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189 Cards in this Set
- Front
- Back
Conducting zone
Consists of |
nose, pharynx, trachea, bronchi, bronchioles, and terminal bronchioles.
|
|
Respiratory zone
Consists of |
respiratory bronchioles, alveolar ducts, and alveoli.
|
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Pneumocytes
Pseudocolumnar ciliated cells extend to the |
respiratory bronchioles;
|
|
Pneumocytes
extend to the respiratory bronchioles |
Pseudocolumnar ciliated cells
|
|
Pneumocytes
goblet cells extend to the |
terminal bronchioles.
|
|
Pneumocytes
extend to the terminal bronchioles. |
goblet cells
|
|
Pneumocytes
%'s |
Type I cells (97% of alveolar surfaces)
Type II cells (3%) |
|
role of
Type I cells |
line the alveoli.
|
|
role of
Type II cells |
-secrete pulmonary surfactant.
-serve as precursors to type I cells and other type II cells. Type II cells |
|
role of
clara cells |
secrete a component of surfactant - degrade toxins - act as reserve cells
|
|
ratio of in amniotic
fluid is indicative of fetal lung maturity. |
A lecithin-to-sphingomyelin
ratio of > 2.0 |
|
bronchopulmonary segment
structure |
3°(segmental) bronchus
- 2 arteries (bronchial and pulmonary) in the center - veins and lymphatics drain along the borders. |
|
what is described by RALS––
|
the heart. The relation of the
pulmonary artery to the bronchus at each lung hilus is described by RALS–– Right Anterior; Left Superior. |
|
Structures perforating diaphragm
what and levels |
-T8: IVC.
-T10: esophagus, vagus (2 trunks). -At T12: aorta (red), thoracic duct (white), azygous vein (blue). |
|
Pain from the diaphragm can be referred to
|
the shoulder.
|
|
Muscles of respiration
in exercise |
Inspiration––external intercostals, scalene muscles, sternomastoids.
Expiration––rectus abdominis, internal and external obliques, transversus abdominis,internal intercostals. |
|
5 Important lung products
|
-Surfactant
-ACE -Prostaglandins -histamine -Kallikrein |
|
Surfactant
aka |
dipalmitoyl phosphatidylcholine
or lecithin |
|
Collapsing pressure =
|
2T/R
T=tension R= radius |
|
what activates bradykinin
|
Kallikrein
|
|
role of Kallikrein
|
activates bradykinin
|
|
role of ACE in lung
|
angiotensin I → angiotensin II; inactivates bradykinin
|
|
lung effects of ACE inhibitors and other effect
|
ACE inhibitors ↑ bradykinin and
cause cough, angioedema) |
|
role of surfactant/mech
|
↓ alveolar surface tension
↑ compliance |
|
TLC =
|
IRV + TV + ERV + RV
|
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VC =
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TV + IRV + ERV
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TV + IRV + ERV
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VC
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IRV + TV + ERV + RV
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TLC
|
|
what causes a shift of the curve
to the right. |
An ↑ in all factors (except pH)
|
|
what causes a shift of the curve to the left.
|
A ↓ in all factors (except pH)
|
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Pulmonary circulation
normal resistnace and compliance |
Normally a low-resistance, high-compliance system.
|
|
Pulmonary circulation
A ↓ in PaO2 causes |
a hypoxic vasoconstriction that shifts blood away from
poorly ventilated regions of lung to well-ventilated regions of lung. |
|
Pulmonary circulation
Perfusion limited what molecules / when / describe / how to change |
O2 (normal health),
-CO2, -N2O. Gas equilibrates early along the length of the capillary. Diffusion can be ↑ only if blood flow ↑. |
|
Pulmonary circulation
Diffusion limited what molecules / when / describe |
–O2 (exercise, emphysema,
fibrosis), -CO. -Gas does not equilibrate by the time blood reaches the end of the capillary. |
|
Normal pulmonary artery pressure =
and when is it changes |
Normal pulmonary artery pressure = 10–14 mm Hg; or >35 mm Hg during exercise.
-pulmonary HTN ≥25 mm Hg |
|
Pulmonary hypertension
primary vs secondary |
Primary––unknown etiology, poor prognosis.
