Lectures 22 & 23 (endocrine intro + pituitary) Flashcards

1
Q

how endocrine hormonal messages function vs neural messages

A
  • hormones circulate through the entire body whereas neurons only deliver signals to specific areas
  • they last from minutes to days whereas neural is less than a second to minutes
  • slow to begin signalling (s to m) whereas neural is milliseconds
  • blood borne
  • many are also neurotransmitters
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2
Q

Endocrine glands

A
  • hypothalamus
  • pineal gland
  • pituitary gland
  • thyroid gland
  • parathyroid glands
  • adrenal glands
  • pancreas
  • testes or ovaries
    **placenta (temporary, only during pregnancy)
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3
Q

Pathology associated with endocrine system

A
  • gigantism or acromegaly (excess growth hormone)
  • hyper/hypothyroidism (excess/defficient thyroid hormone)
  • hyper/hypoprolactinaemia (excess/deficient prolactin)
  • diabetes (low/insensitivity to insulin)
  • adissons disease (deficient cortisol or ACTH)
  • cushing’s syndrome (excess cortisol)
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4
Q

Hunger hormone communication

A
  • fat cells make leptin when ‘full’ to signal the hypothalamus –> stop eating
    (leptin deficiency can cause individual to overeat)
  • empty stomach produces ghrelin to signal the hypothalamus –> start eating
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5
Q

Endocrine cell hormone communication (pathway + types)

A
  • hormones made in endocrine cell, travels through blood, captured by receptor on distant cell, trigger hormone effect, hormone detaches, effects dissipate
  • hydrophillic (most common) and lipophillic
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6
Q

Paracrine cell hormone communication

A
  • hormones made in paracrine cell only effect nearby cells
    (eg: prostaglandins and nitric oxide)
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7
Q

Autocrine cell hormone communication

A
  • hormones made in autocrine cell only effect the cell itself
    (eg: IGF1 - growth factors work as autocrine at times)
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8
Q

hydrophillic circulating hormones

A
  • water soluble, travel through blood
  • bind to extracellular receptors
  • message must be transduced to effect the cell
  • often leads to production of second messengers (eg. cAMP, IP3)
  • second messengers alter cellular function (one H hormone can cause many SM)
  • SM concentration fluctuates depending on H hormone receptor binding
    *some hormones (eg: insulin) do not need second messengers
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9
Q

lipophilic endocrine hormones

A
  • travel through blood
  • pass through phospholipid bilayer (intracellular or even intranuclear)
  • bind to intracellular receptors
  • hormone-receptor complex binds to DNA
    (steroid hormones)
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10
Q

Controlling hormone secretion (loop)

A

all hormones work with negative feedback
(stimulus –> increased hormones –> signal decreased stimulus –> decreased hormones)
eg:
- chemical alteration in blood (exercise)
- nervous stimulation (fear response)
- other hormones can signal hormone production

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11
Q

Posterior pituitary gland hormone circulation

A
  • hormones made by neurosecretory cells in hypothalamus
  • hormones travel in axons to the PPG
  • enter bloodstream through hypophyseal veins and arteries
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12
Q

Anterior pituitary gland hormone circulation

A
  • releasing hormones made by neurosecretory cells in hypothalamus
  • travel in axons to hypophyseal portal system
  • travel through blood to APG
  • triggers stimulating/tropic or non-tropic/direct hormone production in APG release into blood
  • stim. h. goes to target area (may produce another direct/non-tropic hormone)
  • hormones travel back to hypothalamus and APG, inhibiting hormone production
    (fluctuating cycle of hormones)
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13
Q

Thyroid hormone regulation

A
  • hypothalamus: thyrotropin releasing hormone (TRH)
  • anterior pituitary: thyroid stimulating hormone (TSH)
  • thyroid gland: thyroid hormone
  • triggers increased metabolic rate, protein synthesis and fat breakdown
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14
Q

Inhibiting hormones

A
  • inhibits production of stimulating hormone
    (eg: growth hormone inhibiting hormone GHIH inhibits GH and TSH)
    (prolactin is almost completely regulated by its inhibiting hormone PIH (dopamine), little bit by releasing hormone TRH)
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15
Q

