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Exam 1 Flashcards

1
Q

Embryology

A

study of embryo until time of parturition

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2
Q

Parturition

A

Birth

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3
Q

Development

A

morphological, biochemical and physiological differentiation of an individual (embryology & gametogensis & after birth)

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4
Q

Differentiation

A

generation of cellular diversity (fertilized egg specialized into different cell types)

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5
Q

Morphogenesis

A

creation of form and structure

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6
Q

Growth

A

increase in size

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7
Q

Germinating

A

giving life

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8
Q

Ontogeny

A

growth and development of individual from fertilization to birth

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9
Q

Zygote

A

the fertilized egg

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10
Q

Embryo

A

developing organism form cleavage to birth (2 cells)

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11
Q

Fetus

A

developing embryo (in human after 3 mo.)

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12
Q

What are the two major accomplishments of the developmental process?

A
  1. Generates cellular diversity and order with each generation
  2. Ensures the continuity of life from one generation to the next
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13
Q

What are the 7 stages of embryogenesis?

A
  1. Fertilization (zygote formation)
  2. Cleavage (embryo, morula)
  3. Blastulation
  4. Gastrulation
  5. Organogenesis
  6. Germ cell formation
  7. Larval stage
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14
Q

What are the three layers formed in gastrulation?

A
  1. Ectoderm
  2. Mesoderm
  3. Endoderm
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15
Q

How do we approach the study of embryos (3)?

A
  1. Anatomical
  2. Experimental
  3. Genetic
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16
Q

What are the four parts of the anatomical study of embryos?

A
  1. Comparitive
  2. Teratology/Medical Embryology (limited since we can’t experiment on human embryos)
  3. Evolutionary
  4. Fate Mapping
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17
Q

Historical Perspective: the anatomists. How did they believe the embryo formed?

A

Epigenesis

Parts of the embryo arise in succession

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18
Q

What did Aristotle believe in?

A

Oviparity, vivipaarity, oviviparity
Major cleavage patterns
Functions of placenta and umbilical cord
Mensus gave material, semen gave form and animation

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19
Q

Historical perspective: who was William Harvey? What did he believe? He was the first to observe what?

A 
Ex ovo omnia
All animals from eggs
1st to observe chick blastoderm
Blood islands form before heart
Amniotic fluid functions as shock absorber
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20
Q

Epigenesis vs Preformation

A

Epigenesis: organs of embryo develop de novo
(aristotle / harvey)

Performation: tiny babies live inside of us. all generations that will ever be are within you. All orgas are pre-formed, simply required growth

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21
Q

What are two supporting contemporary theories of preformation?

A
  1. Infinite divisibility (things can be infinately small to serve their purpose)
  2. Limited time (creation to apocalypse)

Predate cell theory (didn’t understand there was a limit to how small things can be)

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22
Q

What are the two schools of preformation?

A
  1. Ovist

2. Spermists

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23
Q

What did Spallanzani believe?

A

Preformation
Experimented with frogs; put pants on them and stopped semen from transferring = no offspring
Established that sperm was needed to trigger the generation of offspring

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24
Q

Who were the Baltic Boys? What did they do?

A

Rathke, von Baer, Pander
Rathke - proposed how pharyngeal pouches, reproduction/extretory/respiratory system developed

von Baer - mammalian egg and notochored

Pander - primary germ layers induction

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25
Q

What were the 4 von Baer’s Principles?

A
  1. General features appear earlier in development than specialized features (general features of all vertebrates (arches, notochord)
  2. Generalized features give rise to more specialized (general skin gives rise to scales, feathers, hair, etc)
  3. Embryos do not possess adult features of lower animals (gill slits of mammals don’t look like adult gill fish)
  4. Higher animals are never like lower animals, only like their early embryos (I was never a monkey)
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26
Q

Medical Embryology has no experimental data, so what do physicians utilize?

A

Physicians utilize nature’s “experiments”

2-5% of infants have observable anatomical abnormalities

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27
Q

What are the 3 main causes of birth defects?

A
  1. Malformations (genetic events)
  2. Disruptions (exogenous causes)
  3. Random Chance
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28
Q

Malfomraitons often appear as ______

A

Syndromes

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29
Q

What is Piebaldism? What gene contains the defect? What is the result?

