Flashcards in 2/25&2/26 Deck (166):
Velocity of air vs turbulence.
-whats the relation?
Higher the velocity = more turbulence possible.
Where is the least airway resistance in bronchial tree?
-large number in parallel, resistance reduced, airflow reduced, least turbulence.
*dont forget about adding resistance in parallel. It reduces the resistance.
How far do the cartilage & goblet cells extend?
-To end of bronchi
-bronchioles dont have it.
Pseudostratified ciliated columnar cells extends to:
-Beginning of terminal bronchioles, then transition to cuboidal cells.
Airway smooth muscle extends to:
-end of terminal bronchioles.
epithelium of repiratory bronchioles
-epithelium of alveolar ducts?
-what type of cell are type 1 pneumocytes?
-type 1 pneumocytes = squamous
-what type of cell is type 2 pneumocyte?
Where are clara (club) cells found?
-are they ciliated?
-secrete component of surfactant, degrade toxins.
*has cytochrome P450 enzymes
Whats the most important lecithin in surfactant?
-at what age are mature levels of surfactant reached?
-production starts at 25 weeks.
-what ratio signals mature fetal lungs?
Which lung has lingula?
-homologous to right lung's middle lobe.
Aspirate a peanut:
-lower portion of right inferior lobe.
-superior portion of right inferior lobe, posterior segment of right upper lobe.
Relation of the pulmonary artery to the bronchus at
each lung hilus is described by:
-Right Anterior; Left Superior.
What travels w/aorta thru diaphragm?
-thoracic duct & azygos vein.
Vital capacity vs total lung capacity
-total lung capacity includes residual volume.
What is the greatest contributor to functional dead space?
- apex of healthy lung.
physiologic dead space
-what does it include
-whats the equation?
-includes both anatomic and functional dead space.
-Taco, Paco, Peco, Paco
-VD = VT × (Paco2–Peco2)/Paco2
Does relaxed or taut Hb have high affinity for O2?
-Relaxed in respiratory tract
-Taut in tissues
Inc. or dec. Cl- favors Taut form of Hb (right shift on curve).
-just like inc. H (dec pH), inc temp, inc 2,3 BPG, etc.
-cyanosis & chocolate colored blood.
Treating cyanide poisoning: steps:
1-Oxidize Hb to metHb using nitrites (not nitrates).
2-metHb bill bind to cyanide
3-Use thiosulfate to bind this cyanide forming thyocynate which is renally excreted.
What drugs can lead to metHb formation?
(aka which drugs can oxidize Hb)
-nitrites, TMP, procaine, metoclopramide.
What does O2 graph look like when CO bound to Hb?
-dec efficacy and loses its sigmoidal curve.
O2 content equation
-(O2 binding capacity * % sat) + PAO2
*O2 binding capacity = (Hb)(1.34)
O2 sat = ?
O2 satured Hb.
-fraction of oxygen saturated Hb relative to total Hb.
Anemic: whats her O2 stats like?
-Hb will be dec, but O2 sat will be fine b/c theres less Hb total but still they're all gonna be saturated w/O2.
-PAO2 will be normal.
-O2 content, however, will be decreased.
O2 delivery to tissues =
=CO * O2 content
Is a healthy persons lungs perfusion or diffusion limited?
In the diffusion equation
-what does emphysema do?
-what pulmonary fibrosis do?
-dec. surface area of diffusion = dec diffusion
-inc. thickness = dec diffusion
Is big A or little a for alveoli?
Big A = Alveolar
What can chronic sleep apnea potentially cause?
pulmonary HTN and right heart failure.
-blocks arabinosyltransferase: carb polymerization of mycobacterium cell wall.
-optic neuropathy, red-green colorblindness
Ethambutol sounds like ethanol. Arabs drink a lot of ethanol. When you're hammered you cant see straight.
-Arabs = arabinosyltransferase
-Cant see straight = optic neuropathy
Influenza vaccine: how does it prevent infection?
-inhibition of viral entry into cells.
-neutralizing Abs against hemagluttinin.
-patchy inflam. of a number of lobules.
-inflam. infiltrate confined to walls of alveoli.
-involves an entire lobe.
4 stages of lobar pneumonia
1- first 24 hrs - congestion: Bacterial alveolar exudate.
2- days 2-3 - red hepatization: Alveolar exudate = RBCs, fibrin, neutros.
3- days 4-6 - gray hepatization: RBCs disintegrate. Alveolar exudate = neutros & fibrin.
4- Resolution: enzymatic degradation of exudate.
