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Resp Flashcards

1
Q

What 5 resp structures are lined by stratified squamous epithelium instead of pseudostratified ciliated columnar cells?

A

True vocal cords, oropharynx, laryngopharynx, anterior epiglottis, upper half of posterior epiglottis

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2
Q

Tracheal pO2 = 150 mm Hg
Alveolar pO2 = 140 mm Hg
Alveolar pCO2 = 5 mm Hg
What’s the problem?

A

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

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3
Q

Pt w/ COPD. Resp rate decreases after supplementing w/ cannular oxygen. This is because what stimulation is decreased?

A

Carotid bodies (main stimulation is hypoxemia, unlike central chemoreceptors in medulla whose main stimulation is increased CO2 -> main resp drive in HEALTHY ppl)

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4
Q

Pt w/ dyspnea, bibasillar crackles, and S3 w/ a recent hx of MI. What property of the lungs is responsible for dyspnea?

A

Pt is having classic sx of left HF -> fluid backs up -> fluid in pulm interstitium
So the property would be decreased lung compliance

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5
Q

How does panic attack cause dizziness, weakness, and blurred vision?

A

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

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6
Q

Sign of cor pulmonale?

A

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

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7
Q

Give 3 changes in vessels when you have pulm HTN

A

Vasoconstriction (due to pulm venous congestion -> endothelial damage and leakage -> decreased NO synthesis and increased endothelin synthesis -> increased vascular tone)
Intimal thickening
Medial hypertrophy

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8
Q

What happens to the pulmonary artery flow in the setting of left HF?

A

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

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9
Q

Give formula for calculating PAO2 and the normal values for A-a gradient

A

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)

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10
Q

What 2 circumstances would you have increased tissue CO2 production?

A

Exercise

Severe infection

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11
Q

What 2 circumstances would you have increased mixed venous O2 content?

A

Conditions obstructing O2 unloading -> abnormal Hb binding O2 w/ greater affinity
Conditions where oxidative metabolism is affected -> cyanide toxicity

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12
Q

How does silicosis increase susceptibility to TB?

A

It impairs macrophage killing by disrupting phagolysosomes

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13
Q

Give lung primary main of defense against diff sizes of particles

A

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)

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14
Q

AA w/ hilar adenopathy + pulm infiltrates + noncaseating granuloma + elevated ACE + hypercalcemia. Dx?

A

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.

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15
Q

Paroxysmal episodes of breathlessness + wheezing w/ no hx of aspirin, pulm infection, inhaled irritants, stress, exercise. What should you suspect?

A

Extrinsic allergic asthma

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16
Q

Granule-containing cells and crystalloid masses in sputum. What are you thinking?

A

Eosinophils and Carcot-Leyden crystals (containing eosinophil membrane protein) -> think IL-5 role
Extrinsic allergic asthma

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17
Q

Severe SOB + prolong expiration + prominent wheezing + pulsus paradoxus. Dx? Tx?

A

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

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18
Q

3 risk factors of OSA?

A

Obesity
Tonsillar hypertrophy
Hypothyroidism

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19
Q

CD4+/CD8+ ratio in sarcoidosis and hypersensitivity pneumonitis? What are their similarity?

A

CD4+/CD8+ ratio > 2:1 (so CD4+ predominance) in sarcoidosis
CD8+ predominance in hypersensitivity pneumonitis
Both sarcoidosis and hypersensitivity pneumonitis have noncaseating granulomas

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20
Q

Where does aspirated content go if it happens when you’re lying down? Standing up?

A

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

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21
Q

What lecithin-sphingomyelin ratio means lung has matured? What hormone has the greatest effect on lung development?

A

> 1.9

Cortisol

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22
Q

2 mediators in atopic asthma that can actually be effectively targeted by pharmacotherapeutic agents

A
  1. Leukotrienes: LTD4, LTE4, LTC4 -> montelukast and zafirlukast
  2. ACh -> ipratropium
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23
Q

Finding expected from pt who died from sudden death after being on appetite suppressant

A

“-fenfluramine” and phentermine for more than 3 months -> secondary pulm HTN -> cor pulmonale and RV hypertrophy

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24
Q

What is sudden death from PE due to?

A

Electromechanical dissociation (heart is pumping but blood can’t go any further)

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25
Q

What’s koilonychia and what is it a sign of?

