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SOI2 > PHYSIOLOGY ENDOCRINE > Flashcards

PHYSIOLOGY ENDOCRINE Flashcards

1
Q

What are the endocrine signalling mechanisms?

A

1) Regulated secretion of hormones into ECF
2) Diffusion into vasculature
3) Binding to specific receptor in target organ

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2
Q

What are the types of message transmission (with examples)?

A

Paracrine (adjacent) –> neurotransmitters

Hormonal (endocrine) –> neurohormone

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3
Q

What does the exocrine pancreas mainly secrete?

A

Adiponectin

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4
Q

What does the endocrine pancreas mainly secrete?

A

Insulin
Glucagon
PP

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5
Q

What does the thyroid gland mainly secrete?

A

T3 & T4

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6
Q

What do the parathyroid glands mainly secrete?

A

PTH

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7
Q

What does the cortex of the adrenal glands secrete?

A

Cortisol
Aldosterone
Sex hormones

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8
Q

What does the medulla of the adrenal glands secrete?

A

Catecholamines (adrenaline, dopamine, noroepinephrin)

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9
Q

What is another name for adrenaline?

A

Epinephrine

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10
Q

Where are the hormones secreted by the hypothalamus directed to?

A

Pituitary gland

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11
Q

What is the main classification of hormones?

A

Peptides
Glycoproteins
Steroids
Amines

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12
Q

Where are peptide hormones produces?

A

Hypothalamus

Hypophysis

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13
Q

5 examples of peptide hormones?

A 
Growth hormone
Vasopressin (ADH)
Insulin/Glucagon
Parathyroid hormone (PTH)
Adrenocorticotropin (ACTH)
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14
Q

How are peptide hormones stored?

A

As INACTIVE polypeptides (pre-hormones) inside of vesicles

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15
Q

What peptide hormone is used as a marker for insulin and why?

A

C-peptide & insulin are released simultaneously (and in similar amounts) from the pancreas

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16
Q

Where are glycoprotein hormones mainly produced?

A

Hypohphysis

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17
Q

What is the common subunit of glycoprotein hormones?

A

a-subunit

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18
Q

What is the specific subunit for glycoprotein hormones?

A

B subunit

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19
Q

What are the 4 glycoprotein hormones?

A

Thyrotropin (TSH)
Follicle stimulating hormone (FSH)
Luteinising hormone (LH)
Chorionic Gonadotropin (HCG)

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20
Q

What is chronic gonadotropin (HCG) used for?

A

Pregnancy indicator

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21
Q

Description of the action of peptide hormones

A

Water-soluble
Fast effect
Short half-life

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22
Q

What are the 5 steroid hormones?

A 
Estradiol
Progesterone
Testosterone
Cortisol
Aldosterone
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23
Q

What is the common precursor of steroid hormones?

A

Cholesterol

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24
Q

Where are steroid hormones produced?

A

Cortex of adrenal gland

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25
Q

Where do steroids act on, on a cell?

A

Receptor of the nucleus of a cell

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26
Q

Water affinity and implications for steroid hormones

A

Hydrophobic

Require transport proteins to bind in target cells

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27
Q

What is the common site for hormonal binding and what is the exception?

A

Common site: cell membrane

Exception: steroids

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28
Q

What are the amine hormones?

A

Thyroid hormones

Catecholamines

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29
Q

Where do thyroid hormones act on, on a cell?

A

INSIDE the nucleus of a cell

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30
Q

Where do catecholamines act on?

A

Medulla of adrenal gland

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31
Q

What is the common structure in amine hormones?

A

Tyrosine amino acid

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32
Q

Which hormone is the only which has a positive feedback mechanism?

A

Estrogen

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33
Q

What is the implication of hormonal binding in membrane of a cell?

A

Faster effect

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34
Q

What is the implication of hormone binding inside the cell/cell nucleus?

A

Slower effect

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35
Q

What part of the hormone is able to interact and penetrate the target organ?

A

Free-fraction

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36
Q

What is the difference between the circadian & ultradian rythms?

A

Circadian: daily
Ultradian: monthly

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37
Q

When are cortisol levels highest?

A

In the morning, after waking up

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38
Q

When are growth hormones produced?

A

During sleep

Peak within 2 hours of sleep onset

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39
Q

What is the main determinant of sex hormones?

A

Pulsatility of hypothalamic GnRH

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40
Q

What is ACTH can its rapid degradation be prevented?

A

Precursor of cortisol

By conserving it in ice

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41
Q

Which disease requires the cortisol levels to be measured at night?

A

Cushing’s disease

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42
Q

In a patient with polycystic ovary syndrome, when is the most appropriate time to measure sex hormones?

A

During 1st part of menstrual cycle

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43
Q

What transporters do lipophilic hormones (thyroxine and cortisol) require?

A

Globulin - lipoproteins

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44
Q

What is the main lipoprotein transporter for thyroxine?

A

Thyroxine-binding globulin (TBG)

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45
Q

What is the main lipoprotein transporter for cortisol?

A

Cortisol-binding globulin (CBG)

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46
Q

What are the clinical implications of the transport of hormones?

A

Alterations in binding proteins
Free-hormone fractions
Therapeutic modulation of transporter proteins

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47
Q

What kind of hormonal alteration can occur during pregnancy?

A

False hypothyroidism

Increased levels of estrogen –> increased levels of TBG

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48
Q

What is the therapeutic modulation for the condition of polycystic ovaries?

A

Increased levels of androgens –> bind androgens (steroid) to transporters so that they are not free and cannot act

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49
Q

What is the most relevant membrane receptor family?

A

G-protein coupled receptors

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50
Q

What are the 1st and 2nd messengers, respectively?

A

1st: hormones
2nd: cAMP

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51
Q

What is the mechanism of action of hormones via G-protein coupled receptors?

A

Hormones bind
Dissociation of alpha subunit from beta and gamma subunits
Alpha subunit triggers cascade of events to form cAMP
cAMP produces mediators (adenylcyclases, phosphorylases, kinases)
Mediators activate transcription factors that alter gene expression

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52
Q

What are the 5 main characteristics of peptide hormones?

