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Quarter 3 > Physio Exam 2 > Flashcards

Physio Exam 2 Flashcards

1
Q

Gonadotropin dependent precocious puberty

A

Blame the Anterior Pituitary
Tx: Long acting GnRH Agonist
(causes desensitization)

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2
Q

Gonadotropin independent precocious puberty

A

Blame the gonads

Tx: Remove the tumor on the ovaries/testes

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3
Q

LH and FSH

A

tell the gonads to do their job during puberty

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4
Q

LH and FSH are controlled by

A

Anterior Pituitary

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5
Q

Hypogonadotropic

A

problem is in CNS

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6
Q

Hypergonadotropic

A

problem is with gonads

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7
Q

Kallmans

A

can’t smell
Tx: Estrogen or Testosterone replacement
Later, can start with GnRH to help Ant Pit work again for fertility

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8
Q

Kallmans

A

Kall can’t smell

problem with Ant Pit

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9
Q

Turner syndrome

A 
absence of X chromo [XO]
No gonads 
Short stature or delayed/absent puberty
Amenorrhea
LH and FSH really high bc no negative feedback from Estrogen from gonads

Tx: Estrogen supp and then supplemental sex steroids

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10
Q

Turner syndrome

A

will never be fertile

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11
Q

Klinefelters

A

XXY
Failure of normal testicle function (no testosterone release)—> absence of negative feedback to the pituitary
Feminization occurs
Complications: germ cell tumor, breast CA, osteoporosis

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12
Q

Klinefelters

A

Tx: GH first (Testosterone) and then supplemental steroids

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13
Q

Tx for Turner and Klinefelters

A

the same

GH first and then supplemental sex steroids

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14
Q

Acrosome reaction

A

After sperm has passed Zona Radiata, it reaches the Zona Pellucida (gel)

Hydrolytic enzymes are released into Pellucida so that sperm can pass through

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15
Q

Zona Pellucida (gel)

A

has ZP3 protein that Sperm receptors bind to

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16
Q

Sperm (fertilin) binds to

A

Integrin receptor on Ovum

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17
Q

A bunch of sperm help to degrade the Pellucida (gel), BUT once the sperm reaches the cell membrane,

A

only one contributes its genetic material

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18
Q

Zona Reaction

A

Release of granules containing enzymes to degrade the ZP3 protein so that the Pellucida (gel) layer will harden back up!

prevent multiple sperm from getting to the final step

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19
Q

Zona reaction

A

granules degrade ZP3
ALSO,
Final maturation of oocyte- signals for completion of 2nd Meiotic division

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20
Q

After Zona reaction

A

Head of sperm is fully inside of Oocyte

Pronuclei of sperm will eventually fuse with Pronuclei of Oocyte

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21
Q

Binding of Integrin on Ovum to Fertilin on Sperm triggers

A

Zona reaction

harden gel layer back up and complete 2nd meiotic division of ovum

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22
Q

Estrogen during pregnancy

A

requires healthy Placenta AND baby

uses baby Adrenal gland to convert Chol –> DHEA Sulfate –> Estriol

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23
Q

Estrogen during pregnancy functions:

A 
Growth of myometrium (muscles for delivery)
Develop ductile system of breasts
Prolactin release
Relax pelvic ligaments
Inhibit lactation
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24
Q

Progesterone during pregnancy

A

Requires only healthy placenta

made from mother cholesterol

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25
Q

Progesterone functions

A

Makes the uterus a secretory gland
Inhibit premature contractions
Inhibit premature Lactose (baby milk) synthesis

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26
Q

First two trimesters

A

Progesterone keeps the uterus quiet (aka no contractions)

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27
Q

Levels of High Estrogen as women prepare for parturition (birth)

A
  • Gap jx increase uterus
  • Oxytocin receptors increase
  • Prostaglandins –> cervical softening
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28
Q

Placenta carries

A

CRH –> Fetal Ant Pit –> ACTH –> Fetal Adrenal Cortex –> Cortisol and DHEA production

