Endocrine system Flashcards

1
Q

How does endocrine transmission occur

A

Chemical secreted​

Low concentration​

By a cell or group of cells​

Sent to all parts of body​

Via blood stream​

Hormone acts only in cells with correct membrane receptor protein (target cells)​

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2
Q

What are the properties of hormonal communitcation

A

Many cells in different parts of body​

Coordinated, body-wide actions​

Slow to act​

Effect persists

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3
Q

What are the endocrine glands in the body

A

Hypothalamus​
Pituitary​
Thyroid​
Parathyroid​
Pancreas (Islets)​
Adrenal (supra-renal)
GI tract endocrine cells​
Gonads (ovaries and testes)​
Placenta​
Pineal gland​
Thymus

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4
Q

How can hormones be classified

A

Steroids​

Non-steroids​
-Amino acid derivatives​
-Peptides​
-Glycoproteins

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5
Q

What are some steroid hormones

A

Based on cholesterol ring structure
-Cortisol​
-Aldosterone​
-Testosterone​
-Oestrogen​
-Progesterone

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6
Q

What are some non-steroid amino acid derivative hormones

A

Amines​
-Adrenaline (epinephrine)​
-Noradrenaline (norepinephrine)​
-Melatonin​

Iodinated amino acids​
-Triiodothyronine​
-Tetraiodothyronine (thyroxine)

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7
Q

What are some non-steroid short chain peptide hormones

A

Antidiuretic hormone​
Oxytocin​
Melanocyte stimulating hormone​
Somatostatin

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8
Q

What are some non-steroid long chain peptide proteins

A

Growth hormone​
Prolactin​
Parathyroid hormone​
Calcitonin

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9
Q

Where is the pre-prohormone converted to prohormone

A

Endoplasmic reticulum

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10
Q

Where is prohormone packaged

A

Golgi apparatus

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11
Q

What is prohormone converted to

A

Active hormone

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12
Q

What secretes active hormone

A

Vesicles

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13
Q

What are glycoproteins

A

Protein with attached carbohydrate groups to amino acids

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14
Q

What are some non-steroid glycoprotein hormones

A

Follicle stimulating hormone​
Luteinizing hormone​
Thyroid stimulating hormone​
Chorionic gonadotrophin

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15
Q

What hormone-like substances have a local (paracrine) effect

A

Prostagrandins​

Leucotrienes​

Thromboxanes

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16
Q

What are the functions of local effect hormones

A

Blood flow regulation​

Haemostasis​

Mucosal protection (stomach)​

Inflammation

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17
Q

What are common second messengers

A

cAMP and Ca2+

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18
Q

Where are hormones metabolised

A

Liver

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19
Q

What is hypersecretion

A

Excess secretion

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20
Q

What is hyposecretion

A

Decreased secretion

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21
Q

What is upregulation

A

More receptors

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22
Q

What is downregulation

A

Fewer receptors over time

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23
Q

What occurs during hyperfunction

A

Excess production & secretion​

Upregulation of receptors​

Failure to metabolise hormone

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24
Q

What occurs during hypofunction

A

Decreased production & secretion​

Downregulation of receptors​

Receptors non functioning

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25
Q

Can prohormone produce response

A

Yes - much less of a response

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26
Q

Why do we have prohormone and the hormone if they can both produce a response

A

Prohormone produces a much lesser response allowing the hormone to be stored in concentrations which would otherwise be dangerous in the full hormone

i.e. Insulin would be too dangerous to store in high conc as if it was released unnecessarily this could be fatal to the person

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27
Q

What are the sections of the pituitary gland

A

Anterior pituitary
Posterior pituitary
Infundibulum

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28
Q

What does the hypothalamus control

A

Thermoregulation​

Hormone secretion​
-Primary hormones​
-Trophic hormones​

Circadian rhythms​

Motivation​
-Thirst, feeding, sexual behaviour​

Emotions

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29
Q

What causes hormones secretion from the anterior pituitary

A

Releasing hormones are produced in the hypothalamus which pass to the anterior pituitary via hypothalamic-pituitary portal vessels and trigger secretion of hormones from the AP

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30
Q

How do hormones in the hypothalamus pass to the PP

A

Nerve axons

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31
Q

What are some hypothalamic hormones

A

Corticotropin releasing hormone (CRH)​

Gonadotrophin releasing hormone (GRH)​

Thyrotropin releasing hormone (TRH)​

Growth hormone releasing hormone (GHRH)​

Somatostatin (SS) (GH inhibiting hormone)​

Prolactin releasing hormone (PLRH)​

Dopamine (DA) (also PLIH)

