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BI211 > Exam 2-2 > Flashcards

Exam 2-2 Flashcards

1
Q

3 types of muscle

A

skeletal, cardiac, muscle

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2
Q

skeletal muscle ells

A 
long
multinucleated
composed of many myofibrils
is striated--from arrangement of protein fibers in cells
voluntary contraction
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3
Q

Muscle cell life

A

born from merging of undifferentiated cells called myoblasts

once matured–no mitosis

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4
Q

Satellite cells

A

adult muscle stem cells, triggered to divide by injury– can repair some injured muscles (since muscles can’t fix themself–no mitosis)

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5
Q

hypertrophy

A

swelling of individual muscle cells– happens with exercise

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6
Q

sarcoplasmic reticulum

A

specialized endoplasmic reticulum that can sequester and store Ca.
It stores it in the ER and is will be used to spread signal throughout the muscle cell

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7
Q

T-tubules

A

invaginations of the plasma membrane that transmits the membrane depolarization into the cell

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8
Q

sarcoplasm

A

cytoplasm of a muscle cell

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9
Q

sarcoplasmic reticulum

A

endoplasmic reticulum of a muscle cell-stores Ca

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10
Q

Sarcolemma

A

the plasma membrane of a muscle cell

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11
Q

Sarcomere

A

contractile unit of a muscle cell
is the smallest functional unit of a muscle
consists of thick and thin filaments–myofilaments

1 sarcomere=z line to z line

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12
Q

Myosin

A

Thick filament
Have heads and tails– the heads are gathered and the tails are wrapped together
have 2 sites: ATP binding site and actin binding sites

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13
Q

What are the 2 sites on myosin

A 
ATP site (binds and cleaves ATP-->ADP)
Actin binding site
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14
Q

thin filament

A

Actin, troponin and tropomyosin

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15
Q

Tropomyosin

A

long- string like

hides myosin binding site, preventing myosin from binding to actin

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16
Q

Troponin

A

bound to tropomyosin, binds Ca which triggers a shape change that moves typopmyosin out of the way, revealing the myosin binding site and allowing actin and myosin to interact

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17
Q

During contraction, what is in high conc. in the sarcoplasm?

A

Ca

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18
Q

Sliding filament theory

A

filaments fo not get shorter, they slide across each other, shortening the length of the cell

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19
Q

Crossbridges

A

myosin binds to actin, pulling the actin framework closer together, Z lines get closer together and H and I zones are eliminated.
Requires ATP
Happens multiple times along the actin filament
Sarcomere shortens

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20
Q

Excitation contraction

A
  1. AP reaches motor neuron terminal
  2. AP opens Ca channels, Ach is released
  3. ACh binds receptors of sarcolemma of muscle cell
  4. Na channels open
  5. Na moves in to muscle fiber causing a small local depolarization
  6. If threshold is reached– a muscle AP occurs
    Muscle AP travels along the sarcolemma and down T-Tubules
  7. AP on t-tubules excited receptors on sarcoplasmic reticulum– opening Ca channels
  8. Ca is released into sarcoplasm
  9. Ca binds troponin causing s shape change, which moves tropomyosin out of the way.
  10. Myosin binds to actin– cross bridge
  11. Cross bridge formation triggers a shape change in myosin, cocking head to an abgle, sliding the filaments past each other
  12. ADP is released from myosin head, and a new ATP binds and releases the cross bridge
  13. Myosin binds to next available actin binding site
  14. ATP breaks down to ADP, energy is transfered to myosin head, cocks again and the filaments slide
  15. continues as long as intracellular Ca is high, and ATP is available
  16. In synapse- AChE is degradding ACh
  17. Chem gated Na channels close
  18. Ca pump in sarcoplasmic reticulum re-sequesters Ca
  19. Removal of Ca from troponin restores blocking of actins binding sites
  20. Cross bridge cycling stops, relaxation occurs
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21
Q

In muscles– do we use intra or extracellular Ca?

A

Intra cellular, while in normal AP in neurons we use extracellular Ca

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22
Q

What is ATPs role in filament binding?

A

ATP binds and releases the crossbridge.

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23
Q

Muscle motor units

A

functionally all the same– can’t contract q/o the others.