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29
Q

Cortisol

A

Fetal lungs –> increase pulmonary surfactant –>

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30
Q

DHEA

A

placenta –> DHEA –> Estrogen

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31
Q

CRH

A

“placental clock”

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32
Q

Triggers to premature pregnancy

A

Bacterial infection
Allergic rxn
Multiple fetal pregnancies (twins, triplets)

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33
Q

Role of Nuclear Factor in uterus

A

NF-B caused by stretching, increased production of Macrophages as a result of increased Pulm Surfactant

NF-B stimulates production of inflammatory cytokines (IL-8) and prostaglandins –> cervical softening

PREMATURE DELIVERY

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34
Q

Prolactin

A

enzymes for Milk synthesis

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35
Q

Estrogen and Progesterone

A

helps develop mammary glands but inhibits milk synthesis until baby is born

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36
Q

Prolactin

A

stimulates secretion of milk

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37
Q

Oxytocin

A

milk ejection

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38
Q

Removal of steroids at birth

A

initiate lactation

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39
Q

Estrogen and Progesterone

A

block the action of Prolactin on the breast DURING pregnancy

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40
Q

Estrogens

A

Ductal growth

DUCTS

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41
Q

Progesterone
Prolactin
Hcs

A

Lobules and Alveoli of breast

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42
Q

Prolactin and Hcs

A

milk enzymes

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43
Q

Anterior pituitary

A

release Prolactin (leading to more milk production)

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44
Q

Posterior pituitary

A

release Oxytocin (leading to contraction and milk “let down”)

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45
Q

Stress can affect the Post Pit and inhibit

A

Oxytocin release

inhibiting “let down”

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46
Q

Prolactin (milk synthesis) release is regulated by

A

Dopamine (inhibitory)

Thyrotropin-releasing hormone: TRH (stimulatory)

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47
Q

Prolactin

A

inhibits GnRH
thus inhibiting FSH and LH
No ovarian cycling!!

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48
Q

Irreg menses, very heavy
Dark coarse hair on face, upper arm, abdomen
Persistent acne
Cant get pregnant

A

High testosterone levels
High LH and FSH
Ovarian enlargement with too MANY follicles, but none dominant (eventually they turn into cysts)
PCOS

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49
Q

PCOS

A

The follicles turn into cysts

Cysts produce many Androgens

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50
Q

PCOS

A

“Stein-Leventhal Synd”
Primary product of ovary is Testosterone instead of normal hormones

Testosterone interferes with normal female cycle

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51
Q

46XX

21 hydroxylase deficiency
Virilization

A

Virilization (masculinization)

Extra levels of Testosterone –> DHT (enlarged clitoris)

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52
Q

46XX

A

Low glucose and Low cortisol

High ACTH and Testosterone

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53
Q

46XX

21 hydroxylase def

A

Low cortisol
d/t lack of 21-hydroxylase

cannot be converted into Cortisol, so the precursors instead get made into Testosterone

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54
Q

46XX

21 hydroxylase def

A

more precursors left over SO
Low Cortisol
High Testosterone

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55
Q

46XX

A

can be lethal if low levels of Cortisol are not corrected

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56
Q

Optimal Spermatogenesis requires both sufficient levels of

A

Testosterone

FSH

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57
Q

Spermatogenesis also requires sufficient

A

Sertoli cells (which are stimulated by both Testosterone and FSH)

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58
Q

Hormone with a pleiotropic effect

A

meaning several effects

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59
Q

Hormone with a trophic effect

A

meaning regulates:

  • Hormone secretion by ANOTHER gland
  • Growth and integrity of that endocrine gland
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60
Q

TRH example of hormone with a Trophic effect

A

tells pit to stimulate TSH, goes into bloodstream, targets thyroid gland, releases thyroid hormone (secretory) and maintains normal growth of thyroid gland

