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Physiology > Exam 9: March 20-24 > Flashcards

Exam 9: March 20-24 Flashcards

1
Q

What is a withdrawal response spinal reflex?

A

involuntary contraction like when something is too hot

we have to have the threshold reached to get the involuntary response from our spine rather than wait and have our cerebral cortex response

we can’t inhibit the extensor directly because it’s a skeletal muscle but we need to inhibit the motor neuron for the extensor so our flexor can do its job

contraction: flexor - contralateral extensor
relax: extensor - contralateral flexor

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2
Q

where is smooth muscle located?

A

1) digestive tract lining
2) vessels
3) urogenital tract
4) glands

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3
Q

what does smooth muscle do in digestive tract lining, vessels, urogenital tract and glands?

A

1) digestive tract lining: to squeeze space and change volume and pressure to move things through digestive system
2) vessels: to change blood pressure - can have different BP in each of your arms by changing the pressure in the vessels
3) urogenital tract: to urinate and reproductive components
4) glands

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4
Q

how do smooth muscles contract?

A

3D movement/contractions

the actin is connected via dense bodies*

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5
Q

what are dense bodies/what do they do?

A

actin in smooth muscles is connected via dense bodies

instead of having linear pull with z lines like in skeletal muscles you get a radial pull with our dense bodies

instead of pulling in one line, you extend in a circular motion like an octopus playing tug o war – the radial pull is what you need because you need a 3D tension

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6
Q

is there tropomyosin in smooth muscles?

A

tropomyosin is associated with smooth muscle but it doesn’t block

it’s always there but it’s always allowing myosin to interact with actin

there’s no troponin associated with the tropomyosin

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7
Q

do smooth muscles depend on calcium?

A

you still need Ca in the cytosol for a contraction even though there’s no troponin associated with tropomyosin

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8
Q

how do you increase calcium levels in smooth muscles?

A

smooth is controlled by autonomic nervous system – NT again are what get Ca to increase

unlike skeletal where the only thing that can control it is somatic efferents

with smooth muscle you can have endocrines that can cause contraction because they’ll bind to chemically gated channels that will allow Ca to come in

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9
Q

what are pacemakers?

A

pacemakers can also impact smooth muscles by setting up a regular pattern

they can trigger a regular activity of that muscle

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10
Q

do chemicals impact smooth muscles?

A

yes

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11
Q

how does stretch impact smooth muscles?

A

some of our muscles as they get stretch opens channels and causes movement due to mechanically gated channels

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12
Q

what is calmodulin?

A

a protein in smooth muscle that is activated by calcium = calcium modulated protein

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13
Q

what happens when calcium binds to calmodulin?

A

binding of Ca causes a shape change and activates it

activated calmodulin goes and activates myosin light chain kinase

myosin light chain kinase impacts myosin by doing equation 1 and giving myosin energy by phosphorylating myosin - myosin needs ATP

myosin deflexes and reaches out to do another pull

actin is radially arranged and gives you a 3D pull

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14
Q

what does myosin light chain kinase do?

A

it phosphorylates myosin to give it ATP

the relaxed position is when myosin is in the “flexed” position so we need to energize it so it can deflex and do another pull to get CBC

actin is radially arranged so you get a 3D pull by combining a bunch of different linear pulls in different directions

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15
Q

does smooth muscle have a sarcoplasmic reticulum?

A

no

you need to get rid of Ca in the cell to get a relaxation

smooth muscles doesn’t have an SR so Ca is coming from outside the cell into the cytosol so we have to pump it back out of the cell

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16
Q

what happens during a smooth muscle relaxation?

A

1) pump Ca out of the cell since there’s no SR

decreased [Ca] means that calmodulin won’t be activated and will return to inactive form

w/o active calmodulin, myosin light chain kinase also becomes inactive and we no longer have the “reach out” part of CBC

2) get rid of ATP bound myosin heads with myosin light chain phosphatase

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17
Q

what are the two things that need to happen to get a smooth muscle relaxation?

A

1) pump Ca out out of the cell to deactivate calmodulin

2) get rid of any myosin heads that have ATP bound to them

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18
Q

what is the relaxed position of smooth muscles?