-binds ergosterol & pokes holes in membrane
*same as amphotericin B, except this is topical form.
-Why do COPD pts wheeze?
-what will breath sounds sound like?
-air being forced through narrow, congested airway.
-diminished breath sounds b/c overall dec in airflow.
-What are the two types of asthma?
-Which one is a skin test useful for Dxing?
*skin test can help Dx atopic asthma.
2-non-immune mediated asthma (bronchial hypersensitivity)
*both involve mast cell degranulation (pretty sure thats true).
What molecule is released specifically by mast cells & can be used as marker for mast cell activation/degranulation?
Where do umbilical arteries originate from?
fetal internal iliac arteries
Umbilical arteries & vein are derived from..
-mixed venous blood oxygen content, inc or dec.
-less aerobic metabolism = less O2 used.
-pleural plaques more freq on which pleural layer?
*just b/c you have pleural plaques doesn't mean u have mesothelioma.
-predisposes to what cancer?
-found in alanin dyes & rubber industry.
What is the normal PAO2 (alveolar)?
What is normal PaO2 of incoming venous blood?
*will normally be equilibrated w/alveolar PO2 after only the first 1/3 of pulm caps. That shit equilibrates fast.
What is the normal PaO2 (arterial)?
-104 mmHG before entering the LA
-100 mmHG after entering the LA
*diluted w/deoxy bronchial blood.
What is the PaO2 cutoff for hypoxemia?
Normal A-a gradient?
-not higher than 10-15 mmHG
Does physiological shunting lead to inc/normal/dec A-a gradient?
-inc. A-a gradient
(but I believe that CO2 levels remain normal).
-binds mostly unbound, free serum IgE.
Alveolar gas equation =
PAO2 = PIO2 - PaCO2/.8
-apex: V/Q = 3
-base: V/Q = .3
Both ventilation and perfusion increase from apex to base (base has highest of both). Perfusion inc. to a greater degree though. Thus; as one moves down the lung, the V/Q ratio will decrease b/c Q increasing more so than V!
What happens to V/Q ratio during exercise?
-With exercise (inc. cardiac output), there is vasodilation of apical capillaries, resulting in a V/Q ratio that approaches 1.
What is a shunt?
V/Q = 0
-no ventilation, so even 100% oxygen wont help b/c its not reaching the alveoli for some reason.
-ie. someone choking
In lungs, oxygenation of Hb promotes dissociation of H+ from Hb. This shifts equilibrium toward CO2 formation; therefore, CO2 is released from RBCs.
-protons attached to Hb help stabilize the taut form *which is why low pH (lots of H) causes right shift.
In peripheral tissue, H+ from tissue metabolism shifts curve to right, unloading O2.
Reponse to high alt
-dec PaO2, dec PaCO2 (hypervent)
-inc. EPO, inc 2,3-DPG
-inc. renal excretion of bicarb (comp for resp alk)
-chronic hypoxia => pulm vasoconstrict => RVH
*can augment loss of bicarb w/acetazolamide.
Blood gas changes during exercise
-No change in Pao2 and Paco2
-inc. venous CO2 content
-dec. venous O2 content.
*your tissues extracting more O2 and producing more CO2.
-most common causes?
-Most common acute cause is viral URI
-may cause superimposed bacterial infection
-triad = stasis, hypercoag, endothelial damage.
-sign = dorsiflexion of foot = pain.
thrombophilia means what
inc. susceptibility to forming thrombi.
-long bone fxs, liposuction
-hypoxemia, neurologic abnormalities, and petechial rash.
-Pre-capillary AV-shunts will open up due to inc. pulm pressure. This is how fat emboli get thru and land in the CNS.
-fat molecules get coated by platelets which leads to thrombocytopenia and then petechiae.
amniotic fluid emboli
-can lead to what?
-amniotic fluid has thromboplastin = activates extrinsic system.
*Squamous cells & keratin debris in new mothers lungs = amniotic fluid pulm. emobolus. From babies skin cells that come off in the amniotic fluid.
-how does it usually happen?
-how do you treat it?
-Divers ascending too fast & nitrogen bubbles.
-Or laparoscopic surgery, when we pump air in.
-Tx: hyperbaric O2.
Lines of Zahn
-interdigitating areas of pink (platelets, fibrin) and red (RBCs) found only in thrombi formed before death. Help distinguish pre- and postmortem thrombi.
Obstructive pulm disorders
-air trapping refers to what?
