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Nur 209 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What marks the beginning and the ending of the conducting airway.

A

Conducting airway:

  • beginning: trachea
  • ending: beginning at the alveoli
  • alveoli are not part of the conduction airway
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2
Q

What marks the beginning of the respiratory unit:

A

beginning of the alveoli

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3
Q

What are the advantages of the conducting airway:

A

humidify the airways during winter, protect/clean/filter due to the ciliated cells epithelial layer

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4
Q

big function of the respiratory system

A

gas exchange

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5
Q

what cells are responsible for producing the mucus layer ?

A

club cells of the epithelial lining

mucus is good for humidifying the air

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6
Q

What happens to the smooth muscle of the respiratory tract as we pass: trachea/bronchus-bronchiole-resp bronchiole-alveoli…

A

It tickens, the smaller the airway becomes, the more control we can have on the diameter (diallate, constrict) to modify the Flow of air.

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7
Q

Why is it better to have millions of alveoli instead of 1 big sac?

A

(curvature) surface is bigger = more gas exchange

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8
Q

On alveoli, the smaller the ____, the bigger the ____ is.

A

radius, pressure

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9
Q

What is responsible for the millions alveoli we have?

A

Surfactant produced by type 2 cells. People who’s type 2 cells don’t fonction as well have more alveoli that collapse and that causes resp problems

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10
Q

What allows alveoli to communicate?

A

Pore of Kohn

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11
Q

Lungs have 2 type of pleura. ____that is in the inside and ____ that is outside. They create a ______ that has negative atmospheric pressure.

A

visceral
parietal
pleura cavity

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12
Q

Why do we say that in the left heart, there is mixed blood.

A

Because in the bronchial circulation (branch of the systematic circulation) , the blood that is deoxygenated in the lungs has no venous return. It goes back directly to the left part of the heart.

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13
Q

What are the 3 main goals of pulmonary systems

A
  1. ventilate alveoli (change the air in there)
  2. exchange of O2 and CO2
  3. Alveoli perfusion: making sure that there is blood going to the alveoli
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14
Q

what is the residual volume:

A

volume that can’t get out of your lungs

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15
Q

What’s the equation for Minute Ventilation

A

Minute ventilation (L/Min) = Tidal volume (L/Breath) x Ventilation Rate (Breath/min)

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16
Q

Equation of total lung capacity:

A

Residual Volume + Vital Capacity = TLC (total lung capacity)

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17
Q

Goal of ventilation

A
  1. Get O2 in

2. Push CO2 out

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18
Q

The tidal volume is an ______ neurochemical control.

A

involuntary

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19
Q

The autonomic nervous system separates in 2 categories: ________ and _______. The DRG is controlled by the ______ and _____ and _____ info and is localized in the medulla. The VRG, localized in pons, is only used when there is _________.

A 
Dorsal respiratory group
Ventral respiratory
Automatic Nervous System 
recieves
sends
increase in ventilatory efforts
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20
Q

What centers are the modulators of respiratory rate and depth. They modulate from:

A
  1. apneustic and pneumotaxic centers

2. Cortex, hypothalamus and Limbic system

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21
Q

3 lungs receptors explain

A
  1. Stretch: SLOW ADAPTING, how stretch lungs are, smooth muscles, detects increase in volume/size (if deeper breaths taken than decrease in frequency of resp).
  2. Irritant: FAST ADAPTING, ex food goes in airway and I cough. Thx to irritant receptors.
  3. Juxta-Pulmonary Capillary:
    Close to the pulmonary capillaries, detect pulmonary edema.
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22
Q

2 types of chemoreceptors what are they:

difference:

A
  1. Central chemoreceptors (CC): detects changes of PH in CSF and mesures O2 and CO2.
  2. Peripheral Chemoreceptors (PC). Mesure arterial levels of oxygen.
    difference: CC detects change in ph (indirect mesurment of O2) in CSF and PC detects arterial Po2
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23
Q

Scenario: CC detects increase in Pco2 explain next

A

means there is decrease in PH. CC relays the info the Dorsal Respiratory group (in the brain) and the DGR builds a response: increase ventilation rate and depth to reduce Pco2.

