Physiology 3051 Part 3 (3Rd Midterm)

Front 1

intrapleural pressure

Back 1

later

Front 2

Upper respiratory System

Back 2

Front 3

Lower respiratory system

Back 3

Front 4

Respiratory System Functions

Back 4

•Exchange of gases between the atmosphere and the blood

•Homeostatic regulation of body pH

•Protection from inhaled pathogens and irritating substances (IGA, the antibodies that are in mucus)

•Vocalization

•Conditions air

-Warming air to body temperature

-Adding water vapor

-Filtering out foreign material (cilia trap and get rid of pathogens)

Front 5

External respiration hpic

(2 circulation series, one for using oxygenated blood, one for moving the blood back to heart)

Back 5

Hint 5

Front 6

Epithelial Cells hpic

Back 6

Hint 6

Front 7

Branching of airways

Back 7

as divisions increase...

-Diameter gets smaller

- number of airpockets increase exponentially

-Cross sectional area increases exponentially (more air can be held)

Front 8

Alveoli hpic

Back 8

80-90% of alveoli covered in capilaries

covered in bedding of blood, needs a way to get in touch with blood to oxygenate it.

Hint 8

Front 9

Rat vs Frog

Back 9

Rat has more Surface Area for Alveoli (more SA = more diffusion)

Frogs=cold blooded, metabolism slows down, and oxygen need decreases. can breath through skin, so SA of lungs evened out

Rats are warmblooded, need oxygen all the time in order to stay that temp

Front 10

Pulmonary Edema (fluid increase in interstitial space)

Back 10

•An increase in capillary permeability->intercellular clefts widen

•Albumin leaks from the capillaries

•Increase in interstitial protein osmotic pressure draws water into the interstitium

•However, the interstitial space is small

•Fluid spills into the alveoli, interfering with diffusion and exchange

Front 11

The pleural Sac (hpic)

Back 11

The pleural sac forms a double membrane surrounding the lung,

similar to a fluid-filled balloon surrounding an air-filled balloon.

Hint 11

Front 12

Air in the Lungs

Back 12

Front 13

surface tension

Back 13

the interface between water and air. for the lungs its known as the Law of LaPlace. (the difference in wall tension in different parts of the lung)

Front 14

Complience hpic

Back 14

-The change in pressure needed to inflate the lungs to a particular volume, essentially, the ability ot stretch.

high compliance: stretches easily, requires a lower pressure change to inflate lungs. if its too compliant, then its a disease that kills tissue.

low compliance: requires more force, stiff, requires a larger pressure change to inflate the lungs to the same extent as compliant lungs. Fibrosis(lungs have scar tissue)

Hint 14

Palv= alveolar pressure

Pip= interplueral pressure

Front 15

Elastance

Back 15

The ability to return to resting volume when stretching force is released.

Front 16

Compliance has two aspects hnotes

Back 16

•Characteristics of the tissue

-Compromise of the rib cage (broken rib/muscles)

-Scaring of lung tissue (fibrosis)

-Swelling and inflammation (edema)

-pneumothorax (air in interpleural space, and lungs collapse)

•Surface tension

-Lack of surfactant

Hint 16

emphysema: high compliance, low elasticity (can breath in easily, but cannot force air out)

Front 17

Surface tension

Back 17

•Allows water particles to stick together–like beading of water on a slick window

•High surface tension makes alveoli more likely to collapse.

•Different sized alveoli have different collapsing pressures with equal ST

•Surfactant lowers ST and lowers it more in the small alveoli so that pressures are equal

Front 18

Law of LaPlace (if Surface tension is same, then smaller bubble has higher pressure) hpic

more surfactant = less surface tension= equalize of pressures

Back 18

Hint 18

Front 19

Surfactant

Back 19

•More concentrated in smaller alveoli

•Mixture containing proteins and phospholipids

•Newborn respiratory distress syndrome

-Premature babies

-Inadequate surfactant concentrations

Front 20

Airway

Resistance

Back 20

•Single respiratory cycle consists of one inspiration followed by one expiration

•Airway resistance influenced by the same principles as vascular resistance

•Flow∝∆P/R <-- WHAT LAW IS THIS? (Ohm's law)

•Most important influence on the airways is the radius of the airways

•In Asthma and COPD, airway resistance is pathologically high. (chronic obstructive pulmonary disease, like emphysema)

Hint 20

Front 21

Local control of blood flow

Back 21

Vasodilation decreases resistance, increases bloodflow to that area

Hint 21

Hypoxic vasoconstriction. Local control mechanisms try to Keep ventilation and perfusion matched

Front 22

Hypoxic vasoconstriction

Back 22

•Local responses in the lung are different!