A

Syndrome
Defect in KIT
Specific neural crest cells, RBC, germ, peripheral nerve cells fail to proliferate
Loss of pigment cells (white on forehead and stomach), loss of ear cells, loss of gut neurons
Overall: deafness, digestion issues, anemic, sterile, lack of pigment

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30
Q

99% of Dwarfism is a result of what malformation? What does this cause? (Peter Dinklage)

A

Defect in FGF4, FGFR3
Cartiledge cells lay the formation of bone develope,ent
FGF4 inhibits cartilege cell production > achondroplasia > limited bone growth (weiner dogs too)

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31
Q

What are teratogens?

A

Exogenous agents causing abnormalities

ex. chemicals, viruses, radiation

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32
Q

Tell me the story of Thalidomide. How many infants were affected? How many pills did it take? When was the susceptibility period for the mother? What did the children develop (symptoms)?

A

It was given as a mild sedative to alleviate morning sickness, effected 7,000 infants
1 pill was sufficient
Susceptibility during day 35-50 of menstaul cycle (20-36 days post conception)
Children developed phocomelia (long bones deficeint/absent)
Heart defects, absence of external ears. malformed intestines

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33
Q

What was the big developmental biology lesson form Thalidomide?

A

The symptoms the child faced (absence of ear, absence of arms, etc) was dependent on the days after last menstruation

So, it told us when different parts of the embryo were developing at day 34, 38, 42 and so on

It also told us that exogenous agents in general will effect different pieces of development depending on when it is introduced

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34
Q

What is gestational age?

A

The gestatial age is how long a woman has been pregnant
Gestatial age = 10 weeks
Embyro age = 8 weeks

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35
Q

Who is Thomas Quasthoff?

A

A thalidomide baby that is now an opera singer

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36
Q

Homology vs Analogy

A

Homology: Evolutionarily linked, same face bones from forengial arches

Analogy: not embryologically linked, developed separately, wing of a bird and butterfly

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37
Q

What is Fate Mapping?

A

Tracing cell lineages through development to figure out what they will ultimately become

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38
Q

What are the two types of cell movements?

A
  1. Mesenchyme cells

2. Epithelial cells

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39
Q

How do mesenchyme cells move?

A

Move independently as a herd

ex. Zebra

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40
Q

How do epithelial cells move?

A

Move as a unit

ex. people linked arms and moved together

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41
Q

What are the 6 fundamental professes driving morphogenesis?

A
  1. Direction and number of cell divisions
  2. Cell shape changes
  3. Cell migration
  4. Cell growth
  5. Cell death
  6. Changes cell membrane or secreted products
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42
Q

When was the first fate map created? From what organism?

A

1906
Conklin
He mapped a chicken egg

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43
Q

What are the different ways you can fate map?

A

Flourecent, dyes, GFP in genetics

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44
Q

What are the 4 major techniques of Experimental Embryology?

A
  1. Defect: destroy portion of embryo (how does it develop lacking these cells?)
  2. Isolation: remove portion & observe development (how do singular cells develop)
  3. Recombination: replace original part with part from another region (diff part of same embryo)
  4. Transplantation: one portion replaced by part from another embryo
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45
Q

What are the three fundamental forces of experimental embryology?

A
  1. Forces outside the embryo
  2. Forces within the embryo/cells
  3. Forces ordering cells into tissues
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46
Q

What is an example of a force outside of the embryo affecting development?

A

Temperature
In reptiles
Higher temperatures (above 34) are males

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47
Q

How does climate change affect reptiles that rely on temperature to determine sex?

A

Increasing temperatures and fewer trees > increased number of male reptiles

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48
Q

What is another example of a force outside of the embryo affecting development?

A

Development of both females and males in the same Echiuroid worm
Female: if larvae land in sand, larger
Male: if larvae land on female proboscis, lives symbiotically inside female reproductive organs and acts as a gonad

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49
Q

What are sequential hermaphrodites?

A

Organims that transition from one sex to the other or to a combination of both

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50
Q

Protandry

A

Male to larger female

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51
Q

Protogyny

A

Female to larger male

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52
Q

Protogynous hermaphroditism

A

Female to hermaphrodite

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53
Q

Protandrous hermaphroditism

A

Male to hermaphrodite

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54
Q

Dimorphism

A

Females and males look different

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55
Q

Which sex is typically higher energy?