Helps control how much of a msucle you need to use– done by fine tuning the number of motor units

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24
Q

Neuromuscular junction overview

A

Only one NT: ACh
One form of NT clearance: AChE
Only excitatory

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25
Q

twitch

A

A response of a single muscle fiber to a single AP

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26
Q

latent period

A

can be different for different muscle fibers
depend on speed of Ca pump
Slow pump–> Ca stays longer->twitch lasts longer
Fast pump–>Ca removed faster–?twitch ends quickly

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27
Q

isotonic contraction

A

muscle contracts and creates enough force to move a load–> like lifting your keyys
Initiate as isometric contraction until the tension matches the load

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28
Q

Isometeri contraction

A

When you can’t move the load. Like pushing a wall thats not going to move no matter how hard you push

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29
Q

ATP is muscle contraction

A
  1. ADP–>ATP by creatine phosphate
  2. Oxidative phosphorylation of ADP in the mitochondria
  3. ADP–>ARP by anaerobic glycolysis in cytosol
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30
Q

Creatine phosphate

A

builds up in muscle
At start of contraction, CP can phosphorylate ADP to make ATP
Conversion is so fast that during intiial contraction, ATP rates barely change, while CP levels drop (aka ATP is being made as fast as its being used)

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31
Q

Oxidative phosphorylation/glycolysis for ATP

A

Glycolysis– 2 ATP/glucose
OP-36 ATP/glucose– needs O2

Both are slower than CP mediated ADP, OP is slower than glycolysis

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32
Q

myoglobin

A

can store oxygen for muscles

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33
Q

How long does glycogen storage last?What happens when you run out?

A

lasts for 5-10 minutes. After that circularory system must meet demands. Glycogen sfrom liver is broken down, adter 40 minutes, fatty acids begin to be broken down

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34
Q

Central fatigue

A

your CNS tells you to stop– deelings of tiredness, psychological factors

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35
Q

Peripheral fatigue

A

factors within muscle cells tell you to stop

includes conduction problems and lactic acid build up, inhibition of cross bridge formation

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36
Q

Conduction problems

A

K+ builds up in the t-tubules, no K+ gradient, no repolarization

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37
Q

Lactic acid buildup

A

lactic acid results from anaerobic glycolysis. It does not effect contractile proteins, but can slow re-sequestration of Ca, leading to prolonged contraction

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38
Q

Inhibition of cross bridge formation

A

an excess of ADP and Pi may inhibit formation od new cross bridges.Impaired full contraction and impaired relaxation may result.

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39
Q

How are skeletal muscle fibers classified?

A

Cross bridge cycling speed, based on ATPase on myosin

How they get most of their ATP, oxidative phosphorylation of anaerobic glycolysis

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40
Q

Fast v. Slow fibers

A

fast fiber cross bridge formation occurs 4X faster than slow fiber
force produced is the same
depends on ATPase

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41
Q

Oxidative Fibers

A

get ATP from oxidative phosphorylation–much more efficient
Requires lots of mitochondria
Myoglobin is the oxygen source
referred to as red fibers

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42
Q

Glycolytic Fibers

A

Gets ATP from glycolysis- less efficient, need more glucose, less oxygen
-few blood vessels
-few mitochondria
-much higher glycogen stores– since each glucose only gives 2 ATP
WHITE FIBERS

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43
Q

Type 1 Muscle

A

Slow oxidative

-low myosin ATPase, high oxidative capacity

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44
Q

Type IIa muscle

A

Fast oxidative glycolytic

high myosin ATPase, high oxidative capacity, intermediate glycolytic capacity

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45
Q

Type IIb

A

Fast glycolytic

high myosin ATPas, high glycolytic capacity

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46
Q

If looking at a dead body, with no ATP where will Ca be found?

A

In sarcoplasm, muscles will be contracted myosin can’t unbind from actin without binding a new ATP

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47
Q

If you block ACh in the NMJ what happens?

A

The cell would never have a graded potential

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48
Q

Slow oxidative fibers and fatigue

A

Slow use of ATP, can generate ATP
Doesn’t fatigue easily.
Used in muscles that are always on, back legs etc

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49
Q

Fast oxidative fibers and fatigue

A

Lasts a a while, then fatgues

fast ATP- can contract faster legs

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50
Q

Fast glycolytic fibers and fatigue

A

fast use of ATP minimal ability to replenish ATP, fatigues quickly.

In fingers and hands

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51
Q

Motor units

A

all the same fiber type, controled by one motor neuron.

Proportions of motor units vary based on need

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52
Q

Plasticity of skeletal muscle

A
  • fiber type
  • mitochondrial concentration
  • capacity for glycogen storage
  • local capillary concentration
  • myoglobin concentration
  • size of muscle cell
  • concentration of actin and myosin microfilaments
  • neural pathways

These changes can be gained OR lost

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53
Q

Soreness

A

exercising beyond capacity

  • damage to muscles triggers inflammatory response
  • lengthening muscle (going down stairs, lowering weights slowly) produces more soreness

NOT DUE TO LACTIC ACID BUILD UP

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54
Q

Cramps

A

persistent, high frequency AP
Elecytrolyte imbalance
Caused by overexercise, persistant dehydration

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55
Q

Changes with endurance exercise

A

Increased mitochondria
increase in capillary network feeding the muscles
slight decrease in fiber diameter and maximal strength
also leads to associated changes in the cardiovascular and repiratory system

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56
Q

Changes with strength exercise

A

Primarily affects fast twitch fibers–increase in diameter, increased synthesis of actin and myosin, increase in enzymes in glycolysis pathway.
Gain strength, but not endurance– fatigue rapidly
Sometimes fains in strength without gains in size

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57
Q

Poliomyelitis

A

Polio
A virus that infects motor neurons
90% of cases have no symptoms, 10% milkd disease, 1% paralysis

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58
Q

Muscular dystrophy

A

Genetic or autoimmune defects in costamere protein.

