Week 4-Endocrinology Flashcards

1
Q

What’s fast adaptations in endocrinology?

A

1.Neural control of behaviour
2.Brain and its divisions
3.Neurons, synapses, plasticity

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2
Q

What’s slow, lasting adaptations in endocrinology?

A

1.Reproductive Behaviour
2.Stress, emotions (agression)
3.Social, affiliative behaviour
4.Eating behaviour and eating disorders

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3
Q

Define a hormone and name 3 types of hormones

A

A chemical agent secreted by a group of cells and acting at a distance from the site of origin (gland, tissue)
1.Endocrine hormones: secreted into the circulating blood by specialised cells or glands (e.g., insulin, corpus luteum)
2.Neuroendocrine hormones: secreted by neurones into circulating blood (e.g., hypothalamic releasing hormones)
3.Cytokine hormones: peptides secreted by tissues (e.g., leptin)

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4
Q

What are lipid insoluble?

A

-Proteins and peptides (e.g., insulin)
-Derivatives of amino acid tyrosine (e.g., thyroid hormones)
-Lipid insoluble hormones are amino acid chains (e.g., valine, proline etc.,)
-Proteins=>100 amino acids
-Peptides=<100 amino acids

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5
Q

What are lipid soluble?

A

-Common precursor is cholesterol, steroid hormones (e.g., cortisol, testosterone etc.,)
-Cholesterol is a fat-like molecule, abundant in cell membranes

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6
Q

Define a key and a lock

A

hormones can only affect a cell that has a receptor that fits (i.e. is complementary)

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7
Q

True or False: Hormone receptors are large proteins

A

True! a cell usually needs to have 2000+ receptors to be engaged by a hormone

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8
Q

Define down-regulation and up-regulation of receptors

A

A tool to regulate bodily responses to hormones.

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9
Q

What 3 ways can the mechanism of hormone actions depend on their chemistry?

A

1.Via ion channels (rare) and G protein-linked receptors (frequent) e.g., Peptides or Proteins
2.Via binding to intracellular receptors and acting on DNA (Steroids)
3.Via direct actions on the cell nucleus (Thyroid hormones)

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10
Q

How do G protein-linked hormone actions work?

A

-A receptor on the outer side of the membrane is activated by a hormone
-It cause activation of alpha unit of G protein (GDP)
-Alpha unit detaches from beta and gamma units and activates various intracellular enzymes (adenylyl cyclase, phospholipase C and several others).

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11
Q

How do Steroid hormone actions work?

A

-A steroid freely passes the cell membrane and binds to receptors in the plasma
-the hormone-receptor complex binds to the hormone-response element strand of DNA (the promoter)

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12
Q

How do Thyroid hormone actions work?

A

-Thyroid and adrenal medullary
hormones are derived from amino
acid tyrosine.
-The hormones pass the cell membrane via carrier channels and enter the nucleus.
-There is a thyroid receptor on
hormone sensitive element of
some genes causing transcription
of DNA into mRNA.
-Tyrosine-based hormones can
activate or deactivate genes and
lead to synthesis of new proteins.

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13
Q

What are the 9 divisions of hormones based on their effects?.

A

1.Hypothalamic releasing hormones: top level of regulation, growth
2.Anterior pituitary hormones: second level of regulation
3.Posterior pituitary hormones (vasopressin, oxytocin) – smooth muscle contractions
4.Thyroid hormones (thyroxin T4, triiodothyronin) - metabolism
5.Adrenal cortex hormones (aldosterone, cortisol, androgens) – metabolism, stress
6. Adrenal medulla hormones (adrenaline, noradrenaline) – stress, emotions
7. Pancreas (insulin, glucagon) – maintaining glucose level
8. Sex hormones (estrogens, progesterone, testosterone) - reproduction
9. Gastro-intestinal peptides (CCK, leptin, ghrelin, NYP): eating behaviour

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14
Q

Name 6 hypothalamic releasing and inhibitory hormones

A

1.Thyrotropin-releasing hormone = TRH stimulates secretion of thyroid-stimulating hormone in anterior pituitary
2.Gonadotropin-releasing hormone = GnRH stimulates secretion of LH and FSH in anterior pituitary
3.Corticotropin-releasing hormone = CRH stimulates secretion of adrenocorticotropic hormone in anterior pituitary
4.Growth hormone-releasing hormone = GHRH stimulates secretion of growth hormone in anterior pituitary
5.Growth hormone-inhibitory hormone = somatostatin Inhibits secretion of growth hormone in anterior pituitary
6.Prolactin-inhibitory hormone – PIH (dopamine) inhibits secretion of prolactin in anterior pituitary

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15
Q

AP contains cells of different types
specialised for secretion of different pituitary hormones, what are the 5 different hormones?

