Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BIO125 Physiology > Week 3 The endocrine system II > Flashcards

Week 3 The endocrine system II Flashcards

1
Q

What is the Hypothalamo-Pituitary Complex?

A
  • Hypothalamus = part of diencephalon below thalamus
  • The hypothalamus is conntected to the pituitary by the Infundibulum
  • Hypothalamus communicates with anterior pituitary lobe (adenohypophysis) via hypothalamic-hypophyseal portal circulation
  • Adenohypophsis = glandular epithelium - grows up from buccal cavity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are Hypothalamic Hormones?

A
  • 7 hypophysiotropic hormones (peptides)
  • “Hypophysis” = pituitary*
  • “Tropic” = nourishing / directing*
  • Endocrine axis commonly involves 3 hormones in a hierarchical chain (“H-P-gland” axis): HPA, HPG & HPT axes
  • Hypophysiotropic hormone = direct pituitary, 1st member in chain. However…
    • Primary endocrine disorder = defect in final endocrine gland in hierarchy (e.g. thyroid)
    • Secondary endocrine disorder = AP defect (e.g. TSH)
    • Tertiary endocrine disorder = defect in hypothalamus (e.g. TRH)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Hypothalamic Hormones: What are the 7 hypophysiotropic hormones?

A

7 hypophysiotropic hormones (generally peptides – median eminence – 3o ventricle):

  1. PRH = prolactin-releasing hormone (unknown how large it is, not seen even tho inhibiting hormone is present)
  2. PIH = prolactin-inhibiting hormone
  3. TRH = thyrotropin-releasing hormone (3 a.a.)
  4. CRH = corticotropin-releasing hormone (41 a.a.)
  5. GHRH = growth hormone-releasing hormone (44 a.a.)
  6. GHIH = growth hormone-inhibiting hormone (somatostatin) (28 a.a.)
  7. GnRH = gonadotropin-releasing hormone (10 a.a.)

Hypothalamus influenced by neural & hormonal inputs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the AP Hormones?

A

6 AP hormones synthesised within the AP by 5 different cell populations:

  1. TSH (thyroid-stimulating hormone) / thyrotropin
  2. GH (growth hormone) / somatotropin
  3. ACTH (adrenocorticotropic hormone) / corticotropin
  4. FSH (follicle-stimulating hormone) / follitropin
  5. LH (luteinising hormone) / luteotropin
  6. PRL (prolactin)

Of these six hormones, not all are tropic hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

AP Hormone: TSH (thyroid-stimulating hormone) / thyrotropin

A
  • synthesised by AP thyrotropes
  • synthesis & secretion of TSH stimulated by TRH
  • TSH stimulates growth & function of thyroid gland (increased synthesis & secretion of T4 and T3)
  • indirect effects on BMR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

AP Hormone: GH (growth hormone) / somatotropin

A
  • synthesised by AP somatotropes
  • synthesis/secretion of GH stimulated by GHRH; inhibited by GHIH / somatostatin
  • GH stimulates growth & metabolism
  • Some direct effects; some indirect effects (via hepatic IGF1 = somatomedin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

AP Hormone: ACTH (adrenocorticotropic hormone) /corticotropin

A
  • synthesised by AP corticotropes
  • synthesis/secretion of ACTH stimulated by CRH
  • ACTH stimulates growth and function of adrenal cortex (increased synthesis of cortisol + DHEA)
  • indirect effects on metabolism (plasma [glucose]) and development
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

AP Hormone: FSH (follicle-stimulating hormone) / follitropin

A
  • synthesised by AP gonadotropes
  • one of 2 (or 3) gonadotropins (each a heterodimeric glycoprotein: common α-subunit plus specific β-subunit)
  • synthesis/secretion of FSH stimulated by GnRH
  • FSH stimulates growth and function of gonads (germ cell maturation and release)
    • in ovary, stimulates growth of ovarian follicles and synthesis of estradiol (via granulosa cells of ovarian follicles)
    • in testis, stimulates spermatogenesis (via Sertoli cells of testis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

AP Hormone: LH (luteinising hormone) / luteotropin

A
  • synthesised by AP gonadotropes
  • one of 2 (or 3) gonadotropins (each a heterodimeric glycoprotein: common α-subunit plus specific β-subunit)
  • synthesis/secretion of LH stimulated by GnRH
  • LH stimulates growth and function of gonads
    • in ovary, stimulates release of oocyte at ovulation, synthesis of androgens (in theca cells of ovarian follicles) and progesterone (in cells of corpus luteum)
    • in testis, stimulates synthesis of testosterone (in Leydig cells)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

AP Hormone: PRL (prolactin)

A
  • synthesised by AP lactotropes
  • under dominant negative control of PIH (dopamine)
  • PRL stimulates lactation (mammary glands) – sex-specific endocrine action (function unknown in healthy males)
  • Second order feedback loop to hypothalamus; no downstream endocrine gland to exert third order feedback
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Hypothalamo-Pituitary Complex: What does the hypothalamus communicate with (& via) to produce oxytocin (OT) & vasopressin (AVP)?

