Hormones Flashcards

1
Q

What is the endocrine system

A

Organs that secrete a hormone into the blood are called endocrine glands. Release ‘chemical messengers’

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2
Q

Hormone action on a whole body level

A

Regulation and integration of: ionic and fluid balance, energy balance (metabolism), coping with the environment, growth and development, reproduction.

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3
Q

Hormone action on a molecular level

A

Regulation of: gene transcription, prote4in synthesis and degradation, enzyme activity, protein conformation, protein to protein interactions

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4
Q

Hormone action on a cellular level

A

Regulation: cell division, differentiation, death (apoptosis), motility, secretion, nutrient uptake

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5
Q

Steroid hormone examples

A

testosterone, oestrogen and cortisol - cholesterol derived

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6
Q

Peptide hormone examples

A

growth hormone, oxytocin and parathyroid hormone

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7
Q

Amino acid derived hormone examples

A

thyroid hormones and catelcholamines

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8
Q

Steroid hormone - location of receptor

A

cytosol or nucleus

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9
Q

peptide hormone - location of receptor

A

cell surface

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10
Q

Steroid hormone mechanism of action

A

Bind DNA/ modify transcription

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11
Q

Peptide hormone mechanism of action

A

secondary messenger - cAMP

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12
Q

Which hormone has a faster response

A

peptide hormones

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13
Q

Longevity effects of the hormones

A

steroid - more permanent. Peptide - temporary

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14
Q

Hormone negative feedback system

A

hypothalamus stimulates pituitary gland which stimulates an endocrine gland. Negative feedback is seen when the output of a pathway inhibits inputs to the pathway

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15
Q

Examples of some positive feedback loops

A

oxytocin and parturition

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16
Q

Location of the pituitary galnd

A

inferior (below) the hypothalamus with the optic chiasm between

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17
Q

Anterior lobe (pars distalis) of pituitary gland

A

portal blood vessels connect pituitary and hypothalamic capillary beds

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18
Q

Posterior lobe (pars nervosa) - pituitary gland

A

nerve fibers originate in the hypothalamus and transport hormones to posterior pituitary

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19
Q

Sections of the anterior pituitary

A

pars tuberalis, pars intermedia, pars distalis

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20
Q

Sections of the posterior pituitary

A

infundibular stalk, pars nervosa

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21
Q

Which 2 hormones does the posterior pituitary scerete

A

oxytocin and vasopressin (anti-diuretic hormone, ADH)

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22
Q

Oxytocin function

A

controls milk release from lactating breast. Controls uterine contraction at onset of labout

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23
Q

ADH function

A

acts on kidneys to reabsorb water

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24
Q

Cell bodies of the posterior pituitary

A

paraventricular nucleus and supraoptic nucleus - both produce hormones

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25
Q

What does the interaction of oxytocin with its receptors do

A

raises the levels of intracellular calcium in the myoepithelial cells of the mammary gland causing myoepithelial cells to contract foricng milk into ducts

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26
Q

Oxytocin timeline of events

A

Suckling -> hypothalamus -> posterior pituitary -> oxytocin -> milk squeezed out = neuro-endocrine reflex

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27
Q

Effect of ADH on collecting duct

A

collecting duct is permeable to water so there is increased plasma osmolarity. Dehydration stimulates osmoreceptors in hypothalamus

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28
Q

What are tropic hormones

A

hormones which regulate the secretions of other endocrine organs

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29
Q

What 6 hormones does the anterior pituitary gland produce

A

Growth hormones, prolactin, adenocorticotropic hormone (ACTH), thyroid stimulating hormone (TSH), folicle stimulating hormone (FSH), luteinising hormone (LH)

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30
Q

Prolactin target organs

A

mammary glands

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31
Q

Which hormone is a corticotroph

A

ACTH

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32
Q

Which hormone is from somatotrophs

A

Growth hormones

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33
Q

Which hormones are from gonadotrophs

A

FSH and LH

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34
Q

Which hormones are from thyrotrophs

A

Thyroid stimulating hormone

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35
Q

Stimulatory compounds that the hypothalamus secretes to control anterior pituitary

A

corticotrophin releasing hormone (CRH), gonadotropin releasing hormone (GRH), thyrotropin releasing hormone (TRH), growth hormone releasing hormone (GHRH)

