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Primary Physiology > Endocrine Physiology > Flashcards

Endocrine Physiology Flashcards

1
Q

Classification of hormones and examples

A

Polypeptides - vasopressin, oxytocin, insulin, glucagon, prolactin
Glycoproteins - TSH, FSH, KH
Steroids - corticosteroids, aldosterone, sex hormones
Amines - thyroxine, adrenaline
Fatty acid derivatives - prostaglandins

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2
Q

How are polypeptide and glycoprotein hormones transported in the blood

A

Hydrophilic so unbound in blood stream

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3
Q

How are polypeptide hormones stored and released

A

Stored in granules, released by exocytosis

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4
Q

Where are steroid hormones synthesised? From what?
How are they stored
How are they transported

A

Mitochondria from cholesterol
Produced on demand, not stored
Transported bound to proteins as lipophilic

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5
Q

How are amine hormones produced? How are they stored

A

From amino acid tyrosine
Stored in follicles or granules

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6
Q

How can hormones exert a change on cellular function

A

Changes in membrane permeability
Release of second messenger
Changes in intracellular protein synthesis

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7
Q

How do hormone receptors adapt to hormone concentration

A

Downregulate or upregulate to counter hormone amount

Nb down regulation can be drop in receptor number or in receptor response

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8
Q

Where are hormone receptors located

A

Hydrophilic hormone receptors on cell membrane
Lipiophilic hormone receptor in cytoplasm or nuclear

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9
Q

What is hormone permissiveness

A

When a hormone requires small amounts of another hormone to exert its effect
Eg glucocorticoids are required for catecholamines to have their lipolytic effecet

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10
Q

How do hormones alter membrane permeability?
Examples

A

Via GPCRs
Growth hormone, prolactin, insulin

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11
Q

Examples of second messenger mechanisms involved in hormone signalling

A

GPCR increasing cAMP causing intracellular protein phosphorylation (Gs)
GPCR decreasing cAMP reversing above (Gi)
GPCR activating PIP2 degradation to IP3 and DAG - IP3 causes calcium release DAG activates protein kinase c causing cell division and multiplication

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12
Q

Examples of hormones activating Gi receptors

A

Oxytocin, vasopressin, LH, FSH, TSH, ACTH, adrenaline beta receptors, PTH, glucagon

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13
Q

Examples of hormones activating Gi receptors

A

Somatostatin, alpha 2 adrenaline

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14
Q

Examples of hormones acting via PIP2

A

Alpha 1 adrenaline, vasopressin

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15
Q

What hormones act directly on protein synthesis?
How

A

Thyroixine, steroid hormones
Lipophillic so enter cell, bind to receptor in cytoplasm then cross into nucleus and bind to dna upregulating transcription

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16
Q

What factors can stimulate hormone release

A

Ion levels eg. Sodium dependent release of vasopressin
Organic molecules eg glucose dependent release of insulin
Physical/chemical stimulation eg gut hormones

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17
Q

Example of direct and indirect negative feedback on hormones

A

Direct - low glucose, decreased insulin
Indirect - glucocorticoids inhibit acth-rh, reducing acth, reducing cortisol secretion

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18
Q

Why does gland hypertrophy/atrophy occur

A

Continued low or high levels of hormone despite max or min production in an attempt to compensate

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19
Q

Where is the pituitary gland located

A

Sella turcica

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20
Q

Where do the anterior and posterior pituitary glands develop?

A

Posterior directly from hypothalamus
Anterior from rathkes pouch on roof of mouth.

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21
Q

What are the connections between the hypothalamus and the pituitary

A

Both via the pituitary stalk
Anterior via portal circulation
Posterior direct neuronal connection,

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22
Q

What is the portal circulation of the anterior pituitary
Function

A

Arrises from superior hypophyseal artery, primary capillary plexus on floor of hypothalamus absorbs releasing hormones, drains into portal vein to the secondary capillary plexus in the anterior lobe where the releasing hormones trigger release of trophic hormones into blood stream.

