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Semester 1 > Metabolism Sessions 7-11 > Flashcards

Metabolism Sessions 7-11 Flashcards

1
Q

What methods of communication can be used in a control system?

A

Action potentials
Endocrine hormones
Paracrine hormones
Autocrine hormones

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2
Q

What is the function of a control centre in a control system?

A

Determines set point, analyses input and determines response

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3
Q

Which pathway does the receptor of a control system use?

A

Afferent

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4
Q

Which pathway does the effector of a control system use?

A

Efferent

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5
Q

What happens in a negative feedback loop?

A

Effector opposes stimulus

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6
Q

Which feedback regulates most homeostatic systems?

A

Negative

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7
Q

What is positive feedback?

A

Stimulus produces response which increases its effects causing rapid catastrophic change which can result in a change in state e.g. blood clotting

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8
Q

What does blood cortisol have to be measured at the same time each day?

A

Follows a circadian/diurnal rhythm

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9
Q

What controls the biological clock in the body?

A

Suprchiasmatic nucleus (collection of neurones) in the hypothalamus

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10
Q

Why is the body clock cycle reset by external stimuli?

A

It is naturally slightly longer the 24 hours

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11
Q

What causes jet lag?

A

External stimuli and biological clock indicate different times

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12
Q

What is released from the pineal gland as soon as eyes are closed to regulate the light/dark cycle?

A

Melatonin

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13
Q

Why does melatonin release need optic nerve input?

A

Pineal gland it is released from is buried right at the centre of the brain

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14
Q

Where is the pituitary gland located?

A

Hangs down from hypothalamus

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15
Q

How are the parts of the pituitary gland related to its function?

A 
Anterior = endocrine supplied by veins
Posterior = neuroendocrine supplied by veins and arteries
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16
Q

What percentage of body mass is water in makes and females respectively?

A

50-60% males

45-50% females

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17
Q

Why do females have a lower percentage mass of water?

A

They have more fat

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18
Q

What is osmolality?

A

Solvent expressed per weight of solvent

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19
Q

What is measured along with sodium ion concentration by osmoreceptors in the hypothalamus?

A

Osmolality

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20
Q

How does the body counteract and increase in blood plasma osmolality?

A

Released ADH from posterior pituitary to increase reabsorption of water from urine in collecting ducts

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21
Q

What is the name given to a biologically active signalling chemical?

A

Hormone

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22
Q

Which organs make up the endocrine system?

A 
Hypothalamus
Pituitary gland
Parathyroid glands
Heart
Adrenal glands
Kidneys
Pineal glands
Thyroid glands
Stomach
Pancreas
Intestines
Ovaries/testes
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23
Q

What type of responses is the endocrine system good for?

A

Coordinated multiple

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24
Q

What blood system does the hypothalamus release factors into?

A

Portal

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25
Q

What is considered as the ‘master gland’ of the endocrine system?

A

Anterior pituitary

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26
Q

What does the anterior pituitary gland release on stimulation from the hypothalamus?

A

Trophic (stimulating) hormones

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27
Q

Which axis is the classic stress response?

A

Hypothalamic-pituitary-adrenal (HPA)

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28
Q

What controls the HPA axis?

A

-ve feedback

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29
Q

Which hormones are elevated in the classic stress response?

A

Corticotrophin releasing hormone (CRH)
Adrenocorticotrophin releasing hormone (ACTH)
Cortisol

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30
Q

What is the rate of secretion in the endocrine system usually controlled by?

A

-ve feedback

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31
Q

Why are hormones very difficult to measure in the body?

A

Circulate in very low concentrations

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32
Q

What is the solubility of hormones like?

A

Some peptide and amine are water soluble

Steroid and thyroid are lipid soluble

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33
Q

How are steroid and thyroid hormones carried in the blood?

A

Steroid by specific steroid binding globulins

Thyroid by thyroid binding globulins (TBG)

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34
Q

What is there between the biologically inactive bound form and biologically active free form of hormone?

A

Dynamic equilibrium

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35
Q

What is the function of carrier proteins in hormone transport?

A

Increase solubility in plasma
Increase half-life
Create readily accessible reserve

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36
Q

Why is a readily accessible reserve of hormone provided by carrier proteins important for thyroxine?

A

It is tightly bound

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37
Q

What are the four classes of human hormones?

A

Peptide
Glycoprotein
Steroid
Amine

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38
Q

Which is the largest class of human hormones?

A

Peptide

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39
Q

How many known peptide hormones are there?

A

~20 but often increases due to new gut discoveries

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40
Q

What are all steroid hormones derived from?

A

Cholesterol

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41
Q

Which two steroid hormones is there one group difference between?

A

Testosterone and progesterone

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42
Q

Give some examples of steroid hormones.

A 
Vitamin D
Corticosteroids 
Progestins
Androgens
Oestrogens
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43
Q

How many major amine hormones are there?

A

3

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44
Q

What is a main precursor of amine hormones?

A

Tyrosine

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45
Q

Give two examples of locally acting amine hormones.

A

Histamine and serotonin

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46
Q

What is the precursor of histamine?

A

Histidine

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47
Q

What is the precursor of serotonin?

A

Tryptophan

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48
Q

What is the structure of glycoprotein hormones?

A

2 polypeptides and a carbohydrate side chain

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49
Q

Where are all glycoprotein hormones released from?

A

Anterior pituitary gland

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50
Q

Give four examples of glycoprotein hormones.

A

TSH
FSH
LH
hCG

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51
Q

What does the magnitude of a hormonal response depend on?

A

Concentration of active hormone at target tissue
Receptor number
Affinity of receptor for hormone
Degree of signal amplification

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52
Q

Which type of hormones can cross the CSM?

A

Steroid

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53
Q

Where do steroid hormones bind to cellular receptors?

A

In nucleus or in cytosol (heat shock protein) which moves into the nucleus

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54
Q

What effects do steroid hormones have in the nucleus?

A

Alters transcription process - either switches on or off enzyme expression to affect enzyme action of cell

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55
Q

What happens upon binding of a hormone that cannot cross the CSM to a receptor on the cell surface?

A

Activates second messenger whose products affect enzyme action in cell

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56
Q

Can steroid hormones bind to CSM receptors and affect enzyme action in a cell?

A

New research says yes

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57
Q

What do control systems in the body require?

A

Communication
Control centre
Receptor
Effector

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58
Q

What controls appetite?

A

Appetite centre/satiety centre located in the arcuate nucleus in the hypothalamus

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59
Q

How many types of neurones are there in the arcuate nucleus?

A

2

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60
Q

What is the function of the primary neurones in the arcuate nucleus?

A

Sense glucose and FA in the blood

Respond to hormones

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61
Q

What is the function of secondary neurones in the arcuate nucleus?

A

Synthesise input
Coordinate a response
Signal to higher sensors in the brain

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62
Q

Which hormones are excitatory in the control of appetite?

A

Neuropeptide Y

Agouti-related peptide

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63
Q

Which hormones are inhibitory in the control of appetite?

A

POMC
Beta-endorphin
Alpha-melanocytes stimulating hormone

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64
Q

What is ghrelin?

A

Peptide hormone released from stomach wall when empty which is the only known hormone to stimulate appetite

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65
Q

When is ghrelin inhibited?

A

When stomach is filled

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66
Q

What is cleaved off POMC which suppresses appetite?

A

Alpha-MSH

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67
Q

Which peptide hormone is released from the wall of the small intestine that suppresses appetite?

A

PYY

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68
Q

What is released from adipocytes to signal appetite suppression?

A

Lepton

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69
Q

How does lepton cause excess energy in stores to be dissipated as heat?

A

Induces uncoupling protein expression

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70
Q

Which peptide hormone is secreted by beta cells in the pancreas to suppress appetite?

A

Amylin

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71
Q

Which peptide hormone uses the same mechanism as leptin but is less important in its role of suppressing appetite?

A

Insulin

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72
Q

How does glucagon-like peptide cause weight loss?

A

Released from gut to enhance insulin release

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73
Q

Which gut hormone causes weight loss and ‘cures’ T2DM?

A

Oxyntomodulin

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74
Q

What does an injection of leptin into deficient patients treat?