Progressive weakness, inability to walk by age 12 Death by 20-25

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59
Q

Atrophy

A

Use it or lose it

Muscle cell loss by decrease in nerve use, or decreased muscle use

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60
Q

Myasthenia gravis

A

Autoimmune activity against ACh receptors, muscle fatigue and weakness
Therapies:
AChE inhibitors, autoimmune drugs, removal of antibodies from plasma

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61
Q

Smooth muscle

A

no banding pattern
NO TROPONIN
innervation comes from autonomic– not voluntary
spindle shaped
contract as a sheet
uni-nuclear– can undergo mitosis and repair
in gut, uterus, blood vessels and pulmonary

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62
Q

Role of Ca in smooth muscl

A

CA binds to and activates calmodulin
Ca-calmodulin activates a kinase
The kinase phosphorylates myosin, activating it
Myosin binds actin and cross bridge cycling occures
as long as Ca is entering the cell, the contraction will occur.

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63
Q

Sources of Ca for smooth muscle

A

Can come from sarcoplasmic reticulum (inracellular) and from extracellular fluid
Smooth muscle cells have voltage gated and chemically gatedCa
There is NO ROLE for Na in smooth muscle contracition
Amount of Ca=amount of contraction

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64
Q

Removal of Ca in smooth muscle

A

removed by ATP dependent pumps

rate is very slow (3+ sec. compared to <1 sec. for skeletal muscle)

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65
Q

Smooth muscle gradation and tone

A

Ca channels only let in enough Ca to activate a portion of the cross bridges
more stimulus=stronger contraction
Can alter how much cystolic Ca is kept inside to maintain tone– helpful with always on muscles, like sphincters

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66
Q

The role of stretch in smooth muscle

A

Stretch does not effect force possible. Stretch can increase contraction because stretch can open mechanically gated ion channels

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67
Q

What do smooth muscle cells contract in response to?

A

autonomic inputs can be excitatory or inhibitory

  • in response to depolarization from a neuron
  • spontaneously
  • spontaneously depolarize and contract without nueronal input– waves
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68
Q

Pacemaker cells

A

the tendancy to spontaneously depolarize at regular intervals.
Some smooth muscle cells work this way for regular contraction– like GI tract

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69
Q

Varicosities

A

string of NT filled bumbs of autonomic axons

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70
Q

Factors that indfluence smooth muscle cells

A 
Hormones
--ex. hormonal control over utering contraction
--ex. epinepherine and gut motility
Paracrine signalling
Acidity
O2 availability
Extracellular ion composition
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71
Q

Single unit smooth muscle

A

gap junctions link the cells, many cells contract as a sheet stretching often induces contraction
ex. GI tract(full stomach=contraction), Uterus (braxton hicks), arterioles(high BP)

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72
Q

Multiunit smooth muscle

A

each cell responds on its own, no gap junctions

ex. Arteries, pulmonary system, haid associated muscle

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73
Q

Cardiac Muscle

A
  • striated
  • troponin AND tropomyosin
  • T-tubules and SR
  • single nucleated cells, forked
  • specialized fused ends called intercalated disks
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74
Q

intercalated discs

A

in cardiac muscle
make stronger, and have gap junctions to quickly pass a contraction
So when one depolarizes, they all depolarize

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75
Q

Desmosomes

A

join cells tightly– at intercalated discs

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76
Q

Gap junctions

A

allow cytoplasmic flow of ions. So when one cell depolarizes, they all depolarize

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77
Q

Contraction in Cardiac muscle

A

-involves Ca and Na channels
Na channels provide initial depolarizeion (graded potential)
Voltage gated Ca channels open and Ca flows into the cell.
—these are called L-type channels, long lasting depolarization- elongates refractory period
Ca floods cytosol from SR and extracellular fluid
once in it binds to troponin and works the same way as skeletal muscle.
Ca pump redurns Ca to SR and exracellular fluid

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78
Q

Initiation of depolarization in cardiac muscle

A

Specialized cardiac muscle cells have pacemaker potential
These exist at only 2 plasces in the heard
Wave of depolarization spreads down through conducting fibers throughout the heard

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79
Q

Does skeletal muscle have striations?