A

1.somatotropes
2.corticotropes
3.thyrotropes
4.gonadotropes
5.lactotropes

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16
Q

Name 6 anterior pituitary hormones

A

1.Growth hormone-somatotropin
2.Adrenocorticotropic hormone – ACTH
3.Thyroid stimulating hormone – TSH
4.Follicle-stimulating hormone – FSH
5.Luteinizing hormone – LH
6.Prolactin – PRL

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17
Q

State the function of the growth hormone-somatotropin

A

Stimulates body growth, cell multiplication and differentiation

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18
Q

State the function of the adrenocorticotropic hormone – ACTH

A

Stimulates secretion of glucocorticoids and androgens in the adrenal cortex

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19
Q

State the function of the thyroid stimulating hormone – TSH

A

Stimulates the secretion of thyroid hormones

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20
Q

State the function of the follicle-stimulating hormone – FSH

A

Stimulates development of ovarian follicles and spermatogenesis in testis

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21
Q

State the function of the luteinizing hormone – LH

A

Causes ovulation and stimulates the corpus luteum; stimulates secretion of estrogens and progesterone in the ovaries; stimulates testosterone in testis

22
Q

State the function of the prolactin – PRL

A

Stimulates milk secretion and development of mammary glands

23
Q

Define portal system

A

2 capillary beds just following each other

24
Q

What 2 things does the posterior pituitary (neurohypophysis) store?

A

1.Vasopressin (arginin-vasopressin antidiuretic hormone)-primarily in the supraoptic nucleus
2.Oxytocin-primarily in paraventricular nucleus

25
Q

What happens after the birth of a baby in regards to Prolactin (PRL, anterior pituitary)?

A

-Sudden loss of estrogen and progesterone from placenta which causes PRL to stimulate lactation in postpartum females
-PRL inhibited in non-pregnant women via hypothalamatic prolactin inhibitory hormone (dopamine)
-Mechanical stimulation of nipples during nursing stimulates PRL secretion
PRL suppresses GnRH and consequently estrogen and progesterone
-PRL facilitates parenting behaviour and monogamy

26
Q

What happens after the birth of a baby in regards to Prolactin (PRL, anterior pituitary)?

A

-Sudden loss of estrogen and progesterone from placenta which causes PRL to stimulate lactation in postpartum females
-PRL inhibited in non-pregnant women via hypothalamatic prolactin inhibitory hormone (dopamine)
-Mechanical stimulation of nipples during nursing stimulates PRL secretion
PRL suppresses GnRH and consequently estrogen and progesterone
-PRL facilitates parenting behaviour and monogamy

27
Q

What’s the link between prolactin (PRL) and the brain?

A

-PRL can pass the blood-brain barrier and the brain has PRL receptors in the hypothalamus and other regions
-PRL has anxiolytic effects
-PRL counteracts the effects of the stress hormone (glucocorticoids)
-PRL improves the mood after parturition and opposes detrimental effects of stress during pregnancy on depression-like behaviour on offspring (Smith et al., 2004)

28
Q

What are the effects of PRL on anxiety according to Torner et al., J. Neurosci., 2001?

A

-PRL has anxiolytic effects: rats exposed to elevated-plus maze showing more exploratory behaviour if PRL was injected into the ventricles
-Blocking PRL receptors in rats increased anxiety levels

29
Q

What did Groer (2005) find about PRL levels in breast-feeding mothers

A

-PRL sig. higher in breastfeeding mothers than formula-feeding mothers
-PRL levels correlated negatively with perceived stress but only in the breastfeeding group

30
Q

What is Vasopressin or Arginine-vasopressin (posterior
pituitary)?