A

Hyperphagia

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75
Q

What conditions comprise metabolic syndrome?

A

Insulin resistance
Dyslipidaemia
Impaired glucose tolerance
Hypertension

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76
Q

What three methods of bariatric surgery are available?

A

Adjustable gastric band
Roux-en-Y gastric bypass
Vertical sleeve gastrectomy

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77
Q

Why is Roux-en-Y gastric bypass the most effective type of bariatric surgery?

A

Reroutes small intestine so gut hormones no longer act

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78
Q

What benefits can Roux-en-Y gastric bypass have?

A

Rapid weight loss
Reversal of T2DM due to signalling changes
Reverses infertility caused by obesity

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79
Q

What is gut microbiome composition associated with?

A

Obesity
T2DM
CVD
Non-alcoholic fatty liver disease

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80
Q

What does the strong association between CHD, hypertension, T2DM (adult disease) and low birth and placenta weight suggest?

A

Foetal programming

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81
Q

What is foetal programming?

A

Foetus adapts to conditions in utero –> biochemical adaptations are ‘programmed in’ predisposing to adult diseases

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82
Q

What genetic mechanism explains foetal programming?

A

Epigentics

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83
Q

What is epigenetics?

A

Inherited phenotype resulting from change in a chromosome w/out change in the DNA sequence

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84
Q

What changes to histones can cause suppression of gene transcription?

A

DNA methylation changes histone structure

‘Tails’ on histones affected by surroundings which alters DNA

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85
Q

What is diabetes mellitus?

A

Hyperglycaemia which over years leads to damage of small and large blood vessels causing premature death from CVD

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86
Q

What is diabetes mellitus characterised by?

A

Hyperglycaemia but may have other metabolic abnormalities

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87
Q

How can the insulin levels be affected in diabetes mellitus?

A

Beta-cell failure so not produced

Production is fine but resistance prevents it from working properly

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88
Q

How do patients with diabetes present?

A 
Polyuria
Polydipsia
Tiredness
Weakness
Blurring of vision
Urinary tract infections
Weight loss
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89
Q

What is needed to diagnose diabetes?

A

Either symptoms and 1 abnormal blood test or asymptomatic with 2 abnormal tests

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90
Q

What blood tests can be used to diagnose diabetes?

A

Fasting glucose
Oral glucose tolerance test
HbA1C

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91
Q

What is a long term indicator of glycaemic control?

A

Glycosylated haemoglobin - HbA1C

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92
Q

How is a patient in the impaired glucose tolerance range often treated?

A

Same as if they were in the diabetic range

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93
Q

What is type I diabetes?

A

Autoimmune or non-immune deficiency of insulin

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94
Q

How does T2DM differ from T1DM?

A

Characterised by insulin deficiency and resistance

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95
Q

What can cause T2DM?

A 
Iron overload
Pancreactectomy
Genetic beta-cell defects
Drug induced - steroid, diuretics, beta-blockers
Hormone disorders e.g. cortisol
Genetic defects of insulin action
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96
Q

How does type I diabetes mellitus present?

A 
Rapid onset
Weight loss
Polyuria
Polydipsia
Late presentation --> vomiting from ketoacidosis
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97
Q

Why must identified cases of T1DM be urgently referred?

A

High risk of ketoacidosis and death

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98
Q

What diagnostic feature can be used to differentiate between T1 and T2 diabetes?

A

T1 has ketones present in the urine, T2 does not

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99
Q

What are the functions of insulin on fuel metabolism?

A

Enhance glucose uptake by the liver
Inhibit liver glycogen breakdown
Enhance glucose uptake by muscle and adipose

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100
Q

What effects does insulin have in amino acids?

A

Inhibits catabolism
Inhibits gluconeogenesis in liver
Stimulates active transportation into cells

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101
Q

What effect does insulin have on FA?

A

Promotes their clearance

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102
Q

What treatment is given in ketoacidosis?

A

SC injection of exogenous insulin w/fluids and potassium

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103
Q

What causes diabetic ketoacidosis?

A

Hyperglycaemia and dehydration lead to production of serum acetone

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104
Q

How does obesity cause hyperglycaemia?

A

Increases insulin secretion –> pancreatic exhaustion

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105
Q

What occurs in T2DM that can cause beta-cell failure?

A

Amyloid type deposits

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106
Q

What can be considered as a potentially reversible metabolic disorder which is precipitated by chronic intraorgan fat?

A

T2DM

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107
Q

How does bariatric surgery or hypocalorific diet cause reversal of T2DM?

A

Calorific intake falls –> profound change in [fat metabolites] –> fat mobilised first from liver then other ectopic sites rather than subcutaneous –> pancreatic fat content decreases normalising bet-cell function

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108
Q

Which two pathologies must both happen to cause T2DM?

A

Insulin resistance and relative lack of insulin

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109
Q

Is T2DM caused by genetic or environmental factors?

A

Both

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110
Q

How do T2DM patients present?

A

Variably due to slow rise in blood glucose
Polyuria
Polydipsia
Weight loss

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111
Q

Can T2DM patients be asymptomatic?

A

Yes

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112
Q

In what age group is T2DM usually seen?

A

40+ but increasingly seen in the young

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113
Q

Why are no ketones seen in the urine in T2DM?

A

Beta cells still produce some insulin, just not enough

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114
Q

Why do even asymptomatic T2DM patients have to maintain good blood glucose control?

A

To reduce risk of complications e.g. significant morbidity, mortality

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115
Q

How is T2DM treated?

A 
Change lifestyle factors
Metformin
Sulphonylureas
GLP1 to suppress appetite
Insulin as a last resort
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116
Q

What life-long monitoring methods are used in T2DM?

A 
Well being
Glucose control - capillary vs urinary glucose testing
HbA1C
Vascular risk factors
Surveillance for chronic complications
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117
Q

How is the function of the pancreas split?

A

~1% of tissue is endocrine

~99% of tissue is exocrine

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118
Q

What are the exocrine secretions of the pancreas?

A

Digestive enzymes directly into duodenum

Alkaline secretions through pancreatic duct into duodenum

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119
Q

How does the pancreas develop embryologically?

A

As an outgrowth of the foregut

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120
Q

What are the five major cell types and their respective functions in the endocrine pancreas?

A 
Alpha - glucagon
Beta - insulin
Delta - somatostatin
F - pancreatic polypeptide
Unnamed - ghrelin
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121
Q

What is the combined function of insulin and glucagon?

A

Regulation of metabolism of carbohydrates, proteins and fats

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122
Q

What are the target tissues of insulin?

A

Liver
Adipose
Skeletal muscle

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123
Q

What does insulin affect the metabolism of?

A

Carbohydrates
Lipids
Proteins

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124
Q

Is insulin anabolic or catabolic?

A

Anabolic

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125
Q

What are the target tissues of glucagon?

A

Liver

Adipose

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126
Q

What does glucagon affect the metabolism of?

A

Carbohydrates

Lipids

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127
Q

What would cause swelling/shrinking of cells in the brain, thus causing detrimental damage?

A

Changes in blood glucose altering osmolarity

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128
Q

What can alter the renal threshold?

A

Elderly increases

Pregnancy decreases it

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129
Q

How are insulin and glucagon carried in the blood?

A

Dissolved in plasma

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130
Q

What is the half life of insulin and glucagon?

A

5 minutes

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131
Q

What happens when glucagon and insulin reach target cells?

A

Interact w/cell surface receptors and form a complex which can be internalised

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132
Q

Why does insulin have a rigid structure?

A

Has 2 sulphide bridges

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133
Q

How is insulin mRNA translated?

A

Single chain precursor called preproinsulin

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134
Q

What happens to preproinsulin on insertion to the ER?

A

Pre cleaved off

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135
Q

What happens to proinsulin in the ER?

A

Exposed to specific endopeptidases which excise C peptide

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136
Q

What happens to the mature insulin in the Golgi and cytoplasm?

A

Insulin and free C peptide packaged in Golgi into secretory granules which accumulate in cytoplasm

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137
Q

What is the process of margination in insulin secretion?

A

Storage vesicles –> CSM –> exocytosis

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138
Q

Why is rapid turnover of insulin needed?

