Exam 2 Flashcards
1-why learn lung path
2-broad classification of lung disorders
3-disorders in the airways
4-obstructive pulmonary disease
1- many of diseases occur in patients
- manage dental problems w/ special care
- empower you to help patients avoid
- some disease you can cause
2-disease affecting:
airways, interstitium, & pulm vascular system
3-atelectasis
acute lung injury (ARDS)
obstructive pulmonary diseases
4-emphysema
chronic bronchitis
asthma
bronchiectasis
1-Atelectasis
2-acute lung injury
3-acute respiratory distress syndrome ARDS
1-collapse
-loss of lung volume caused by inadequate expansion of airspaces
-shunting of inadequately O2 blood from
pulm arteries into veins
2-spectrum of pulm lesions
endothelial & epithelial
-acute dyspnea
-hypoxemia
-bilateral pulm infiltrates (radiographs)
-no evidence of primary l. sided heart failure
-non cardiogenic pulm edema
3-MEDICAL EMERGENCY
- rapid onset of life threatening resp insufficiency, cyanosis, & severe arterial hypoxemia
- 85% patients= clinical syndrome w/ 72 hrs of insult
- prognosis= grim…mortality rate=100%
- mortality now=60%
- chronic sequalae= diffuse interstitial fibrosis
- those who survive acute insult & dont develop chronic sequelae…norm function w/in 12 mo
- –common cause pneumonia & gastric contents
1-obstructive disease
2-restrictive pulm disease
1-diffuse pulm disease
- airway disease
- limitation of airflow—emphysema, chronci bronchitis, bronchiectasis, asthma
- FVC norm or slightly reduced
- *-dec FEV1= much more than FVC reduction
- FEV1/FVC = dec**
2-diffuse pulm disease
- reduced expansion of lung parenchyma
- *-chest wall disorders
- acute or chronic interstitial lung diseases**
- FVC reduced
- FEV1 norm or reduced proportionately to FVC
- FEV1/FVC = norm ratio
1-chronic bronchitis
2-bronchiectasis
3-asthma
4-emphysema
5-small airway disease, bronchioles
1-bronchus
- mucous gland hypertrophy/hyperplasia/hypersecretion
- tobacco, smoke, air pollutants
- cough / sputum production
2-bronchus
- airway dilation & scarring
- severe infections
- cough, prulent sputum, fever
3-bronchus
- SM hypertrophy, hyperplasia, excessive mucus, inflam
- immunologic
- wheezing, cough, dyspnea
4-acinus
- air space enlargememnt, wall destruction
- tobacco smoke
- dyspnea
5-bronchiole
- inflam scarring, partial obliteration of bronchioles
- tobacco smoke, air poluutants
- cough, dyspnea
Small airway diseases
1-emphysema
2-chronic bronchitis
3-asthma
1-alveolar wall destruction overinflation
2-productive cough
airway inflam
3-reversible obstruction
-bronchial hyperresponsiveness triggered by allergens & infections
1-emphysema
2-centriacinar
3-panacinar
4-distal acinar—paraseptal
1-**abnormal perm englargement of airspaces
- distal to term bronchioles
- destruction of alveolar walls w/o obvious fibrosis**
- enlargement when no destruction present= overinflation—opposite lung after unilateral pneumonectomy
2-in upper lobes of lung
- cigarette smoking
- no a1 antitrypsin
3-in lower lung
-a1 antitrypsin deficiency
4-adjacent to pleura, along lobular CT septa
- upper half of lungs
- *-cyst structures= bullae
- underlies spontaneous pneumothorax in young adults**
Emphysema Clinical Features
1-dyspnea
- weight loss over time
- *-reduced FEV1/FVC**
- pink puffers—pure emphysema & blue bloaters (chronic bronchitis)
- secondary pulm hypertension
1-chronic bronchitis
1-common in cig smokers & city dwellers
- 20-25% of men btween 45-60
- persistant productive cough for at least 3 consecutive mo in 2 consecutive years
clinically= cough & sputum production w/ no ventilation disturbance—
- chronic obstructive bronchitis/outflow obstruction
- severe may have COPD w/ cyanosis blue bloaters
- differntiated w/ emphysema- pink puffers
Complications= pulm hypertension & cardiac failure
-recurrent infections & resp failure
Asthma