A

Spoon-shaped nail

One of the signs of iron deficiency anemia

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26
Q

2 conditions where you see elevated FEP (free erythrocyte protoporphyrin)

A

Heme = Fe (defects) + Protoporphyrin (more float unbound) -> so find in
Iron deficiency anemia
Anemia of chronic disease (iron locked up by hepcidin)

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27
Q

2 ways that hepcidin sequesters iron in storage

A
  1. limits iron transfer from macrophages to erythroid precursors
  2. suppresses EPO production
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28
Q

PE signs and sx of airway obstruction?

A

Rhonchi, wheezing -> turbulent airflow 2ndary to obstruction

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29
Q

Most common cause of acute small airway obstruction in infants? What’s the tx?

A

RSV bronchiolitis

Ribavirin only if severe

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30
Q

Steps leading to adaptation when living in high altitude?

A

High alt means lower PO2 -> lower PaO2 -> carotid and aortic bodies tell your body to hyperventilate -> PaCO2 goes down (resp alkalosis) ->
48 hrs later: renal compensation (so now gets low HCO3-)
10-14 days: increased production of EPO -> so now PaO2 is almost restored (compensation only effective up to about 4000 m)

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31
Q

What kinds of things will be present in lung hamartoma?

A

Aka pulmonary chondroma -> most common benign lung tumor
Will see mature islands of hyaline cartilage, fat, smooth muscle and clefts lined by resp epithelium
Well-defined lesion w/ popcorn calcification

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32
Q

Where are club cells (Clara cells) and what is their fx?

A

Bronchioles (starts replacing goblet cells as the secretory cells from this level onward)
Regenerative source of ciliated cells in the bronchioles, helps detoxify inhaled substance by cytochrome P450 mechanism, prevents BRONCHIOLAR collapse (more upstream stuff)

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33
Q

A person w/ lung mass complains of shoulder pain, persistent hiccups, and dyspnea. What nerve roots are affected?

A

C3-5 -> think phrenic n. whenever you have pain at shoulder
Don’t think about pancoast tumor affecting brachial plexus (if that’s the case, C8-T2 would be affected and sx would be different)

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34
Q

What lung cancer is assc. w/ SVC syndrome?

A

Small cell lung cancer

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35
Q

Lung infiltrates w/ dry cough on a pt who was on cruise ship (or exposed to some kind of contaminated water like spas, hospitals, A/C hotels)?

A

Legionnaire’s disease -> so will see hyponatremia, high fever w/ relative bradycardia, transaminitis -> gram stain will show many neutrophils but no org (intracellular)

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36
Q

Pulmonary infiltrates + eosinophilia?

A

Loffler -> suspect helminthic infections

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37
Q

What are 2 upper resp sx of CF?

A

Bilateral sinusitis and nasal polyps

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38
Q

Why does blood arriving in the LA have lower O2 content than blood in the pulmonary capillaries (that just freshly picked up O2 from alveoli)?

A

Venous admixture -> b/c only a little of blood in bronchial arteries (2nd blood supply to lungs) goes back in bronchial veins; most actually gets carried back in bronchial arteries which are then mixed w/ pulmonary veins (the freshly oxygenated) before returning to LA -> so really bronchial blood gets to bypass the right side of the heart

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39
Q

What should you always assc. insufficient surfactant production w/?

A

Patchy atelectasis! (think of neonatal resp distress syndrome)
NOT pulm HTN (hypoxic pulm vasoconstriction created from this condition alone is not enough to cause pulm HTN)

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40
Q

URI followed 2 days later by brassy cough and difficulty breathing. What’s the org?

A

Parainfluenza (paramyxoviridae)

Brassy cough = croup

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41
Q

Major cause of spontaneous pneumothorax?

A

Rupture of apical blebs

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42
Q

Differences in distribution of 2 types of emphysema

A

Centriacinar (smoking): likes upper lobe

Panacinar (A1AT def): likes lower lobe

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43
Q

How is bronchial hyperreactivity (BHR) quantified?

A

Conc of bronchoconstrictive substance (ie methacholine) required to produce > 20% reduction in FEV1

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44
Q

Law of Laplace and its implication?

