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Year 2 Semester 2 > endocrine physiology LOL > Flashcards

endocrine physiology LOL Flashcards

To learn the very basics

1
Q

Lecture: introduction to the endocrine system 1 and 2

A
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2
Q

Lecture: hypothalamus and the pituitary

A
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3
Q

What is the endocrine system?

A

This is a collective term for the cells which produce chemical messenger substances that are
regarded as hormones.

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4
Q

Classify hormones according to their chemistry and mechanisms of action upon target cells

A
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5
Q
  • Define the terms: troph; trophic hormone; hypophysiotropic hormone.
A
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6
Q

List the neurohormones produced by the hypothalamus - including those secreted via
the neurohypophysis (posterior pituitary lobe).

A
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7
Q

Describe diagrammatically the compartmentation and routes of communication within
the hypothalamus-pituitary gland complex.

A
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8
Q

The feeding centre promotes feelings of hunger, whilst the satiety centre promotes feeling of fullness. These are hypothalamic centres.

What affect do they have on each other?

A

Satiety centre suppresses the feeding centre

but not vice verse obvs

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9
Q

Is the satiety centre or the feeding centre sensitive to insulin

A

satiety.

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10
Q

is the feeding centre and satiety centre just endocrine, or also neural?

A

neuroendocrine

neural and chemical

chemical being hormones AND from the food we eat

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11
Q

What are the two theories of hunger

A

1) Glucostatic theory
2) Lipostatic theory

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12
Q

whats glucostatic theory

A

hunger controlled by blood glucose levels- rise switches off feeding centre, switches on insulin/satiety centre

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13
Q

what is lipostatic theory

A

hunger controlled by amount of fat stores- rise switches off feeding centre, switches on insulin/satiety centre

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14
Q

What does leptin do

A

depresses feeding centre in hypothalamus

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15
Q

Where is leptin released from

A

adipose tissue/ fat stores

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16
Q

When does obesity result (endocrinally speaking)

A

when there is a disruption in the feeding and satiety pathways, i.e. satiety centre no longer switches off feeding centre

fact of interest: 2/3 of people in Scotland are considered overweight vs not

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17
Q

what are the 3 categories of energy output (easy peasy)

A

cellular work
mechanical work
heat loss

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18
Q

Metabolism how many of the biochemical reactions in the body

A

‘integration of all biochemical reactions in the body’.

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19
Q

anabolic pathways are pathways that…

A

build up

think about anabolic steroids

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20
Q

is cortisol an anabolic or catabolic steroid

A

catabolic (not building up muscle!)

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21
Q

What happens in the absorptive state after eating (to ingested nutrients)

A

Ingested nutrients that are used to supply energy are stored, so any excess energy is stored in that absorptive state.

so glucose as glycogen in muscle

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22
Q

is the absorptive state an anabolic or catabolic one

A

it’s anabolic- we’re BUILDING UP stores

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23
Q

what’s happening in the post absorptive/fasting state

A

body starts to rely on stores/ nutrients in the plasma, built up in absorptive state (catabolic)

release glucose from glycogen, AND make new glucose from amino acids

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24
Q

what does it mean, that the brain is the obligatory glucose user

A

brain can only use glucose

but other cells can use carbs, protein.

That’s why hypoglycaemia leads to coma and death.

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25
Q

when can the brain metabolize ketone bodies

A

starvation

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26
Q

Before excess glucose becomes fat, what does it become?

A

any excess glucose is broken into free fatty acids, then fat. Through glycogenesis.

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27
Q

what hormone initiates gluconeogenesis and glycogenolysis when glucose levels are low?

A

glucagon

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28
Q

what happens when glucagon stimulates the liver

A

new glucose is created from amino acids,and glycogen into glucose

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29
Q

Insulin is an anabolic hormone that does what (2)

A

stimulates process of glycogenesis to admit glycogen from glucose in the blood. i.e. stimulates formation of glycagon.

And stimulates uptake of glucose

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30
Q

What’s happening to insulin in type 1 diabetes

A

No insulin is being made by the pancreas. Glucose builds up in the blood, can’t be converted to glucagon or fat stores.

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31
Q

What’s happening to insulin in type 2 diabetes

A

Body stops responding to insulin. Glucose builds up in the blood.

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32
Q

what part of the pancreas releases glucagon and insulin. Nb, insulin and glucagon exist IN BALANCE

A

islets of langerhans (islands of endocrine cells)

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33
Q

alpha, beta, delta cells of the pancreas produce what

A

alpha = glucagon
beta = insulin
delta = somatostatin

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34
Q

affect of insulin on fat synthesis

A

increases fat synthesis i.e. converting glucose into fat.

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35
Q

If levels of insulin rise, what will be happening to glucagon levels?

