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Physiology exam 5 (Sabryna) > Lecture 66 > Flashcards

Lecture 66 Flashcards

1
Q

Growth hormone is also called

A

somatotropin

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2
Q

Growth hormone is the number 1 most important thing for

A

GROWTH (bones, muscle, etc)

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3
Q

Growth hormone (somatotropin) is a single chain _______

A

polypeptide (AA sequence varies by species)

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4
Q

GH secretion is described as

A

Pulsatile (burst of release every 2-4 hrs)

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5
Q

GH secretion: _______ pattern in fish and mammals

A

circadian (depends on species nocturnal pulses)

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6
Q

Sexual dimorphism in GH secretion for _______ 3 groups of animals

A

Humans, rodents, fish

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7
Q

Growth hormone (somatotropin): Large, nocturnal pulses in _______, more sustained secretion in _______

A

males; females

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8
Q

Growth hormone (somatotropin): (Decreases/ increases) with age

A

decreases

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9
Q

_______ explains the “growth spurt” at puberty

A

Growth hormone (somatotropin) increases in frequency and magnitude of pulses

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10
Q

Regulation of GH secretion: Stimulators of GH

A

GHRH, Decreased glucose, Decreased FFA, Increased AA (ex: arginine), Puberty (estrogen/testosterone)

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11
Q

Does Hypoglycemia/fasting/starvation stimulate or inhibit GH

A

STIMULATE

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12
Q

Regulation of GH secretion: Inhibitors of GH

A

Somatostatin, Increased glucose, FFA, GH, Obesity, Somatomedins (IGFs)

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13
Q

_______ 3 stimulators of GH are in the “nutrient regulation” category

A

Decreased glucose, Decreased FFA, Increased AA (ex: arginine)

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14
Q

why is nutrient regulation important

A

we need building blocks for growth (decrease in nutrients is stimulatory because that means they’ve been used up)

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15
Q

How can GH be its own inhibitor

A

negative feedback (prevent us from making too much)

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16
Q

Somatomedins (IGFs): _______ is it? _______ does IGF stand for?

A

hormones produced by the liver that stimulate somatostatin from Hypothalamus; IGF= insulin-like growth factor

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17
Q

where do Somatomedins (IGFs) inhibit

A

at anterior pituitary

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18
Q

GH has metabolic actions on (4)

A

liver, muscle, adipose, bone

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19
Q

_______ synthesis carbohydrate and lipid _______

A

linear and organ; protein; metabolism

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20
Q

Actions of GH: Direct anabolic actions of GH (GH acting on self)

A

Increased Ca absorption from gut, P reabsorption from kidney, protein synthesis in liver

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21
Q

Define anabolic and catabolic

A

anabolic is build up; catabolic is break down

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22
Q

Actions of GH: Indirect anabolic actions via somatomedins (insulin-like growth factors - IGF) _______ are the IGF’s involved

A

IGF-1 (somatomedin C); IGF-2(somatomedin A); stimulated by GH**

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23
Q

Actions of GH: Indirect anabolic actions via somatomedins (insulin-like growth factors - IGF) _______ do these lead do (3)

A

Increased lean muscle mass, linear bone growth, organ size/function

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24
Q

Where are IGF 1 and 2 made _______ receptors do they act on

A

made in liver; act on receptors similar to insulin receptors (TYROSINE KINASE activity)

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25
Q

Explain the general process of indirect anabolic actions via somatomedins (insulin-like growth factors - IGF)

A

GH stimulates IGF or Somatostatin then IGF or somatostatin then acts on tissue

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26
Q

Direct catabolic effects of GH: Increased _______ in liver

A

gluconeogenesis (break down to make glucose)

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27
Q

Direct catabolic effects of GH: Increased gluconeogenesis in liver helps maintain _______ within normal range

A

blood glucose

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28
Q

Direct catabolic effects of GH: Increased gluconeogenesis in liver Maintains blood glucose within normal range _______ decreases because of this? _______ results because of the decrease

A

Decreases glucose uptake in skeletal muscle has temporary insulin resistance (means the glucose is available for other organs)

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29
Q

Direct catabolic effects of GH: Increase _______ in adipose tissue

A

lipolysis

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30
Q

Direct catabolic effects of GH increases lipolysis in adipose tissue _______ 2 things does this lead to When there is a release of FFA into blood. _______ does FFA bind to?

