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Physiology 1B > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What are the different types of hormones action?

A

Endocrine- cells release hormones from vesicles which then are secreted into the blood where they travel to tissues far away
Paracrine- hormones released act on nearby cells in same tissue
Autocrine- hormones released act on receptors on the same cell

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2
Q

What are hormones?

A

Chemical messengers of the endocrine system

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3
Q

How do hormones circulate in the body?

A

Either free or bound to binding protein

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4
Q

What is the purpose of binding proteins to hormones?

A

Provide reservoir of hormone to avoid fluctuations
Extend hormone life
Allow insoluble hormones to circulate

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5
Q

How are peptide hormones produced and what are some examples?

A

Protein sysnthesis in endocrine cells, often produced as prohormones/inactive precursors and then processed into active form
Insulin, oxytocin

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6
Q

What are steroid hormones derived of and what are some examples?

A

Cholesterol

Cortisol

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7
Q

How do peptide hormones act on target cells?

A

At cell surface receptor causing downstream signalling within a cell

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8
Q

How long to peptide hormone responses take?

A

Seconds to minutes

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9
Q

How to steroid hormones act on target cells?

A

At cytoplasmic or nuclear receptors
Circulate with binding protein due to being hydrophobic then are released through cell membrane alone due to being lipophilic
Cause regulation of gene transcription

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10
Q

How long do steroid hormone responses take?

A

Hours-days

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11
Q

How are hormone releases regulated?

A

Feedback mechanisms- negative feedback loops
Tropic hormones- stimulate release of another hormone from other endocrine glands
Neuronal control- neuronal stimulation causes stimulation or inhibition of hormone release

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12
Q

Describe the structure of the hypothalamus pituitary organ axis

A

Hypothalamus contains neuroendocrine cells
Posterior pituitary is continuous with hypothalamus so is neuronal and glandular
Anterior pituitary is only glandular and connects to hypothalamus by the hypophyseal portal circulation

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13
Q

How does the hypothalamus signal via the anterior pituitary?

A

Neuroendocrine cells release hypothalamic hormone into hypophyseal portal circulation
Hypothalamic hormone hormone binds to glandular cells in anterior lobe which secretes anterior lobe hormone into circulation

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14
Q

Explain how the hypothalamus signals via the posterior pituitary

A

Neuroendocrine cells secrete posterior lobe hormone into posterior lobe which enters the general circulation

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15
Q

What is the importance of the hypothalamus?

A

Focus point of information on internal wellbeing and produce hormones in response to changes

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16
Q

What is neuroendocrine function in the hypothalamus?

A

Neuroendocrine cells reside in nuclei in hypothalamus and detect levels on circulating hormones, metabolites, nutrients and electrolytes
Also respond to physiological stimuli such as stress and pain

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17
Q

What is the role of oxytocin?

A

Cause uterine contractions in labour and let down milk in lactation

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18
Q

What is the role of antidiuretic hormone?

A

Changing the rate of water reabsorption in the kidney

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19
Q

Explain the structure of the thyroid gland cells

A

Follicles with colloid/viscous proteinated centre surrounded by follicular/cuboidal epithelium

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20
Q

How are thyroid hormones synthesised?

A

Derived from tyrosine amino acid and incorporates iodine in the thyroid epithelial cell

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21
Q

Where does the tyrosine amino acid come from for thyroid hormone synthesis?

A

In polymer thyroglobulin

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22
Q

What are the two different thyroid hormones?

A

T4- thyroxine

T3- triiodothyronine

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23
Q

What is the features of T3?

A

Cause most physiological effects
Active receptor affinity
Loosely bound to protein in circulation

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24
Q

What are the features of T4?

A

Most of hormone released by thyroid gland
Less active receptor affinity
Tightly bound to protein in circulation
Acts as a pool for T3 as is converted to T3 in tissues

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25
Q

How does thyroid gland morphology change with activity of gland?

A

Unstimulated gland- cuboidal epithelium with follicles full of colloid
TSH stimulated- columnar epithelium with follicles collapsed due to increased colloid uptake for T3 and T4 production

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26
Q

How do thyroid hormones act on target cells?

