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JMP Semester 2 > Week 22 > Flashcards

Week 22 Flashcards

1
Q

What are the two pituitary hormone functional groups?

A
  1. Directly act in non-endocrine tissues- Growth hormone, prolactin, ADH, vasopressin, oxytocin, melanocyte stimulating hormone (MSH)
  2. Modulate secretory activity of other endocrine glands (trophic hormones) - Thyroid stimulating hormone (TSH), Adrenocorticotrophic hormone (ACTH), FSH, Luteinising hormone (LH)
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2
Q

What are the glands that are pituitary dependant?

A

Thyroid
Adrenal cortex
Gonads

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3
Q

What is energy homeostasis?

A

Maintenance of food intake against energy expenditure.

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4
Q

What is energy intake described as and what can influence this?

A

What we eat:

1. Socio economic
2. Genetic
3. Cultural
4. Psychological factors
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5
Q

What is the definition for energy expenditure?

A

Sum of internal heat and external work

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6
Q

What is classified as internal heat?

A
  1. Basal Metabolic Rate (BMR) - minimal energy expenditure at rest to maintain life
    1. Thermic effect of food - energy investments in digestion and absorption of nutrients
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7
Q

What happens in positive energy balance?

A

Energy intake higher than expenditure leads to weight gain

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8
Q

What happens in negative energy balance?

A

Energy intake lower than expenditure leads to weight loss

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9
Q

What are the general components of an average daily intake?

A

Protein, fat, carbohydrates, simple sugars, sodium, dietary fibre.

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10
Q

What are the main controllers for appetite regulation?

A
  1. GIT
    1. Key hormones
    2. CNS
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11
Q

What is the main effector organ for appetite?

A

Hypothalamus

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12
Q

What are the main GIT sensors involved in appetite regulation?

A
  1. Ghrelin
    1. Cholecystokinin (CCK)
    2. Peptide YY and pancreatic polypeptide
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13
Q

How does Ghrelin regulate appetite?

A
  1. It acts on the hypothalamus to increase hunger (increase food intake)
    1. Also increases gastric acid secretion and GIT motility.
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14
Q

Where and when is Ghrelin released?

A

Produced by the stomach when it is empty, production stops when stretch receptors are activated. (increases food intake)

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15
Q

How does Cholecystokinin (CCK) regulate appetite?

A
  1. Acts on hypothalamus to inhibit food intake

2. Also stimulates pancreatic/gall bladder secretion and GIT motility.

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16
Q

Where and when is Cholecystokinin (CCK) released?

A

Released from the GIT postprandially (post meal) (inhibits food intake)

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17
Q

Where and when is Peptide YY released?

A

Released by the distal intestine in proportion to the amount of calories ingested (inhibits food intake)

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18
Q

Where and when is pancreatic polypeptide released?

A

Released by the pancreas in the same way as peptide YY.

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19
Q

What is the effect of peptide YY and pancreatic polypeptide release?

A

Suppressed food intake

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20
Q

What are some other tissue sensors outside the GIT that regulate appetite?

A

Insulin

Leptin

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21
Q

How does exercise and physical activity regulate appetite?

A
  1. Increase in BMR (basal metabolic rate)
    1. Increased muscle mass (muscle has a higher resting metabolic rate)
      The increase in BMR increases need for intake
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22
Q

How is insulin related to adipose tissue?

A

Circulates in proportion to fat mass.

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23
Q

How does insulin regulate appetite?

A

It circulates the blood at levels equivalent to fat mass and suppresses appetite

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24
Q

What is the main adipokinin produced by adipose tissue?

A

Leptin

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25
Q

How is circulating leptin related to fat mass?

A

Circulating levels proportional to fat mass.

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26
Q

How does Leptin regulate appetite?

A

When levels are high the hunger response in inhibited

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27
Q

How is leptin believed to be related to obesity?