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36
Q

Inhibitory compounds the hypothalamus secretes to control the anterior pituitary

A

dopamine (DA) (inhibits prolactin) and somatostatin (SS) (inhibits growth hormone)

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37
Q

Growth hormone target

A

bone and skeletal muscle

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38
Q

Growth hormone function

A

Stimulates growth in children and adolescents but continues to exert important effects throughout adult life

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39
Q

Other hormones that effect growth and their affects

A

Thyroxine (lack inhibits growth)

Cortisol (excess inhibits growth)

Insulin (excess stimulates growth

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40
Q

Do growth hormones have an anabolic or catabolic effect on metabolism

A

anabolic

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41
Q

How do growth hormones protect against hypoglycaemia

A

it is glucose sparing with an anti-insulin action so can conserve growth for CNS

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42
Q

Growth hormone affect on muscle

A

decrease glucose uptake, stimulates aa uptake/protein synthesis, inhibits protein breakdown = increased muscle mass

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43
Q

Growth hormone effect on adipose tissue

A

decrease glucose uptake, increase lipolysis = decrease in fat tissue

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44
Q

Growth hormone effect on liver

A

increase glycogenesis, increase protein synthesis, stimulates IGF production

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45
Q

Indirect effects of growth hormone - insulin

A

GH actions via insulin like growth factors: growth hormone -> liver -> IGF ->

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46
Q

Indirect effect of growth hormone on skeletal growth

A

cartilage formation, bone deposition – lengthening and thickening

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47
Q

Indirect effect of growth hormone on soft tissue growth

A

protein synthesis, cell proliferation

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48
Q

When does growth-promoting bone response to growth hormones cease

A

when growth plates fuse

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49
Q

Somatopause (decrease in GH) effects

A

Decrease in lean body mass. Decline in bone mineral density. Increase in body fat

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50
Q

What can cause growth hormone disorders

A

result of pituitary tumours

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51
Q

What occurs in people with gigantism (GH excess)

A

abnormally high linear growth due to excessive action of IGF while the epiphyseal growth plates are open during (children)

Normally body proportions as soft tissues are also affected

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52
Q

What is acromegaly

A

Increases growth hormone later in life after fusion of epiphyses (growth plates)

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53
Q

Symptoms of acromegaly

A

course facial features, enlarged hands and feet, protruding jaw and separation of teeth, enlarged tongue and thickened lips, deep voice, cardiomegaly, diabetes

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54
Q

Effects of GH insufficiecny in children (pituitary dwarfism)

A

Slow growth rate below 3rd centile on age/height or bone chart

Normal body proportions

Poor muscle development, excess subcutaneous fat

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55
Q

Thyroid gland structure

A

adhered to the trachea. 2 large (asymmetrical) flat lobes connected by isthmus

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56
Q

What regulates the thyroid gland

A

by hypothalamus and pituitary

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57
Q

Development of the thyroid gland

A

Fully developed by week 12 of gestation

Responsive to TSH at 22 weeks

Capable of producing T3/T4 at 14 weeks

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58
Q

What is the function of theyroid hormones

A

subsequent for fetal growth and development

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59
Q

Thyroid gland blood supply

A

left superior and inferior thyroid artery. Left superior, middle and inferior thyroid vein

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60
Q

Histology if thyroid gland

A

Functional unit = follicle (200-300um in diameter)

1000’s in each gland

Each follicle consists of a layer of follicular cells (simple cuboidal epithelial) surrounding a colloid-filled cavity

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61
Q

Components of thyroid follicle

A

C cells secrete calcitonin, follicular cells secrete thyroid hormone, capillary, colloid is a glycoprotein, capsule of connective tissue

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62
Q

What are the 2 thyroid hormones

A

Triiodothyronine (T3) and thyroxine (T4)

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63
Q

Which thyroid hormone has a greater biological activity

A

T3 (about 10 x more than T4)

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64
Q

How many iodine molecules does T4 contain

A

4

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65
Q

How many iodine molecules does T3 contain

A

3

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66
Q

What does the thyroid secrete per day

A

about 80-100 ug of T4, but only 5ug of T3 per day

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67
Q

Why 2 raw materials is required for the synthesis if T4 and T3

A

tyrosines and iodine

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68
Q

Sources of tyrosines

A

Provided by thyroglobulin

Secreted by follicular cells into lumen of follicle as colloid

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69
Q

Iodine in the synthesis of T4 and T3

A

Iodine is pumped into follicular cells against concentration gradient (40 x blood concentration)

Dietary iodide is oxidized to iodine.