A

Thyroid hormones diffuse or move through transporter into cell
Most T4 is converted to T3 by removal of one iodine
T3 diffuses into nucleus and binds to thyroid hormone receptor
Thyroid hormone receptor binding to promotor elements activate gene transcription and protein production

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27
Q

What systems do thyroid hormones cause affect on the body?

A

Normal childhood growth and critical CNS development
Cardiovascular
Basal metabolic rate

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28
Q

What is the cardiovascular effects of thyroid hormones?

A

Increased manufacture and incorporation of beta 1 adrenergic receptors causing increased responsiveness and sets sensitivity of heart to adrenaline and noradrenaline
Long term sensitivity of cardiac cells regulated by plasma levels of TH

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29
Q

What are the effects of thyroid hormone on basal metabolic rate and how does it happen?

A

Most important action
Increases basal metabolic rate
Oxidative metabolism increased in most cells as increased Na-K pump activity which uses more energy
Stimulates anabolic and catabolic reactions regarding fat, protein and carbohydrates
Stimulates protein synthesis
More glucose available and lipid metabolism for increased metabolic demand`

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30
Q

What is hypothyroidism and how is is caused?

A

Underproduction of TH

Caused by iodine deficiency or hashimotos disease (autoimmune destruction of thyroid cells)

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31
Q

What are the symptoms of hypothyroidism?

A 
Weight gain
Decreased metabolic rate
Low appetite
Cold intolerance
Mental sluggishness
Fatigue
Low cardiac output
Low force and rate of contraction
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32
Q

How is hypothyroidism treated?

A

Increased iodine

Replacement thyroid hormone

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33
Q

Why does the thyroid gland enlarge in hypothyroidism?

A

No T3 or T4 formation so no feedback control of TSH

TSH high which continues stimulation of production of thyroglobulin

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34
Q

What is hyperthyroidism and how is it caused?

A

Overproduction of thyroid hormone

Graves disease or follicular cell tumours

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35
Q

What are the effects of hyperthyroidism?

A 
Goiter
Increased metabolic rate
Weight loss
Nervousness
Irritability
Sleeplessness
Fatigue
Heat intolerance
Increased force and rate of heart contractions
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36
Q

What is graves disease?

A

Thyroid stimulating immunoglobulin produced which binds to TSH receptor
Triggers overstimulation of thyroid increasing T3 and T4 synthesis

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37
Q

How is graves disease treated?

A

Antithyroid drugs
Thyroidectomy
Radioactive iodine to kill some thyroid cells

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38
Q

What is growth?

A

Increase in cell size/hypertrophy or increase in cell number/hyperplasia

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39
Q

How is growth controlled?

A

Hormones and growth factors to provide fuel and cell components

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40
Q

When is somatostatin released for growth hormone release inhibition?

A

Increases blood glucose
Increased free fatty acids
Obesity
Aging

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41
Q

When is growth hormone releasing hormone released for growth hormone release stimulation?

A 
Decreased blood glucose
Decreased free fatty acids
Starvation
Protein deficiency
Trauma
Stress
Excitement
Sleep 
Exercise
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42
Q

What is meant by dimal and pulsatile release of growth hormone?

A

Dimal- increased GH release in sleep

Pulsatile- pulses release across the day

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43
Q

Why is pulsatile release important?

A

Helps maintain homeostatic balance needed for essential processes

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44
Q

Acute effects of growth hormone?

A

Reduced lipogenesis and fat storage
Reduced glucose uptake and oxidation
Increased gluconeogenesis and glycogenolysis
Increased blood glucose
Increased amino acid uptake and protein synthesis
Reduced protein catabolism

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45
Q

What are the long term effects of growth hormone?

A

Causes insulin like growth factor 1 release from liver which mediates local growth

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46
Q

Explain the causes and effects of excess growth hormone

A

Causes- pituitary tumours

Giantism in childhood and acromegaly in adults

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47
Q

Explain the symptoms and causes of acromegaly

A

Symptoms- soft tissue swelling, generalised skull expansion

Causes- insulin resistance

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48
Q

What is the effect of growth hormone defecit?

A

Dwarfism- short stature in appropriate proportions, delayed maturation

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49
Q

What are the causes of growth hormone defecit?

A

Pituitary tumour

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50
Q

Explain what gene therapy is and what is its effects

A

Injections of recombinant hGH to increase muscle mass, bone density and decrease body fat
Doesn’t increase strength, functionality or performance
Can cause complications such as diabetes, hypertension and can increase cancer risk

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51
Q

What are the layers of the adrenal glands?