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32
Q

What anterior pituitary hormones would you expect to find

A

Adrenocorticotropic hormone (ACTH)​

Follicle stimulating hormone (FSH)​

Luteinising hormone (LH)​

Thyroid stimulating hormone (TSH)​

Growth hormone (GH)​

Prolactin (PL)

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33
Q

How many hormones are involved in creating an action to resolve a stimulus

A

3
hypothalamus - 1
Anterior pituitary gland - 2
Target organ - 3

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34
Q

How will the body react to ‘stressors’

A

Hypothalamus- Corticotropin RH
AP - ACTH
Adrenal cortex - Cortisol

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35
Q

What controls the release of FSH and LH

A

Gonadotrophins

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36
Q

What hormons stimulates testosterone production and ovulation production of oestrogen & progesterone

A

LH - luteinising hormone

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37
Q

What does FSH stimulate

A

Sperm production and ovum maturation, oestrogen production

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38
Q

What does thyrotrophins release

A

Thyrotropin
Thyroid stimulating hormone
Thyroid hormones

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39
Q

What are somatotrophins

A

Growth hormones RH and IH both released from hypothalamus which lead to the release of growth hormone at the APG

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40
Q

What does the release of prolatin stimulate

A

Breast development and milk production

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41
Q

How is Prolactin released

A

Prolatin RH is produced in the hypothalamus leading to the release of Prolactin in the APG

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42
Q

What hormones are released in the PP

A

Antidiuretic hormone (ADH)
Oxytocin

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43
Q

Where asre ADH and oxytocin produced initially

A

These are produced by neurons in the hypothalamus and pass along the axons to the posterior part of the pituitary​

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44
Q

Which nucleus produces ADH

A

Paraventricular

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45
Q

Where is oxytocin produced

A

Supraoptic nucleus

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46
Q

What are the steps to releasing ADH

A

Stimulus
Hypothalamus - ADH axonal transport
PPG - ADH in plasma
Kidney - Water reabsorbed in collecting ducts

47
Q

What stimulus lead to release of oxytocin

A

Infant suckling and strech of uterus

48
Q

What action does the release of oxytocin into plasma promote when stimulated by the stretch of uterus

A

Contraction of uterus

49
Q

What does infant suckling encourage when oxytocin is released

A

Milk ejection

50
Q

What are some endocrine glands

A

Thyroid gland​

Parathyroid glands​

Pancreas (Islets of Langerhans)​

Adrenal (suprarenal) glands​

Gonads: ​
-ovaries​
-testes​

Placenta

51
Q

What hormones does the thyroid gland produce

A

Thyroid hormones T3, T4
Calcitonin

52
Q

What produces calcitonin

A

C cells

53
Q

What are the actions of T3 and T4

A

Increase metabolic rate of all cells​

Determines basal metabolic rate​

Essential for normal fetal and childhood growth​

Permissive effect on action of adrenaline by upregulating adrenoreceptors

54
Q

What is the name of T4

A

tetra-iodo-thyronine (‘thyroxine’)

55
Q

What causes disorders of thyroid hormones

A

Undersecretion​
-Hypothyroidism​
-Cretinism, Myxoedema​

Oversecretion:​
-Hyperthyroidism​
-Grave’s disease

56
Q

What are the symptoms of simple goitre

A

Thyroid swelling associated with iodine deficiency​

Low levels of thyroxine result in increased secretion of TSH​

Iodide added to salt

57
Q

What hormones do islets of langerhans produce

A

Insulin
Glucagon
Somatostatin

58
Q

When is insulin released

A

In response to raised [blood glucose], [amino acid], glucose-dependent insulinotropic peptide, vagus nerve