A

Release of FFA into blood, Increased formation of ketones

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31
Q

_______ does it turn into?

A

Albumin; NEFA’s

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32
Q

An increase in ketone bodies can lead to

A

metabolic acidosis

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33
Q

Abnormal secretion of GH: A deficiency/lack of GH secretion leads to

A

dwarfism

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34
Q

_______ are the 2 types of dwarfism we discussed

A

pituitary dwarfism & disproportional dwarfism

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35
Q

_______ is pituitary dwarfism

A

autosomal recessive common in GSD

36
Q

_______ is disproportional dwarfism

A

shortened long bones common in dachshunds, corgis, basset hounds

37
Q

which of the following will STIMULATE GH secretion

A

Decreased FA’s

38
Q

Excessive GH secretion leads to

A

acromegaly

39
Q

Where/ how do we see acromegaly (excessive GH secretion) in cats

A

Pituitary tumor in cats

40
Q

Excessive GH secretion (acromegaly) in dogs causes

A

Increased progesterone during diestrus in dog

41
Q

Increased progesterone during diestrus in dog _______ type of dogs experience this

A

ALL intact females go through a period after estrus when progesterone increases, regardless of being pregnant or not

42
Q

Increased progesterone during diestrus in dog and _______ does this lead to

A

High progesterone which antagonizes insulin, stimulates GH; LEADS to : Insulin resistance

43
Q

_______ will inhibit ADH

A

Hypervolemia

44
Q

_______ are the 2 hormones released from posterior pituitary

A

Antidiuretic hormone (ADH;vasopressin/arginine vasopressin) and Oxytocin

45
Q

ADH and Oxytocin are classified as _______ kind of hormone

A

neuropeptide (hormone made in neurons)

46
Q

_______ hormone is synthesized primarily by neurons in supraoptic nuclei of hypothalamus

A

Antidiuretic hormone (ADH;vasopressin/arginine vasopressin)

47
Q

_______ is the peptide precursor for ADH

A

prepropressophysin

48
Q

_______ makes up prepropressophysin

A

ADH, neurophysin 2, signal peptide

49
Q

_______ hormone is synthesized primarily by neurons in paraventricular nuclei of hypothalamus

A

Oxytocin

50
Q

_______ is the Peptide precursor for oxytocin

A

prepro-oxyphysin

51
Q

_______ makes up prepro-oxyphysin

A

oxytocin, neurophysin 1, signal peptide

52
Q

Hormones released from posterior pituitary: Secretion of _______ in posterior pituitary

A

vesicles

53
Q

Hormones released from posterior pituitary: Action potential from cell body in _______

A

hypothalamus

54
Q

Hormones released from posterior pituitary: _______ does the AP from the hypothalamus cause to happen

A

Causes Calcium to enter nerve terminal, and exocytose vesicles where they’ll be picked up by the capillary plexus

55
Q

Hormones released from posterior pituitary : After each hormone is synthesized _______ steps does it go through (3)

A

Golgi removes signal peptide and packages pro-hormone into vesicles, Neurophysin will be removed as it travels down the axon to the posterior pituitary, Ready to be released once in posterior pituitary

56
Q

Stimulation of oxytocin secretion: _______ is the main stimulus for oxytocin? Where are the receptors?