Iodine binding to tyrosine of the thyroglobulin, cuts bits off

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70
Q

How much iodine is required per day

A

minimum of 75ug per day

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71
Q

T4 and T3 synthesis (steps 1 -4)

A
  1. Thyroglobulin is synthesized and discharged into follicle lumen
  2. Iodide is actively transported in
  3. Iodide is oxidized to iodine
  4. Iodine is attached to tyrosine in colloid, forming DIT and MIT
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72
Q

T4 and T3 synthesis (steps 5-7)

A
  1. Iodinated tyrosines are linked together to form T3 and T4
  2. Thyroglobulin colloid is endocytosed and combined with a lysosome
  3. Lysosomal enzymes cleave T4 and T3 from thyroglobulin and hormones diffuse into bloodstream
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73
Q

Advantages to the thyroid production system

A
  1. Can stores week’s worth of thyroid hormones
  2. Thyroid secretion can be maintained if no iodine is available
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74
Q

What are rich sources of iodine

A

processed food that contains iodized salt, seaweed, eggs, cows milk

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75
Q

how much of thyroid hormone release is T4

A

90%

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76
Q

Where does conversion of T4 into T3 occur

A

in peripheral tissues (liver, kidneys and skeletal muscle)

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77
Q

Thyroid hormone mechanism of action

A

bind to intracellular receptors. Complex with thyroid response elements (TRE) that bind to DNA and influence gene expression (stimulates transcription/translation)

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78
Q

Transcription of T4 and T3

A

Triiodothyronine moves into the nucleus where it binds to the THR. The T3-THR complex acts as a transcription factor and is able to bind directly to the DNA at sequences known as TREs. With the help of additional transcription-regulating proteins, transcription of messenger RNA (mRNA) occurs with mRNAs encoding a number of proteins involved in metabolism.

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79
Q

What do the transcribed proteins triggered by thyroid hormones usually do

A

Increase cellular metabolism, Increase cellular oxygen consumption, Increase cellular glucose, Increase circulation and respiration, Promote nervous system and skeletal development

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80
Q

What do the thyroid hormones help maintain

A

Energy levels, Weight, Thermoregulation, Heart rate, GI motility, Mood

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81
Q

Thyroid hormone cardiovascular effects

A

increased cardiac output, increased heart rate and contractility

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82
Q

Thyroid hormones - increased basal metabolic rate

A

important in temperature regulation and adaptation to cold environments. O2 consumption and heat production, increases mobilization and utilization of glucose, fat, protein.

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83
Q

Thyroid hormones - growth and maturation

A

bone growth, synergy with growth hormone, CNS development and function, thyroid hormone deficiencies can result in mental impairment and short stature.

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84
Q

Thyroid hormones - other effects

A

respiratory effects, skeletal muscle function, regulation of reproductive function, synergy with catecholamines.

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85
Q

What does TSH do

A
  1. Promotes release of thyroid hormones
  2. Increases activity of iodide pump and iodination of tyrosine to increase production of thyroid hormones
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86
Q

What is hypothyroidism

A

underactive thyroid. In general metabolic rate decreases and weight gain

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87
Q

Hypothyroidism symptoms

A

dry, cold skin, sensitivity to cold, weight gain despite loss of appetite, impaired memory, mental dullness, lethargy

88
Q

hypothyroidism clinical exam

A

reduced metabolic rate, reduced cardiac output

89
Q

Hypothyroidism diagnosis

A

low plasma levels of ‘free’ T3 and T4

90
Q

Hypothyroidism treatment

A

thyroxine. Dose determined by TSH monitoring

91
Q

Hypothyroidism causes

A

iodine deficiency -> endemic goitre. Autoimmune disease -> Hashimoto’s thyroiditis. Others: congenital, post radiation/surgery, medications, stress

92
Q

What is hyperthyroidism

A

overactive thyroid. In general metabolic rate increases and weight loss

93
Q

Iodine deficiency (endemic goitre)

A

Insufficient dietry iodine. Insufficient amounts of T3 and T4. Abnormally high TSH. Abnormal growth of the thyroid due to trophic effects of TSH

