31
Q

Why is there an impact/effect of the organs, since there is not actually inflammation in Metabolic syndrome?

A
  • Since organs don’t know what they actually are receiving isn’t actually inflammation (they don’t have the info.
    • Eg. don’t know they have diabetes, don’t know that they have eating a lot)
  • Pro-inflammatory factors activated (usually release during infection)
  • All body’s cells react as though there is an inflammation
  • Becomes chronic inflammation –> damages cells, organs and tissues
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32
Q

________ carry lipids in the bloodstream

A

Lipoproteins

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33
Q

Protein component is called _______

A

apolipoprotein

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34
Q

What are the 4 types of lipoproteins?

A
  1. Very low density lipoproteins (VLDL)
    • Known as “bad cholesterol”
  2. Intermediate density lipoproteins (IDL)
  3. Low density lipoproteins (LDL)
  4. High density lipoproteins (HDL)
    • Known as “good cholesterol”
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35
Q

What are the 2 important types of lipoproteins out of ?

A
  1. Very Low density lipoproteins (VLDL)
  2. High density lipoproteins (HDL) – Known as “good cholesterol”
36
Q

Elevated lipids can lead to _________ such as atherosclerosis

A

cardiovascular disease

37
Q

Lipids can travel across the membrane through _______ (type of transport)

A

Passive diffusion (they can cross the layer of the cells present in muscosa)

38
Q

Fat is _____ (hydrophobic/hydrophilic)

A

hydrophobic

39
Q

Fats are carried as lipoproteins. Why do we need protein?

A
  • Hydrophilic (okay to be around liquid)
  • Being around the lipids = able to carry them around the body
40
Q

What if we needed have proteins around fats (lipoproteins)?

A

Eg. Oil in water

  • Small drops
  • If didn’t have proteins around –> fat droplets would fuse together –> clog artery –> implications (possible death)
41
Q

Why is too much fat not good for you?

A

Blocks arteries

42
Q

Bad cholesterol can have an impact on the ______ of the artery and this can create ______.

A

epithelium; plague

43
Q

Atherosclerotic lesions initiate with _______ causing modification of apolipoproteins containing _____ and _____

A

endothelial cell dysfunction; LDL; VLDL

44
Q

What are 3 processes that occur as a result of lesions of epithelium of arteries? What is the consequence/problem of this?

A
  1. Damage of system
  2. Macrophages (immune system) activated
  3. But fat sits at the site of damage
    • Since its made of proteins –> penetrate and form all together (bubble of fat together)

Problem: small arteries (eg. heart) ○ Site of inflammation (pro-inflammatory factors) Blocks arteries –> no blood flow through

45
Q

What are 3 hormones that the endocrine pancreas secrete (produced in the pancreatic islets)?

A
  1. Insulin
  2. Glucagon
  3. Somatostatin
46
Q

What are 2 cells of the exocrine pancreas?

A
  1. Chief
  2. Parietal
47
Q

What cell type is insulin produced by?

A

β cells

48
Q

What cell type is glucagon produced by?

A

α cells

49
Q

What cell type is somatostatin produced by?

A

δ cells)

50
Q

What is the function of insulin?

A

Lowers blood glucose levels

51
Q

What is the function of glucagon?

A

Increases blood glucose levels

Impacts glycogen stores in liver and muscles –> break down –> glucose

52
Q

What is the function of somatostatin in endocrine and exocrine parts?

A

Inhibits insulin and glucagon secretion

Regulation to disinhibit/reduce amount of gastric juices (in exocrine)

53
Q

Why does pancreatic cancer have such a high mortality rate?

A

• Affects both exocrine and endocrine system ○ GIT (digestion and absorption of nutrients) Metabolism

54
Q

What is Diabetes Mellitus (DM) due to?

A

Due to lack of insulin secretion or action or both

55
Q

What is Diabetes Mellitus characterised by?

A

chronic hyperglycaemia Unable to activate insulin –> constantly high glucose levels

56
Q

What is the effect of chronic hyperglycaemia?

