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Flashcards in Repiratory Tract Deck (70):


Inflammation of the nasal mucosa
Rhinovirus most common cause
Sneezing, congestion, runny nose (common cold)


Allergic Rhinitis

Type I hypersensitivity reaction (ex pollen) characterized by inflammatory infiltrate with eosinophils
assoziated with asthma and eczema


Nasal Polyp

Protrusion of edematous, inflamed nasal mucosa
Usually secondary to repeated bouts of rhinits
Also can be one of first signs of CF!!!!! and also seen in aspirin intolerant asthmatics


Aspirin Intolerant Asthma

Triad of asthma, aspirin induced bronchospasm, and nasal polyps



Benign tumor of nasal mucosa composed of large blood vessels and fibrous tissues classically seen in adolescent males that present with profuse epistaxis


Nasopharyngeal Carcinoma

Malignant tumor of nasopharyngeal epithelium associated with EBV and classically seen in african children or chinese men that often also present with enlarged cervical lymph nodes
Pleomorphic KERATIN+ epithelial cells in a background of lymphocytes


Acute Epiglottitis

Inflammation of the epiglottis usually due to Influenza b
High fever, sore throat, drooling with dysphagia, muffled voice, and inspiratory stridor



Croup. Inflammation of upper airway due to parainflueza virus
hoarse, "barking" cough and inspiratory stridor


Vocal Cord Nodule

Singer's Nodule
Nodule that arises on the true vocal cord due to excessive use.
Usually bilateral and presents with hoarseness


Laryngeal Papilloma

Benign papillary tumor of the vocal cord
Due to HPV 6 and 11.
Single in adults, multiple in children
Presents with hoarseness


Laryngeal Carcinoma

Squamous cell carcinoma arising from epithelial lining of the vocal cord
Alcohol and tobacco are risk factors but can also arise from a laryngeal polyp
Presents with hoarseness, cough, and stridor



Infection of the lung parenchyma
Occurs when normal defense are impaired (lack of mucocilliary elevator, no cough reflex, mucus plug)
Clinical features include: fever and chills, productive cough with yellow or rusty color, tachypnea, pleuritic chest pain (when breath in), decreased breath sounds, dullness on percussion, and elevated WBC
Diagnose with Chest X-Ray, sputum stain, or blood cultures


Lobar Pneumonia

Conolidation of entire lobe of lung.
Usually bacterial (strep or klebsiella pneumonia)
1) Congestion = congested vessels and edma
2)Red hepatization = exudate, hemmorhages, and neutrophils fill alveolar space turning lung from spngy to solid
3) Gray hepatization = degradation of red cells within the exudate
4) Recovery = Type II pneumocytes act as stem cells and divide to repair the lung



Characterized by pathy consolidation centered around the bronchioles.
Often multifocal and bilateral
Bacteria include (staph aureus, haemophilus influenza, pseudomonas aerginosa, moraxella catarrhalis, legionella pneumophilia)


Interstitial Pneumonia

Atypical in that it presents with diffuse interstitial infiltrates, minimal sputum production, mild fever, small cough)
caused by mycoplasma pneumonia, chlamydia pneumonia, Respiratory syncitial virus, CMV, influenza virus, and coxiella burnetti)


Aspiration Pneumonia

Seen in alcoholics and comatose
Usually due to anaerobic bacteria in the oropharynx (bacteriodes, fusobacterium, and peptococcus)
classically presents as right lower lobe abscess


staph aureus

2nd most common cause of secondary pneumonia
complicated by absecess or empyema (pus in pleural space)


haemophilus influenza

common cause of secondary pneumonia and pneumonia superimposed on COPD


pseudomonas aerginosa

see in CF patients


moraxella catarrhalis

Community acquired and superimposed on COPD


legionella pneumophilia

Community acquired and superimposed on COPD
best visualized by silver stain


mycoplasma pneumonia

Interstitial/atypical pneumonia
affects young adults (military recruits or college kids in dorms)
Complications include autoimmune hemolytic anemia (IgM against I antigen on RBCs cause cold hemolytic anemia) and erythema multiforme
Not visible on gram stain cus lacks cell wall


chlamydia pneumonia

Interstitial/atypical pneumonia
2nd most common cause of atypical pneumonia in young adults


