Lung Flashcards
Community acquired pneumonia
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Hospital acquired pneumonia
Ok
Healthcare acquired pneumonia
Ok
Ventilator associated pneumonia
Ok
Aspiration pneumonia
Ok
Right factors PNA
Ok
Patient population susceptible to PNA
Ok
Aspiration PNA
Ok
Local pneumonia
Alveoli
CXR/CT-dense consolidation , air bronchospasm
US-consolidation , dynamic air broncograms
Micro of lobar
Strep pneumonia
Klebsiella pneumonia
Legionella
Bronchopneumonia
Bronchi
CXR/CT-Patchy opacities
US-Patchy B lines
May have consolidation
Micro of bronchopneumonia
Wide variety (mycoplasma, chlamydia, staph, pseudomonas
Interstitial pneumonia
Interstitial
CT/CXR-diffuse hazy opacities, septal thickening
US-patchy B lines, may have some consolidation
Micro interstitial pneumonia
Viruses, PJP, mycoplasma
Discuss preventative practices for CAP. What are contraindications
Ok
Two indices used to determine if a patient needs to be admitted to the hospital for PNA
Ok
Outline the following in regards to aspiration PNA and lung abscesses: risk factors, patient presentation, common causative agents, lab findings, imaging, and a generic empiric treatment plan
Ok
Orthomyxovirus PNA
Ok
Adenovirus PNA
Ok
H5N1 PNA 240, 250
Avian flu virus great risk for human pandemics
MPV PNA 303 -paramimyxoviridaevirus
Second most common etiology of lower respiratory infection in young.
Upper and lower respiratory tract infections-young kids and old adults
Slightly older as than RSV, 1 year vs 6 months
Winter early spring
Bronchiolitis, croup, pneumonia in kids
Old-cold
Reverse transcriptase PCR
Supportive treatment
Hantavirus PNA 299, 308 a bunyviridae
New Mexico, Arizona, Colorado, Utah
Influenza like followed by sudden respiratory failure, lot causing death
In previously health adults
Hemorrhagic fever with renal failure , pulmonary syndrome
Deer mouse-sin nombre south west USA
Pulmonary syndrome-high fever, muscle aches, cough, nausea, vomiting, rapid HR and RR< high WBC, low platelets, elevated RBC
Diagnosis-IgM and IgG to sin nombre
Lung capillary permeability leak-need intubation
40% die
Young adults flu like symptoms who develop pulmonary edema*** just supportive therapy
Define antigenic drift and shift, provide an example of each
Ok
Outline diagnostic and treatment methods for influenza. Include in you discussion: supportive care and neuraminidase inhibitors
Ok
Strep pneumonia morphology, metabolism, clincial presentation, diagnostics 33, 38
Capsule
Smooth S colonies cause rapid death in mice
R-no capsule -lost virluence
India ink stain -no taken up by capsule appears as a transparent halo around the cell. Usually for crypto coccus
Quelling reaction-mixed with antibodies to bind to capsule
Optichin sensitivity
Most common cause of pneumonia in adults
Sudden-shaking chills , high fevers, chest pain with respiration’s, and SOB, alveoli in one or more lung lobes fill up with white blood cells, bacteria and exudate. Seen as white consolidation
Cough up yellow green phlegm
Gram positive lancet shaped diplococci
Most common cause of otitis media in kids and most common bacteria meningitis in adults
Haemophilus influenza morphology, metabolism, clincial presentation, diagnostics 96 ,100
Rod negative
HACEK
Blood loving, blood again
Hematin found in blood is necessary for the bacterium’s cytochrome system. Blood also contains NAD needed for metabolism
B bad-nonencapsulated strains can colonize UR tract of kids and adults. They lack the virluence invasiveness of their encapsulated cousins and can only cause local infection . Cause otitis media and respiratory disease in adults with weaker prezinsting lung disease
-COPD GET IT worsens wheezing and SOB
Antibodies not in infants 6 mo-3 years, window
B-meningitis , acute epiglottis, septic arthritis, sepsis,
Vaccination
Moraxella 68,71
Neisseriaceae
Causes otitis media, and URI in patients with COPD or old
COPD exacerbation
Staph aureus 43, 46
Enterotoxin-lipases, penicillinase, staphylokinase, leukocidin, exfoliation, factors that bind complement. Hydrolyzes lipids, destroying penicillins, activates plasminogen to lyse fibrin clots, loses white blood cells, epithelial cell loses,
Klebsiella 75, 94
Ok
Pseudomonas 92, 94
Ok
Coxiella burnetti 120
Ok
Typical pneumonia
Strep p, HE< moraxella cat, klebsiella, pseudomonas, coxiella burnetti
Atypical bacterial pneumonia
Mycoplasma, chlamydia pneumonia’s, legionella pneuophilia, chlamydia psittacosaurus, burkholderia cepacia
Mycoplasma pneumonia 156, 158
Ok
Chlamydia pneumoniae 115, 122
Atypical bacteria TWAR, which is transmitted from perso to person by the respiratory route and causes an atypical pneumonia in young adults worldwide.