- MED EMERGENCY
- recurrent episodes of wheezing, breathlessness & chest tightness
- clinical triad= intermittent & reversible airway obstruction
- chronic bronchial inflam & eosinophils
- bronchial SM hypertrophy & hyperreactivity
- extrinsic or atopic—70%, environental, IgE & TH2
- intrinis or non-atopic= 30%—non immune stimuli, aspirin, infections, cold, exercise
-path===th2 inflam response & airway remodeling
1-atopic asthma
2-asthma morph
3-asthma clinical
1-in childhood, fam history
- asthma attack by allergic rhinitis, urticaria, eczema
- environmental antigens
- skin test= wheal & flare type 1 hypersensitivity
2-gross= mucus plugs in bronchi & bronchioles
histo= curshmann spiral-whorls of shed epi
numerous eosinophils
charcot-layden crystals-crystalloids of eosinophilic proteins
-airway remodeling features in bronchial wall
3-dyspnea, wheezing, & difficulty expiration
- 1-several hours
- reduces spontaneously or after therapy
- intervening times normal
- paroxysm irrespnsive to therapy
- status asthmaticus—days or weeks
- hypercapnia, acidosis, hypoxia= fatal
Bronchiectasis
1-perm dilatation of bronchi & bronchioles= destruction of muscles & elastic tissues
- obstruction
- chronic infection= necrotizing/suppartive= s.aureus & k. pneumoniae
- one leads to the other
morph= affects lower lung lobs, bilaterally, vertical air passage
- dilated airways can be traced close to pleura
- normal airways= only upto 2-3 cm away from pleura
Bronchiectasis Clinically
1-severe, persistent cough
- mucopurulent, fetid sputum
- specks of blood & frank hemoptysis
- episodic, precipitated by infection
- clubbing of fingers
severe=
- widespread bronchiectasis
- ventilatory defects
- pulm hyperetnsion
-brain abscess & reactive amyloidosis
1-diffuse interstitial lung diseases
- *-restrictive, infiltrative
- reduced lung compliance, dyspnea, & hypoxia**
- chest radiographs= small nodules, ground glass shadows
-progressive= resp failure, pulm hypertension,
cor pulmonale
Idiopathic Pulm Fibrosis IPF
- cryptogenic fibrosing alveolitis
- agent unknown
- males > females over 60 yrs at presentation
- *-histologic—usual interstitial pneumonia=diagnostic**
- exclude other causes before calling idiopathic
Gross Morph= cobblestone of pleura & cut surface shows fibrosis (firm, rubbery white)
Histological= usual interstitial pneumonia—patchy interstitial fibrosis
-early & late lesions—temporal heterogeneity
-dense fibrosis—hoenycomb fibrosis
Idiopathic Pulm Fibrosis IPF Clinical
- insidious onset= non productive cough= progress dyspnea
- dry, velcro like—crackles during inspiration
- late stages= cyanosis, cor pulmonale
- surgical biposy—gold standard for diagnosis
- mean survival= therapy 3 years
- treatment= lung transplant
1-Pneumoconioses
2-sarcoidosis
1-inhaled mineral dusts & inorganic particulates
- coal duse= anthracosis-coal macules & coal nodules
- silica= silicosis—silicotic nodules & silica particles
- asbestos= effusions & plaques, lung/laryngeal cancers—asbestos bodies
2-multisystem disease—non caseating granulomas
- restictive lung disease
- *-diagnosed= exlusion= mycobacterial& fungal infections, berryliosis—granulomatous lesions**
- bilateral hilar lymphadenopathy
- 25% cases- eye + skin—erythema nodosum
- lung transplant needed
- no etiology—adults <40, danish & swedish, blacks
- interstitial & intra-alveolar—Th1 type CD4 T
- oligoclonal expansion of T cells
- Polyclonal hypergammaglobulinemia= B cells
- association with HLA-A1 & HLA B8—CD8
Disease of Vascular Origin
- pulm embolism
- hemorrhage
- infarction
- pulm hypertension
- goodpasture syndrome
- idiopathic pulm hemosiderosis
- wegener granulomatosis
1-Pulm Embolism
2-Pulm Hypertension
1-arise from deep vein thrombi in legs
- prolonged bedrest, CHF, high estrogen birth control
- –inc in pulm artery pressure & ischemia of downstream lung parenchyma