A

Short half life

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139
Q

How does [glucose] in beta-cells rise?

A

Enters by facilitated diffusion through GLUT2

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140
Q

How does increasing [glucose] in beta-cells cause release of insulin?

A

Allows more ATP to be formed so ATP sensitive potassium channel can function –> membrane depolarised –> V-G calcium channel opens and calcium influx triggers exocytosis of insulin

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141
Q

What effect can metabolic insulin have in GLUT4?

A

Increases insertion to increase glucose uptake into target cells and increase glycogen synthesis

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142
Q

What is the structure of an insulin receptor?

A

Alpha-chain on exterior of cell membrane
Beta-chain spans cell membrane in single segment
2 units held together by a disulphide bond
Receptor is a dimer

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143
Q

What causes the insulin receptor to become active tyrosine kinase?

A

Alpha-chains move together and fold round insulin which moves beta-chains together

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144
Q

What effects does tyrosine kinase activation by insulin have in the cell?

A

Initiates phosphorylation cascade which results in increased GLUT4 expression so cells can take up more glucose

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145
Q

What causes glucagon secretion?

A

Low glucose levels within alpha-cells

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146
Q

How is glucagon synthesised?

A

In RER and transported to Golgi where it is packaged into granules

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147
Q

Why is glucagon more flexible than insulin?

A

No disulphide bridges

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148
Q

How are granules of glucagon secreted?

A

Move to cell surface by margination and exocytosis

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149
Q

What is the only case where glucagon is not antagonistic to insulin?

A

When it increases gluconeogenesis when a protein rich meal is consumed

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150
Q

Is glycolysis and amino acid and glucose uptake into muscle and adipose rapid, intermediate or delayed?

A

Rapid

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151
Q

What are the delayed effects of insulin and glucagon?

A

Lipogenesis
Lipolysis
Ketogenesis

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152
Q

What happens initially in insulin resistance in the young?

A

Beta-cells compensate by increasing insulin production which maintains normal blood glucose but kills beta-cells off

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153
Q

What happens eventually in insulin resistance in the young to cause impaired glucose tolerance?

A

Beta-cells are unable to maintain increased insulin production

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154
Q

What happens finally in insulin resistance in the young causing overt T2DM?

A

Beta-cell dysfunction leads to relative insulin deficiency

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155
Q

What is decreased in the adipose tissue in addition to decreased lipogenesis in chronic hyperglycaemia?

A

Esterification

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156
Q

What are the long-term consequences of chronic hyperglycaemia?

A

Muscle wasting
Weight loss
Ketosis
Hyperglycaemia

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157
Q

What are chronic long-term microvascular consequences of chronic hyperglycaemia?

A

Neuropathy
Nephropathy
Retinopathy

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158
Q

What are acute metabolic consequences of choroid hyperglycaemia?

A

Glycosuria - exceeds renal threshold
Polydipsia
Poolyuria

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159
Q

What are chronic microvascular consequences of chronic hyperglycaemia?

A

Stroke
Coronary artery disease
Poor peripheral circulation esp. feet

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160
Q

How does the development of the anterior and posterior pituitary gland vary?

A

Anterior derives from primitive gut tissue

Posterior is brain tissue

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161
Q

Why are tumours seen in the gut and pituitary similar?

A

Derived from same primitive tissue

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162
Q

What is the link between the endocrine and nervous system?

A

Hyothalamo-pituitary axis

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163
Q

What is a slower metabolic response than the neurological response to the external environment?

A

Endocrine response

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164
Q

What characteristic symptom does upward tumour growth in the pituitary gland cause?

A

Tunnel vision due to optic chiasm disruption

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165
Q

Why does sideways tumour growth in the pituitary gland cause headaches and vision problems?

A

Cranial nerves disrupted

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166
Q

What hormones does the anterior pituitary gland secrete?

A 
ACTH
Prolactin
Growth hormone
TSH
LH
FSH
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167
Q

Which hormone released by the anterior pituitary gland is the only one under inhibitory control?

A

Prolactin

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168
Q

Which two hormones are secreted by the posterior pituitary gland?

A

Oxytocin

ADH

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169
Q

What stimulates lactation after birth?

A

Oxytocin

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170
Q

Do correctly managed benign pituitary tumours reduce life expectancy?

A

No

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171
Q

What are the five anterior pituitary axes?

A 
Growth hormone
ACTH
LH/FSH
TSH
Prolactin
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172
Q

Which anterior pituitary axis is abused by athletes/body builders?

A

Growth hormone

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173
Q

Which growth axis that is important for growth and metabolism increases blood glucose like adrenaline but for longer?

A

Growth hormone

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174
Q

Which tissues does GH act on?

A

All

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175
Q

How does the growth hormone axis work?

A

Via insulin-like growth factor (IGF-1) produced by the liver which on binding to receptor stimulates secondary messenger by dimerisation of receptor

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176
Q

What is secreted by the hypothalamus to increase and suppress growth hormone action?

A

GRH increases

Somatostatin decreases

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177
Q

Why does somatostatin inhibit lots of hormones, especially gut hormones?

A

Due to their origin

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178
Q

When is GH normally released?

A

Few pulses each day, mostly during sleep

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179
Q

What does a high mean GH level cause?

A

Acromegaly

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180
Q

What are the functions of GH?

A 
Skeletal growth
Metabolism
Muscle strength
Bone density
Cardiac function
Quality of life
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181
Q

How do the changes seen in growth hormone differ in adults and children?

A

Changes more subtle in adults than children

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182
Q

Which anterior pituitary axis is the most important to preserve life and why?

A

Hypothalamo-pituitary-adrenal axis as lack of ACTH is potentially fatal

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183
Q

In what rhythm are CRH and ACTH secreted in?

A

Circadian

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184
Q

What gives a positive hypothalamic control in the hypothalamo-pituitary-adrenal axis?

A

CRH

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185
Q

What external factor causes ACTH release?

A

Stress

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186
Q

How do cortisol deficient patients feel all the time?

A

Sick and groggy

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187
Q

What is used to treat cortisol deficient patients?

A

Hydrocortisone

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188
Q

When would you measure cortisol levels in suspected Addison’s and why?

A

Early in the morning when cortisol level is highest

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189
Q

When would you measure cortisol levels in suspected Cushing’s and why?

A

Midnight as this is when cortisol levels are at their lowest

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190
Q

Which axis is controlled by the action of LH/FSH?

A

Hypothalamo-pituitary-gonadal axis

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191
Q

What stimulates LH/FSH release from the pituitary gland?

A

GnRH

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192
Q

What feedback mechanism do LH/FSH use in men?

A

Simple -ve feedback

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193
Q

What action do LH and FSH have in men?

A

LH drives testosterone secretion

FSH drives sperm production

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194
Q

When would you measure LH and FSH levels in men and why?

A

Highest in morning due to circadian rhythm so measure then

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195
Q

Which method of feedback do LH and FSH use during their mid-cycle surge?

A

+ve

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196
Q

What does LH cause in the follicular phase in women?

A

Pulses cause oestrogen release

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197
Q

What do LH pulses cause in the mid-late luteal phase in women?

A

Progesterone release

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198
Q

Which type of feedback does the hypothalamo-pituitary-thyroid axis use?

A

Simple -ve

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199
Q

How is production of T3 and T4 stimulated?

A

TRH stimulates pituitary to secrete TSH which activates follicular cells in thyroid

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200
Q

What is the function of prolactin?

A

Initiate and maintain lactation

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201
Q

What is the target of the lactotroph axis?

A

Peripheral tissues with no target gland

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202
Q

What do high levels of prolactin cause?

A

Lactation and menstrual disturbance - inhibits menstruation

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203
Q

What tonically inhibits prolactin?

A

Dopamine

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204
Q

What increases prolactin levels?

A

Minor positive control by TRH

Oestrogen

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205
Q

What pattern of secretion does prolactin follow?

A

Pulsatile, slightly higher at night

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206
Q

When can you measure prolactin?

A

Any time of day

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207
Q

What are high levels of prolactin caused by?

A

5Ps: pregnancy, physiological (stress), pharmacological, pituitary, polycystic ovaries

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208
Q

What is primary gland failure?