A

A decreased sensitivity in leptin leads to inability to detect satiety (increases risk of obesity)

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28
Q

What is satiety?

A

Feeling of being full after a meal

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29
Q

What is the hypophyseal portal system?

A

The link between the hypothalamus and the pituitary gland which allows rapid hormonal communication between the two structures

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30
Q

What organs receive the drug first after first part metabolism?

A

Well perfused ones - liver, kidney, brain

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31
Q

What is volume of distribution (Vd)?

A

It is the amount of drug in the body/ concentration

Used to represent the extent of drug distribution to tissues and not plasma.

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32
Q

What drugs would have a low Vd?

A

Drugs retained in the vascular compartment (eg warfarin)

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33
Q

What drugs would have a high Vd?

A

Drugs that are highly distributed into adipose and other non vascular compartments.

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34
Q

How does the plasma concentration of a drug change post IV administration?

A
  1. Initially falls sharply with time (Distribution phase)

2. Then decreases more slowly as drug has been distributed (elimination phase)

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35
Q

What barriers are in the blood brain barrier?

A
  1. There is tight junctions between endothelial cells
    1. There is also a lot of efflux transporters to pump xenobiotics such as drugs out of the brain- meaning they may not reach therapeutic levels in the brain.
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36
Q

What do the tight junctions of the blood brain barrier achieve?

A

Prevents diffusion through these spaces

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37
Q

What molecules can get through the blood brain barrier?

A
  1. Small non polar molecules may move across lipid membrane by passive diffusion (lipophilic)
    1. Large and/or polar drugs need to be transported actively or they are excluded
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38
Q

How does the placenta interact with medications?

A
  1. Generally does not exclude drugs
    1. Exposed to drugs to some extent
    2. Does have p-glycoprotein efflux pumps to limit exposure to potentially toxic agents.
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39
Q

What effects can higher proportions of adipose tissue have on drug distribution?

A
  1. There will be a high proportion of lipophilic drug being distributed to adipose tissue
    1. There may be reduced tissue perfusion to further affect distribution
    2. Cardiac structure and function may be changed in obesity- affect distribution
40
Q

How is drug dose changed in some cases of obesity?

A
  1. Yes sometimes increased to reach therapeutic levels- a drug dose may be increased to account for obesity level and for altered Vd.
    1. Can also be decreased to account for fatty build up in liver –> altered hepatic flow –> altered drug metabolism and clearance.
41
Q

What would low blood flow/ poor perfusion have on drug distribution?

A

Will take longer for the drug to reach that tissue

42
Q

What is the effect of low blood flow/perfusion on drug clearance?

A

Clearance would also be reduced from those tissues with less perfusion.

43
Q

What is the term for low blood sugar?

A

Hypoglycaemia

44
Q

What is the term for high blood sugar?

A

Hyperglycaemia

45
Q

What are the most susceptible organs to hypoglycaemia?

A

Brain, retinas

46
Q

How is hypoglycaemia treated?

A

Glucose, can take hours.

47
Q

What is normally mainly involved in correcting hyperglycaemia?

A

Insulin

48
Q

What are some of the main issues with untreated hyperglycaemia?

A

Vascular disease:

1. Glycation or glycosylation of structures in vessel walls

49
Q

What is the general time frame for hyperglycaemia?

A

It is usually a chronic problem lasting moths to years.

50
Q

What Is one way to indicate long term hyperglycaemia?

A

Concentration of glycated Hb (haemoglobin)- gives a snapshot of 10-12 weeks (the lifespan of a RBC

51
Q

What is the two major divisions of the Pancreas?

A

Exocrine (98%, endocrine (2%)

52
Q

What do the islets of langerhan/ pancreatic islets produce?

A

Endocrine Peptide hormones (comprised of many cells types)

53
Q

What do alpha-cells produce?

A

Glucagon

54
Q

What is the role of glucagon?

A

Acts to increase blood glucose via liberation and manufacture of glucose

55
Q

What do Beta-cells produce?