59
Q

What does insulin promote the formation of

A

Glycogen​

triglycerides​

Facilitates protein synthesis

60
Q

Where does insulin facilitate glucose entry into

A

Muscle cells, adipocytes

61
Q

What factors inhibit insulin secretion

A

Adrenaline​

Sympathetic nerves​

somatostatin

62
Q

What factors promote insulin secretion

A

Increase Blood glucose​

Increase Blood amino acids​

Glucose-dependent, insulinotropic peptide​

Vagus nerve activity

63
Q

When is glucagon released

A

Released in response to low blood glucose concentration​

acts to raise blood glucose

64
Q

What are the actions of glucagon

A

Glycogenolysis in liver, ​

Gluconeogenesis in liver,​

Lipolysis and ketone synthesis

65
Q

What inhibits glucagon secretion

A

Insulin
Somatostatin

66
Q

What promotes insulin secretion

A

increased Blood glucose​

Increased Blood amino acids​

Cholecystokinin​

Autonomic nerve activity

67
Q

What are the clinical features of diabetes

A

Polyuria (increased urine production)​

Polydipsia (increased fluid intake; thirst)​

Glycosuria (glucose in urine)​

Diabetic neuropathy​

Skin and oral diseases, incl. periodontitis, xerostomia

68
Q

What is diabetes

A

Elevated blood glucose concentration​

Decreased glucose uptake by cells​

Metabolic changes​

Gluconeogenesis; lipolysis​

Two basic types

69
Q

What is type 1 diabetes

A

Insulin-dependent​

decreased Insulin secretion​

Destruction of beta-cells​

Autoimmune?​

10% of cases​

“Early” onset​

Insulin injections and diet

70
Q

What is type 2 diabetes

A

Insulin-independent​

Insulin levels “normal”​

Decreased target cell responsiveness to insulin​

Related to overweight​

“Late” onset​

Diet, oral hypoglycaemic agents

71
Q

What hormones does the adrenal glands secrete

A

Cortex hormones (‘corticosteroids’)
-aldosterone​
-cortisol​
-androgens
Medulla​

Modified sympathetic ganglion​
-adrenaline (epinephrine)

72
Q

What is cortisol

A

Glucocorticoid hormone​

Produced by cells of zona fasciculata of adrenal cortex​

Controlled by ACTH from Ant pituitary​

Actions:​
-Metabolic effects​
-Permissive effects​
-Anti-inflammatory, immunosuppressant

73
Q

What is aldosterone

A

Mineralocorticoid​

Produced by cells of zona glomerulosa​

Release controlled by the renin-angiotensin system

74
Q

What are the actions of aldosterone

A

promotes reabsorption of Na+ and H2O in kidney (DCT)​

Increases excretion of H+, K+

75
Q

What is the Renin-angiotensin-aldosterone system

A

Renin from the juxta-glomerular apparatus is used toconvert angiotensinogen to angiotensin 1 which is then converted to angiotensin 2 with angiotensin converting enzyme which moves to the adrenal cortex and increases the aldosterone released in turn increasing the Na+ reabsorption in cortical collecting ducts

76
Q

What are androgens

A

Gonadocorticoids from zona fasciculata and reticularis of adrenal cortex​

The main hormones are androgens, which contribute to growth and 2o sexual characteristics in boys and girls​

Pubertal growth spurt

77
Q

What does excess glucocorticoid cause

A

Cushing’s syndrome
-fat pads
-pendulous abdomen
-moon face
-thin skin
-poor wound healing
-poor muscle development
-striae
-bruisability with echymoses

78
Q

What may excess androgens cause

A

Adreno-genital syndrome
-Heavy arms and legs
-Hirsutism
-Androgenic flush
-Small breasts
-Baldness, receeding hairline
-Enlarged clitoris
-Male escutcheon

79
Q

What is the adrenal medulla

A

This is a modified sympathetic ganglion​

Controlled by pre-ganglionic sympathetic nerves ​

The cells mostly produce adrenaline​

Adrenaline release augments the action of the sympathetic nervous system

80
Q

What does adrenal insufficiency cause

A

Addison’s disease ​

Decreased adrenal function and reduced levels of adrenal hormones:​
-Glucocorticoids​
-Mineralocorticoids​

Very serious condition

81
Q

How do we lose and gain water

A

Gains​
Water ingested (food and drinks)​
Water formed in metabolism​

Losses​
Excretion: urine, faeces​
Evaporation: sweat, in expired air

82
Q

How much water approx do we lose via each process

A

Losses (ml/day)​
Urine (1500)​
Faeces (100)​
Evaporative sweat, breathing (800)​

Total = (2400)

83
Q

What is the only factor of water balance under homeostatic control

A

Urinary secretion

84
Q

What are the sections of a nephron

A

Glomerulus
Proximal convuluted tubule
Distal convuluted tubule
Loop of henle
Collecting duct

85
Q

What is the conc of renal blood flow

A

1200ml/min

86
Q

What is the function of the glomerulus

A

Filtration of plasma 120ml/min

87
Q

What are the variing filtration pressures within the glomerulus

A

Pressures vary along length of glomerular capillary from afferent arteriole - efferent arteriole)​

Capillary hydrostatic (blood) pressure 45-50mmHg​

Plasma protein oncotic pressure 25-35mmHg​

Capsular pressure 10mmHg​

Net filtration pressure 10-15mmHg

88
Q

What occurs in the proximal convoluted tubule

A

Obligatory reabsorption of 60 – 70% of the glomerular filtrate​

Ions, small organic molecules are reabsorbed​

Secretion of H+ (acid-base balance)​

Active transport; facilitated diffusion​

Relatively little control over what is reabsorbed

89
Q

What determines the conc of urine

A

The active transport pumps in the ascending limb of loop of henle

90
Q

What corrrelates wih the length of the loop of hele

A

Ability to conc urine

91
Q

Why do we have a loop of henle

A

Important for conc of urine
Some net reabsorption of fluid (10% of GFR)

