Exam 4: ch 26 reproductive ch 22 respiratory Flashcards

1
Q

pathway of sperm thru the male reproductive tract

A

-formed in seminiferous tubules(site of meisosis) - straight tubule (tubule rectus)-rete testis- efferent ductule-epididymis-ductus deferens-urethra-exterior

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2
Q

% of semen volume made up of prostatic fluid

A

-30% of total volume of semen

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3
Q

nutrient fuel for sperm

A
  • fructose
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4
Q

prostaglandins function

A
  • decrease the viscosity of mucus in the cervix and stimulate reverse peristalsis in the uterus to facilitate sperm movement in the female reproductive tract
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5
Q

normal pH of semen

A

7.3-7.7

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6
Q

other substances in semen

A
  • substances to help suppress the immune response in the female’s reproductive tract and antibiotic chemicals to destroy bacteria as well as clotting factors to help coagulate semen after it is ejaculated to help stick to the walls of the vagina until sperm become mobile
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7
Q

how many sperm in normal ejaculate

A
  • 2-5 ml/ 20-150 million per mL
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8
Q

what branch of ANS controls erection and ejaculation

A
  1. -erection- parasympathetic

2. -ejaculation- sympathetic

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9
Q

what chemical is released into the penile tissue during erection and function?

A

NO(Nitric Oxide)- it relaxes the smooth muscles in the blood vessel walls; let’s them dilate and fill w/ blood.

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10
Q

what function does expansion of the CORPORA CAVERNOSA and CORPUS SPONGIOSUM perform during erection?

A

1) CORPORA CAVERNOSA- compresses drainage veins -keeps blood there
2) CORPUS SPONGIOSUM- expands to keep the urethra open for ejaculation

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11
Q

After ejaculation, what arteries constrict to allow blood to leave the penis?

A

1- internal pudendal arteries

2- penile arterioles

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12
Q

What causes ED-erectile dysfunction?

A

-caused by a deficient release of NO

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13
Q

During___________, a primary diploid spermatocyte gives rise to 4 haploid spermatids. Where does the process take plac?

A
  • Meiosis

- takes place in seminiferous tubules of the testes

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14
Q

Process sperm undergoes before being capable of fertilizing an egg, 3 major events

A

Spermatid in spermiogenesis:

1) elongation
2) shedding excess cytoplasm
3) forming a tail

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15
Q

function of acrosome on the sperm

A
  • the acrosome, located on the tip of the head contains hydrolytic enzymes that enable sperm to penetrate and enter the egg
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16
Q

Why is blood-testis barrier important?

A
  • the blood-testis barrier occurs between the sustentacular cells and the bloodstream. This barrier prevents membrane antigens of the sperm from escaping into the blood stream.
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17
Q

What 2 hormones stimulate spermatogenesis indirectly, and how do they work?

A

1- FSH- stimulates spermatogenesis indirectly by causing sustentacular cells to release androgen-binding proteins, which allows spermatogenic cells to bind and concentrate testosterone (stimulates spermatogenesis directly)
2- LH- stimulates the interstitial cells to make testosterone.

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18
Q

What does testosterone stimulate at puberty?

A

spermatogenesis, as well as anabolic effects on the body

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19
Q

Differentiate: Primordial Follicle, primary follicle, secondary follicle, late secondary follicle, vesicular follicle

A

1) A PRIMORDIAL FOLLICLE becomes a primary follicle
2) A PRIMARY FOLLICLE becomes secondary follicle, with multiple cell layers(granulosa cells)
3) A SECONDARY FOLLICLE becomes late secondary follicle, with with a THECAL FOLLICULI (layer of connective tissue) around the follicle.
4) A LATE SECONDARY FOLLICLE becomes a vesicular follicle

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20
Q

What is ovulation?

A
  • the secondary oocyte (with its surrounding ring of granulose cells or corona radiate) is expelled from the ovary wall into the peritineal cavity.
  • ovulation is stimulated directly by the hormone LH.
  • when the dominant follicle ovulates, other follicles usually degenerate and are reabsorbed
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21
Q

What is corpus luteum?