A

Unable to activate insulin –> constantly high glucose levels

57
Q

What are the 3 types of diabetes?

A
  1. Type 1
  2. Type 2
  3. Gestational (women during pregnancy)
58
Q

What are the 2 circumstances in diabetes?

A
  1. Decrease secretion of insulin but receptors (B cells are fine) –> type I 2. Production of insulin but receptors don’t respond –> type II
59
Q

What is the prevalence of type I diabetes?

A

Most common form of diabetes in children “juvenile diabetes” (5% of all diabetes adult cases)

60
Q

What is the prevalence of type II diabetes?

A

Most common form of diabetes (90-95% of all diabetes)

61
Q

What is the prevalence of gestational diabetes?

A

Pregnant women (3-8%)

62
Q

What is the cause of Type I diabetes?

A

Autoimmune disorder where the body’s immune system mistakenly destroys its insulin-producing cells, making the person unable to produce insulin which delivers sugar from bloodstream into cells

63
Q

What is the cause of Type II diabetes?

A

A dual effect of resistance to action of insulin, combines with an inability to make enough insulin to overcome the resistance

64
Q

What is the cause of gestational diabetes?

A

The hormones of pregnancy or a shortage of insulin

65
Q

What are 5 characteristic information about Type I diabetes?

A
  1. Biggest impact
  2. No/very little production of insulin since “day” 1
  3. Very dangerous –> eating lollies (high sugar) –> no insulin to help the system–> system goes into shut down –> “diabetes induced coma”–> possible death
    • Cure: injections of insulin for the rest of your life
  4. Rely on insulin
    • Constantly need to check levels –> injections
  5. While insulin injections help, still have pro-inflammatory factors –> cause long term problems
66
Q

What are 4 characteristic information about Type II diabetes?

A
  1. Lifestyle
  2. Obesity
  3. Have had a normal life and then get diabetes –> some changes
  4. Usually take tablets
67
Q

What are 5 characteristic information about gestational diabetes?

A
  1. Quite common and increasing
  2. Imbalance of hormones during pregnancy
  3. Stop producing insulin –> baby might want lots of sugar/food (wants to grow)
  4. Mother constantly has high glucose levels
  5. After birth –> usually goes back to normal levels
  6. If poor lifestyle/obesity –> can remain permanent
68
Q

What is the characteristic of insulin secretion in Type I DM?

A

None

69
Q

What is the characteristic of insulin secretion in Type II DM?

A

Normal or increased

70
Q

What is the age of onset in Type I DM?

A

Early

71
Q

What is the age of onset in Type II DM?

A

Late-adult/obesity

72
Q

What is the speed of onset in Type I DM?

A

Rapid

73
Q

What is the speed of onset in Type II DM?

A

Slow

74
Q

What is the percentage total diabetics in Type I DM?

A

10-20%

75
Q

What is the percentage total diabetics in Type II DM?

A

80-90%

76
Q

What is the defect in Type I DM?

A

destruction of β cells

77
Q

What is the defect in Type II DM?

A

Insulin resistance

78
Q

What is the treatment and management in Type I DM?

A

Insulin, exercise, diet

79
Q

What is the treatment and management in Type II DM?

A

Weight reduction, diet, exercise, drug

80
Q

What are the 3 long term effects of diabetes?

A
  1. Vascular damage
  2. Renal failure and blindness
  3. Neuropathies
81
Q

Diabetics have a _____ (shorter/same/longer) life expectancy than the general population

A

shorter

82
Q

How does life expectancy change with people with diabetes?

A

Depends on the patients ability to control circulating glucose levels.

83
Q

Why is vascular damage a long term effect of diabetes?

A
84
Q

Why is renal failure and blindness a long term effect of diabetes?

A
85
Q

Why is neuropathies a long term effect of diabetes?

A

impaired blood flow damages nerves of the CNS and PNS

86
Q

What are the 4 classes of oral anti-diabetics agents?

A