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61
Q

Endocrine

A

dumped into plasma to act distally on receptor cell

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62
Q

Paracine effect

A

hormone regulates processes in NEIGHBORING cells

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63
Q

Autocrine effect

A

hormone “acts back” , leaves cell but comes back to to regulate process WITHIN CELL OF ORIGIN

acts on those receptors

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64
Q

Intracrine

A

act on cell of origin but DOESNT EVEN LEAVE CELL at all

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65
Q

Neurocine

A

hormone that is released from neuron, travels down axon

carried distally either by blood vessel or synaptic transmission

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66
Q

“Classic” endocrine glands

A 
Hypoth
Pit
Pineal
Thyroid and Parathyroid
Placenta, ovaries, testes
Pancreas
GI tract
Thymus
Adrenal cortex and medulla
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67
Q

“Novel” endocrine glands

A

Adipose tissue
Heart (epicardial fat)
Skeletal muscle

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68
Q

Chemical structure categories

A

Peptide (gene is transcribed into mRNA)
Amine (tyrosine)
Steroid (cholesterol)

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69
Q

Peptide (the majority)

water loving

A

gene mRNA

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70
Q

Amine

A

derived from tyrosine

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71
Q

Steroid

A

derived from cholesterol

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72
Q

Majority of hormones are:

A

Peptide hormones (produced from gene that is transcribed into mRNA)

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73
Q

Peptide hormones
hydrophillic
water loving

A

gene, mRNA

derived from Amino Acids

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74
Q

Tyrosine is in

A

Adrenal medulla,

used to make Catecholamines

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75
Q

Tyrosine is the parent A.A. for

A

Catecholamines and Thyroid hormones

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76
Q

Thyroid hormone is made by

A

Two tyrosine and Iodine atoms

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77
Q

Catecholamines are made by

A

modifying the side groups of Tyrosine

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78
Q

Amines

A 
Epi
NE
Dopamine
T4 (Thyroxine)
T3 (Triiodothyronine)
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79
Q

Steroids

A 
Aldosterone
Cortisol
Estradiol
Estrogen
Testosterone
DHEA
Vit D
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80
Q

Majority or hormones are

A

PEPTIDE

Glycoproteins fall under the peptide family

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81
Q

Glycoproteins (type of peptide)

A 
FSH
TSH
LH
hCG
have a slight modification: CARB moiety critical in secretion and activity of this hormone
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82
Q

Hydrophillic- water loving- reach target tissue via Cardiovascular system

A

Peptide hormones and Catecholamines

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83
Q

Hydrophobic

A

Steroid and Thyroid- need carrier protein

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84
Q

Hydrophillic

A

dissolved and transported in bloodstream

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85
Q

Concentration of hormone in plasma is determined by:

A

Production/release of plasma binding proteins
Feedback mechanisms
Glucuronidation
Sulfate conjugation (increases water solubility for excretion)
Peripheral conversion
Internalization of hormone/receptor in peripheral tissue

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86
Q

Group 1 mechanism: Steroid and Thyroid

STD goes right through
steroid and thyroid

A

Hydrophobic

Dissolve RIGHT THROUGH membrane and bind to nucleus

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87
Q

Group 1 mechanism: Steroid and thyroid

A

do not have any fancy signal transduction mechanisms bc they can dissolve through and go right to the nucleus

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88
Q

Steroid hormone synthesis

A

Cholesterol –> Cytosol, ER, mitochondria –> immediately dumped into circulation (no storage)

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89
Q

Amines

A

Tyrosine –> Enzymatic in cytosol (catecholamines) and Follicular cell and colloid (for thyroid) –> stored in granules or inside the Follicular cells

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90
Q

Follicular cells are found

A

in the Thyroid gland

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91
Q

Peptide hormone synthesis (the big class)

A

Specific gene that directs mRNA –> Ribosomes, golgi, ER –> stored in granules until needed

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92
Q

Synthesis of peptide

A

Gene for hormone transcribed into mRNA (in nucleus) then leaves

Preprohormone –> prohormone (in Endoplasmic Reticulum)

Prohormone –> hormone (in Golgi)