Chronic bronchitis (blue bloaters)
-Hyperplasia of mucus secreting glands due to smoking. All this mucus will either be coughed up or back up and cause obstruction.
-disease of smaller airways.
-Reid index > 50% (gland layer:total thickness)
*productive cough > 3 months (not necessarily consecutive) for >2 years.
-histologically what do you see?
Inflammatory infiltrate w/lymphocytes, squamous metaplasia, and fibrosis. Monocytes and CD8 cells seen.
*squamous metaplasia due to smoking.
-chronic inflamm so you see monocytes/lymphocytes.
Which lung problem associated w/barrel chest?
-destroy lung elastic tissue to FRC is increased.
Which lung problem associated w/pursed lips?
-emphysema (pink puffers)
-create a back pressure so bronchioles wont collapse upon exhalation.
*these pts lose weight b/c pursing your lips to breath takes energy!
Normal allele for A1At? Mutated allele?
-what sort of dominance?
-normal = PiM
-abnormal = PiZ
Centriacinar emphysema: worse in lower or upper lobes?
-worse in upper lobe.
Distal acinar (paraseptal) emphysema
-localized, beneath pleura typically in an upper lung lobe, and may occurin an area of fibrosis or scar formation.
-Prone to rupture with minor trauma, leading to spont. pneumothorax.
A1AT trypsin problem
-ER or hepatocytes
-promotes switch to IgE.
-class switch to IgA
-calls in eosinophils.
“Hot T-bone stEAK”
IL-1: fever (hot).
IL-2: stimulates T cells.
IL-3: stimulates bone marrow.
IL-4: stimulates IgE production.
IL-5: stimulates IgA production.
IL-6: stimulates aKute-phase protein
-Smooth muscle hypertrophy
-Curschmann spirals (shed epithelium forms mucus plugs)
-Charcot-Leyden crystals (formed from breakdown of eosinophils in sputum, major basic protein).
-purulent, foul smelling sputum, hemoptysis, recurrent infections
-bronchial obstruction, poor ciliary motility (smoking), Kartagener syndrome, cystic fibrosis, allergic
*its a chronic inflammatory state, and any chronic inflammatory state can lead to amyloidosis.
-autopsy, what will u see?
-large dilated bronchi in periphery.
-normally by time everything branches to periphery, its just tiny bronchioles/alveolar ducts, you dont typically find large bronchi in the periphery.
Wegeners leads to what type of lung problem?
-obstructive or restrictive?
Any granulomatous disease in the lung leads to what?
-restrictive lung disease.
-sarcoidosis, wegeners, langerhans histiocytosis.
Asteroid body found in what disease?
-Mixed type III/IV hypersensitivity reaction to environmental antigen.
-Often seen in farmers and those exposed to birds.
*granulomas may occur since its type 4
*farmers lung & actinomycetes.
Rheumatoid arthritis and pneumoconioses with intrapulmonary nodules.
*intrapulm nodule = rheumatoid nodules.
Pleural plaques in asbestos exposure
How do pneumoconioses lead to restrictive lung disease?
key = macrophages phagocytosing these environmental
dust particles causes they to release cytokines which
promote collagen deposition by fibroblasts.
-inhibit phagolysosome formation & impair macrophags, leading to inc. susceptibility to TB.
-also inc. risk of bronchogenic carcinoma, like asbestos.
“Eggshell” calcification of hilar lymph nodes
-Risk factors for NRDS?
-risks for O2 treatment?
-prematurity, maternal DM (fetal insulin dec surfactant), C-section (dec glucocorticoids which promote surfactant).
-retinopathy of prematurity, bronchopulmonary dysplasia. These are due to free radical damamge.
Whats responsible for the green color of put and sputum in a bacterial infection?
-myeloperoxidase released from azurophilic granules of neutrophils.
-it is a blue-green heme-based pigmented molecule.
Azoles (ie. itraconazole, ketoconazole)
-inhibit ergosterol synthesis by inhibiting a P450 enzyme that converts lanosterol to ergosterol.
-enzyme = 14-alpha-demethylase
-side effects: Testosterone synth. inhibition & liver dysfunction. It inhibits P450 system.
*P450 enzyme used to make testosterone.
How far down respiratory tree does ciliated epithelium extend?
-goes until start of respiratory bronchioles.
Are goblet cells found in terminal bronchioles?
-so then you know cilia must be in terminal bronchioles b/c cilia must extend past last spot you find goblet cells.
whats the most common lung cancer?
Tx for small cell carcinoma?
-no surgery possible.
