Intro to Pulm B&B

Question 1

which type of pneumocytes regenerate following injury?

Answer 1

Type 2: produce surfactant, key for regeneration after injury

[Type 1: most common, thin for gas exchange]

Question 2

what is surfactant made of?

Answer 2

mix of lecithins, esp. dipalmitoylphosphatidylcholine

Question 3

what changes in fetal alveoli for them to be considered mature?

Answer 3

lungs are considered mature once enough surfactant is present, ~35 weeks

when there is more lecithin than sphingomyelin in the surfactant

Question 4

what is the use of betamethasone in improving preterm lung function?

Answer 4

betamethasone: steroid that stimulates surfactant production in lungs

(lungs considered mature once enough surfactant is present for alveoli to not collapse)

Question 5

neonatal respiratory distress syndrome, aka ______, often leads to which congenital heart defect?

Answer 5

neonatal respiratory distress syndrome = hyaline membrane disease, because there is not enough surfactant (so alveoli look clear)

severe hypoxemia due to poor ventilation (surfactant keeps alveoli from collapsing)

complications: patent ductus arteriosus, bronchopulmonary dysplasia, retinopathy (via ROS)

risk factors: maternal diabetes, C-section, prematurity

Question 6

into which lung is aspiration of a foreign body most likely?

Answer 6

right lung because right bronchus is wider and more vertical than left

if upright - right inferior lobe
if supine - right inferior or right upper

Question 7

at which vertebral level are the following openings into the diaphragm, and what passes through them?
a. caval opening
b. esophageal hiatus
c. aortic hiatus

Answer 7

a. caval opening (T8): IVC
b. esophageal hiatus (T10): esophagus, vagus nerve
c. aortic hiatus (T12): aorta, thoracic duct, azygous vein

Question 8

which nerves innervate the diaphragm?

Answer 8

C3, C4, and C5 keep the diaphragm alive!

(C5 = phrenic nerve)

also innervate shoulder, which is why diaphragm irritation (gallbladder disease) can cause referred shoulder pain

also, if a nerve is cut, may seem diaphragm elevation (rather than depression) with inspiration (“sniff test”)

Question 9

which accessory muscle raise the ribs and sternum, respectively, in exercise breathing?

Answer 9

scalenes - raise ribs
sternocleidomastoids - raise sternum

Question 10

what is summed to give total lung capacity vs inspiratory capacity vs vital capacity vs functional residual capacity?

Answer 10

total lung capacity = RV + ERV + IRV + TV

inspiratory capacity = TV + IRV

vital capacity = TV + IRV + ERV

functional residual capacity = RV + ERV

Question 11

how is total lung capacity calculated

Answer 11

sum of all volumes:

RV (residual volume), air that can’t be blown out no matter how hard you try

ERV (expiratory reserve volume), extra air pushed out with force beyond TV

IRV (inspiratory reserve volume), extra air that can be drawn in with force beyond TV

TV (tidal volume), air that moves in/out with each quiet breath

Question 12

how is vital capacity calculated?

Answer 12

vital capacity = most air you can exhale at max

vital capacity = TV (tidal volume) + IRV (inspiratory reserve volume) + ERV (expiratory reserve volume)

Question 13

how is functional residual capacity calculated?

Answer 13

functional residual capacity = residual volume after quiet expiration = RV + ERV

basically, the volume of air in the lungs when they are relaxed

chest wall pulling out = lungs pulling in
[remember chest wall has tendency to expand/spring outward, lungs have tendency to collapse/recoil]

Question 14

anatomic vs physiologic dead space

Answer 14

anatomic dead space: volume of conducting portions of respiratory tract (nose, trachea)

physiologic dead space: anatomic dead space + volume of alveoli that don’t exchange gas well due to insufficient perfusion (mostly in the apex)
*may be increased during disease

Question 15

when is pressure inside the respiratory system zero?

Answer 15

functional residual capacity: volume where lungs rest after quiet exhalation

chest wall pulling out = lungs pulling in

[remember chest wall has tendency to expand/spring outward, lungs have tendency to collapse/recoil]

Question 16

how does intrapleural vs alveolar pressure change during inhalation and exhalation? (during quiet breathing)

Answer 16

intrapleural pressure remains negative at all times (always more negative than alveolar)

alveolar pressure becomes negative during inhalation, then positive during exhalation

Question 17

how does pleural pressure change during forced exhalation?

Answer 17

normally (tidal breathing), pleural pressure is negative at all times

in forced expiration, pleural pressure becomes positive to put pressure on the alveoli, which causes the air to be pushed out

Question 18

what occurs during the equal pressure point in the lungs?

Answer 18

equal pressure point: pleural pressure = airway pressure, and beyond this point airways collapse (pleural should be more negative than alveoli pressure)

in healthy lungs, this occurs proximally in the cartilaginous airways, which prevents collapse

in disease (bronchitis, emphysema), EPP can move towards alveoli and cause collapse/obstruction

Question 19

where is resistance to air flow highest in the respiratory system?

