Pulmonology 5

zwinthrop's version from 2015-04-16 02:53


Question Answer
Define dyspnea.“uncomfortable awareness of one’s own breathing”→ Reflects imbalance btw current afferent/efferent neurological state and body’s “memory” of relationship.
What are the 3 primary symptom categories of dyspnea?(1) Air hunger or suffocation, (2) Increased effort or work of breathing, (3) Chest tightness.
What is happening neurally during dyspnea?Feedback loop. Mechanoreceptors--> Afferent: resp muscles sense tension/contraction and are innervated by the anterior horn cells of spinal motor neurons and project o somatosensory cortex. Efferent: Diaphragm innervated by phrenic nerves. Sensory Afferents from the lungs are transmitted via the vagus nerves to brainstem. All innervated by myelinated fibers of the vagus nerve, and unmyelinated vagal C fibers, present in the entire respiratory tract. Chemoreceptors in aortic arch stimulate neural output of CNS respiratory drive to increase rate/depth of respiration.
What dictates the intensity of dyspnea?The extent of the mismatch between the new afferent/efferent information and preexisting memory of the relationship between central respiratory drive and output determines the intensity of dyspnea. Magnitude of mismatch = intensity of dyspnea.
What are the 5 things included in the physiologic "differential" for dyspnea?(1) Increased work of breathing- Airway obstruction (3) Hypoxia (3) Hypercapnia (4) Metabolic Acidosis (5) Anxiety/Pain/Psychosomatic disorders.
For each of the following state what lung sound is heard, whether it is heard on inspiration or expiration, and why that is when it is heard- (1) An extrathoracic airway obstruction, (2) An intrathroacic large airway obstruction, and (3) An intrathoracic small airway obstruction.(1) Extrathoracic→ Inspiratory stridor. Larynx being pushed on by ambient pressure and pressure inside the airway. Exhale→ intrathoracic pressure > outer→ airway dilates → airflow moves out. When inhale→ airway pressure lower then ambient (negative pressure)→ airway contricts. Thus, partial blockage during inspiration, increased obstruction (collapse)→ inspiratory stridor.
(2) Intrathoracic- trachea/bronchi→ Expiratory stridor. Intrapleural pressure this time. When exhale, intrapleural pressure greater than ambient (to push on lungs). If large enough, intrapleural pressure can compress on lungs to cause sound. On inhalation, the airway pressure is greater then the intrapleural b/c air coming in. Keeps airway distended→ no wheezing.
(3) Intrathoracic- small airways→ expiratory wheeze. Same reason but in alveoli so hear wheez.
What are some examples of VQ mismatches?Pneumonia, pulm edema, pneumothorax, pulm embolism.
Name 6 ways hypoxia can lead to dyspnea.(1) Low FiO2 (altitude) (2) Shunt (Eisenmenger's) (3) V/Q mismatch (4) Alveolar Hypotension (5) IMpaired O2 transport (anemia) (6) Cheyne-Stokes Breathing (CHF).
A 45 yo male presents having awoken with headache and dyspnea. He is previously healthy, no signficant PMH. BP 130/80 P 120 R 24 T 37 SaO2 99%. He is somnolent but lungs are clear and he appears to be moving air well. Physical exam is otherwise unremarkable. (1) What test(s) might be useful? ABG: 7.44, 37, 77, 24, 93%. (2) The dyspnea is most likely due to? What other tests? Do carbon monoxide test with venous blood gas→CO% = 44%. (3) What does this mean?(1) EKG, radiograph (CXR), PFT (pulmonary function test), ABG (acid-base status), BMP (basalmetabolic profile). (2) Resp alkalosis due to pH and decreased PCO2/PO2.. HYPOXIA. Other tests: CBC, BMP, ABG, DLCO, CO test. (3) Carbon monoxide poisoning is cause of hypoxia.


Question Answer
Define hemoptysis.Expectoration of blood from the lower respiratory tract (larynx and down). Originally classified as mild (blood streaked sputum) to massive (100-1000ml of blood per 24 hours-no specific volume is universally accepted). Hemoptysis is NEVER normal
What is meant by the "Functional Definition of Hemoptysis?"Functional definition: Large volume of expectorated blood should not define “massive” hemoptysis, rather an amount sufficient to cause a life threatening condition for the patient is considered massive hemoptysis.
What is the cause of death from hemoptysis?Cause of death is ASPHYXIA rather than exsanguination→ Oxygenation issue not blood loss. Mortality rate from untreated massive hemoptysis is >50%
(1) What are the 2 arterial blood supplies to the lung? (2) Which one is the principle source of hemoptysis?(1) Pulmonary Arterial System (low pressure system-<10% of hemoptysis) and (2) Bronchial Arterial System (higher pressure- 90%).
What are the 6 most frequent diseases causing hemoptysis?Bronchiectasis, Tuberculosis, Fungal infection, Cancer, Arteriovenous malformations, Rheumatologic conditions.
What is the optimal workup for hemoptysis?CT scan and bronchoscopy
What do you do to initially manage hemoptysis?Stabilize bleeding--> position with BLEEDING SIDE DOWN--> minimizes spillover.
What do you do to stabilize MASSIVE hemoptysis?Preservation of oxygenation, Resuscitation of intravascular volume, Reversal of coagulopathies. PROTECTION OF THE NONBLEEDING LUNG. Identify bleeding source as soon as possible. Intubation strategies: bronchial blocker, or mainstem intubation of nonbleeding side, double lumen tubes have disadvantages. Bronchoscopic: Balloon tamponade of bleeding site–Iced saline lavage–Topical epinephrine or vasopressin–Laser therapy, electrocautery, cryotherapy of a visualized tumor or other lesion.

