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Clinical Medicine 2 > Dr. Houston (pulm) -Exam 2 > Flashcards

Dr. Houston (pulm) -Exam 2 Flashcards

1
Q

What are factors that affects gas exchange?

A
  • Surface area (large for gas exchange)
  • Respiratory membrane (thin)
  • Blood supply
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2
Q
A

Mucous, dust in alveolar space will compromise diffusion
* Lining of alv and endothieal blood vessels: Simple squamous

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3
Q

What are all the different cells in the alevolus

A

type 1: Gas exchange
* type 2: surfactant
* Marcophages: degrade pathogens

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4
Q

⭐️

In a normal person, what are the volumes of tidal volume, dead space and alveolar ventilation?

A
  • TV: 500ml
  • Dead: 150 ml (no gas exchange)
  • Alv: 350ml (where gas exchange happens)
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5
Q

⭐️

How does the airway divide?

A

Airway tree divides repeatedly.
* The airway tree consists of a series of highly branched hollow tubes that become narrower, shorter, and more numerous as they penetrate the deeper parts of the lung.
* The airways are divided into two functional zones with the first 16 generations of branches comprising the conducting zone and functioning to conduct air to the deeper parts of the lungs.
* The last seven generations participate in gas exchange and comprise the respiratory zone.

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6
Q

⭐️

What muscles are for normal (eupneic) inspiration and expiration?

A
  • Inspiration: External intercostals (elevates ribs 2-12 widen thoracic cavity) and diaphragm (descends and increases depth of thoracic cavity)
  • Expiration: no muslces, just the recoil back
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7
Q

⭐️

As we move down the resp. trees in the lungs, what happens to the diameter, cilia, goblet cells, cartilage and smooth muscle?

A

Going down the lung braches:
* Decreases in: Diameter (smallest being alveolar sac), cilia (for propeling dust/debris out), cartilage, goblet cells
* Increases in: Smooth muscle (the most being in bronchioles and terminal brochioles)
* Smooth muscle replaces cartilage

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8
Q

⭐️

What muscles are for FORCED inspiration and expiration?

A
  • Inspiration (SIPS): SCM (elevates sternum), Scalenes (fix or elevate ribs 1-2), pectoralis minor (elevates ribs 3-5), Internal internals, intercartiagionous part (aid in elevating ribs)
  • Expiration: Intercostals, interosseous part (depress ribs 1-11 narrow thoracic cavity), Rectus abdominis (depresses lower ribs, pushes diaphragm upward by compressing abdominal organs), external abdominal oblique (same effects as rectus abdominis)
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9
Q

What are the sequence of events for inspiration?

A

You need to increase volume to decrease pressure (think about molecules in a small and large container)

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10
Q

What are the sequence of events for expiration?

A

Increase pressure by decreasing volume

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11
Q

⭐️

What is the size of bronchioles?

A

0.5-1mm

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12
Q

What prevents the lung and airways to not collapse?

A

Negative intrapleual pressure

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13
Q

Pressures:
* Atmospheric:
* Intrapleual pressure:
* Intra-alveolar pressure:
* Transpulmonary pressure:

A
  • Atmospheric: 760 mmHg (or 0mmHg)
  • Intrapleual pressure: 756 mmHg (or -4 mmHg)
  • Intra-alveolar pressure: 760 mmHg (or 0 mmHg)
  • Transpulmonary pressure: Palv-Pip = 4 mmHg
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14
Q

What causes the pleural sac negative pressure?

A

Lungs want to recoil in and chest wall wants to recoil out therefore causing the negative intrapleural pressure (ALLOWS the chest wall and lungs to move together)

If we do not have this, then the lungs will win and cause the lungs to collapse.

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15
Q

Explain the changes in alveolar pressure move air in and out of the lungs

A
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16
Q

ELASTIC PROPERTIES OF LUNG AND CHEST WALL

  • What does elastic recoil of the lungs directly affect?
  • Lung compliance measures what? What is the lung complicance equation?
  • What does increase compliance cause?
  • What does decrease elasticity cause?
A
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17
Q

How does obstructive and restrictive diseases alter lung compliance?