Secondary––usually caused by COPD, also can be caused by L → R shunt. |
|
O2 content =
|
(O2 binding capacity × % saturation) + dissolved O2.
|
|
O2 changes as Hb falls
|
O2 content of arterial blood ↓ as [Hgb] falls,
but O2 saturation and arterial PO2 do not. |
|
Arterial PO2 ↓ with
|
chronic lung disease; physiologic shunt ↓ O2 extraction ratio
not decrease in Hb |
|
-Normally 1 g Hgb can bind
-normal Hgb amount in blood -Normal O2 binding capacity |
-1 g Hgb can bind 1.34 mL O2;
-Hgb amount in blood is 15 g/dL. -O2 binding capacity ≈ 20.1 mL O2 / dL. |
|
↑ A-a gradient may occur in
|
-hypoxemia; causes include
shunting, high V/Q mismatch, fibrosis (diffusion block) |
|
CO2 transport forms
|
1. Bicarbonate (90%)
2. Bound to hemoglobin as carbaminohemoglobin (5%) 3. Dissolved CO2 (5%) |
|
Haldane effect
|
In lungs, oxygenation of hemoglobin promotes dissociation of CO2 from hemoglobin
|
|
Bohr effect
|
In peripheral tissue, ↑ H+ shifts curve to right, unloading O2
|
|
7 Response to high altitude
|
1. Acute ↑ in ventilation
2. Chronic ↑ in ventilation 3. ↑ erythropoietin 4. ↑ 2,3-DPG 5. Cellular changes (↑ mitochondria) 6. ↑ renal excretion of bicarbonate to compensate for the respiratory alkalosis 7. Chronic hypoxic pulmonary vasoconstriction results in RVH |
|
Emphysema
types with causes |
Centriacinar: caused by smoking.
Panacinar: α1-antitrypsin deficiency |
|
α1-antitrypsin deficiency leads to
|
Panacinar Emphysema and liver cirrhosis
|
|
Paraseptal emphysema: what and who
|
associated with bullae →can rupture →pneumothorax;
often in young, otherwise healthy males. |
|
associated with bullae →can rupture →pneumothorax;
often in young, otherwise healthy males. |
Paraseptal emphysema
|
|
Emphysema
pathology |
↑ elastase activity.
Enlargement of air spaces and ↓ recoil resulting from destruction of alveolar walls. |
|
Chronic Bronchitis
pathology |
Hypertrophy of mucus glands in the bronchioles →Reid index = gland depth / total thickness of bronchial wall; in COPD, Reid index > 50%.
|
|
Reid index
|
gland depth / total thickness of bronchial wall; in COPD, Reid index > 50%.
|
|
Bronchiectasis
pathology |
Chronic necrotizing infection of
bronchi →permanently dilated airways, |
|
Bronchiectasis
complications |
purulent sputum, recurrent infections, hemoptysis.
|
|
causes of Bronchiectasis
|
Associated with bronchial obstruction, CF, poor ciliary motility, Kartagener’s
syndrome. |
|
Asthma triggers
|
Can be triggered by viral URIs, allergens, and stress.
|
|
Restrictive lung
disease causes Poor breathing mechanics (extrapulmonary): |
a. Poor muscular effort––polio, myasthenia gravis
b. Poor structural apparatus––scoliosis, morbid obesity |
|
Restrictive lung
disease 8 types Interstitial lung diseases (pulmonary): |
1. (ARDS) 2. Neonatal RDS
3. Pneumoconioses 4. Sarcoidosis 5. Idiopathic pulmonary fibrosis 6. Goodpasture’s syndrome 7. Wegener’s granulomatosis 8. Eosinophilic granuloma |
|
Pneumoconioses
name some |
coal miner’s silicosis, asbestosis
|
|
Neonatal respiratory distress
syndrome Tx |
maternal steroids before birth;
artificial surfactant for infant. |
|
Adult acute respiratory distress syndrome (ARDS)
pathophys |
Diffuse alveolar damage →↑ alveolar capillary permeability →protein-rich leakage into alveoli. Results in formation of intra-alveolar hyaline membrane.
|
|
Adult acute respiratory distress syndrome (ARDS)
initial damage due to |
-neutrophilic substances toxic to alveolar wall,
-activation of coagulation cascade, -oxygen-derived free radicals. |
|
Sleep apnea
types |
Central sleep apnea––no respiratory effort.