Taiwan and acute respiratory TWAR
Legionella pneumophilia 99-101, 102
Aerobic gram negative rod that is famous for causing an outbreak of pneumonia
Pontiac fever, legionnaires disease,
CAP, accounting for .2-10% of all admitted pneumonia cases
Local consolidation , but with fever with pulse temperature dissociation, (high fever, low HR), severe HA, confusion, myalgia, rhabdomyolysis, cough, hyponatremia, diarrhea,
Chlamydia psittacosaurus 115 122
Infects 130 species of birds
Human infected by inhaling chlamydia laden dust from feathers or dried out feces. This infection is an occupational hazard for breeders of carrier pigeons, veterinarians, and workers in pet shops or poultry slaughterhouse. Infection most commonly results in an atypical pneumonia called psittacosis, which occurs 1-3 weeks after
Burkholderia cepacia 93, 94-95
Gram negative rods in soil, water, plants, animals, lungs of CF, transmit on medical devices, hands of healthcare workers, between cystic fibrosis, oxidase positive, non lactose fermenter, antibiotic and disinfectant resistant
Pulmonary fungi
Aspergillus Histoplasma capsulatum Coccidiodes immitis Blastomycoses dermatidis -like Tb inhaled, primary infection int he lung, asymptomatic, mild, severe, or chronic lung infections, lung granulomas, calcifications and/or cavitation, can disseminate hematogenously to distant sites
Unlike-no person to person, fungi with spores not acid fast bacteria
Aspergillus 201, 2140215
Most common allergic bronchopulmonary aspergillosis, aspergillosis, invasive aspergillosis
Inhaling spores -ABPA, increase IgE, eosinophilia
Type IV,
Ppl with lung cavitation form TB can grow an aspergillus call called aspergillosis which needs surgery
Invasive-immunocompromised , bloody sputum may occur, due to blood vessel wall invasion by aspergillus hyphae (neutropenia after chemo or patients on highs teroids AIDS….multiple nodular infiltrateson chest CT, IgG mortality, voriconazole)
Mycotoxin-liver damage called AFLATOXIN…prob since grows in peanuts africa liver cancers
Histoplasma capsulatum 205-207, 212
Non encapsulated
Bird and bat droppings, (chicken cou)
AIDS disseminated \myxelial forms with spores at 25C, yeast at 37, no capsule,
Asymptomatic-most
Pneumonia-lesions calcific, which can be seen onc hest x ray (may look similar to tb)
Disseminated-can occur in almost any organ, espicially in the lung , spleen, or liver
Coccidiodes immitis 205-212
Mild pneumonia in normal southwest common in AIDS disseminated
Desert, respiratory transmitting
Mycelial forms at 25C, yeast at 37C
Asymptomatic most
Pneumonia
Disseminated-lints, skin, bones, meninges,
-erythema nodosum
Blastomycoses dermatidis 205-207
Soil, rotten wood, NOT MILD, weight loss, night sweats, lung involvement, skin ulcers, BBB
Mycelial forms 25 years 37
Asymptomatic-most
Pneumonia-lesions rarely calcify
Disseminated-present with weight loss, night sweats, lung involvement and skin ulcers
Cutaneous-skin ulcers
Harrisons 132 pneumonia Nd lung abscess,
101 influenza and other common viral respiratory infections
Ok
What is pneumonia
Infection of lung parenchyma, classified as community acquired (CAP) or health care-associated (HCAP)
HCAP
Hospital acquired and ventilator associated
Associated with current hospitalization for >48 h, hospitalization for > 2 days in the prior 3 months, chronic dialysis, home infusion therapy, home wound care, and contact with a family member who has multi drug resistant infection
How get pneumonia
Microorganisms gain access to the lower respiratory tract via microaspiration fromt he oropharyngeal (most common), inhalation of contaminated droplets, hematogenous spread , or contiguous extension from an infected pleural or mediastinal space
Before disease manifests, the size of the organism burden must overcome the ability of ___and other components of innate immunity (surfactant proteins A and D) to clear bacteria
Macrophages
Classic pneumonia presentation
Step p
Lobar pattern and evolves through four phases characterized by changes int he alveoli
Edema: proteinaceous exudates are present
Red hep-erythrocytes and neutrophils are present int he intraalveolar exudate
Gray hep-neutrophils and fibrin deposition are abundant
Resolution-macrophages are the dominant cel type
In VAP, respiratory bronchiolitis can __ a radiographically apparent infiltrate
Precede
Typical community acquired pneumonia
S pneumoniae, haemophilus influenza, staph aureus, and gram negative bacteria like klebsiella p and pseudomonas a
Atypical PNA
Mycoplasma pneumoniae, chlamydia pneumoniae, legionella, respiratory viruses (influenza, adenovirus, human metapneumovirus, RSV)
A virus may be responsible for a large proportion fo CAP cases that require ____, even in adults
Hospital admission
10-15% of PNA are ___
Polymicrobial
Combo of typical and atypical
When do anaerobes play a big role in CAP
Aspiration precedes presentation by days or weeks, often results in significant empyema
CAP epidemiology
> 5 million a year in US, 80% treated outpatient
> 55000 deaths annually
12 billion dollars
Who gets CAP most
<4 >60
Risk factors CAP
Alcoholism, asthma, immunosuppression, institutionalization, >70
Factors CPA
Tobacco smoke, copd, colonization with MRSA, recent hospitalization or antibiotic therapy-influence the types of pathogens that should be considered in etiology disease
Clincial manifestation CAP
Fevers, chills, sweat, cough, pleuritic chest pain, dyspnea
Nausea, vomiting, diarrhea, fatigue, HA< myalgia, arthralgias
Old patients with CAP presentation
Atypical, with confusion but few other manifestations
PE CAP
Tachypnea, increased or decreased tactile fremitus; dull or flat percussion reflecting consolidation and pleural fluid, respectively; crackles; bronchial breath sounds ; pleural friction rub
Diagnose CAP-want bc empiric tratment better for specific , also public safety implications
Chest radiography (need sensitivity and specificity not perfect from PE)
- CT for postobstructive PNA or suspected cavitary disease
- some radiographically patterns suggest an etiology (pneumatoceles suggest s aureus)
Sputum samples must have WBC>25 and <10 squamous epithelial cells per high-power field to be appropriate for culture. The sensitivity of sputum cultures is highly variable; in cases of proven bacteremic pneumococcal pneumonia, the yield of positive cultures form sputum samples<50%
Blood cultures are positive in 5-14% of cases, most commonly yielding s pneumoniae. Blood cultures are optional for most CAP pots but should performed for high risk pts (pts with chronic liver disease or asplenia)
Urine antigen tests for S pneumiae and legionella pneumophila type 1 can be helpful
PCR of nasopharyngeal swabs has become the standard for diagnosis of respiratory viral infection and is also useful for detection of many atypical bacteria
Serology: a fourfold rise in titer of specific IgM antibody can assist in diagnosis of pneumonia due to some pathogens; however, the time required to obtain a final result makes serology of limited clincial utility
What are the two sets of criteria that identify pts who will benefit from hostpail care
Pneumonia severity index
CURB-65
Complications CAP
Respiratory failure, shock, multiorgan failure, coagulopathy, and exacerbation of comorbid disease. Metastatic infection occurs rarely and requires immediate attention
-lung abscess may occur in association with aspiration or infection from single CAP pathogen (P. Aeruginosa).