A

They decrease. Remember that it’s all a balance

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36
Q

What 4 actions increase when insulin levels rise? remember its an anabolic state

A

Glucose oxidation (being used)
Glycogen synthesis (stores built up)
Fat synthesis
Protein synthesis

It’s an anabolic state, (building) and blood glucose decreases.

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37
Q

What three actions increase when glucagon levels rise? (During the fasted state)

A

Glycogenolysis
Gluconeogenesis
Ketogenesis

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38
Q

What’s Glycogenolysis, which occurs in the fasting state?

A

Breakdown of glycogen

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39
Q

What’s Gluconeogenesis, which occurs in the fasting state?

A

Glucose formed from amino acids

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40
Q

What type of hormone is insulin?

A

Peptide hormone

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41
Q

How is insulin synthesised?

A

As a large preprohormone, preproinsulin, when is then converted into proinsulin. These are packaged as granules, and then cleaved again to give insulin.

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42
Q

Insulin is stored until what

A

The beta cell it’s in is activated and secretion occurs

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43
Q

Where in the beta cell is preproinsulin, converted to pro insulin?

A

In the endoplasmic reticulum

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44
Q

One Proinsulin, that packaged in granules, is later converted into insulin by being cleaved. How many copies of insulin does that produce?

A

Granules of proinsulin broken up to release active form of insulin. Multiple, not just one insulin molecule. And also c-peptide fragments that intersperse the copies of insulin.

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45
Q

By what method is insulin and c peptide releases into the plasma, following stimulates of the beta cells?

A

Exocytosis

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46
Q

Why is c peptide a useful indicator of pancreatic beta cell function, versus insulin?

A

Because c peptide resists degradation much more than insulin does, and c peptide can be independent of any exogenous insulin that your patient might be injecting

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47
Q

During what state is insulin released?

A

Absorptive state

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48
Q

When blood glucose levels rise, that triggers the release of insulin from the pancreas. What else triggersa release of insulin?

A

When amino acid levels go up

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49
Q

What is the only hormone that stimulates the uptake of glucose out of the blood?

A

Insulin

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50
Q

Excess glucose can be stored as glycogen in the liver and muscle tissue, but also as what in liver tissue and adipose tissue?

A

Triacylglycerols

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51
Q

Amino acids being consumed in our diet is being used how?

A

New protein, with any excess being converted to fat
We can also use amino acids as an energy source during starvation (breaking down muscle)

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52
Q

Why does using your amino acids/proteins in your diet, as energy during starvation, affect your immunity?

A

Your antibodies are proteins so if they’re gone, more vulnerable to infection

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53
Q

Mechanism by which insulin is released by the pancreas, depends on the activity of which channel?

A

The potassium ATP channel in the beta cells- so potassium ion channels that’s are sensitive to the levels of ATP that are in the cells (like, glucose).

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54
Q

Glucose enters the pancreatic beta cell through transporters known as what

A

GLUT transporters

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55
Q

How is potassium ATP channel involved in the exocytosis of insulin vesicles?

A

Glucose coming in, = increase in ATP. Which means said channels close, so k builds up. So that increases positive charge therefore cell is depolarised, therefore voltage gated Ca channels open and = exocytosis.

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56
Q

Insulin vesicle exits beta cell into circulation via what channel

A

Voltage dependant Ca2+ channels.

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57
Q

How does insulin lower BG?

A

Binds to tyrosine kinase receptors on the cell membrane of insulin dependant tissues, to increase glucose uptake of these tissues.

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58
Q

In muscle and adipose tissue, insulin stimulates mobilisation of which specific glucose transporter?

A

GLUT-4

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59
Q

When do GLUT-4 transporters move to the cell membrane from the cytoplasm?

A

In response to insulin binding to tyrosine kinase receptors on the surface of cells, so that glucose can be transported INTO the cell

Nb I feel like: insulin binds to cell, GLUT-4 transporters are triggered to move to membrane, meaning glucose can come into the cell.

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60
Q

True or false, there is an exocytosis of the GLUT4 transporters

A

Yes

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61
Q

Which cells can take up glucose independent of insulin and when?

A

Muscle cells
During exercise

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62
Q

How many tissue types require insulin to take up glucose?

A

Only adipose and muscle

But this makes up a large proportion of the body so like 65%

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63
Q

Muscle tissue mainly uses what instead of glucose

A

Free fatty acids, so don’t need insulin that way

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64
Q

Glut 1 transporters are found where? Are these insulin dependant?

A

Brain, kidney, red blood cells

whereas insulin dependant cells have GLUT 4. Like adipose and muscle cells.

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65
Q

Where are Glut 2 transporters? Are they insulin dependant/ found in cytoplasm?

A

Beta cells of the pancreas and in the liver

They are present in the cell membrane all the time therefore.

So: if they’re insulin dependant, they’re found in the cytoplasm > need insulin for the transporters to be exocytosed, if you get me. They are the GLUT 4.

Non insulin = GLUT 2- pancreas and liver
and GLUT 1- brain, kidney and red blood cells

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66
Q

Is the liver insulin dependant?