94
Q

What is Hashimoto’s disease

A

Most common cause of hypothyroidism

Autoimmune disease

95
Q

Hashimoto’s disease effects

A

Antibodies against thyroglobulin or thyroid peroxidase

Interferes with thyroid hormone synthesis

Antibodies also against TSH receptor

Prevents stimulation of T3 and T4 release

96
Q

Congenital hypothyroidism cause

A

Lack of gland or incorrect hormone biosynthesis

97
Q

Congenital hypothyroidism effects

A

Intellectual disability. Short disproportionate body. Thick tongue and neck. Intellectual disability if treatment later than 3 months

98
Q

Hyperthyroidism symptoms

A

loss of weight, excessive sweating/intolerance to heat, Palpitations and an irregular heartbeat, anxiety and nervousness, exophthalmos

99
Q

Hyperthyroidism clinical exam

A

raised metabolic rate and oxygen consumption, increased heart rate, hypertension

100
Q

Hyperthyroidism treatment

A

surgical removal of all/part of thyroid gland, ingestion of radioactive iodine that selectively destroys the most active thyroid cells, drugs that interfere with the gland’s ability to make T3/T4

101
Q

Hyperthyroidism cause

A

Autoimmune disease -> Grave’s disease

102
Q

Graves disease symptoms

A

Muscle weakness, heart palpitations, irritability

103
Q

What causes grave’s disease

A

Autoimmune B cell makes antibodies against TSH receptor that stimulate thyroid hormone production and T3/T4 release

104
Q

What charcterizes grave’s disease

A

goitre, exophthalmos and lid retraction

105
Q

Location of adrenal glands

A

a pair - lie above each kidney

106
Q

Structure of adrenal glands

A

Each gland enclosed in a fibrous capsule surrounded by fat. Inner: adrenal medulla. Outer: Adrenal cortex – under hormone control

107
Q

What do the adrenal glands respond to

A

atreaa

108
Q

Adrenal development

A

At 7 weeks of life, the primitive adrenal medullary tissue begins to invade the cortex. At birth, the medullary cell mass is fully surrounded by the cortex. However, cortical differentiation into a zona glomerulosa, zona fasciculata, and zona reticularis is not complete until later in childhood

109
Q

How much does each adrenal gland weigh

A

6-10g

110
Q

Adrenal glands blood supply

A

Rich blood supply – adrenal arteries arise directly from the aorta. Blood flows through the cortex and drains into the medulla

111
Q

Zones of the adrenal cortex

A

capsule, zona glomerulosa, zona fasciculata, zona reticularis

112
Q

Which nervous system controls the adrenal medulla

A

sympathetic nervous system - has an enlarged and specilaized sympathetic ganglion

113
Q

What does the adrenal medulla secrete

A

catecholamine hormones: Adrenaline (epinephrine) and noradrenaline (norepinephrine)

114
Q

Why isn’t the adrenal medulla a true endocrine gland

A

its not under hormonal control

115
Q

What does the adrenal medulla contain

A

CHROMAFFIN CELLS

SPECIALISED POSTGANGLIONIC NEURONS

Preganglionic = splanchnic nerve fibers

116
Q

What is the neurotransmitter for adrenal medulla

A

acetylcholine

117
Q

What does the adrenal medulla secrete

A

adrenaline and noradrenaline

118
Q

Cardiovascular effects of adrenaline

A
  1. Increases Heart rate and stroke volume
  2. Increase in blood pressure (systolic)
  3. Vasodilation of coronary and skeletal muscle blood vessels
  4. Vasoconstriction of blood vessels to ‘non-essential’ tissues (GIT, skin, kidneys)
  5. Bronchodilation
119
Q

Metabolic effects of adrenaline

A
  1. Increases the amount of energy for immediate use
  2. Liver converts glycogen to glucose
  3. Metabolic rate increases
  4. Blood flow changes, reducing digestive system activity and urine output
120
Q

Adrenaline receptors

A

alpha 1, alpha2, beta 1,2,3. Adrenaline interacts primarily with beta receptors

121
Q

What is released in response to prolonged stress

A

mineralcorticoids and glucocorticoids

122
Q

Long-term stress response effects

A

Kidneys retain sodium and water. Blood volume and blood pressure rise. Proteins and fats converted to glucose or broken down for energy. Blood glucose increase immune system supressed