Any significant pleural effusion should be tapped for diagnostic and therapeutic purposes.
Pleura effusion pH<7, glucose<2.2 LDH >1000 or if bacteria seen or cultured
Fluid should be drained, a chest tube is usually required
Follow up CAP
CXR abnormalities may require 4-12 weeks to clear. Pts should receive influenza and pneumococcal vaccines, as appropriate
Ventilator associated pneumonia micro
Potential etiology agents include MDR and non MDR pathogens; the prominence of various pathogens depends not he lengthof hospital stay at the time of infection
Epidemiology VAP
-26-52 cases per 100 pts, with the highest hazard ration in the first 5 days of mechanical ventilation
Three factors important in the pathogenesis of VAP
Colonization of the oropharynx with pathogenic microorganisms, aspiration of these organisms to the lower respiration tract, and compromise of normal host defense mechanism
Clincial manifestation
Are similar to those in other forms of pneumonia
Diagnosis VAP
Application of clinical criteria consistently results in overdiagnsis of VAP. Use quantative culture to discriminate between coloniazation and true infection by determining bacterial burden may be helpful; the more distal int he respiratory tree the diagnostic sampling, the more specific the results
What if use wrong treatment
Higher mortality rate
Treatment failrue VAP
Common, espicially MRSA, P aeruginos
VAP complications
Prolonged mechanical ventilation, increased length of ICU stay and necrotizing pneumonia with pulmonary hemorrhage or bronchiectasis. VAP is associated with significant mortality risk
Hostpital acquired pneumonia
MDR usually
Anaerobes may also be more commonly involved in non-VAP pts bc of the increased risk of macro aspiration in pts who are not incubated
Bronchiectasis etiology
Irreversible airway dilation that involves the lung in either a focal or a diffuse manner
Epidemiology bronchiectasis
Older age women
25-50% idiopathic disease
Vicious cycle of bronchiectasis
Susceptibility to infection and poor mucocele are clearance results in microbial colonization of the bronchial tree.
Noninfections bronchiectasis
Immune mediated reactions that damage the bronchial wall and parenchymal distortion as a result of lung fibrosis
Clinical manifestation bronchiectasis
Persistent productive cough with ongoing production of thick, tenacious sputum
Crackles and wheezing on lung auscultation and occasionally reveals clubbing
Acute exacerbations are associated with increased purulent sputum production
Diagnose bronchiectasis
Clincial presentation with consistent radiographically findings such as parallel tram tracks a signet ring sign, lack of bronchial tapering, bronchial wall thickening or cysts emanating from bronchial wall
Treat bronchiectasis
Control of active infection and at improving in secretion clearance
Lung abscess what is it
Necrosis and cavitation of the lung following microbial infection -can be categorized as primary )80%) or secondary; alternatively, it can be categorized as acute (<4-6 weeks in duration) or chronic (40%)
What causes primary lung abscesses
Usually arise from aspiration int he absence of an underlying pulmonary or systemic condition, are often polymicrobial (primarily including anaerobic organisms and microaerophilic streptomcin) and occur preferentially in dependent segments (posterior upper and superior lower lobes) of the right lung.
Secondary cloud abscesses
In setting of underlying condition (post obstructive process, an immunocompromised condition) and can be due to a number of different organisms among which P aeruginosa and other gram negative rods are most common
Clinical manifestations lung abscess
Similar to pneumonia.
Anaerobic lung abscess presentation
More chronic and indolent presentation, with night sweats, fatigue, and anemia, in addition, pts may have discolored phlegm and foul tasting or foul smelling sputum
Lung abscess from non anaerobic organisms (s aureus)
Present with a more fulminant course characterized by high fevers and rapid progression
Diagnose lung abscess
Chest CT is the preferred radiographically study for precise delineation of the lesion
Secondary lung abscess diagnosis
Sample collection (lovage, CT guided percutaneous aspiration) are recommended for secondary lung abscesses or when empirical therapy fails
Treat primary lung abscess
Clindamycin or amoxacilllin
Secondary lung abscess treat
Specific pathogen
When stop treat lung abscess
When cleared or small scar
Influenza A< B, C
Viruses RNA and orthomyxoviridae that have different nucleoprotein and matrix protein antigens
Major human influenza
A and B (morphologically similar)
A or B more severe
A
Influenza A subtypes by ___ and ____
Hemagglutinin(H) and neuraminidase(N) antigens
How does influenza infect
Attaches to Salic acid cel receptors via the hemagglutinin.neuraminidase degrades the receptor and plays a role in the release of virus from infected cells after replication
What is major determinant of influenza a immunity
H antigen antibodies
N antibodies
Limit viral spread and contribute to reduction of the infection
How influenza a acquired
Aerosolized respiratory secretions of acutely ill individuals and possibly by hand to hand contact or other personal or fomoterol contact. Viral shedding usually stops 2-5 days after disease onset
Epidemiology influenza A
Each year an vary in extent/severity
Winter. In temperate climates
Year round in tropics
Epidemics begins abruptly, peak over2-3 weeks, last 203 months, and then subside rapidly
Global pandemics
2009 A H1N1
Multiple locations, high attack rates, beyond normal seasonality patterns, and are duein part to the propensity of the H and N antigens to undergo periodic antigenic variation
Major changes
Antigenic shirt (INFLUENZa a only
Minor variations
Antigenic drifts
Avian influenza virus A/H51
Cause sporadic human cases, but sustained human to human transmission has not been observed; infection is linked to direct contact with infected poultry
Swine
Can sustain simultaneous infection with swine, human, and avian
Thesis multiple. Virus infections facilitate reassortment of genetic segments of different viruses.