Hormone is stored in secretory vesicles until it is released

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93
Q

Leaving the ER

A

we have Prohormone

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94
Q

Leaving the Golgi

A

we have normal Hormone

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95
Q

ER

A

preprohormone–> prohormone

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96
Q

Peripheral conversion

A

transfer to something else to increase biological activity

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97
Q

Skin: Vitamin D3

A

hydroxylation on Liver and Kidney–> 1,25 Dihydroxyviamin D3

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98
Q

Testes: testosterone

A

Androgens formed

conversiont ot E2 in brain and testes

DHT and E2 final products

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99
Q

Thyroid: Thyroxine T4

A

Conversion in most tissues to make T3 (final product) Triiodothyronine

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100
Q

T3

A

active form

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101
Q

Humoral release

A

activated by blood borne substrate

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102
Q

Humoral release

A

the concentration of substrate is above or below “setpoint”

i.e. Ca levels low, trigger PTH release from Parathyroid gland

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103
Q

Neural release

A 
Psychological stress
Emotion
Fight or flight
Exercise
Hypoglycemia
Shock
Hemorrhage
Heart dz
CNS is secreting the hormones
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104
Q

Examples of Humoral release

A

Calcium and PTH

Glucose and Insulin

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105
Q

Neural release

A

Adrenal gland releases hormones (Epi and NE)

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106
Q

Hormonal release

A

Classic endocrine gland

Network of hormonal connection starting at Hypoth

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107
Q

Hormonal release

A

Hormones regulate the secretion of OTHER hormones

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108
Q

Long example of Hormonal release

A

TRH stimulate pituitary secretion of TSH which stimulates endocrine gland (thyroid) to release thyroid hormone (T3/T4)

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109
Q

What types of hormones have to bind to receptor on the cell surface?

A

Peptides and catecholamines (hydrophobic, cant get through)

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110
Q

What types of hormones diffuse through and go straight to nucleus?

A

Steroid and Thyroid hormones

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111
Q

Decrease in max response

A

Decrease in target cells

Decrease signal transduction mechanisms

112
Q

Decrease in sensitivity (max response can still be reached)

A

More hormone needed in order to get max response

Decrease in affinity
Decrease in receptor #

113
Q

Example of decrease in sensitivity

A

Insulin and obesity

114
Q

Permissiveness

A

Hormone cannot exert its effect unless it has help from another (needing a bathroom buddy in order to be able to pee)

115
Q

Autologous up/down regulation

A

hormone regulates its own receptor affinity/number

116
Q

Heterologous up/down regulation

A

hormone regulates number/affinity of ANOTHER hormone’s receptor

117
Q

Anterior pituitary

A 
Metabolism
Growth
Reproduction
Lactation
Response to stress
118
Q

Posterior pituitary

A 
Water balance
Birth and lactation (lactation is in both)
Regulate BP
Cardiac fx
Diuresis
119
Q

Main products of posterior pituitary

A

Oxytocin

AVP/ADH

120
Q

Main products of Anterior Pituitary

A 
ACTH
Growth hormone
TSH
Prolactin
FSH
121
Q

Post pit

A

Magnocellular neurons –> downt Infundibular process –> end in Post pit –> hormones into capillary bed

122
Q

Ant Pit

A

Parvicellular neurons –> median eminence with releasing hormones–> hypothalamo-hypophyseal portal vessels –> Ant Pit –> regulate secretion of Tropic hormones

123
Q

Ant pit

A

either inhibiting or releasing hormones

Vascular link from hypothalamus and Ant PIt

124
Q

Parvicellular

Ant Pit

A

Secrete hormones that are either inhibitory or stimulatory

125
Q

GHRH

A

Growth hormone releasing hormone

Act on somatotrophs, which release Growth Hormone

126
Q

TRH

A

stimulating hormone
Thyrotropin releasing hormone
acts on Thyrotrophs

Target thyroid gland

T3 and T3

Also maintains growth (trophic effect)

127
Q

Somatostatin

A

INHIBITORY

causes decrease in GH and TSH

128
Q

TRH

A

also involved in Prolactin glands- mammary glands- breast development and milk synth