A

No you have glut-2 transporters found there. But insulin DOES enhance glucose uptake by hepatocytes

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67
Q

Why is glucose transport into hepatocytes affected by insulin status, if the liver isn’t insulin dependant (due to the presence of glut 2)?

A

Insulin stimulates hexokinase enzyme (after binding to tyrosine kinase receptor) which lowers the intracellular glucose concentration by converting glucose to glucose 6 phosphate
therefore maintaining concentration gradient.

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68
Q

What does the liver do to glucose when no insulin present?

A

Insulin was needed for the enzyme hexokinase to create concentration gradient.

If no gradient? Liver actually synthesises glucose via glycogenolysis- breaking down hepatic glycogen.

And gluconeogenesis from amino acids.

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69
Q

How does insulin increase glycogen synthesis in muscle and liver tissue?

A

In a roundabout way. By stimulating the enzyme glycogen synthase and inhibiting an enzyme that breaks down glycogen.

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70
Q

Three actions of insulin to liver

A

Stimulate uptake of glucose by helping create concentration gradient (converting glucose)

Increase glycogen synthesis by:
Switching on enzymes that synthesise glycogen, and switching off enzymes that would break down glycogen.

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71
Q

Does insulin inhibit or increase amino acid uptake and synthesis in muscle?

A

Increase by switching on and off relevant enzymes.

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72
Q

What affect of insulin onto enzymes of gluconeogenesis?

A

Inhibit
To stop the liver creating new glucose

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73
Q

Which three hormones are needed for growth?

A

Insulin and growth hormone
Because you need insulin to “permit” growth hormone

But also thyroid hormone

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74
Q

How does insulin have an affect on potassium entry into cells?

A

Stimulating sodium potassium ATPase

We want k to build up incell, so that cell is depolarised.

That would make the exit Ca channels to open to release insulin

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75
Q

Any protein that is a target for the insulin receptor is known as what

A

Insulin receptor substrate

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76
Q

Half life of insulin

A

5 mins

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77
Q

Location of degradation of insulin

A

In liver (and kidneys) by enzyme insulinase

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78
Q

What 5 stimuli increase insulin release?

A

1) increased blood glucose
2) increased amino acids
3) glucagon

4) other hormones controlling GI secretion eg gastrin, secretin, CCK, GIP.

5) vagal nerve activity (helps control GI function, doesn’t it?!)

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79
Q

Gluconeogenesis is stimulated by what

A

Glucagon

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80
Q

Why is insulin released when stimulated by GI hormones, like gastrin, secretin and CCK?

A

In preparation for the increase in blood glucose that it knows is coming

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81
Q

What stimuli (3) inhibit insulin release?

A

Low blood glucose
Somatostatin
Stress e.g. hypoxia

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82
Q

Why is is good the the vagus nerve directly stimulates insulin release?

A

It means we get an insulin response faster than we would if we had to wait for glucose to be absorbed and get into the bloodstream

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83
Q

The amount of insulin that is released in response to intravenous glucose- more or less than oral administration of the same amount?

A

Less

Only blood response, not also vagal and incretin hormone response to the same amount

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84
Q

How does glucagon increase blood glucose in simpler terms? (3)

A

Releasing glucose from stores into the plasma by breaking it down (glycogenolysis)
The formation of new glucose from amino acids (glucaneogenesis)
Formation of new ketones (ketogenesis)

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85
Q

How is glucagon produced (considering it’s a peptide hormone like insulin)?

A

Starts off with preprohormone
That gets cleaved to a prohormone
That’s stored in vesicles until required for release from alpha cells, following stimulation

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86
Q

What is glucagon degraded by?

A

Liver

Also mainly acts on the liver
Half life of 5-10 mins

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87
Q

When is glucagon most active?

A

Post absorptive state
In between meals, FASTING state. (When you’re about to get hungry again)

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88
Q

Insulin receptors are tyrosine kinase receptors. What about glucagon receptors?

A

G-protein couples receptors that are linked to the adenylate cyclase/cAMP system.

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89
Q

Gluconeogenesis us s substrates from the breakdown of

A

Proteins
Amino acids
Lactate
Pyruvate

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90
Q

Triglyceride stores in adipose tissue can be broken down to release what

A

Glycerol and free fatty acids

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91
Q

If glucose is spare se what does the brain use

A

Ketones

Eg starvation or poorly controlled diabetes

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92
Q

Amino acids are also a potent stimulus for glucagon secretion. What would happen if they weren’t?

A

Hypoglycaemia
Because amino acids stimulate insulin release, which in the absence of glucagon uptake into cells, dramatically lowering BG.

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93
Q

Amino acids stimulate release of glucagon or insulin?

A

Trick question
Both
They’re in balance

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94
Q

Eat a meal high in protein. That triggers lots of insulin. What do we need therefore

A

Well the body will release glucagon as well, so it’s all okay, because glucagon will maintain BG

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95
Q

What does low insulin levels mean for adipose and muscle tissue?