Pandemic A/H1N1 virus 2009-2010
Quadruple reassortment among swine, avian and human influenza viruses
Interpandemic outbreaked
226,000 hospitalizations and 23,000 deaths per year in US. Chronic cardiopulmonary disease and old age are the most prominent risk factors for severe illness
Clincial manifestation influenza
Mild cold like, abrupt HA< fever, chills, myalgia, malaise
Deserves every within 2-3 days, but respiratoy symptoms accompanied by sub sternal pain can persist for >1 week. Postinfluenza asthenia may persist for weeks, particularly int he elderly
Complications influenza
Pneumonia and extrapulmonary
Common patients under 5 and over 65, pregnant women, or patients with chronic disease
Pneumonia from influenza
Primary influenza pneumonia is the least OMMonday but most severe of the pneumonic complications, most often affecting patients with mitral stenosis and pregnant-pts with progressive pulmonary disease and high timers of virus in respiratory secretions
Secondary bacterial pneumonia
Usually due to strep pneumoniae, strep aureus, or haemophilus influenza and presenters as the reappearance of fever ANS respiratory symptoms after 2-3 days of clinical improvement
Most common pneumonic complication involves aspects of viral and bacterial pneumonia
Extrapulmonary complications : Reyes’s, myositis, rhabdomyolysis, myoglobinuria, and CNS disease can occur as complications of influenza infection
Reye’s syndrome
Serious complication in children that is associated with influenza B virus (and less commonly wth influenza A virus), varicella zoster virus, and asprin therapy for the antecedent viral infection
Diagnose influenza
Reverse transcription PCR of respiratory samples
Rapid tests that detect viral antigens
Fast results, can distinguish influenza a and b viruses, and are relatively specific but variably sensitive
Serologic testing
Requires availability of acute and convalescent phase sera and is useful only retrospectively
Prophylaxis influenza
Annual vaccination with either an inactivated or a live attenuated vaccine is the main public health measure for prevention
How make vaccine
Strains are generated from influenza a and b viruses that have circulated during the previous influenza season and whose circulation during the upcoming season is predicted
Inactivated vaccines
50-80% protection against influenza is expected if the vaccine virus and the currently circulating viruses are closely related
Who gets influenza vaccine
> 6 months
Chemoprophylaxis against influenza
Should be reserved for individuals at high risk of complications who have had close contact with a pt sick with influenza. Chemoprophylaxis can be administered simultaneously with inactivated-but not with live-vaccine
Acute viral respiratory illness
> 50% of all acute illnesses; adults have 3-4 cases per person per year.
Clincial presentation acute viral respiratory illness
Not specific enough to allow an etiology diagnosis, and viral illnesses are typically grouped into clinical syndromes
Microbiology rhinovirus
Non enveloped, SsRNA viruses int he family picornaviridae that together are the major cause of the common cold
Epidemiology rhinovirus
Spread by direct contact with infected secretions, usually respiratory droplets
Clinical manifestations rhinovirus
After an incubation period of 1-2 days, pts develop rhinorrhea, sneezing, nasal congestion and sore throat that lasts for 4-9 days. Fever and other systemic signs and symptoms are unusual in adults.
-severe disease, including fatal pneumonia, is rare but has been described in immunocompromised pts, particularly bone marrow transplant recipients
Diagnose rhinovirus
PCR and tissue availbe, but not ususlal attempted
Treat rhinovirus
Symptom-antihistamines and decongestants
Coronovirus
Pleomorphic, SsRNA viruses
What coronavirus cause
Common cold SARS
Incubation period coronavirus and duration
3 days
6-7 days
2002-2003
Coronavirus SARS developed in >8000 pts in 28 countries and was associated with 10% fatality rate, no case since 2004
SARS incubation period and duration
2-7 days after which patients develop fever, malaise, HA< myalgia, and then a nonproductive cough and dyspnea
SARS patients can develop what in second week of illness
ARDS and multiorgan dysfunction
Middle East respiratory syndrome coronavirus
First identified in 2012 and has caused more than 1600 cases, with a 36% case fatality rate. All cases have been associated with contact or travel to the Arabian peninsula
-after an incubation period of 5 days, patients develop cough and fever that progress to respiratory failure
Diagnose coronavirus
ELISA, IF< reverse transcription PCR
SARS and MERS detected by R-PCR or viral culture of respiratory samples
Treat coronavirus
Common cold-symptom relief
SARS MERS-aggressive supportive care is most important . No specific therapy has been established as efficacious
Human respiratory syncytial virus
Enveloped SsRNA and a member of the paramyxoviridae
Epidemiology HRSV
With an attack rate approaching 100% among susceptible individuals, HRSV is a major respiratory pathogen among young children (2-3 months) and the foremost cause of owner respiratory disease among infants
-30-35% of hospital admissions of young children for pneumonia and for 75% of cases of bronchiolitis in this age group
Transmission HRSV
Contact with contaminated fingers or fomites and by spread of coarse aerosols. Incubation 4-6 days
Clincial manifestation HRSV
Infants typically develop rhinorrhea, low grade fever, cough, and wheezing; 35-40% of infections resul in lower tract disease, including pneumonia, bronchiolitis and tracheobronchitis
In adults HRSV typically presents as the common cold, but is can cause
Lower respiratory tract disease with fever, including severe pneumonia in patients who are elderly or immunosuppressed or who have cardiopulmonary disease. HRSV pneumonia has a case-fatality rate of 20-80% among transplant pts
Diagnosis HRSV
Rapid viral diagnosis available IF, ELISA, RTPCR of nasopharyngeal washes, aspirates or swabs
Treat HSRV
Symptom based for upper tract disease and mild lower tract disease
Incubation-if severe lower tract disease
Prevention HRSV
Monthly give palivizumab <3 years old who have bronchopulmonary dysplasia or cyanosis heart disease or who were born prematurely. In settings with high transmission rates, contact precautions are useful to limit spread of the virus