24
Q

What are major muscles of expiration:

A

there is none.

25
Q

The major muscles need to _____ to bring air in. There is 2 of them: ______ and ______.

A

contract
diaphragm
external intercostals

26
Q

Accessory muscles you ______ at rest. Only during ______. ____ and ____ are accessory muscles. The

A

don’t use
forced expiration
scalenus muscle
sternocledomastoid

27
Q

_____ of accessory muscles of expiration allow air to go out. They are only used during ______. _______ and _______ are both opposite to major muscles.

A

Relaxation
forced expiration
internal intercostals
abdominal muscles

28
Q

Lung and chest wall work together. Because your ____ wants to expand, it keeps your lungs from _____. These 2 opposite forces create ______,

A

expand
collapsing
negative pressure

29
Q

What is the definition of compliance of the lungs and is it always the same?

A

C = variation of volume / variation of pressure. Pressure required to change volume of the lungs. A high compliance= decreased elasticity = difficulty exhaling. At rest (end of expiration) it is easier to inflate lungs so the compliance is high. At the end of inspiration the lung compliance is the lowest. Compliance varies depending on where you are in your breathing cycle.

30
Q

Depending on how you sit (your position), what is the effect on your lungs?

A

The air molecules will go to the part of the lungs that are closest to the ground (se ppt). So it’s important to lead most of the blood to go to that region to optimize gas exchange.

31
Q

What part of your lungs are responsible for the most gas exchange?
ROLE OF GRAVITY

A

bottom: the blood pressure is higher than the pressure of air in your alveoli. More blood = more gas exchange. Ventilation and perfusion ratio is greater.

32
Q

Describe O2 pathway:

(40-100 mmHg)

deoxygenated blood: 40 mmHg

A
  1. Heart to pulmonary artery: pressure increases (40 mmHg to 100 mmHg).
  2. Pulmonary vein to heart.
  3. Heart to tissues (100 mmHg to 40 mmHg).

O2 pressure increases in the lungs.

33
Q

Describe CO2 pathway:

(46-40 mmHg)

oxygenated blood: 100 mmHg

A
  1. Tissues to heart. Heart to pulmonary artery (46 mmHg to 40 mmHg).
  2. From pulmonary vein to heart and systematic circulation.
  3. From heart to tissues (40 mmHg to 46mmHg).

Co2 concentration decreases in lungs.

34
Q

The has exchange depends on 2 things:

A
  1. Thickness of capillary walls

2. Blood flow speed

35
Q

Bohr effect: normal thing

A

relationship between amount of ox present in blood and amount of saturation at different steps. Close to 100% = fully charged with 4 oxygen. If it’s a low number it means the oxygen ot out of blood into tissues. The more the blood gets to tissues and the more affinity decreases. The more affinity increases the more oxygen binds to hemoglobin.

36
Q

Bohr effect stats that there is 3 things _____, _____ and _____ can affect the normal curve of hemoglobin saturation.

A

pH, CO2 and temperature

37
Q

What are symptoms of decrease in metabolism:

IF LESS METABOLISM, LESS NEED OF OXYGEN.

A

increase pH, decrease T° and PCO2.

38
Q

pH and metabolism always opposed.

A

If pH goes up it’s because decrease in metabolism. Should I need more oxygen? NO.

39
Q

The reason why oxygen exits the hemoglobin to go inside the tissues or not depends on the level of metabolism and this level of metabolism depends on 3 factors :

A

pH, T° and PCO2.

40
Q

Metabolism and dissociation do the same:

A

increase in metabolism, increase in dissociation. Ex: exercises boosts metabolism. Tissues need more oxygen and perfusion cause a lot of lactic acid produced. Affinity decreases to release oxygen in tissues and dissociation of O2 increases cause more oxygen dissociates from blood cells.
affinity and dissociation are opposed always.

41
Q

Halden effect states that :

A

there is more Co2 transported deoxygenated blood than in oxygenated blood.