A 
Synthesized as pre-hormones
Stored in secretory vesicles/granules
Regulated at level of secretion
Can circulate in blood freely
Hydrophilic --> no need for binding proteins
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53
Q

What are the 5 main characteristics of steroid hormones?

A 
Derived from cholesterol
Regulated at level of enzymatic pathway
Transported in blood bound to binding globulins
Signal through intracellular receptors
Oral administration
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54
Q

What are the 5 main characteristics of thyroid hormones?

A 
Derived from tyrosine/iodothyronines
Lipophilic but stored in thyroid follicular cells
Regulated at all levels 
Transported bound to proteins
Signal through intracellular mechanisms
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55
Q

What do tyrosines couple to form?

A

Iodothyronines

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56
Q

What is the difference between the primary and secondary gene transcription mechanisms?

A

Primary: thyroid hormones act directly on gene transcription
Secondary: steroid hormones act by mediators on gene transcription

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57
Q

What is the classification of diseases as primary, secondary and tertiary diseases like?

A

Primary diseases in target organ
Secondary diseases in anterior pituitary gland
Tertiary disease in hypothalamus

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58
Q

What is the mechanism of feedback regulation for ADH?

A

Via changes in ion concentration (osmolarity)

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59
Q

What allows ovulation?

A

Positive feedback

LH increased production by pituitary gland triggers ovulation

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60
Q

What is another name for pituitary gland?

A

Hypophysis

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61
Q

What is the best indicator of hypothyroidism?

A

TSH (thyroid stimulating hormone) not T3 nor T4

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62
Q

What happens from the days 12-14 of the menstrual cycle?

A

Hypothalamus releases GnRH –>
Adrenal gland releases FSH, LH –>
Ovaries (glands) secrete Estradiol –>
Estradiol acts on endometrium (target organ)
Estradiol ENHANCES release of more FSH & LH by adrenal gland

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63
Q

What region gives rise to the adenohypophysis and what is its orientation?

A

Epithelium

Anterior

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64
Q

What region gives rise to the neurohypophysis and what is its orientation?

A 
Neural origin (nervous tissue)
Posterior
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65
Q

What bone and structure house the pituitary gland?

A

Sphenoid bone

Sella Turcica

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66
Q

What does the invagination of the oral cavity form?

A

Rathke’s Pouch

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67
Q

What forms the pars tuberalis?

A

The infundibulum (diencephalic prolongation) and the Rathke’s Pouch

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68
Q

What hormones does the adenohypophysis secrete?

A 
TSH
ACTH
Prolactin
GH
FSH
LH
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69
Q

How do the hormones secreted by the adenohypophysis reach the anterior pituitary gland?

A

Via the pituitary portal system

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70
Q

What hormones does the neurohypophysis secrete?

A

ADH

Oxytocin

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71
Q

How do the hormones secreted by the neurohypophysis reach their target organs?

A

Move down axon to axon endings

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72
Q

How do hypothalamic hormones affect the anterior pituitary hormones?

A

By inhibiting or stimulating their production and secretion
(“certain situations such as mental stress or mood disturbances have repercussions on pituitary hormonal secretion, and consequently function of the peripheral glands”)

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73
Q

Via which artery are oxytocin & ADH released into the general circulation?

A

Inferior hypophyseal artery

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74
Q

What regulates the secretion of pituitary hormones?

A

Hypothalamus (CNS)

Hormones produced by peripheral glands

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75
Q

What is/are the main stimulators and inhibitors of GH?

A

Stimulator: GHRH
Inhibitor: Somatostatin

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76
Q

What is/are the main stimulators and inhibitors of TSH?

A

Stimulator: TRH
Inhibitor: Somatostatin

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77
Q

What is/are the main stimulators and inhibitors of Prolactine?

A

Stimulator: VIP, SER
Inhibitor: Dopamine!!

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78
Q

What is/are the main stimulators and inhibitors of ACTH?

A

Stimulator: CRH, Vasopressin (ADH)
Inhibitor: -

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79
Q

What is/are the main stimulators and inhibitors of FSH & LH?

A

Stimulator: LNRH (AKA GNRH)
Inhibitor: GnIH (Gonadotropin inhibitory hormone)

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80
Q

The levels of which hormone would increase if the infundibular stalk were cut and why?

A 
Prolactine 
Dopamine (its inhibitor) would not be able to inhibit its production (since dopamine is produced in the hypothalamus) therefore prolactine levels would increase
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81
Q

How can an adenoma (benign tumor) of GH be treated?

A

By administering an analogue of somatostatin (since it inhibits the action of GH)

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82
Q

What is the relation between prolactine and the menstrual cycle?

A

Prolactine inhibits gonadotropin releasing hormone (gnrH) which results in the abscence of the menstrual cycle

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83
Q

What produces inhibin?

A

Sertolli cells
(In men in the testicles & adrenal glands)
(In women only in adrenal glands)

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84
Q

What is the “feedback-loop” of GH (pituitary hormone) with its corresponding peripheral hormone?

A

GH stimulates IGF-I

IGF-I inhibits GH

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85
Q

What is the “feedback-loop” of TSH (pituitary hormone) with its corresponding peripheral hormone?

A

TSH stimulates T3 & T4

T3 & T4 inhibits TSH

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86
Q

What is the “feedback-loop” of ACTH (pituitary hormone) with its corresponding peripheral hormone?

A

ACTH stimulates cortisol

Cortisol inhibits ACTH

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87
Q

What is the “feedback-loop” of FSH (pituitary hormone) with their corresponding peripheral hormone?

A

FSH & LH stimulate Estrogens, Progesterone, Testosterone and Inhibin
Estrogens, Progesterone, Testosterone and Inhibin!! inhibit FSH

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88
Q

What is the “feedback-loop” of LH (pituitary hormone) with its corresponding peripheral hormone?

A

LH stimulates release of Estrogens, Progesterone, Testosterone and Inhibin
Estrogens, Progesterone and Testosterone inhibit LH
Inhibin DOES NOT inhibit LH

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89
Q

What are the levels of FSH like in a menopausal woman?