123
Q

What does the zona glomerulosa secrete

A

mineralocorticoids (Aldosterone) SALT

124
Q

What does the zona fasciculata secrete

A

glucocorticoids (cortisol) SUGAR

125
Q

What does the zona reticularis secrete

A

gondocorticoids (androgens) SEX

126
Q

What do steroid hormones initiatw

A

transcription of mRNA -> protein synthesis

127
Q

How is enzyme expression vairable within the zones of the adrenal cortex

A

the zona glomerulosa lacks 17-hydroxylase. Zona fasciculata and zona reticularis lack 18-hydroxylases

128
Q

What do high levels of circulating testosterone levels lead to

A

masculinization of fetal external genitalia to variable degrees

129
Q

What do adrenal glands produce

A

Dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEA-S), and androstenedione - which are testosterone and estrogen precursors

130
Q

Binding of DHEA and DHEA-S

A

they bind less efficiently to the androgen receptors (weak steroids) compared to testosterone.

131
Q

Where are the testosterone precursors converted into testosterone

A

in peripheral tissues

132
Q

Where are testosterone precursors controlled

A

by ACTH - anterior pituitary

133
Q

Role of testosterone in males

A

male secondary characteristics and aggression in young boys - adrenal glands secret little compared to testes so role not fully understood

134
Q

Adrenal androgens over/under secretion effect

A

no noticeable consequences

135
Q

What do females convert testosterone produced by the adrenal glands into

A

oestrogen

136
Q

Function of estrogen

A

Responsible for growth of pubic and axillary hair and sex drive

Kick start puberty

Maintain muscle and bone mass

137
Q

How much testosterone do adrenal glands secrete in females

A

half of the total androgenic requirement

138
Q

What can cause excess production of adrenal androgen

A

overproduction of ACTH, adrenal tumor, Cushing’s syndrome

139
Q

symptoms of excessive adrenal androgen production

A

Acne, hirsutism, irregular periods, breast shrinkage…..

Play a role in polycystic ovary syndrome (PCOS)

Patients with PCOS have adrenal androgen excess

140
Q

Examples of anti androgens and what do they do

A

they block androgen receptors e.g., cyproterone acetate and ethinylestradiol

141
Q

Is there more or less SHEA/DHEA-S with age

A

less as u get older

142
Q

How is aldosterone secretion regulated

A

by plasma levels of sodium and potassium via the renin - angiotensin aldosterone system (RAAS)

143
Q

What does it mean when there is renin secretion

A

Low sodium in the distal tube

144
Q

Principle actions of aldosterone - control ECF volume

A

Conserve body sodium

Stimulates reabsorption of sodium in renal distal convoluted tubules in exchange for potassium

145
Q

Principle actions of aldosterone - control of release

A

Response to renin-angiotensin system (RAAS)

Decreased ECF volume (hypovolaemia or hypotension) and decreased renal blood flow

Response to high plasma potassium

146
Q

What can stimulate cortisol production

A

stress

147
Q

What is stress

A

physical trauma, intense heat or cold, infection, mental or emotional trauma

148
Q

What does cortisol do to mediate the body’s response to stress to endocrine signals

A

Metabolic effects. Cortisol increases plasma glucose and FFA concentration. Provide energy substrates to body tissues for their response to the stressful event that stimulated cortisol production

149
Q

Cortisol function - increased catabolism

A

Cortisol increases skeletal muscle protein catabolism. Amino acids are then converted to glucose (gluconeogenesis)

150
Q

Cortisol function - increased lipolysis

A

Liberate free fatty acids & triglycerides from adipose tissue. Used as an energy source

151
Q

Cortisol function - increased intake

A

Stimulates appetite. If the stressful event doesn’t involve physical activity – weight gain. Decreased cortisol leads to weight loss and increased cortisol leads to increased apetite and weight gain

152
Q

Other actions of cortisol

A
  1. May contribute to emotional instability
  2. Anti-inflammatory – blocks the processes which lead to inflammation (in high doses)
  3. Immunosuppressive – fall in antibody production and number of circulating lymphocytes
153
Q

What does ACTH do to affect production of cortisol

A

stimulates enzymes involved in cortisol and andorgen synthesis

154
Q

What is cushing’s disease

A

overproduction of cortisol

155
Q

What can cause cushing’s disease

A

adrenal or pituitary tumour

156
Q

Symptoms of cushing’s disease

A
  1. Redistribution of body fat
  2. Muscle wastage
  3. Thin skin, bruising abnormal pigmentation
  4. Changes in CHO and protein metabolism
  5. Hyperglyceamia
  6. Hypertension - Cortisol has weak mineralocorticoid activity
157
Q