Obstructive sleep apnea––respiratory effort against airway obstruction. |
|
Sleep apnea
define |
Person stops breathing for at least 10 seconds
repeatedly during sleep. |
|
Sleep apnea
complications |
- systemic/pulmonary hypertension,
-arrhythmias, -possibly sudden death. -chronic fatigue |
|
Asbestosis
mech |
Diffuse pulmonary interstitial fibrosis caused by inhaled asbestos fibers.
|
|
asbestos
wrt malignancy |
↑ risk of:
pleural mesothelioma bronchogenic carcinoma. |
|
pneumoconioses
where in lungs |
Asbestosis Mainly affects lower lobes. Other pneumoconioses
affect upper lobes (e.g., coal worker's lung). |
|
Asbestos and smoking
|
Asbestosis and smoking greatly
↑ risk of bronchogenic cancer (smoking not additive with mesothelioma). |
|
Asbestosis
histo |
Ferruginous bodies in lung (asbestos fibers coated with hemosiderin). Ivory-white pleural plaques
|
|
Bronchial obstruction
-Breath Sounds -Resonance -Fremitus -Tracheal Deviation |
-Absent/↓ over affected area
-↓ -↓ -Toward side of lesion |
|
Pleural effusion
-Breath Sounds -Resonance -Fremitus -Tracheal Deviation |
-↓ over effusion
-Dullness -↓ - NC |
|
Pneumonia (lobar)
-Breath Sounds -Resonance -Fremitus -Tracheal Deviation |
-May have bronchial
breath sounds over lesion -Dullness -↑ -NC |
|
Pneumothorax
-Breath Sounds -Resonance -Fremitus -Tracheal Deviation |
-↓
-Hyperresonant -Absent -Away from side of lesion |
|
Breath Sounds, Resonance, Fremitus, Tracheal Deviation
-Absent/↓ over affected area -↓ -↓ -Toward side of lesion |
Bronchial obstruction
|
|
Breath Sounds, Resonance, Fremitus, Tracheal Deviation
-↓ over effusion -Dullness -↓ - NC |
Pleural effusion
|
|
Breath Sounds, Resonance, Fremitus, Tracheal Deviation
-May have bronchial breath sounds over lesion -Dullness -↑ -NC |
Pneumonia (lobar)
|
|
Breath Sounds, Resonance, Fremitus, Tracheal Deviation
-↓ -Hyperresonant -Absent -Away from side of lesion |
Pneumothorax
|
|
Lung cancer
complications |
SPHERE of complications:
-Superior vena cava syndrome -Pancoast’s tumor -Horner’s syndrome -Endocrine (paraneoplastic) -Recurrent laryngeal symptoms (hoarseness) -Effusions (pleural or pericardial) |
|
Lung cancer
which types are central |
-Squamous cell carcinoma
-Small-cell |
|
Lung cancer
which types are peripheral |
Adenocarcinoma:
Bronchial Bronchoalveolar Large cell carcinoma |
|
Lung cancer
describe Squamous cell carcinoma (gross) |
Hilar mass arising from bronchus; Cavitation;
|
|
Lung cancer
which have strong smoking association |
-Squamous cell carcinoma
-Small-cell |
|
Lung cancer
Undifferentiated → very aggressive |
Small-cell (oat-cell) carcinoma
|
|
Lung cancer
ectopic production of ACTH or ADH |
Small-cell (oat-cell) carcinoma
|
|
Lung cancer
Lambert-Eaton syndrome. |
Small-cell (oat-cell) carcinoma
|
|
Lung cancer histology
Small-cell (oat-cell) carcinoma |
Neoplasm of neuroendocrine
Kulchitsky cells → small dark blue cells. |
|
Lung cancer histology
Squamous cell carcinoma |
Keratin pearls and intercellular
bridges. |
|
Lung cancer histology
Neoplasm of neuroendocrine Kulchitsky cells → small dark blue cells |
Small-cell (oat-cell) carcinoma
|
|
Lung cancer histology
Keratin pearls and intercellular bridges |
Squamous cell carcinoma
|
|
Lung cancer histology
Clara cells → type II pneumocytes multiple densities on x-ray of chest. |
both types of Adenocarcinoma:
Bronchial and Bronchoalveolar |
|
Lung cancer histology
Pleomorphic giant cells with leukocyte fragments in cytoplasm. |
Large cell carcinoma
|
|
Lung cancer histology
Adenocarcinoma |
Both Types: Clara cells → type II pneumocytes multiple densities on x-ray of chest.