A

posterior pituitary lobe (neurohypophysis) via neural tract

(cell bodies of magnocellular neurones in hypothalamus – terminate in posterior lobe – secrete oxytocin (OT) & vasopressin (AVP))

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the PP hormones?

A

oxytocin (OT) & vasopressin (AVP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

PP hormones: what does OT stimulate?

A
  • stimulates contraction of smooth muscle
    • mammary glands [suckling reflex]
    • myometrium [Fergusson reflex])
  • behavioural / emotional actions
    • bonding + hugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

PP hormones: what does AVP stimulate?

A
  1. stimulates contraction of blood vessels to increase blood pressure (vasopressor)
  2. facilitates water resorption in renal collecting ducts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

In fish, amphibians and birds – vasotocin does what?

A

Vasotocin combines OT and AVP actions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the cells present in the ardenal coretx and adrenal medulla, and what do they synthesis?

A
  • Adrenocortical cells - synthesise corticosteroid hormones
  • Adrenomedullary chromaffin cells – synthesis and secrete catecholamines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

The structure of Adrenal Glands:

A
20
Q

Corticosteroids: What do Mineralocorticoids (e.g. aldosterone) do?

A

influence salt and water balances (electrolyte balance and fluid balance)

  • increases resorption of Na+ ions (in distal nephron, colon and salivary glands) / anti-natriuresis, then drives water resorption to increase plasma volume / BP
  • increases secretion of K+ ions (into urine) in distal nephron / kaliuresis (hypokalemia can cause tetani)
21
Q

Corticosteroids: How are Mineralocorticoids (e.g. aldosterone) synthesised?

A
  • synthesised in ZG (zona glomerulosa)
  • synthesis stimulated by electrolytes:
    • directly by increased plasma [K+]
    • indirectly by decreased plasma [Na+]
  • (fall in BP increases secretion of renin - converts*

angiotensinogen to angiotensin I, metabolised to

angiotensin II by ACE; activates AT2 receptors in ZG)

22
Q

Point of clinical interest: What are the clinical therapies for hypertension?

A
  1. ACE inhibitors (e.g. ramipril) decrease conversion of Ang I to Ang II
  2. AT2R antagonists (e.g. losartan) – inhibit stimulation of aldosterone synthesis by Ang II
  3. Aldosterone synthase (CYP11B1) inhibitors (e.g. metyrapone) inhibit conversion of corticosterone to aldosterone
  4. Mineralocorticoid receptor antagonists (e.g. spironolactone) prevent aldosterone from increasing renal and colonic Na+ resorption
23
Q

Corticosteroids: What do Glucocorticoids (e.g. cortisol) do?

A
  • increase plasma [glucose] for brain
  • increase plasma [NEFA] and amino-acids
  • mediate chronic stress response - suppress all “non-essential” body functions (e.g. reproduction) and immune system (anti-inflammatory steroids)
  • circulate in association with albumen and CBG (transcortin)
  • exert negative feedback on CRH and ACTH
24
Q

Corticosteroids: How are Glucocorticoids (e.g. cortisol) synthesised?

A
  • synthesised in ZF (zona fasciculata)
  • stimulated by ACTH in HPA axis
25
Q

Point of clinical interest:

“Mineralocorticoid” receptor (MR) = type 1 corticosteroid receptor is non-specific – equal affinities for glucocorticoids & mineralocorticoids

A
  • Cortisol acts as MR ligand
  • Cortisol present at 100 to 1000X higher concentrations than aldosterone
  • Cortisol has to be inactivated (by 11βHSD2) to confer specificity for aldosterone on MR
  • Enzymatic inactivation of cortisol defective in patients with HSD11B2 mutations or following intoxication with liquorice
26
Q

Corticosteroids: What do Adrenal androgens (e.g. dehydroepiandrosterone / DHEA) do?

A
  • adrenal DHEA metabolised in peripheral tissues (e.g. skin, adipose tissue and bone) to more potent androgens (e.g. androstenedione and testosterone) and estrogens (e.g. estradiol) – implicated in pubertal development & ageing
  • DHEA circulates in association with albumen and SHBG
  • DHEA-S (sulphate) has no affinity for SHBG
27
Q

Corticosteroids: How are Adrenal androgens (e.g. dehydroepiandrosterone / DHEA) synthesised?

A
  • synthesised in ZF & ZR (zona reticularis)
  • stimulated by ACTH in HPA axis
28
Q

What is the Adrenal Medulla?

A

Modified part of sympathetic autonomic nervous system (ANS) – chromaffin cells = modified post-ganglionic neurones (lack axons)

29
Q

What does the Adrenal Medulla synthesis and secrete?

A
  • Synthesises and secretes catecholamines – 80%:20% adrenaline:noradrenaline (epinephrine:norepinephrine)
    • methylation of noradrenaline to adrenaline catalysed by PNMT enzyme – upregulated by glucocorticoids from overlying adrenal cortex
    • secretion of adrenaline (chromaffin granules) triggered SOLELY by sympathetic innervation (NOT under endocrine control!)
30
Q

Adrenal Medulla: What do Catecholamines act via?