Radiology of the lung

Question Answer
What are the 4 categories of assessing radiograph adequacy?(1) Rotation: Asses by looking at spinous processes. Clavicular heads, clavicular and rib symmetry. Trachea and all anterior structures move to the side of rotation. Posterior structures move to the opposite side. (2) Inflation (Inspiration): Adequate Inflation: should see 9.5 posterior spaces above diaphragm, or 5-7 anterior ribs before diaphragm at mid clavicular line. (3) Exposure (Penetration): Must see vertebral endplates through heart. (4) Projection (AP or PA): Heart looks bigger on AP. Lung vessels sharper on PA. PA usually better exposed.
Run through the "systematic Approach."Heart, Mediastinum, Hila, Vessels, Lung Parenchyma (make sure spine gets progressively darker), pleura, bones, soft tissue, review.
What are the 3 features of Airspace Disease?(1) Cloud-cotton-like, fluffy opacities. (2) Air bronchogram sign- bronchi normally not very visible, air space disease in lung parenchyma surrounds air-filled bronchi rendering them visible-seen in ARDS. (3) Silhouette sign- outline occurs due to contrast btw air-filled lung parenchyma and soft tissue.
What are the features of interstitial disease?Linear, reticular, and/or nodular opacities--> sharper than airspace disease. Can usually see through abnormal lung.


Question Answer
Outline the cough reflex arc.(1) Receptors: chemical, mechanical, thermal, or inflammatory→(2) Afferent Nerve (Vagus)→(3) Cough Center (Medulla)→Efferent Nerves (Phrenic, spinal motor, recurrent laryngeal nerves) →Expiratory Muscles, Diaphragm, Laryngeal muscles, Abdominal muscles, Intercostal Muscles→COUGH.
Where do "volitional" coughs come from?Cerebral cortex.
What are C Fibers?Majority of bronchopulmonary vagal afferent nerves- unmyelinated C fibers. Conduction velocity <2 m/s. Distinguished from lung stretch receptors based on relative insensitivity to mechanical stimulation and lung inflation. High sensitivity to a wide variety of agents such as bradykinin, TRPV1 (capsaicin), TRPA1 (ozone, allyl isothiocyanate), prostaglandins, adenosine, serotonin, nicotine.
What are Widdicombe Cough Receptors?Subtype of myelinated vagal afferent nerves innervating the larynx, trachea, mainstem, and segmental bronchi. They are mechanically sensitive, capsaicin insensitive. Conduction velocity 5 m/s, faster than C-fibers but slower than lung stretch receptors (>/ 15m/s).
What is meant by "Nasal Afferent Regulation of Cough?"While nasal mucosa does not illicit cough (maybe sneeze), it is possible that rhinosinusitis stimulates nasal afferents which sensitize effect that lowers the cough threshold.
What is a pharynx initiated cough?Infusion of fluids into the pharynx can iniiate cough under certain circumstances. This seems to occur in settings where fluid is unexpected--if brain expects it, then no cough. This may be how cough is initiated with postnasal drip.
What is the "Arnold Reflex?"Small subset of people (<5%) can have cough initiated by stimulation of the tympanic membrane.
What are the 3 phases of coughing?. 1. Inspiratory phase. 2. Compression phase. 3. Expiratory phase: larynx opens and air exists. Intrathoracic pressures may reach 300 mm Hg and expiratory velocities approach 800 kilometers per hour (500 mph).
What are the 3 major causes of CHRONIC cough?1- Upper airways cough syndrome (UACS-post-nasal drip). 2- Asthma (cough-variant asthma). 3- Gastroesophageal Reflux (GERD).
What is Non Asthmatic Eosinophilic Bronchitis (NAEB). Only eosinophilic patho of asthma→ cough outside the U.S. found in 13-33%. In U.S. studies either an uncommon cause, or not a cause of chronic cough. Symptoms: Cough, Eosinophilic infiltration of the bronchial tree, Normal spirometry, Lack of bronchial hyperresponsiveness. Treatment: Resolution of cough and eosinophilia with steroid treatment. ACCP- Inhaled corticosteroids mainstay. lBTS- Follow asthma guidelines→ Except no role for LABA. Long term treatment may be necessary, Risk of progression to asthma, airflow obstruction
Describe clinical, patho, assessment, and treatment of UACS.Clinical: post nasal drip-dripping down throat, nasal discharge, mucoid drainage, cobblestoning. Patho: maybe actitation of cough receptors in hypopharynx/larynx.
Asses: rhinoscopy, sinus xray.
Treatment: Allergic Rhinitis-nasal corticosteroids, antihistamines (1st gen), leukotriene decongestant, Vasomotor rhintis-antihistamines; post viral URI-1st gen antihistamine and decongestant.
Describe clinical, patho, assessment, and treatment of ASthma induced CC.Clinical: no wheezing, nocturnal cough, post allergen exposure. Work-up: peak flow monitor, bronchodilator test, bronchoprovocation challenge (methacholine). Treatment: ICS+BA, leukotriene inhibitors
Describe patho, assessment, and treatment of GERD. What is the GERD-cough cycle, Silent GERD? Patho: may occur multiple levels, may irritate lower respiratory tract receptors or esophogeal bronchial cough reflex. GERD-cough cycle is when cough induces GERD episodes and GERD causes cough, so self-perpetuating. Silent GERD: Cough may be only sing of GERD. Tx: Omeprazole.
What is acute vs. sub-acute, vs chronic cough?<3 wk, 3-8 wks, >8 wks.
What are the 5 less common causes of cough?(1) Bronchiectasis-dilated damaged airways w/ impaired mucus clearance. (2) Tracheobronchial Foreign Body. (3) Arrhythmia induced- PVCs. (4) Obstructive Sleep Apnea (5) Psychogenic.