|
|
Lung cancer histology
Large cell carcinoma |
Pleomorphic giant cells with
leukocyte fragments in cytoplasm. |
|
Lung cancer characteristics
Adenocarcinoma: Bronchial |
Develops in site of prior pulmonary inflammation or injury
|
|
Lung cancer characteristics
most common lung CA in non-smokers |
Adenocarcinoma: Bronchial
|
|
Lung cancer characteristics
Develops in site of prior pulmonary inflammation or injury |
Adenocarcinoma: Bronchial
|
|
Lung cancer characteristics
Not linked to smoking. |
Adenocarcinoma: Bronchoalveolar
|
|
Lung cancer characteristics
parathyroid-like activity → PTHrP |
Squamous cell carcinoma
|
|
Lung cancer characteristics
Hilar mass arising from bronchus; Cavitation |
Squamous cell carcinoma
|
|
Lung cancer characteristics
Highly anaplastic undifferentiated tumor; poor prognosis. |
Large cell carcinoma
|
|
Lung cancer characteristics
Large cell carcinoma |
Highly anaplastic undifferentiated tumor; poor prognosis.
|
|
Lung cancer characteristics
Carcinoid tumor |
Secretes serotonin, can cause carcinoid
syndrome (flushing, diarrhea, wheezing, salivation). |
|
Lung cancer characteristics
flushing, diarrhea, wheezing, salivation |
Carcinoid tumor
|
|
Lung cancer characteristics
most common. Brain (epilepsy), bone (pathologic fracture), and liver (jaundice, hepatomegaly). |
Metastases
|
|
Lung cancer common presentation features
|
cough, hemoptysis, bronchial
obstruction, wheezing, pneumonic “coin” lesion on x-ray film. |
|
cough, hemoptysis, bronchial
obstruction, wheezing, pneumonic “coin” lesion on x-ray film. |
Lung cancer
|
|
Pancoast’s tumor
where and findings |
Carcinoma that occurs in apex of lung and may affect cervical sympathetic plexus, causing
Horner’s syndrome. |
|
Carcinoma that occurs in apex of lung and may affect cervical sympathetic plexus, causing
Horner’s syndrome. |
Pancoast’s tumor
|
|
Kulchitsky cells
|
Enterochromaffin (EC) cells (Kulchitsky cells) are a type of enteroendocrine cell[1] occurring in the epithelia lining the lumen of the gastrointestinal tract. also implicated in the origin of small cell lung cancer.
|
|
Lambert-Eaton syndrome
findings |
progressive weakness that does not usually involve the respiratory muscles and the muscles of face. In patients with affected ocular and respiratory muscles, the involvement is not as severe as myasthenia gravis. The proximal parts of the legs and arms are predominantly affected.
|
|
Lambert-Eaton syndrome
causes |
small-cell lung cancer, lymphoma, non-Hodgkin's lymphoma
|
|
progressive weakness that does not usually involve the respiratory muscles and the muscles of face. In patients with affected ocular and respiratory muscles, the involvement is not as severe as myasthenia gravis. The proximal parts of the legs and arms are predominantly affected.
