Oxytocin and ADH Flashcards

1
Q

What is the difference between OT and AVP?

A

Two different AA side chains

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2
Q

Where are both AVP and OT synthesized?

A
Supraoptic nucleus (mainly AVP)
Paraventricular nucleus (mainly OT)
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3
Q

How is OT transported?

A

Created in the paraventricular nucleus and sent in vesicles down the magnocellular axon to the posterior pituitary

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4
Q

When does OT have a burst in males?

A

At ejaculation to produce contractions for sperm release

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5
Q

Mechanism which OT binds and causes smooth muscle contraction?

A

OT bind OTR-> GPCR-> IP3 (Ca channels open) and DAG-> Prostaglandin (PGF2a)-> uterine and smooth muscle contraction

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6
Q

What is the Ferguson reflex?

A
  1. ) Head of baby pushes against cervix
  2. ) Nerve impulses from cervix transmitter to brain
  3. ) Brain stimulates release of oxytocin (hypothalamus)
  4. ) Oxytocin carried in bloodstream to uterus
  5. ) Oxytocin simulates uterine contractions and pushes baby towards cervix
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7
Q

What is the secretory unit of the breast?

A

The alveolus

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8
Q

What surrounds the alveolus of the breast?

A

Myoepithelial cells

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9
Q

What does OT cause contraction of to cause the let down reflex?

A

Myoepithelial cells

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10
Q

Characteristics of the four stages of labor:

A

0: Uterine tranquility and refractoriness
1: Uterine awakening, extending to complete cervical dilation
2: Active labor, from complete cervical dilation to delivery of newborn
3: From delivery of fetus to expulsion of placenta

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11
Q

What physiologically is occurring during each of the four stages of labor?

A

0: Progesterone and relaxin promote inactivity
1: Estrogens increase OT receptors by 80x at 36 weeks
2: Oxytocin, prostaglandins, estrogen increases OT receptors 200X during early labor
3: Oxytocin increases especially in last stage of labor

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12
Q

What effect does estrogen have in the OT cycle?

A

It up regulates OT

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13
Q

What affect does progestogens have in the OT cycle?

A

Decreases response of smooth muscle from OT

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14
Q

How does suckling cause OT release?

A

Suckling stimulates PRL release by removing the inhibition of DA

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15
Q

How does suckling affect the menstrual cycle?

A

GnRH is inhibited by suckling reducing LH and FSH release inhibiting the ovarian menstrual cycle

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16
Q

When is relaxin released and what are its affects?

A

It is released during pregnancy to keep the uterus in a quiet state also during labor in the cervix to dilate it

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17
Q

What is the half-life of OT?

A

3-6 minutes

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18
Q

Where is ADH mainly produced?

A

Supraoptic nucleus

19
Q

What is ADH produced as?

A

A preprohormone

20
Q

What does the preprohormone of ADH consist of?

A

Signal peptide
ADH
Neurophysin II

21
Q

What causes the most cases of hereditary hypothalamic diabetes insipidus?

A

A point mutation in neurophysin II

22
Q

What is neurophysin II?

A

A carrier of ADH

23
Q

What is the primary signal for secretion of ADH?

A

An increase in ECF osmolality

24
Q

What inhibits ADH release?

A

High fluid volume or blood pressure

25
Q

What transports AVP from hypothalamus to neurohypophysis?

A

Magnocellular neurons

26
Q

What are the receptors for AVP?

A

V2R in the renal collecting duct

27
Q

Sequence of events for AVP action in renal tubules?

A
  1. ) ADH binds V2R
  2. ) Activates PKA
  3. ) Phosphorylation of CREB stimulates transcription of mRNA to produce more AQP2
28
Q

What is the threshold at which ADH can be released?

A

When osmolality increases as little as 1% from 280 mEq/L

29
Q

ADH is also released when blood volume is decreased by what percent and what senses this?

A

Reduced by 10% by baroreceptors in the atria

30
Q

ADH half-life:

A

18 minutes

31
Q

What breaks down ADH and what can occur in this organ failure?

A

Kidneys and Liver

Failure in these organs can lead to high ADH levels

32
Q

In pregnancy, what hormone causes the changes in osmolarity and volume?

A

Relaxin

33
Q

What occurs to ADH in aging adults?

A

The kidneys become less sensitive to nocturnal plasma levels of ADH

34
Q

Two types of diabetes insipidus:

A

Central

Nephrogenic

35
Q

What causes central DI?

A

Failure of AVP secretion

36
Q

What causes nephrogenic DI?

A

Kidneys not adequately responding to ADH levels

37
Q

What is the differential diagnosis following water deprivation in DI?

A

Central: decreased plasma ADH low urine osmolality
Nephrogenic: increased plasma ADH extremely low urine osmolality

38
Q

What does SIADH stand for?

A

Syndrome of inappropriate ADH secretion

39
Q

What is SIADh essentially?

A

The opposite of DI

40
Q

What occurs in SIADH?

A

Secretion of inappropriately high levels of ADH

41
Q

What is the sign of SIADH?

A

Any urine with greater than 100 Osm with hyponatremia is SIADH

42
Q

Why is urine Na osmolality so high in SIADH?

A

Because the volume expansion causes a release of ANP increasing natriuresis

43
Q

Treatment of SIADH?

A

Fluid restriction

44
Q

Drug treatment of SIADH?

A

V2 receptor antagonists: Conivaptan and Tolvaptan