•Low oxygen in the airways causes the blood vessels going to that part of the lung to constrict.

•Why is this helpful? (diverts path from poor alveoli to a good one, maximizes oxygenation)

•How could it be harmful? If you have hypoxia everywhere, vasoconstriction occurs, then pressure goes up. afterload in ventricle increases

Front 23

Vital capacity

Back 23

•Total amount of air that can be moved in and out of the lungs

•3.5 to 4.5 liters

•Reduced with any kind of pulmonary disease

Hint 23

Front 24

%FEV1

Back 24

•Measure of airway resistance

•Volume of forced expiration in one sec divided by

forced vital capacity

•FEV1/FVC

•3 liters/4 liters = 75%

•70-80% normal

•Decreased with obstructive disease like asthma or COPD

*does not show for restrictive diseases.

Front 25

restrictive vs obstructive

Back 25

•Restrictive

•Low compliance or stiff lungs

•Small tidal volume with high RR

•Fibrosis, tuberculosis, interstitial lung disease,

ARDS, pulmonary edema

Hint 25

•Obstructive

•High airway resistance

•Must be taught to take large TV with a low RR

(called pursed lip breathing)

•Asthma, emphysema, chronic bronchitis

Front 26

Commonalities

Back 26

•Both would have a reduced vital capacity

-R–difficulty expanding to get air in

-O–difficulty recoiling to get the air out

•Both would have a reduced flow rate

-See explanations above

•Both would have an increased work of breathing

(WOB)

Front 27

Saturation vs oxygen

Back 27

saturation only applies to CO2 content,

Oxygen content = both CO2 and O2 and also hemoglobin as well.

Front 28

Dalton’s Law (hnotes)

Back 28

Hint 28

normal atmosphere has around 20% O2, CO2 is only .03%

therefore of that 760 torr, 20% of that comes from O2.

Front 29

oxygen pathway in pulmonary and systematic circulation

Back 29

Front 30

Movement of Gases hpic

Back 30

•Pressure gradient (aka: concentration gradient)

•Solubility

•Temperature

Hint 30

Front 31

What if we didnt have hemoglobin?

Back 31

our cardiac output would have to be 67 liters/min to maintain tissue life.

*its normally just 5 liters/min, even at highest exercise 20-25liters/min

Hemoglobin carries a truckload of oxygen in our blood

Front 32

Oxyhemoglobin saturation curve

hnotes

Back 32

Hint 32

at 40% PO2, saturtaion still at 75,

but between 20-40% PO2, changes the shape of hemoglobin, and becomes a releaser of oxygen rather than a binder of oxygen (the normal PO2 found in capillaries)

Front 33

Alveolar gas exchange hnotes

Back 33

Hint 33

Front 34

amount of oxygen bound to Hb hnotes

Back 34

Hint 34

Oxygen cannot be calculated unless you know exactly how much hemoglobin you have.

Front 35

Normal blood values for medicine hnotes

Back 35

Hint 35

the capilaries have a PO2 between 20-40 mm Hg

Front 36

Effect of pH on hemoglobin saturation (bohr effect) hnotes

Back 36

Hint 36

note: more acidic means easier to release oxygen from hemoglobin. high CO2, means more acidic right shift, and vice versa

Front 37

Effect of Temp on hemoglobin saturation

Back 37

Front 38

Effect of PCO2 on hemoglobin saturation

Back 38

Front 39

Total arterial O2 content hpic

Back 39

Hint 39

Front 40

Carbon Monoxide

Back 40

•240 times the affinity for Hb than O2

•Decreases content with normal arterial Blood

gases (ABGs)

•NO SHORTNESS OF BREATH

•Left shift (more basic, latched, harder to release oxygen from hemoglobin)

Front 41

Carbon Dioxide Transport

Back 41

•Dissolved: 7%

•Converted to bicarbonate ion: 70%

•Bound to hemoglobin: 23%

–Hemoglobin also binds H+

–Hb and CO2: carbaminohemoglobin

•CO2 + H20 -> H2CO3 -> H+ + HCO3-

•NOTE: a build up of CO2 causes a build up of acid

Front 42

Carbon dioxide transport hpic

Back 42

Hint 42

Front 43

What have you learned about content and saturation?

Back 43

•Mary has 12 gm% of hemoglobin and Frank has 13gm%

•At a pO2 of 100 mmHg of mercury

–who is more saturated?

-who has a higher content? Who has higher dissolved content? Bound content?

•What about at a pO2 of 60 mmHg?

Hint 43

frank higher content

both have same dissolved content and same saturation

bound content is hemoglobin dependant

Front 44

reflex control of ventilation

Back 44

medulla oblongata and pons have pacemaker like functions

pons: deepness of breath and rapidity.