A

Insulin

56
Q

What is the role of insulin?

A

Acts to reduce blood glucose via storage of energy

57
Q

What do delta cells produce?

A

Somatostatin/GHIH

58
Q

What do F-cells produce?

A

Pancreatic peptide

59
Q

Can other stress hormones increase blood glucose?

A

Yes- adrenaline, cortisol, GH, thyroid hormone.

60
Q

How is insulin synthesised?

A

In a pre-pro peptide form (inactive form)

61
Q

What is required to get synthesised insulin ready for use?

A

Two cleavage events and then it is stored in vesicles ready for exocytosis.

62
Q

What is the mechanism of insulin release?

A
  1. Increased blood glucose detected at the Pancreas by Glut2 channels
    1. Glut2 facilitates glucose transport into the Beta cells.
    2. Rising glucose levels are used to make ATP to power K+ channels to pump K+ out of the cell.
    3. Ca+ then able to enter the cell
    4. Ca+ concentration drives exocytosis of insulin
63
Q

How can the excretion be described by one word?

A

Biphasic - first stored insulin secreted - second newly synthesised secreted

64
Q

What are the approximate levels of insulin secreted over time?

A

Initial insulin spike (first phase) (stored)

Secondary steady curve (less than peak) (second phase) (synthesised)

65
Q

How do water soluble hormones usually cause cellular change?

A

Activation of extracellular receptors as they cannot cross the phospholipid bilayer.

66
Q

What is the key factor in a cells sensitivity to a hormone which is affected by up and down regulation?

A

The number of receptors
Upregulation –> more receptors –> more sensitive
Downregulation –> less receptors –> less sensitive

67
Q

What is a way drugs are non effective long term?

A

Downregulation

68
Q

What is the general mechanism flow of a hormone binding to an extracellular receptor?

A
  1. Binding
    1. Activation of G-protein
    2. Recruitment of secondary messenger molecules
    3. Signal amplification
    4. Cellular response
69
Q

What is the specific effect of insulin on target cells?

A
  1. Translocation of Glut (glucose transporters) (particularly glut4 insertion into the plasma membrane)
    1. Allow facilitated diffusion of glucose into cells
    2. Decreases blood glucose concentrations
70
Q

How is facilitated diffusion maintained so glucose continues to enter the cell?

A

Concentration gradient needs to be sustained (as non-energy transport)
Glucose-6-phosphatase phosphorylates glucose to maintain gradient to allow for continued influx.

71
Q

What is the specific mechanism of glucagon signaling?

A

Stimulates the breakdown of stored glycogen in the liver

Glucose then released by the liver

72
Q

What are the main tissues/organs involved in blood glucose levels?

A
  1. Adipocytes
    1. Skeletal muscle
    2. Liver
73
Q

What can the liver do to control blood glucose levels?

A

Release and produce glucose

74
Q

What are the two methods the liver uses to produce glucose?

A

Glycogenolysis –> break down of glycogen to glucose

Gluconeogenesis –> synthesis of glucose

75
Q

Where is glycogen mainly stored?

A

Mainly in the liver but also stored in skeletal muscle for use.

76
Q

What are the ways blood glucose is reduced?

A

Glycogenesis –> production of glycogen (in liver and skeletal muscle)
Adipogenesis –> triglyceride synthesis in adipocytes

77
Q

Describe Glycogenolysis

A

Glycogen –> glucose

Glycogen –> glucose 1 phosphate –> glucose 6 phosphate –> glucose –> blood

78
Q

Describe Gluconeogenesis

A

Lipids and protein –> Glucose
Cortisol –> on adipocytes (lipolysis) or on other tissue (proteolysis) provides substrate for glucose production
Pyruvic acid –> glyceraldehyde 3 phosphate –> glucose 6 phosphate –> glucose

79
Q

Describe what is produced by lipolysis

A

Hormone sensitive lipase –> breaks down triglycerides into Free fatty acids and glycerol –> released and attached to lipoproteins/albumin to the liver.