A

Distending pressure = T/2r
So smaller radius sphere -> more pressure -> so will collapse into larger radius sphere b/c air flows from high pressure to low pressure
Surfactant decreases surface tension as the sphere decreases in size -> so you get proportional reduction in T as you go down in r -> keep distending pressure operable

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45
Q

Differences bet. Lambert-Eaton myasthenic syndrome (LEMS) assc. w/ small cell lung cancer and ocular myasthenia gravis?

A

Both have ocular stuff

but LEMS pts have hypo/areflexia, autonomic sx, classic incremental response to repetitive stimulation

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46
Q

What does graph of work of breathing (y) vs. respiratory rate (x) tell you?

A

Looking at the RR at which the graph takes the most dip can tell you whether it’s restrictive or obstructive lung disease!
Normal dip is at RR = 15 breaths/min
In restrictive lung diseases (increased elastic resistance) -> the optimum RR is higher -> meaning pt will take rapid and shallow breaths b/c the work of breathing is minimum with high RR and low tidal volume -> think of stiff elastic band swinging back and forth quickly for increased elastic resistance
In obstructive lung disease (increased airflow resistance) -> optimum RR is lower -> meaning pt will take slow, deep breaths b/c the work of breathing is minimum w/ low RR and high tidal volume

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47
Q

What 2 cells play a role in centriacinar emphysema?

A

Neutrophils -> secretes elastase, which is inhibited by serum a1 antitrypsin
Macrophages -> secretes elastase, which is inhibited by TIMPs (tissue inhibitors of metalloproteinases) -> so unaffected by A1AT!

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48
Q

2 mechanisms behind pulm and CNS sx of fat embolism?

A
  1. Platelets coat fat emboli and release mediators

2. Systemic activation of LPL and intravascular release of oleic acid

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49
Q

What levels do you perform thoracentesis if you do it mid-clavicular, mid-axillary, and paravertebral?

A

All performed in top margin of rib (if do it on inf margin -> risks striking subcostal neurovascular bundle)
Mid-clavicular: above 7th rib (bet. 5th-7th)
Mid-axillary: above 9th rib (bet. 7th-9th)
Paravertebral: above 11th rib (bet. 9th-11th)
If do it lower than the levels indicated -> risk puncturing liver (assuming right side)
If do it higher -> risk puncturing lungs (levels given are borders of pleura)

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50
Q

What do you give in asthma resistant to steroids?

A

Omalizumab (anti-IgE Ab subQ injection) -> useful in moderate-severe allergic asthma

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51
Q

What’s tachyphylaxis and what do you do when this happens?

A

Tachyphylaxis = decrease in effect due to negative feedback
Example 1: using a1 antagonist nasal decongestants decreases NE release from nerve terminal due to neg feedback -> rebond rinorrhea (rhinitis medicamentosa) when using it past >3 days
Stop the drug when this happens
Example 2: nitroglycerine -> maintain drug-free interval of 8-10 hrs to prevent this

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52
Q

What will sputum gram stain for Mycoplasma pneumonia show?

A

Won’t detect orgs in sputum gram stain -> don’t have peptidoglycan cell wall! just phospholipid bilayer cell membrane

53
Q

Mechanism behind dyspnea and exercise limitation in COPD?

A

Dynamic hyperinflation -> increasing amount of air becomes trapped in lungs during rapid breathing, leading to further reduction in tidal volume

54
Q

What would PFTs look like in thromboembolic disease?

A

Normal b/c only perfusion is limited (no effect on ventilation)

55
Q

How do you tell whether unilateral opacities is from pleural effusion or lesion in mainstem bronchus?

A

Look at eso -> if deviates away from affected side -> it’s from pleural effusion
If deviates toward the affected side -> obstructive lesion in mainstem bronchus causing lung collapse
OPACITIES is not the same as fluffy appearing infiltrates, which are seen in pulm edema

56
Q

What’s the complication of oxygen therapy in NRDS?

A

Retinopathy of prematurity (retrolental fibroplasia)

57
Q

How does aspirin and NSAIDs precipitate asthma attacks?

A

By overproducing leukotriene in airways

Acetaminophen is a weak inhibitor of COX and doesn’t precipitate asthma

58
Q

Examples of conditions w/ paroxysmal cough relieved by sputum production?

A

Pink frothy sputum w/ pts w/ LV failure&severe pulm edema that’s followed by rupture of bronchial veins
Infectious or inflammatory condition assc. w/ bronchial exudation

59
Q

In what context does obstructive hyperinflation occur?