129
Q

GnRH

A

stimulates production of LH and FSH (in gonads)

130
Q

LH

A

Synth of Estrogen

Secretion of Testosterone form Leydig cells

131
Q

FSH

A

Development of follicle

Initiate spermatogenesis

132
Q

CRH

A

acts on Corticotrophs, makes ACTH which then acts on Adrenal glands

Trophic Result: growth of Adrenal gland, synth of Corticosteroids

133
Q

PRF

A

Prolactin releasing factor

mammary glands

breast develop and milk synth

134
Q

Dopamine

A

INHIBITORY

inhibits prolactin release (inhibits milk synth and breast development)

135
Q

Hormones of post pit

A

ADH and Oxytocin

136
Q

Oxytocin and ADH are made by two types of neurons in the Hypoth

A

Supraoptic

Paraventricular

137
Q

ADH and Oxytocin

A

Peptide hormones

138
Q

Oxytocin

A

binds NP1

139
Q

ADH

A

binds NPII

140
Q

Central Diabetes Insipidus

A

absence of NeurophysinII can lead to no ADH being released into blood

141
Q

Neurophysins

A

keep the hormone in the axon for as long as it needs to be, then allows it to be released

142
Q

messed up Neurophysins or deficiency

A

leads to low levels of the hormone
ADH example
Diabetes Insipidus

143
Q

ADH

A

VERY sensitive to changes in Plasma Osmolarity

anything above 280-284

144
Q

Homeostatic adjustments for dehydration

Re-establish plasma osmolarity

A

ADH secretion
Water reabsorp
Decrease urine output
Stimulate thirst

145
Q

ADH is less sensitive to volume depletion

A

than osmolarity

146
Q

Changes in blood volume (specifically loss here)

A

Baroreceptors

also activates ADH secretion if BP is too low

147
Q

Distention of cervix and Uterine contraction

A

Stimulates Oxytocin release

148
Q

Oxytocin is also important cardiovascular and cardiometabolic

A

cardio renal axis

Regulating BP

149
Q

Oxytocin

A

produced in heart
receptors in heart
Part of Oxytoxin- natriuretic peptide NO axis

150
Q

OT in heart

A

stimulates ANP/BNP release from cardiomyocytes and then ANP stimulates release of NO from vascular endothelium

Protective

151
Q

Nucleus Tractus Solitarius NTS

A

is in the Medulla Oblongata

152
Q

What activates the Cardio-Renal axis? baroreceptors?

A

HTN and

Hypervolemia

153
Q

Oxytocin is cardioprotective because

A

decreases work of heart by decreasing BOTH Chronotropy and Ionotropy
Opening up blood vessels
opening up flood gates of Kidney to allow diuresis

154
Q

Local oxytocin system in the heart

A

OT receptors
Locally produced oxytocin
Pituitary produced oxytocin

Either one causes same effect: NO release

Bradycardia
Negative ionotropy
Increased glucose uptake

155
Q

Oxytocin effect in heart

A

like insulin!!! but different mechanism.

increased in glucose uptake BY THE HEART!

156
Q

Sertoli cells secrete:

A

Anti-mullerian hormone
Androgen binding protein
Inhibin

157
Q

Leydig cells secrete:

A

Testosterone

158
Q

Where are germ cells and Sertoli cells?

A

Seminif tubule

159
Q

Where are leydig cells?