A
  • The remaining granulose cells increase in size and long with the internal thecal cells, form the corpus luteum.
  • the corpus luteum produces progesterone and some estrogen
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22
Q

What occurs in the oviducts?

A
  • The uterine tubes, also called fallopian tubes or oviducts, form the initial part of the female duct system.
  • they receives the ovulated oocyte and are the site where fertilization generally occurs
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23
Q

traditionally it is believed that women have how many primary oocytes at puberty

A

250k

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24
Q

What are the 2 cells formed at the end of Meiosis I of an oocyte?

A
  • First Polar Body and the Secondary Oocyte
  • At the end of Meiosis II ?
  • The polar body may produce 2 additional polar bodies and the secondary oocyte produces a second polar body and a large ovum.
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25
Q

What are the 2 phases of ovarian cycle?

A
  1. The Follicular Phase (follicle growth from days 1-14) and the…
    2) Luteal Phase (corpus luteum activity from days 14-28)
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26
Q

3 phases of the uterine cycle

A

1) Menstrual Phase -days 1-5- uterine lining is shed. Ovarian hormones at the at their lowest layers
2) Proliferative Phase- days 6-14- the endometrium (inner lining of the uterus) is rebuilding as blood estrogen levels rise. SPIRAL ARTERIES increase in #. In the ovary. ovulation, which only takes 5 min, occurs at the end of this phase. Cervical mucus thins to aid sperm in entering uterus
3) Secretory Phase-days 15-28- this phase is the most constant, timewise. Uterine lining continues to build up, and cervical mucus thickens again, to form a cervical plug that blocks entry to the uterus in case an embryo is implanting. If fertilization did not occur, the corpus luteum degenerates ~day 25, LH levels fall, spiral arteries kink and go into spasms, and menstruation begins.

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27
Q

atelectasis

A
  • lung collapse
  • can occur of a bronchiole becomes plugged (following pneumonia) or if a chest wound allows air into the pleural cavity or a tear in the visceral pleura lets air from the respiratory tract out
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28
Q

infant respiratory distress syndrome IRDS

A

-if infant is born prematurely - they often do not produce enough surfactant, they have to work hard to reinflate their lungs

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29
Q

tidal volume TV

A

what goes in and out of lungs in a single normal breath

~500mL

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30
Q

Inspiratory Reserve Volume IRV

A

amount that can be inspired forcibly beyond tidal volume

~2100-3200mL

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31
Q

expiratory reservce volume ERV

A

amount you can breath out -expire- after tidal expiration

~1000-1200mL

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32
Q

residual volume RV

A

extra 1200mL of air remaining in the lungs, reserves air in the lungs -keep our lungs from collapsing

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33
Q

inspiratory capacity IC

A

total amount of air that can be inspired after tidal expiration
IC= TV+ IRV

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34
Q

functional residual capacity FRC

A

amount of the air in the lungs after tidal expiration

FRC= RV+ERV

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35
Q

Vital Capacity VC

A

amount of exchangeable air
~4800 mL
VC= TV+ IRV+ ERV

36
Q

Total Lung Capacity TLC

A

sum of all your lung volumes, except TV

~6000mL

37
Q

Dalton’s Law of Partial Pressures

A

the total pressure exerted by a mixture of gases is the sum of all pressure exerted by individual gases in the mixture

38
Q

Henry’s Law

A

when a gas contacts a liquid, that gas will dissolve in the liquid in proportion to its partial pressure
- the greater the concentration of a particular gas in the gas phase, the more and faster it will go into solution in the liquid

39
Q

Bohr effect

A

acidosis and increasing Pco2 weaken the Hb-O2 bond, so O2 is dropped where it is needed most

40
Q

hypoxia

A

inadequate O2 delivery to the tissues

41
Q

ischemic (stagnant) hypoxia

A

impaired or blocked circulation

42
Q

histotoxic hypoxia

A

cells can’t use oxygen ; ex. cyanide poisining

43
Q

hypoxemic hypoxia

A

reduced arteriole blood oxygen , can be caused by abnormal ventilation , perfusion coupling, pulmonary diseases and breathing air with low O2