Human metapneumovius
Pleomorphic, single stranded RNA virus of the family paramyxoviridae
Epidemiology Human metaneumovirus
1-5% of childhood upper respiratory tract infections and for 2-4% of acute respiratory illnesses in ambulatory adults
Clincial human metapneumovirus
Disease manifestations are similar to those caused by HRSV
Diagnose human HRSV
IF, PCR< tissue culture of nasal aspirates or respiratory secretions
Treat human metapneumovirus
Supportive and symptom based
Parainfluenza virus
Enveloped SsRNA virus of the family paramyxoviridae ranks second only to HRSV as a cause of lower respiratory tract disease among young children and is the most common cause of croup (laryngotracheobronchitis)
Clinical manifestations parainfluenza virus
Infections are milder among children and adults, but severe , prolonged and fatal infection has been reported among pts with severe immunosuppression, including transplant recipients
Diagnosis paramyxoviridae
Infections are milder among children and adults but severe prolonged and fatal infection has been reported among pts with severe immunosuppression, including transplant recipients
Diagnoses paramyxoviridae
Tissue culture, rapid testing with immunofluorescence or ELISA (both of which are less sensitive) or PCR of respiratory tract secretions, throat swabs, or nasopharyngeal washing can detect virus
Treat parainfluenza virus
Treat URI symptom based.
For cases of croup with respiratory distress, intermittent racemis epinephrine and glucocorticoids are beneficial
Adenovirus
DsDNA virus 10% of acute respiratory infections among children and <3% of respiratory illness among civilian adults. Some serotypes are associated with outbreaks among military recruits. Transmission takes place primarily from fall to spring cia inhalation of aerosolized virus through inoculation of the conjunctival spaces, and probably via the fecal oral route
Clincial adenovirus
In children, causes upper and lower respiratory tract infections and outbreaks of pharyngojunctical fever
Adults-type 4 and 7 cause an acute respiratory disease consisting of a prominent sore throat, fever on the second or third day of illness, cough, Cory a, and regional adenoma they. Pharyngeal edema and tonsillar hypertrophy with little or no exudate may be seen
In addition to respiratory disease, adenovirus can cause diarrheal illness, hemorrhagic cystitis and epidemic keratoconjuctivitis. In patients who have received a solid organ transplant, adenovirus can affect the transplanted organ and disseminate to other organs
Diagnose adenovirus
Isolation fo the virus in tissue culture; by rapid testing of nasopharyngeal aspirates, conjunctival or respiratory secretions, urine, or stool, or by PCR testing
Treatment adenovirus
Supportive ribavirin cidofovir
Tb Harrison
Ok
Compare and contrast primary , progressice primary, latent and active Tb
Ok
Outline signs and symtpoms indicative of pulmonary Tb
Ok
Outline lab findings that are consistent with M Tb
Ok
Familiarize yourself with PPD skin testing, place emphasis on interpreting results, how the BCG vaccination affects PPD skin testing, and highlights false negative and false positive test results
Ok
Table 94-2
Ok
Describe imaging finding for primary Tb, active Tb, and Millard Tb
Ok
Define a nervy and discuss which patient populations are most likely to exhibit this phenomenon
Ok
Outline basic principles of anti Tb treatment, outline the 5 drugs used for the initial treatment of Tb . Include in your discussion potential side effects of each drug
Ok
In regards to monitoring treatment of TB, outline labs that are used to assess treatment progression and potential AE of medication
Ok
Define MDR-TB and XDR TB
List reasons for resistance
Mycobacterium TB
Acid fast
Mycotic acid, mycoside, cord factor , sulfatides, wax D MIKE WAX SURF CORD
Facultative intracellular growth in macrophages, cell mediated immunity, caseous necrosis
PPD skin test, type IV, (false positive BCG)
Mycobacterium Adium complex
AIDS-disseminated infection with fever, weight loss, hepatitis, and diarrhea
Immunocompromised-upper lung cavitary disease in elderly smokers, middle and lower lung nodular and bronchiectasis disease in middle aged femalenon smokes
Lymphadenitis-most commonly in kids
Mycobacterium kansaii
Gram positive acid fast, obligate aerobes, facultative intracellular organisms,
Pulmonary: upper lung cavitary disease
Disseminated disease in immunocompromised
Microbiology TB
Caused by organisms of the mycobacterium TB complex, which includes M Tb, most common and important agent of human mycobacteria disease, and M Boris, which is acquired via ingestion of unpasteurized milk. M Tb is a thin aerobic bacillus that is neutral on gram staining but that nice stained is acid fast. It cannot be decolonized by acid alcohol bc th cell walls high content of molecules acids and other lipids
Epidemiology TB
9 million new cases every year 1.5 million deaths-usually glow income, TB stable and falling worldwide
US T
HIV, immigrants, old, poor
MDR M TB
Resistant o at least rifampin and isoniazid and extensively drug resistant are increasing in frequency=480000 causes in 2013
How spread T
Droplet nuclei that are aerosolized by coughing, sneezing or speaking
<5-10 microV in diameter may be suspended in air for several hours
How determine intimacy of Tb and duration of contact with pt
Degree of infectiousness of the pt, and the shared environment
Cavitary or laryngeal disease
Most infectious, with as many as 10^5-10^7 acid fast bacilli in sputum
Risk factors for active TB
Recent acquisition, comobidity (HIV..), malnutrition, tobacco smoking, and presence of fibrotic lesions
Pathogenesis T
AFB that reach alveoli are ingested by macrophages. The bacilli impair phagosome maturation, multipl, lyse the macrophages, and spread to regional lymph nodes, reform which they may disseminate thought the body. Thesis initial stages of infection are generally asymptomatic and induce cellular and humoral immunity
2-4 weeks after Tb infection