|
Lambert-Eaton syndrome
|
|
Small-cell carcinoma
aka |
oat-cell carcinoma
|
|
oat-cell carcinoma
aka |
Small-cell carcinoma
|
|
Pneumonia types with different organism causes
|
Lobar - Pneumococcus usually
Bronchopneumonia - S. aureus, H. flu, Klebsiella, S. pyogenes Interstitial (atypical) pneumonia - viruses (RSV, adenoviruses), Mycoplasma, Legionella, Chlamydia |
|
Lobar pneumonia Characteristics
|
Intra-alveolar exudate → consolidation; may involve entire lung
|
|
Bronchopneumonia Characteristics
|
Acute inflammatory infiltrates
from bronchioles into adjacent alveoli; patchy distribution involving ≥ 1 lobes |
|
Interstitial (atypical)
pneumonia Characteristics |
Diffuse patchy inflammation
localized to interstitial areas at alveolar walls; distribution involving ≥ 1 lobes |
|
Which type of pneumona
Intra-alveolar exudate → consolidation; may involve entire lung |
Lobar
|
|
Which type of pneumona
Acute inflammatory infiltrates from bronchioles into adjacent alveoli; patchy distribution involving ≥ 1 lobes |
Bronchopneumonia
|
|
Which type of pneumona
Diffuse patchy inflammation localized to interstitial areas at alveolar walls; distribution involving ≥ 1 lobes |
Interstitial (atypical)
pneumonia |
|
Which type of pneumona
Pneumococcus most frequently |
Lobar
|
|
Which type of pneumona
S. aureus |
Bronchopneumonia
|
|
Which type of pneumona
Viruses (RSV, adenoviruses) |
Interstitial (atypical)
pneumonia |
|
Which type of pneumona
Mycoplasma, Chlamydia |
Interstitial (atypical)
pneumonia |
|
Which type of pneumona
Legionella |
Interstitial (atypical)
pneumonia |
|
Interstitial pneumonia
aka |
atypical pneumonia
|
|
atypical pneumonia
aka |
Interstitial
pneumonia |
|
Which type of pneumona
S. aureus |
Bronchopneumonia
|
|
Which type of pneumona
H. flu |
Bronchopneumonia
|
|
Which type of pneumona
Klebsiella |
Bronchopneumonia
|
|
Which type of pneumona
S. pyogenes |
Bronchopneumonia
|
|
what are Lung abscess and who gets them
|
Localized collection of pus within parenchyma, usually resulting from bronchial
obstruction (e.g., cancer) or aspiration of gastric contents (especially in patients predisposed to loss of consciousness, e.g., alcoholics or epileptics). |
|
Pleural effusions what and causes of
Transudate |
↓ protein content.
Due to CHF, nephrotic syndrome, or hepatic cirrhosis. |
|
Pleural effusions what and causes of
Exudate |
↑ protein content, cloudy. Due to malignancy, pneumonia, collagen vascular disease,
trauma. |
|
Which type of Pleural effusion
↓ protein content |
Transudate
|
|
Which type of Pleural effusion
CHF |
Transudate
|
|
Which type of Pleural effusion
nephrotic syndrome |
Transudate
|
|
Which type of Pleural effusion
hepatic cirrhosis |
Transudate
|
|
Which type of Pleural effusion
↑ protein content, cloudy |
Exudate
|
|
Which type of Pleural effusion
malignancy |
Exudate
|
|
Which type of Pleural effusion
pneumonia, |
Exudate
|
|
Which type of Pleural effusion
collagen vascular disease |
Exudate
|
|
Which type of Pleural effusion
↑ protein content |
Exudate
|
|
Which type of Pleural effusion
cloudy |
Exudate
|
|
Which type of Pleural effusion
trauma |
Exudate
|
|
1st generation H1 blockers
names |
Diphenhydramine, dimenhydrinate, chlorpheniramine.
|
|
1st generation H1 blockers
Clinical uses |
Allergy, motion sickness, sleep aid.
|
|
1st generation H1 blockers
Toxicity |
Sedation, antimuscarinic, anti-α-adrenergic.
|
|
1st generation H1 blockers
mech |
Reversible inhibitors of H1 histamine receptors.
|
|
2nd generation H1 blockers
mech |
Reversible inhibitors of H1 histamine receptors.
|
|
2nd generation H1 blockers
names |
Loratadine, fexofenadine, desloratadine.
|
|
2nd generation H1 blockers
names |
Allergy.