Front 45

Regulation of Ventilation

Back 45

•Peripheral chemoreceptors

–Located in carotid and aortic arteries

–Sense changes in PO2

, pH, and PCO2

–Specialized glomus cells respond to low PO2 when drops to 60 mmHg or less

•Central chemoreceptors

–Respond to changes in CO2

Front 46

chemoreceptors 2,3 DPG

Back 46

respond to one thing, 2,3 DPG signifies that glycolysis is occuring.

Front 47

Protective Reflexes Guard the Lungs

Back 47

•Respond to physical injury or irritation

•Bronchoconstriction

–Irritant receptors in airway mucosa send signals through

sensory neurons

•Sneezing

•Coughing

•Hering-Breuer inflation reflex

-these are stretch receptors that are responsible for inflation reflex

-if lungs are not stretched, causes inspiration, otherwise if too stretched, expiration

Hint 47

Which of the following stimuli would most likely

to cause BOTH the central and peripheral

chemoreceptors to stimulate ventilation?

–Arterial blood pH of 7.3.

–PaCO2 of 44 mmHg.

–PaO2 of 105 mmHg.

–PvCO2 of 48 mmHg

Front 48

uhoh

Back 48

increases as temp, CO2, (2,3 DPG), and H-ions increases(pH goes down)

and decreases in the vice versa scenario.

as the graphs move to the right, metabolism is increasing because oxygen is being released from hemoglobin more easily

Front 49

lung facts

Back 49

dissolved CO2 goes into the alveoli

oxygen binds to hemoglobin, hemoglobin goes up.

normal atm = 79% N2, 20% O2, 1% random

Front 50

fatigue and oxygen

Back 50

if brain has so litle oxygen, will start changing saturation release factors.

O2 and CO2 have to dissolve into blood to exhibit PO2 and PCO2. losing hemoglobin doesnt mean PCO2 increases. PCO2 affects hemoglobin, but hemoglobin does not effect PCO2

Front 51

Hormones: Definition and Function

Back 51

•A chemical signaler secreted into the blood or interstitial fluid by one cell or group of cells and

has a physiologic control effect through a specific receptor.

•Examples of physiologic control effects

–Affecting rates of enzymatic reactions

–Transport of ions or molecules across cell membranes

–Changes in gene expression and protein synthesis

Front 52

Important characteristics of

hormones

Back 52

•Potent in small concentrations

–amplification

•Regulate biologic functions

•Work through receptors that are specific for

certain classes of hormones

–Example estrogen receptors bind estrogens like estradiol, estriol or estrone

Front 53

Hormones: Classification by Chemical Class

Back 53

•Peptide or protein hormones

•Steroid hormones

•Amino acid

–derived or amine hormones

–Catecholamine = characteristics in common with

peptides

–Thyroidhormone = characteristics in common with steroids

Front 54

Hormones: Peptides or Proteins

Back 54

•Preprohormone (the gene is a lot bigger than the active peptide)

–Large, inactive precursor

•Prohormone

–Smaller, inactive

–Proteolytic, post-translational modification

•Peptide/protein/glycoproteinshormones

–Biologically active ( activate the hormone requires modification by changing the peptide, or adding the other stuff)

Front 55

Preprohormones

Back 55

Front 56

Prohormones

Back 56

Front 57

Peptides/Proteins/Glycoprotein

Back 57

•Large protein molecules which dissolve well in blood (water soluble)

•Broken down quickly by peripheral enzyme systems (topic of research) (they disappear quickly)

–Ex: chemical half life of GH 20 -30 minutes

–Ex: chemical half life of epinephrine 2 minutes

•Bind surface membrane receptors

•Cellular response through signal transduction system

–Most commonly second messenger systems

–Can affect gene transcription

Front 58

Peptide hormone synthesis and processing (hpic)

Back 58

Hint 58

Front 59

Hormones: Steroid hnotes

Back 59

•Cholesterol-derived

–Lipophilic and easily diffuse cross membranes

•Bind carrier proteins in blood (shields from degradation)

–Longer half-life

•Cytoplasmic or nuclear receptors

–Genomic effect to activate or repress genes for protein synthesis

–Slower acting

•Cell membrane receptors

–Nongenomic responses

Hint 59

why are steroids slow acting long lasting?
because transcription takes time, but they have a long half life.