Respiratory syncitial virus

Interstitial/atypical pneumonia
most common in infants



Interstitial/atypical pneumonia
See in posttransplant people receiving immunosupressive therapy


influenza virus

Interstitial/atypical pneumonia
see in elderly, immunocompromised, and preexisting lung disease
Also increases risk for superimposed S aureus or H influenzae bacterial pneumonia


coxiella burnetti

Interstitial/atypical pneumonia
atypical but with high Q fever.
See in farmers and verterinarians
is a ricketsial organism but does not cause typical skin rashand does not require a arthropod becuase it can survive as highly heat resistant endospore


Primary TB

Inhalation of aerosolized Mycobacterium tuberculosis
Results from initial exposure and leads to focal, caseating necrosis in lower lobeof lung and hilar lymph nodes that udnergoes fibrosis and calcification to form the "ghon complex"
Generally asymptomatic but will have a postive PPD


Secondary TB

reactivation in AIDS or elderly
Occurs at apex of lung where lymph drainage is poor and high oxygen tension
forms cavitary foci of caseous necrosis, may lead to miliary TB or tuberculous pneumonia
high fevers, night sweats, cough with hemoptysis, weight loss
Biopsy reveals caseating granulomas and AFB stain reveals acid fast bacilli


Sytsemic complication of TB

Meninges - meningitis at BASE of brain
Kidneys- sterile pyuria
Lumbar vertebrae - Pott disease



Group of diseases characterized by airway obstruction, lung does not empty air
decreased FVC, and even greater decrease in FEV1 (air breathed out in 1second)
Total loung capacity is usually higher as well


Chronic Bronchitis

Chronic productive cough lasting at least 3 months over a minimum of 2yrs.
Characterized by hypertrophy of bronchial mucinous glands (Reid index increases to >50%)
Clinically see productive cough, cyanosis (blue bloaters), and increased risk of infection and cor pulmonale



Destruction of alveolar air sacs due to either excess production of proteases or lack of alpha1 antitrypsin.
Get a loss of elastic recoil and collapse of airways during exhalation.
Clinically see
1)dyspnea and cough with minimal sputum
2) prolonged expiration with purse lips "pink-puffer"
3) weight loss
4) Increased anterior-poterior diameter of chest (barrel chest)
5) Hypoxemia from desturction of capillaries in alveolar air sacs)
6) cor pulmonale is a late complication


Normal handling of inflammation in the lungs

Inflammation in the lung normally leads to release of proteases by neutrophils and macrophages.
Alpha 1 antitrypsin neutralizes proteases
excessive inflammation or lack of A1AT leads to emphysema


Emphysema from smoking

Smoking introduces a lot of pollutants which leads to excessive inflammation and protease mediated damage
results in CENTRIACINAR emphysema mostly in UPPER LOBES


Emphysema from A1AT deficiency

Lack of antiprotease leaves air sacs vulnerable to protease mediated damage.
Liver cirrhosis may be present as mutant A1AT accumulates in ER of hepatocytes resulting in liver damage
Biopsy shows pink, PAS+ globules in hepatocytes
PiM is normal allele. PiZ is abnormal allele
PiMZ is susceptible to emphysema if smoke
PiZZ significant risk for panacinar emphysema



Reversible airway bronchoconstriction most often due to allergic stimuli and often associated with allergic rhinitis, eczema, and family history of atopy.
Presents with wheezing, dyspnea, productive cough with spiral shaped mucus plus = "Curschmann spirals" and eosinophil derived crystals = "Charcot-Leyden crystals.