A
  • Blue line: obstructive
  • Doted black: restrictive
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18
Q
  • What directly affects inflation and deflation of the lungs?
  • What is distensibility?
  • What is elatic recoil?
A
  • Elastic recoil of lungs
  • Distensibility - ease with which the lungs can be stretched or inflated.
  • Elastic recoil - ability of a stretched or inflated lung to return to its resting volume (FRC).
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19
Q

⭐️

  • Surfactant lowers what? What does that do?
  • Surfactant is more concentrated where? and why?
A
  • Surfactant lowers surface tension and stabilizes alveoli at low lung volumes.
  • Surfactant is more cont in smaller alveoli than larger ones because they tend to collapse dt to higher pressures (atelectasis).
  • Surfactant lowers surface tension proportionately more in the smaller alveolus. As a result, pressures in the two alveoli are equal, and alveoli of different diameters can coexist
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20
Q
  • Increased surfactant =
  • Increased compliance =
A
  • Increased surfactant = compliance
  • Increased compliance = increased volume at a given pressure
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21
Q
A
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22
Q

What ventation values cannot be determined directly by spirometry?

A

Residual lung volume, FRC, and TLC (since you need RV)

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23
Q
A
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24
Q
A
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25
Q

What are the partial pressures of Po2 and Pco2 when entering alveolar capillaries, alveoli, and leaving alveolar capillaries?

A
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26
Q

What is the approximate percentage for inhaled and exhaled (N2, CO2, O2, H2O) ?

A

Nitrogen stays the same because it comes from digestion and not from vent.
O2 decreases in exhalation
CO2: increase in exhalation

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27
Q

Fill in

A
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28
Q

What is the chloride shift?

A
  • The reaction mostly occur inside RBCs because CA is abundant there
  • In RBCs, CO2 reacts with water of the cytoplasm with the presence of CA to form carbonic acid
  • The carbonic acid is a weak acid, which undergoes partial dissociation to yield H+ and bicarb
  • The bicarb ion then diffuses outside of the RBC in the plasma and combines with Na ions to form sodium bicarbonate
  • The loss of bicarb ions from RBC causes a positive charge inside RBC which is balance by diffusion of Cl ions from the plasma into the RBC

IN SYSTEMIC GAS EXCHANGE

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29
Q

What is the reserve Cl shift

A

happens in the pulmonary capillaries
* Oxygen entering the blood (RBC) leads to release of protons
* Increasing protons level causes HCO3- to enter the RBC and in return Cl- is removed from the RBC to maintain electrical neutrality
* HCO3- can combine with the H+ ions from O2 coming in to form Carbonic acid
* Carbonic acid is then broken into CO2 and H2O via Carbonic anhydrase
* CO2 then diffuses out of the capillary and into alv.

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30
Q

⭐️

What is the minute ventilation equation?

A
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31
Q

⭐️

What is the alveolar ventilation per minute equation?

A
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32
Q

How is alveolar ventilation determined?

A

By measuring the patient’s volume of expired CO2

33
Q

If alv. ventilation is halved, the PCO2 is what? This is called what?

A
  • If alv. vent is halved, arterial PCO2 will double (assuming a steady-state and constant carbon dioxide production)
  • This decrease in alv vent below normal is called hypoventilation
34
Q

What happens with PaCO2 when you increase ventilation? What is this called?

A
  • If alv. vent is increased, arterial PCO2 will fall (assuming a steady-state and constant carbon dioxide production)
  • This increase in alv vent below normal is called hyperventilation
35
Q
  • What allows for distribution of pressure in alveoli?
  • What cell reduce surface tension?
  • What cell is the squamous epithelial cell?
A
  • Alveolar pores
  • Type 2
  • Type 1
36
Q

What is oxyhemoglobin and deoxyhemoglobin?

A
  • Oxyhemoglobin:O2 bound to hemoglobin
  • Deoxyhemoglobin: hemoglobin with no O2
37
Q
  • Oxyhemoglobin–dissociation curve illustrates what?
  • Each hemoglobin molecule can do what?
A
  • Oxyhemoglobin–dissociation curve illustrates the effect that plasma PO2 has on the loading and unloading of oxygen from hemoglobin
  • Each hemoglobin molecule can bind four O2 molecules. There is cooperative binding of O2 so that each additional O2 binds more easily, producing the sigmoidal shape of the O2 dissociation curve.