A

connective tissue

160
Q

Two essential products of testes

A

Sperm

Testosterone

161
Q

Spermiogenesis occurs in the walls of:

A

Seminif tubules

162
Q

Spermatogonia (diploids) become

A

Spermatozoa sperm (haploid)

163
Q

After 2 rounds of Mitosis in males

A

Create 4 diploid spermatocytes

Double strand DNA

164
Q

After 2 rounds of MEIOSIS in males

A

Now have 16 haploid spermatocytes/spermatids

Single strand DNA

165
Q

Tight jxb /w Sertoli cells

A

Blood-testes barrier

Prevents immune cells from accessing spermatozoa, REQUIRED for fertility

166
Q

Early sperm cells have more communication with outside world, but once they pass the Blood-Testes barrier,

A

Now entirely dependent on the Seminiferous Tubules for nutrients

an EXLUSIVE area inside the seminif tubules

167
Q

Gap jx

A

allow for nutrients to be exchanged b/w sertoli cells

168
Q

tight jx

A

hold young sperm in place together, not ready to be released yet

169
Q

Cytoplasmic bridge

A

allows genetic info txr from X–> Y

170
Q

What two hormones stimulate Sertoli cells?

A

Testosterone

FSH

171
Q

From “cell like” Spermatids –> “animal like” Spermatozoa

A

SpermIOgenesis

172
Q

Spermiation

“Release!”

A

release sperm from sertoli cells syncytium into the Seminif tubules

173
Q

Spermiation

A

pass thru Rete testes

174
Q

Where are sperm stored and further matured?

A

Epididymis “maturation area”

175
Q

SpermATOgenesis

A

germ cells –> spermatozoa

176
Q

SpermIOgenesis

A

packaging “cell like” spermatids –> “animal like” spermatozoa

177
Q

SpermIATION

A

release from Sertoli cells tight jx

178
Q

Kiss1 neuron in ARC nucleus in MALES

A

always stimulate GnRH

179
Q

Kiss1neuron in ARC nucleus in FEMALES

A

can be inhibitory or stimulatory

180
Q

FSH

A

Tells Sertoli cells to secrete Inhibin and Androgen binding protein

181
Q

LH

A

tells Leydig cells to produce Testosterone

182
Q

Inhibin regulates

A

FSH

183
Q

Testosterone regulates

A

LH and FSH by negative feedback

184
Q

What enzyme is vital for any steroid hormone?

A

Cholesterol desmolase- rate limiting

185
Q

What stimulates Cholesterol desmolase to do its thing?

A

LH

186
Q

T –> DHT via

A

5-a-reductase

187
Q

T–> E2 via

A

Aromatase

188
Q

DHT effects

external

A

Diff of penis, scrotum, and prostate
Hair/baldness
Prostate
Sebaceous

189
Q

Testosterone effects

A

Diff of Epididymis, vas deferens, and Seminal vesicles
Deep voice
Neg fdbk on Ant pit
Libido (sex drive)

190
Q

Rate of sperm production is set by

A

Retinoic acid signaling within the Sertoli cells

timing controlled by Vit A

191
Q

When do Sertoli cells cease proliferation?

A

End of puberty

192
Q

What determines the spermatogenic potential of the testes?

A

of sertoli cells

193
Q

Average sperm count

A

20-40 million per ml/ejacu

194
Q

Oligospermia (little)

A

<15 million

195
Q

Taking too much Testosterone (Aka steroids) messes with sperm production bc

A

You are causing Testosterone to have a negative feedback on FSH (which would usually tell Sertoli cells to do their thing AKA make sperm)

196
Q

synergistic effect on spermiation? (Release of sperm)

A

FSH and Testosterone

197
Q

DHEA

A

An androgen produced from Adrenal glands

198
Q

DHT

A

Male pattern baldness

199
Q

ppl with deficiency of 5-a-reductase

A

DONT GO BALD

bc they cant convert T–> DHT

200
Q

5-a-reductase activity

A

leads to baldness

201
Q

Beard growth

A

DHT and IGF-1

202
Q

Who does NOT go bald?

A

Androgen-insensitivity
Castrated
5-a-reductase deficient

203
Q

DHT and TGF-B1

A

Lead to thinning of hair!!