Cushing’s syndrome treatment

A

surgery, radiation and medication

158
Q

What is Conn’s disease

A

adrenal cortex hyperfunction - mineralcorticoid excess

159
Q

Effect of Conns disease

A

Overproduction of Aldosterone. Retention of sodium, loss of potassium and alkalosis. Hypertension through expansion of plasma volume

160
Q

What is addison’s disase

A

adrenal cortex hypofunction

161
Q

What can cause addison’s disease

A

Damage to adrenal glands, autoimmune disease or pituitary damage

162
Q

What does addison’s disease cause

A

Deficits in glucocorticoids and mineralocorticoids (i.e., low cortisol, hypoaldosteronism, low sex hormone)

163
Q

Symptoms of addison’s disease

A

Progressive weakness, lassitude and weight loss. Pigmentation of the skin and mucosal membranes

164
Q

What is calcium involved in

A
  1. Structural component of bones and teeth (99% total calcium)
  2. Maintains normal excitability of nerve and muscle cells
  3. Involved in neurotransmitter and hormone release
  4. Muscle contraction (skeletal and cardiac)
  5. Activation of many enzymes
  6. Coagulation of blood
  7. Milk production
165
Q

Calcium’s occurrence in nature

A

Does not exist freely, occurs mostly in soil systems as limestone (CaCO3), gypsum (CaSO42H2O) and fluorite (CaF2)

166
Q

Calcium’s occurrence in the body

A

The most abundant mineral. The average adult body contains app 1kg. 0.1% in the extra cellular fluid (ECF). 1% in the cells. The rest (app. 99%) in the skeleton – hydroxyapatite. (Bones can serve as large reservoirs, releasing calcium when extracellular fluid contraction decreases and storing excess calcium).

167
Q

What us plasma calcium concentration

A

2.2-2.6 mM

168
Q

What are the 3 forms calcium is found in the plasma

A
  1. protein bound calcium
  2. ionized or free calcium
  3. complex or chelated calcium
169
Q

Protein-bound calcium

A

calcium cannot diffuse through membranes and thus is not usable by tissues (41%)

170
Q

Ionized or free calcium

A

the physiologically active form (50%)

171
Q

Complex of chelated calcium

A

bound to phosphate, bicarbonate, sulfate, citrate and lactate (9%)

172
Q

What does too low calcium levels cause

A

involuntary muscle contraction. Neuronal hyper - excitability (tetany)

173
Q

How does low calcium levels cause involuntary muscle contraction

A

Low ionized calcium levels in the extracellular fluid increase the permeability of neuronal membranes to sodium ion, causing a progressive depolarization, which increases the possibility of action potentials.

174
Q

What is hypercalcemia

A

calcium levels are too high so neurons are less excitable (Na channels are less likely to open so harder to depolarise) and therefore slower muscle contraction

175
Q

Symptoms of hypercalcemia

A

slower/absent reflexes, muscle weakness, confusion, hallucination

176
Q

What are the 3 control points for calcium

A
  1. Absorption – via intestines
  2. Excretion – via kidney/urine
  3. Temporary storage – via bones
177
Q

Osteoblast cell role

A

synthesize and secrete collagen and promote deposition of calcium phosphate (hydroxyapatite - (Ca10(PO4)6(OH)2)) crystals. Secrete factors that activate osteoclasts

178
Q

Osteoclast role

A

promote resorption of bone

179
Q

Osteocytes role

A

essential role in exchange of calcium between ECF and bone

180
Q

Acute control of calcium

A

Must maintain constant free Ca2+ concentration in the plasma

Mostly by rapid exchange between bone and ECF

181
Q

Chronic control of calcium

A

Maintain total level in the body long term

Adjust GIT absorption and urinary excretion

182
Q

What determines plasma Ca2+ concentration

A
  1. Net absorption of Ca2+ from the GIT
  2. Net excretion of Ca2+ in urine
  3. Exchange of Ca2+ with bone
183
Q

What 3 hormones control plasma Ca2+ concentration

A
  1. Parathyroid hormone
  2. 1,25 – dihydroxycholecalciferol – calcitriol (activated vitamin D)
  3. Calcitonin
184
Q