A

Failure of actual organ

209
Q

What hormone levels are seen in primary gland failure?

A

End organ hormone low

Pituitary hormone high

210
Q

What is lost in primary gland failure which results in high pituitary hormone levels?

A

-ve feedback

211
Q

Which organ fails in secondary gland failure?

A

Pituitary

212
Q

What hormone levels are seen in secondary gland failure?

A

End organ hormone low

Pituitary hormone low

213
Q

Why is the thyroid not stimulated in secondary hypothyroidism?

A

Loss of TSH

214
Q

What hormone levels are seen in excess hormone production by the primary gland?

A

End organ hormone high

Pituitary hormone low

215
Q

What hormone levels are seen in excess hormone production by the pituitary gland?

A

End organ hormone high

Pituitary hormone high

216
Q

What controls water retention using osmoreceptors which measure serum osmolality and rising sodium levels before thirst occurs?

A

Posterior pituitary

217
Q

When a rise in serum osmolality and sodium is detected, what is released?

A

ADH

218
Q

What happens when blood concentration increases?

A

ADH released –> water recycled into bloodstream

219
Q

What happens if osmolality decreases?

A

ADH is switched off –> water is not recycled to the bloodstream

220
Q

What happens in diabetes insipidus?

A

Water is not reabsorbed by the kidneys which causes an increase in serum osmolality and decrease in urine osmolality

221
Q

Why are the symptoms of diabetes insipidus?

A

Polyuria

Polydipsia

222
Q

What can cause diabetes insipidus?

A

ADH deficiency due to disease of hypothalamus or pituitary stalk
ADH resistance

223
Q

What are the S/S of acromegaly?

A 
Large hand and feet
Sweating
Headaches
Coarse features
Hypertension and diabetes
224
Q

What are the S/S of Cushing’s disease?

A 
Central obesity
Striae
Easy bruising
Rounded moon-shaped face
Diabetes and hypertension
Proximal myopathy
225
Q

What are prolactinomas?

A

Prolactin-secreting pituitary tumours

226
Q

What are the S/S of prolactinomas?

A

Infertility
Menstrual disturbances
Glactorrhea

227
Q

What does a a big tumour squashing the pituitary gland cause?

A

Decreased hormone levels of all pituitary hormones except prolactin which increases

228
Q

What are the clinical features of hypopituitarism?

A

Lethargic
Pallor
Loss of body hair
Poor growth in children

229
Q

What are gonadotropinomas?

A

LH/FSH secreting pituitary tumours

230
Q

What do gonadotropinomas cause?

A

Increases of sex steroids

Increased LH/FSH

231
Q

What are basal endocrine tests used in pituitary disease to measure prolactin and testosterone?

A

Tests carried out at any time of day due to stable hormone levels

232
Q

What are dynamic endocrine tests in pituitary disease?

A

Tests where the time of day they are conducted is important due to cyclic or pulsatile hormone release

233
Q

Which hormones are measured by dynamic endocrine tests?

A

LH
FSH
GH
ACTH

234
Q

What do you do to a gland if there is a hormone deficiency or excess in order to identify pituitary disease?

A

Deficiency - try to stimulate gland into action

Excess - try to suppress gland

235
Q

What is growth hormone stimulation test used for?

A

Suspected GH deficiency

236
Q

What does the GH stimulation test investigate?

A

Pituitary GH reserve to identify growth disorders in children and pituitary tumours in adults

237
Q

What is the best test of GH reserve?

A

Insulin tolerance test

238
Q

What happens in an insulin tolerance test?

A

IV insulin –> hypoglycaemia –> somatostatin inhibited so GH is stimulated (testing for deficiency) –> GH doesn’t rise –> unpleasant sensation/hot and sweaty/tachycardia/faint

239
Q

Why is medical supervision important when conducting an insulin tolerance test?

A

Positive results from the test can be prolonged

240
Q

When is the insulin tolerance test not used?

A

If patient has ischaemic heart disease, epilepsy or unexplained blackouts

241
Q

When is the growth hormone suppression test used?

A

Suspected GH excess e.g. Acromegaly

242
Q

What happens in the GH suppression test?

A

75 g of oral glucose –> increases somatostatin which should suppress GH –> no suppression of GH = acromegaly

243
Q

How often are glucose and GH measured in the GH suppression test?

A

Every 30 mins starting 30 mins prior to oral glucose dose

244
Q

When is the ACTH stimulation test used?

A

Suspected ACTH deficiency caused by hypopituitarism or another isolated condition

245
Q

Wha can be used to conduct an ACTH stimulation test if the patient does not suffer from IHD, epilepsy or unexplained blackouts?

A

Insulin tolerance test

246
Q

What happens in an ACTH stimulation test?

A

Stress –> CRH rises –> ACTH should rise and cause cortisol release to prevent hypoglycaemia –> hypoglycaemia occurs

247
Q

When is a dexamethasone suppression test used?

A

Suspected excess ACTH e.g. Cushing’s

248
Q

What happens in a dexamethasone suppression test?

A

Dexamethasone should act in hypothalamus to decrease CRH and subsequently decrease cortisol but ACTH remains high so cortisol remains high

249
Q

What treatments are available for pituitary disease?

A

Controlled removal of tumour by surgery, radiotherapy or medical therapy
Reduce increased hormone secretion
Replace hormone deficiencies

250
Q

What are the advantages of using radiotherapy to treat pituitary tumours?

A

Prevents tumour and protects vision

Can damage gland and increase risk of stroke

251
Q

What medical therapies can be used to remove pituitary tumours?

A

GH receptor antagonists
Dopamine (D2) agonists
Somatostatin analogues

252
Q

What effects do dopamine agonists have in pituitary tumour treatment?

A

Reduce prolactin

Shrink pituitary tumour enough to prevent need for surgery

253
Q

Which axis do somatostatin and its analogues act on?

A

GH

254
Q

What is given as a monthly injection to treat acromegaly?

A

Somatostatin and its analogues

255
Q

How do GH receptor blockers work I treating acromegaly?

A

Normalise IGF-1 (not GH) levels

256
Q

What controls are the cortex and medulla of the adrenal gland?

A

Cortex - endocrine

Medulla - neurological

257
Q

What is the only source of testosterone in women?

A

Androgens released from the reticularis of the adrenal cortex

258
Q

What is the most common enzyme deficiency causing absent mineralocortcoids or glucocorticoids?

A

21-hydroxylase

259
Q

What causes a newborn to have indistinguishable sex?

A

Build up of androgens due to deficiency of 21-hydroxylase

260
Q

What allows the dramatic change in shape of mediator proteins due to steroid hormone binding?

A

Alteration of DNA transcription

261
Q

What happens in mineralocortcoid deficiency?

A

Decreased sodium
Dehydration
Hyperkalaemia

262
Q

What happens in mineralocortcoid excess?

A

Increased sodium
Hypertension
Hypokalaemia

263
Q

What actions do glucocorticoids have?

A

Increase glucose production
Breakdown protein
Redistribute fat

264
Q

What does redistribution of fat due to glucocorticoid action depend on?

A

Enzyme specific concentration in tissues

265
Q

Where is fat usually distributed in glucocorticoid excess?

A

Centrally

Dorso-cervical

266
Q

Why happens in glucocorticoid excess?

A

Decreased glucose
Weight loss
Nausea
Hypotension

267
Q

What happens in glucocorticoid excess?

A 
Increased glucose
Weight gain
Increased appetite
Hypertension
Cushingoid
268
Q

What is aldosterone controlled by?

A

Rennin-cycle

269
Q

What gland failure does increased pigment around knuckles, scars and bucchal mucosa indicate?

A

Primary adrenal

270
Q

What tumour can cause ectopic ACTH secretion?

A

Small cell lung

271
Q

What does a Cushingoid appearance but low ACTH levels indicate?

A

Autonomous cortisol secretion

272
Q

What precursor is ACTH secreted as?

A

POMC

273
Q

What is POMC broken down into?

A

Amino terminal fragment –> alpha-MSH
ACTH
Beta-lipoproteins –> meta-MSH and met-enkephalin

274
Q

What does ACTH stimulate in the adrenal glands?