The oxyhemoglobin equilibrium curve is nonlinear. The oxygen saturation (left vertical axis) or oxygen content (right vertical axis) is plotted against the partial pressure of oxygen (horizontal axis) to generate an oxyhemoglobin equilibrium curve. The curve is S shaped and can be divided into a plateau region and a steep region. The dashed line indicates the amount of oxygen dissolved in the plasma. a, arterial; v, venous; Hb, hemoglobin; SO2, oxygen saturation; P50, partial pressure of O2 required to saturate 50% of the hemoglobin with oxygen.

38
Q
  • A left shift in the oxyhemoglobin dissociation curve causes what?
  • A right shift in the oxyhemoglobin dissociation curve causes what?
A
  • A left shift in the oxyhemoglobin dissociation curve causes hemoglobin to become saturated at lower Po2. Loading O2 into blood at the lung is easier, but it is more difficult to unload O2 at the tissues.
  • A right shift in the oxyhemoglobin dissociation curve causes hemoglobin to become saturated at higher Po2. O2 loading at the lungs is reduced and the proportion of hemoglobin saturated with O2 (Sao2) may be reduced, but O2 is unloaded more readily at the tissues.
39
Q

What are several factors that cause a right shift in the O2 dissociation curve?

A
  • Increased temperature (e.g., exercise). Higher temperature increases O2 unloading in working muscle.
  • Increased CO2. High levels of CO2 in metabolically active tissues indicate high O2 demand, and more O2 unloading is needed.
  • Increased [H+]. Buffering of H+ by hemoglobin reduces its O2 affinity (known as the Bohr effect). For example, anaerobic metabolism produces lactic acid, indicating that more O2 delivery to tissue is needed.
  • Increased concentration of 2,3-bisphosphoglycerate (BPG) in erythrocytes. BPG is an end product of metabolism in erythrocytes. Hypoxemia increases BPG formation, causing more unloading of O2 from hemoglobin.
40
Q

What are the factors that would cause a left shift and right shift in O2 dis. curve?

A

.

41
Q

What happens when not all of the inspired air reaches the alveloi? Give examples

A

not all of the inspired air reaches the alveloi will become wasted air
* Some of the air in the tidal volume does not participate in gas exchange.The volume of air in the conducting airways does not participate in gas exchange and constitutes dead space volume (VD)
* Total wasted air in the lungs is computed from the physiologic dead space volume. Dead space volume occurs in the conducting airways and in alveoli with poor capillary circulation. For A, There is no blood flow to an alveolar region. For B, There is reduced blood flow. In both cases, a portion of alveolar air does not participate in gas exchange and constitutes alveolar dead space volume.

42
Q
  • What is the V/Q ratio?
  • If the breathing rate, tidal volume, and cardiac output are normal, the V/Q ratio is what?
  • This V/Q ratio results in an arterial Po2 of _ mm Hg and an arterial Pco2 of _ mm Hg.
A
  • V/Q ratio is the ratio of alveolar ventilation (V) to pulmonary blood flow (Q). Ventilation and perfusion (blood flow) matching is important to achieve the ideal exchange of O2 and CO2.
  • If the breathing rate, tidal volume, and cardiac output are normal, the V/Q ratio is approximately 0.8. This V/Q ratio results in an arterial Po2 of 100 mm Hg and an arterial Pco2 of 40 mm Hg.
43
Q

⭐️

V/Q ratios in different parts of the lung
* Blood flow, or perfusion, is highest and lowest where?
* Ventilation is lower and higher where?
* the V/Q ratio is higher and lower where?
* As a result of the regional differences in V/Q ratio, there are corresponding differences in the efficiency of what?
* At the apex (higher V/Q) and at the base (lower V/Q), what are the Po2 and Pco2 levels?

A
44
Q

How is ventilation adjusted to changes in perfusion?

A
45
Q

How is perfusion adjusted to changes in ventilation?

A
46
Q

What is wasted air and blood?