Front 60

Steroids synthesis process

Back 60

Front 61

Steroid transport

Back 61

•Because lipid soluble, must have a protein carrier, like a blood reservoir of steroid

•Some carriers are specific

–androgen binding globulin

•Some carriers are general

–albumin

•Free hormone is biologically active

Front 62

Sex determination

Back 62

•Sex organs

–Gonads contain germ cells and produce gametes and sex

hormones

–Male gonads->testes->sperm

–Female gonads->ovaries->eggs

–Internal genitalia

–External genitalia

•Nucleated cells contain 46 chromosomes

–22 pairs of autosomes

–1 pair of sex chromosomes

Front 63

Embryology hpic

Back 63

•Sex is genetically determined (XX vs XY)

•Reproductive system starts out undifferentiated (in early fetal development, cant determine sex)

•Y chromosome contains SRY gene ->testes and testosterone production ->differentiation of male

structures (mutations in this gene can cause ambiguous child gender)

•In absence of SRY->female structures

Hint 63

Front 64

Male structures hpic

Back 64

•Testes produce sperm and testosterone

•Pathway

–Seminiferous tubules (sperm made here)

–Epididymis (sperm are stored here)

–Vas Deferens (tube takes sperm out)

–Ejaculatory duct (where the sperm leaves testes around bladder)

–Glands (seminal vesicles, prostate, Cowper’s glands)

–Urethra (tube down shaft of penis)

–Penis (the name for said tube)

Hint 64

Front 65

More male structures hpic

Back 65

Hint 65

Front 66

Testes and sperm hpic

Back 66

The testes contain: Seminiferous tubules in which all levels of spermatogenesis is found. Developing cells are protected by Sertoli cells. The interstitial Leydig cells are source of testosterone production

Hint 66

Front 67

hormonal control of spermatogenesis

hnotes

Back 67

Hint 67

Spermatogonium: stem cells, are able to go through mitosis. sperm can bypass the blood bypass barrier

L path goes through testosterone.

SFH to testes, activates sertoli cells, make sperm.

LH goes to leydig cells, makes testosterone and transports everywhere. testosterone feedbacks to the anterior pituitary and GnRH

Front 68

Puberty

Back 68

•As boy ages–brain seems to notice the lack of sex hormone

•Role for Kisspeptin in puberty (helps brain sensitization to testosterone levels)

•Increased GnRH -> LH ->testosterone (GnRH is secreted in pulses, depending on which hormone is needed)

•Development of male organs

•First sign of puberty is growth of the testicles (then the penis)

•Testosterone accelerates growth

–sealing of epiphyseal plate ->adult height

Hint 68

SRH and testosterone are in synergy with each other

Front 69

Androgens Influence Secondary Sexual Characteristics

Back 69

•Primary sex characteristics are internal organs and external genitalia that distinguish males from females

•Secondary sex characteristics are other traits that distinguish males from females

–Body shape

–Beard and body hair

–Muscular development

–Lowering of voice

–Libido

•Anabo ]lic steroids are used illegally by athletes

Hint 69

if decreased anterior pituitary gland function causes decreased sperm and testosterone, will injecting testosterone make more sperm? no, need other hormones too.

Front 70

Pelvis cross section (not important)

Back 70

Hint 70

all external female genitalia = vulva

Front 71

Embryology

Back 71

•In female fetus –stem cells called oogonia undergo mitotic division

•At birth 2-4 million oocytes in ovaries

•About 400 may be ovulated over lifespan

•Traditional view–all stem cells(oogonia) enter meiosis and stop, no remaining stem cells in ovary

•New challenges to this way of thinking

Front 72

The Ovary Produces Eggs

Back 72

•Primary follicle

–Primary oocyte

–Granulosa cells produce estrogens

–Theca cells produce androgen precursor used by granulosa cells

(2step process to making estrogen. theca cells require requires granulosa cells as precurser)

estrodial=main form of estrogen, made by granulosa cells

Front 73

Ovarian events hnotes

Back 73

•Under the influence of FSH, a few(12?) ovarian follicles containing primary oocytes develop

•Follicular cells produce estrogens

•Tertiary/Dominant follicle is chosen about day 7

•Ovulation occurs about day 14 of a 28 day cycle*

•Follicle remnant->corpus luteum

•Corpus luteum lasts about 14 days

Hint 73

Lutenizing hormone ruptures the follicle for ovulation and turns it into a corpus luteum.

Front 74

Cycles are Variable

Back 74

•Important to note that cycles are variable...

ovulation occurs about 14 days from the end of the cycle..

•In other words.. Variability is in the follicular phase.

•Many women do not have a 28 day cycle

Front 75

Two cell process to make estrogen from androgen

Back 75

Front 76

Uterine Events

Back 76

•Menstrual Phase –loss of endometrium because of low levels of estrogen and progesterone

•Proliferative phase –growth of endometrium because of estrogen, causes endometrium to grow

•Secretory phase–differentiation of endometrium into glands because of progesterone,

Hint 76

Day 1-3? (endometrium is dying, not enough hormones)