- diminished cardiac output= r. heart failure
- hypoxemia develops
2-norm pulm BP= 1/8 systemic BP
pulm hypertension BP= 1/4 systemic BP
-secondary to other causes
-idiopathic pulm hypertension
-pulm endothelial cell or vascular SMC dysfunction
-reduced production of vasodilators—NO, prostacyclin
-migration & growth factors for SMC
1-pulm infection
2-classification
1-infection of lung
- bronchopneumonia= patchy, multilobar, bronchioles
- lobar pneumonia= contiguous air spaces, consolidation
- anatomic distinction —based on pathogen
2-community acquired acute pneumonias—S. pneumoniae
- community acquired atypical pneumonia= mycoplasma
- nosocomial
- aspiration
- chronic
- necrotizing
- pneumonias in immunocrompised host
Community Acquired Acute Pneumonias
- mostly bacterial= after viral
- strep pneumoniae
- lobar or bronchopneumonia=latter at age
- aspiration of pharyngeal floras= lower & middle lobes
4 stages pre antibiotic= congestion, red hepatization, gray hepatization, & resolution
-early antibiotic treatment eliminates stages
- bronchopneumonia= patchy inflam, confluence to consolidation
- pleural involvement more in lobar
- complications= lung abcess, empyema, fibrosis, & infection—meningitis & arthritis
Community Acquired atypical Pneumonias
- gram staining of sputum
- blood cultures
- hemophilus influenza, catarrhalis, staph aureus, pseudomonas, legionella, klebsiella
- inflam reaction confined w/in walls of alveoli
- mycoplasma pneumoniae, chlamydia, & coxiella burnetti
1-nosocomial pneumonia
2-aspiration pneumoniae
1-hospital acquired
- chronic immune depression, immunodeficiency, prolonged antibiotic therapy
- mechanical ventilation= high risk
- **gram neg rods (enterobacteria & pseudomonas)
- staph aureus
- typically not s. pneumoniae**
2-debilitated patients
- *-unconscious anesthesia/repeated vomiting
- **aspiration of gastric contents
- partly chemicals (gastric)
- partly bacterial
- necrotizing/fulminant course, leading to death
1-lung abcess
2-chronic pneumonia
3-tuberculosis
1-formation of 1 or more large cavities
2-aerobic & anaerobic bacteria—latter common in abcesses
-pleural cavity—pneumothorax or empyema
-embolization of septic material= meningitis or brain abcess
-symptoms= bronchiectasis
2-localized lesion in immunocompetent patient
- bacteria= mycobacterium tuberculosis
- fungi
- HIV
- mortality 6% from TB alone
3-communicable franulomatous disease= m. tuberculosis
-centers of granuloma= caseous necrosis
- –parenchymal lesion & node= ghon complex
- –calcified parenchymal lesion & nodals= Ranke complex
1-secondary tuberculosis
2-fungal infections
3-pneumonia in immunocompromised
1-clinical= insidious & low grade fever in late afternoon, night sweat
- cough, mucoid, purulent sputum, hemoptysis
- pleuritic pain
- diagnosis= consolidation/cavitation in upper lobes of lung
- *-isolation of tubercle bacilii**
- non tuberculous mycobacteria= m. avium in HIV patients
2-histoplama, immitis, blastomyces dermatidis= dimorphic fungi
- *-isolated lesions= immunocompetent
- disseminated when immunocompromised**
- t cell mediated immunity
- diagnosis= identification of fungi in tissue
3-cytomegalovirus
pneumocystitis jiroveci
candida albicans
mucormycosis
cryptococcus sporidium
HIV
1-lung tumors
2-carcinoma of lung
1-lung common site for metastasized tumors
- benign= most common= hamartomas or coin lesions
- malignant= common bronchial epithelial carcinoma—95
- Ca lung = common cancer in western world
2-85% of patients die w/in 5 yrs
- localized disease 5 yr survival only 45%
- incidence in male reducing, females inc
- cig smoking= strong risk factor…casual relationship-peak incidence= 50s & 60s
Carcinoma of Lung
histo= squamous cell carcinoma
adenocarcinoma
small cell carcinoma
large cell carcinoma
- adenocarcinoma= greater than squamous cell carcinoma