204
Q

Propecia (finasteride)

A 
block 5-a-reductase
Non-competitive blocker (does not let go)
blocks T --> DHT
Treats:
Enlarged prostate
Baldness
205
Q

Propecia (finasteride)

A

Baldness

Enlarged prostate

206
Q

Propecia (finasteride)

A

Erectile dysfx
Loss libido
Reduced ejaculate

207
Q

Propecia (finasteride) DO NOT GIVE TO PREGNANT WOMEN

A

dangerous bc blocking DHT in utero can have profound effects on MALE BABY DEVELOPMENT

208
Q

What organ makes up most of the ejaculate? (60%)

A

Seminal vesicles

  • Fructose
  • Prostaglandins
  • Clotting factors
209
Q

Prostate produces 20% of ejaculate

A

Secretes

-Alkaline fluid to counteract acidic vagina

210
Q

Bubourethral glands produce 10% of ejaculate

A

Lubrication

211
Q

Seminal vesicles

A

Fructose
Prostaglandins
Clotting factor

212
Q

Prostate

A

Alkaline fluid (for pH)

213
Q

Bulbourethral glands

A

Lubrication

214
Q

3 main dz of prostate

A
  1. BPH
  2. Prostatitis- infection
  3. CA of prostate
215
Q

How many corpus cavernosa do males have?

A

Two

216
Q

How many corpus spongiosum do males have?

A

One

217
Q

Integration site in CNS of erectoin

A

MPOA- medial preoptic area

218
Q

Order of information in erection

A

Amygdala info –> MPOA integration –> Paraventricular nuclei of hypoth –> grey matter S2-S4

219
Q

Erection achieved by (3 possibilities)

A

Higher brain activity (thinking)
Mechanical stimulation of glans provides sensory fdback to S2-S4
Periodic parasymp impulses from sacral erection generation center

220
Q

NO

A

activates guanyl cyclase
increases cGMP
LOWERS ca release
vasodilation

221
Q

Increase of flow into cavernosa and prevent blood flow out

A

Increase BF to cavernosa thanks to cGMP
AND
contraction of muscles around base of penis to keep blood from getting out

222
Q

Flaccid state

A

BF into penis is limited d/t contraction of Helicine arteries and Trabecular sm.muscle

223
Q

Erection state

A

Relaxation of Helicine arteries

224
Q

Compression of what reduces venous outflow during erection?

A

Subtunical venules

225
Q

Pathway of sperm ejaculation

A

Vas deferens –> Ampulla –> Urethra

226
Q

Role of the Internal urethral muscle/sphincter

A

Prevents retrograde sperm ejaculation into the bladder

227
Q

What degrades cGMP?

A

Phosphodiesterase

228
Q

PDE5

A

Phosphodiesterase inhibitor can treat Erectile Dysfx

229
Q

PDE5

A

Viagra/Sildenafil
Cialis/Tadalafil
Levitra/Vardenafil

Maintain high levels of cGMP

230
Q

Vasectomy

A

ligation of vas deferens
accessory gland functions are unnaffected
semen (BUT NO SPERM) are still produced
T not affected

231
Q

Vasectomy

A

Sperm can no longer move thru the ejaculatory duct- are degraded by phagocytosis

232
Q

Vasecotomy, what will semen have in it?

A

everything normal but NO SPERM (sperm was degraded by phagocytes bc it could not get through the ejac duct)

233
Q

LH stimulates Thecal cells to convert Cholesterol ——chol.desmolase—-> Androgens

A

Androgens then diffuse over to Granulose cells where FSH stimulates the conversion of Androgens ——-aromatase—–>Estradiol

234
Q

FSH

A

less frequent pulse from GnRH hypoth

235
Q

LH

A

more frequent pulse from GnRH hypoth

236
Q

As follicular phase proceeds, the levels of Estrogen in amtrum are building up

A

eventually causes a switch from negative feedback (-) to positive feedback (+) on the anterior pituitar

237
Q

Buildup of Estrogen during follicular phase and switch to positive feedback (+) leads to

A

More GnRH released –> more FH and LSH released as a result, BUT Inhibin is keeping FSH in check so we just have a LH SURGE

238
Q

Thx to LH surge

A 
Primary --> Secondary oocyte
Meiosis resumed
Enzymes help follicle get thru 2 layers
Increase prostaglandins
Remainder parts turn into Corpus Luteum
239
Q

What restores the normalcy of feedback after LH surge?