A

Catecholamines act via GPCR’s:

  • α1AR and α2AR (modulate [Ca<b>2+</b>]i)
  • β1AR and β2AR (modulate [cAMP]i; activate PKA)
31
Q

What response does the adrenal medulla mediate?

A

Mediate acute stress response – aspects of the “fight or flight response”

• e.g. vasoconstriction / increased peripheral resistance

plus increased heart rate increases blood pressure /

flow

  • e.g. increase plasma [glucose] and [NEFA]
  • e.g. sensitise the CNS and exert autonomic functions

(sweating and dilation of the pupils)

32
Q

What is are the features of the pancreas?

A
33
Q

What are the features of the pancreas: duct and acinar cells?

A
34
Q

The features of the pancreas: What does the Exocrine pancreas do?

A

pancreatic acini secrete “pancreatic juice” (amylase, lipase, nuclease and protease enzymes plus HCO3- ions) via ducts into GI tract

35
Q

The features of the pancreas: What does the Endocrine pancreas do?

A

Regulate plasma [glucose]

  • ​endocrine glands
  • account for 1-2% of pancreas (by mass)
  • secrete hormones directly into plasma:
    • glucagon - raises plasma [glucose]
    • insulin - lowers plasma [glucose]
    • somatostatin - inhibits secretion of pancreatic hormones
    • pancreactic polypeptide (PP) - appetite control
36
Q

What are the Islets of Langerhans?

A
  • α cells – glucagon
  • β cells – insulin
  • δ cells – somatostatin
  • PP cells – PP!
37
Q

Point of Clinical Interest: Plasma [glucose] has to be kept between 4 and 8 mmol L-1 (typically 5 mmol L-1) in humans

A
  • hypoglycaemia (<4mmol L-1) – insufficient glucose to support brain function (coma)
  • hyperglycaemia (>8mmol L-1) – excess glucose causes:
    • disturbance to osmolarity
    • damage to membrane proteins and lipids (advanced glycation end-products) culminating in diabetic nephropathy, neuropathy and retinopathy
38
Q

Glucose Homeostasis: Insulin and glucagon serve as _____ _____ to control _____ (glucose, NEFA & a.a.) usage and storage

A

Insulin and glucagon serve as antagonistic pair to control metabolic fuel (glucose, NEFA & a.a.) usage and storage

39
Q

Glucose homeostasis: Insulin and glucagon serve as antagonistic pairto control metabolic fuel (glucose, NEFA & a.a.) usage and storage

What is an anabolic state?

What is an catabolic state?

A
  • anabolic state (polymer synthesis – excess energy stored as glycogen {liver and skeletal muscle} and triglyceride {adipose tissue})
  • catabolic state (polymer breakdown – energy stores mobilised through glycogenolysis and/or lipolysis)
40
Q

Glucose homeostasis: What is the Absorptive state?

A

Absorptive state – raised [glucose] 3-4 hours post-feeding (anabolic) (elevates insulin)

41
Q

Glucose homeostasis: What is the Post-Absorptive state?

A

Post-absorptive state – decreased [glucose] between meals (catabolic) (elevates glucagon + …)

42
Q

What is the Antagonistic Control in glucose homeostasis?

A
43
Q

Anatagonistic Control in the Endocrine Pancreas:

A
44
Q

How is Insulin Secretion controlled?

A
  • β cells respond directly to plasma [glucose]
  • Mechanism of excitation-secretion coupling for insulin relies on 2 types of plasma membrane ion channel:
  1. ATP-sensitive K+ channel ​​​​​​​(closed by ATP binding) (drug target for sulphonylureas)
  2. Voltage-gated Ca2+ channel (closed at resting potential but opened by depolarisation of β cell)
45
Q

What are the 2 types of channel in the beta cell?

A

2 types of channel in the beta cell:

  1. ATP sensitive K+ channel (remains open unless ATP binds to it)
  2. Voltage gated Ca2+ channel (closed at resting potential)
    * Relevant in relation to the mechanism of excitation-secretion coupling of insulin*
46
Q

What is Excitation-Secretion Coupling?

  • Increase plasma [glucose] –> _____
  • Glucose phosphorylated to_____ by _____ – committed to glycolysis
  • Increased ATP:ADP ratio closes _____
  • Decreased efflux of K+ _____
  • Opens _____ – facilitates _____
  • Increased [Ca2+]i triggers _____
A
  • Increase plasma [glucose] –> More glucose admitted to β-cell via GLUT2
  • Glucose phosphorylated to glucose-6phosphate by glucokinase – committed to glycolysis
  • Increased ATP:ADP ratio closes K+ channels
  • Decreased efflux of K+ depolarises cell
  • Opens voltage-gated Ca2+ channel – facilitates Ca2+ influx
  • Increased [Ca2+]i triggers exocytosis of secretory
47
Q
A

BIO125 Physiology (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions