Pulmonology, part 3 Flashcards
Pneumoconiosis/silicosis
Lung dz caused by inhalation of mineral dust.
Silicosis is caused by inhalation of dust containing crystalline silica
Pathophys of silicosis
Small particles are dangerous because they deposit distally in the bronchiole, ducts, and alveoli. The inflammation leads to fibroblast and collagen formation that leads to fibrosis
Other causes of pneumoconiosis
Asbestosis
Coal dust
Other chemical exposures
Occupation risk for pneumoconiosis
Mining or tunneling Quarrying Drilling Crushing stone Chipping Grinding/sandblasting Pottery or stone work Cement manufacturing Masonry
Tx of pneumoconiosis
Prevent exposure Quit smoking Immunize- flu and pneumococcal No known cure Lung transplant for severe pt Treat complications (airflow obstruction, cor pulmonale, resp failure)
Silicosis sx
SOB Fever Bluish skin at the earl lobes or lips As the dz progresses: Fatigue Extreme shortness of breath Loss of appetite CP Respiratory failure
Respiratory distress syndrome
Used to be called hyaline membrane disease
An acute lung dz caused by surfactant deficiency.
Seen in neonates <36 wks gestation and weighing <3 lbs
Prognosis of resp distress syndrome
Outcome has improved with use of antenatal steroids to improve pulm.
Maturity, early postnatal surfactant tx, and gentle techniques of ventilation to reduce barotrauma to the immature lungs
F/u of respiratory distress syndrome
Support IV nutrition within 24 hrs of birth once breathing is stabilized
Prevent hypothermia with a double-walled incubator
Start oral feedings with small feedings through an orogastric tube as soon as tolerated
Support circulatory status which may require blood transfusion
Start abx in all infants who present with resp distress at birth after BCx are drawn. D/c within 2-5 days if cultures are neg
Cause of immune compromise/fungal PNA
Candida
Aspergillus
Cryptococcus
Complications of fungal PNA
Disease dissemination to other sites
Blood vessel invasion, which can lead to pulmonary hemoptysis
Conditions that predispose pts to immune compromise/fungal PNA
Leukemia Lymphoma Bone marrow transplant Organ transplant Prolonged high-dose steroids HIV Congenital immune deficiency syndrome
Tx for immune compromise/fungal PNA
Amphotericin B- treat for Histoplasmosis, Coccidiodomycosis, Cryptococcosis, Candidiasis
-Then azoles after improvement
Itraconazole- treat Blastomycosis
When is viral PNA more common?
Childhood PNA
Elderly
What are the four most frequent viruses in PNA?
Influenza
RSV
Adenovirus
Parainfluenza
Presentation of viral pneumonia
Fever Chills Nonproductive cough Rhinitis Myalgias HA Fatigue
PE of viral PNA
Wheezes Crackles Increased fremitus Bronchial breath sounds Rapid antigen detection of viruses can be ordered along with viral culture
Tx of viral pneumonia
Tamiflu for influenza A and B
Ribavirin used for RSV PNA
Cidofovir is being studied for adenovirus
Ribavirin has shown some benefit with parainfluenza
What is the MC opportunistic infection in persons with HIV infection
Pneumocystis carinii pneumonia
Tx of PCP
Abx are primarily recommended and TMP-SMX has been shown to be as effective than IV abx
Mortality rate of PCP and tx duration
10-20% in pts with HIV infection
Tx with TMP-SMX is 21 days
Smear of PCP
Crinkled cyst with a crushed ping pong shape
Air entrance in pneumo
Air can enter the intrapleural space through a communication from the chest wall or through the lung parenchyma across the visceral pleura
When does primary spontaneous pneumo?
Secondary?
Occurs in people without underlying lung dz and in the absence of an inciting event
Occurs in pts with a wide variety of lung dz
What lung cancer accounts for about 85% of all lung CA?
Non-small cell lung CA
How is non-small cell lung cancer further divided?
Adenocarcinoma
Squamous cell carcinoma
Large cell carcinoma
Progression of non-small cell lung cancer
Often insidious, and it may produce no sx until well advanced
Small cell lung CA
A neuroendocrine carcinoma that is aggressive with rapid growth, early spread, but sensitive to chemo and radiation
Spread and consequences of small cell lung CA
Spread to adrenal glands and brain
Can also cause SIADH and the syndrome of ectopic ACTH production
Hx/PE of non-small cell lung CA
Most are asymptomatic in early stages Wt loss Only subtle findings on exam Check supraclavicular nodes Hemoptysis SOB Wheezing SVC obstruction Horner syndrome
Hx/PE small cell lung CA
95% asymptomatic at presentation SOB Cough Bone pain Wt loss Fatigue Neurologic dysfunction
RFs for lung CA
Quit smoking Asbestos exposure Radon exposure Chromium, nickel exposure Vinyl chloride exposure
Lung CA work up
CXR PA and lateral Sputum cytology Bronchoscopy Chest CT CBC with diff CMP PFT PET scan to determine metastasis
Tx/prognosis of non-small cell lung CA
Stage I and II: surgical resection then chemo
Stage III: Chemo radiotherapy and surgical resection
Stage IV: Cisplatin-based chemo. Surgical resection if solitary metastatic lesion along with resectable primary tumor
Prognosis: 5 yr survival rate 50-70% Stage I-IIA
Stage II_IV: 5-15%
Tx/prognosis of small cell lung CA
Cisplatin + etoposide Early stage I may benefit from surgical resection, then chemo Prognosis: Stage I-IIA: 40% Late stages: <5%
What types of pulmonary nodules are considered masses?
> 3 cm and are treated as malignancies until proven otherwise
Why do nodules need to be investigated?
To answer:
Is the nodule benign or malignant?
Should it be investigated with bx or observed?
Should it be surgically removed?
What constitute most benign nodules?
Adenomas and hamartomas
What does a nodule have to be to be identified on a CXR?
> 1 cm