|
|
2nd generation H1 blockers
names |
Far less sedating than 1st generation.
|
|
Asthma drugs
name the Nonspecific β-agonists |
Isoproterenol
|
|
Asthma drugs
Isoproterenol mech and uses |
Nonspecific β-agonists relaxes bronchial smooth muscle (β2).
|
|
Asthma drugs
Isoproterenol toxicity |
Nonspecific β-agonists Adverse effect is tachycardia (β1).
|
|
Asthma drugs
name the β2 agonists |
Albuterol and Salmeterol
|
|
Asthma drugs
Albuterol mech and uses |
β2 agonist relaxes bronchial smooth muscle (β2). Use during acute exacerbation.
|
|
Asthma drugs
Salmeterol mech and uses |
β2 agonist long-acting agent for prophylaxis.
|
|
Asthma drugs
Salmeterol toxicity |
Adverse effects are tremor and arrhythmia.
|
|
asthma drug
Adverse effects are tremor and arrhythmia. |
Salmeterol
|
|
Asthma drugs
name the Methylxanthines |
Theophylline
|
|
Asthma drugs
Theophylline mech and uses |
Methylxanthine - likely causes bronchodilation by inhibiting phosphodiesterase, thereby ↓
cAMP hydrolysis. |
|
Asthma drugs
Theophylline tioxicity |
Usage is limited because
of narrow therapeutic index (cardiotoxicity, neurotoxicity). |
|
Asthma drugs
Usage is limited because of narrow therapeutic index (cardio and neuro toxicity). |
Methylxanthines: Theophylline
|
|
Asthma drugs
name the muscarinic antagonists |
Ipratropium
|
|
Asthma drugs
Ipratropium mech and uses |
competitive block of muscarinic
receptors, preventing bronchoconstriction. |
|
Cromolyn
mech and uses |
Prevents release of mediators from mast cells. Effective
only for the prophylaxis of asthma. Not effective during an acute asthmatic attack. |
|
Asthma drugs
7 different Tx drug classes |
1. Nonspecific β-agonists
2.β2 agonists 3. Methylxanthines 4. Muscarinic antagonists 5. Cromolyn 6. Corticosteroids 7. Antileukotrienes |
|
Cromolyn
toxicity |
Toxicity is rare.
|
|
Asthma drugs
name the corticosteroids |
Beclomethasone, prednisone
|
|
Asthma drugs
Beclomethasone, prednisone mech |
inhibit the synthesis
of virtually all cytokines. Inactivate NF-κB, the transcription factor that induces the production of TNF-α, among other inflammatory agents. |
|
1st-line therapy for chronic asthma.
|
Beclomethasone, prednisone
|
|
name the Antileukotrienes
|
Zileuton
Zafirlukast, montelukast |
|
Zileuton
mech and uses |
A 5-lipoxygenase pathway inhibitor. Blocks conversion of arachidonic acid to leukotrienes.
asthma |
|
A 5-lipoxygenase pathway inhibitor. Blocks conversion of arachidonic acid to leukotrienes.
|
Zileuton
|
|
Zafirlukast, montelukast
mech and uses |
Zafirlukast, montelukast––block leukotriene receptors.
Especially good for aspirin induced asthma. |
|
block leukotriene receptors.
|
Zafirlukast, montelukast
|
|
Especially good for aspirin induced asthma.
|
Zafirlukast, montelukast
|
|
Expectorants
names |
-Guaifenesin (Robitussin)
-N-acetylcystine |
|
Guaifenesin
aka |
Robitussin
|
|
Robitussin
aka |
Guaifenesin
|
|
Guaifenesin
mech and uses |
Removes excess sputum but large doses necessary; does not suppress cough reflex.
Expectorants |
|
Removes excess sputum but large doses necessary
|
Guaifenesin
|
|
Mucolytic → can loosen mucus plugs in CF patients.
|
N-acetylcystine
|
|
N-acetylcystine
mech and uses |
Mucolytic → can loosen mucus plugs in CF patients.
also used as an antidote for acetaminophen overdose |
|
antidote for acetaminophen overdose
|
N-acetylcystine
|