A

yes

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80
Q

does cardiac muscle have striations?

A

yes

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81
Q

does smooth muscle have striations?

A

no

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82
Q

Does skeletal muscle have thick and thin filaments?

A

yes

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83
Q

Does cardiac muscle have thick and thin filaments?

A

yes

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84
Q

Does smooth muscle have thick and thin filaments?

A

yes

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85
Q

Is skeletal muscle control voluntary or involuntary?

A

voluntary

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86
Q

Is cardiac muscle control voluntary or involuntary?

A

involuntary

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87
Q

Is smoothmuscle control voluntary or involuntary?

A

involuntary

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88
Q

What shape are skeletal muscles cells

A

long and cylindrical

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89
Q

What shapre are cardiac muscle cells?

A

short and chubby

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90
Q

What shape are smooth muscle cells?

A

Spindle

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91
Q

Are skeletal muscle cells uni or multi nucleated?

A

multi

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92
Q

Are cardiac muscle cells uni or multi nucleated?

A

uni

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93
Q

Are smooth muscle cells uni or multi nucleated?

A

uni

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94
Q

What is the source of Ca for skeletal muscle?

A

Intracellular

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95
Q

What is the source of Ca for cardiac muscle?

A

intra and extracellular

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96
Q

What is the source of Ca for smooth muscle?

A

intra and extracellular

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97
Q

What is the site of Ca regulation in skeletal muscle?

A

troponin

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98
Q

What is the site of Ca regulation in cardiac muscle?

A

troponin

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99
Q

What is the site of Ca regulation in smooth muscle?

A

Myosin

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100
Q

What is the refractory period duration for skeletal muscle?

A

very short

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101
Q

What is the refractory period duration for cardiac muscle?

A

very long

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102
Q

What is the refractory period duration for smooth muscle?

A

short

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103
Q

What is the contraction control for skeletal muscle?

A

only somatic motor neurons

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104
Q

What is the contraction control for cardiacmuscle?

A

innervation, autorhythmc, endocrine

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105
Q

What is the contraction control for smooth muscle?

A

innervation, autorhythmic, endocrine

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106
Q

What is the effect of K+ channel blocker on NMJ?

A

Lots of ACh in the synapse

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107
Q

What happens if you leave ACh in the synapse?

A

Prolonged muscle contraction

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108
Q

What would adding an Ach antagonist to NMJ do?

A

no muscle contraction

109
Q

Which type of muscle uses calmodulin?

A

Smooth

110
Q

Tropic hormones

A

stimulate other glands to make and release hormones. Usually also trigger growth of the target gland

111
Q

Hormone synthesis

A

most hormones are built in the cell as large inactive molecules
They are stored in their inactivated state and can be activated before release or activated in the blood or at the target tissue

112
Q

In what ways can endocrine gands be stimulated to release a hormone?

A
  1. Monitor blood and release the hormone in response to a change
  2. Neuron stimulates the release of the hormone
  3. Controlled by a tropic hormone.
113
Q

Humoral stimulus

A

When a hormone is released in response to a change in the blood..
Ex. insulin and glucose changes

114
Q

hormones and allosteric inhibition

A

the presence of a hormone can inhibit the step of a pathway by acting as an allosteric nhibitor of an enzyme. This will turn off a pathway resulting in negative feedback

115
Q

GnRH/testosterone feedback loop

A

GnRH–>LH–> testosterone. Testosterone then inhibits the release of more GnRH

116
Q

Amines

A

derived from amino acids
help build thyroid hormones, epinephrine and norepinephrine
Are water soluble, so need transport into cells

117
Q

Peptide hormones

A

larger than amine hormones
built from polypeptides
the majority of hormones are peptide hormones
they are typically water soluble, need transport into the cell

118
Q

steroid hormones

A

lipid based, built from cholesterol
ex. corisol, aldosterone, tersosterone, estradiol, vitamin D

Are hydrophomic, so need plasma protein transporters, but easily diffure in and out of cells

119
Q

Hyposecretion

A

When not enough hormone is secreted

120
Q

Hypersecretion

A

too much hormone released

121
Q

Hyporesponsiveness

A

not enough reception by target cells

Ex. type 2 diabetes

122
Q

Hyperresponsiveness

A

More reception by target cells

123
Q

Primary hyposecretion

A
  • damage to gland=less hormone
  • enzyme deficiency=less hormone
  • dietary deficiency of iodine=less hormone produced
124
Q

Secondary hyposecretion

A

too little tropic hormone produced/released. Results in reduction of hormone secretion