A

Females - takes more energy to make eggs than sperm

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56
Q

What are simultaneous hermaphrodites?

A

both reproductive parts at the same time

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57
Q

Differentiation

A

development of specialized cell types

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58
Q

Commitment

A

developental fate of cells is restricted

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59
Q

Go from differentiation through the stages of commitment to a fully differentiated cell

A

True

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60
Q

What are the two stages of commitment

A
  1. Specification

2. Determination

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61
Q

Specification

A

Autonomous differentiation in a neutral environment

Still reversible

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62
Q

Determination

A 
Autonomous differentiation regardless
Assumed irreversible (regardless of outside influence)
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63
Q

What are the only cells in your body that are not fully differentiated?

A

Stem Cells

Stem cells can differentiate OR make more of themselves

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64
Q

What are the three basic mechanisms of specification? What organisms do we see these mechanisms in?

A
  1. Autonomous specification (most invertebrates, inherited transcription factors, asymmetrical eggs)
  2. Conditional specification (all vertebrates & some invertebrates)
  3. Syncytial Specification (most insects)
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65
Q

What is autonomous specification?

A
  • mosaic development
  • determinal specification
  • Fate is set from very beginning, predetermined
  • Morphogens
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66
Q

Morphogens

A

Generates morphology (ex. TF)

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67
Q

Who was L. Chabry? What did he do?

A

1st to demonstrate autonomous specification

Pull it apart and it will still develop into specified pieces

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68
Q

Summary - Autonomous Specification. It is characteristic of what kind of organism? The specification is achieved by what? where? Cells can’t change fate if _____ is lost

A
  1. Characteristic of most invertebrates
  2. Specification by the differential acquisition of cytoplasmic molecules present in egg
  3. Cells can’t change fate if blastomere lost
    (You get half a person if you split the cell)
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69
Q

What are the 2 characteristics of conditional specification?

A
  1. Each cell has the potential to become any of the many different cell types
  2. Interactions with other cells/factors restricts fate
    (You get twins if you split the cell)
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70
Q

Who was Wilhelm Roux? What was his big achievement?

A

Frog Mosaic development
At the two-cell stage, he killed one cell > the dead tissue was still able to influence the living cell > still end up with dead half and live half

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71
Q

What is something unique about the nine-banded armadillo?

A

They have 4 identical twins every time they reproduce

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72
Q

Who was Hans Dreisch? What was his big achievement?

A

Urchin development
Echinoderms = only group of invertebrates that are conditional specification
If you split up the 4 cells > get 4 fully formed structures

Also noted, location in the blastomere dictates fate!

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73
Q

What is syncytial specification?

A

Seen in insects
Multinucleate cell structure
Nucli replication > multiple nuclei > signal gradient > different development

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74
Q

What are the three typesof cell-cell interactions in development?

A
  1. Cell Adhesion
  2. Cell Migration
  3. Cell Signaling
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75
Q

What is differential cell affinity?

A

When germ layers are developing you can scramble them up and they will still cluster on the inside and outside the way they should

This is because the endoderm has the strongest cell adhesion (surface tension) and the epiderm has the weakest

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76
Q

What is surface tension?

A

The strength it takes to seperate two cells

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77
Q

What generates surface tension between cells? (2)

A
  1. Cadherins (cell-cell)

2. Integrins (cell-ECM)

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78
Q

What are cadherins?

A

Calcium dependent adherein molecules

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79
Q

What is one way to cause cells to dissociate?

A

Remove calcium > targets cadherins > lose cell-cell adhesion

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80
Q

What are catenins?

A

Linked to actin in the cytoskeleton to give the cell strength
Connect Cadherins to the cytoskeleton

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81
Q

What are two factors that can affect Cadherin strength?

A
  1. Number of cadherins

2. Types of cadherins

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82
Q

What is a homotypic binding? Example?

A

When two of the same molecules bind together

ex. Cadherin-Cadherin binding

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83
Q

What are the 4 types of cadherins?

A
  1. E-cadherin
  2. N-cadherin
  3. P-cadherin
  4. VE-cadherin
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84
Q

What is the main location of E-cadherins?

A

epithelia

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85
Q

What is the main location of N-cadherins?