Pituitary gland development

A

anterior: outgrowth of the ectoderm of the roof of the mouth (pars distalis)
posterior: outgrowth of the ectoderm at the base of the hypothalamus (pars nervosa)
pars intermedia: seperates ant. and post.
(develops at 5 - 16 weeks of pregnancy, W13, the pituitary, 3:00)

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16
Q

alternate names for posterior and anterior pituitary

A

anterior: adenohypophysis
posterior: neurohypophysis
pituitary: hypophysis

17
Q

bone of the skull where the pituitary is located

A

Sphenoid –> hypophyseal fossa

18
Q

structures that form turk’s saddle/sella turcica

A

tuberculum (front), hypophyseal fossa, dorsal (back) sellae
(part of sphenoid)

19
Q

Pituitary tumour

A

pituitary adenoma –> can cause a depression in the hypothalamus (called mass effect)

symptoms: visual defects (optic chiasm, bitemporal hemianopia) and headaches

removal: transsphenoidal hypophysectomy, remove tumour through sphenoid sinus (up nose), replace with fat and seal in with cartilage and glue

20
Q

Pituitary blood supply

A
  • Ant: superior hypophyseal artery –> hypophyseal portal veins –> ant. hypo. v.
  • Post: inferior hypophyseal artery –> post. hypophyseal veins

issues: BP extremely low in AHV, if BP drops in body (eg: extreme blood loss) it’s easy for blood flow to stop here, APG can die –> panhypopituitarism

21
Q

Main hormones in Anterior pituitary

A

Tropic (stimulating):
- FSH: follicle stimulating hormone - promotes follicle and sperm development
- LH: luteinizing hormone - promotes ovulation, sex steroid production
- ACTH: adrenocorticotropic hormone - promote production of glucocorticoids
- TSH: thyroid stimulating hormone - stims thyroxin release
Non-tropic (direct):
- PRL: prolactin: stimulates milk production in F
- hGH: human growth hormone - promote protein synthesis + bone growth + glycogen –> glucose
- MSH: melanocyte stimulating hormone - increase pigmentation (pars intermedia)
(FLAT PeG M)

22
Q

Main hormones in Posterior pituitary

A

**produced in hypothalamus, just travel through PPG
- Oxytocin: increase uterine contraction + ejection of milk
- ADH: Antidiuretic hormone (vasopressin) causes water re-uptake in kidneys (suppresses urination) - triggered by high Na in blood

23
Q

Hormones produced in Hypothalamus

A
  • TRH –> produce TSH
  • CRH –> produce ACTH
  • GnRH –> produce FSH and LH
  • GHRH –> produce hGH
  • GHIH –> inhibit hGH
  • PIH –> inhibit PRL
24
Q

stimuli that regulate growth hormones

A

hypoglycemia (low blood glucose) –> release GHRH (promote (hGH)
hyperglycemia (high BG) –> release GHIH (inhibit hGH)
- normal BG is about 90mg/mL

25
Q

growth of long bones stimulus

A
  • hGH stimulates formation of new cartilage at epiphyseal line
  • growth plate is ‘closed’ by testosterone and estrogen
26
Q

hGH secreting tumors

A

before growth plate closes: gigantism (very tall)
after growth plate closes: acromegaly (thick skin, broad nose…)
both diabetic due to high BG

27
Q

Main sex steroids

A

progesterone, estrogens, androgens (testosterone, DHEA)
*act as inhibitors for GnRH

28
Q

Prolactin regulation

A

TRH promotes PRL
PIH inhibits PRL
suckling inhibits PIH
- domperidone (dopamine receptor blocker) inhibits PIH since it is dopamine

29
Q

excess/deficient prolactin issues

A

hyperprolactinaemia (excess)
- galactorrhea (large amount of milk/milk outside pregnancy)
- amnenorrhea (lack of menstrual cycles)
- infertility
- impotence (inability to get erect - males)
hypoprolactinaemia (deficient)
- sub/infertility in both men and women (cause unclear)

30
Q

development of lactating (active) mammary glands

A

high levels of estrogen and progesterone trigger activation
- that’s why breaks are needed from hormonal birth control pills