44
Q

Haldane Effect

A

the lower the Po2 and the lower the extent of Hb saturation with O2, the more CO2 that can be carried in the blood

45
Q

hypercapnia

A
  • rise of CO2 in the blood
  • when CO2 accumulates in the brain, it is hydrated to form carbonic acid which then dissociates to release H+
  • increase in H+ excites the central chemoreceptors. which synapse to the respiratory centers; this results in increasing depth and rate of breathing
46
Q

chronic obstructive pulmonary disease COPD

A

permanent decrease in ability to expire

- often caused by cigarette smoking

47
Q

emphysema

A

permanent enlargement & destruction of alveoli

- this causes lungs to become less elastic, and breathing takes much more energy

48
Q

chronic bronchitis

A
  • excessive mucous production, esp. in lower passages
  • this impairs ventilation and gas exchange and provides an environment for bacteria to grow, increasing infections
  • ex. cystic fibrosis
49
Q

asthma

A

reversible obstructive condition caused by immune response that inflames & constricts air passageways, causing the person to gasp for breath

50
Q

tuberculosis TB

A

infectious disease caused by airborne bacteria, it affects the lungs

51
Q

cystic fibrosis CF

A

the most common fatal hereditary disease in North America results from abnormal CFTR protein; fails to form chloride channels

  • the result is thick mucus that clogs the respiratory system and invites infection
  • the thorax becomes more rigid & lungs less elastic with age, causing vital capacity to decline
52
Q

what is intrapulmonary pressure? How does is compare to atmospheric pressure?

A

Intrapulmonary pressure Ppul- pressure the alveoli changes during breathing but always evetually going to equalize with atmospheric pressure

53
Q

What is interpleural pressure? How does it compare to intrapulmonary pressure?

A

Interpleural pressure Pip: pressure in the pleural cavity; always about 4mmHg<Ppul
- this means that Pip is always negative, lower relative to Pul

54
Q

What is transpulmonary pressure?

A

Difference between Pip and Ppul (4mmHg); prevents lung collapse
- transpulmonary pressure is related to lung size so the greater the pressure, the larger the lungs

55
Q

What is Boyle’s Law and how does it relate to our ability to breathe?

A

Boyle’s Law: Relationship between pressure and volume : P1V1=P2V2

  • pulmonary ventilation- breathing in and out, depends on volume changes in the thoracic cavity
  • volume changes lead to pressure changes, and pressure changes lead to the flow of gases to equalize pressure
56
Q

Steps of Inspiration

A

1) inspiratory muscles (intercostals) contract, lifting the rib cage and pushing the sternum outward; the diaphragm also gets pushed downward
2) Together, these actions cause an increase of thoracic volume of 500mL
3) Lungs are stretched and the intrapulmonary volume increases
4) This causes intrapulmonary pressure to decrease by ~ 1mmHg, making it lower than atmospheric pressure
5) This change in intrapulmonary pressure causes air to flow down its pressure gradient to enter the lungs until the intrapulmonary is 0 (equal to the atmospheric pressure)

57
Q

Steps of Expiration

A

1) Inspiratory muscles relax causing the rib cage to descend and the diaphragm to rise
2) This leads to a decrease in thoracic volume
3) Elastic lungs recoil passively, causing intrapulmonary volume to decrease as well
4) this causes an increase in intrapulmonary pressure of 1mmHg
5) This change in Pip allows air to leave the lungs flowing down its pressure gradient until intrapulmonary pressure is 0.
* During inspiration Pip actually declines to about 6mmHg relative to Patm; and it increases during expiration back up to 4mmHg relative to Patm (its normal pressure).

58
Q

How does air flow relate to resistance and pressure?

A

-Airway resistance: Major nonelastic source of resistance to gas flow is friction encountered in respiratory passageways
-F= (change in P)/R
F=gas flow
P=pressure
R=resistance

59
Q

perfusion

A

perfusion is the process of a body delivering blood to a capillary bed in its biological tissue

60
Q

Where in the lungs is the greatest resistance to gas flow?