Is a Type I hypersensitivity where
1) allergens induce TH2 phenotype in CD4+ Tcells --> TH2 cells secrete IL4(mediates class switch to IgE) IL5 (attracts eosinophils) and IL10 (stimulates TH2 cells and inhibits TH1)
2) Reexposure to allergen leads to IgE mediated activation of mast cells that release preformed histamine granules (vasodilation and increased vascular permeability) and generation of leukotrienes C4, D4, and E4 lead to bronchoconstriction, inflammation, and edema
3) Inflammation and release of major basic protein derived from eosinophils damages cells and perpetuates bronchoconstriction



Permanenet dilation of bronchiloes and bronchi due to necrotizing inflammation with damage to airway walls
Cuases include: CF, Kartanger syndrome defect in dynein arm in cilia), tumor or foreighn body, necrotizing infection, or allergic bronchopulmonary aspergilliosis

Presents with cough, dyspnea, and foul-smelling sputum
Complications include hypoxemia and cor pulmonale and secondary (AA) amyloidosis


Idiopathic Pulmonary Fibrosis

Fibrosis of lung interstitium with unknown etiology but likely related to cyclical lung injury; TGF-beta from injured pneumocytes induces fibrosis.

Present with progressive dyspnea and cough, fibrosis on CT (subpleural plaques progress to diffuse fibrosis with "honeycomb" appearance"


Drugs that can causepulmonary fibrosis

radiation therapy



Interstitial fibrosis due to occupational exposure
Alveolar macrophages engulf foreign particles and induce fibrosis


Coal Workers Pneumoconiosis

Carbon dust in coal minors.
Massive exposure leads to diffuse fibrosis
Associated with Rheumatoid Arthritis / Caplan Syndrome



Mild exposure to carbon results in collects on carbon-laden macrophages but not clinically significant



Seen in sandblasters and silica miners
Fibrotic nodules in UPPER lobes
Increased risk for TB
Silica impairs phagolysosome formation by macrophages



Beryllium miners and Aerospace workers
Noncaseating granulomas in the lung, hilar lymph nodes, and systemic organs
Increased risk for lung cancer
Resembles sarcoidosis



Construction workers, plumbers, and shipyard workers
Fibrosis of lung and pleura with increased risk for lung CARCINOMA and also mesothelioma
See Asbestos bodies = long, golden brown fibers with associated iron



SYSTEMIC disease characterized by NONCASEATING granulomas in multiple organs.
African American Females most commonly
Unkown etiology but likely CD4+ Helper T-Cells response to unknown antigen
Most commonly affects the hilar lymph nodes and lung
See characteristic stellate inclusions/asteroid bodies within giant cells of the granuloma
Can mimic sjorgen syndrome with granulomas in lacrimal and salivary glands
Present with dyspnea or COUGH, elevated serum ACE, hypercalcemia (due to increased 1-alpha hydroxylase activity of epitheliod histocytes converting vitamin D to its active form)


Hypersensitivity Pneumonitis

Granulomatous reaction to inhaled organic antigens (pigeo breeders lung).
Fever, cough and dyspnea after exposure and resolve with removal of exposure.
Chronic exposure however leads to interstitial fibrosis
see granulomas with EOSINOPHILS


Pulmonary Hypertension

High pressure in pulmonary circuit (>25mmHg)
Characterized by atherosclerosis of pulmonary trunk, smooth muscle hypertrophy of pulm arteries, and intimal fibrosis
Presents with exertional dyspnea and right sided heart failure


Primary Pulmonary Hypertension

Classically seen in young adult females
Etiology Unknown
Familial forms are related to inactivation mutations of BMPR2, leading to proliferation of vascular smooth muscle


Secondary Hypertension

Due to hypoxemia (close arteries to shunt blood elsewhere but increases pressure)
Increased volume in pulmonary circuit
Recurrent pulmoanry embolisms


Acute Respiratory Distress Syndrome

Diffuse damage to the alveolar-capillary interface
Leakage of protein rich fluid leads to edema and formation of hyaline membranes in alveoli
Presents with hypoxemia, cyanosis, (thickened diffusion barrier and collapse air sacs), and white out on chest x-ray
Activation of neutrophils induces protease and free radical mediated damage of type I and II pneumocytes
Ventilate with Positive End Expiratory Pressure(PEEP) to keep the alveoli open
Loss of Type II leads to scarring and fibrosis