Do you typically find atopic asthma in infants?
-atopic asthma is rare in infants.
Ribavirin given for what diseases?
-RSV & chronic Hep C
MAC vs TB
-CD4 < 50
-anemia, hepatosplenomegaly, elevated ALP & LDH.
-grows optimally at 41 C.
Which acid fast bacteria grows optimally at 41 C?
-whats prophylaxis for it?
-for persistent asthma.
What is the most common side effect of inhaled glucocorticoids?
-Tx for pulm. HTN
-endothelin 1 competetive antagonist.
-decreases pulm vascular resistance.
Fish bone in piriform recess can damage what nerve and lead to what problem?
-internal laryngeal n. (branch of superior laryngeal n. which is CN10 branch).
-afferent limb of cough reflex
-CN9 = afferent
-CN10 = efferent
-blood can pass thru entire capillary length w/o blood gas and alveolar gas equilibrating.
-can happen in emphysema, pulm fibrosis, or very high pulmonary flow (ie. exercise, b/c blood just moving too fast).
Diffusion capacity of CO2 relative to O2.
Diffusion capacity of CO2 is about 20x higher than O2.
-So CO2 levels are not nearly as affected as O2 levels in diffusion-limited states.
How does emphysema lead to decrease diffusion capacity?
-By straight up decreasing the surface area for diffusion to occur. Destroys both alveoli and the associated capillary beds.
-that means more blunt has to be shunted to areas that still have vent and perfusion and these areas might get overloaded and not work as well.
PCWP in ARDS?
-distinguishes it from cardiogenic causes of heart failure.
-Name some causes of dec. pulm compiance.
-dec lung compliance will lead to what change in FRC?
-insufficient surfactant, pulm fibrosis, pulm edema.
-dec. FRC. Lungs = more fibrosed/more elastic force so pulls chest wall in.
-associated w/dec. levels of what?
-high or low EPO?
-associated w/myeloproliferative disorder.
Causes of ARDS
-uremia, sepsis, shock, gastric aspiration, acute pancreatitis, amniotic fluid embolus.
-Initial damage in ARDS due to:
-which cells are being damaged?
-neutrophils, activation of coag cascade, and O2 free radicals.
-What is normal pulm. art pressure?
-what pressure defines pulm HTN?
-25mmHG + at rest
-changes to artery?
Arteriosclerosis, medial hypertrophy, and intimal fibrosis of pulmonary arteries. Results in luminal narrowing.
Primary pulm HTN.
-what kind of mutation in which gene?
-inactivating mutation in the BMPR2 gene (normally functions to inhibit vascular smooth muscle proliferation).
-Central sleep apnea
-Obstructive sleep apnea
-neuro problem leading to no respiratory effort.
-respiratory effort against airway obstruction. Associated with obesity, loud snoring.
Risk factors for obstructive sleep apnea.
-obesity, tonsillar hypertrophy, hypothyroidism.
Obesity hypoventilation syndrome
-they'll have abnormal blood gases throughout the day. Unlike sleep apnea which has normal blood gases during the day.
-these pts also have concomitant obstructive sleep apnea.
-fremitus inc or dec?
Atelectasis (bronchial obstruction)
-percussion: hyper-resonant or dull
Bronchial breath sounds heard when?
Atrophic skin + raynauds =
interstitial pulm. fibrosis.
CFTR channel is what sort of protein?
-what chromosome is the mutation usually on?
-ATP-gated transmembrane protein.
Anaerobes part of normal mouth flora
*if they get into lungs, can cause lung abscess.
Foul smelling sputum: think what?
-anaerobes (think aspiration)
Whats the most common cause of lung abscess?
-whats the major stimulator
-inc PaCO2 => inc in respiration
-whats the major stimulus
-found in carotid & aortic bodies.
--hypoxemia (dec. PaO2) => inc respiration.
--hypercapnia (inc. PaCO2) & inc. H => inc respiration.
Pulmonary stretch receptors
-myelinated & unmyelinated C fibers in lungs/airways.
-regulate duration of inspiration depending on degree of lung inflation.
-protect against hyperinflation.
-only stimulated when..
you need to breath more.
What is airway pressure at FRC?
-the (-) pressure of expanding chest is equal to the (+) pressure of the collapsing elastic lungs.
-this is why at FRC no air is flowing in the lungs (in or out).
What is the intrapleural pressure at FRC?
-5 cm H20
*negative 5, thats not a dash.
*when the chest wall and lungs directions are opposing each other, the intrapleural pressure becomes more negative. This induces a slightly negative alveolar pressure = sucks air into lungs.