A

medium-sized bronchi

61
Q

how do histamine and epinephrine affect bronciole diameter?

A
  1. histamine- cause bronchiconstriction when irritants are inhaled, dramatically reducing air passage
  2. epinephrine- dilate bronchioles, released during sympathetic nervous system, reducing airway resistance
62
Q

What is the importance of surfactant in the lungs?

A

Surfactant, a detergent-like, complex of lipids & proteins, decreases the cohesiveness of water in the lung fluid, decreasing surface tension and allowing the alveoli to overcome it when they expand during inspiration

63
Q

What is lung compliance and what conditions decrease it?

A

Lung Compliance- distensibility of the lungs

  • the higher the lung compliance, the easier it is to expand the lungs at any given transpulmonary pressure
  • LC is decreased when: chronic infection can cause inelastic scar tissue to form or not producing enough surfactant, or deformoties, ossification of costal cartilages, paralysis of intercostals=all reduce LC
64
Q

what contributes to dead space in the lungs?

A
  • Anatomical dead space- where air is filling conducting zones but it doesn’t contribute to gas exchange , ~150mL
  • Alveolar dead space- any alveoli that have collapsed are added to the anatomical dead space to get total dead space
65
Q

How are partial pressures of gases related to atmospheric pressure?

A

As altitude increases (atmospheric pressure decreases) partial pressures also decrease.
- as altitude decreases below sea level (atmospheric pressure increases) partial pressures also increase

66
Q

Which respiratory gas is most soluble? The least?

A

most soluble: CO2

least soluble: N2

67
Q

How does the composition of alveolar gases compare to that of atmospheric gases?

A

Composition of alveolar gases are very different from that of atmospheric gases, much higher proportions of CO2 & WATER VAPOR

68
Q

What are the approx. partial pressures of O2 and CO2 in deoxygenated blood and in the alveoli?

A

O2: Alveoli (104mmHg) Deoxygenated blood (40mmHg)
CO2: Alveoli (40mmHg) Deoxygenated blood (45mmHg)

69
Q

ventilation-perfusion coupling: mismatch where low ventilation (little gas) and/or high perfusion of alveoli (lots of blood flow)

A

1) If there is a mismatch where low ventilation(little gas) and/or high perfusion of alveoli (lots of blood flow) cause local Pco2 to be high and local Po2 to be low
-Pulmonary arterioles serving those alveoli constrict and local bronchioles dilate
RESULT: Arteriolar constriction decrease blood flow (perfusion) and bronchiolar dilation allows more air flow/(increase in CO2 leaving the lungs).
-both ventilation and perfusion are now matched and excess CO2 that has built up can leave

70
Q

ventilation-perfusion coupling: mismatch where high ventilation (much gas) and/or low perfusion of alveoli (low blood flow)

A

2) If there is a mismatch where high ventilation (much gas) and/or low perfusion of alveoli (low blood flow) lead to a build up of Po2 and low Pco2
-pulmonary arterioles will dilate and bronchioles will constrict
RESULT: Arteriolar dilation increases blood flow (perfusion) and bronchiolar constriction decreases the CO2 leaving the lungs
- both ventilation & perfusion are now matched and CO2 levels are increased

71
Q

What is the thickness and the area of the normal respiratory membrane and why is it important?

A

Thickness & surface area of the respiratory membrane: the healthy respiratory membrane is usually ~0.50-1micrometer thick and has an area of about 90m^2
- if the lungs become waterlogged such as from pneumonia or left heart failure, the effective thickness of the lungs is increased so the time the RBCs are in transit through the lungs is not enough for adequate gas exchange

72
Q

Why does gas diffusion allow O2 and CO2 to go into the proper direction between lungs and blood and between blood and tissues?

A
  • Po2 in the tissues (40mmHg) is lower than that in the blood (100mmHg); thus O2 diffuses out of the blood into the tissues
  • Pco2 is higher in the tissues than the blood and thus CO2 diffuses out of the tissues into the blood
  • gas exchange that occurs between the blood and alveoli and between the tissues and blood takes place by simple diffusion across gradients of O2 and CO2 that exist on opposite sides of the exchange membrane
73
Q

What is the main transport mechanism for O2 and why?