A

They cannot readily access glucose because they’re insulin dependant tissues of the body

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96
Q

Affect of cortisol on glucagon release?

A

Stimulates it

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97
Q

What level does BG have to fall for glucagon release?

A

Below 5 millimolar

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98
Q

What affect does glucose have on glucagon release? And free fatty acids and ketones?

A

Well obvs inhibits

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99
Q

What affect does insulin have on glucagon release?

A

Inhibits

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100
Q

What affect does somatostatin have on glucagon release?

A

Inhibits

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101
Q

If we know vagus activity causes increase in insulin release, (and to a lesser extent glucagon).

On the other hand, what affect does sympathetic have on activity in islet cells/ release of glucagon?

A

We’re saying para increases insulin.

But Sympa increases glucagon and therefore inhibits insulin

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102
Q

Release of glucagon prevents

A

Hypoglycaemia

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103
Q

Growth hormone antagonises the action of what?

A

Insulin

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104
Q

Glucagon stimulates breakdown of glycogen in the liver, but not in the muscle. Which hormone does both?

A

Epinephrine

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105
Q

Which two hormones inhibit glucose uptake?

A

Growth hormone and cortisol

whenstressed, these AND epinephrine and glucagon rise

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106
Q

Why do you look diabetic in Cushing disease?

A

Because you have loads of cortisol, which inhibits glucose uptake/ makes tissues less sensitive to insulin, therefore elevation of blood glucose

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Perfectly
107
Q

Where are the two places somatostatin is released?

A

Delta cells of the pancreas
Released by the hypothalamus

108
Q

Main action of pancreatic somatostatin?

A

Inhibit activity in the GI tract, released in response to nutrients coming.

Prevent exaggerated peaks

alsoinhibit glucagon and somatostatin

109
Q

Why is synergetic somatostatin used in life threatening diarrhoea?

A

It slows the motility of the GI tract

110
Q

Affect of somatostatin on insulin and glucagon?

A

Suppresses release- local affect on alpha and beta cells

111
Q

Patients who have somatostatin secreting rumours often develop what kind of symptoms?

A

Diabetic like symptoms (loss of insulin release from beta cells)

112
Q

The insulin independent mechanism of skeletal muscle that can take up glucose during exercise, increases the number of which transporters?

Nb exercise also increases insulin sensitivity

A

GLUT-4

113
Q

Why is exercise strongly advised for individuals with type two diabetes?

A

Because exercise increases glucose uptake in an independent mechanism, and the effect has been found to persist for several hours after exercise.

114
Q

In non active muscle, insulin must bind to its receptor why?

A

To stimulate the exocytosis of the GLUT 4 containing vesicles on the membrane

115
Q

During starvation, the body can break down adipose tissue to release fatty acids to use as energy. Except for which organ?

A

The brain

116
Q

In starvation, how does the body supply the brain with energy?

A

The liver will convert any excess free fatty acids to ketone bodies by beta oxidation, by the hormone glucagon

Meaning we don’t need to use protein

117
Q

Which is the last store that is depleted in starvation?

A

Protein

118
Q

Is the uptake of ketone bodies insulin dependant or independant?

A

Independant

Therefore for diabetes, not good. Because ketones are acidic. = ketoacidosis

119
Q

What type of hormone is growth hormone

A

Peptide

120
Q

What is growth hormone also known as

A

Somatotropin

121
Q

Where is growth hormone released from

A

Anterior pituitary

122
Q

Release of growth hormone is controlled via NEUROhormones, with the same or opposing action?

A

Opposing

123
Q

Release of growth hormone is controlled via NEUROhormones, with the opposing action. Name these two:

A

Growth hormone inhibiting hormone aka somatostatin (think statin like stasis) GHIH

Growth hormone releasing hormone GHRH

124
Q

Factors affecting what part of the body, determines the balance between GHRH : GHIH?

A

Hypothalamus

125
Q

Permissive action from where is required before GH can stimulate growth?

A

Thyroid hormones and insulin

126
Q

Why would children with poorly controlled diabetes have stunted growth, despite normal GH levels?

A

Because GH requires permissive action of thyroid hormones and insulin before it will stimulate growth

127
Q

Why does GH secretion continue throughout adult life?

A

It continues to be essential in the maintenance and repair of tissue

128
Q

What exact affect does GH have on cells?

A

Cell size (hypertrophy)
And
Cell division (hyperplasia)

129
Q

What receptors does GH act on?

A

Tyrosine kinase receptors

130
Q

What are the two main B-road actions of GH?

A

Growth of long bones- (indirect action mediated via IGF-I)
Regulation of metabolism (direct action)

131
Q

I know that growth hormone has a direct affect on metabolism, but it only has an indirect affect on growth of long bones/ skeletal system. Through which hormone is that achieves?