What secretes parathyroid hormone

A

the parathyroid gland (beneath the thyroid gland)

185
Q

What type of hormone is the parathyroid hormone

A

peptide hormone

186
Q

where is parathyroid hormone stored

A

within chief cells

187
Q

parathyroid hormone half life

A

5 minutes

188
Q

When is parathyroid hormone secreted

A

continuously at a kw rate but in response to loe blood calcium

189
Q

Parathyroid hormone target

A

bone, gut, kidney

190
Q

Parathyroid hormone function

A
  1. Increases reabsorption of calcium from the urine. Fast acting. Decreases urinary calcium in minutes
  2. Increases the expression of the enzyme 1 alpha – hydroxylase (activates vitamin D)
  3. Bone: increases osteoclast activity (indirectly) causing increase in bone resorption
191
Q

Vitamin D2 (Ergocalciferol) source

A

plant sources

192
Q

Vitamin D3 (cholcalciferol) sources

A

Obtained from the diet (animal sources), food supplements and synthesized in the skin in the presence of sunlight

193
Q

What is D2 and D3 converted into

A

1,25 dihydroxycholecalciferol or 1,25 - (OH)2D3

194
Q

What type of hormone is vitamin D

A

steroid

195
Q

What regulates production of vitamin D

A

Liver – dietry intake

Kidney – 1 alpha hydroxylase

196
Q

1,25 – hydroxyvitamin D3 function

A

maintains calcium balance in the body

197
Q

How does calcitriol (1,25 dihydroxycholecalciferol) increase calcium stores

A

Acts on cells on the GIT to increased production of calcium transport proteins. Leads to an increase in Calcium uptake from GIT

198
Q

calcitriol (1,25 dihydroxycholecalciferol) effect on bone

A

Increasing rate of bone resorption – increases the secretion of osteoclast activating factors (Indirect effect)

199
Q

calcitriol (1,25 dihydroxycholecalciferol) effect on kidney

A

Minor effect in decreasing urinary loss of calcium

200
Q

Which enzyme converts vitamin D3/D2 into (1,25 dihydroxycholecalciferol)

A

1 alpha - hydroxylase

201
Q

How does calcitriol work on kidney failure patients

A

by increasing how much caclium we can absorb from food

202
Q

What secretes calcitonin

A

Secreted by the C-cells (parafollicular cells) of the thyroid gland.

203
Q

Calcitonin function

A
  1. Lowers the level of free plasma calcium
  2. Inhibition of osteoclast activity: bone resorption reduced (direct effect)
  3. Increased excretion of calcium and phosphate by the kidneys
204
Q

What can calcitonin be used to treat

A

osteoporosis in postmenopausal women

205
Q

What increases plasma calcium

A

PTH and vitamin D

206
Q

Hormones involved in regulation of plasma calcium

A

Major hormonal regulators: PTH, 1,25 - (OH)2D3 and possibly calcitonin

Others: Growth hormone, adrenal glucocorticoids and thyroid hormones. Oestrogen and androgens

207
Q

What is hyperparathyroidism

A

hypercalcemia - too much vitamin D

208
Q

What is hypocalcaemia

A

vitamin D defficiency

209
Q

Primary hy[erparathyroidism effects

A

Inappropriate (autonomous) secretion of PTH, resulting in hypercalcaemia

Elevated PTH and raised serum calcium (and low serum phosphate)

210
Q

What can cause primary hyperparathyroidism

A

by a single parathyroid adenoma

211
Q

Presentation of primary hyperparathyroidism

A

bones, stones, abdominal groans and psychic moans

Increases bone resorption, increased GIT absorption, decreased renal excretion

212
Q

Presentation of primary hyperparathyroidism

A

painful bones, renal stones, abdominal groans and psychic moans

Increases bone resorption, increased GIT absorption, decreased renal excretion

213
Q

Vitamin D deficiency: rickets

A

Bone remodeling impaired

Failure of calcification

skeletal deformities of weight bearing bones in children

214
Q

Causes of a vitamin D deficiency

A

poor diet, malabsorption, decreased sunlight, liver or kidney disease

215
Q

What does hypocalcaemia lead to

A

increased excitability of nervous tissue. Pins and needles, tetany, muscle cramps, convulsions

216
Q

What does a vitamin D deficiency lead to

A

reduction in intestinal calcium absorption