Where does lung cancer most commonly metastasize to?
Which is the only lung cancer not associated w/smoking?
What is hypertrophic osteoarthropathy?
-what are some activating mutations that cause this?
-whats another name for adenocarcinoma in situ?
-k-ras, EGFR, ALK.
-bronchioalveolar subtype, excellent prognosis, grows along alveolar septa (apparent "thickening" of alveolar walls.
Squamous cell carcinoma
-cells being pulled apart, stretched desmosomes make "intercellular bridges".
-PTHrP: causes hypercalcemia.
Classic cells seen in small cell carcinoma?
-stains (+) for what?
-Kulchitsky cells = small dark blue cells.
Amplification of what oncogene is common in small cell carcinoma?
Large cell carcinoma
-less responsive to chemo, remove surgically.
Bronchial carcinoid tumor
-whats it look like?
-stains + for what?
-polyp like mass in bronchus.
*can occasionally cause carcinoid syndrome.
Which lung pathology has psammoma bodies?
How can pancoast tumor result in hoarseness?
compress on recurrent laryngeal n.
Which bugs cause lobar pneumonia?
-S. pneumoniae most frequently, also Legionella, Klebsiella
Which bugs cause bronchopneumonia?
-whats bronchopnuemonia look like?
-S. pneumoniae, S. aureus, H. influenzae, Klebsiella.
-patchy involving at least 1 lobe.
-classic S. aureus.
Lobar & bronchopneumonia
Interstitial (atypical) pneumonia
-atypical bacteria or viral
Common causes of interstitial pneumonia:
-Viruses (influenza, RSV, adenoviruses)
-Mycoplasma, Legionella, Chlamydia
-1st gen: name them
- Diphenhydramine, dimenhydrinate, chlorpheniramine, promethazine.
*Names contain “-en/-ine” or “-en/-ate.”
-Use: Allergy, motion sickness, sleep aid.
-Tox: Sedation, antimuscarinic, anti-α-adrenergic.
-2nd gen: name them
*no CNS entry like 1st gen.
-Loratadine, fexofenadine, desloratadine, cetirizine.
*Names usually end in “-adine.”
-tox: far less sedation than 1st gen.
-Antitussive (antagonizes NMDA glutamate receptors).
-Synthetic codeine analog. Has mild opioid effect when used in excess.
-Naloxone can be given for overdose. Mild abuse potential.
-what does it do to cerebral perfusion?
-CO2 is a potent cerebral vasodilator.
-so a decrease in CO2 (hypervent) will lead to a decrease in cerebral perfusion (and thus decreased ICP).
*pts w/cerebral edema often hyperventilated to reduce CO2 and therefore reduce cerebral perfusion and reduce ICP.
O2 effect on chemoreceptors
-oxygen has a relatively small effect on respiratory
drive if its PaO2 > 70mmHG.
-unless you have long-standing COPD pts who have decreased sensitivity to CO2 and H. These pts also have profound hypoxemia (PaO2 < 60mmHG). In this case, PaO2 becomes a significant contributor to the respiratory drive.
--in this case, giving a COPD pt O2 can reduce respiratory drive b/c the low PaO2 was stimulating the peripheral chemoreceptors.
-cyclic breathing in which apnea is followed by gradually increasing tidal volumes, and then gradually decreasing tidal volumes until the next apneic period.
-commonly seen in cardiac disease (ie. advanced CHF) & neuro diseases (ie. inc ICP).
-usually has a poor prognosis once this is present.
slow respiratory feedback loop
-CO2 gets low, so respiratory drive depressed. So you get apneic. CO2 levels rise but the feedback to the respiratory drive to kick in is slow. Once the resp drive kicks it the CO2 levels are higher than they should be and you hyperventilate to make up for it.
-The hyperventilation causes lowers the CO2 to the extent that a period of apnea is induced.
-Then the cycle continues.
-use: long-acting agents for asthma prophylaxis.
-tox: tremor and arrhythmia.
Theophylline (a Methylxanthines)
-blocks action of which drug?
-phosphodiesterase inhibitor = inc cAMP levels which leads to bronchodilation (smooth muscle relaxation).
-Narrow therapeutic index: cardiotoxicity, neurotoxicity
*mostly Seizures! Also abdominal pain, vomiting.
-metabolized by P-450.
-Blocks actions of adenosine.
-LTB4 = chemotactant for neutrophils. If you are
blocking this then you're immunosuppresive.