A

Insulin-like growth factor (IGF-1) aka somatomedin C

As it mediates the action of growth hormone

132
Q

Somatomedin (IGF-1) mediates the action of GH for long bones.

Name can be confused with:
Somatostatin -stasis- is the GH inhibiting hormone. GHIH. There is a constant balance between GHIH and what other hormone?

A

Growth hormone releasing hormone (GHRH).

Nb IGF acts on both bottom two hormones

133
Q

IGF-1 aka somatomedin is secreted primarily by what, in response to what?

A

By the liver, in response to GH release.

134
Q

Why is GH not secreted in urine? But rather has like 50% remain like a reservoir in the blood?

A

Because it is transported in the blood bound to carrier proteins. Means there is a reservoir to smooth out effects of the erratic pattern of secretion.

135
Q

IGF exhibits negative feedback on GH by inhibiting what hormone, and stimulating what hormone?

A

Inhibits GHRH
Stimulates GHIH (somatostatin)

136
Q

IGF is the ‘insulin like hormone’. It exhibits negative feedback on GH. Has it hyper or hypoglycaemic action on IGF-1?

A

Hypoglycaemic

137
Q

Which dominates: the hypoglycaemic action of IGF-1, or the hyperglycaemic properties of GH?

A

The hyperglycaemic properties of GH

138
Q

Affect of GH on insulin, and gluconeogenesis by the liver?

A

Increases gluconeogenesis
Reduces ability of insulin to stimulate glucose uptake by muscle and adipose tissue

Basically GH is releasing energy stores to support growth (has anti-insulin effect, like cortisol)

139
Q

Why is GH said to be anti insulin

A

Basically GH is releasing energy stores to support growth (has anti-insulin effect, like cortisol)

140
Q

What’s the difference in the action between cortisol and GH?

A

Unlike cortisol (and just like insulin) GH increases amino acid uptake and protein synthesis in almost all cells = anabolic effect.

141
Q

Does cortisol stimulate protein anabolism or catabolism?

A

Catabolism

GH and insulin is anabolism of proteins.

cause remember cortisol

142
Q

Both insulin and GH cause increased amino acid uptake, and protein synthesis. What’s the difference between them?

A

Only GH causes increased glucose uptake.

143
Q

What time of day is the most GH released?

A

Majority of GH released during first 2 hours of sleep (deep delta sleep)

144
Q

How does amount of amino acids in the plasma, affect GHRH amounts?

A

Up = up

145
Q

(Considering we have a growth spurt in puberty). What affect does oestrogen and testosterone have on GH release?

A

Stimulates GH release from the pituitary

146
Q

What affect does stress and illness have on growth? (Two hormones)

A

Increases GHRH, but growth may be stunted due to catabolic action of cortisol

147
Q

3 stimuli that increases GHIH (somatostatin secretion therefore down GH)?

A

Ageing
Glucose (more sugar = less growth!)
Cortisol

148
Q

What’s the normal cause of hyper secretion?

A

Endocrine tumours

149
Q

Difference in pathology between gigantism and acromegaly?

A

Hyper-secretion of GH in both. But in gigantism, due to a pituitary tumour BEFORE Epiphyseal plates of long bones close. = excessive growth.
Vs after

150
Q

What are the two physiologically active forms of the thyroid hormone?

A

(They have long names, but like, just know them as:)
T3
T4

151
Q

What are the two cells types in the thyroid gland?

A

C cells
Follicular cells

152
Q

What do the c cells of the thyroid gland secrete?

A

Calcitonin, a calcium regulating hormone

153
Q

What do the follicular cells of the thyroid gland do?

A

The cells support thyroid hormone synthesis and surround hollow follicles

154
Q

Most of the thyroid gland is made up of which cell?

A

The follicular cells

155
Q

The follicular cells of the thyroid form follicles- basically a hollow ball. What is that filled with?

A

Colloid

156
Q

What’s colloid?

A

A sticky, glycoprotein substance, where we find thyroid hormones in precursor form

157
Q

How many months supply of precursor thyroid hormones are stored in the follicles?

A

Like a few months

158
Q

Follicular cells manufacture the enzymes that make thyroid hormones, as well as what?

A

Thyroglobulin, a large protein rich in tyrosine residues, that basically form the backbone of those thyroid hormones.

159
Q

Involvement of follicular cells with iodine?

A

Concentrate iodine from plasma and transport it to the colloid to combine with tyrosine

160
Q

What combines to form the thyroid hormones?

A

Thyroglobulin (produced by follicular cells, and rich in tyrosine residues)
Iodide from the plasma

161
Q

Where is tyrosine and iodide derived from?

A

The diet

162
Q

How does the iodide enter the follicular cells, through the action of which transporter? (Even against a concentration gradient!)

A

Sodium iodide transporter

163
Q

How is iodide oxidised to iodine?

