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Physiology > Lecture 12- The HP Unit > Flashcards

Lecture 12- The HP Unit Flashcards

1
Q

What are the two embryological structures that meet to form pituitary

A

Rathke’s pouch and infundibulum process

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2
Q

What is Rathke’s pouch

A

Forms in roof of oral ectoderm, forms anterior pituitary

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3
Q

What is the infundibulum process

A

Descends from the diencephalon, forms posterior pituitary

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4
Q

What part of the pituitary is the pars nervosa, and neurohyophysis

A

Posterior pituitary

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5
Q

What part of the pituitary is pars distalis and adenohypophysis

A

Anterior pituitary

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6
Q

What part of the pituitary is the intermediate lobe that is the source of melanocyte stimulating hormone

A

Pars intermedia

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7
Q

What part of the pituitary is made of a fatty sheath of tissue that supports the pituitary stalk

A

Pars tube rails

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8
Q

What are the two pathways from hypothalamus to pituitary

A
  1. Neural pathway
  2. Portal pathway
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9
Q

What’s is the neural pathway

A

Magnocellular neuron that project to the posterior pituitary to release hormones

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10
Q

What is the portal pathway

A

Small blood portal system to transport releasing hormones from the median eminence of the hypothalamus

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11
Q

What hypothalamic nuclei are responsible for releasing oxytocin and vasopressin

A

Paraventricular nuclei and supraoptic nuclei

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12
Q

What are the two hormones released in neural pathway

A

Oxytocin and vasopressin

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13
Q

Oxytocin and vasopressin differ by two amino acids. What amino acids?

A

Oxytocin has leucine and isoleucine whereas vasopressin has arginine and phenylalanine

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14
Q

What is the target of vasopressin

A

Collecting ducts of the kidney

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15
Q

What are the effects of vasopressin

A

Increase number of aquaporins in collecting duct, increase water reabsorption in collecting duct, decrease urine production

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16
Q

Is vasopressin a diuretic or antidiuretic

A

Antidiuretic

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17
Q

What is the intracellular mechanism (G-proteins…) of vasopressin

A

GPCR (Gs)—> increase cAMP—> translocation of vesicles—> exocytosis of aquaporins—> insertion in epithelial cell plasma membrane

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18
Q

What is the major stimuli for vasopressin release

A

Increased blood osmolarity sensed by osmorceptors in hypothalamus

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19
Q

What is the other mechanism that stimulates vasopressin release, more so in emergency, large volume loss

A

Decreased stimulation of carotid and aortic stretch receptors

20
Q

How do hypothalamic osmoreceptors restore normal osmolarity and ECF volume

A

Osmorecptors act on hypothalamus to increase thirst, increase water intake, and decrease ECF osmolarity and increase ECF water volume

21
Q

How do atrial baroreceptors act to increase ECG volume and decrease ECF osmolarity

A

Atrial baroreceptors act on hypothalamus to release vasopressin, causing ateriolar vasoconstriction, increase H20 permeability of CD, increase H20 reabsorption in CD, decrease urine output, increase ECF volume and decrease ECF osmolarity

22
Q

What does vasopressin bind to in distal tubule and collecting duct of kidney to stimulate exocytosis of aquaporins

A

V2 receptors, activating cAMP—> AQP-2 channels inserted into luminal membrane

23
Q

During an emergency response, decrease BP due to blood loss which receptor does vasopressin act on

A

V1A receptor present in vascular smooth muscle tissue

24
Q

What stimulates release of vasopressin

A

Decreased blood volume and increase blood osmolarity

25
Q

Describe how central diabetes insipidus affects the levels of vasopressin, water intake, and urine

A

Posterior pituitary is unable to release VP so serum VP is low

Collecting ducts are impermeable to water due to VP not exocytosing aquaporins

Urine: diluted and large volumes

26
Q

What is a potential treatment for central DI

A

Exogenous VP or synthetic analogues (because problem isn’t receiving VP at kidneys, problem is producing it)

27
Q

Describe the role of nephrogenic diabetes insipidus in relation to VP, water permeability, body fluids

A

Collecting duct is not responsive to VP (defect in V2 receptor, GPCR, or intracellular signaling)

Water not reabsorbed, large dilute urine

Body fluids concentrated

High serum VP

28
Q

What is a possible treatment for nephrogenic DI

A

Thiazide diuretics: decreases GFR and decrease Na+ reabsorption in distal tubule

29
Q

Why would exogenous VP be ineffective in treating nephrogenic DI

A

Problem is not with vasopressin release, VP is released normally but can’t act on V2 receptor

30
Q

What test can you run for Diabetes insipidus

A

Water deprivation test

31
Q

How does water deprivation test work

A

After 3-8hrs test USG if > 1.025 animal is normal to partial DI

If urine remains dilute (1.003-1.024) lack of ADH activity

  • does not distinguish whether central or nephrogenic
32
Q

What test can you run to differentiate between nephrogenic and central DI

A

VP response test

33
Q

How does a VP response test work

A

Administer exogenous VP and then test USG, if >1.026 animals have primary/central VP deficiency, with little change (0.003-0.025) they have nephrogenic diabetes

34
Q

What is desmopressin acetate

A

Synthetic analogue of ADH that can be used to treat primary/central DI

35
Q

What is syndrome of inappropriate ADH (SIADH)

A

VP released from autonomous source (ex: tumor)

36
Q

What are some symptoms of SIADH

A

Hyponatremia: low serum, high urine
Reduced serum osmolarity
Confusion, disorientation
Generalized muscle weakness, tremors, ataxia
Seizures, coma

37
Q

What are some treatment options for SIADH

A

Hypertonic saline
Diuretics
V2 antagonists (demeclocycline, conivaptan or tolvaptan)
Fluid restriction

38
Q

Oxytocin promotes ___ and ___

A

Social bonding and reproduction

39
Q

Does oxytocin promote monogamy or polygamy

A

Monogamy

40
Q

In voles oxytocin increases partner preference in ___ females and OT antagonist blocks that response in ___ females

A

Unmated, mated females

41
Q

In voles VP increases partner preference in ___ males and VP antagonists increases partner preference in ___ males

A

Unmated and mated

42
Q

What hormone strengthens uterine contractions, causes milk release during nursing and facilitates sperm transport

A

Oxytocin

43
Q

What hormone promotes the maternal offspring and mate bonds

A

Oxytocin

44
Q

How does oxytocin affect heart rate and BP

A

Slows heart and reduces blood pressure

45
Q

Labor is initiated when….

A

Uterine oxytocin receptor concentration reaches a critical threshold, positive feedback cycle progressively increases until cervical dilation and delivery of baby are complete

46
Q

What is the role of oxytocin in milk let down demand

A
  1. Suckling/milking- mechano and temperature receptors
  2. PVN releases oxytocin via posterior pituitary
  3. Myoepithelial cells contract, oxytocin causes contraction of myoepthelial cells which moves the milk into ducts and cistern
  4. Milk let down result
  5. Not milk production!

Positive feedback mechanism

Physiology (10 decks)

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