A

neurons, heart, skeletal muscle

86
Q

What is the main location of P-cadherins?

A

placenta, epidermis, breast

87
Q

What is the main location of VE-cadherins?

A

endothelial cells

88
Q

What are protocadherins?

A

No strong connection to the cytoskeleton (in comparison to classical cadherin)

Function is more directional than strength

89
Q

What are integrins?

A

Connect ECM-Cytoskeleton inside cell

Has two subunits (alpha and beta)

90
Q

What does the alpha component of integrins bind to? The beta?

A

Alpha: binds ECM to cell membrane
Beta: binds ECM to Talin to Actin (cytoskeleton)

91
Q

What does integrin-binding require?

A

Divalent ions (ex Ca2+)

92
Q

What are talin, vinvulin, a-actinin protiens?

A

Linker proteins connecting integrins to the actin

93
Q

Talk me through epithelial to mesenchyme transition

A

To move from epithelial to mesenchyme the cell needs to lose cadherin connections from paracrine factors

94
Q

Metastasis is an example of what?

A

Epithelial to mesenchyme transition

95
Q

What are the four stages of cell migration?

A
  1. Polarization (2 distict sides; leading and lagging)
  2. Protrusion of leading-edge (uses actin; globular > filamentous)
  3. Adhesion to ECM
  4. Release of lagging edge
96
Q

Invagination

A

infolding of region of cells

97
Q

Involution

A

in-turning of an expanding outer layer

98
Q

What are the two driving forces for Involution?

A
  1. Intercalation

2. convergent extension

99
Q

Ingression

A

Migration of individual cells to interior

100
Q

Delamination

A

Splitting one cell layer into two or more

101
Q

Epiboly

A

Spreading of epithelial surface sheets to enclose deeper layers of embryo

102
Q

Intercalation

A

Going from 2 layers to 1 longer layer

103
Q

Convergent Extension

A

Going from lots of layers to fewer longer layers

104
Q

What are the 4 types of cell signaling?

A
  1. Juxtacrine: 2 cells that are touching (homo or heterotypic)
  2. Paracrine: general area
  3. Endocrine: (via blood)
  4. Autocrine
105
Q

Define induction, inducer, and responder

A

Induction: message
Inducer: sender
Responder: responser

106
Q

Competence

A

The cells have to have the capacity to do their job

107
Q

Time regulation can place a role in making sure everything is in place in regards to cell signaling and development

108
Q

Sequential cell signaling

A

a > b > B > c > C

109
Q

Reciprocal cell signaling

A

a > b > B ……. back to a > A

110
Q

Placode

A

a region that’s going to form something else

111
Q

Talk me through the formation of the eye (cell signaling)

A

lens placode > signals to neural ectoderm to become optic cup > optic cup signals to lens placode to become lens (reciprocal signaling) > developing lens signals to epidermis to become cornea (sequential signaling)

112
Q

What are the two types of cell signals?

A
  1. Instructive interactions “do this”

2. Permissive interactions “you can do this”

113
Q

Tell me about the experiment with the heart and cell signaling

A
  1. Removed cells with detergent, so just ECM is left
  2. Introduced progenitor cells
  3. ECM gives progenitor cells permission to become heart cells
114
Q

What are the two types of specificity of induction?

A
  1. Regional Specificity

2. Genetic Specificity

115
Q

What is an example of regional specificity of induction?

A

If you take the dermis from the wing, thigh, and foot and then layer the wing epidermis over it, the epidermis will become the wing, thigh, and foot despite being wing epidermis because the dermis is telling the epidermis what to become

116
Q

What is an example of genetic specificity of induction?

A

If you take a section of the frog gastrula and put it in the newt gastrula > the newest will have frog tadpole suckers

Likewise if you take a section of the newt gastrula and put it in the grog gastrula > the frog will have newt balancers

both have competent cells, so they received the signal to develop, but they can only develop into the cells they have the genetics for

117
Q

What is a morphogen gradient?

A

The concentration of the morphogen will determine the type of cell

118
Q

What are the 5 major families of signaling pathways?

A
  1. FGF
  2. Hedgehog
  3. Wnt
  4. TGF-beta
  5. RTK pathway
119
Q

Talk me through RTK pathway

A

Ligang > RTK > GEF > Ras > Raf > MEK > ERK > Transcription Factor > Transcription

120
Q

Talk me through FGF & JAK-STAT pathway

A

Ligand > receptor > JAK > STAT > STAT dimerization > transcription

121
Q

A mutation in the gene for FgfR3 causes what?