A

High levels of FSH because inhibin and estrogens are inhibited (inhibitors of FSH inhibited, therefore levels of FSH rise)

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90
Q

What factors stimulate GH secretion?

A

Sleep
Stress
Exercise

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91
Q

What does GH produce in the liver?

A

IGF-1

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92
Q

What is the most important transport protein linked to IGF-1?

A

IGFBP3

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93
Q

What factors inhibit GH secretion?

A

Starvation
Acute hypoglycaemia
Aging

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94
Q

What condition results from the hyper-secretion of GH?

A

Acromegaly

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95
Q

In a person without acromegaly, what is the effect of glucose overload on GH secretion?

A

Decrease (inhibition)

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96
Q

In a person with acromegaly what is the effect of glucose overload?

A

No effect on GH release

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97
Q

What test is done to confirm diagnosis of acromegaly (GH hyper-secretion)?

A

Oral glucose overload

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98
Q

At what time of the sleep do GH levels increase?

A

2 hours after sleep is initiated

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99
Q

What are the main physiological effects of GH and IGF-1?

A

Cell growth

Anabolism

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100
Q

What is the main difference (in terms of physiological effects) between GH and IGF-1?

A

GH has lipolytic effect (thereby reducing adiposity)

IGF-1 increases insulin sensitivity

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101
Q

What molecules are the main inhibitors of growth plate chondrocytes?

A

Glucocorticoids

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102
Q

What are the main functions of IGF-1?

A

Development of:

  • Thymus
  • Neural
  • Cardiovascular
  • Musculoskeletal
  • Glomerular
  • Fetus
  • Ovarian folliculogenesis
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103
Q

What is the main controller of the hypothalamic-pituitary-adrenal axis?

A

Suprachiasmatic nucleus receiving afferences (sensory fibers) from retina

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104
Q

What are the hormones responsible for the secretion of ACTH on the pituitary gland?

A 
Mainly CRH (corticotropin-releasing hormone)
Also ADH
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104
Q

What are the hypothalamic hormones responsible for the secretion of ACTH on the pituitary gland?

A 
Mainly CRH (corticotropin-releasing hormone)
Also ADH
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105
Q

What is the main function of ACTH and where does it carry this function out?

A

Stimulate synthesis of cortisol

Adrenal cortex

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106
Q

What is the effect of cortisol on the pituitary gland and on the hypothalamus?

A

Negative feedback

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107
Q

What are the main molecules secreted by cortisol?

A

Pro-inflammatory cytokines (IL-1, IL-2, IL-6, TNF-a) which stimulate the hypothalamic-pituitary-adrenal axis

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108
Q

What is the global stimulator of the hypothalamic-pituitary-adrenal axis?

A

Stress

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109
Q

What is the best time of the day to measure cortisol levels?

A

After waking up (8am)

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110
Q

What stimulates the release of prolactin?

A 
Sleep
Stress
Food
Exercise
Pregnancy
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111
Q

What drugs (pharmacological) inhibit the release of prolactin?

A

Antipsychotics

H2-blockers

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112
Q

What hormones regulate the release of prolactin from the pituitary gland?

A

Serotonin stimulates

Dopamine inhibits

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113
Q

What effects does prolactin have?

A

Lactation (postpartum period)
Mammary gland development
Kidney sodium reabsorption (Electrolytic homeostasis)

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114
Q

How do estrogens stimulate the production of prolactin?

A

Via inhibition of TIDA (tuberoinfundibular dopamine)

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115
Q

What is the most common cause of hyperprolactinemia?

A

Pharmacological hyperprolactinemia (antipsychotics, H2-blockers)

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116
Q

When are prolactin levels (ideally) measured?

A

First thing in the morning (fasting state)

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117
Q

When are prolactin levels (ideally) measured in WOMEN?

A

Follicular phase of menstrual cycle

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118
Q

What hormones have a circadian rythm?

A

GH
Prolactin
TSH

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119
Q

How is T4 converted into T3?

A

Deiodination (removal of iodine) of T4

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120
Q

What is the effect of stress on the hypothalamic-pituitary-gonadal axis?

A

Inhibition on secretion of gonadotropins

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121
Q

What effect does LHRH (leutinising hormone releasing hormone) AKA GnRH (gonadotropin releasing hormone) on the secretion of FSH and LH?

A

Stimulation

LH > FSH

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122
Q

What is the importance of a pulsatile secretion of GnRH?

A

Every 90 minutes to maintain bioactivity of LH and FSH

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123
Q

What hormones inhibit the release of FSH and LH from the pituitary gland?

A

Testosterone
Inhibin
Estradiol
Progesterone

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124
Q

In what part of the menstrual cycle does estradiol have a stimulating effect on the release of FSH and LH?

A

Follicular (periovulatory) phase

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125
Q

What is the effect of inhibin (of gonadal origin) on the hypothalamus-pituitary-gonadotropin axis?

A

SELECTIVELY inhibit the release of FSH

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126
Q

What are FSH levels like in menopausal women or after a gonadectomy? Why?

A

FSH levels are elevated because inhibin is decreased

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127
Q

What is the effect of kisspeptin on GnRH-neurons?

A

Stimulatory effect –> stimulates secretion of FSH and LH

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128
Q

What are the receptors for vasopressin and where are they found?

A

V1 - blood vessel
V2 - kidney
V3 - pituitary gland

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129
Q

What is the effect of V1 (vasopressin 1) receptor?

A

Vasoconstriction

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130
Q

What is the effect of V2 (vasopressin 2) receptor?

A

Increased reabsorption of water

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131
Q

What is the effect of V3 (vasopressin 3) receptor?

A

Stimulates ACTH producing cells

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132
Q

What is cranial diabetes insipidus due to?

A

ADH deficiency

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133
Q

What is nephrogenic diabetic insipidus due to?

A

Defects in collecting tubule

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134
Q

What is the best imaging test to investigate the causes of pituitary dysfunctions?

A

MRI

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135
Q

What is the campimetry test used for?

A

Pituitary macroadenoma

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136
Q

What is the effect of hypopituitarism on GH?

A

Growth delay

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137
Q

What is the effect of hypopituitarism on PRL?