A

98.5% of O2 is transported bound to hemoglobin and only 1.5 % dissolved in plasma because oxygen is poorly soluble in water

74
Q

Does hemoglobin release all of its O2 with each circuit through the body?

A
  • normally only 20-25% of O2 is unloaded in one systemic circuit, so if O2 drops to very low levels in the tissues, such as vigorous exercise, more O2 can be unloaded to compensate
75
Q

What factors affect hemoglobin unloading at a particular partial pressure?

A
  • temperature
  • blood pH
  • pressure of Pco2
  • BPG in the blood
76
Q

What are the ways that CO2 is transported in the body and in what percentages?

A

CO2 is transported from tissues to the lungs 3 ways:
1) Dissolved in plasma (7-10%)
2) Bound to hemoglobin (just over 20%); it is bound and carried in the RBCs as carbaminohemoglobin. CO2 + HbHbCO2
3) Bicarbonate in plasma (70%)
CO2 +H2O H2CO3 H+ + HCO3-

77
Q

What factors affect CO2 loading and unloading to and from hemoglobin?

A

CO loading and unloading to and from Hb are directly influence by Pco2 and the degree of oxygenation on the Hb

78
Q

CO2 +H2O H2CO3 H+ + HCO3-

A

CO2 +H2O H2CO3 H+ + HCO3-

Carbon dioxide + water Carbonic Acid hydrogen ion + bicarbonate

79
Q

How does carbonic acid/bicarbonate buffer system work to maintain pH in the blood?

A

If H+ concentration becomes too high in the the blood, excess H+ is removed by combining with HCO3- (a weak base) to form H2CO3 (a weak acid)
-If H+ becomes to low, H2CO3 dissociates releasing H+

80
Q

How does depth and rate of breathing affect blood pH?

A
  • SLOW SHALLOW BREATHING- lets CO2 accumulate in blood, increasing carbonic acid and decreasing blood pH
  • RAPID DEEP BREATHING-flushes CO2 out of the blood; reducing carbonic acid levels and increasing blood pH
81
Q

What are the medullary and pontine respiratory centers responsible for?

A
  1. MEDULLARY- rhythm of breathing
  2. PONTINE RESPIRATORY CENTERS- impulses to the VRG modify the fine tune breathing rhythm during activities such as vocalization, sleep and exercise
82
Q

What do central and peripheral chemoreceptors respond to?

A

CENTRAL CHEMORECEPTORS, found in the brainstem, and PERIPHERAL CHEMORECEPTORS , found in the aortic arch and carotid arteries, are sensors that respond to fluctuations in CO2, O2 and H+

83
Q

How do the presence of Pco2, level of Po2 and level of pH influence breathing depth and rates?

A
  1. High Pco2-hypercapnia-increase depth & rate of breathing
  2. Low Pco2-hypocapnia- slow & shallow breathing
  3. low Po2 (<60mmHg)- increase ventilation
  4. low pH- respiratory rate and depth increase
84
Q

how can the hypothalamus influence respiratory centers?

A

Strong emotions and pain can act through the hypothalamus and the rest of the limbic system to signal the respiratory centers
ex. jump into really cold water, you gasp-pain response

85
Q

What is inflation (Hering-Breurer) reflex?

A

Stretch receptors in the lung passageways are stimulated when the lungs are inflated, these stimulate the respiratory centers via the afferent fibers of the vagus nerve, sending inhibiting impulses, end inspiration and start expiration.
-As lungs recoil, these receptors quiet, allowing inspiration again

86
Q

How doe exercise & altitude affect respiration?

A
  1. Exercise-hypernea-as exercise begins ventilation abruptly increases, this is followed by a more gradual increase
    - when exercise stops, there is am abrupt decrease in ventilation then a gradual decline to baseline values
  2. High altitude- at higher elevation, both arteriol Po2 & hemoglobin saturation decrease because of decrease in atmospheric pressure
    - increased ventilation helps increase partial pressure of O2