A

Cortex- glomerulosa, fasciculata and reticularis

Medulla

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52
Q

What does each layer of the adrenal glands produce?

A

Glomerulosa- mineralocorticoids
Fasciculata- glucocorticoids
Reticularis- androgens and oestrogens
Medulla- adrenaline/noradrenaline

53
Q

What is the precursor for adrenal steroid synthesis and where is is acquired and stored?

A

Cholesterol

Acquired from GI tract or synthesised from acetate and stored in cortical cells

54
Q

How do steroid hormones cause effect?

A

Act on cytoplasmic receptors in target tissues then translocates to nucleus where it modulates gene transcription of certain genes to cause protein synthesis to cause effect

55
Q

What are the features of cortisol?

A

Hydrophobic so circulate bound to plasma protein

60-90 minute half life

56
Q

What controls the release of glucocorticoids?

A

Tropic hormones and circadian release

57
Q

What systems do glucocorticoids effect in the body?

A

Metabolic
Muscular
Nervous system
Inflammatory and immune response

58
Q

How do glucocorticoids effect metabolism?

A

Stimulates gluconeogenesis and inhibits effects of insulin so decreased tissue uptake of glucose
Stimulates protein catabolism causing gluconeogenesis
Increased lipolysis in times of stress or starvation
Hyperglaecaemia

59
Q

How does glucocorticoid insufficency effect cardiac, smooth and skeletal muscle?

A

Muscle fatigue
Cardiac insufficiency
Loss of vasomotor tome
General muscle weaknedd

60
Q

What is the effect of different levels of glucocorticoids on nervous system?

A

Excess- hyperactivity, insomnia, euphoria, increased sensory activity
Insufficiency- lethargy, apathy, lack of concentration

61
Q

How do glucocorticoids effect inflammatory and immune responses?

A

Inhibit cytokine secretion, immune cell proliferation and antibody synthesis
Increase susceptibility for infections

62
Q

What is an example of a glucocorticoid?

A

Cortisol

63
Q

What is an example of mineralocorticoids?

A

Aldosterone

64
Q

What are the features of aldosterone?

A

Bound to plasma protein

15-30 minute half life

65
Q

What is the role of aldosterone?

A

Regulate Na+ and K+ concentration in ECF

66
Q

What stimulates release of aldosterone?

A

Changes in electrolyte and water balance

67
Q

How are glucocorticoids used therapeutically?

A

Anti-inflammatories
Anti-allergic
Immunosuppression

68
Q

Why do you need to be weaned off therapeutic glucocorticoids?

A

Withdrawal can cause hypocorticism as synthetic steroids reduce natural cortisol so the gradual decrease allows natural cortisol levels to build back up

69
Q

What diseases are associated with hypercortisism and hypoadrenocorticism?

A

Hyper- cushings disease

Hypo- addisons disease

70
Q

What are the different types of hypercortisism?

A

Primary- adenoma of adrenal cortex causing uncontrolled production of cortisol
Secondary- pituitary tumours causing uncontrolled ACTH so uncontrolled cortisol production
Latrogenic- widespread synthetic cortisol use

71
Q

What are the symptoms of hypercortisism?

A 
Upper body obesity
Round face
Extra neck fat
Thin skin
Weak bones
Hyperglycaemia
72
Q

What are the different types of hypoadrenocortisism?

A

Primary- autoimmune attack causing atrophy of adrenal cortex
Secondary- pituitary mutation
Latrogenic- abrupt withdrawal from steroid therapy

73
Q

What are the symptoms of hypoadrenocortisism?

A

Muscle weakness
Poor CV function
Low blood pressure

74
Q

What hormones are known as catecholamines?

A

Adrenaline and noradrenaline

75
Q

What do catecholamines act on?

A

Receptors on adipose and pancreatic tissue and the CNS

76
Q

How are adrenergic receptors for catecholamines regulated?

A

Affinity
Concentration of receptor
Receptor signalling and activation of second messengers

77
Q

How are catecholamines secreted?