A

Major stimulus is suckling; Sensory receptors on myoepithelial cells of alveoli in mammary gland

57
Q

_______ does suckling result in?

A

Results in milk let-down

58
Q

Other than suckling, _______ is the other stimulus for oxytocin

A

Stimulation of cervix by fetus

59
Q

Stimulation of oxytocin secretion: Stimulation of cervix by fetus results in

A

Results in uterine contractions (Oxytocin acts on smooth muscle of uterus)

60
Q

T/F Uterine contractions is an example of negative feedback

A

F; positive feedback

61
Q

Oxytocin effect on males

A

acts on testes, epididymis and prostate to aid in sperm movement and ejaculation

62
Q

Regulation of ADH secretion: Stimulators (7)

A

Increased plasma osmolarity, Decreased blood volume(hypovolemia), Decreased blood pressure, Pain, Nausea, Hypoglycemia, Nicotine, opiates

63
Q

Stimulation of ADH results in _______ of water

A

REABSORPTION

64
Q

Regulation of ADH secretion: Inhibitors (5)

A

Decreased plasma osmolarity, Increased blood volume(hypervolemia), Increased blood pressure, Ethanol, Glucocorticoids

65
Q

Regulation of ADH secretion: _______ happens when plasma osmolarity is increased

A

increase water reabsorption; increase urine concentration

66
Q

Regulation of ADH secretion : _______ happens when blood volume decreases (ex: hemorrhage)

A

stimulates baroreceptors

67
Q

decreases blood pressure

A
68
Q

Loss of _______ percent of ECF will result in a decrease in blood volume (hypovolemia)

A

10

69
Q

Regulation of ADH secretion: How does pain stimulate ADH

A

We actually don’t know, we know that pain stimulates the hypothalamus

70
Q

Regulation of ADH secretion: How does nausea stimulate ADH

A

there is a loss of fluids

71
Q

Regulation of ADH secretion: How does hypoglycemia stimulate ADH

A

weak stimulus- probably acting with osmotic triggers

72
Q

Regulation of ADH secretion: How does Glucocorticoids inhibit ADH

A

they decrease renal sensitivity to ADH

73
Q

_______ 2 areas of the nephron are water permeable

A

Distal convoluted tubule and collecting duct are permeable to water (water can be reabsorbed into blood)

74
Q

In the nephron, under the influence of _______ water can be reabsorbed into blood

A

UNDER THE INFLUENCE OF ADH

75
Q

_______ are the 2 main actions of ADH

A

kidney and vascular smooth muscle

76
Q

_______ ADH-V receptor does the kidneys use? Vascular smooth muscle?

A

Kidney and V2 receptor (adenylyl cylase and cAMP) VSM and V1 receptor; increases BP

77
Q

Vascular smooth muscle contraction causes constriction of

A

arterioles

78
Q

How does ADH affect the kidney and free water absorption

A

Increase water permeability of principal cells in distal convoluted tubules and collecting ducts of kidney

79
Q

_______ are the 3 main abnormal ADH secretion diseases we discussed in class

A

Central diabetes insipidus; Peripheral or nephrogenic diabetes indipidus; Syndrome of inappropriate ADH secretion

80
Q

_______ disease is caused by a lack of ADH secretion likely due to a head injury

A

Central diabetes insipidus

81
Q

_______ disease is caused by the posterior pituitary being normal, but principal cells in collecting duct are unresponsive to ADH

A

Peripheral or nephrogenic diabetes insipidus

82
Q

_______ disease is caused by a defect in V2 receptor or G protein/ andenylyl cyclase

A

Peripheral or nephrogenic diabetes insipidus

83
Q

_______ syndrome is related to excess ADH released from posterior pituitary or not at all (Ex: disorders in brain, certain medications)

A

Syndrome of inappropriate ADH secretion (there is no feedback inhibition)

84
Q

Central diabetes insipidus: _______ happens to ADH, Urine, ECF osmolarity

A

ADH decrease; Urine increase; ECF osmolarity increase (something is inhibiting ADH release)

85
Q

Peripheral or nephrogenic diabetes insipidus: _______ happens to ADH, Urine, ECF osmolarity

A

ADH increase; Urine dilute; ECF osmolarity increased

86
Q

Syndrome of inappropriate ADH secretion: _______ 3 things result from this

A

Hypervolemia and hyponatremia; Urine very concentrated

Physiology exam 5 (Sabryna) (18 decks)

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