A

Postpartum agalactia (reduced lactation)

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138
Q

What is the effect of hypopituitarism on ACTH?

A

Secondary (cortical) adrenal insufficiency

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139
Q

What is the effect of hypopituitarism on TSH?

A

Secondary hypothyroidism

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140
Q

What is the effect of hypopituitarism on FSH/LH?

A

Secondary hypogonadism

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141
Q

What is the effect of hypopituitarism on ADH?

A

Cranial diabetes insipidus

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142
Q

What are hyper-functioning syndromes of GH?

A

Acromegaly (gigantism in children)

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143
Q

What are hyper-functioning syndromes of Prolactin?

A

Hyperprolactinemia

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144
Q

What are hyper-functioning syndromes of ACTH?

A

Cushing’s disease

Hypercortisolism

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145
Q

What are hyper-functioning syndromes of TSH?

A

Secondary hyperthyroidisim

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146
Q

What are hyper-functioning syndromes of FSH/LH?

A

Gonadotropinomas

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147
Q

What are hyper-functioning syndromes of ADH?

A

Inadequate secretion of ADH

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148
Q

What joins the two lobes to form the thyroid gland?

A

Isthmus

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149
Q

Should thyroid gland be palpable under physiological conditions?

A

No (palpation must be painless)

150
Q

Where is the thyroid gland located?

A

In front of the trachea

151
Q

How many parathyroid glands are there?

A 
Usually 4 (2 upper and 2 lower)
10% of people have a 5th (variable location)
152
Q

What nerve is located posterior to the thyroid gland?

A

Recurrent laryngeal nerve

153
Q

What can cutting the recurrent laryngeal nerve cause?

A

Dysphonia

154
Q

What does the hypothalamus pituitary thyroid axis consist of?

A

Hypothalamus produces TRH
Pituitary gland produces TSH
Thyroid gland produces T3 (10%) and T4 (90%)

155
Q

How is TRH conducted from the hypothalamus to the anterior pituitary gland?

A

Via the hypothalamic-pituitary portal system

156
Q

What amount of T4 undergoes deiodination to become T3?

A

90%

157
Q

What hormone mediates the feedback mechanism of the hypothalamus-pituitary thyroid axis?

A

T3

158
Q

What hormones inhibit the secretion of TSH?

A

Dopamine
Somatostatin
Glucocorticoids
Stress (not a hormone, I know)

159
Q

What does a thyroid follicle consist of?

A

Follicular cells and a colloid

160
Q

What is the colloid of a thyroid follicle?

A

Reservoir of:

  • Thyroglobulin
  • Iodothyrosines
  • Thyroid hormones
161
Q

What is thyroglobulin?

A

Protein made of thyroxine and iodine

162
Q

What is the main function of the capillaries surrounding the thyroid follicles?

A

Iodine transport

163
Q

What supplementation must pregnant women take?

A

Folic acid

Iodine salt

164
Q

What is the iodine turnover rate?

A

Iodine intake = iodine excretion (daily)

165
Q

What is TSH’s receptor?

A

G-protein coupled receptor

166
Q

What is the final effect of TSH?

A

Synthesis of thyroid hormones

167
Q

What does the chronic elevation of TSH promote?

A

Goiter: growth of thyroid gland

168
Q

What is the most frequent cause of hyperthyroidism?

A

Grave’s disease (TSHR antibody - overstimulates TSH receptor to overproduce thyroid hormones)

169
Q

What is the 1st step in the synthesis and secretion of thyroid hormones?

A

Iodine (circulation) active transport by NIS (Na+/I- symporter) in basolateral membrane of thyroid epithelial cells

170
Q

What is the 2nd step in the synthesis and secretion of thyroid hormones?

A

Iodine travels through thyroid epithelial cells to apical membrane
Transported to colloid via Pendrin (I-/Cl-) transporter

171
Q

What is the 3rd step in the synthesis and secretion of thyroid hormones?

A

Iodination
Iodine binds to tyrosine residues (in thyroglobulin)
Thyroid peroxidase (TPO) catalyses conversion into MIT and DIT

172
Q

What is the 4th step in the synthesis and secretion of thyroid hormones?

A

Coupling (catalysed also by TPO)
MIT + DIT = T3 (10%)
DIT + DIT = T4 (90%)

173
Q

What is the 5th step in the synthesis and secretion of thyroid hormones?

A

Endocytosis of vesicles with TG bound to MIT, DIT, T3, T4 into follicular cells
Release of T3 & T4 in circulatory system
Recycling of iodine and tyrosine

174
Q

What does TPO stand for?

A

Thyroid peroxidase

175
Q

What is the effect of excessive iodine intake?

A

TPO blockage known as Wolff-Chaikoff effect

176
Q

Why is iodine prescribed to patients with hyperthyroidism?

A

Because it blocks TPO action thereby reducing release of T3 and T4

177
Q

How is thyroid hormone transported in circulation?

A

99% bound to proteins

1% free (active)

178
Q

How must thyroid be measured in blood?

A

In the free form (active)

179
Q

Why can a pregnancy be a false indication of hypothyroidism?

A 
Estrogens (elevated in pregnancy) increase TBG (thyroid binding globulin)
More TBG = less free thyroid
Less free (active) thyroid = hypothyroidism
180
Q

What are the “transport” proteins found in the 99% of thyroid protein-bound?

A

70% TBG
20% Albumin
10% Transthyretin

181
Q

Why is T4 prescribed preferably to T3?

A

Half life of T4 is longer

T4 is more stable

182
Q

What does the largest proportion of circulating T3 come from?

A

From T4!!

183
Q

What is the site of conversion of T4 into T3?

A

Mainly peripheral circulation

184
Q

What enzymes catalyse the conversion of T4 into T3?

A

Deiodinase (D) - D1, D2, D3

185
Q

What is the function of D1?

A

Peripheral conversion of T4 into T3

186
Q

What is the function of D2?

A

Peripheral and HYPOTHALAMIC conversion of T4 into T3

187
Q

What is the function of D3?

A

Conversion of T4 into REVERSE T3 (inactive)

Found in sick euthyroid syndrome

188
Q

How do T3 and T4 enter the target cells?