A

Adrenaline produced in adrenal medulla
Noradrenaline synthesised by chromaffin cells and noradrenergic receptors
Both produced by tyrosine undergoing enzymatic changes
Stored in granules until release on demand

78
Q

What is hyperfunction of adrenal medulla?

A

Pheochromocytes are tumours arising from chromaffin cells, benign but secrete large quantities of catecholamines causing increased blood pressure and heart rate

79
Q

What are the effects of glucose imbalance?

A

Excess- dehydration, microvascular damage such as blindness

Deficiency- CNS function effected as heavily glucose dependent

80
Q

What are the two stages of glucose metabolism?

A

Anabolic

Catabolic

81
Q

Explain the anabolic stage of glucose metabolism

A

Starts at food ingestion and several hours after
Caloric intake exceeds caloric demand
Plasma glucose levels increase
Energy gets stored

82
Q

Explain the catabolic stage of glucose metabolism

A

4-6 hours after food intake
Caloric demand exceeds caloric intake
Plasma glucose decreases
Endogenous fuel mobilised from the liver, muscle and adipose and stored anabolic fuel released

83
Q

Define glycogenesis

A

Glucose to glycogen which gets stored

84
Q

Define glycogenolysis

A

Glycogen to glucose which is released into blood

85
Q

Define glycolysis

A

Glucose to pyruvate

86
Q

Define gluconeogenesis

A

Pyruvate to glucose

87
Q

Which type of islet of langerhans cells produce which hormone

A

Alpha- glucagon

Beta- insulin

88
Q

What do insulin and glucagon do?

A

Insulin- stores fuel in anabolic phase

Glucagon- mobilises fuel in catabolic phase

89
Q

Describe key features of insulin

A

Peptide hormone
Receptor is receptor tyrosine kinase
Mainly targets liver, muscle and adipose

90
Q

What stimulates insulin secretion?

A

Glucose, GI hormones and parasympathetic nerves which are activated on eating

91
Q

What inhibits insulin release?

A

Sympathetic nervous system

92
Q

What is the action of insulin of the blood?

A

Reduces glucose, amino acid and fatty acid levels

93
Q

What is the action of insulin on the liver?

A

Binds to insulin receptor on target tissue when glucose enters hepatocyte
Glucose storage is increased due to increased glycogenesis and glycolysis and decreased gluconeogenesis
Lipogenesis increases so more fatty acids converted to lipid storage
Proteogenesis increased so more proteins are formed from amino acids

94
Q

What is the effect of insulin on muscles?

A

Binds to receptor activating GLUT4 to insert into membrane so more glucose can enter the cell
Increased glucose storage from increased uptake, glycolysis and glycogenesis
Increased amino acid uptake and proteogenesis

95
Q

What is the effect of insulin on adipose?

A

Increased glucose removal from the blood due to increased uptake and glycolysis
Increased fatty acid synthesis
increased lipogenesis

96
Q

What is the main regulator of glucagon concentration?

A

Glucose concentration as glucose inhibits glucagon

97
Q

Describe the action of glucagon?

A

Liver is main target
Increases glucose output by increased glycogenolysis and gluconeogenesis
Increases lypolysis by increasing fatty acids and ketone bodies to be used as fuel by muscles and CNS when glucose low

98
Q

What are regulators of blood glucose, not insulin or glucagon?

A

Growth hormone
Glucocorticoids
Adrenaline

99
Q

How does growth hormone regulate blood glucose?

A

Inhibition of insulin induces glucose utilisation
Inhibits lipogenesis and glucose uptake in adipose
Increases glycogenolysis and gluconeogenesis but protects protein
Increased blood glucose

100
Q

How do glucocorticoids regulate blood glucose?

A

Protects from hypoglycaemia during stress
Stimulates gluconeogenesis and enhances glucagon and adrenaline
Inhibits effects of insuline

101
Q

How does adrenaline regulate blood glucose?

A

Maintains glucose supply to the brain
Stimulates liver gluconeogenesis and glycogenolysis
Stimulates adipose lipolysis

102
Q

What are the two types of diabetes?

A

Type 1- autoimmune disease destroying beta cells so are unable to produce insulin
Type 2- reduced beta cell function or insulin resistance in target cells

103
Q

What are the symptoms of diabetes?

A 
Dehydration
Thirst
Excessive urination
Tiredness
Weightloss
Hunger
Ketoacidosis
104
Q

How does type 1 diabetes work?