A

with the myosin heads in the flexed position

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19
Q

what does myosin light chain phosphatase do?

A

gets rid of ATP energy without resulting in movement

it makes sure all the myosin heads are in the flexed position but without doing the pull to get them there

aka you use the ATP energy to reach out and grab on to be in the flexed position BUT there’s no pull because phosphatase takes the left over energy so you can’t do the pull

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20
Q

how does the endocrine system communicate?

A

blood carried communication

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21
Q

how fast does the endocrine system work?

A

slower because it travels over farther distances via the blood so you see the results LATER

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22
Q

does the speed that the endocrine system work at make sense?

A

yes!

in sympathetic nervous system you get the NT there quickly and get an immediate response like heart rate change because you’re in fight or flight and need to react quickly

adrenal medulla releasing epinephrine in our system kicks in later because it’s slower

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23
Q

how long do endocrine system effects last?

A

longer lasting effect

if we’re studying and roommate walks in and scares you you’re heart rate will go up really quickly but adrenaline rush will stay around longer even though your heart rate will go back down

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24
Q

how is the endocrine system regulated?

A

negative feedback regulation

we need to shut down the process of a certain endocrine being released

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25
Q

what is the key of the endocrine system?

A

the messengers themselves are the key to the system – it’s called the endocrine system not the glandular system – you need a bunch of messengers to get a gland to work

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26
Q

what varies between endocrine messengers?

A

messengers have different production

they types of endocrines are determined by how they’re made

binding of ligand to the receptor is determined by shape and charge which is determined by how the endocrine is put together

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27
Q

what are the types of endocrine messengers?

A

1) amines
2) steroids
3) peptides

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28
Q

what is the structure of amines? what are they all derived from?

A

they all have cyclohexane rings because they all come from the same amino acids

they’re all derived from tyrosine!

if you become tyrosine deficient you’ll wipe out this class of endocrines

they’re polar (except T3 and T4)

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29
Q

what are types of amine endocrine messengers?

A

1) T3/T4
2) dopamine
3) epinephrine and norpeinephrine

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30
Q

what are T3 and T4?

A

amine endocrine messengers

produced by the thyroid gland

they’re different because they have two rings which tips them from being polar to non polar

non polarity is important because they are going to have problems traveling through polar plasma

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31
Q

what is dopamine?

A

amine endocrine messenger

it’s a neurotransmitter in our bioamine group but here it’s acting as an endocrine within our mammary gland component

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32
Q

what are epinephrine and norepinephrine?

A

amine endocrine messengers

the only difference between the two is a methyl group so they act pretty similarly

fight or flight

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33
Q

what’s the structure of steroids?

A

they’re all derived from cholesterol

aka all of them have a series of carbon rings

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34
Q

what is the polarity of steroids?

A

they’re all derived from steroids which is amphipathic, however it’s primarily no-par

so all steroids are nonpolar

they have problems traveling within the blood plasma!

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35
Q

what are types of steroids?

A

1) cortisol
2) aldosterone
3) testosterone/estrogen
4) placental endocrines

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36
Q

what is cortisol?

A

steroid

comes from cortex of the adrenal gland

regulates stress levels

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37
Q

what is aldosterone?

A

steroid

released from adrenal gland

regulates sodium levels

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38
Q

what are testosterone/estrogen?

A

sex steroids

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39
Q

what are placental endocrines?

A

steroids

placenta is the structure that allows for exchange between mom and fetus

majority of the encodrines created by placenta are in the steroid category

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40
Q

what are peptides?

A

a group of endocrine messengers

they’re just small proteins

they largest group of endocrines

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41
Q

how are peptides made?

A

they’re created as proteins

they get made with too many AA in the string so they’re made too big - when this happens they can’t do their job

that’s okay because we want them to do their job outside in the system, not inside the cell that’s making them aka it’s a safety mechanism

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42
Q

what is a prohormone?

A

it’s a safety mechanism on the protein, specifically peptides, we refer to it as prohormone because it’s initially inactive

they can later be activated

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43
Q

how are peptides transported?