A

Production of steroid hormones

275
Q

What is ACTH broken down into which leads to pigmentation?

A

Alpha-MSH

CLIP

276
Q

What can cause corticosteroid excess?

A

Cushing’s disease
Ectopic ACTH
Primary adrenal tumour
Exogenous steroids

277
Q

What must be considered when testing the HPA-axis?

A

Its circadian rhythm

278
Q

What social factor might alter testing time of the HPA-axis?

A

Shift work

279
Q

What test is used for primary adrenal failure?

A

Synacthen

280
Q

What happens in a synacthen test that indicates primary adrenal failure?

A

Primary adrenal failure or disease of adrenal cortex means there is no cortisol response to synthetic ACTH

281
Q

What test is used in suspected secondary adrenal gland failure?

A

Insulin tolerance test

282
Q

How long does there have to be absent pituitary stimulation to cause the adrenal gland to atrophy?

A

~month

283
Q

What are two causes of pseudocushing’s?

A

Alcohol

Psychiatric disease

284
Q

What tests are used in suspected corticosteroid excess?

A

24hr urine free cortisol

Dexamethasone suppression test

285
Q

What is Addison’s disease?

A

Far endocrine disorder due to auto-immune destruction of adrenal cortex causing a deficiency of all hormones

286
Q

Why are lymphocytes seen in the adrenal cortex of Addison’s patients?

A

Causes inflammatory infiltrate in adrenal cortex

287
Q

What do Addison’s disease patients often also present with?

A

Other auto-immune diseases

288
Q

Is Addison’s more common in women or men?

A

Women

289
Q

What are the S/S of Addison’s disease?

A 
Weight loss
Anorexia
Malaise
Weakness
Fever
Depression
Impotence
Amenorrhea
Low libido
Abdominal pain
Myalgia
Arthralgia
Nausea
290
Q

What are the specific clinical features of Addison’s disease?

A

Pigmentation
Postural hypotension
Salt cravings

291
Q

What are the biochemical features of Addison’s disease?

A

Decreased sodium
Increased potassium
Increased urea (due to dehydration)
Decreased glucose

292
Q

What confirmatory tests can be used in Addison’s disease?

A 
0900 cortisol
Short synacthen test
ACTH
Plasma renin
Adrenal antibodies
293
Q

What can cause primary adrenal failure?

A 
Adrenal leucodystrophy
Tuberculosis
Surgical removal
Meningitis
Haemorrhage/infarction
294
Q

Is acute primary adrenal failure an emergency?

A

Yes

295
Q

How is glucocorticoid replacement monitored?

A

Improvement in clinical symptoms
Restoration of normal weight
Cortisol measurements throughout the day

296
Q

How is fludrocortisone replacement monitored?

A

Restoration of serum electrolytes to normal
Blood pressure response to posture
Suppression of plasma renin to normal

297
Q

How do the S/S of primary and secondary hypoadrenalism compare?

A

Primary: high ACTH, pigmented, gluco and mineralcorticoids raised
Secondary: low ACTH, pale, glucocorticoids only raised

298
Q

What results is exogenous steroids cause hypo-adrenal crisis?

A 
Hypotension
Hypoglycaemia
Hyponatreamia
Hyperkalaemia
Severe dehydration and death if untreated
299
Q

Why are long-term steroid use patients at an increased risk of peri-operative hypoadrenal crisis?

A

Cannot mount an endogenous stress response

300
Q

What is endogenous Cushing’s syndrome?

A

Rare endocrine disorder caused by pituitary disorder, adrenal tumour/hyperplasia, ectopic ACTH secretion or abnormal receptors in adrenal cortical cells

301
Q

What is the main cause of endogenous Cushing’s syndrome?

A

Pituitary source

302
Q

What are the clinical features of endogenous Cushing’s syndrome?

A 
Central weight gain
Change in appearance
Depression
Insomnia
Menstrual disturbance
Poor libido
Thin skin
Easy bruising
Hair growth
Acne
Muscle weakness
Growth arrest in children
Back pain
Psychosis
303
Q

What is found on examination in endogenous Cushing’s syndrome?

A 
Moon face
Plethora
Buffalo hump
Striae
Central obesity
Thin skin
Bruising
Hypertension
Proximal myopathy
304
Q

What confirmatory tests can be used in endogenous Cushing’s syndrome?

A

24 hour urinary free cortisol
Midnight cortisol
Adrenal CT or MRI

305
Q

What happens if endogenous Cushing’s syndrome is left untreated?

A 
High mortality
Hypertension
MI
Infection
Heart failure
306
Q

What is congenital adrenal hyperplasia?

A

Rare endocrine disorder causing deficiency of an enzyme that causes a block in the cortisol pathway

307
Q

What are the clinical features of congenital adrenal hypertension?

A 
Virilisation of female baby
Neonatal salt-losing crisis
Hypotension
Hypoglycaemia
Hyponatraemia
308
Q

Why is urgent confirmation of congenital adrenal hypertension needed?

A

To identify before gender assignment

309
Q

What is tested for in congenital adrenal hyperplasia?

A

High 17-hydroxyprogesterone
High androstenedione
High testosterone
High ACTH

310
Q

How is congenital adrenal hyperplasia treated?

A

Emergency with steroids

311
Q

What is the function of the thyroid gland?

A

Secrete thyroid hormone to maintain energy homeostasis

312
Q

What is the functional anatomy of the thyroid gland?

A 
Wraps around trachea at base of neck below cricoid cartilage
2 lobes connected by isthmus
Ductless
Alveolar
~20 g
313
Q

What is the structure of a thyroid follicle, the secretory unit of the thyroid gland?

A

Polarised cell thyroid epithelia around colloid filled centre

314
Q

How are the epithelial cells of the thyroid polarised?

A

Transporters on side that face colloid are different from the that face interstitium

315
Q

What accounts for 30% of thyroid mass?

A

Colloid

316
Q

What is thyroglobulin?

A

Large glycoprotein rich in tyrosine that is important in thyroid hormone synthesis and secretion

317
Q

What type of cells make up the thyroid epithelium?

A

Cuboidal or columnar

318
Q

Is there a standard size of thyroid follicle?

A

Nope

319
Q

How is blood supplied to the thyroid gland?

A

Superior and inferior thyroid arteries

320
Q

How is blood drained from the thyroid?

A

Superior, middle and inferior thyroid veins

321
Q

How can the lymphatic system of the thyroid be described?

A

Rich

322
Q

What innervation is abundant in the thyroid?

A

Sympathetic and parasympathetic

323
Q

What has a minor role in overall regulation of the thyroid gland in comparison to its cascade stimulus?

A

Sympathetic stimulation

324
Q

What does TRH binding to Gq receptors on the anterior pituitary cause?

A

Stimulation of PLC which causes an increase in intracellular calcium levels resulting in exocytosis of TSH

325
Q

Where are the receptors for TSH located on the thyroid follicular cell?

A

Basolateral membrane

326
Q

What does binding of TSH on thyroid receptors cause?

A

Stimulation of iodine uptake
Acutely: Stimulate synthesis and storage of T3 and T4
Production and release of thyroglobulin
Chronically: hyperplasia and hypertrophy

327
Q

What electrolytes are found in the fluid that bathes the basolateral membrane of epithelial cells in the thyroid?

A

Sodium
Potassium
Iodine

328
Q

What creates a sodium gradient in iodine uptake in the thyroid?

A

Active pumping of sodium out of follicle

329
Q

How is iodine moved against its concentration gradient I tot eh third follicles?

A

Taken with sodium as it moves down its concentration gradient

330
Q

What happens to the iodine transported into a thyroid follicle on the follicular lumen?

A

Activated into reactive form by oeroxidase enzyme

331
Q

What associates with thyroglobulin in thyroid follicles?

A

Reactive iodine

332
Q

Why is the storage of thyroglobulin as colloid in the thyroid follicle considered to be an iodide trap?

A

Follicular cells concentrate iodine to 20-50x the naturally occurring amount

333
Q

Why is it necessary for the colloid in thyroid follicles to act as an iodide trap?