A

Lung expands from ball valve/subtotal obstruction of bronchiole/bronchus supplying it -> like mucus plug or bronchogenic carcinoma

60
Q

Why do you have to be careful w/ O2 supplementation in COPD pts?

A

Hypoxia drives their resp fx (whereas pCO2 does in normal individuals) so O2 supplementation can lead to resp depression and coma

61
Q

What happens to pulm vasculature in COPD?

A

Chronic hypoxia causes pulm vasoconstriction

62
Q

What’s the last feature to disappear as the epithelium changes along resp tube?

A

CILIA
The goblet cells, glands (serous or mucous), and cartilage disappear by the time you reach bronchioles
But you still have simple cuboidal up to the level of terminal bronchioles, and ciliated epithelium persists up to end of resp bronchioles

63
Q

Orgs most often responsible for secondary bacterial pneumonia after viral pneumonia?

A

Strep pneumonia > Staph aureus > H. influenzae

64
Q

Differences bet. PaO2, SaO2, and O2 content?

A

PaO2 = dissolved O2 (regardless of Hb conc) -> decreased in CO poisoning
SaO2 = % Hb saturation -> increased in venous blood in cyanide intoxication (fail to unload O2 in tissues)
O2 content = affected by above 2 AND Hb concentration -> so get decreased content w/ normal PaO2 and SaO2 in anemia

65
Q

Regulatory molec in gluconeogenesis?

A

Acetyl CoA!
B/c you first need to convert pyruvate (various substrates feed into here) to oxaloacetate, and pyruvate carboxylase which catalyzes this step is upregulated by acetyl CoA

66
Q

Which tx for allergic rhinitis causes flushed cheeks and dilated pupils?

A

Think anti-muscarinic -> so tx must have been H1 blockers (have anti-muscarinic activities)
a1-adrenergic agonists are also used for this tx and it would cause mydriasis in large does, but it will NOT cause flushing like H1 blockers do

67
Q

What kind of vaccine is a lyme disease vaccine?

A

Recombinant outer surface protein

68
Q

When is total PVR lowest?

A

At FRC
If you draw out a graph of PVR (y) vs. lung volume (x), you’ll see that
1. increasing in vol increases PVR for ALVEOLAR capillaries (line goes up as you go right) b/c of longitudinal stretching by expanding alvoli (breathing in)
2. decreasing in vol increases PVR for EXTRA-alveolar capillaries (line goes down as you go right) b/c of decreased radial traction from adjacent tissues & compression by positive intrathoracic pressure (breathing out)
3. so draw a line that’s a sum of these 2 lines, and the minimum point will be in the middle at FRC (left is RV, right is TLC)

69
Q

2 major risk factors for ARDS?

A

Acute necrotizing pancreatitis (so in alcoholics w/ elevated amylase and lipase)
Sepsis an shock

70
Q

Stab wound to 5th intercostal space at midclavicular line. What do you injure first?

A

Left lung (it’s in front of cardiac apex, which is formed by LEFT ventricle)

71
Q

What happens to ventilation and perfusion when healthy ppl exercise?

A

BOTH increase

72
Q

What happens to expiratory flow rate in restrictive lung diseases and obstructive lung diseases?

A

Restrictive lung diseases: increased elastic recoil pressure & INCREASED RADIAL TRACTION on conducting airways by fibrotic pulm interstitium -> high expiratory flow rates (despite low lung vol)
Obstructive lung diseases: increased wall thickness of small airways (think bronchial asthma) -> reduces radius of conducting airways -> lower expiratory flow rates

73
Q

What kind of HSR is present in sarcoidosis?

A

Type IV HSR

74
Q

What does A1AT globules in liver stain w/?

A

PAS -> reddish-pink stuff in periportal hepatocytes

75
Q

What happens to pulm circulation in acute airway obstruction?

A

hypoxic vasocontriction leads to pulm ARTERIAL HTN

76
Q

What are 2 clinical assc. of large cell carcinoma of the lungs?

A

Gynecomastic

Galactorrhea

77
Q

What are distinct features of silicosis?

A

Eggshell calcification of hilar nodes
Birefringent silica particles surrounded by fibrous tissue
Upper lung involvement

78
Q

Classic locations of extrapulm TB?