A

Via diffusion

189
Q

What does T3 interact with once inside the target cell?

A

Thyroid hormone receptor (TR) - nuclear receptor of thyroid hormones

190
Q

What is the main outcome of gene transcription by T3?

A

Stimulates B-adrenergic receptors

191
Q

What is the main mechanism of metabolism/excretion of thyroid hormones (T3 and T4)?

A

T4 and T3 metabolised into T2 (inactive) via deiodinases & excreted in urine, feces or bile

192
Q

What are the main actions of thyroid hormones in cardiovascular system (MUST KNOWS)?

A

Positive inotropic and chronotropic effects

193
Q

What are the main actions of thyroid hormones in metabolic system (MUST KNOWS)?

A

Increase basal metabolism

Indirectly increasing brown adipose tissue

194
Q

What are the main actions of thyroid hormones in hormonal systems (MUST KNOWS)?

A

GH modulation
Regulation of gonadal function
E2/T ratio (estrogen/testosterone)

195
Q

What are the main actions of thyroid hormones in bones (MUST KNOWS)?

A

Aid in bone maturation

Decrease glycosaminoglycans

196
Q

What are the main actions of thyroid hormones in respiratory system (MUST KNOWS)?

A

Increase respiratory rate

197
Q

What are the main actions of thyroid hormones in muscular system (MUST KNOWS)?

A

Muscle trophism

198
Q

What are the main actions of thyroid hormones in autonomous nervous system (MUST KNOWS)?

A

Synergy with catecholamines

199
Q

What are the main actions of thyroid hormones in nervous system (MUST KNOWS)?

A

Aid in neuronal development
Increase alert, memory, cognition
Osteotendinous reflexes
Gastrointestinal motility

200
Q

What is the main functional difference between calcium and phosphorus?

A

Phosphorus is a component of phospholipid membranes (calcium is not)

201
Q

What are the main functions carried out by calcium and phosphorus?

A

Enzymatic activation
Muscle contraction
Coagulation
Bone mineralization

202
Q

What is the effect of pH on ionic calcium quantities in blood plasma?

A

Acidosis INCREASES ionic calcium

Alkalosis DECREASES ionic calcium

203
Q

What percentage of calcium is ionised and what percentage is free in plasma?

A

50% ionised

50% free

204
Q

What are the key elements of calcium and phosphorus homeostasis?

A

Intestinal absorption
Renal elimination
Bone exchange

205
Q

What calciotropic hormones are involved in the regulation of calcium metabolism?

A

PTH

Vitamin D

206
Q

What are the only 2 regulative elements of Ca2+ and bone metabolism that has an anabolic function?w

A 
Growth hormone (GH)
Insulin like growth factor (IGF-1)
207
Q

What is the effect of thyroid hormones, cortisol and cytokines in the BONES?

A

Induce catabolism

208
Q

What is the effect of sex steroids and somatotropic axis (growth-hormone axis) in the BONES?

A

Induce catabolism

209
Q

What 2 things does bone remodelling involve?

A

1) Bone formation (osteoblasts)

2) Bone destruction (osteoclasts)

210
Q

What is an osteoid?

A

Bone matrix that is yet to be mineralised

211
Q

What controls the mineralization of osteoids?

A

Calcium and Pi (inorganic phosphate)

212
Q

Where is PTH (parathyroid hormone) synthesised and secreted?

A

Parathyroid glands (4 or 5 - 10% of population-)

213
Q

What is the predominant parenchymal cell type in the parathyroid gland?

A

Principal or chief cell

214
Q

Where does the biological activity reside in the peptide chain of PTH?

A

First 34 amino acids

215
Q

How long is the half-life of PTH?

A

Short (2 min)

216
Q

What stimulates PTH secretion via interaction with CaSR (calcium-sensing receptor) in the principal/chief cells?

A

Hypocalcemia

Catecholamines

217
Q

What factors suppress PTH release?

A

Hypercalcemia
Hypomagnesemia
Vit D administration

218
Q

What effect does activation of beta2-adrenergic receptor have on PTH secretion¿

A

Stimulates PTH secretion

219
Q

What is the pathway of Vitamin D from the moment of its intake to the moment it carries out its function?

A

Food & skin “absorb” Vit. D
25-hydroxylase catalyses Vit.D into 25(OH) D
1 a-Hydroxylase catalyses 25(OH)D into 1.25(OH)2D
1.25(OH)2D acts in GI tract to stimulate calcium and phosphorus absorption

220
Q

What is the active form of Vitamin D?

A

1.25(OH)2D

221
Q

What stage of vitamin D is measured in blood tests?

A

25(OH)D

222
Q

What is the action of PTH related to calcium, phosphorus and phosphate?

A

Stimulates calcium and phosphorus resorption
Stimulates release of 1 a-hydroxylase
Stimulates phopshate excretion

223
Q

What is the main modulator of calcium absorption in small intestine?

A

1 a-hydroxylase

224
Q

What is the effect of PTH on osteoclasts and on osteoblasts?

A

DIRECT activation of osteoblasts

INDIRECT activation of osteoclasts

225
Q

How are osteoclasts formed?

A

Prosteoclasts (osteoclast precursors) have RANK
RANK ligand binds to RANK
Induces osteoclastogenesis –> osteoclasts

226
Q

What generates RANK ligands?

A

Osteoblasts

227
Q

What occurs when there is an excess secretion of PTH?

A

Increase in resorption that translates into osteoporosis

228
Q

What effect does osteoprotegerin have?

A

Inhibits osteoclastogenesis by acting as a decoy receptor (inhibitor) for RANKL

229
Q

What is the effect of Denosumabe?

A

Human monoclonal antibody that acts on RANKL to inhibit osteoclastogenesis Administered in situations of osteoporosis

230
Q

What effect does PTH have on the proximal tubule of the kidneys?

A

Promotes destruction of phosphate co-transporter IIa –> stimulates phosphate excretion (instead of reabsorption)
Activates 1 a-hydroxylase –> Vit. D synthesis

231
Q

What effect does PTH have on distal tubule of the kidneys?