A
  • All of the inspired air does not participate in gas exchange, resulting in some “wasted air.”
  • All of the blood entering the lung is not fully oxygenated, leading to some “wasted blood.”
47
Q

What are example of wasted blood? What is the Po2 and Pco2 levels?

A

Airway obstruction causes a low regional ventilation/perfusion ratio. A partially blocked airway causes this region to be underventilated relative to blood flow. Note the alveolar gas composition. A low regional ratio causes venous admixture and will increase the physiologic shunt.

48
Q

What are examples of wasted air? what are the Po2 and pco2 level?

A

A partially obstructed pulmonary arteriole (right panel) will cause an abnormally high ratio in a lung region. Restricted blood flow causes this region to be overventilated relative to blood flow, which leads to an increase in physiologic dead space

49
Q

Right-to-left shunts
* always result in a decrease in what? why?
* defining characteristic of the hypoxemia caused by a right-to-left shunt is that it cannot be corrected by what?

A
  • always result in a decrease in arterial Po2 because of the admixture of venous blood with arterial blood.
  • defining characteristic of the hypoxemia caused by a right-to-left shunt is that it cannot be corrected by having the person breathe a high-O2 gas (e.g., 100% O2) because the shunted blood never goes to the lungs to be oxygenated.
50
Q

The respiratory centers are located within what?

A

pons and medulla

51
Q

The basic rhythm of breathing is controlled by what?
The medullary center has what?

A
  • The basic rhythm of breathing is controlled by groups of neurons in the medulla.
  • The medullary center has a dorsal respiratory group (DRG) of neurons in the nucleus of the tractus solitarius and a ventral respiratory group (VRG) in the nucleus ambiguus and nucleus retroambiguus.

somatic motor neurons= diaphragm with phrenic nerve

52
Q

The DRG is thought to be what?
The VRG is what?

A

The DRG is thought to be the main integrator of sensory information and to have primarily inspiratory neurons.

The VRG is larger and has primarily motor neurons that mediate both inspiration and active expiration.

53
Q
A
54
Q

Central and peripheral chemoreceptors respond to changes in what?

A

in arterial blood gases and hydrogen ion concentration
* Look at picture for which does what

55
Q

What are J receptors? What are they activated by?

A
  • J receptors = “juxtaposed” to the pulmonary capillaries.
  • Activated by physical engorgement of the pulmonary capillaries
56
Q

P2 Chronic Obstructive Pulmonary Disease (COPD) = Chronic Bronchitis and Emphysema
* causes?
* Features:
* Chronic bronchitis defined by what?
* Emphsema defined by what?
* Can occur how?
* COPD: airways become what?
* What are the PFTs?
* Increased what and why?

A

Causes: Smoking, air pollutants, genetics

COPD Features
* Chronic bronchitis defined by clinical features (e.g. productive cough)
* Emphysema defined by structural changes (e.g. enlargement of the air spaces).
* Can occur separately, but often co-exist – major risk factor smoking
* COPD: airways become obstructed, lungs don’t empty properly, leaves air trapped
* Low FVC, Very Low FEV1
* Thus, Low FEV1:FCV ratio i.e. <70%
* Also, air trapping = increased TLC

57
Q

Pathophysiology - Chronic Bronchitis
* What is the cough situation?
* Inflammation of what?
* Smoke=
* Stimulates what? What does that cause?
* What does smoking cause?
* Cough becomes a mechanism to do what?
* _ bloaters?
* Vasoconstriction =

A
  • chronic productive cough (w/ mucus) 3 months, 2 years or more
  • inflammation of the bronchial tubes
  • smoke = irritants and chemicals
  • stimulate hypertrophy & hyperplasia of mucinous glands & goblet cells = increased mucus production = obstructs bronchioles = air trapping
  • Smoking = Cilia shorten = inhibits mucus escalator
  • Cough becomes mechanism to clear mucus
  • Hypoxemia, Hypercapnia = cyanosis = “Blue Bloaters”
  • Vasoconstriction = Cor pulmonale
58
Q

Pathophysiology - Emphysema
* Smoke triggers Inflammatory reactions which does what?
* What breaks down collagen and elastin?
* What happens when there is no elastin? Compliance?
* What happens to the lungs?
* Furthermore, loss of elastin also leads to a breakdown of what?
* _ puffers
* Chest/
* Cor pulmonale?