A

In the colloid, catalysed by the enzymes produced by the follicular cells, which are then exocytosed into the colloid.

164
Q

1 iodine to tyrosine =

A

MIT

165
Q

2 iodines plus tyrosine =

A

DIT

166
Q

MIT and DIT can u servo conjugation reactions.
MIT + DIT =
DIT + DIT =

A

MIT + DIT = T3
DIT + DIT = T4

167
Q

Name of enzyme that is found on the colloid side of the follicular cells

A

Thyroid peroxidase > oxidising iodide to iodine, adding iodines to tyrosine residues, and conjugating them to become T3 or T4

168
Q

Why can’t we store thyroid hormones in their active form?

A

Because they’re lipophilic, so they’d just cross the cell membrane and get into the blood.

169
Q

What stimulates T3&4 to go from colloid to follicular cell, and form vesicles?

A

Thyroid stimulating hormone

170
Q

Where is thyroid stimulating hormone released from?

A

Anterior pituitary (specifically, the thyroglobulin)

171
Q

What is the main carrier protein of T3&4 known as?

A

Thyroxine binding globulin

172
Q

Do we have more T3 or T4 present in the plasma?

A

T4

173
Q

Are thyroid hormones active when bound to thyroxine binding globulin?

A

Yes but not actually physiologically active, they can’t be used

174
Q

Why is there more T4 than T3 in the plasma?

A

T4 has 6 x the longer half life (6 days)

175
Q

As the physiologically active thyroid hormone in the plasma increases, what happens?

A

It switches off the hormones that stimulates the release- antagonists release of TSH from the anterior pituitary.

(So level of own hormone regulates itself, like GH)

176
Q

Most TH circulating is T4. However, which is actually the most physiologically active?

A

DEFO T3

177
Q

T4 is deiodinated to T3 by what

A

Deiodinase enzymes.

178
Q

Where is T4 deiodinated? (To T3)

A

Half in the plasma, half inside target cells

179
Q

Any cell that contains an intracellular receptor for thyroid hormone, also contains what enzymes?

A

Deiodinase enzymes that Deiodinase T4-T3

180
Q

What thyroid hormone are you supplemented with, when you’ve had your thyroid gland removed?

A

T4

(Turns into T3 anyway, and has a longer glad life than T4)

181
Q

Which hormone controls the release of thyroid hormone?

A

Thyrotropin releasing hormone from the hypothalamus

182
Q

Exercise and pregnancy increase release of thyroid stimulating hormone. Why pregnancy?

A

Because thyroid hormones are critical for the growth of the fetus

183
Q

Which two drug are inhibitory on release of thyroid hormones?

A

Glucocorticoids and somatostatin aka growth hormone inhibiting hormone. (Inhibitory on release of thyroid hormone).

184
Q

Why is being cold the primary stimulus for the release of thyroid hormones?

A

Because thyroid hormones promote thermogenesis (by causing futile cycles of simultaneous catabolism and anabolism)

NB this is especially important in infants!

185
Q

Lack of thyroid hormone means what?

A

Retarded growth

Because thyroid hormone stimulates receptor expression

186
Q

What does maternal iodine deficiency result in?

A

Congenital hypothyroidism, which is crazy cuz it’s essential for brain development

187
Q

In the womb, does the baby make its own or receive maternal thyroid hormones?

A

Maternal

188
Q

Two main symptoms of hyperthyroidism?

A

Increased metabolic rate and heat production

189
Q

The adrenal glands sit atop the kidneys. Are they retroperitoneal or intraperitoneal?

A

When considering the kidneys are retro …

190
Q

What are the two parts of the adrenal glands?

A

Adrenal medulla and adrenal cortex

Medulla in the middle about 25%

191
Q

What part of the adrenal gland is a modified sympathetic ganglion?

A

Adrenal medulla, making it a neuroendocrine gland

192
Q

The adrenal medulla secretes from the post ganglionic cell. What does it secrete? (3)

A

Epinephrine aka adrenaline
And also
Norepinephrine
Dopamine

193
Q

Is the adrenal cortex a neuroendocrine gland, or a true endocrine gland?

A

True endocrine gland

194
Q

What 3 hormones does the adrenal cortex secrete?

A

Mineralocorticoid like ALDOSTERONE (involved in regulation of Na and K

Glucocorticoids e.g. cortisol

Sex steroids e.g. testosterone

195
Q

What is cortisol mainly involved with?

A

Maintaining plasma glucose

196
Q

Out of the three steroid hormones that the adrenal cortex secretes, which two are necessary for survival?

A

Aldosterone
Cortisol

So not sex hormones

197
Q

Why do we consider the role of sex hormones secreted from the adrenal gland, as less important?

A

Because there is SO much more sex hormones secreted from gonads instead

198
Q

Which is our areas hormone?