A tissue damaging response resulting from delayed hypersensitivity destroys nonactivated macrophages that contain multiplying bacilli, and a macrophage activating response activates cells capable of killing AFB. A granuloma forms at the site of the primary lesion and at sites of dissemination. The lesions can then either heal by fibrosis or undergo further evolution. Despite helping, viable bacilli can remain dormant within macrophages or in necrotic material for years
______ confers partial protection against BT. Cytokines secreted by alveolar ___c ontribute to disease manifestations, granula formation and mycobacteria killing
Cell mediated immunity
Macrophages
Clinical T
Pulmonary, extrapulmonary or both
Extrapulmonary higher in HIV
Pulmonary TB primary disease
No or mild in contrast to prolonged disease course that is common in post primary or adult type
Primary Tb disease
Middle and lower lobes. Heal spontaneously, and calcified nodule (GHON FOCUS) remains
- transient hilar and paratracheal lymphadenopathy is common
- in immunosuppressed pts and children, primary disease may progress rapidly to significant clincial disease, with cavitation, pleural effusions and hematogenous dissemination (military)
Military disease
Hematogenous dissemination
Adult type TB
Initially with nonspecific and insidious signs and symptoms such as diurnal fever, night sweats, weight loss, anorexia, malaise, and weakness
- as progresses get cough, pursuant sputum with blood streaking, extensive cavitation may develop, with occasional massive hemoptysis following erosion of a vessel located int he wall of a cavity
- disease is usually localized to the apical and posterior segments of the upper lobes and superior segments of the lower lobes
Extrapulmonary T
Any site, usually lymph nodes, pleura, GU, bones, joints, meninges, peritoneum, and pericardium,
HIV and T
2.3 have extrapulmonary
Lymphadenitis T
35% extrapulmonary, esp in kids and HIV infected pts. Painless swelling of cervical and supraclavicular nodes (scrofula)
- nodes are discrete early on but can develop into a matter nontender mass with a fistulas tract
- fine needle aspiration or surgical excision biopsy of the node is requires for diagnosis. Cultures are positive 70=80%.
Pleural TB
20% extrapulmonary, from hypersensitivity response to mycobacteria antigens or contiguous spread of parenchymal inflammation
- pleural fluid is straw colored and exudative, with protein levels >50% of those in serum, normal to low glucose, and pH 7.3, and pleocytosis, the pleural concentration deaminase, of low, virtually excludes
- empyema is uncommon from rupture of a cavity with many bacilli into the pleural space. In these cases, direct smears and cultures are often positive, and surgical drainage us usually required in addition to chemo
GU T
Local symptoms predominate and 75% have a CXR with previous or concomitant pulmonary disease. Occasionally identified only after severe destructive lesions of kidney have developed.
- UA pyuria and hematuria with negative bacterial cultures
- mycobacteria culture of three morning urine specimens is diagnostic 90%
Weight bearing joints T
Most common spinal T(Potts)-often involves two or more adjacent vertebral bodies; in adults , lower thoracic/upper lumbar vertebrae are usually affected. Disease spreads to adjacent vertebral bodies, later affecting the intervertebral disk and causing collapse of vertebral bodies in advanced . Paravertebral cold abscess
Meningitis T
Kids and HIC,
1-2 weeks with paresis of CN, toward coma, with hydrocephalus and ICP high
-CSF can have high lymphocyte count an elevated protein level and a low glucose concentration. Cultures are positive in 8% of cases. PCR sensitive!!!!!
-glucocorticoids enhance survival
GI Tb
Can affect any portion of GI , ab pain, obstruction, hematochezia, palpable mass, peritonitis from ruptures lymph nodes
Pericarditis Tb
Acute or subacute onset of fever, dull retrosternal pain and friction rub, effusion common, chronic is potentially fatal,
Military disease
Hematogenous spread of M Tb through body. Small granulomas may develop in many organs. Hepatomegaly, splenomegaly, lymphadenopathy, and choroidal tubercles of eye
HIV associated TB
Partial Cell mediated compromised-typical upper lobe
Late HIV-diffuse interstitial or Millard infiltrate
Immune reconstitution inflammatory syndrome
1-3 mo after initiation antiretroviral, may exacerbate TB
Diagnose TB
AFB microscopy stained with Ziehl Neelsen basic fuchsin dyes of fluoresce microscopy of samples stained with auramine rhidamine-can provide a presumptive diagnosis in TB , two or three sputum samples need
Definitive diagnosis
Grow M Tb in culture or identification or the organisms DNA in clinical samples
-liquid media and speciation by molecular methods have decreased the time required for diagnostic confirmation 2-3 weeks
Nucleus acid amplification in AFB pos and neg
TST
Limited value active disease but mist widely used screening test for latent
Interferon gamma release assays
Measure the release of interferon gamma by T cells after stimulation with TB specific antigens and more specific for M Tb that TST
Prevent T
Vaccination
Treat latent infection
Tuberculin reaction size >5
HIV infected, recent contacts of a patient with TB , organ transplant recipients, persons with fibrotic lesions consistent with old TB on chest radiography, immunocompromised, persons with high risk medical conditions
Tuberculin reaction size >10 mm
Recent immigrants from high prevalence coutnries, injection drug users, mycobacteriology laboratory personnel; residents and employees of high risk congregate settings, children under 5, low risk
Leprosy
Nonfatal chronic infectious disease from m leprae, an obligate intracellular bacterial species indistinguishable microscopically from other mycobacteria. In humans, armadillos, and sphagnum moss
Can you culture M leprae
Not in vitro, has a doubling time in mice of 2 weeks
What is leprosy associated with
Poverty and rural residence, is a disease of developing world; its global prevalence is difficulty to assess and is variously estimated at .6-8 million
-400 in america
Transmission leprosy
Nasal drops maybe
Clinical leprosy
Polar tuberculoid to polar lepromatous disease is associated with an evolution from asymmetric localized Manuel’s and plaques to nodular and infuriated symmetric generalized skin manifestations, an increasing bacterial loss and loss of M leprae-specific cellular immunity.