A

they’re proteins that are made with too many AA so they can’t just get sent through the PM

we have to put them in a vesicle that we can exocytose so we can secrete the endocrine into the body

once the endocrine is in the vesicle we can activate the prohormone because they’re protected

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44
Q

what happens to peptides before they’re needed in the body?

A

endocrines sit in vesicles until we need them just like how Ach waits in neuromuscular junction waiting to be released once they’re needed

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45
Q

what are endocrines?

A

ligands

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46
Q

what is the most important characteristic of endocrines?

A

they’re ligands so polarity is key

ligands fall into nonpolar or polar which determines which types of receptors in terms of location that they can bind to

nonpolar ligands can bind to intercellular receptors

polar ligands bind to membrane bound receptors

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47
Q

how can endocrines be disrupted?

A

we can disrupt endocrines by messing with their synthesis or release

if you take cholesterol you lose all the steroid or if you take out tyrosine you lose all the amines

if you’re membrane bound then to can exocytose or endocytose receptor to change response but with intercellular you can only catabolize or anabolize the receptor

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48
Q

what is clearing?

A

endocrines are always moving through the blood so if you make changes to the blood you effect the endocrines

endocrines can be removed from the blood by our kidney

this is how pregnancy sticks work!

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49
Q

where is the pituitary gland located?

A

it’s attached to the brain but it’s not part of it

it’s connected to the hypothalamus by a hallow tissue stock called the infundibulum = connective stock

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50
Q

what’s another word for pituitary?

A

hypophysis

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51
Q

what are the parts of the pituitary gland?

A

anterior and posterior pituitary gland

hypothalamus interacts with the pituitary gland in two ways

52
Q

what is the anterior pituitary gland?

A

adenohypophysis = APG

releases 7 endocrines (FLATPEG)

portal vasculature system so blood vessels running down infundibulum from hypothalamus to APG

receives AND released endocrines

it also MAKES endocrines

53
Q

what is the posterior pituitary gland?

A

neurohypophysis = PPG

neural connection so axons come down through infundibulum to release NTs into PPG from brain

just a RELEASE point for Es

2 endocrines are released from PPG

PPG does NOT make Es - they are made by the hypothalamus, come down through the neuron and then gets released by PPG

54
Q

do the APG and PPG receive and release endocrines?

A

APG = receives and released

PPG = releases only because neural connection to the brain so hypothalamus sends Es which go to PPG then get released

55
Q

do the APG and PPG make endocrines?

A

APG makes Es

PPG does NOT make Es

56
Q

how many endocrines do the APG and PPG release?

A

APG = 7

PPG = 2

57
Q

what’s the flow of communication for the endocrine system?

A

1) NT/Es
2) hypothalamus
3) endocrine 1
4) portal vasculature
5) APG
6) endocrine 2
7) circulation
8) gland
9) endocrine 3
10) effector

58
Q

what are endocrine 1?

A

Es always made and released by hypothalamus and affect the hypophysis (pituitary gland)

endocrine 1 always causes the release of endocrine 2

59
Q

what are the endocrine 2 group?

A

Es always made and released by the anterior pituitary

endocrine 2 always goes to a particular gland and causes the release of a 3rd endocrine (one exception)

60
Q

what are the points of negative feedback of the endocrine pathway?

A

endocrine 3 have negative feedback effect on APG and hypothalamus

self regulation!

61
Q

what is there positive feedback in the endocrine pathway?

A

NT and Es have a positive effect on the hypothalamus neuron

portal vasculature has positive effect on APG

circulation has a positive effect on gland

endocrine has positive effect on effector

62
Q

what are the three jobs of the endocrine 3 group?

A

endocrine 3 goes out to effector and:

1) get response/physiological change
2) suppresses E3 release by decreasing endocrine 2 = negative feedback on APG
3) suppresses E3 release by decreased endocrine 1 = negative feedback on hypothalamus

63
Q

what are the benefits of self-regulation by endocrine 3?

A

1) there are many opportunities to alter the path of the endocrine system which allows for specialization (different glands get impacted in different parts of the body to do different things)
2) amplification by E1 and E2 to impact a larger space within the body because you have 3 endocrine types - E1 binds which can release multiple E2 depending on how long it stays bound
3) typically creates quartets

64
Q

can the hypothalamus and pituitary gland change size?