A

Basal meninges: TB meningitis
Lumbar spine: Pott disease
Psoas muscle: psoas abscess
Serous membranes (pericardium and pleura)

79
Q

Bronchial wall pathology in chronic asthmatics vs. chronic bronchitis (from smoking)

A

Chronic asthmatics: thickening of bronchial epithelium, BM, bronchial wall + edema + submucosal mucous gland enlargement, bronchial SMC hypertrophy + inflmmatory infiltrates (eosinophils and mast cells)
Chronic bronchitis: same thickened bronchial walls & mucous gland enlargement but infiltration is by neutrophils & get patchy squamous metaplasia instead

80
Q

Histology see columnar mucin-secreting cells that line alveolar spaces w/out invading stroma or vessels. See pneumonia-like consolidation on CXR. What kind of disease process is this?

A

Malignant neoplasm -> this describes bronchioalveolar carcinoma which is pre-invasion even tho it’s in situ at the time

81
Q

What kind of lung tumor is often detected incidentally on CXR as peripheral coin lesion?

A

Hamartomas

82
Q

What is responsible for CF pts collapsing during sports?

A

Na+ loss w/ sweating (for normal ppl, it would be free water loss w/ sweating)
This is b/c CFTR is supposed to help produce hypotonic sweat in healthy ppl, but CF pts can’t reabsorb Cl and Na so secrete sweat containing high Cl and Na -> get hypovolemia secondary to Na+ loss

83
Q

What is Bohr effect and where does that happen?

A

In peripheral tissues

High CO2 and H+ in RBCs (H+ buffered by histidine residues) -> help decrease affinity for O2 and facilitate O2 unloading

84
Q

What is Haldane effect and where does this happen?

A

In lungs

Binding of O2 to Hb drives release of H+ and CO2 from RBC

85
Q

Timeline for lobar pneumonia?

A

First day: congestion
Day 2-3: red hepatization (liver-like consistency) -> RBCs, neutrophils, and fibrin in alveolar exudate
Day 4-6: gray hepatization -> same histology but grossly see gray-brown lobe
Resolution -> enzymatic digestion of exudate

86
Q

Why is hypoxia caused by CO worse than anemia?

A

Both reduces O2-carrying Hb available, but only CO causes leftward shift of Hb-O2 dissociation curve (so decreases O2 unload in tissue)

87
Q

Important sx of fat emboli besides lung stuff?

A

SKIN AND NEUROLOGIC FINDINGS

petechial rash, altered mentation, seizures

88
Q

Smoker w/ chronic cough w/ O2 sat at 90% at rest and 84% w/ moderate exertion. What’s the likely finding?

A

Increased EPO -> don’t think about 90% being too high, he’s a long-time smoker and probably has COPD and chronic hypoxia

89
Q

What’s the pattern of airway resistance along the bronchial tree?

A

Starting high at around half total airway resistance in upper resp tract -> goes higher and peaks (highest resistance) at medium-sized bronchi b/c of highly turbulent flow (max at bronchial generations 2-5) -> drops as you get to smaller airways b/c cross-sectional area massively increases

90
Q

Diff nerves carrying sensation of diff parts of pleura?

A

Phrenic n.: carries pain fibers from diaphragmatic and mediastinal pleura
Intercostal n.: carries sensation from the remainder of parietal pleura

91
Q

Formula for calculating physiologic dead space?

A

Physiologic dead space = tidal volume x ([PaCO2 - PECO2]/PaCO2)

92
Q

What conditions should you assc. finger clubbing w/?

A

Chronic hypoxia: so lung diseases (except bronchial asthma), cyanotic heart diseases
Other things that might seem unrelated: bacterial endocarditis, IBD, hyperthyroidism, malabsorption
NOT iron deficiency anemia

93
Q

Leading cause of death in lung transplant pts?

A

Infection -> esp by CMV

94
Q

Major cause of morbidity in sarcoidosis?

A

Pulm fibrosis -> cor pulmonale

95
Q

What happens to RV/TLC ratio in obstructive lung diseases?

A

Increases

96
Q

Diff steps of mast cell degranulation and drugs that inhibit them?