A

Thanatophoric dysplasia

Mutation in gene for FgfR3 causes the premature constitutive action of the STAT pathway > premature production phosphorylated Stat1 protein > cartilage growth stops before birth > narrow chest, extremely short limbs > thanatophoric dysplasia

122
Q

Talk me through the hedgehog pathway

A

Hedgehog –| patched inhibits smoothened –| Ci protein made activator > transcription

123
Q

Talk me through the Wnt pathway

A

Wnt > Frizzled/LRP5/6 > Disheveled –| B-catenin –| transcription

124
Q

Talk me through TGF-beta & smad pathway

A

TGF-beta superfamily ligand > receptor II > receptor I > smad activation > smad dimerization > new transcription

125
Q

Talk me through Juxatrcine signaling

A

Delta ligand on singnaling cell > notch receptor > protease cleaves notch > peice of notch acts as TF > activation of CSL

Normally CSL has repressor sitting on it

126
Q

What are the 4 phases of gametogenesis?

A
  1. Formation & Migration of PGCs
  2. Mitotic Increase in Germ Cell Numbers
  3. Meiotic Reduction in DNA/Chromosome Content
  4. Differentitation & Maturation
127
Q

What are PGCs?

A

Primordial germ cells

All gametes are derived from PGCs

128
Q

PGCs can differentiate into what?

A

Either sperm or eggs (dependent on sex of adult)

129
Q

PGCs acts as ____ cells for all future gametes in individuals

A

Stem cells

130
Q

How do PGCs get to the gonads during development?

A

They migrate

131
Q

What do Vasa cells(?) do?

A

bind and activate germ-cell-specific genes

132
Q

What do Nanos & Pumilio do?

A

Block RNA translation for somatic gene expression > prevent replication of germ cells > prevents apoptosis

133
Q

What do Tudor & Piwi do?

A

Silence genes

134
Q

The PCGs are isolated to a specific end of the embryo in a highly conserved process

135
Q

Chromosome diminuation

A

Pieces of chromosome break down > unique cells

136
Q

Stem cells are the only cells with all _______ intact

A

chromosomes

137
Q

Nanos localization

A

Half of the egg with yolk ad half the egg without yolk due to gravity

Nanos will localize in yolk

138
Q

What does DAZL protein do?

A

Regulate mRNA translation = makes PGCs competent

No DAZL = no PGC

139
Q

Why does PGC migration occur?

A

To seperate the events that lead to somatios and germ cells

Germ cells inherit supresed to not be somatic

140
Q

Where do PGC migrate to?

A

Genital ridge along the hindgut

141
Q

What is Retinoic acid? What does it do? What is it produced by?

A

Influences germ cells and gonads
Dictates initiation of meiosis
Produced by mesonephric kidney

142
Q

The re-initiation of meiosis in PGC happens when?

A

In males it starts at puberty

In females it starts before birth

143
Q

What is Stra8?

A

Stimulates DNA replication round and enter into meiosis (works with retinoic acid)

144
Q

How are retinoic acid (RA), Stra8, and meiosis related?

A

RA > Stra8 > Meiosis

145
Q

What is Cyp26b1?

A

Inhibits RA, stops the progression of meiosis in males before day 13.5

146
Q

What sex if Cyp26b1 found in?

147
Q

What is Nanos2? What sex is it found in? When?

A

Inhibits Stra8
In males
After day 13.5
Determines male fate

148
Q

Talk me through spermatogenesis in terms of mitosis and meiosis

A

Primodial germ cells > E12.5 = prospermatogonia = mitotic arrest > birth > proliferation > puberty > meiosis > fertilization > zygote

149
Q

Talk me thorugh spermatogenesis in terms of DNA methylation

A

Low Levels of DNA methylation with primodial germ cells and during prolifertion & migration

High levels of DNA methylation in prospermatogonia (mitotic arrest, proliferation, meiosis)

Low levels after fertilization

150
Q

What does methylation on DNA do?

A

Supresses gene expression

151
Q

What are imprinted genes?