Answer 19

medium bronchi, due to turbulent flow

resistance lowers in terminal bronchioles, slowing laminar flow

Question 20

how is 2,3 BPG generated?

Answer 20

created from diverted 1,3 BPG, which is a substrate of glycolysis

sacrifices ATP from glycolysis in RBC (which have no mitochondria, so can only use glycolysis for energy), but worth it for more O2 delivery

Question 21

how do the following affect the O2 saturation curve?
a. 2,3 BPG
b. H+
c. low CO2

Answer 21

left shift = higher O2 affinity
right shift = lower O2 affinity

a. 2,3 BPG —> R shift
b. H+ —> R shift
c. low CO2 —> L shift

Question 22

how does carbon monoxide affect the oxygen saturation curve?

Answer 22

CO binds iron in heme with MUCH higher affinity than O2 —> blocked O2 binding sites = less O2 absorbed

shifts O2 sat curve to LEFT (higher affinity) and pulls the max % saturation DOWN (less carrying capacity because of less binding sites)

Question 23

what state is iron in methemoglobin and what is the treatment for methemoglobinemia?

Answer 23

methemoglobin: oxidized iron (Fe3+, instead of Fe2+)

Fe3+ cannot bind oxygen

treatment: methylene blue

Question 24

what is the effect of cyanide poisoning on the respiratory system?

Answer 24

blocks electron transport chain in mitochondria

aerobic metabolism stops —> functional hypoxia, especially for brain and heart

anaerobic metabolism occurs —> lactic acidosis

PaO2, CaO2, and SaO2 will all be normal, but oxygen in mixed venous blood will be INCREASED because cyanide is preventing oxygen USE

Question 25

how can the following be used as treatment for cyanide poisoning? a. nitrates b. hydroxocobalamin c. thiosulfate

Answer 25

a. nitrates: generate methemoglobin (Fe3+), which cyanide binds, pulling it away from mitochondria (where it disrupts ETC) b. hydroxocobalamin: precursor of Vit. B12, binds CN and forms cyanocobalamin, which is readily excreted c. thiosulfate: transforms CN to thiocyanate, which is readily excreted

Question 26

how does systemic vs pulmonary circulation respond to low oxygen levels?

Answer 26

system - vasodilation pulmonary - *hypoxic vasoconstriction*, in order to shunt blood away from poorly ventilated areas (important in fetal circulation)

Question 27

what 3 parameters influence the rate of diffusion from air to blood?

Answer 27

1. pressure difference between air and blood 2. area of alveoli for diffusion 3. thickness of alveolar tissue

Question 28

how is O2 uptake limited in healthy vs disease-state patients? (what is the limiting factor)

Answer 28

healthy: O2 uptake is *perfusion* limited - more blood flow in capillaries alongside alveoli = more O2 uptake disease (fibrosis, emphysema): O2 uptake is *diffusion* limited - thickened alveolar walls limit how much O2 can be taken up

Question 29

how does primary pulmonary hypertension classically present?

Answer 29

rare disease, classically affects young women increased endothelin (vasoconstrictor), decreased NO associated with *BMPR2* gene mutation —> abnormal endothelial and vascular smooth muscle proliferation

Question 30

how are each of the following drugs used to lower pulmonary vascular resistance? a. Epoprostenol b. Bosentan c. Sildenafil

Answer 30

a. Epoprostenol: prostacyclin (IV) b. Bosentan: antagonize endothelin-1 receptors (PO) c. Sildenafil: inhibits PDE5 in smooth muscle of lungs (PO)

Question 31

what 3 parameters determine O2 content in the blood?

Answer 31

1. O2 binding capacity (determined by hemoglobin) 2. % saturation (of hemoglobin) 3. dissolved O2 O2 content = (O2 binding capacity)x(% Sat) + (dissolved O2)

Question 32

do the following primarily cause hypoxemia or hypoxia? a. heart failure b. anemia

Answer 32

a. heart failure: low CO —> hypoxia (low O2 delivery to tissues) b. anemia: low O2 carrying capacity —> hypoxemia (low O2 content in blood)

Question 33

how will the following causes of hypoxia affect O2 content and PaO2 (partial pressure of O2 in the blood, reflecting amount of dissolved O2), respectively? a. hypoxemia b. heart failure c. anemia d. carbon monoxide

Answer 33

a. hypoxemia (low O2 content): LOW O2 content, LOW PaO2 b. heart failure (low CO): NORMAL O2 content, NORMAL PaO2 c. anemia (low O2 carrying capacity): LOW O2 content, NORMAL PaO2 d. carbon monoxide (“functional anemia”): LOW O2 content, NORMAL PaO2

Question 34

what would be the cause of hypoxemia with a normal vs high A-a gradient? (Alveolar to arterial O2 partial pressure)

Answer 34

hypoxemia with normal A-a gradient: alveoli are working, but not enough O2 is being inhaled - *hypoventilation*, *high altitude* hypoxemia with high A-a gradient: alveoli are not working - most lung diseases (fibrosis, shunt, V/Q mismatch) [V/Q = ventilation/perfusion]

Question 35

what does a V/Q ratio < 1 indicate?