Incubacliniincubation leprosy
2-40 years, usually 5-7
Tuberculoid leprosy
At the less severe end of the disease spectrum, TT leprosy results in symptoms confined to the skin and peripheral nerves ,
- one or several hypopigmented macules or plaques with sharp margins that are hypesthetic and have lost sweat glands and hair follicles are present. AFB are few or absent
- there is asymmetric enlargement of one or several peripheral nerves-most often the ulnar, posterior auricular, peroneal and posterior tibial nerves-associated with hypesthesia and myopathy
LL leprosy
Pts develop symmetrically distributed skin nodules, raised plaques and diffuse dermal infiltration that can cause leonine fancies, loss of eyebrows and lashes, pendulous earlobes and dry scaling
- numerous bacilli are present in skin, nerves, and all organs except the lungs and CNE
- nerve enlargement and damage are usually symmetric and due to bacillary invasions
Complications leprosy
Reactional states-immune mediated inflammatory states(can be deadly)
-erythema nodosum -painful erythematous papules that resolve spontaneously in 1 week
Extremities-neuropathy (insensitive to stuff, and LOSE distal digits as result),
Eyes-CN palsies, legophthalmos and corneal insensitivity may complicate …blindness
Nerve abscess-urgent surgery
Diagnosis TT
Biopsy, even in normal skin
Others not good
What are nontuberculous mycobacteria
Mycobacteria not Tb or leprosy
Miepidemiology NTM
Cause disease in humans only rarely unless some aspect of host defense impaired
Mainly M kansasii, MAC M abscesses
Clincial manifestations NTM
Broad
Dieesminated
Pulmonary disease
Isolated cervical lymphadenopathy
Skin and ST
Disseminated NTM
Rare, HIV, spread from bowel to the bone marrow and bloodstream, but disease is indolent, and it can take weeks or months for the pt to present for medical attention with malaise, fever, weight loss, organometallic, and lymphadenopathy, >3 organ systems should be evaluated for interferon y pathway defect
Pulmonary NTM
Industrialized
MAC in North America
Present with months or years of throat clearing, nagging cough, and slowly progressice fatigue. M kanassii can cause a TB like syndrome with hemoptysis, chest pain and cavitary lung disease
Isolated cervical lymphadenopathy NTM
Most common in kids in NA, MAC
Nods typically firm and painless and develop in absence of systemic symptoms
Skin ST NTM
Requires break in skin for introduction of organisms. Different NTM associated with exposures
M fortuitous
Lined to pedicure bath-skin abrasions has imediatde pedicure (like if shaved legs before pedicure)
M marinum
Acquires from fish tanks
M ulverans
Waterborne tropical and africa
Diagnose NTM
Acid fast or fluorocarbons smears of clincial samples and cultured on mycobacteria medium. Isolation of NTM from a clincial specimen may reflect colonization and requires an assessment of the organisms clincial significance
Isolation of NTM from blood specimens is clear evidence of disease; many NTM species require special media and not grown on blood culture medium
MAC
Two of three sputum samples, a positive lovage, or a pulmonary parenchyma biopsy with granulomatous inflammation or mycobacteria found on section and NTM in culture.
Antibiotic NTM
Clarromycin, MAC
Kansassi-rifampin
MAC
Macrolides bc MDR
Kansassi
Isoniazid.
M Mary I’m
Rifamycin treat extrapulmonary disease
Pulmonary htn
Describe the common cause of pulmonary HTN
Outline clinical findings of patients with pulmonary HTN, and describe the basis for assigning patients to a group
Describe common management principles in patients with pulmonary HTN
Medication induced pulmonary HTN
Fen-phen, the weight loss drug that suppresses appetites
Releases serotonin
Fatigue dizzy, SOB, primary pulmonary HTN, idiopathic pulmonary arterial HTN, heart valve disease, HF
Causes pulmonary HTN and heart disease
.smoker, normal vitals, but low O2 sat. , bibasilar inspiratory crackles. No wheeze or prolongation of the expirations phase, no neck vein distention. S4
Normal vitals but low o2, has crackles, has s4 gallop
Hypovascularoty peripheral
Right descending pulmonary artery
prominent central artery
RV enlargement
X ray of PAH
Peripheral hypovascularity, prominent central pulmonary artery (right and left prominent), right descending pulmonary artery, RV enlargement(see on lateral)-from increased workload
Classic PFT pulmonary HTN
May have features of primary cause -severe COPD low DLCO
Low diffusion capacity for CO….
Classis PAH with no DLCO
Normal PFT except isolated reduction in DLCO
ECG PAH
RVH, RV strain, RAD
Right axis deviation, right ventricular hypertrophy
May see peaking of p wave—-right atrial enlargement .
Echo PAH
Increased estimated PA pressure
RA enlargement
RV enlargement
Is pulmonary HTN common
Pretty common
Idiopathic uncommon
Treat pulmonary HTN
Treatment is the treatment of underlying disease
Idiopathic HTN is common?