125
Q

Primary hypersecretion

A

Endocrine cell tumor=produces hormone out of control

126
Q

Secondary hypersecretion

A

excressive stimulation by tropic hormones

127
Q

Roles of the hypothalamus

A
  1. influences hormone secretion activity of the anterior pituitary– with tropic hormones
  2. Produces hormones itself
  3. Oversees hormone secretion by the adrenal medulla
128
Q

Anterior pituitary

A

hormone secretion from this is influenced by tropic hormones from the hypothalamus
releases 6 hormones
is regulated through secretion of hypophysiotropic hormones into the hypothalamo-pituitary portal system

129
Q

posterior pituitary

A

stores hypothalamic hormones, then releases them into the local capillary network

130
Q

Hypothalamus releases corticotropin releasing hormone (CRH)…

A

triggers release of adrenocoticotropic hormone from the anterior pituitary (ACTH)

131
Q

Hypothalamus releases Growth hormone releasing hormone (GHRH)

A

which releases growth hormone (GH) from the anterior pituitary

132
Q

Hypothalamus releases thyrotropin releasing hormone (TRH)

A

which releases thyroid stimulating hormone from the anterior pituitary

133
Q

Hypothalamus releases gonadotropin releasing hormone (GnRH)

A

which releases Luteinizing hormone (LH) and follicle stimulatin hormone (FSH) from the anterior pituitary

134
Q

Hypothalamus releases somatostatin (SS)

A

which INHIBITS the release of GH from anterior pituitary

135
Q

,Hypothalamus releases dopamine (DA)

A

which inhibits the release of prolactin from the anterior pituitary

136
Q

Thyroid stimualting hormone

A

anterior pituitary hormone
Is tropic
Stimulates the release of thyroid hormone from the thyroid gland

137
Q

Prolactin

A

is an anterior pituitary hormone

regulates breast milk production, and is anti-libido released during stress

138
Q

Adreocorticotropic hormone

A

is an anterior pituitary hormone

Stimulates the adrenal cortex to produce cortisol

139
Q

Growth hormone

A

is an anterior pituitary hormone

Causes the growth of bones, muscles and most body cells

140
Q

Follicle stimulating hormone and luteinizing hormone

A

anterior pituitary proteins

influence reproductive stuff by regulating hormone synthesis by the gonads

141
Q

What regulates the hypothalamus?

A

CNS stimulation- stress, environmental influences, NT

Hormone levels in the blood

142
Q

Oxytocin

A

Posterior pituitary hormone
positive feedback loop for cervical opening in labor and milk let-down in lactation.
plays a role in bonding an social stuff

143
Q

Vasopressin

A

posterior pituitary protein
aka antidiuretic hormone
constricts smooth muscle cells around blood vessls, increasing blood vessels, increasing blood pressure and decreasing urine output

144
Q

Thyroid gland

A

butterfly shaped gland in neck

secretes 2 hormones: Thyroid hormone and calcitonin

145
Q

Thyroid hormone

A

released by thyroid gland
maintains metabolism/body temperature
iodine is an important part of TH production

There are 2 versions of TH: T4 and T3 (based on # of iodine molecules

Production and secretion is regulated by TSH`

146
Q

TH production

A

TRH (hypothalamus)–>TSH (ant. pit.) –> TH (thyroid gland

TH then negative inhibits TSH and TRH

147
Q

Hypothyroidism

A

low metabolic rate, weight gain, lethargy, feeling cold

Happens because

148
Q

Goiter

A

due to low iodine in diet, thyroid can’t produce enough TH, but pituitary continues to make TSH

149
Q

Action of thyroid hormone

A
  • increase carb intake from intestine and fatty acid release by horone=more fuel in blood stream
  • increase activity of Na/K pumps=increase use of calories and increase of heat
150
Q

Symptoms of hypothyroidism

A 
decrease in overall metabolism
cold intolerance
weight gain
fatigue
loss of concentration
151
Q

Symptomes of hyperthyroidsim

A 
overall metabolism increases
heat tolerance
weight loss
twitchiness
anxiety
152
Q

Calcitonin

A

produced by thyroid glad
encourages calcium deposition into bone from blood
“calcium to the bone”
release is controlled by blood Ca levels

153
Q

parathyroid hormone

A 
released by parathyroid
encourages less calcium to be deposited in blood
stimulated formation of vt. D
opposes the action of calcitonin
regulated directly by blood Ca levels
154
Q

Viamine

A

organic compound present in minute amounts in the diet that are essential to metabolism

155
Q

Vit. D3

A

formed by action of UV light on a cholesterol molecules in the skin

156
Q

Vit. D2

A

derived from plants

157
Q

Vit. D function

A

targets the small intestine
increases uptake of Ca
Parathyroid hormone increases synthesis
is the most common deficiency in the US.

plays a role in reducing inflammation

158
Q

Vitamin D and TB

A

vit. d helps to speed the recovery of TB patients, reducing markers of inflammation
increase in sun, decrease of TB symptoms.