Answer 35

V/Q ratio = ventilation (V) to perfusion (Q) ratio low V/Q ratio indicates reduced ventilation relative to perfusion - blood going where not enough O2 is present in the lungs (such as physiologic dead space) if V/Q = 0 —> shunting (venous blood to arterial system without oxygenation)

Question 36

explain physiologic shunting as caused by atelectasis

Answer 36

atelectasis = collapsed airway (alveoli) physiologic shunting: blood perfuses alveoli that doesn’t work, so venous blood is shunted to arterial system without oxygenation —> hypoxemia

Question 37

what does a V/Q ratio > 1 indicate?

Answer 37

V/Q ratio = ventilation (V) to perfusion (Q) ratio high V/Q ratio indicates reduced perfusion relative to ventilation - gas is going in where there is insufficient blood flow extreme example: anatomic or physiologic dead space

Question 38

Inadequate gas exchange can be caused by shunting, V/Q mismatch, or dead space. Which of these will NOT respond to 100% O2 administration?

Answer 38

shunting (venous blood to arterial system without picking up O2) won’t correct with 100% O2 because functional alveoli are already extracting max O2 dead space and V/Q mismatch will be corrected with 100% O2, because increasing O2 content in alveoli will increase PaO2

Question 39

Inadequate gas exchange can be caused by shunting, V/Q mismatch, or dead space. Which of these will present with hypercapnia (high PaCO2)?

Answer 39

dead space: classic cause of hypercapnia, due to perfusion problem and ventilation is wasted shunting and V/Q mismatch rarely cause increase in PaCO2 (increased ventilation resolves hypercapnia)

Question 40

describe the Bohr effect

Answer 40

CO2 + H2O <> HCO3- + H+ via carbonic anhydrase H+ can bind to hemoglobin and convert Hgb to tense form which releases O2 this shifts O2 saturation curve to the right —> more O2 offload for a given PO2

Question 41

explain why RBC have a high Cl- content in venous blood

Answer 41

RBC convert CO2 to HCO3- via carbonic anhydrase HCO3- inside RBC leave cell to plasma, and Cl- enters to maintain electrical neutrality

Question 42

describe the Haldane effect and how it works in synergy with the Bohr effect

Answer 42

in low O2 environments, hemoglobin is more likely to bind CO2, such as in the tissues low O2 and high CO2 in tissues favors O2 unloading (Bohr effect) and CO2 loading (Haldane effect), while high O2 and low CO2 in lungs favors O2 loading (Bohr effect) and CO2 unloading (Haldane effect)

Question 43

explain why high altitude causes alkalosis

Answer 43

high altitude = lower pO2 hypoxia —> hyperventilation —> decrease pCO2 —> respiratory alkalosis (leftward shift) after 24-48h, renal excretion of HCO3- causes pH to fall back to normal 2,3 BPG production will also increase, shifting curve back to normal

Question 44

how does exercise affect O2 and CO2 levels in veins vs arteries?

Answer 44

exercise —> increase ventilation and blood flow more O2 consumed/ CO2 produced by muscle veins: O2 falls, CO2 rises arteries: NORMAL O2 and CO2

Question 45

what is the major stimulus for breathing, and where are the central vs peripheral chemoreceptors?

Answer 45

PaCO2 is major stimulus for breathing central chemoreceptors in medulla most important, some input from peripheral chemoreceptors in carotid and aortic bodies (these are more sensitive to O2) high PaCO2 —> increase respiration

Question 46

what do rales indicate on physical exam?

Answer 46

rales = crackles heard when small airways pop open after collapse classic causes: pulmonary edema, pneumonia, interstitial fibrosis

Question 47

what do wheezes indicate on physical exam?

Answer 47

wheezes = air flow through narrowed bronchi classically caused by asthma, can also be caused by heart failure (cardiac asthma), chronic bronchitis, or obstruction (tumor - *localized wheeze*)

Question 48

what is the classic cause of rhonchi being heard on physical exam?

Answer 48

rhonchi = course breath sounds due to secretions in large airways classically caused by COPD

Question 49

what does stridor indicate on physical exam?

Answer 49

stridor = wheeze that is almost entirely inspiratory, usually heard loudest over neck indicates partial obstruction of larynx or trachea classic causes: laryngotracheitis (croup), epiglottitis (Hib virus in children), retropharyngeal abscess, diphtheria (pseudomembrane)