A

no, they’re in a confined space (your skull)

if you want more of an endocrine in the system you need a bigger space to do that production - if you want more E3 in the system you need a bigger gland to produce it and it’s possible to have a bigger liver and thyroid gland

if it was just the hypothalamus running everything, if you needed more of an endocrine you’d have to increase the size of the hypothalamus but you can’t do that so it wouldn’t work

65
Q

what is a quartet?

A

3 Es + gland

E1 is always made and released by hypothalamus
E2 is always made and released by APG
E2 then goes to gland which releases E3

66
Q

what are hypophysiotropic endocrines?

A

there’s 7 of them from the hypothalamus that cause the APG to do something

E1 from hypothalamus –> release of E2 from APG

the endocrines released from hypothalamus that are causing the hypophysis APG to do something

67
Q

what are the 5 stimulatory hypophysiotropic endocrines?

A

1) thyrotropin releasing hormone (TRH)
2) corticotropic releasing hormone (CRH)
3) growth hormone releasing hormone (GHRH)
4) gonadotropin releasing hormone (GnRH)
5) prolactin-releasing peptide factor (PrRP/F)

68
Q

what does TRH effect?

A

E1: Thyrotropin-releasing hormone (TRH)

E2: thyroid-stimulating hormone (TSH)

E1 goes to APG and stimulates release of E2

69
Q

what does CRH effect?

A

E1: corticotropic releasing hormone (CRH)

E2: adrenocorticotropic hormone (ACTH)

70
Q

what does growth hormone releasing hormone effect?

A

E1:
Growth hormone-releasing hormone (GHRH)

E2: growth hormone (GH)

71
Q

what does GnRH effect?

A

E1:
Gonadotropin-releasing hormone (GnRH)

E2: follicle stimulating hormone (FSH)

luteinizing hormone (LH)

causes release of 2 endocrine 2

72
Q

what does PrRP/F effect?

A

E1: Prolactin-releasing peptide/factor (PrRP/F)

E2: prolactin (PRL)

PrRP/F is different because it doesn’t say hormone aka it’s new

73
Q

what are the 2 inhibitory hypophysiotropic endocrines? why are they needed?

A

1) somatostatin (SS)
2) dopamine

E1 that go to APG and limit the release of a particular E2

GH and prolactin have ways to circumvent feedback process from E3 so you need another way to regulate the system

74
Q

what does somatostatin effect?

A

E1: somatostatin

E2: inhibits GH

75
Q

what’s another name for somatostatin?

A

growth hormone inhibiting hormone (GHIH)

76
Q

what does dopamine effect? what’s another name for it?

A

E1: dopamine

E2: decreases prolactin (PRL)

aka prolactin-inhibiting hormone

77
Q

what is quartet 1?

A

hypophysiotropic endocrines

7 endocrines

E1 –> E2

78
Q

what is quartet 2?

A

APG endocrines

E2 –> glands –> E3

79
Q

what are the endocrines in quartet 2?

A

1) TSH
2) ACTH
3) GH
4) FSH
5) LH
6) PRL
7) Beta-lipotropin
8) beta-endorphine

80
Q

what is TSH quartet 2?

A

TSH –> thyroid –> T3 and T4

TSH came from TRH

T3 and T4 are nonpolar amines

81
Q

what is ACTH quartet 2?

A

quartet 2

ACTH –> adrenal cortex –> corticosteroids

cortisol is a type of corticosteroid

82
Q

what is GH quartet 2?

A

GH –> liver + others –> IGF-1

GH –> many tissues –> growth
GH can bypass E3 and stimulate growth so it needs somatostatin to inhibit it

83
Q

what is IGF-1? what’s its problem?

A

insulin-like growth factor 1

IGF-1 has problems doing it’s job as an E3 that’s supposed to inhibit E1 and E2 release via negative feedback

this is because unlike other endocrine 2s that just go to a gland and get E3 release, we have receptors in many of our cells that respond directly to GH and get those tissues to immediately respond so our E2 is getting a physiological response directly and kind of acting like an E3

GH can bypass E3 and stimulate growth directly so now there isn’t a negative feedback happening which is why you need somatostatin

84
Q

what is FSH quartet 2?