A
  • Smoke triggers Inflammatory reactions attract various immune cells which release inflammatory chemicals & proteases
  • Proteases break down collagen and elastin
  • No elastin = airway walls weak = collapse during exhalation = air-trapping
  • Also, loss of elastin makes lungs more compliant
  • easily expand, hold onto air instead of expelling
  • lungs start to look like large thin plastic bags.
  • Furthermore, loss of elastin also leads to a breakdown of alveolar walls = neighboring alveoli coalesce into larger and larger air spaces= decreased surface area = decreased gas exchange
  • Pursed lips exhale (to increase pressure in airways) = “Pink Puffers”
  • Barrel chest
  • Cor pulmonale
59
Q

What are the three types of emphysema:
?

A
  1. Centriacinar
  2. Panacinar
  3. Paraseptal
60
Q

Pneumonia
* Epithelial cells are covered with what? Blanketed by a layer of what?
* Most bacteria are 0.5–2 μm in size and can reach where in resp tract? What happens when they get there?
* Macrophages recognize the pathogen via what?
* This signaling cascade recruits what?
* Another important role of the immune response is the activation of what?

A
61
Q

Pneumonia
* Infection in lung tissue caused by microbes results in what?
* The inflammation brings water where?
* Microbes typically do what?
* The tissue quickly fills with what?

A
  • Infection in lung tissue caused by microbes results in inflammation response
  • The inflammation brings water into the lung tissue, and that extra water can make it harder to breathe.
  • Microbes typically multiply and cross over from the airways into the lung tissue, creating an inflammatory response.
  • The tissue quickly fills with white blood cells as well as proteins, fluid, and even red blood cells if a nearby capillary gets damaged in the process.
62
Q

⭐️

Pleural effusion
* What is it?
* Normally, lymphatic vessels in pleura allow what?
* Pleural effusion = excess fluid where? What are two mechanisms?

A
  • A disease process causes fluid to start to collect in the pleural space
  • Normally, lymphatic vessels in pleura allow drainage of plasma that leaks into intrapleural space = constant interstitial fluid volume

Pleural effusion = excess fluid in the pleural space
* too much pleural fluid is produced (transudative or exudative effusion)
* or lymphatics can’t effectively drain away the fluid (lymphatic effusion).

63
Q

Transudative Pleural Effusion:
* Thoracentesis produces what?
* When does this happen?
* What are the three causes?
*

A
  • Thoracentesis produces clear fluid
  • when too much fluid starts to leave the capillaries either because of increased hydrostatic pressure or decreased oncotic pressure in the blood vessels.

Causes
* Common cause = heart failure.
* Blood backs up into the pulmonary vessels and causes the blood pressure in those vessels to rise.
* The high pressure forces fluid out of the capillaries and into the pleural space.

64
Q

What is the pathophysio of transudative pleural effusion?

A
  • Oncotic pressure results from the inability of solutes like large proteins - albumin for example - to move across through the capillary.
  • Fluid therefore flows out of capillaries and leaks into the pleural space when there is decreased oncotic pressure in the blood vessels.
  • Two causes of low oncotic pressure are cirrhosis, where the liver makes fewer proteins and nephrotic syndrome, where proteins are lost through the urine.
65
Q

Exudative Pleural Effusion
* What are the causes (3)
* What is the pathophyio?

A

Causes
* vary - trauma, malignancy, inflammatory condition e.g. lupus, infection e.g. pneumonia.
* If infection can spread into the pleural space forming enormous abscess - infected pleural space can develop fibrinous walls and have loculations.
* Thoracentesis produces cloudy fluid (immune cells)

Pathophysiology
* inflammation of the pulmonary capillaries makes them much more leaky.
* larger spaces between endothelial cells allows fluid, immune cells and large proteins e.g. lactate dehydrogenase (LDH) to leak out of the capillaries.
* Water follows solutes into pleural space

66
Q

Lymphatic Pleural Effusion
* What does Thoracentesis produces? What is it called?
* What are the causes?
* What is the pathophys?