A

Stimulates calcium resorption

232
Q

What receptor senses alterations in calcium levels?

A

CaSR (calcium-sensing receptor)

233
Q

What is the effect of 1,25 Vitamin D on PTH gene?

A

Inhibitory effect of PTH gene

Stimulation of synthesis of CaSR

234
Q

What is the most important effect of Vitamin D?

A

Increase intestinal absorption of calcium

235
Q

Where does Vitamin D come from?

A

Synthesis of cholecalciferol from provitamin D from UV light

236
Q

Via hydroxylations of which molecule is Vitamin D transformed into its active form?

A

Successive hydroxylations of Cholecalciferol

237
Q

What is FGF23? Where is it produced? What is its function?

A

Fibroblast growth factor 23
Produced by mature osteoblasts
Phosphate and Vit.D metabolism and regulation

238
Q

Where does FGF23 mainly act on?

A

Proximal tubules of kidneys via FGFR/Klotho receptor

239
Q

What are the main effects of FGF23?

A

Decreases active Vit.D and causes phosphaturia (phosphate excretion) by inhibiting 1 a-hydroxylase

240
Q

What occurs with the Klotho receptor (FGFR/Klotho) in kidney diseases?

A

Decreased expression of klotho receptor

241
Q

Why is PTH not used to measure hypocalcemia?

A

Because it is very expensive

242
Q

What is the effect of increased PTH levels on cytochrome p450 1a?C

A

Rapid stimulation (increase)

243
Q

What condition produces PTHrp (PTH related peptide)?

A

Cancerigenous (malignant) tumors

244
Q

What is the effect of PTHrp (PTH related peptide)?

A

Hypercalcemia by stimulating renal calcium resorption & bone resorption

245
Q

What is calcitonin used for in medical exams?

A

Biomarker for medullary thyroid cancer

246
Q

What is the main effect of calcitonin?

A

Reduces blood calcium levels

Opposes effect of PTH (antagonists)

247
Q

In what condition was calcitonin previously administered and why?

A

Osteoporosis because it has an antiresorptive effect at bone level

248
Q

What is the most common secondary disease of patients with kidney complications?

A

Cardiovascular problems

249
Q

What types of hormones are produced by adrenal glands?

A

Steroids

Catecholamines

250
Q

What is the origin of the cortex and the medulla of the adrenal glands?

A

Cortex - mesodermal origin (epithelial)

Medulla - ectodermal origin (neural)

251
Q

What is the venous drainage of the right adrenal gland?

A

Right suprarenal vein drains directly onto vena cava

252
Q

What is the venous drainage of the left adrenal gland?

A

Left suprarenal vein drains into left renal vein which then drains onto inferior vena cava

253
Q

What are the 3 zones of the adrenal cortex?

A

Zona glomerulosa
Zona fasciculata
Zona reticularis

254
Q

What do each of the 3 zones of the adrenal cortex secrete, respectively?

A

Zona glomerulosa - mineralocorticoids
Zona fasciculata - glucocorticoids
Zona reticularis - sex hormones

255
Q

Where are 50% of circulating androgens of women produced?

A

In the adrenal glands

256
Q

How do ACTH and cortisol levels relate?

A

Parallel

257
Q

What is axis regulates cortisol synthesis?

A

Hypothalamic-pituitary-adrenal (HPA) axis

258
Q

What does cortisol exert a negative feedback on?

A

CRH (corticoid releasing hormones) and ACTH (adrenocorticotropic hormone)
All hormones of the HPA axis

259
Q

What situations stimulate the release of CRH and ACTH?

A

Cold
Injury
Hypoglycemia
Pain

260
Q

What is the effect of increased glucocorticoid levels in the menstrual cycle?

A

Absence of menstrual cycle

261
Q

What is the mechanism via which CRH stimulates ACTH production?

A 
CRH reaches pituitary corticotrope cells via portal system 
Triggers intracellular signalling pathways 
Activates CREB (protein) & AP-1 (transcription factor) to generate ACTH
262
Q

Where is CRH produced?

A

In the paraventricular nucleus of the hypothalamic nuclei

263
Q

How does calcium affect ACTH release?

A

Direct stimulation

264
Q

How does ADH (Vasopressin) affect ACTH release?

A

Indirect stimulation

Stimulates intracellular calcium mobilization therefore ACTH secretion

265
Q

In which part of the adrenal cortex does ACTH interaction cause a greater hormonal response?

A

Zona fasciculata - secretes cortisol

266
Q

What does the interaction of ACTH with the receptors of the zona fasciculata stimulate?

A

Entry of LDL-cholesterol

Synthesis of of StAR protein

267
Q

What is the StAR protein responsible for and why?

A

Transfers cholesterol to inner mitochondria membrane because mitochondria is the site of steroid production

268
Q

What does the interaction of ACTH with receptors in the zona fasciculata of the cortex of the adrenal glands ultimately generate?

A

Pregnenolone (precursor of most steroid hormones)

269
Q

What condition is related to increased aromatase?

A

Obesity

270
Q

What component do people with congenital adrenal insufficiency lack?

A

21-Hydroxylase

271
Q

What is the function of the aromatase enzyme?

A

Androgens conversion into estrogens

272
Q

What is the function of 21-Hydroxylase?

A

Catalyses glucocorticoid and mineralocorticoid pathways to produce cortisol and aldosterone, respectively

273
Q

What hormone induces virilizartion (in a girl)?

A

Androstenedione

274
Q

What is transcortin?

A

Cortisol binding globulin

275
Q

What is the function of transcortin?

A

Balancing free fraction of cortisol

Preventing loss of cortisol in urine

276
Q

What hormone increases the concentration of transcortin?

A

Estrogens

277
Q

What are the main functions of cortisol?

A

Lipolysis
Catabolism
Stress reactivity regulation
Anti-inflammatory properties

278
Q

What type of intracellular receptors does cortisol interact with?

A

Glucocorticoids

Mineralocorticoids

279
Q

Why are glucocorticoids prescribed?

A

Most potent anti-inflammatory

280
Q

How can the metabolic effects of cortisol be increased via pharmacological treatment?