A

FSH –> gonads –> sex Es

**causes development of gametes (sperm and egg)

gonads = ovaries and testes

85
Q

what is LH quartet 2?

A

LH –> gonads –> sex Es

not associated with gametes

86
Q

what is PRL quartet 2?

A

PRL –> mammaries –> milk

(prolactin…lactin = lactation)

not producing endocrine, they’re producing an exocrine

prolactin needs dopamine to disrupt it because there’s no E3 being produced that can go back and cause negative feedback because milk is going to the kid

87
Q

what is beta-lipotropin?

A

quartet 2

see these functional in animals but not in us, want them in us! animal’s fat levels increase in the winter because resources are limited but we stay active in the winter and aren’t as reliant on this one

dieting industry is trying to activate this pathway - if you can activate this pathway by putting all those fats into your system rather than having them be stored

we don’t know what it’s E1 is or what gland they go to or what their effect is

88
Q

what is beta-endorphin?

A

quartet 2

don’t know E1 or their effect

makes us happier w/o needing drugs

in other animals this is a natural pain killer

89
Q

where is the 2nd place that releases endocrine 2s?

A

posterior pituitary gland

E1 made in hypothalamus then go through axon and get released by PPG

E1 from hypothalamus goes out to the body and gets us our effect, there is no quartet

90
Q

does the PPG use a quartet?

A

no

PPG doesn’t make any new endocrines so it just skips the rest of the template

immediately get effects from E1 from hypothalamus

91
Q

what does oxytocin do?

A

helps with lactation and labor contractions

92
Q

do males have oxytocin?

A

it’s primarily in females but it’s also circulating in males

it also serves as a NT which is why males need it too

93
Q

what behavior is related to oxytocin?

A

oxytocin plays a big role in our attachment behavior

in the animal world, bringing together 100s of us that are reproductively active all in the same room is unheard of in the animal world

when we see individuals with deficits in oxytocin they have problems with social situations where they’re not comfortable

one section of autism is caused by a problem with oxytocin communication system

94
Q

what are the two PPG endocrines?

A

oxytocine and vasopressin

don’t use a quartet, they immediately get a response in the body

95
Q

what is vasopressin?

A

causes vessel to contract so it’s related to blood pressure

it’s an antidiuretic hormone (ADH) so it causes you not to lose water

conserves water in association with how much urine we produce so vasopressin causes us to produce less urine

96
Q

how fast are the effects of vasopressin and oxytocin?

A

they’re PPG endocrines so they don’t go through a quartet so they have immediate effects in the body

both also serve as NTs within the CNS

97
Q

where is the thyroid located?

A

below the larynx (voice box)

it’s 2 lobes straddling your trachea

98
Q

does the thyroid gland change?

A

as we age it gets smaller

it’s biggest when we’re in utero

99
Q

what does the thyroid gland look like?

A

it’s kind of a lumpy structure which is caused by the fact that it’s made up of structures called follicles

if we do a cross section of thyroid gland, it looks like individual cells but it’s actually just follicles and there’s individual cells creating the walls of the follicles

follicles aren’t cells because they don’t have a PM, they still have a barrier around them but it’s actual cells – the inside of the follicle is full of fluid

100
Q

what is the thyroid composed of?

A

follicles

101
Q

what are follicles?

A

follicles make up the thyroid gland

follicles aren’t cells because they don’t have a PM

they still have a barrier around them but it’s actual cells

the inside of the follicle is full of fluid

102
Q

what are follicular cells?

A

cells that create the barrier around the follicles in the thyroid

103
Q

what is colloid?

A

the fluid inside the follicles of the thyroid

colloid is interstitial fluid because it’s outside the cell

104
Q

what endocrines does the thyroid produce?

A

T3 and T4

T4 is the most abundant form in circulation

105
Q

what is T3?

A

triiodothyronin

has 3 iodines associated with it

106
Q

what is T4?

A

thyroxine

has 4 iodines associated with it

107
Q

is T3 or T4 more abundant?