A

Thoracentesis produces milky fluid (fats)
called a chylothorax.

Causes
* damage during surgery, tumors

Pathophysiology
* Thoracic duct is disrupted and lymphatic fluid accumulates in the pleural space.

67
Q

Pulmonary Hypertension (and Cor Pulmonale)
* What is the normal mean pul arterial pressure?
* What is htn?
* How does left heart disease cause this?

A
  • Normal mean pulmonary arterial pressure = 15 mmHg.
  • Hypertension > 25 mmHg

Causes/Types of Pulmonary
Left heart disease:
* pulmonary blood vessels are normal and undamaged
* heart failure or valvular dysfunction.
* backup of blood in the pulmonary veins and capillary beds
* which can increase the pressure in the pulmonary artery.

68
Q

Causes/Types of Pulmonary Hypertension:
* how does chronic lung disease cause it?
* How does Chronic thromboembolic pulmonary hypertension cause it?

A

Chronic lung disease:
causes hypoxic vasoconstriction
* to compensate, the pulmonary arterioles in that area, start to constrict
* this shuttles blood away from damaged areas and towards healthy lung tissue.
* However, if problem widespread (e.g. emphysema) can lead to widespread vasoconstriction of pulmonary arterioles
* = increased pulmonary vascular resistance = increased pulmonary artery afterload
* = right side of the heart has to generate increased pressure = pulmonary hypertension.

Chronic thromboembolic pulmonary hypertension:
* recurrent blood clots in their pulmonary vessels (via some underlying clotting disorder)
* clots block pulmonary vessels = increased resistance to blood flow
* also cause vessel endothelial cells to release histamine and serotonin = constricts the pulmonary arterioles.
* thus, blockage + narrowing blood vessels = pulmonary hypertension

69
Q

Pulmonary Arterial Hypertension
* What is it?
* What are the causes?
* What is the pathophy?

A
70
Q

Pulmonary Arterial Hypertension
* What are the consquences?

A
71
Q
A
72
Q

Interstitial lung disease (Pulmonary fibrosis)
* What is it?
* What are the causes?
* What is the patho?
* What does it result in?

A
73
Q

Asthma
* Asthma =
* Chronic what?
* What are the causes?
* What are the types?

A
  • Asthma = “panting”.
  • Chronic inflammation and narrowing of airways

Causes
* Specific causes unknown – air pollution, smoking, allergens (dust, mold, dander), medications (aspirin, beta blockers).
* Predicted combination of genetic and environmental factors
* Hygiene hypothesis: reduced early immune-system exposure to bacteria and viruses increases risk of later developing asthma, possibly by altering overall proportion of immune cell subtypes.

Types
* childhood asthma (<12 y.o.) stronger genetic influence
* adult onset asthma is more likely environmental factors.
* status epilepticus (severe asthma exacerbation).
* cough variant - presents solely with cough (non-productive)
* exercise-induced

74
Q

what is extrinic and intrinsic asthma?

A
75
Q

What cells are involved in asthma?

A

Th2 cells, are an immune cell subtype, which are known to be involved in asthma, as well as atopic dermatitis, and allergic rhinitis, making up what’s called the atopic triad

76
Q

Pathophysiology (Timeline) of asthma:
* What happens within minutes and then a few hours?

A

Minutes
* smooth muscle around the bronchioles start to spasms and increased mucus secretion.
* Thus asthma type of obstructive pulmonary disease.
* also an increase in vascular permeability and recruitment of additional immune cells from the blood.

Few hours
* immune cells, particularly eosinophils, release chemical mediators that physically damage the endothelium of the lungs.
* Initially inflammatory changes reversible, but over the years irreversible changes start to take place—edema, scarring, and fibrosis build up, leading to thickening of the epithelial basement membrane, which permanently reduces the airway diameter.
*

77
Q

Acute Respiratory Failure (ARS)
* Also called what?
* Form of what?
* Disease of what?
* What type of inflammation?
* What are the causes?
* What is the pathophy?

A
78
Q

What is the acute and chronic phase of ARS?

A

Clinical Medicine 2 (16 decks)

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