A

Thyroid hormones contain large amounts of iodine that is not abundant in the diet

334
Q

How is thyroglobulin synthesised?

A

Synthesised on ribosomes –> glycosylated on ER cisternae –> translocated to Golgi for packaging into secretory vesicles of follicular epithelium cells

335
Q

Are T3 and T4 fat or water soluble?

A

Fat

336
Q

Which thyroid hormone is more potent, very biologically active and has a shorter half life?

A

T3

337
Q

How is T3 made ineffective?

A

Deiodinated to T2

338
Q

What carries T3 and T4 around the circulation?

A

Thyronine binding globulin
Albumin
Prealbumin

339
Q

How are T3 and T4 degraded?

A

Deiodination in the liver and kidney

340
Q

Which thyroid hormone is produced in larger volume, has a greater affinity for binding proteins and has a longer half life?

A

T4

341
Q

Where can T4 be deiodinated?

A

Liver or peripheral tissues

342
Q

Which thyroid hormone is given in tablet form as a treatment for hypothyroidism?

A

T4

343
Q

Which thyroid hormone can shrink thyroid tumours but is a possible growth factor for adenoma?

A

T4

344
Q

How is BMR increased by thyroid hormones?

A

Increased number and size of mitochondria
Increased oxygen consumption and heat production
Increased nutrient utilisation

345
Q

What metabolic pathways are stimulated by thyroid hormones?

A

Lipolysis
Glycolysis
Glycogenolysis
Proteolysis

346
Q

How do thyroid hormones promote normal growth and development of tissues?

A

Increase synthesis of specific proteins

347
Q

What do thyroid hormones increase responsiveness of tissues to?

A

Sympathetic nervous system

Various metabolic and reproductive hormones

348
Q

How do thyroid hormones increase functional capacity of the nervous system in adults?

A

Increased myelination of nerve fibres
Increased development of neurones
Increased speed of reflexes
Increased mental activity - alertness, emotional tone, memory

349
Q

How do thyroid hormones cause an increase in cardiac output?

A

Direct effect in heart and increased effect of noradrenaline

350
Q

Where is increase in turnover of proteins and glycoproteins seen due to action of thyroid hormones?

A

Skin and subcutaneous tissues

351
Q

What is seen with hypothyroidism in the neonate?

A

Irreversible severe mental retardation due to failed CNS development
Coarse features
Protruding tongue
Diminished linear growth due to failure of genetic aging
Delayed sexual development

352
Q

How soon after birth does hypothyroidism have to be treated in order for it to be reversible?

A

21 days

353
Q

What is conducted on neonates to look for hypothyroidism?

A

Heel price test to assay for TSH

354
Q

What can hyperthyroidism cause to be early but not elevated in children?

A

Maturation

355
Q

Why is hyperthyroidism not usually seen in children?

A

Exceedingly rare and/or symptoms are not noticeable

356
Q

What are the S/S or hyperthyroidism?

A 
Heat intolerance, increased perspiration
Clammy hands
Weight loss (lipid and protein)
Tachycardia
Increased bowel movements
Increased appetite
Nervousness, irritability, emotional liability
Hyper-reflexive
Exophthalmos (anterior bulge of eye)
357
Q

What is Grave’s disease?

A

Autoimmune disease which produces antibody that stimulates TSH receptor

358
Q

How does carbimazole treat Grave’s disease?

A

Inhibits incorporation of iodine with thyroglobulin

359
Q

What treatments are available for Grave’s disease?

A

Carbimazole
Radioactive iodine
Surgery

360
Q

How does radioactive iodine treat Grave’s disease?

A

Destroys follicular cells

361
Q

Are males or females more commonly affected by Grave’s disease?

A

Females, there is 10/1 ratio

362
Q

What are the S/S of hypothyroidism?

A 
Cold intolerance
Deceased perspiration, cold dry hands
Mild weight gain
Bradycardia
Constipation
Mood swings
Poor concentration, memory and initiative
Oedema and myxoedema
Dry skin
Brittle nails
Hair loss
363
Q

What is Hashimoto’s disease?

A

Autoimmune disease that destroys thyroid follicles and produces antibody that blocks TSH receptor and inhibits peroxidase enzyme

364
Q

Is Hashiomot’s disease more common in men or women?

A

Women, 10/1 ratio

365
Q

How is Hashimoto’s disease treated?

A

Oral T4

366
Q

How do you know oral T4 treatment of Hashimoto’s disease is effective?

A

Measure TSH to ensure pituitary function is normal and there will be a loss of s/s with no development of hyperthyroid s/s

367
Q

How can an ectopic thyroid at the back of the tongue arise?

A

If it does not migrate down to its position in the neck from the back of the tongue by week 12 of development

368
Q

Why does an ectopic thyroid gland at the back of the tongue have a reduced function?

A

Lack of proper blood supply

369
Q

What subunits form TSH?

A

Alpha and beta

370
Q

Which portion of thyroid hormones has any biological affect?

A

Free concentration

371
Q

What two features of T3 and T4 form a combined mean which causes the overall activity of the hormones to be slit equally?

A

Respective half lives and comparative activity

372
Q

How can the comparative activity of T3 and T4 be explained at the cellular level?

A

T3 can act directly in mitochondria to increase synthesis of enzymes and structural proteins
T4 must bind to cell membrane receptors

373
Q

Where are there receptors for both T3 and T4 present in the cell?

A

Nucleus

374
Q

What can cause hypothyroid disease?

A 
Autoimmune disease
Post-surgery
Radioactive iodine treatment
Anti-thyroid drug treatment
Secondary - due to lack of TSH
Congenital
Iodine deficiency
375
Q

What is the most common cause of hypothyroidism in the UK?

A

Autoimmune disease

376
Q

What is the most common cause of hypothyroidism worldwide?

A

Iodine deficiency

377
Q

What cause of hypothyroidism always triggers goitre formation?

A

Iodine deficiency

378
Q

What can cause hyperthyroid disease?

A

Autoimmune: Grave’s, toxic multinodular goitre, solitary toxic adenoma
Excessive T4 therapy
Thyroid carcinoma
Ectopic thyroid tissue
Excess iodine due to treatment with anti-arrhythmic drug amioderone

379
Q

Is thyroid disease more common in men or women?

A

Women

380
Q

Why are used to diagnose hyper, hypo or euthyroid?

A

Thyroid function tests

381
Q

Why are free T4 and TSH both looked at in thyroid function tests rather than just one hormone level?

A

Individual variation is smaller than population variation so what may be in population range may be unusually for an individual

382
Q

What are free T4 and TSH levels like in the thyroid function test of euthyroid?

A

Both normal

383
Q

What are free T4 and TSH levels like in the thyroid function test of hypothyroid?

A

Free T4 is low and TSH is elevated

384
Q

What are free T4 and TSH levels like in the thyroid function test of hyperthyroid?

A

Free T4 is high and TSH is low

385
Q

What is the spectrum of hyperthyroidism from most to least severe?

A

Thyroid storm
Gross hyperthyroidism
Mild hyperthyroidism
Autonomous thyroid function

386
Q

What is the spectrum of hypothyroidism from least to most severe?

A

Compensated euthyroidism
Mild hypothyroidism
Gross hypothyroidism
Myxoedema coma

387
Q

What condition on the spectrum of hypothyroid disease may not require treatment but should be continually monitored?

A

Compensated euthyroidism

388
Q

What exacerbates myxoedema coma?

A

Biological stress

389
Q

What is sick euthyroid syndrome?

A

Sick in-patients often have abnormal TFTs despite being euthyroid

390
Q

What do you need to have in order to carry out a TFT in ill in-patients due to the occurrence of sick euthyroid syndrome?

A

String clinical suspicion of gross thyroid disease

391
Q

Will all thyroid disease patients have obvious disease?

A

No

392
Q

How is calcium found in the bloodstream?

A

1.0-1.3 M free and 0.9-1.3 M bound to plasma proteins or complexed w/citrate

393
Q

Where is most of the calcium in the body stored?

A

Skeleton

394
Q

What is calcium needed for in the body?