159
Q

Roles of Ca in the body

A 
important in signalling pathways
muscle function
NT release
BONES
cardiac and smooth muscle function
160
Q

Bones

A

rebuild 20% of our skeleto each year
is a type of connective tissue
Is a collagen matrix upon which calcium salts are deposited
Works as a bank-calcium is deposited and withdrawn as needed

growing bones contain cartilage connective tissue

161
Q

epipheyseal growth plate

A

proliferating cartilage

bones can’t grow, cartilage at growth plates grow, then becomes bone

162
Q

Osetoprogenitor cells

A

stem cells that become osteoblasts

163
Q

osteoblasts

A

become new bone

164
Q

osteocytes

A

mature bone cells in matrix

165
Q

Osteoclasts

A

large multinuclearclls that eat/reabsorb bone

166
Q

Bone growth

A

chondroblasts in epiphyseal plate generate new cartilage

osteoblasts at the shaft of the plate convert cartilage to bone

167
Q

Growth rate

A

childre undergo 2 periods of intense growth
before 2 years, and during puberty
boys enter puberty 2 years later than girls, during puberty boys grow more due to the action of testosterone

168
Q

factors that limit growth

A

persistent disease
lack of AA, fatty acids, vitamins, minerals
Physical or psychological stress

169
Q

Growth hormone

A

stimulates maturation and mitosis of chondrocytes

elongates epiphyseal plates, more material for bone conversion

170
Q

acromegaly

A

growth after plates fuse—just cartilage grows

171
Q

IGF

A

insulin like growth factors
secreted by liver and osteoprogenitor cells
triggered by GH
autocrine, paracrin and hormonal functions to dive the mitosis of chondrocytes

172
Q

Growth hormone stimuli

A

only secreted during exercise and 1-2 hours after sleep begins

173
Q

Sex hormones and growth

A

At low levels: promote growth by increasing GH and IGF1

At high levels: promote ossification directly, cause ossification of epiphyseal plates

174
Q

Testosterone

A 
is an anaboilc steroid
used to increase protein synthesis in muscles
Side effects: 
liver damage
prostate cancer
infertility
aggression
175
Q

Cortisol

A

Antigrowth
inhibits DNA synthesis and bone growth
Use of cortisol in children to precent/treat asthma etc can temporarily stunt growth– have to take breaks to alow growth catch up

176
Q

Stress and bone formation

A

high levels of cortisol (released when stressed) can temporarily hault growth

177
Q

Gametes

A

cells that fuse with other cells to make an embryo

178
Q

gametogenesis

A

making gametes

179
Q

gonads

A

organs that produce gametes

180
Q

Male reproductive goals

A

make gametes, get them to the egg

181
Q

Female reproductive goals

A

make gametes, prepare place to receive gametes, prepare place to house the developing embryo, get give birth, feed offspring

182
Q

leydig cells

A

in testes, secrete testosterone

183
Q

sertoli cells

A

aid in spermatogenesis in semineferous tubules
filter nutrients for developing sperm
bind testosterone and transport it into the lumen
is triggered by FSH, make prosperm paracrine signaling molecules which help sperm mature

184
Q

seminiferous tubules

A 
unbroke ring of sertoli cells
make blood-testes barrier
sperm stem cells at periphery
developing cells b/w sertoli cells are locked into place by tight junctions
fully differentiated sperm at the lumen
185
Q

how many sperm released in 1 ejaculation?

A

30-300 million

186
Q

Items required for success of sperm

A

speed, envionmental conditions, direction, adequate digestion of egg coat

187
Q

acrosome

A

on head of sperm. has enzyme that digests the coating of eggs

188
Q

How does the egg prevent multiple sperm from entering?

A

once a sperm gets in , there is an exocytosis of the corticol granuales, the contents are released the the zona pellucida hardens so nothing else can pentrate it

189
Q

testosterone functions

A

required for spermatogenesis
development and maintainance of male reproductive organs
required for maintenance of male secondary sex characteristics
opposes action ot estrogen on breat development
sex drive
muscle growth

190
Q

what impact does endogenous testosterone have?