A

T4

108
Q

what is the problem with T3 and T4?

A

they’re nonpolar

our blood is polar so they don’t travel well

109
Q

does T3 or T4 travel better in the blood?

A

T4 because it has an extra iodine so it’s a little less nonpolar than T3

if you lose an iodine off T4, you get T3 but if T3 loses an iodine you get T2 and it’s no longer an effective endocrine – those two reasons are why T4 is a better traveler

110
Q

does T3 or T4 bind better?

A

ironic part is that T3 binds to the receptors better and gets a better response than T4

however we don’t have T3 traveling as much but it’s the more active part

so what happens is most effectors for T3/T4 have receptors than can instantaneously switch from T4 to T3

111
Q

what controls production of T3/T4?

A

controlled by TSH from anterior pituitary

follicular cells have receptors for TSH which trigger production of T3 and T4

112
Q

where are T3 and T4 made?

A

unlike almost every other protein in your body, these endocrines are not made inside of a cell, they’re made in the colloid; they’re made extracellularly

all the enzymes and components that make them get moved into the colloid

113
Q

what gland makes us a mammal?

A

our thyroid!

it’s what makes us “warm blooded” = homeothermic

when T3 and T4 are in our system we do equation 2 which generates heat!

114
Q

what do T3/T4 do?

A

it increases our metabolism when T3 and T4 are in our system

it causes our equation 2 to happen more

equation 2 generates heat so our thyroid gland makes more T3 and T4 to stimulate metabolism and generate more heat when necessary

thyroid also increases metabolic fuels; makes sure glucose and lipids and proteins are present and available so equation 2 can happen

115
Q

what do T3/T4 help with?

A

1) sympathetic nervous system
2) neural development
3) growth hormone

116
Q

how do T3/T4 help with the sympathetic nervous system?

A

SNS needs fuel to be active and do fight or flight activity

if T3 and T4 have already primed the system with metabolism it’s easier to succeed in fight or flight

triggering sympathetic is easier when thyroid is in play

117
Q

how do T3/T4 help with neural development?

A

bigger thyroid in babies than us

many deficits in kids when they’re born can be linked to thyroid problems when in utero

can cause nervous system problems

118
Q

how do T3/T4 help with growth hormone?

A

thyroid helps growth hormone do it’s job

if we don’t have a good thyroid gland, then a person could end up being shorter

if it’s overactive thyroid gland then GH could be overactive

119
Q

what are the three jobs of every endocrine with respect to the thyroid?

A

1) get physiological effects
2) do negative feedback on endocrine 2 (TSH)
3) endocrine 1 (TRH)

120
Q

what is hypothyroidism?

A

low T3 and T4 levels

121
Q

what is the most common cause of hypothyroidism?

A

iodine deficiency

salt has iodine added to it to make sure we have good iodine levels

122
Q

what are the effects of hypothyroidism?

A

if we aren’t making T3 and T4, they can’t do negative feedback because they aren’t there to impact TSH or TRH so lots of TSH and TRH get made

TSH levels are going to be crazy high so TSH keeps going to follicular cells and telling them to ramp up production – to have more production we need a bigger space so follicles will grow bigger and the overall thyroid will get bigger too so you end up with an enlarged gland

123
Q

what are goiters?

A

• Before we added iodine in our salt, individuals would get visible thyroid glands called goiters (big chunky necks)

this is still present in poor countries and it can also happen in livestock being born (she made a sheep joke)

124
Q

what are symptoms of hypothyroidism?

A

1) cold intolerance: we aren’t generating heat because metabolism isn’t working
2) putting on weight because metabolism isn’t working and they’re saving fuels for later
3) tired because equation 2 generates ATP so without it you can’t move muscles and you’re tired

125
Q

what are the components of our endocrine system?

A

hypothalamus and pituitary gland

126
Q

what does our hypothalamus do for the endocrine system?

A

hypothalamus is part of the diencephalon

it’s our integration point between the afferent to getting a response happening by having endocrine system be efferent part

hypothalamus communicates directly with pituitary gland

127
Q

are there more E1 or E2?

A

more endocrine 2 compared to endocrine 1

Physiology (15 decks)

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