80
Q

What is Adipogenesis?

A

Insulin stimulated
Increases glucose uptake and free fatty acid uptake
Increases triglyceride synthesis

81
Q

Where is excess energy stored?

A

Liver and muscle –> as glycogen
Adipocytes –> as triglycerides
All cells –> proteins/amino acids

82
Q

What is the general mechanisms stemming from a rise in blood glucose levels?

A

High blood glucose–> insulin secreted by Beta cells –> insulin binds to extracellular receptors (G-protein coupled) –>secondary messengers carry signal into cell –> glucose transporters translocated and inserted into the plasma membrane –> cells then take in glucose via facilitated diffusion –> glucose is converted to Glucose 6 phosphate inside the cells to sustain gradient for facilitated diffusion –> glucose 6 phosphate is used to produce glycogen (in liver and muscles) –> glucose uptake in adipocytes used to synthesise triglycerides. –> blood sugar levels fall.

83
Q

What is the general mechanisms stemming from a fall in blood sugar levels?

A

Low blood glucose –> Glucagon secreted by Alpha cells –> binds to extracellular receptor in the liver –> drives glycogenolysis and gluconeogenesis –> glucose released –> blood sugar levels increase

84
Q

What is the definition of overweight and obesity?

A

Excessive fat accumulation that presents a risk to health

85
Q

What is the prevalence of overweight and obese Australians?

A

63.4% obese and overweight
35% overweight, 28% obese
70% of men and 56% of women are overweight

86
Q

What are some of the health consequences of obesity?

A 
Hypertension
Liver disease
Cardiovascular disease
Increased cancer risk
GORD
Hypercholesterolemia 
Metabolic syndrome 
Type 2 Diabetes
Phycological abnormalities
87
Q

What does obesity have an effect on chance of sleep apnea?

A

Soft tissue in the mouth/throat can obstruct breathing when sleeping (for 10 seconds or more in sleep apnea) can cause intermittent hypoxia etc etc

88
Q

What is the impact of obesity on adipose?

A

Adiposopathy (sick fat) - hypertrophy and hyperplasia of adiposities
Vascular infrastructure cannot keep up to supply adipocytes –> hypoxia –> fibrosis –> necrosis –> attracts macrophages –> pro inflammatory response –> chronic low grade inflammation

89
Q

What is the effect of obesity on the liver?

A

Non alcoholic fatty liver disease –> visceral adipose tissues secrete free fatty acids, hormones (leptin and adiponectin) and adipokines (cytokines) –> increases intrinsic apoptosis in the hepatocytes –> leads to inflammation

90
Q

Effects of obesity on a persons lipid profiles?

A 
Higher total cholesterol
Lower HDL
Higher LDL
Insulin resistance
Increases risk of heart disease from atherosclerosis from cholesterol deposits
91
Q

What is the term for atherlosclerosis driven by fatty deposits?

A

Atheroma –> wall degeneration by fatty deposits accumulation driving scarring.

92
Q

What is type 1 diabetes?

A

Insulin dependent diabetes- extensive damage to Pancreatic Beta islet cells via autoimmune attacks.

93
Q

What is type 2 diabetes?

A

Non insulin dependant diabetes - dysfunctional release of insulin accompanied by insulin resistance and decreased sensitivity to insulin.
So in short insulin still there but not having a good effect.

94
Q

How is obesity linked with inflammation?

A

Is associated with numerous pro inflammatory molecules

95
Q

What are the clinical symptoms of hyperglycaemia?

A 
Increased thirst
Frequent urination
Fatigue
Headaches
Trouble concentrating 
Numbness or tingling in feet
96
Q

What is the clinical relevance of subcutaneous fat vs visceral fat?

A

Visceral fat is a lot more dangerous

JMP Semester 2 (8 decks)

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