A

IgE binding: inhibited by omalizumab (keep in mind that stimulus can also be non-Ag and not IgE)
Effectors in the cell: glucocorticoids (inhibits PLA2), Zileuton (inhibits lipoxygenase)
Mast cell degranulation (regardless of stimuli): cromolyn and nedocromil (prevention of acute attacks rather than treating acute bronchoconstriction itself)
Leukotriene receptor antagonist: zafirlukast and montelukast

97
Q

Best long-term drug for asthma for preventing cellular rxn in pt’s airway?

A

Glucocorticoids -> strongest and most predictable effects on the inflammatory component of asthma
Great at PREVENTING acute exacerbation but no role in tx of acute episodes

98
Q

What is “small bowel obstruction by inspissated green mass”?

A

Meconium ileus -> suspect CF (most common cause)

99
Q

What is “exudation and alveolar hepatization” a feature of?

A

Pneumonia caused by strep pnuemo

100
Q

What are 2 causes of progressively weakening diaphragmatic contractions during max voluntary ventilation & intact phrenic nerve stimulation?

A

Neuromuscular jx pathology (like myasthenia gravis)

Abnormally rapid diaphragmatic muscle fatigue (from restrictive lung or chest wall disease)

101
Q

Difference in how sweat glands and other exocrine glands use CFTR?

A

Sweat glands: use CFTR to ABSORB luminal NaCl -> so get NaCl wasting in CF
Exocrine glands: use CFTR to SECRETE NaCl -> so get negative transepithelial potential difference in CF from increased Na+ ABSORPTION

102
Q

What structures do you go thru when you do cricothyrotomy?

A

Skin -> superficial cervical fascia (subQ fat and platysma) -> deep cervical fascia (investing and pretracheal layers) -> cricothyroid membrane

103
Q

What do you have to suspect in sudden onset dyspnea in the setting of recent calf swelling?

A

PE! -> also remember that ABGs won’t have renal compensatory response b/c it’s acute
Don’t be distracted by the smoking status, heart conditions, etc.

104
Q

What is AIRWAY pressure at FRC? INTRATHORACIC pressure?

A

Airway pressure is 0

Intrathoracic pressure is -5 cm H2O -> decreases to -7.5 during inspiration

105
Q

What creates positive transmural pressure? Negative transmural pressure? When do they balance out?

A

Positive transmural pressure: alveolar -> always wants to collapse
Negative transmural pressure: chest wall -> always wants to expand
These 2 balance out creating 0 AIRWAY pressure at FRC

106
Q

What would you see on recorded tidal volume (airflow), PaCO2, and PaO2 during Cheyne-Stokes respiration?

A

It’s a cycle of hyperventilation and apnea -> related to slow resp feedback loop w/ enhanced resp response to PaCO2 levels -> so airflow will be cyclic (waves make crescendo decrescendo shape, followed by flat line, then repeat)
Where the flat line on airflow happens (apnea), you’ll see a gradual rise in recorded PaCO2 (and thus fall in recorded PaO2) -> once PaCO2 rises high enough the cyclic breathing comes back (hyperventilation) -> this happens on repeat

107
Q

What are Cheyne-Stokes respiration seen in?

A 
Cyclic breathing (hyperventilation alternating w/ apnea)
Sign of poor prognosis -> seen in cardiac disease (advanced CHF), neurologic disease (stroke, brain tumors, traumatic brain injury)
108
Q

Difference in recorded tidal volume (airflow) bet. OSA and Cheyen-Stokes?

A

OSA: airflow remains constant during apneic periods (no cyclical variation -> so airflow shape looks like a rectangle followed by flat line which is apneic period)
Cheyen-Stokes: airflow makes cycle pattern (gradually increasing tidal volume then gradually decreasing it then flat line)

109
Q

Diff in how mesothelioma look under EM vs. adenocarcinoma?

A

Mesothelioma: tumor cells w/ long, slender microvilli and abundant tonofilaments
Adenocarcinoa: short, plump microvilli

110
Q

Diff in pulm profile bet. A1AT deficiency and asthma?

A

Both are obstructive disease so will see decreased FEV1/FCV ratio and increased lung volume
But get decreased DLCO in A1AT deficiency (both capillary and alveoli destroyed) and increased DLCO in asthma (increased pulm blood volume)

111
Q

What are DDs for combined restrictive and obstructive pulm profiles (so like decreased FEV1/FCV, lung vol, and DLCO)?