A

decrease in GnRH, LH and testosterone

191
Q

production of testosteron

A

endocrine cells in testes have enzymes to convert:
Cholesterol–>androstenedione–>testosterone
androstenedione- is also found in the adrenal cortex
small amounts of testosterone are converted to estradiol

192
Q

aromatase

A

converts testosterone to estradiol

193
Q

semen

A

combination of sperm and secretions from accessory glands
takes 2 weeks to prepare
lives 48-72 hours once in the female reproductive tract

194
Q

testosterone decline

A

occurs around age 40

slow and steady decline

195
Q

Ovaries

A

make gametes

196
Q

uterus

A

houses the fetus

197
Q

fallopian tubes

A

transports egg to uterus, site of fertilization

198
Q

vagina

A

entrance/exit to system

199
Q

cervix

A

“doorway” from vagina to uterus

200
Q

Gamete production

A

produce oocytes in the ovary during the fetal period
oocytes are encased in follicles
each month a few follicles mature, the one that matures the fastest is the one that releases the egg

201
Q

ovulation

A

when the egg is released from the follivle and availabel for fertilization

202
Q

corpus luteum

A

what the follicle is called after ovulation when it remains in the ovary (light body) , if pregnancy does not occur it dies and triggers menstruation
is an active endocrine gland- makes progesterone

203
Q

perimetrium

A

outer membrane of uterus

204
Q

myometrium

A

thick smooth muscle layer of uterus– is most powerful muscle in the body

205
Q

endometrium

A

lining of the uterus composed of thick connective tissue, which is sloughed off and regrown every 28 days in menstruation

206
Q

Preparing for pregnancy

A
  1. First half of ccyle: maturing an egg
  2. ovulation
  3. enriching uterine lining for implantation
  4. shedding lining if implantationdoes not occueqw
207
Q

which cells release estrogen?

A

granulosa cells

208
Q

what releases progesterone?

A

a small amount is made by theca cells, most is made by he corpus luteum

can also be made by the adrenal cortex

209
Q

Progesterone synthesis location

A

made by corpus luteum and placenta in women, and in the adrenal cortex

210
Q

progesterone functions

A

maintain uterine lining , water and ion balance, regulation of synaptic activity associated with mood, memory and immune functions, promotes schwann cells,

211
Q

Progesterone and MS

A

progesterone promotes schwaan cells, so is helpful in relieving symptoms of MS

212
Q

what triggers ovulation?

A

a surge in LH (which is released by anterior pituitary and controlled by estrogen levels)

213
Q

What do birth control pills do with regard to LH

A

prevent the surge in LH this preventing ovulation

214
Q

what triggers LH surge?

A

estrogen peak

215
Q

what role does estrogen have in menstruation?

A

triggers LH secretion, builds endometrium and prepares for pregnancy

216
Q

what role does progesterone have in menstruation/pregnancy?

A

progesterone prevents the shedding of the lining

menstruation occures when progesterone levels fall

217
Q

how does progesterone based birth control pills work?

A

it inhibits LH surge

218
Q

Basic role of FSH in female reproduction

A

stimulates development of follicles.

There is no role for this in the luteal phase

219
Q

basic role of LH in female reproduction

A

triggers ovulation

There is no role for this in the luteal phase

220
Q

basic role of estrogen in female reproduction

A

prepares uterine lining, breasts for lactation

SURGE IN ESTROGEN TRIGGERS THE LH SECRETION

221
Q

basic role of progesterone in female reproduction

A

maintains uterine lining. Theres is no role for this in the follicular phase

222
Q

How does the body make sure we only have one baby at a time?

A

Follicular phase and ovulation hormones are inhibited by the corpeus luteum

progesterone inhibits LH and GnRH

223
Q

Mestruation

A

Corpeus lutum degrades–> decrease in estrogen and progesterone–>prostoglandin secreting in endometrium–>vasoconstriction and uterine contractions= menstruation

224
Q

prostoglandins

A

triggers vasoconstriction and uterine contractions, released due to decrease in estrogen and progesterone.

Redues blood flow, causing endometrial tissue to die. and contractions trigger sloughing

225
Q

In vitro

A

grow blastocyte in test tube, then implant it into uterine lining

226
Q

fraternal twins

A

one egg ovulates from each ovary

227
Q

Fertilization

A

occurs in fallopian tube
egg divides and develops as it travels to the uterus
if endometrium is primed, it implants and begins to grow.

228
Q

tend and befriend

A

release oxytocin during stress events

229
Q

oxytocin

A

promotes the resolution of stress by activating parasympathetic system
promotes bonding and social behavior during stress response to keep track to offspring and find friends

230
Q

male hormanal profile during stress

A

epinephrine, corisol and testosterone

231
Q

female hormonal profile during stress

A

epinephrine, cortisol and oxytocin

232
Q

Needs in a stress situation

A

O2, blood to muscles, glucose

233
Q

What physiologically changes in a stress event

A

Increase: breathing, hear rate, shift blood flow to skeletal muscles, mobilize glycogen, protein breakdown

Decrease: urine output, shift blood aaway from digestion, decrease inflammation and immunity, decease sex drive, decrease bone growth