42
Q

Halden effect

A

blood travels to tissues where affinity to o2 decreases. O2 is relieved in blood and H+ that also has affinity to hemoglobin steals O2’s free space. This way there is less H+ in the plasma. Result: the co2 will come bind to oxygen to form Co2 - and will come bind to H+. More C02 from tissues can dissolve on plasma.

43
Q

What pulmonary pathology is due to inadequate gas exchange and inadequate alveolar ventilation?

A

Acute Respiratory Lung Failure. It is always secondary to an other condition (COPD, cystic sclerosis, stroke
, etc) and can lead to hypoxemia (not enough o2 sat) and hypercapnia.

44
Q

What is pneumothorax:

A

when you ave a rupture/puncture in the lungs (parietal or visceral pleura) . Air moves into the pleural space and lungs collapse.

45
Q

Respiratory diseases are separated in 2 categories

A
  1. Restrictive lung diseases

2. Obstructive lung diseases

46
Q

Respiratory diseases are separated in 2 categories

A
  1. Restrictive lung diseases

2. Obstructive lung diseases

47
Q

Pulmonary fibrosis (scaring of lungs)

A

Scar tissue decreases elasticity so becomes more rigid, more difficult to inflate so low compliance.

48
Q

Cystic fibrosis

sensation: “ breathing through a straw “

A

genetic disease (CFTR gene), decrease in resp capacity, decrease in digestion (pancreatic enzymes)., decrease in reproductive function. excessive chloride excretion. Leads to dehydrate mucus cause a lot of sodium is rehabsorbed. Form mucus plung and that is a good place for the bacteria to multiply (chronic bacterial infection). Club cells will go hyperplasia and athropy to replace mucus. Chronic inflammation leads to neutrophilic chronic inflammation.

49
Q

Cystic fibrosis

sensation: “ breathing through a straw “

A

genetic disease (CFTR gene), decrease in resp capacity, decrease in digestion (pancreatic enzymes)., decrease in reproductive function. excessive chloride excretion. Leads to dehydrate mucus cause a lot of sodium is reabsorbed. Form mucus plug and that is a good place for the bacteria to multiply (chronic bacterial infection). Club cells will go hyperplasia and atrophy to replace mucus. Chronic inflammation leads to neutrophilic chronic inflammation.

50
Q

Pulmonary edema

A

More fluid, less place, harder for lungs to inflate. Can lead to left-heart failure, toxic gases, growth of tumor.

51
Q
  1. Obstructive lung diseases
A

spirometry: FEV test : do poor.
Difficult to exhale, the lung volume is greater than for a normal person. not good cause you can’t exhale it proprely. A lot of air remains in lungs. The ventilation point is to exchange it. Trapped with a lot of CO2 in lungs which is not useful.

52
Q

Difference between asthma and COPD.

A

Asthma is reversible

COPD is not reversible

53
Q

Asthma

A

chronic inflammation of bronchial mucosa, reversible.

54
Q

Acute Asthma

3 THINGS MAKE IT MORE DIFFICULT TO BREATH:

A
  1. antigen comes in and makes it way to the airways.
  2. It’s gonna activate mast cells meaning it’s going to degranulate releasing it content filled with histamine. Histamine and other mediators have effects on airways: massive vasodilatation (edema), club cells produce more mucus (accumulate in airways), smooth muscles constrict, activates other inflammatory cells.

3 THINGS MAKE IT MORE DIFFICULT TO BREATH:

  1. mucosa accumulation
  2. vasodilatation
  3. airways constriction
55
Q

Late asthma pathology

what does it cause

A

The more you wait to treat asthma and the less chances you have to return to normal because of the remodeling. It means that the cells of the airways change function: more smooth muscle cells, airways less ciliated, thickening of walls, mucus accumulation. Space restricted and can become irreversible.

  1. decrease in perfusion
  2. decrease in ventilation
56
Q

Acute asthma leads to _____. As chronic asthma leads to ______.

A

alkalosis

acidosis

57
Q

Pathophysiology of asthma:

A

increase in alveolar gas pressure can obstruct airway leading to decrease of perfusion (blood supply) and decrease in ventilation. This mismatch can lead to improper reoxygenation of blood and alveolar dead space (no perfusion).

Nur 209 (2 decks)

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