A

CF and bronchiectasis

112
Q

PFT w/ restrictive profile + paraseptal and subpleural cystic airspace enlargement (honeycomb lung) + progressive exertional dyspnea. Dx?

A

Idiopathic pulmonary fibrosis

113
Q

If you see air-fluid level in lung on CXR, what cells should you immediately think about?

A

Neutrophils and macrophages releasing lysosomal enzymes! (b/c this is abscesses)

114
Q

What is plexiform lesion?

A

In severe pulm HTN, arteriolar medial hypertrophy and intimal fibrosis can progress to form interlacing tufts of small vascular channels

115
Q

What is the main pulm effect of increased vagus nerve efferent activity?

A

Increased work of breathing from bronchoconstriction and increased mucous secretion -> both increase airflow resistance
NO significant direct effect on pulm circulation!

116
Q

Normal value of Reid index?

A

40% -> elevation correlates w/ severity of chronic bronchitis
Reid index = mucous gland thickness / thickness of wall bet. epithelium and cartilage

117
Q

Timeline for primary TB infection?

A

Up until a couple of weeks before: just get intracellular bacterial proliferation
2-4 weeks following infection: get interferon secretion and T cell response

118
Q

What’s vasomotor rhinitis?

A

Chronic nasal congestion in response to temp changes, humidity, odors or alcohols -> might get anosmia, headache, and sinusitis too

119
Q

Hay fever vs. allergic rhinitis?

A

Hay fever is allergic rhinitis provoked by pollens of specific plants

120
Q

Exudate vs. transudate parameters?

A

Higher proteins in exudate (pleural/serum ratio > 0.5)
Higher LDH in exudate (pleural/serum ratio > 0.6 or > 2/3 upper limit of normal serum LDH)
Transudate (like in HF) has lower proteins and LDH

121
Q

Exercise intolerance + breathlessness + wheezing + sensitivity to cold weather. Dx and tx?

A

Exercise-induced asthma

Tx: montelukast (antagonizes bronchoconstricting LTD4)

122
Q

RV hypertrophy + bilateral ankle pitting edema in young female (30 yo). What’s the mechanism of damage?

A

This is idiopathic pulm ARTERIAL HTN (IPAH) - suspect in young females
Pathogenesis: pulm endothelial dysfx -> thickening of endothelium, SMC, intima -> RV hypertrophy -> backs up to peripheral circulation

123
Q

Tx of emergent asthma attack?

A

Supplemental O2 + inhaled B2 agonist -> most fast-acting (antimusca taks a while) -> so the effect will be mediated by increased cAMP
Most common type of asthma is extrinsic allergic asthma btw -> so suspect this in ppl developing sx after moving to a new home (don’t just think about lead poisoning)

124
Q

What’s a foam stability index? What is it used to assess?

A

Mix amniotic fluid w/ ethanol and shake -> the index is the highest value well that contains ring of stable foam
Assess surfactant -> fetal lung maturity

125
Q

Pt w/ pneumonia on respirator was put on antibiotics for 10 days. ABGs on 9th day shows pH 7.36, pCO2 42, and pO2 85. On 11th day it’s pH 7.24, pCO2 60, pO2 68. What’s happening?

A

Key thing here is he’s on respirator, so we know central hypoventilation or anything like that is not a problem since total minute ventilation, FIO2, and CO are constant
So new onset resp acidosis and hypoxemia in this setting has to be pulmonary pathology that increases both physiologic dead space and/or physiologic right-to-left shunt -> in this case it’s probably worsening infection w/ increased dead space formation

126
Q

Most specific sign of pulm arterial HTN?

A

P2 louder than A2

127
Q

6-yo child brought into ER for coughing, wheezing, and rapid breathing for 6 hr. He was dx w/ URI 2 days ago. Temp is 37.2 C, pulse is 120/min, resp 44/min, BP 90/60. Hear inspiratory and expiratory wheezes throughout lung fields. Decreased tactile fremitus. What’s the dx?

A

Asthma
Don’t think about strep pneumo pneumonia -> you will have INCREASED tactile fremitus w/ pneumonia. And don’t forget that the BP isn’t necessarily considered hypotension b/c he’s a child.

128
Q

What’s Caplan syndrome?

A

RA + pneumoconioses w/ intrapulm nodules

Question Bank (10 decks)

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