A

Administration of synthetic glucocorticoids

281
Q

Why is cortisol considered an anti-inflammatory?

A

Inhibits transcription factor NF kappa beta involved in inflammatory & immune responses exerted on T lymphocytes and macrophages

282
Q

What is the half-life of cortisol in blood?

A

100 minutes

283
Q

What is the pharmacological treatment used in primary adrenal failure?

A

Fludrocortisone (oral preparation of mineralocorticoid)

Or cortisol as hydrocortisone

284
Q

What are the main effects of angiotensin II in the RAAS system?

A

1) Aldosterone secretion
2) ADH secretion
3) Arteriolar vasoconstriction
4) Sympathetic activation

285
Q

What is the main trigger for the secretion of aldosterone?

A

Elevated potassium levels (hyperkalemia)

286
Q

What are the most important enzymes in the synthesis of aldosterone?

A

21-Hydroxylase
11-b-hydroxylase
18-hydroxylase

287
Q

What can excess aldosterone cause?

A 
Oxidative sterss
Cardiac fibrosis
Hypertension
Dyslipidemiia
Obesity
288
Q

What does hyperaldosteronism lead to?

A

Alkalosis

289
Q

What type of innervation does the adrenal medulla receive?

A

Preganglionic innervation

290
Q

What is a pheochromocytoma and where is it found?

A

Neuroendocrine tumor in adrenal medulla

291
Q

What are the proportions of the production of hormones by the adrenal gland?

A

20% - noradrenaline

80% - adrenaline

292
Q

What is paracrine vs endocrine action?

A

Endocrine: acts on distant target cells
Paracrine: acts on target cells at point of release

293
Q

What is the mechanism of action of adrenaline and that of noradrenaline?

A

Adrenaline - endocrine action

Noradrenaline - paracrine action

294
Q

What enzyme catalyses the conversion of tyrosine into dihydroxyphenylalanine (DOPA)?

A

Tyrosine hydroxylase

295
Q

From what amino acid is epinephrine biosynthesized upon?

A

Tyrosine

296
Q

In what part of the adrenal medulla is noradrenaline converted into adrenaline?

A

Cytoplas

296
Q

In what part of the adrenal medulla is noradrenaline converted into adrenaline?

A

Cytoplasm

297
Q

What enzyme catalyses the conversion of norepinephrine into epinephrine?

A

PNMT (phenylmethanotamine-N-methyltransferase)

298
Q

What is the effect of cortisol on PNMT?

A

Stimulation

299
Q

Where are the catecholamines stored?

A

In vesicles in chromaffin cells of adrenal medulla

300
Q

With which other molecules are catecholamines CO-SECRETED?

A

Chromogranin A (notably), B, C neuropeptide Y….

301
Q

What is the clinical relevance of chromogranin A?

A

Screening of catecholamine-producing tumors (due to feedback on catecholamine production)

302
Q

On what receptor does adrenaline preferentially act on?

A

Beta receptors

303
Q

On what receptor does noradrenaline preferentially act on?

A

Alpha receptors

304
Q

What is the main effect achieved via A1 receptor?

A

Vasoconstriction

305
Q

What is the main effect achieved via A2 receptor?

A

Decreased insuline release

306
Q

What ARE the main effectS achieved via B1 receptor?

A

Cardioacceleration

Increased myocardial strength

307
Q

What ARE the main effectS achieved via B2 receptor?

A 
RELAXATION (and vasoconstriction)
Intestinal and bladder wall relaxation 
Uterus relaxation 
Bronchodilation 
Calorigenesis
Glycogenolysis
Lipolysis
308
Q

What is the primary mechanism of action of A2 receptor?

A

Decreased cAMP (inhibition)

309
Q

What is the mechanism of action of ventolin (albuterol) for asthma?

A

Acts on B2 adrenergic receptors
Relaxes bronchial smooth muscle
Secondary effect: increased HR

310
Q

What ENZYME (notably) catalyses the metabolism of of epinephrine and norepinephrine?

A

COMT (catechol-orthomethyl transferase)

311
Q

What are the resultant molecules from the metabolism of epinephrine and norepinephrine?

A

Metanephrine and normetanephrine

312
Q

What is the clinical relevance of metanephrine and normetanephrine?

A

Diagnosis of pheocromocytoma and paranganglioma

313
Q

What axis and nervous system does stress activate?

A

Hypothalamic-pituitary-adrenal axis

SNS

314
Q

Via which nucleus are the HPA axis and SNS activated?

A

Locus ceruleus

315
Q

What is the effect of the activation of the locus coeruleus nucleus?

A

Insulin resistance

Hypertension

316
Q

What is the effect of ACUTE physical exercise on adrenergic receptors?

A

Activation of ALL of them

317
Q

What are the general consequences of stress?

A

Obesity development
Carbohydrate intolerance
Dyslipidemia
Arterial hypertension

318
Q

Why can stress cause irregular menstrual cycles?

A

Releases corticotropin releasing hormone which:

Inhibits GnRH –> inhibits LH/FSH –> inhibits gonadrotropins

319
Q

What is the effect of an increase in cortisol?

A

Inhibitory effect on total secretion of anterior pituitary gland

320
Q

What do the a cells of the islet of langerhans release?

A

Glucagon

321
Q

What do the b cells of the islet of langerhans secrete?

A

Insulin

322
Q

What do the delta cells of the islet of langerhans secrete?

A

Somatostatin

323
Q

What do the F cells of the islet of langerhans secrete?

A

Pancreatic polypeptide (AKA PP cells)

324
Q

What do the epsilon cells of the islet of langerhans secrete?

A

Ghrelin

325
Q

What is the most prevalent type of islet of langerhans?

A

B-cells

326
Q

What molecule is measured to differentiate between type 1 and type 2 diabetes and why?

A

C peptide because it is produced at the same rate as insulin but has a longer half-life

327
Q

What enzyme breaks down C-peptide?

A

Proinsulinases by breaking sulfide bridges

328
Q

What is the main mechanism for adjustment of insulin secretion?

A

Phosphorylation of glucose into glucose-6-phosphate

329
Q

What is the pattern of insulin secretion?