A

-A peptide (9 amino acids) causing decreased secretion of water (antidiuresis) via creating water channels (aquaporins) in collective ducts of kidneys
-The latency of this effect is 5-10 min
-The signals for secretion of vasopressin: increased conc. of solutes (ions) due to low water intake or due to loss of fluids (detected in the atria of the heart)
-The osmalilty of fluids is detected in the hypothalamus and in the third ventricle (stria terminalis of organus vasculorum)
-Vasopressin is a powerful vasoconstrictor agent: increases blood pressure

31
Q

What are the mechanisms of thirst?

A

-Osmoreceptor cells in supraoptic nucleus and stria terminalis of organus vasculorum shrink in response to increase of plasma osmalarity (plasma sodium concentration)
-Shrinking causes action potentials in the supraoptic nucleus which stimulates the release of vasopressin from secretory granules in posterior pituitary
-Dryness in the mouth, dehydration and loss of fluids stimulates sensation of thirst

32
Q

What’s Oxytocin – posterior pituitary?

A
  • Also a small peptide (9 amino acids) causing contractions of smooth muscles in the breast during milk ejection and in uterus during
    parturition
  • The amount of oxytocin increases during parturition. The signal for
    release of oxytocin comes from the increased pressure on uterine
    cervix during later stages of parturition.
  • Milk ejection: suckling stimulates the nipple of the breast and the
    somatosensory signals are being transmitted to hypothalamic
    supraoptic and paraventricular nuclei. Oxytocin stimulates the myoepithelial cells around the alveoli of milk glands.
  • Oxytocin is a hormone of social affiliation: OT increases both in men and women after the birth of a baby – promotes parenting.
33
Q

How do Mono- (Prairie) and polygamous (Montana) voles differ in their ability to increase production of oxytocin and vasopressin during the familiarisation period?

A

-monogamous voles activate the dopaminergic reward system (first D2 receptors, later D1 receptors) along with the 2 hormones
-Monogamous prairie voles showed stronger expression of vasopressin and OT receptors in nucleus accumbens than polygamous volves.

34
Q

What are T3 (triioidothyronine) and T4 (thyroxine)? (thyroid hormones)

A

-cleaved from a colloid (thryoglobulin) making up the bulk for thyroid gland
Widespread effects include:
-increased metabloism
-increased heart rate and strength of heart contractions
-increased respiration
-growth, CNS development

Regulation: TRH and TSH in the form of a double-feedback loop
-T3 and T4 have very slow effects (days, weeks)

35
Q

What are T3 (triioidothyronine) and T4 (thyroxine)? (thyroid hormones)

A

-cleaved from a colloid (thryoglobulin) making up the bulk for thyroid gland
Widespread effects include:
-increased metabloism
-increased heart rate and strength of heart contractions
-increased respiration
-growth, CNS development

Regulation: TRH and TSH in the form of a double-feedback loop
-T3 and T4 have very slow effects (days, weeks)

36
Q

What’s hypersecretion of thyroid hormones?

A

-Excitation of CNS, increased speed of cognitive at the cost of being disorganised
-Nervousness, anxiety, restlessness, impaired concentration, worries, paranoia,, depression, manic episodes in severe thyrotoxicosis

37
Q

What’s hyposecretion of thyroid hormones?

A

Cognitive: cognitive impairment, lack of concentration, memory deficits, psychomotor slowing

Psychiatric: delusions, hallucinations, depression, impaired sleep, apathy

38
Q

How do thyroid hormones affect mood and depression?

A
  • Animal experiments showed presence of thyroid receptors in many brain areas, especially in phylogenetically younger regions.
  • Thyroid hormones increase the turnover of serotonin (5-hydroxitryptamin, 5-HT) in brain stem nuclei, and hypothyroid states show a decrease in 5-HT production.
  • 5-HT and noradrenaline are the main mood regulatory systems, with depression showing a decreased serotoninergic activity
39
Q

Where are T3 and T4 hormones found from animal experiments?

A

They’re found in the cerebral cortex.

40
Q

What is Insulin?

A

-Secreted from beta-cells of Langerhans Islets in the pancreas
-Hormone of energy abundance: allows transport of glucose into cells in the presence of high blood glucose level, formation of glucose stores (glycogen) and fat stores (adipose tissues) and supports proteosynthesis
-Secretion initiated in the presence of high blood glucose, amino acids, parasympathetic stimulation, and gastrointestinal hormones gastrin, CCK and other factors.

41
Q

What is type 1 and type 2 diabetes caused by?