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23
Q

Cell types in anterior pituitary, hormones they release and proportion of total cell number for top 2

A

Somatotropes - growth hormone, 50%
Lactotropes - prolactin 10-30%
Corticotropes - ACTH
Thyrotopes - TSH
Gonadotropes - FSH and LH

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24
Q

Where are posterior lobe pituitary hormones produced? How are they released

A

Produced in median eminance of hypothalamus.
Form granules passed down axons in pituitary stalk into posterior pituitary for storage
Released into the blood stream when stimulation occurs

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25
Q

What hormones are produced for release int he posterior pituitary? Precisely where?

A

Vasopressin - supraoptic nucleus
Oxytocin - paraventricular nucleus

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26
Q

Functions of TSH
Type of hormone, mechanism

A

Stimulates production of thyroid hormone from thyroid and stimulates growth of thyroid gland
Glycoprotein, Gs

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27
Q

Functions of ACTH
Type of hormone, mechanism
Pattern of release

A

Increased corticosteroid production from adrenal cortex
Stimulates melanocytes to produce melanin
Polypeptide, Gs
Diurnal highest in mornings, lowest in evenings.

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28
Q

Functions of GH
Other name
Type of hormone, mechanism

A

Promotes protein synthesis, lipolysis and raised BM promoting growth
Indirect effects from increased release of other factors such as IGF-1 and 2
Somatotropin
Peptide hormone, affects permeability

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29
Q

Effect of high or low growth hormone as child

A

High - gigantism
Low - dwarfism
All in proportion!

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30
Q

Effect of high growth hormone in adults

A

High - acromegaly

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31
Q

Functions of Prolactin
Type of hormone, mechanism

A

Stimulates development of milk producing breast tissue and milk production, suppresses ovulation.
Peptide, increased permeability

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32
Q

Functions of FSH
Type of hormone, mechanism

A

Stimulates ovulation and spermatogenesis
Glycoprotein, Gs

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33
Q

Functions of LH
Type of hormone, mechanism

A

Stimulates ovulation and luteinisation of ovarian follicles
Stimulates testosterone secretion
Glycoprotein Gs

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34
Q

Functions of vasopressin
Mechanism of action

A

Water retention
All PIP2
V1 receptor - vasoconstriction
V2 receptor - insertion of AQP2 into collecting duct
V3 receptor - ACTH-RH release

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35
Q

What stimulates vasopressin release

A

Rise in osmotic pressure
Decreases in extracellular volume
Increased angiotensin II
Pain, stress and exercise
Nausea and vomiting
Smoking

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36
Q

What inhibits vasopressin release

A

Decreased plasma osmotic pressure
Increased extracellular fluid volume
Alcohol

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37
Q

Effect of vasopressin deficiency

A

Diabetes insipidus

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38
Q

Effect of vasopressin excess

A

Fluid retention, hyposomolality, hyponatraemia

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39
Q

What Type of hormone is vasopressin

A

Polypeptide

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40
Q

Functions of Oxytocin
Type of hormone, mechanism

A

Milk ejection from glands, uterine contractionin labour and post partum, sexual arousal
Polypeptide Gs

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41
Q

What is sheehans syndrome

A

Severe bleeding and hypovolaemia in childbirth leading to pituitary necrosis

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42
Q

What are the hormones produced by the hypothalamus that control anterior pituitary secretion? Type?

A

All polypeptides
TRH
ACTH-RH
GH-RH and GH-IH (somatostatin)
PRH and PIH (dopamine)
Gn-RH

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43
Q

Examples of crossover in hypothalamic releasing hormones effect

A

TRH also stimulates prolactin
GRH also inhibits TSH

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44
Q

Effects on hypothalamic hormone output

A

Pos/negative feedback
Stress
Diurnal variation
Emotional factors

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45
Q

Lobes of the thyroid

A

Left and right lobes each with upper and lower pole
Sometimes there’s a third pyramidal lobe anterior to isthmus

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46
Q

Arterial supply to thyroid
Venous drainage

A

Superior and inferior thyroid arteries
Superior middle and inferior thyroid veins

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47
Q

Structure of a thyroid acini (follicle)

A

Central colloid full of thyroglobulin and iodine
Surrounding thyroid epithelial cells
Parafollicular cells (c or clear cells) that secrete calcitonin

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48
Q

How are thyroid hormones produced
What enzyme is required to do this

A

Tyrosine in thyroglobulin (large glycoprotein) combines with iodine in 4-8 residue units (MIT monoiodotyrosine, and DIT diiodotyrosine). MIT combines with DIT to form triiodothyronine (T3) and DIT with DIT to from tetraiodothyronine (T4).
Under control of thyroid perisidase