A

5% is INITIALLY released as PREFORMED - 1st phase
95% is released 2HRS later - 2nd phase (postpandrial = after a meal)
Biphasic curve

330
Q

How does the SNS regulate the release of insulin?

A

Via A2 adrenergic rcp

Inhibitory effect on insulin release

331
Q

What are incretin hormones?

A

Stimulate internal insulin secretion
GLP-1 (glucagon-like-peptide 1)
GIP (gastric inhibitory peptide)

332
Q

Where are GLP-1 and GIP cells released from respectively?

A

GLP-1: L cells of small & large intestine

GIP: duodenal and jejunal K cells

333
Q

What conditions and hormones inhibit insulin secretion?

A

Fasting, hypoglycemia, glucagon, adrenaline, GH, cortisol,

334
Q

What is the composition of the insulin receptor?

A

2 alpha subunits + 2 beta subunits held together by disulfide linkages

335
Q

What are the only type of cells that can use glucose without the intermediation of insulin?

A

Brain cells because they are PERMEABLE to glucose

336
Q

What is the treatment for diabetes type 2?

A

Blockage of SGLT-2 (sodium-glucose cotransporter)

337
Q

What is the main function of GLUT2 (apart from transporting glucose)?

A

Stimulate release of insulin in beta cell

338
Q

What is the main function of GLUT4 (apart from transporting glucose)?

A

Intracellular metabolisation of glucose

339
Q

What is THE MAIN effect of insulin?

A

Anabolism!!!!

340
Q

What is the product of the conversion of proglucagon by alpha cells (islet of langerhans)?

A

Glucagon

341
Q

What is the product of the conversion of proglucagon by intestinal L cells?

A

GLP-1

GLP-2

342
Q

What are the main actions of glucagon?

A 
Thermogenic effects on brown adipose
Appetite inhibition 
Can be used to assess pancreatic reserve of insulin
Hepatic glucose production
Proteolysis, ketogenesis, contractility
343
Q

Why does GLP-1 not cause hypoglycemia?

A

Because their effect is dependent on glucose levels (irregularity) - they stop acting as soon as glycemia normalises

344
Q

What is the effect of an increase in ghrelin (fasting state)?

A 
Appetite stimulation
Increases glucagon
Reduces insulin
Favours lipolysis 
Favours hepatic glucose production
345
Q

What are the consequences of obesity?

A

Adipocytes hypertrophy
Dysfunctional adipocyte (insulin sensitivity, secretory function, lipid storage)
Subcutaneous tissue can sometimes not accommodate all of the fat

346
Q

What are the types of adipocytes?

A

White
Beige
Brown

347
Q

What confers thermogenic capacity in adipocytes?

A

Uncoupling protein 1 (UCP 1)

348
Q

Where are the essential and non-essential WHITE adipocytes located?

A

Essential - subcutaneous

Non-essential - visceral

349
Q

Why is white adipose tissue in the visceral compartment not good?

A

White adipose tissue in visceral compartment (abdominal location) drains FFA to portal vein of liver –> releases TNF (inflammatory marker) –> insulin resistance

350
Q

What type of adipocyte expresses UCP1?

A

Brown adipose tissue

351
Q

What are the main differences between white and brown adipocytes?

A

Brown: highly vascularised and SNS innervation

352
Q

What percentage of the population with normal and overweight BMI meet diagnostic criteria for obesity?

A

29% of people with normal BMI

80% of people with overweight BMI

353
Q

What is the total daily energy expenditure based upon from most to least?

A

Basal metabolic rate
Thermic effect of food
Non exercise activity
Exercise activity

354
Q

What transporter is needed for beta-oxidation?

A

Carnitine

355
Q

What are the 3 main pathways of lipid metabolism?

A

Exogenous pathway
Endogenous pathway
Reverse transport pathway

356
Q

What does the exogenous pathway consist of?

A

Fat intestinal digestion and absorption –> liver

357
Q

What does the endogneous pathway consist of?

A

Fat from liver that reaches tissues

358
Q

What does the reverse transport pathway consist of?

A

HDL collects FA from tissues and takes it to liver

359
Q

Characteristics of chylomicrons (lipoprotein)

A

Transport triglycerides

Lowest density

360
Q

Which lipoproteins are atherogenic?

A

Apo B100 and Apoa

361
Q

Which lipoproteins contain the apoprotein ApoB48?

A

Chylomicrons

Chylomicron remnants

362
Q

Which lipoproteins contain the apoprotein B100?

A

VLDL
IDL
LDL
LpA

363
Q

What apoproteins does lipoprotein A contain?

A

Apo B 100

Apo a

364
Q

Elevated value of which cholesterol value is associated with cardiovascular protection?

A

HDL

365
Q

What are chylomicrons composed of?

A

Triglycerides
ApoB-48
Cholesterol
Phospholipids

366
Q

What is the exogenous pathway of lipid metabolism?

A

Chylomicron (thoracic duct –> vena cava) –> FA and chylomicron remnant
FA to muscle and adipose tissue
Chylomicron remnant to liver for cholesterol recycling

367
Q

What is the endogenous pathway of lipid metabolism?

A

Liver: synthesis of VLDL –> circulation
VLDL –> FFA (by lipoprotein lipase) that accumulates in adipose tissue
High concentration of chylomicrons –> VLDL remnants that reach liver

368
Q

What happens if LDL receptors in hepatocytes decreases?

A

LDL particles remain in circulation
Increase LDL concentration
Oxidation & glycosylation of LDL makes it more atherogenic

369
Q

What is the self-regulatory mechanism in a situation of dyslipidemia?

A

Statins inhibit HMG-CoA reductase –> cholesterol production is inhibited –> increase in LDL rcp. –> lower LDL in macrophages

370
Q

Why can PCSK9 inhibitors be used in hypercholesterolemia?

A

PCSK9 degrades LDL receptor

371
Q

What is the function of the SR-BI receptor?

A

Mediate selective uptake of HDL-derived cholesteryl esters into tissues

372
Q

What is SR-BI receptor?

A

Type of HDL

SOI2 (9 decks)

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