A 
Signalling
Activity of some enzymes and hormone receptors
Normal kidney function
Blood clotting
AP transmission at NMJ 
Regulate heart rhythm
395
Q

Where is 99% of calcium found in the adult human?

A

Hydroxyapatite crystals of bone

396
Q

Why do we need a calcium store in the skeleton if calcium levels can be regulated by uptake in the GI and excretion in the urine?

A

This regulation cannot be guaranteed

397
Q

What is the rapid modulator of calcium levels?

A

Parathyroid hormone

398
Q

What is the action of parathyroid hormone?

A

Stimulate bone resorption and release of calcium into circulation
Stimulate calcium reabsorption in kidney and excretion of phosphate
Stimulate final hydroxylation of vitamin D

399
Q

What is a long-term modulator of calcium levels?

A

Dietary vitamin D

400
Q

What action does dietary vitamin D have?

A

Increase intestinal absorption of dietary calcium
Increase renal reabsorption of calcium
Increase bone resorption

401
Q

What is the name of active vitamin D?

A

Calcitriol

402
Q

Where is calcitonin produced?

A

Thyroid gland

403
Q

What is the action of calcitonin?

A

Counteracts effects of PTH but is not particularly effective in humans

404
Q

Typically how many parathyroid glands are there per lobe of the thyroid?

A

2

405
Q

Where may extra parathyroid glands be located?

A

Anywhere in the thorax

406
Q

What is the appearance of chief cells in the parathyroid?

A

Round
Clear cytoplasm
Large nucleus
Lots of mitochondria

407
Q

What is the function of chief cells?

A

Secrete PTH

408
Q

What are oxyphil/principle cells of the parathyroid?

A

Assumed old chief cells that are not associated with PTH secretion

409
Q

How does the number of mitochondria present differ between chief cells and oxyphil cells?

A

Oxyphil have less

410
Q

What cells are found in a parathyroid gland?

A

Chief
Oxyphil/principle cells of the parathyroid
Adipose

411
Q

Why does PTH stimulate calcium reabsorption but phosphate excretion in the kidney?

A

Reduce risk of urinary stones forming

412
Q

How does PTH act in the small intestine?

A

Increases calcium absorption by activating vitamin D

413
Q

What is the structure of PTH?

A

Straight chain polypeptide

Pre-pro-hormone

414
Q

What accelerates cleavage of the pre- section of PTH in the liver?

A

High serum calcium levels

415
Q

Describe the production and storage of PTH.

A

Continuously produced but not stored

Broken down immediately if not needed by chief cells

416
Q

How is the mRNA of PTH affected by serum calcium?

A

Prolongs its survival

417
Q

What is the half life of PTH?

A

4 mins

418
Q

What effect do low and high serum calcium levels have on PTH synthesis?

A

Low increases gene transcription

High downregulates production

419
Q

How is PTH release controlled?

A

-ve feedback loop - calcium binds to receptor which leads to inhibition of PTH secretion

420
Q

Is there always a degree of basal PTH?

A

Yes

421
Q

How are basal PTH secretions maintained if calcium is within normal limits?

A

2 secondary messenger pathways are balanced

422
Q

What is found on cell surface of chief cells, kidney tubule cells and C cells of thyroid gland?

A

Unique G-protein calcium receptors

423
Q

What happens to the G-protein receptors when there are high calcium levels present?

A

Phospholipase is activated which inhibits adenylate cyclase leading to reduce cAMP and reduced PTH release

424
Q

What other ion levels regulate PTH release?

A

High phosphate –> increased PTH secretion

High magnesium –> low PTH secretion

425
Q

Levels of which molecule other than calcium ions are important in chronic kidney disease?

A

Phosphate

426
Q

How do osteoclasts cause bone resorption?

A

Produce acid micro-environment which dissolves hydroxyapatite crystals

427
Q

How is calcium stored in bone?

A

Calcium phosphate crystals within collagen fibrils

428
Q

How do osteoblasts create new bone?

A

Produce collagen matrix which is mineralised by hydoxyapatite

429
Q

Which function of bone is its main priority and what is the consequence of this?

A

Maintaining serum calcium which results in soft bendy bones in order to maintain calcium levels

430
Q

What is the action of PTH on bone?

A

1-2 hrs stimulates osteolysis

431
Q

How does PTH affect osteoblastic cells?

A

Induces them to synthesise and secrete cytokines on CSM which stimulate differentiation and activity in osteoclasts and prevent them from undergoing apoptosis
Decreases their activity

432
Q

Which part of the kidneys does PTH affect?

A

PCT
Loop of Henle
DCT

433
Q

Where does PTH increase calcium reabsorption in the kidney?

A

Ascending limb

DCT

434
Q

How does PTH act on the PCT?

A

Withdraws phosphate transporters from the surface

435
Q

How much dietary intake of calcium is absorbed by para cellular uptake when calcium is not limited due to PTH action on the gut?

A

30%

436
Q

What significantly increases transcellular uptake of calcium in the gut upon PTH stimulation?

A

Vitamin D

437
Q

How is calcium absorbed in the gut?

A

Carriers in the luminal membrane of the duodenum and jejunum move calcium down concentration gradient extruded across basolateral membrane of epithelial cells

438
Q

What effect does having secretions from the gut rich in calcium have on the minimum load that must be taken in to the diet to maintain calcium balance?

A

Additive

439
Q

What is vitamin D?

A

Lipid soluble vitamin derived from plants or action of sunlight on cholesterol in skin

440
Q

How is D3 (cholecalciferol) made?

A

In skin from dairy product intake and using sunlight

441
Q

Where is D2 obtained from in the human body?

A

Ingestion of yeast and fungi which is often added to margarine as a supplement

442
Q

Do D2 and D3 form calcitriol?

A

Yes

443
Q

What can be said about the calcitriol forms from D2 and D3?

A

Equipotent

444
Q

What are the intermediates of calcitriol formation?

A

7-dehydrocholesterol
Precalciferol
Cholecalciferol
Calcitriol

445
Q

Where does the first hydroxylation reaction of calcitriol take place?

A

C25 on molecule in the liver

446
Q

How long can the product of the first hydroxylation reaction in vitamin D activation circulate in plasma for?

A

15-20 days until it is filtered by the kidneys

447
Q

Where does the second hydroxylation reaction occur if PTH is present?

A

At C1 on molecule in PCT of kidneys

448
Q

What does D3 bind to in the blood?

A

Transcalciferin

449
Q

How does the first hydroxylation reaction in vitamin D activation affect the half life of the molecule?

A

Extends it to ~2 weeks

450
Q

What enzyme catalyses conversion of calcitriol in the PCT?

A

1-alpha-hydroxylase a

451
Q

What is the half life of calcitriol?

A

0.25 days

452
Q

Why can the pre-vitamin in vitamin D activation be filtered by the glomerulus?

A

Bound to carrier small enough

453
Q

What regulates C1 hydroxylation in vitamin D activation?

A

Negative feedback from serum calcium levels

454
Q

What effect does high PTH have on C1 hydroxylation?

A

Stimulators

455
Q

What action does calcitriol have in the gut?

A

Active uptake and extrusion of calcium ions
Transcellular transport
Endocytosis and exocytosis of calcium-CaBP complex

456
Q

What action does calcitriol have on bone?

A

Stimulates osteoclast formation from haemopoietic stem cells

457
Q

What affect does calcitriol have on the kidney?

A

Stimulates calcium reabsorption

458
Q

What abolished rickets in the UK during WWII?

A

Adding calcium carbonate to flour and vitamin D to margarine

459
Q

What secretes calcitonin?

A

Sporadic parafollicular cells or C cells of thyroid gland

460
Q

What is the importance of calcitonin in pregnancy?

A

May have role in protecting maternal skeleton

461
Q

Does thyroidectomy in humans demonstrate a marked calcium level affect?

A

Nope

462
Q

What are the S/S of hypocalcaemia?

A 
Hyper excitability of NMJ so:
Pins and needles
Tetany
Paralysis
Convulsions
Death
463
Q

What is the normal response to hypocalcaemia?

A

Increase osteoclast activity and increase C1 hydroxylation in vitamin D activation

464
Q

What is rickets?