A

1=Lack of insulin secretion
2=Decreased sensitivity of insulin receptors knowns as insulin resistance

42
Q

What can increase insulin resistance and what can it lead to?

A

-Psychological stress can potentiate insulin resistance via the stress hormone cortisol
-It manifests in weight gain, obesity, fasting hyperglycemia and hypertension, poor sleep, reduced memory
-Exercise, calorie restriction and weight reduction can often help with type 2 diabetes with no meds required

43
Q

What’s the link between insulin and the brain?

A
  • Insulin penetrates the blood-brain barrier and brain has insulin receptors in a number of regions (hypothalamus, hippocampus, cortex, basal ganglia)
  • In humans, intranasal spraying of insulin allows insulin to enter the brain without affecting plasma glucose levels – used in behavioural experiments
  • In hypothalamus, arcuate nucleus, paraventricular nucleus and both lateral and ventromedial hypothalamus have insulin receptors in abundance:
  • Insulin inhibits orexigenic neurotransmitters such as Agouti-related Protein and Neuropeptide Y
  • Insulin promotes cleavage of alpha-melanocyte-stimulating
    hormone a-MSH which inhibits eating and stimulates energy expenditure
44
Q

Adrenal glands: What hormones are in the cortex and the medulla?

A

Cortex:
Glucocorticoids
(cortisol, corticosterone)
Aldosterone
Androgens
(dehydroepiandrosterone) (all steroid hormones)
Medulla: adrenalin, noradrenalin

45
Q

What are glucocorticoids: cortisol and corticosterone and what are their functions?

A

Hormones that help to cope with stress (trauma, cold, infection, surgery, psychological stress)
Functions:
-increase glucose levels (for muscles)
-supports genesis of new glucose
-mobilises free fatty acids (energy)
-mobilises amino acids (new proteins?)
-decreases immune response
-increases proteins in liver and plasma (healing of injured tissues?)
-decreases inflammation

46
Q

What does hypothalamic-pituitary-adrenal axis do?

A

Supports the adaptions to stress

47
Q

How does cortisol affect the brain via mineralo- and
glucocorticoid receptors?

A
  • Brain regions having receptors for cortisol are: hypothalamus, hippocampus, amygdala and prefrontal cortex
  • Slow, genomic effects of cortisol in the brain include synthesis of important neurotransmitters (dopamine, serotonin, noradrenaline, glutamate, acetylcholine)
  • Fast, non-genomic effects refer to modulation of membrane-associated proteins and rapid changes in monoamine levels – not known too well.
  • Effects of cortisol on brain and behaviour are usually in form of an inverted U
48
Q

What are the short-term effects of cortisol on behaviour (after
onset of acute stressor or after application of hydrocortisone)?

A

-Increases subjective arousal, activity and mood (euphoria)
-Self reported level ofn attention is related to increased cortisol concentraion, possibly via stimulating secretion of noraadrenaline
-Cortisol improves encoding of threat-relevant memories
-Cortisol enhances responses to negative stimuli , e.g., acoustic startle reaction
-Cortisol increases sensiticvity to rewards but decreases it for losses
-Decreased sensitivity to pain= stress induced analgesia

49
Q

What are the behavioural and brain effects of chronically
elevated cortisol?

A
  • Chronically elevated cortisol is associated with fatigue, anxiety,
    depression, apathy and impaired concentration.
  • Prolonged periods of increased cortisol alters the structure of neurons in prefrontal cortex, amygdala and hippocampus.
  • Atrophic changes in hippocampus manifest in impaired verbal and declarative memory.
  • Note: amygdala, prefrontal cortex and hippocampus are three brain regions that modulate the activity of the hypothalamic paraventricular nucleus.
  • Chronically elevated cortisol initiates a cycle of imbalances within the HPA.
50
Q

Adrenal medulla – What are the hormones adrenalin and noradrenalin and what are there effects?

A
  • Stimulated by the sympathetic nerve system
  • AD and NAD survive in blood for only 2 min
    Effects:
  • Increased heart rate and strength of cardiac contractions
  • vasoconstriction in abdominal region
  • vasodilation in skeletal muscles
  • increased metabolism
  • glycogenolysis
  • increased CNS arousal

Effects of adrenaline/noradrenaline depends on the type of receptors in a particular organ or tissue (alpha or beta receptors)