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49
Q

How is iodine moved into the thyroid colloid

A

Dietary iodine converted to iodide (I-) in gut
Transported to thyroid where concentrated into the thyroid by sodium iodide pumps
Secreted into the colloid and oxidised back to iodine

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50
Q

Key functions of a thyroid cell

A

Absorption and concentration of iodide with secretion into colloid
Production of thyroglobulin and thyroid peroxidase and secretion into cokkkid
Absorption of thyroid hormone back from colloid and into blood stream

51
Q

How is thyroid hormone secretion controlled
What is secreted and what circulates?
What exerts most end organ effect?

A

By TSH levels.
90% of secreted hormone is T4 with rest T3
33% T4 converted to T3 with T3 making up 25% of the circulating amount
T3 exerts 5x the effect of T4 on tissues and most T4 is converted to inactive rT3

52
Q

How do thyroid hormones travel in the blood

A

Bound to protiens including albumin and thyroxine binding prealbumin or thyroxine binding globulin.
Albumin has largest capacity but TBG has highest affinity so most is in TBG
<1% is unbound.

53
Q

Effects of TSH

A

Release of t3 and t4
Increase size and number of cells in thyroid gland
Increase thyroglobulin synthesis, increased colloid Endocytosis,

54
Q

How do thyroid hormones exert their efffect

A

Enter cells
Bind with receptor in nuclei
Hormone receptor complex binds to dna upregulating transcription and protein synthesis.

55
Q

Main effects of thyroid hormone

A

Increased proteins breakdown and lipolysis
Increased carbohydrate absorption
Increased beta adrenoceptors in heart, increased sensitivity of heart to catecholamines, thus increased iontrophy and chronotrophy with decreased pvr
Increased mitochondria with increased metabolic rate, energy utilisation and heat production.

56
Q

Causes of hypothyroidism (broadly)

Effects

A

Pituitary failure
Thyroid failure
Iodine deficiency

Myxoedema, lethargy, slowness, weight gain, cold intolerance, thick stiff skin (lack of protein breakdown)
In children cretinism (mental retardation, dwarfism, pot belly, large protruding tongues)

57
Q

Causes of hyperthyroidism
Effects

A

Pituitary overproduction of TSH
Thyroid disease

Nervousness, tremor, weight loss, sweating, heat intolerance, af, wide pulse pressure

58
Q

What is Graves’ disease

A

Thyroid autoantibodies that stimulate TSH receptors
In 50% also cause tissue deposition behind eye and exophthalmos

59
Q

Types of cells in parathyroid glands

A

Chief cells containing secretory granules of pth
Oxyphil cells with unknown function

60
Q

What is pth

A

A polypeptide produced in chief cells of parathyroid
Converted from preprohormone to prohormone to pth before release from granules into blood

61
Q

Function of PTH

A

Mobilisation of ca from bones raising plasma Ca
Reabsorption of ca in DCT of kidney
Decreased reabsorption of phos in pct of kidney
Increase phosphate absorption in gi tract
Increase production of 1,25dihydroxycholecalciferol

62
Q

Mechanism of action of pth on cells

A

Gs receptor activation

63
Q

Stimulus for pth release

A

Low ca levels

64
Q

Vitamin d pathway

A

7-dehydroxycholestrol
[sunlight]
Cholecalciferol
[liver]
25 hydroxycholecalciferol
[kidney]
1.25 dihydroxycholecalciferol

65
Q

How does Vit d exert its effect

A

Binding to cell nucleus receptors exposing dna binding site altering transcription

66
Q

Effect of Vit d

A

Increases gi calcium and phosphate absorbtion
Increases ca absorption in kidney
Increases osteoblast activity laying down ca in bones

67
Q

Where is calcitonin produced
Effect

A

C cells (clear cells, parafolicular cells) of thyroid
Reduces ca and phos levels by reducing bone reabsorption

68
Q

Effect of glucocorticoids on calcium

A

Inhibit bone breakdown reducing calcium but may cause osteoporosis long term

69
Q

Effect of pth deficiency

A

Hypocalcaemia
Hyperphosphatemia
Neuromuscular excitability and tetany

70
Q

What is pseudohypoparathyroidism

A

Resistance to pth leading to similar clinical picture to primary hypoparathyroidism.