92
Q

What occurs in the distal convoluted tubule

A

Reabsorption of water, Na+, Cl–, Ca2+
Secretion of H+, K+

93
Q

What hormones control the activity in the DCT

A

Aldosterone​

Atrial natriuretic hormone​

ADH (in most distal parts) ​

Parathyroid hormone

94
Q

What is metabollic acidosis

A

When acids build up in the body fluids (too many H+ ions)

95
Q

What is the purpose of the collecting ducts

A

Water reabsorption, under the influence of ADH​

ADH  provides membrane channels for water reabsorption​

Water moves along osmotic gradients created by the counter current exchange mechanism​

96
Q

What is responsible for regulating water and electrolytes

A

Antidiuretic hormone (ADH)
Renin-angiotensin-aldosterone
Atrial Natriuretic Hormone (ANH,ANF,ANP)

97
Q

What is another name for Vasopressin

A

ADH

98
Q

How does ADH control water reabsorption

A

Acts on distal convoluted tubules (distal end) and collecting ducts to increase water permeability​

By insertion of aquaporin channels​

Water moves passively along osmotic gradient between tubule lumen and interstitial fluid​

99
Q

What is octapressin

A

Also known as viniopressin which is an analogue of vasopressin which acts as a vasoconstrictor

Used in conjunction with Citanest

100
Q

What stimulates ADH secretion

A

Decreased plasma volume
Decreased baroreceptor distension
OR
Increased plasmaosmolarity
Increased osmoreceptor activation

RESULTING IN:
Increased ADH release
Increased water permeability

101
Q

Why is it names vaso-press-in

A

Vasoconstrictor - decreases size of lumens

102
Q

How is ADH secretion increased

A

Decreased ECF volume (low pressure receptors in atria and great vein
Increased ECF osmolarity (Osmoreceptors in hypothalamus)

103
Q

What happens to ADH as plasma osmolarity increases

A

Increases

104
Q

What happens to ADH levels when blood volume or pressure increases

A

Decreases

105
Q

What ions are present in ICF and ECF and what are they called

A

Electrolytes
Na+, K+, H+, Ca2+

106
Q

What controls the levels of electrolytes

A

Homeostasis, much of which operates through the kidneys which determine secretion volumes

107
Q

What hormones are responsible for Na+ levels

A

Renin-angiotensin-aldosterone system​
-Promotes reabsorption of Na+ (and water) in DCT; exchange for K+, H+​
-Angiotensin is a potent vasoconstrictor​

Atrial Natriuretic Hormone​
-Increases excretion of Na+ (and water)​
-Opposite effects to aldosterone

108
Q

Why do we need K+ and how is it regulated

A

Cell membrane potentials depend on ECF [K+]
Small changes in [K+]ECF can have big effects on nerve/muscle function​

K+ is regulated by aldosterone; Na+ is swapped for K+ or H+

109
Q

What can hypo and hyper ADH secretion result in

A

Hypo-secretion:​
-Diabetes insipidus​
-Large volumes of insipid (tasteless) urine (cf. diabetes mellitus)​

Hyper-secretion:​
-Syndrome of inappropriate ADH (SIADH)​
-Excess ADH  water retention

110
Q

What are the effects of K+ on nerve function

A

Increasing ECF [K+] - depolarisation​

Depolarisation causes axons to fire AP​

But the MP does not return to ‘resting’ levels​

Result is that axon remains in an extended ‘refractory period’​

K salts are used in toothpastes to desensitise ‘hypersensitive dentine’

111
Q

Does sensodine toothpaste actually reduce sensitivity

A

Exposure of dentinal tubules poses threat when brushing, causing production of tertiary dentine reducing sensitivity in teeth ​

Toothpaste actually has little effect on the reduction of sensitivity

112
Q

How does K+ ions reduce sensitivity

A

K+ ions diffuse from paste along tubules
Raise [K+] at inner end of tubule
Nerves depolarised;
Na+ channels inactivated; prolonged refractory period

Problem: K+ build-up does not persist

113
Q

How does a decrease in plasma volume increase renin secretion

A

Decreased plasma volume
Increased sympathetic nerve activity
Decreased renal blood flow - greater flow rate (decreased Na+ in tubular fluid), macula densa
Decreased stretch of J-G baroreceptors
Juxta-glomerular apparatus
Increased renin secretion