A

Cortisol

199
Q

Which hormones secreted by the adrenal medulla, are associated with the stimulation of the sympathetic nervous system? (Fight and flight)

A

Epinephrine
Norepinephrine

200
Q

Why would animals that have their adrenal glands removed, due within weeks?

A

Because aldosterone and cortisol together are essential for survival

201
Q

The adrenal cortex, surrounding the medulla, is arranged in 3 concentric zones, why?

A

They’re producing different hormones

Aldosterone
Cortisol (glucocorticoid)
Sex hormones

202
Q

So which part of the adrenal gland is secreting the ‘catecholamine neurohormone’?

A

Adrenal medulla

203
Q

If all steroid hormones are made of cholesterol, and we have 3 different types made in the adrenal cortex, how are there different end products?

A

Different enzymes for different zones, so for the outermost zone, only enzymes like aldosterone synthase, that can make cholesterol into aldosterone, are there

204
Q

21 hydroxylase is an enzyme required for the synthesis of which two steroid hormones from the adrenal cortex?

A

Aldosterone and cortisol

205
Q

How are cortisol levels controlled?

A

A negative feedback loop within the hypothalamic-pituitary-adrenal pathway

206
Q

Why does a deficit in 21-hydroxylase cause adrenal hyperplasia?

A

Increased ACTH secretion responsible.

Because there body is over stimulated to try and fix the break in the negative feedback system (so this happens, despite no cortisol or aldosterone being made)

207
Q

What does ACTH do?

A

Stimulates release of the steroid hormones from the adrenal cortex

208
Q

ACTH stimulates release of the steroid hormones from the adrenal cortex. What about the adrenal medulla?

A

No, that’s controlled by the sympathetic nervous system

209
Q

Cortisol is a glucocorticoid hormone that influences what

A

Glucose metabolism

210
Q

95% of plasma cortisol is bound to what?

A

A carrier protein, cortisol binding globulin (CBG)

211
Q

How many cells of the body have cytoplasmic glucocorticoid receptors?

A

All nucleated cells

212
Q

What happens after the hormone receptor complex migrates to the nucleus? (Eg cortisol)

A

Binding to DNA, to alter gene expression transcription and translation

213
Q

Why do the effects of cortisol persist for a relatively long time?

A

Because we’ve either increased protein synthesis or we’ve switched off protein synthesis- so basically a change in protein synthesis that persists for a relatively long period of time, days or weeks.

214
Q

How long is the response to peptide hormones usually?

A

Usually only present for only minutes usually

215
Q

Which type of hormone from the adrenal gland is well known for their anti inflammatory effect?

A

Glucocorticoids

216
Q

Which type of hormone from the adrenal gland is well known for their use in suppressing the immune system?

A

Glucocorticoids

217
Q

How often is cortisol released throughout the day?

A

Plasma levels of cortisol show a very characteristic pattern- following by a preceding pattern of ACTH release

So there is a peak in the morning

218
Q

Effect of cortisol on blood pressure?

A

Increases blood pressure

219
Q

Is cortisol hyper or hypoglycaemic?

A

Hyper

220
Q

Cortisol has what action on glucagon?

A

It had a permissive action on glucagon, helping to protect the brain from hypoglycaemia

221
Q

How to describe the action of cortisol on insulin?

A

Opposing

222
Q

What affect does cortisol have on muscle protein?

A

Stimulates breakdown of muscle protein to provide gluconeogenic substrates for the liver

223
Q

Cortisol stimulates formation of gluconeogenic enzymes from where, leading to what?

A

Enhancing gluconeogeneis and glucose production.

Enzymes from the liver.

224
Q

What’s lipolysis?

A

Breakdown of triacyglycerols into glycerol and free fatty acids

225
Q

Cortisol has what affect on adipose tissue?

A

Stimulates lipolysis, which creates an alternative fuel supply that allows blood glucose levels to be protected

226
Q

What affect does cortisol have on insulin sensitivity?

A

Decreases insulin sensitivity

Cortisol is acting to oppose glucose, and increase glucose levels

227
Q

Negative affect on bones of cortisol?

A

Decreases calcium absorption from the gut, and increases bone resorption- so basically stimulates breaking down of bone which leads to osteoporosis

228
Q

Too much cortisol has what affect on mood

A

Increases depression and causes impaired cognitive function- hyper cortisolaemia

229
Q

What are the three side effects of high levels of cortisol?

A

Osteoporosis
Depressive mood
Hypertension

230
Q

Low levels of cortisol are association with hyper or hypotension?

A

Hypotension

231
Q

Affect of cortisol on the immune system?

A

Suppression

232
Q

Why would you give cortisol following an organ transplantation?

A

Because it suppresses the immune system.
It reduces circulating lymphocyte count
Reduces antibody formation
Inhibits inflammatory response.

233
Q

Why do you end up with a loss of percutaneous fat when taking glucocorticoid therapy like cortisol?

