Resp Flashcards
What 5 resp structures are lined by stratified squamous epithelium instead of pseudostratified ciliated columnar cells?
True vocal cords, oropharynx, laryngopharynx, anterior epiglottis, upper half of posterior epiglottis
Tracheal pO2 = 150 mm Hg
Alveolar pO2 = 140 mm Hg
Alveolar pCO2 = 5 mm Hg
What’s the problem?
Poor alveolar perfusion (perfusion-limited gas exchanged)
Know this because tracheal pO2 is normal, alveolar pO2 is increased (normal should be 104 mm Hg), and alveolar pCO2 is decreased (normal should be 40 mm Hg).
If the problem had been related to diffusion-limited gas exchange (such as emphysema or fibrosis), you would see relatively normal alveolar pCO2 compared to pO2 because CO2’s diffusion capacity is much higher than O2 (CO2 is not a diffusion-limited gas)
If the problem had been poor alveolar ventilation, you would see alveolar gas composition close to venous blood (pO2 = 40 mm Hg and pCO2 = 45 mm Hg) because your problem isn’t that you don’t have enough time or perfusion to equilibrate, you just don’t have gas in to equilibrate with
Pt w/ COPD. Resp rate decreases after supplementing w/ cannular oxygen. This is because what stimulation is decreased?
Carotid bodies (main stimulation is hypoxemia, unlike central chemoreceptors in medulla whose main stimulation is increased CO2 -> main resp drive in HEALTHY ppl)
Pt w/ dyspnea, bibasillar crackles, and S3 w/ a recent hx of MI. What property of the lungs is responsible for dyspnea?
Pt is having classic sx of left HF -> fluid backs up -> fluid in pulm interstitium
So the property would be decreased lung compliance
How does panic attack cause dizziness, weakness, and blurred vision?
Hyperventilation leads to reduced PaCO2 in brain -> reduced blood flow to brain (think of central chemoreceptors detecting mainly PaCO2 level)
Has nothing to do w/ O2
Sign of cor pulmonale?
It’s right HF due to pulmonary HTN
so will see RV wall thickening w/ eventual dilation of RV chamber as pumping begins to fail
Give 3 changes in vessels when you have pulm HTN
Vasoconstriction (due to pulm venous congestion -> endothelial damage and leakage -> decreased NO synthesis and increased endothelin synthesis -> increased vascular tone)
Intimal thickening
Medial hypertrophy
What happens to the pulmonary artery flow in the setting of left HF?
Normal or decreased
NOT increased, b/c the problem would be backed up to LA -> pulm veins -> pulm congestion -> so the worse the condition, the lower the flow
Pulm arterial PRESSURE increases in left HF tho
Give formula for calculating PAO2 and the normal values for A-a gradient
PAO2 = 150 - PaCO2/0.8
Normal A-a gradient is PAO2 - PaO2 = 10-15 mmHg
(if increased, consider shunting, V/Q mismatch, fibrosis, R-to-L shunt, cyanotic congenital heart defects)
What 2 circumstances would you have increased tissue CO2 production?
Exercise
Severe infection
What 2 circumstances would you have increased mixed venous O2 content?
Conditions obstructing O2 unloading -> abnormal Hb binding O2 w/ greater affinity
Conditions where oxidative metabolism is affected -> cyanide toxicity
How does silicosis increase susceptibility to TB?
It impairs macrophage killing by disrupting phagolysosomes
Give lung primary main of defense against diff sizes of particles
Large (10-15 uM): trapped in upper resp tract
Medium (2.5-10 uM): mucociliary clearance (trapped in trachea and up to proximal portion of resp bronchioles)
Small (< 2.5 uM): macrophages (distal to terminal bronchioles)
AA w/ hilar adenopathy + pulm infiltrates + noncaseating granuloma + elevated ACE + hypercalcemia. Dx?
Sarcoidosis (granuloma produce ACE and active vit D)
Will see constitutional sx! Will also see liver granulomas (like portal triads) as well. Don’t let that distract you.
Paroxysmal episodes of breathlessness + wheezing w/ no hx of aspirin, pulm infection, inhaled irritants, stress, exercise. What should you suspect?
Extrinsic allergic asthma
Granule-containing cells and crystalloid masses in sputum. What are you thinking?
Eosinophils and Carcot-Leyden crystals (containing eosinophil membrane protein) -> think IL-5 role
Extrinsic allergic asthma
Severe SOB + prolong expiration + prominent wheezing + pulsus paradoxus. Dx? Tx?
Severe asthmatic episode
Give B-blocker acutely. Corticosteroids (which works by inhibiting eosinophil degranulation) are useful for asthma but take too long to take effects, and mast cell stabilizer is only useful for prophylaxis
3 risk factors of OSA?
Obesity
Tonsillar hypertrophy
Hypothyroidism
CD4+/CD8+ ratio in sarcoidosis and hypersensitivity pneumonitis? What are their similarity?
CD4+/CD8+ ratio > 2:1 (so CD4+ predominance) in sarcoidosis
CD8+ predominance in hypersensitivity pneumonitis
Both sarcoidosis and hypersensitivity pneumonitis have noncaseating granulomas
Where does aspirated content go if it happens when you’re lying down? Standing up?
POS. segment of RIGHT UPPER lobe or SUP. segment of LOWER lobe
NOT middle lobe, because middle lobe is actually situated anteriorly
If standing up, it’ll go to basilar segment of lower lobe
What lecithin-sphingomyelin ratio means lung has matured? What hormone has the greatest effect on lung development?
> 1.9
Cortisol
2 mediators in atopic asthma that can actually be effectively targeted by pharmacotherapeutic agents
- Leukotrienes: LTD4, LTE4, LTC4 -> montelukast and zafirlukast
- ACh -> ipratropium
Finding expected from pt who died from sudden death after being on appetite suppressant
“-fenfluramine” and phentermine for more than 3 months -> secondary pulm HTN -> cor pulmonale and RV hypertrophy
What is sudden death from PE due to?
Electromechanical dissociation (heart is pumping but blood can’t go any further)