A

Beta cells produce little or no insulin so high blood sugar but low glucose uptake
Glucagon breaks down fat, glycogen and proteins further increasing blood glucose
Glucose and ketone produced in huge excess causes high blood osmolality
Ketoacidosis and osmotic stress causes dehydration and glucosuria

105
Q

How is type 2 diabetes caused?

A

Insulin resistant target tissues or impaired beta cell function

106
Q

What are the treatments for diabetes?

A

Type 1- therapeutic insulin and glucose monitoring

Type 2- diet and exercise management, insulin when required

107
Q

What are the roles of calcium in the body?

A 
Component of skeleton and teeth
Muscular contraction
Blood coagulation
Enzyme activity
Neuronal excitability
Hormone secretion
108
Q

Where is calcium stored in the body?

A

99%- inorganic mineralised matrix of bone as hydroxyapatite
0.9%- endoplasmic reticulum
0.1%- extracellular fluid
Tiny amount free in cytosol

109
Q

How is calcium stored in ECF?

A

50%- biologically active ionised Ca2+
5%- calcium salts
45%- protein bound

110
Q

Which storage of calcium is regulated in the body?

A

ECF

111
Q

How does Ca2+ act as a regulatory ion?

A

ECF has huge concentration compared to cytosol
Ca2+ influx into cytoplasm is controlled by Ca2+ ion channels so Ca2+ can act as signalling ion to activate intracellular processes

112
Q

What are the 3 hormones that regulate calcium homeostasis?

A

Parathyroid hormone
Active vitamin D
Calcatonin

113
Q

What are the main tissues involved in calcium regulation?

A

Gut
Bone
Kidneys

114
Q

What is the parathyroid hormone and why and where is it released?

A

Peptide hormone
Released in response to falling circulating levels of calcium
Parathyroid gland (4 on dorsal aspect of thyroid gland)

115
Q

How is parathyroid secretion controlled?

A

Stored in secretory granules of chief cells

Release is regulated by circulating concentration of calcium with low calcium promoting secretion

116
Q

What is the slow and fast exchange effect on bone of the parathyroid hormone?

A

Slow- bone dissolution from osteoblast activity

Fast- release from bone fluid labile pool

117
Q

How does the fast exchange in bone work regarding the parathyroid hormone?

A

Parathyroid hormone activates pathways to increase Ca2+ channels
Allows calcium management in and out of circulation

118
Q

What is active vitamin D?

A

Steroid produced from cholesterol or acquired in the diet

119
Q

When is active vitamin D produced?

A

In response to falling levels of blood calcium via parathyroid hormone

120
Q

What are the actions of active vitamin D?

A

Longer term Ca2+ regulation
Increased absorbtion of Ca2+ from intesting so more Ca2+ can be stored in bone to protect it
Supports protein synthesis of Ca2+ channels, pumps and exchangers

121
Q

What is calcitonin and how and where is it released from?

A

Peptide hormone

Released rapidly in response to high blood Ca2+ from C cells in thyroid gland

122
Q

What is the role of calcitonin?

A

Reduce blood Ca2+ and prevent hypercalcaemia
Target bone and kidneys primarily to inhibit bone resorption and ca2+ absorption in kidneys
Acts as emergency hormone to prevent excess loss from skeleton in pregnancy

123
Q

What disorders are associated with calcium homeostasis?

A

Rickets/osteomalacia
Hyperparathyroidism
Hypoparathyroidism

124
Q

What are the causes and effects of rickets?

A

Causes- diet deficient in vitamin D, lack of sunlight and lack of renal 1 alpha hydroxylase
Effects- un mineralised cartilage, weak bones

125
Q

What is hyperparathyroidism?

A

Excessive parathyroid hormone

126
Q

What are the two types of hyperparathyroidism?

A

Primary- unregulated excessive parathyroid released

Secondary- chronic renal failure causing excess parathyroid hormone secretion

127
Q

What is hypoparathyroidism?

A

Inadequate parathyroid hormone secretion

128
Q

Describe how calcium ions can act as signalling receptors

A

Influx of Ca2+ into cells
Cellular function regulated by interaction with intracellular calcium binding proteins and calcium sensitive protein kinases
Biological response triggers

Physiology 1B (4 decks)

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