A

as a result of stimulating lipolysis in our fat

(Gives skin a thin appearance, and more fragile)

234
Q

Why get muscle wasting with glucocorticoid therapy such as you take when you have asthma, Uc, rheumatoid arthritis.

A

Protein catabolism

235
Q

Care must be required when withdrawing glucocorticoid treatment why??

A

Due to the enhanced negative feedback effects of exogenous cortisol: can lead to atrophy of the adrenal gland

236
Q

Affect of aldosterone on sodium and potassium? (2)

A

Increases reabsorption of sodium
Promotes excretion of potassium

237
Q

Loss of aldosterone leads to life threatening hypo or hypertension

A

Well obviously hypotension

It increases blood volume by increasing Na+ amount in the plasma, and therefore increases blood pressure.

238
Q

Why does a pheochromocytoma (a neuroendocrine tumour of the adrenal medulla) result in increased BP?

A

Results in hyper stimulation of adrenaline acetylcholine and norepinephrine etc.
therefore increase in cardiac output, therefore increase in blood pressure.

239
Q

What happens when there is a problem with the hypothalamus? What affect on CRH, ACTH, and cortisol?

A

Hypersecretion of all three hormones

240
Q

What are the three classifications of the endocrine hormones?

A

Peptide/protein hormones- composed of chains of amino acids (most common)

Amine hormones (just a few amino acids) like tyrosine

Steroid hormones - derived from cholesterol

241
Q

What is the inactive fragment cleaved from insulin pro hormone?

A

C peptide

242
Q

Steroid hormones are most commonly bound to what

A

Albumin

243
Q

What two organs are the principal organisers of the endocrine system?

A

Hypothalamus and pituitary

244
Q

What are the two parts of the pituitary gland?

A

Anterior (front 2/3)
Posterior (back 1/3)

245
Q

Difference in the two parts of the pituitary gland?

A

Front 2/3 is true endocrine tissue
Back 1/3 posterior is neuroendocrine

246
Q

Which are the two hormones of the posterior pituitary gland? (made in hypothalamus remember)

A

vasopressin and oxytocin

247
Q

All hormones that are released by the hypothalamus and the posterior pituitary are what type of hormone?

A

Neurohormone

248
Q

What’s the differences between tropic and non tropic hypothalamic neurohormones?

A

Non-tropic hormones are hormones that directly stimulate target cells to induce effects.
Whereas
Tropic hormones act on another endocrine gland

249
Q

How does the hypothalamus and the pituitary work together?

A

The hypothalamus synthesis hormones

These hormones are transported to the nerve terminal in posterior pituitary, ready for release

The posterior pituitary release

250
Q

Affect of growth hormone onto insulin?

A

Growth hormone inhibits insulin

251
Q

Is this hyper or hypo:

FT3/FT4 high
TSH low

A

Hyperthyroidism aka thyrotoxicosis

252
Q

Is this hyper or hypo?

FT3/FT4 low
TSH high

A

Hypothyroidism

253
Q

Why might a virus trigger diabetes mellitus?

A

Viral mimicry, so the virus surface mimics that of pancreatic beta cells

254
Q

2/3 of islet cells in the pancreas is what type of cell

A

beta cells

255
Q

Why does central adiposity cause diabetes mellitus?

A

Because there is an increase in free fatty acids, (that enter the blood due to leukocytes being stressed) and with more fatty acids in the blood, insulin receptor sensitivity decreases. Therefore glucose remains in the blood.

256
Q

Why might genetic errors lead to type 2 dm?

A

if lots of gene variants code for low insulin production.

Therefore any extra weight as environmental trigger, body can’t keep up with demands of glucose.

257
Q

Commonest cause of death in diabetes mellitus?

A

myocardial infarction

258
Q

Diabetes mellitus accelerates atherosclerosis. How much more likely is stroke, and heart disease?

A

stroke = 3 times more likely
heart disease = 20 times more likely

259
Q

Why does diabetes cause atherosclerosis?

A

Glucose stops LDL from binding to its receptor in the liver, so LDL rises, therefore hyperlipidaemia, therefore deposits around the body.

260
Q

What’s ‘glycosylation’ in diabetes?

A

when glucose gets added to proteins in the blood (bc of a rise). This is initially reversible.

261
Q

Example of proteins that glucose gets added to?

A

collagen (gets stuck in basal lamina of small vessels)

262
Q

Glucose can’t bind to albumin unless

A

It’s also glycosylated to other proteins, leading to hypalbuminaemia

263
Q

Why hypoalbuminaemia in diabetes?

A

Because basically: albumin binds to glucose, which has bonded to proteins (that allows it), because there is excess glucose and the body is like, ‘I don’t know what to do with this’.

264
Q

Why peripheral nerve damage in diabetes?

A

Because of the arterioles supplying the nerves- the arterioles suffer from build ups of collagen that is glycosylated.

NB its the vessels getting damaged!

265
Q
A

Year 2 Semester 2 (8 decks)

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