Neonatal Respiratory Distress Etiology

Inadequate surfactant production by the Type II pneumocytes.
Surfactants normally decreases surface tension so increase leads to alveolar collapse and hyaline formation
Phophatidylcholine (lecthin) ifs the major component of surfactant

Presents as increasing respiratory effort, tachypnea with use of accessory muscles and grunting. See cyanosis and hypoxemia


Causes of Neonatal Respiratory distress syndrome

1)Prematurity = surfactant production begins at 28 weeks and not adequate until 34 weeks. Screen for lung maturity by looking at ratio of Phophatidylcholine (lecthin) to sphingomyelin. Lecthin increases while spoingo remains the same. Ratio > 2 means lungs are mature
2) C-section = lack of stress induced steroids hen have a c-section and these steroids increase synthesis of surfactant
3) Maternal diabetes = insulin decreases surfactant production


Complications of Neonatal Respiratory distress syndrome

hypoxemia can cause a persistent patent ductus arteriosus
hypoxemia can also make necrotizing enterocolitis more likely
Treatment with supplemental oxygen can cause retinal injury that can lead to blindness


Risk factors for lung cancer

Cigarette smoking, radon (formed by decay or uranium which is present in soil so can build up in basements), and asbestos


DDX for "Coin lesion" on x-ray

Granuloma = TB or fungus (especially histoplasma in Midwest)
Bronchial Hamartoma = beign tumor composed of lung tissue and cartiallage that often calcifies to appear on imaging


Treatment of Small cell vs non-small cell carcinoma

Small = chemo
Non-small = surgery


Small Cell Carcinoma

Poorly differentiated small cells arising from neruoendocrine (kulchitsky) cells
Male Smokers
Rapid growth and early mets
May produce ADH or ACTH
Cna also cause an Eaton-Lambert Syndrome = make autoantibodies against presynaptic calcium channels that leads to muscle weakness that improves with use


Squamous Cell Carcinoma

Keratin pearls or intracellular bridges
Most common tumor in male smokers
may produce PTHrP



Flans or Mucin
Most common in non-smokers or female smokers
Can involve the pleura


Large Cell Carcinoma

Poorly differentiated large cells
central or peripheral
poor prognosis


Brochilolalveolar Carcinoma

Columnar cells that grow along preexisting bronchioles and alveoli (arise from Clara cells)
no relation to smkoing
may present with Pneumonia like consolidation on imaging
Good prognosis


Carcinoid Tumor

well differentiated neuroendocrine cells that are chromogranin positive
not related to smoking
central (classically presents as a polyp like mass in the bronchus)
low grade malignancy


Mets to lung

Most common source is breast and colon
get multiple cannon ball nodules
more common than primary lung tumors


Examples of local extension of lung carcinoma

1) adenocarcinoma occurs on periphery and can involve the pleura
2) growth can obstruct the SVC and cause distended head and neck veins with edema and blue discoloration of the arms and face
3) Press on laryngeal nerve = hoarsenss
4) press on phrenic nerve = diaphragmatic paralysis
5) Compress sympathetic chain = pancoast/apical tumor = Hornerys syndrome = ptosis (drooping eyelid), miosis (pinpoint pupil), and anhidrosis (no sweating)


Where primary lung cancer might met to

Adrenal gland


Spontaneous Pneumothorax

Rupture of an emphysematous bleb, usually seen in young adults
Results in collapse of a portion of the lung
Trachea shifts TOWARDS the side of collapse


Tension Pneumothorax

Arises from a penetrating chest wall injury
Air enters the pleural space but cannot exit
Trachea is pushed AWAY from side of injury
Treat with insertion of a chest tube



Malignant neoplasm of mesothelial cells highly associated with asbestos exposure
Presents with recurrent pleural effusions, dyspnea, chest pain
Tumor encases the lung