A

Filature to mineralise long bones leading to deformity as skeleton is sacrificed to maintain serum calcium

465
Q

What are the S/S of rickets?

A 
Head soft spot slow to close
Bony necklace
Curved long bones
Big lumpy joints
Bowed legs
466
Q

What happens in accidental surgical removal of the parathyroid?

A

PTH deficiency causing life threatening hypocalcaemia with rapid onset as PTH is the rapid modulator of serum calcium levels –> convulsions of respiratory system = death

467
Q

What are the S/S of hypercalcaemia?

A 
Renal canaliculi
Kidney damage
Constipation
Dehydration
Tiredness
Depression 
(Stones, moans and groans)
468
Q

What is the normal response to hypercalcaemia?

A

Decrease osteoclast activity

Inhibit transcellular absorption of calcium

469
Q

Is calcitonin used in the normal response to hypercalcaemia?

A

No

470
Q

How is hypercalcaemia treated?

A

Fluids to restore blood volume

Remove causative tumour (likely benign)

471
Q

What do you have to do before you can remove a benign tumour of the parathyroid gland?

A

Find the glands (they can be anywhere in the thorax)

472
Q

What can cause hypercalcaemia?

A

Over secretion of PTH from primary hyperoarathyroidism

PTH analogue secreted from various tumours

473
Q

Is phosphate regulated as tightly as calcium?

A

No

474
Q

What normal activity gives the human body a classic stress response?

A

Exercise

475
Q

What just the body do in order to adapt to exercise?

A

Meet acute oxygen append metabolite needs of muscles
Dispose of carbon dioxide and other metabolic waste
Minimise disturbances to other physiological systems

476
Q

What is the metabolic whole body response to exercise?

A

Mobilise stored fuels at a rate that matches the increased activity whilst preserving blood glucose levels to protect the brain

477
Q

What effects the body’s metabolic response to exercise?

A

Type of exercise - muscles used
Intensity
Duration
Physical condition and nutritional state of individual

478
Q

Why is a muscle store of glycogen needed in a 100 m sprint?

A

To help spare blood glucose as extra glucose cannot be delivered fast enough

479
Q

How is ATP created once phosphate stores have been used up in a 100m sprint?

A

Anaerobic glycolysis

480
Q

How is energy supplied in a 1500m race?

A

40% anaerobic as some oxygen can be delivered but not enough

Aerobic can use FA and glucose

481
Q

How much energy is needed in total for a 100m sprint, a 1500m race and a marathon respectively?

A

30 kJ
500 kJ
10,000 kJ

482
Q

How is energy supplied in a marathon?

A

At least 95% aerobic

Muscle and liver glycogen and FA

483
Q

Describe the timeline of energy usage during a marathon.

A

Muscle glycogen deleted in mins
Glucose from liver glycogen peaks after ~1 hour and steadily declines
After 20-30 mins use FA in addition

484
Q

What are the very short term stores of energy for muscle contraction?

A 
ATP
Creatine phosphate (using creatine kinase)
485
Q

What does muscle glycogen produce without using ATP which can be metabolised anaerobically?

A

Glucose-6-phosphate

486
Q

Why is muscle glycogen available when blood flow is limited?

A

Located within muscle fibres so doesn’t need to cross CSM

487
Q

What limits the capacity of FA usage in providing energy for exercise?

A

Albumin levels in blood

Carnitine shuttle transporting molecules across mitochondrial membrane

488
Q

Describe the aerobic and anaerobic metabolism balance in exercise > 20 mins.

A

0-30 s = 95% anaerobic
2-4 mins = 40-50% anaerobic
>20 mins = 5% anaerobic

489
Q

Describe the phases of response in the initial sprint, long middle section and finishing sprint of running a race.

A

Initial sprint: ATP and creatine phosphate
Long middle: glycogen and FA by aerobic metabolism
Finishing sprint: glycogen by anaerobic mechanism

490
Q

What is needed in order to mobilise energy reserves during exercise?

A

Insulin to increase the number of GLUT4 to move glucose into muscle cells

491
Q

How does glucagon stimulate glycogenolysis in the liver?

A

Stimulates glycogen phosphorylase phosphorylation

492
Q

Remembering that exercise causes a stress response, what other hormone can stimulate glycogenolysis in the liver by the Salem mechanism as glucagon?

A

Adrenaline

493
Q

How do hormones change over the course of running a marathon?

A

Insulin decreases slowly
Glucagon increases
Adrenaline and growth hormone increase rapidly
Cortisol increases slowly

494
Q

What is the action of rapid increase of growth hormone levels when running a marathon?

A

Increases lipolysis which mobilises FA

495
Q

How does cortisol stimulate gluconeogenesis if exercise is long duration?

A

Increases PEPCK and fructose-1,6-bishopshate activity

496
Q

What are the benefits of exercise?

A 
Improve muscle sensitivity to insulin - improve glucose tolerance
Better balance of lean tissue and fat
Lower blood lipids
Lower blood pressure
Lower HR for given cardiac output
497
Q

What are the benefits of exercise to skeletal muscle?

A 
More and bigger fibres
Better FA oxidation capacity
Increased glucose transport capacity
More myoglobin for oxygen storage
More capillaries
Increased glycogen
498
Q

Why is reorganisation of maternal metabolism in pregnancy necessary?

A

So there is a higher concentration of energy and raw materials in maternal circulation so they can diffuse passively and via carrier proteins down a concentration gradient to the developing foetus

499
Q

What is the usually weight gain in pregnancy and how much of this is attributed to energy stores?

A

8-10 kg of which ~3 kg is energy

500
Q

When do maternal energy stores accumulate?

A

First 20 weeks of pregnancy

501
Q

When are maternal stores at their highest?

A

Later pregnancy and during lactation

502
Q

What is the development of maternal stores under?

A

Reproductive hormones mainly from the placenta w/some contribution from the ovaries until the 12th week of pregnancy

503
Q

How does the placenta supersede maternal HPA?

A

Ability to secrete just about every hormone

504
Q

How is the foetus adapted to take over maternal metabolism to ensure its own survival?

A

Via the placenta

505
Q

How are stores built in the first 20 weeks of pregnancy?

A

Stimulus to appetite (also go off harmful foods)
Increased action of insulin in storage tissues
Decreased action of insulin in tissues which use energy

506
Q

Describe the hormone balance in the early half and second half of pregnancy.

A

Early half = insulin dominant

Second half = anti-insulin dominant

507
Q

How do the reproductive steroids enable energy store building during pregnancy?

A

High levels increase sensitivity of beta-cells to blood glucose and increase appetite so more glucose is ingested and there is a specific effect on calorific foods

508
Q

What do the high levels of oestrogens and progesterone sin pregnancy cause in beta-cells?

A

Hyperplasia
Hypertrophy
Increased basal and stimulated insulin synthesis

509
Q

What affect do oestrogens and human placental lactogen have in muscle due to their anti-insulin properties?

A

Make it resistant to insulin

510
Q

What is oestriol?

A

Oestrogen in placenta

511
Q

Where is progesterone secreted from during pregnancy?

A

Ovary their high quantities by placenta

512
Q

What happens to blood glucose levels in pregnancy despite the higher insulin levels?

A

They are higher in average, especially after meals

513
Q

What is the advantage of having elevated blood glucose during pregnancy?

A

Increases glucose gradient so it easier to move across placenta as well as driving into adipose tissue for storage

514
Q

What happens in gestational diabetes?

A

Beta-cells do not respond regularly to increased insulin secretion and blood glucose is seriously elevated as extra demand for glucose is met but not controlled

515
Q

How common is gestational diabetes?

A

Affects 3-10% of pregnancies

516
Q

What are the consequences of gestational diabetes?

A

Maternal effects of hyperglycaemia
Macrosomia (fat baby) w/lots of liver and muscle glycogen
Difficult delivery

517
Q

Why do you always screen a pregnancy after 24 weeks for gestational diabetes?

A

Takes a while to develop so may present late and could require C-section

518
Q

What is the treatment for gestational diabetes?

A

Careful short-term insulin

519
Q

What are the possible sequelae of gestational diabetes?

A

Normally corrects after placental delivery

Can result in T2DM

Semester 1 (7 decks)

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