A

can be tissue specific
certain genes that just aren’t expressed because they’re always methylated
Ex. mom’s is expressed and not dad’s

152
Q

What is Prader-Willi syndrome? What chromosome is affected? Which sex does it affect the most? What are the symptoms/

A

Chromosome 15: dad’s version is defective and mom’s version is imprinted (blocked)
Typically in males
Weak muscles, constant appetite

153
Q

What do the PGCs turn into once they reach the genital ridge? (males)

A

Incorporate into sex cords and remain until maturity and then hallow out into seminferous tubules

154
Q

What is the initiation of spermatogenesis at puberty regulated by? (2)

155
Q

What do Sertoli cells differentiatie from?

A

Epithelium

156
Q

What are spermatogenic germ cells are bound to Sertoli cells by what? (2)

A
  1. N-Cadherins

2. Galactosyltransferase on PGCs

157
Q

What is the role of Sertoli cells?

A

Nourish and Protect spermatogenic germ cells

158
Q

What do galactosyltransferases do?

A

Bind and transfer sugar (how sertoli cells nourish speratogenic germ cells ?)

159
Q

Two sertoli cells can link together to form what? What is this structure important for?

A

Link together to form a testis blood barrier

Important because sperm are haploid and the body might think they’re foreign

160
Q

What is the order from spermatogonia to sperm?

A

Spermatogonia > primary spermatocytes > meiosis I > secondary spermatocytes > meiosis II > spermatid > spermatogenesis > mature sperm

161
Q

Type A, intermediate, and type B spermatogonia are all examples of ____ cells

A

Stem cells

162
Q

What is the first step towards commitment to become sperm?

A

A4 > either become intermediate, replicate, or die off

163
Q

What is the signal for spermatogonia to become spermatocytes?

164
Q

What is GDNF dependent on?

A

Dependent on conc
Low conc = supports spermatogonia to become spermatocytes
High conc = renewal (spermatogonia to more spermatogonia)

165
Q

What supports the transition to spermatogenesis?

166
Q

Spermatogonia, spermatocytes, and spermatids linked?

A

Cytoplasmic bridges

167
Q

Why do developing sperm need to be linked by cytoplasmic bridges (2)?

A
  1. Important for coordination
  2. Need proteins for transcription and translation that come from the X chromosome (which only half the secondary spermatocytes and on would have)
168
Q

What is the difference between cellular and nuclear maturation?

A

Nuclear maturation is the division of the nucleus etc

Cellular maturation begins with spermatid and is the creation of the polar bodies - it is not a cell division

169
Q

What is the point of residual bodies in spermatogenesis?

A
  1. decrease the size of the sperm = eliminate extra size

2. Lose cytoplasmic bridge (so they can move individually)

170
Q

What are the 3 major components of sperm?

A
  1. Head - acrosome & nucleus
  2. Middle piece - mitochondria
  3. Tail - locomotion
    Membrane surrounds the entire thing
171
Q

What is the acrosome? What does it do?

A

Cellular vesicle that releases enzymes to get to egg surface and bind to egg

172
Q

What is the centriole? What does it do? (3)

A

mTOC

  1. Nucleatic center for microtubles
  2. Help assemble tail
  3. Contribute to spindle in zygote
173
Q

What is the acrosomal vesicle?

A

Extratory vessicle

Golgi derived structure

174
Q

In nuclear condensation of spermiogenesis __ histones are replaced by _____

A

H1 histones are replaced by protamines

175
Q

When are protamines translated?

A

Protaamines are translated in early spermatid

176
Q

Histones:solinoid
Protamine: ______

A

Doughnuts (annulus)

177
Q

What are the 3 main functions of the mitochondria in sperm?

A
  1. Produce ATP (for cell life)
  2. Regulate calcium
  3. Clear ROS
178
Q

The flagella uses ATP produced primarily by what?

A

Glycolysis in the cytoplasm

179
Q

What is the structure of the axoneme?

A

9 & 2

with the inner and outer dynein arms connected with radial spokes

180
Q

What is nexin?

A

The space between theinner and outer dyenin arms in the axoneme

181
Q

What are dynein?

A

Motor protein that walk using ATP in the plus direction

182
Q

What are Kinesin?

A

Motor protein that walk in the minus direction

183
Q

What are linker proteins?