71
Q

Effect of Vit d deficiency

A

Rickets in kids
Osteomalacia in adults

72
Q

Effect of excess pth

A

Hypercalaciema
Hypophosphatemia
May be kidney stones or metal symptoms

73
Q

What is secondary hyperparathyroidism

A

CKD
Lack of 1.25 Vit d
Chronically low ca
Parathyroid hypertrophy

74
Q

Effect of excess Vit d

A

High calcium and phosphate

75
Q

Regions of the adrenal gland
What do they secrete

A

Cortex:
Zona glomerulosa - mineralocorticoids
Zona fasciculata - glucocorticoids
Zona reticularis - adrogenic hormones

Medulla:
Catecholamines

76
Q

How do the adrenal steroid hormones work

A

Bind to cytoplasmic receptors
Complex enters nucleus altering dna transcription.

77
Q

What proportion of the mineralocorticoid activity is mediated by aldosterone
What does the rest

A

95%
Glucocorticoids

78
Q

What stimulates aldosterone production

A

High plasma na
Decreased plasma k
Reduced ECF
Trauma, stress, surgery, anxiety

79
Q

Effects of mineralocorticoids

A

Reabsorption of na in kidneys, stomach, sweat, saliva and intestine.
Reabsorption of water from kidneys
Excretion of k and h from kidneys

80
Q

Half life of aldosterone

A

20 minutes

81
Q

Control of aldosterone secretion

A

Mainly angiotensin II as part of RAAS triggered by low na or reduced perfusion to juxtaglomerular apparatus
Minor impact from ACTH

82
Q

What is cortisol known as when given in medication from

A

Hydrocortisone

83
Q

Main glucocorticoids produced by Zona fasciulata

A

Cortisol
Corticosterone
Cortisone

84
Q

Production of aldosterone

A

Cholesterol
[ACTH/angiotensin ii]
Pregane derivatives
Progesterone/corticosteroids
[aldosterone synthase]
Aldosterone

85
Q

How is cortisol transported in plasma?
Half life

A

Bound to a globulin, transcortin, albumin
Half life 100mins but effects last much longer

86
Q

What would be the effect of increased binding proteins on cortisol?

A

More bound, less free
Less negative feedback
More acth-rh, more acth, more cortisol produced until free back to equilibrium

87
Q

Effects of glucocorticoids

A

Increased catabolism of protein and lipids, increased gluconeogenesis
Anti-insulin effect
Increased water excretion
Increased sensitivity to catecholamines
Facilitates na to adrenaline
Increased RBC and pot
Decreased wbcs
Mineralocorticoid effects
Anti inflammatory when at very high levels

88
Q

What adrogenic hormones are released from the adrenal cortex Zona reticularis
Fate of these

A

Dehydroepiandrosteone (dhea)
Androstenedione - converted to testosterone and oestrogen in peripheral tissues and fat

89
Q

Adrenaline synthesis pathway

A

Phenylalanine
Tyrosine
Dopa
Dopamine
Noradrenaline
Adrenaline

90
Q

What proportion of adrenal medulla cells secrete what

A

90% adrenaline
10% NA
Small amounts of dopamine and opioid peptides

91
Q

Where are additional areas of adrenaline synthesis found

A

Along course of aorta

92
Q

What enzyme converts na to adrenaline

A

N methyltransferase

93
Q

What breaks down catecholamines

A

Monoamine oxidase
Catechol-o-methyl transferase

94
Q

Effects of adrenaline and noradrenaline on heart rate

A

Adrenaline increases
Na decreases

95
Q

Effects of adrenaline and noradrenaline on cardiac output

A

A increases
Na - decreases at low dose, increases at high dose

96
Q

Effects of adrenaline and noradrenaline on peripheral vascular resistance

A

A - low levels decrease
Na increases

97
Q

Effects of adrenaline and noradrenaline on MAP

A

A - increase low levels
Na - increase

98
Q

Non cardiovascular effects of adrenaline and noradrenaline

A

Increases glycogenolysis, mobilisation of fatty acids, increased metabolic rate, increased heat production
Nervous system stimulation

