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1507 > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

1-why learn lung path

2-broad classification of lung disorders

3-disorders in the airways

4-obstructive pulmonary disease

A

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

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2
Q

1-Atelectasis

2-acute lung injury

3-acute respiratory distress syndrome ARDS

A

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
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3
Q

1-obstructive disease

2-restrictive pulm disease

A

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
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4
Q

1-chronic bronchitis

2-bronchiectasis

3-asthma

4-emphysema

5-small airway disease, bronchioles

A

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
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5
Q

Small airway diseases

1-emphysema

2-chronic bronchitis

3-asthma

A

1-alveolar wall destruction overinflation

2-productive cough
airway inflam

3-reversible obstruction
-bronchial hyperresponsiveness triggered by allergens & infections

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6
Q

1-emphysema

2-centriacinar

3-panacinar

4-distal acinar—paraseptal

A

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**
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7
Q

Emphysema Clinical Features

A

1-dyspnea

  • weight loss over time
  • *-reduced FEV1/FVC**
  • pink puffers—pure emphysema & blue bloaters (chronic bronchitis)
  • secondary pulm hypertension
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8
Q

1-chronic bronchitis

A

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

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9
Q

Asthma

A
  • 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

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10
Q

1-atopic asthma

2-asthma morph

3-asthma clinical

A

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
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11
Q

Bronchiectasis

A

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
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12
Q

Bronchiectasis Clinically

A

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

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13
Q

1-diffuse interstitial lung diseases

A
  • *-restrictive, infiltrative
  • reduced lung compliance, dyspnea, & hypoxia**
  • chest radiographs= small nodules, ground glass shadows

-progressive= resp failure, pulm hypertension,
cor pulmonale

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14
Q

Idiopathic Pulm Fibrosis IPF

A
  • 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

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15
Q

Idiopathic Pulm Fibrosis IPF Clinical

A
  • 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
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16
Q

1-Pneumoconioses

2-sarcoidosis

A

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
17
Q

Disease of Vascular Origin

A
  • pulm embolism
  • hemorrhage
  • infarction
  • pulm hypertension
  • goodpasture syndrome
  • idiopathic pulm hemosiderosis
  • wegener granulomatosis
18
Q

1-Pulm Embolism

2-Pulm Hypertension

A

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

19
Q

1-pulm infection

2-classification

A

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
20
Q

Community Acquired Acute Pneumonias

A
  • 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
21
Q

Community Acquired atypical Pneumonias

A
  • 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
22
Q

1-nosocomial pneumonia

2-aspiration pneumoniae

A

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
23
Q

1-lung abcess

2-chronic pneumonia

3-tuberculosis

A

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
24
Q

1-secondary tuberculosis

2-fungal infections

3-pneumonia in immunocompromised

A

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

25
Q

1-lung tumors

2-carcinoma of lung

A

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
26
Q

Carcinoma of Lung

A

histo= squamous cell carcinoma
adenocarcinoma
small cell carcinoma
large cell carcinoma

  • adenocarcinoma= greater than squamous cell carcinoma
  • *-adenocarcinomas= more common in women & lifetime nonsmokers**
27
Q

1-Small Cell Lung Cancer SCLC

2-Non Small Cell Lung Cancer NSCLC

3-carcinoma of lung path

A

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
28
Q

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

A

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
29
Q

1-lesions of pleura

2-pleural effusion & pleuritis

A

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
30
Q

1-pneumothorax

2-hemothorax

3-chylothorax

4-malig mesothelioma

A

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
31
Q

1-lesions of upper resp tract

A

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
32
Q

1-nasopharyngeal carcinoma

2-laryngeal tumors

A

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

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