A

Connect the inner and outer dynein arms so that when the microtubles move they bend

184
Q

What is the structure of a microtubule dublin?

A

A ring of 11 dyenins and a ring of 13 dyneins overlapping

185
Q

What is katageners syndrome? What is the cause? What are the symptoms?

A

Flagella lack dynein arms > dysfunctional flagella > effects all cilia in the body

Can lead to detracardio, respiratory problems, infertility

186
Q

What is citus invertus totalis? What causes it? What are the symptoms?

A

Nodal cilia are non-functional

The symmetry of your body is flipped

187
Q

How many days does it take for spermatogenesis? What does that mean in terms of hr/testicle rate?

A

65 days

1x10^8 sperm/hr/testicle

188
Q

How many sperm are in an ejaculationg/ (~2mL)

189
Q

What sperm count is considered sterile?

A

< 1 million

190
Q

How many sperm will a man make in his lifetime?

A

1-10 trillion

191
Q

Why are testes outside of the body?

A

To keep them cool

192
Q

Sperm can have many different morphologies depending on the organism

193
Q

What are the 3 main classes of hormones?

A
  1. Peptides (lipophobic)
  2. Steroids (lipophilic)
  3. Monoamines/amino acids (ex epinephrine and norepi)
194
Q

Peptides have extraceulluar receptors

195
Q

Sterioeds require what to navigate the circulatory system?

196
Q

What is GnRH? Where is it made? What does it target? What does it do?

A

Gonadotrophin releasing hormone
Produced by hypothalamus
Targets anterior pituitary
Stimulates Gonadotrophin release

197
Q

What are the 3 gonadotrophins discussed in class? What class of hormone are they?

A
  1. FSH
  2. LH
  3. ICSH
    Peptides
198
Q

What is FSH? Where is it produced? What does it target?

A

Follicle stimulating hormone
Produced in pituitary
Males: target sertoli cells
Females: target Ovarian follicles

199
Q

What is LH? Where is it produced? What does it target?

A

Lutenizing hormones
Produced in pituitary
Targets ovaries

200
Q

What is ICSH? Where is it produced? What does it target? What does it do? It is the male equivalent of what?

A

Interstitial Cell Stimulating Hormone
Produced in pituitary
Targets Interstitial cell of lytig to produce testosternone
“Male LH”

201
Q

What are the 3 sex hormones?

A
  1. Estrogen
  2. Progesterone
  3. Testosterone
202
Q

What can estrogen be converted into (3)? Where is it produced? What does it target?

A

Estradiol, estriol (placenta), estrone (postmeopause)
Produced in gonads and adrenal gland
Males: targets germinal cells
Females: everything

203
Q

Where is progesteorn produced? What does it targert?

A

Females: produced by ovaries and endometrium/placenta
Males: produced by adrenal/testis
Females: targets breast tissue, endometirum, pituitary
Males: turns into tesosterone

204
Q

What is the most potent form of testosterone? Where is it produced? What does it do?

A

Most potent form is DHT
Produced in gonads and adrenal gland, and in females in ovay
Males: targets everything
Females: controls libido, muslce mass, fat distirbution

205
Q

What are the 4 sex glands?

A
  1. Hypothalamus
  2. Anterior Pituitary
  3. Gonads
  4. Adrenal Glands
206
Q

What does the hypothalamus produce?

207
Q

What does the Anterior Pituitary produce?

A

Gonadotrophins

208
Q

What do the gonads produce?

A

Androgens and Estrogen/Progesterone

209
Q

What do adrenal glands produce?

A

Testosterone and estrogens

210
Q

Talk me through the male hormones from GnRH through the results

A

Hypothalamus > GnRH > anterior pituitary > FSH > blood > sertoli cells > 1. produce ABP (androgen binding protein) 2. produce CYP19 (converts testosterone to estradiol) 3. produce AMH (antimullerian hormone) 4. blood testis barrier 5. produces GDNF

211
Q

Talk me through the male hormones starting with ICSH

A

ICSH > stimulates lydig cells > produce testorsterone > sertoli cells > ABP + testosterone > seminal fluid > effect developement of sperm
sertoli cells > inhibin > block anterior pituitary

212
Q

What does the build up of testosterone do?

A

Build up of testosterone > block hypothalamus and anterior pituitary

Developmental Biology (7 decks)

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