A

Progesterone has a negative feedback on hypoth and pit which suppresses the (+) of Estrogen, SUPPRESSING A 2nd LH SURGE!

240
Q

Suppression of 2nd LH surge

A

Progesterone

241
Q

If any changes in woman cycle occurs, which stage is it?

A

First half

Follicular phase which corresponds to Uterine Proliferative phase

242
Q

After day 14

A

Physiologically, the Luteal and Progestational/Secretory phases are pretty consistent.

243
Q

Rise in Estrogen means

A

Rise in RECEPTORS for Progesterone. Estrogen does a great job at prepping the body for Progesterone.

244
Q

Progesterone

A

“hormone of Pregnancy”

245
Q

Progesterone acts on Estrogen primed tissue and

A

antagonizes Estrogen’s effects

246
Q

Prostaglandins are responsible for

A

Contraction of Uterus during Menses
Cramps
GI discomfort

247
Q

PMDD

A

Premenstrual Dysphoric Disorder
(bloating, wt gain, breast tend, mood swing, depression, unable to work effectively)
5% of women
Meds

248
Q

No TDF

A

Ovaries develop

249
Q

Testes produce

A

Testosterone —> DHT and Wolffian

250
Q

DHT

A

External male genitalia

251
Q

Wolffian ducts

A

Male internal reproductive tract

252
Q

Absence of testoterone

A

female External genitalie

253
Q

Absence of Mull-Inh factor

A

Female internal reproductive tract

254
Q

What secretes Anti- Mull hormone?

A

Seroli cells

255
Q

5-a-reductase deficiency

A

all of a sudden male develops at Puberty

male internally all along, but not enough DHT–> testosterone conversion to make Male external until puberty

256
Q

Hormones important for “growth spurt”

A

IGF-1 and GH

257
Q

Gonadotropin dependent

A

Meaning depending on the gonadotropins- problem with CNS

increased gonadotropins (LH and FSH)

258
Q

Gonadotropin independent

A

Blame the gonads

Increased gonadal hormones

259
Q

Kallmans

A

Can’t smell
CNS problem
Hypo Hypo

260
Q

Klinefelter and Turner

A

Hyper hypo

Blame the gonads

261
Q

Kallman

A

Can’t smell

262
Q

Tx for Kallman

A

Supp sex steroids (FIRST, this is unique) Estrogen or Progesterone

later GnRH

263
Q

Tx for Klinefelter and Turner

A

GH first,

then Supp sex steroids

264
Q

Once sperm reaches the alkaline pH of the cervix (alkaline thx to Estrogen) it is activated by

A

Cholesterol withdraw
Surface protein redistribution
Ca influx (motility)

265
Q

What triggers Acrosomal reaction?

A

Receptors on the sperm bind to ZP3 protein in the Zona Pellucida

266
Q

Acrosomal rxn

A

breakage of this cap so that the enzymes can be release and break down the egg wall

267
Q

Acrosomal rxn

A

an “army” of sperm help break down, but only one gets through to actually fertilize the egg

268
Q

Zona rxn

A

the re-hardening of zona pellucida, making sure only 1 sperm fertilizes the egg

269
Q

Zona rxn

A

degrade ZP3

completion of final maturation of Oocyte!

270
Q

Ovulation

A

day 14

271
Q

Optimal implanatoin

A

day 20-24

272
Q

hCG

A

rescues Corpus luteum and maintains until Placenta takes over

273
Q

In order for the placenta to make Estrogen, requires

A

BOTH fetus and placenta

Needs fetus Adrenal glands (DHEA) and fetal Liver

274
Q

What does the placenta need in order to make Progesterone?

A

only placenta

275
Q

Fetal Adrenal gland

A

DHEA

CRH “placental clock”

276
Q

CRH leads to production of

A

ACTH which tells Adrenal cortex to produce: Cortisol –> pulm surfactant, and DHEA –> Estrogen

Quarter 3 (17 decks)

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