99
Q

Primary receptor stimulated by noradrenaline
Primary effects cardiovascularly

Effect at higher doses

A

Alpha receptors
Increased SVR

Some beta effects at high doses increasing cardiac output

100
Q

Primary receptor stimulated by adrenaline
Primary effects cardiovascularly

Effect at higher doses

A

Beta stimulation
Increased heart rate and cardiac output. Vasodilates

Some alpha effect at higher doses increasing SVR

101
Q

What stimulates medullary hormone production in the adrenal gland

A

Sympathetic stimulation

Needs glucocorticoids to activate n methlytransferase to convert na to a

102
Q

What happens in congenital glucocorticoid deficiency

A

Upregulated acth
Adrenal gland hypertrophy
Excess androgen secretion - virilisation of females and precocious puberty in males
Increased pigmentation

103
Q

What causes secondary hyperaldosteronism

A

High renin production
- cirrhosis, heart failure, some renal diseases

104
Q

Features of Cushing syndrome

A

Muscle waisting, thin hair, poor skin, moon face and bufflo hump
Hyperglycaemia
Hypertension
Hyperlipidaemia
Osteoporosis

105
Q

What functional units are there in the pancreas
Rough function

A

Acini - exocrine function secreting digestive enzymes
Islets of langerhans - endocrine function secreting hormones

106
Q

Cells in the islets of langerhans and what they produce

A

B (or beta) cells - insulin
A (or alpha) cells - glucagon
D (or delta) cells - somatostatin
F cells - pancreatic polypeptide

107
Q

Structure of insulin
Production

A

Polypeptide made of 2 aa chains linked by pair of disulphide bridges
Produced in ER from prepropinsulin, part splits off, folds in two, and disulphide bridges form creating proinsulin. Then c-peptide part is removed forming insulin.

108
Q

How is insulin the medication made

A

Either bovine or porcine (very close to human) or human by dna recombinant technology

109
Q

Structure of insulin receptor
How do they work

A

2 alpha (extracellular) and 2 beta subunits (transmembrane)
Insulin binds to alpha, beta unit activates second messenger by tyrosine kinase.
Main Effect is insertion of glut transporters into cell membrane

110
Q

Main effects of insulin

A

Increased glucose uptake
Increased glycogenesis
Increased amino acid uptake
Increased protein synthesis
Increased fatty acid synthesis
Increased k uptake
Increased ketone uptake
Decreased ketone synthesis

111
Q

Structure and formation of glucagon

A

Polypeptide hormone
Preproglucagon to proglucagon to glucagon

112
Q

Effects of glucagon

A

Opposite to insulin
Main effects glycogenolysis in liver (not muscle), gluconeogenesis, lipolysis, ketogenesis

113
Q

Effects of somatostatin

A

Inhibition of insulin and glucagon
Inhibition of pancreatic polypeptide
Slows down the propulsive movement in the gi tract

114
Q

Effect of pancreatic polypeptide

A

Uncertain
Possibly to smooth out blood levels of glucose and amino acids after a meal by slowing food absorption

115
Q

What stimulates insulin secretion

A

High glucose
Glucagon
Some beta receptor agonists
Acetylcholine
Sulphonyluresas

116
Q

What inhibit insulin release

A

Adrenaline
Somatostatin
Beta blockers
Alpha agonists
Thiazides

117
Q

What stimulates glucagon release

A

Hypoglycaemia
Hunger
Stress
Trauma
Infection
Selective beta agonists

118
Q

What inhibits glucagon release

A

Hyperglycaemia
Somatostatin
Insulin
Ketones
Free fatty acids
Selective alpha agonists

119
Q

Which glut channel is insulin sensitive

A

Glut 4

120
Q

What is the influence of glucocorticoids on carb metabolism
Significance

A

Needed for glucagon to cause gluconeogenesis
Excess causes hyperglycaemia, deficiency hypoglycaemia

121
Q

Effect of growth hormone on glucose metabolism

A

decreases uptake into cells
Increases glycogenolysis
Decreases binding of insulin

122
Q

Likely pathology behind t1dm

A

T lymphocyte attack on beta cells in pancreas

123
Q

Causes of insulin excess

A

Overtreatment with insulin
Sulphonylureas or biguanides
Rarely insulinoma

Primary Physiology (15 decks)

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