234
Q

Stress

A

real or perceived threats to our homeostasis

235
Q

adrenal glands

A

pyramid shaped glands above the kidnesy–is the major stress gland

Release aldosterone, cortisol, androgens and epinepherine

236
Q

Adrenal cortex

A

makes over 25 lipid based steroid hormones– the corticosteroids

(SALT, SUGAR, SEX)

237
Q

mineralocorticoids

A

released by adrenal cortex,
are lipid based
regulate minerals/electrolytes (water salt balance)
released by the outer layers

238
Q

glucocorticoids

A

released by middle section of adrenalcortex
regulate glucose levels in blood
lipid based

239
Q

gonadocorticoids

A

regulate gonadal hormones (androgens)
made by inner section of adrenal cortex
lipid based

240
Q

Epinephrine

A

dialiates airways to increase breathing rate
breakdown glycogen in liver/skeletal muscles, and breakdown fat in adipose tissues
shifts vlood away from digestive system– decreases the need to eat

241
Q

Cortisol

A 
Shifts bloodflow to skeletal muscles
breakdown protein in bone and skeletal muscles and breakdown fat in adipose tissue
turs everything off. 
decreases growth of immune system
increases appetite to replenish stores
increase prolactin to decrease sex drive
breakdowns bone 
increases growth hormone (in order to break down protein)
242
Q

Hyporthalamic pituitary adrenal axis

A

Hypothalmus releases CRH–>ant. pit. releases ACTH–>Adrenal cortex releases cortisol

cortisol has negative feedback on the other two

243
Q

Stress and eating acute stress

A

Epi decreases the need to eat (ex. fen phen )

244
Q

Stress and eating chronic stress

A

Cortisol increases the need to eat

to replenish energy storage.

245
Q

Chronic stress and cardiovascular system

A

cort. causus systemic vasoconstriction and an increase in blood pressure

246
Q

Chronic stress and immune system

A

Cort. decresases cytokine cross talk and decreases the immune cells, means system is vulnerabel and have increased risk of infection

247
Q

need more glucose

A

decrease insulin, increase glucagon

248
Q

decrease need to respond to injury

A

increase beta-endorphin– is a pain killer

249
Q

decrease need to grow

A

decrease GH

250
Q

decrease need to pee

A

increase ADH, increase blood volume– in case of hemmorrhaging

251
Q

decrease need to have sex

A

increase prolactin
decrese sex drive
decrease gonadal hormones
decrease fertility

252
Q

Benefits of cortisol

A

-circadian rhythm
-maintain BP –permissive for epi
-maintain glucose metabolism
brake on the immune system

253
Q

Hyposecretion:Adrenal insufficiency

Causes

A

decreased cort.
decreased adrenal developmet
decreased enzyme synthesis
damage (addisons disease)

254
Q

need more glucose

A

decrease insulin, increase glucagon

255
Q

decrease need to respond to injury

A

increase beta-endorphin– is a pain killer

256
Q

decrease need to grow

A

decrease GH

257
Q

decrease need to pee

A

increase ADH, increase blood volume– in case of hemmorrhaging

258
Q

decrease need to have sex

A

increase prolactin
decrese sex drive
decrease gonadal hormones
decrease fertility

259
Q

Benefits of cortisol

A

-circadian rhythm
-maintain BP –permissive for epi
-maintain glucose metabolism
brake on the immune system

260
Q

Hyposecretion:Adrenal insufficiency

Causes

A

decreased cort.
decreased adrenal developmet
decreased enzyme synthesis
damage (addisons disease)

261
Q

Hyposecretion:Adrenal insufficiency

Symptoms

A

weakness,fatigue
decreased appetite and weight
decrease blood presure, decreased glucose
increase skin pigmentation (ACTH in blood is a precursor to melotoin

262
Q

Hyposecretion:Adrenal insufficiency

Treatment

A

Hydrocortisone or prendisone for life

263
Q

Hypersecretion: Cushing syndrome

Causes

A 
exogenous therapies, increased cort
adrenal tumors (increased cort)
pituitary tumors (increased ACTH and cort)
264
Q

Hypersecretion: Cushing syndrome

symptoms

A 
osteoporosis
decreased muscle mass
odd body fat distribution
hypertension
hyperglycemia
immunosuppression
265
Q

Hypersecretion: Cushing syndrome

Treatment

A

stop exogenous therapy

surgery

266
Q

prolonged heavy exercise

A 
increase epi and cort
decrease insulin, increase glucagon
increase aldosterone and ADH
increase endorphins
increase prolactin
267
Q

Fasting

A

increases epi and cort
decrease insulin, increase glucagon
increase aldosterone and ADH

268
Q

Are neuromuscular junctions inhibitory?

A

No. Only excitatory

BI211 (11 decks)

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