- *-adenocarcinomas= more common in women & lifetime nonsmokers**
1-Small Cell Lung Cancer SCLC
2-Non Small Cell Lung Cancer NSCLC
3-carcinoma of lung path
1-metastasis at diagnosis
not suitable for surgery
chemo & radiation—Rb gene mutations
2-resistant to chemo & radiation
-suitable for surgical resection
p16/CDKN21—gene mutations common
-KRAS & EGFR= adenocarcinoma
3-genetic predisposition= P53, KRAS, EGFR
- environmental factors= cig smoking—squamous & asbestos (inhaled)
- not all people who smoke get cancer, nonsmokers can get it too
- environmental factors may trigger Ca in genetically predisposed
Carcinoma of Lung
1-squamous cell carcinoma
2-adenocarcionma
3-small cell lung carcinoma
4-large cell lung carcinoma
5-clinical of carcinoma of lung
1-men>women—stronger w/ smoking
- arise in main bronchi, spread to hilar lymph nodes
- slow distant spread
- cavitation, hemorrhage
- squamous metaplasia/dysplasia—>carcinoma in situ—>malig
- *-cytobrushings, biposy have keratin pearls—well differentiated**
2-arise centrally but maybe peripheral
- *grow slowly, but metastasize early**
- precursor may be atypical adenomatous hyperplasia AAH
- bronchioalveolar carcinoma= no destruction of alveolar structure
3-derived from neuroendocrine cells of lung
4-undifferentiated malig tumor
- large nuclei, prom nucleoli, moderate cytoplasm
- minimal squamous or glandular differntiation common
5-silent, insidious & spread fast
- chronic cough, expectoration
- hoarse voice, chest pain, superior vencaval syndrome, pericardial/effusion
- segmental atelectasis, pneumonitis
- metastatic
1-lesions of pleura
2-pleural effusion & pleuritis
1-secondary to parenchymal disease
-primary lesions= primary intrapleural bacterial infection &&& malig mesothelioma—(in parietal or visceral pleura—50% bc of asbestos)
2-transudate= hydrothorax due to CHF
- exudate= protein>2.9 gm w/ inflam cells=pleuritis
- transudates resorbed
- exudates = fibrosis & calcification
- principal cause of pleural exudate= suppurative pleuritis, cancer, pulm infarction, viral pleuritis
1-pneumothorax
2-hemothorax
3-chylothorax
4-malig mesothelioma
1-spontaneous & secondary
2-ruptured intrathoracic aorta aneurysm
& blood clots w/in pleural cavity
3-lymph fluid & tumors
4-rare cancer of mesothelial cells
parietal & visceral pleura
-50% cases in asbestos
-cig smoking & asbestos= inc risk for bronchogenic carcinoma but not for malig mesothelioma
- preceded by pleural fibrosis & plaque formation
- sheath of yellow-white, firm, gelatinous, layer around lung
- histo= epithelial, sarcomatoid, biphasic
- basis isnt clear
1-lesions of upper resp tract
1-acute infections
- common cold
- acute pharyngitis= mild pharyngitis= common
- –accompanied by tonsilits, suppuration= b hemolytic strep
- –coxsackie a virus= pharyngeal vesicles & ulcers
- –EBV = infectious mono
- acute bacterial epiglottis= h influenza
- acute laryngitis= tuberculous & cornyebacterium diphth
1-nasopharyngeal carcinoma
2-laryngeal tumors
1-link to EBV & high incidence in chinese
-invades locally, lymph nodes, metastaize to distant sites
-radiosensitive 5 yr survival rate, 50% even for advanced cancer
-histology= keratinizing squamous cell carcinoma
non keratinizing squamous cell carcinoma
undifferentiated carcinoma
- *2-hoarseness of voice**
- non malig tumors= vocal
- –laryngeal papilloma/squamous papilloma
- –multiple papilloma in kids= recurrent resp papillomatosis
- –caused by HPV 6 & 11
- –dont become malignant
-carcinoma of larynx= 2% all tumors
>40 yrs age
men to women= 7:1
60-75% glottic, 20-45% supraglottic, 5% subglottic
—environmental influences= all cases in smokers & alc & asbestos
—95% typical squamous cell lesions= rarely adenocarcinomas
-persistent hoarseness of voice
-can be cured= 1/3rd die
-infection of distal resp passages, metastasis, cachexia