No…specific therapies are changing very rapidly
Group 1 pulmonary HTN
Idiopathic and CTD
Group 2 pulmonary HTN
Heart
Group 3 pulmonary HTN
Lung
Group 4 pulmonary HTN
Pulmonary emboli
Group 5 pulmonary HTN
All others
Similarities between pulmonary HTN and ischemic heart disease
Both have exertional dyspnea, similar lack of associated symptoms, BNP elevated
Differences between pulmonary HTN and ischemic heart disease
P2 increased in PAH
CXR
Other studies-ECG, echo
-ischemic, congestion, Kelley b lines, increased vasc
May not see vascularity in pulmonary HTN
Functional assessment of PAH
Soo, how diagnose PH, how treat
6MWT
Serial testing
-echo, right heart cath
-echo, ekg large RA, RV, but need right heart cath over 40mmHg. P2 loud -idiopathic, vasodilator -other treat cause Stop med Oxygen-why do 6MWT
OSA history clues
Impaired daytime attention
-MVA, diffulty with memory, sleepiness
Snoring
Witnessed apnea
Mood alterations
-obese patients with depression must be screened for OSA
1/4 have complaints of this
Clincial findings OSA
Obesity, large neck circumference (short road), nasal obstruction( talk weird, short airway polyps and stuf congested), enlarged tonsils, narrow oropharynx, macroglossia, micrognathia, retrognathia
Can non obese people get OSA. How diagnose OSA
Yup
Sleep history from parter and patient, morning headaches, fat, postmenopausal women,
Need ****polysomnography(measures respiratory events and hours of sleep to derive the apneahypopnea index, which is the average number of apnea and hypoapnea events per hour >5 per hour confirms OSA) for diagnosis, may get electroencephalogram for sleep staging and assessment to accurately diagnose.
Manage OSA goals
Improve daytime sleepiness and cognitive performance, prevent long term sequelae
Improve mood and depressive symptoms, higher quality of life, lower incidence of traffic accidents, decrease daytime sleepiness
Improved quality of life
Tools to manage OSA
Lifestyle modifications, CPAP
Long term sequelae
Patients with moderatesevere OSA are
-four times more likely to die each year than non affected patients
- 2.5 times more likely to develop cancer
- four times more likely to have a CVA
——get serum TSHwith recent weight gain it may be elevated), chest x ray for heart failure, ECG for heart failure, COC secondary erythrocytosis can be a complication of severe OSA with hypoxemia, overnight oximetry , arterial blood gas to OHS),
Lifestyle modifications OSA
Obese? Lose 10% or more
Avoid etOH and sedatives 3-4 hrs prior to bed
Lateral decubitus sleeping position (keep airways from collapsing)
Intranasal steroids/decongestants-can help congestion
When give CPAP
If symptoms persist after modifications
Pneumatically props airway open
-increased intraluminal airway presssure and FRC-after modifications
Defer driving
Continuous positive atrial airway pressure ,
What is don’t adjust to CPAP
Bi-level PAP (BiPAP)
CPAP has one pressure level; BiPAP has separate pressures for inspiratory and expiratory phases…may improve comfort and adherence
Bi level positive airway pressure nasal ventilation or auto titrations positive pressure devices that modify airflow pressure to a more comfortable level.
Oral device OSA
Mandibular assist device
- can eliminate need for CPAP in mild/moderate cases
- protrudes the jaw and/or holds tongue forward to prevent prolapse
Upper airway surgery OSA
If cant use CPAP, resection of enlarged obstructing tonsils may be beneficial ,
-get fibrosis and things retract and enlarge more
Uvulopalatopharyngoplasty (UPPP)-Respect tonsils and adenoids, make small airway larger
- aleviate obstruction of the hypoglossal space.
- can remove obstruction to airflow
- patient selection important-many co factors involved
- most commonly done of a variety of surgical procedures to alleviate airway obstruction
Variable success
Do polysomnogram after surger or mandibular to see how it works
Obesity hypoventilation syndrome-fat bicarb 48(long term respiratory acidosis-lets try to compensate), non smoker, Hct up (RBC increased…reactive from hypoxemia), pulse ox down, edema, right parasternal lift, JVD, NON SMOKER probably not COPD
Pickwickian syndrome-fat boy breathing disorder
Too much CO3 and too little oxygen
Many have sleep apnea
Sluggish , depressed
Can mimic copD, but PFT demonstrate restrictive not obstructive
90% will have OSA
Risk of HF, hard to get
890% pickwinian have OSA, but restrictive defect rather than
Ondine curse-fell in love with man found out he was cheating so out curse on him so he was aware of his breathing so if he forgot he would die if sleep DIE
Symptoms obesity hypoventilation syndrome we need to do polysomnography!!!!!! Get ideas of what is going on and diagnose
decreased central respiratory drive
Restrictive chest , pulmonary HTN, hypoxemia,
Difficult airway, OSA
CAD, congestive HF
Difficult to position and bad vascular access
Man sleepy during day stops breathing at night, doesn’t use alcohol, stopped smoking eight years ago, is sedentary, OBESSE
He’s fat
Pink puffer
Emphysema thin burning so many calories as try to breathe
Blue bloater
Chronic bronchitis
Symptoms chronic bronchitis -a type of COPD-most have combo-productive cough 3 months for 2 years uncreas in volume of tissue in broncholar wall and accumulation of inflammatory exudate in the airway lumen
Cyanosis, crackles and wheeze, obesity, peripheral edema, CO2 retention, chronic productive cough, purulent sputum
Fat
CO2 narcosis,
Emphysema symptoms THIN-a type of COPD-most ppl have combo-permanent enlargement of airspace’s distal to the terminal bronchioles with destruction of the bronchiole walls without fibrosis-loss of elasticity
Minimal cough, tachypnea and increase minute ventilation , pink skin, pursed lip breathing muscles, barrel chest, decreased breath sounds, cachectic appearance
Increase end expiratory pressure keep from collapsing so pink, prominence of breathing musculature barrel chest
Cytokines, cachetic
Extrapulmonary COPD
Ischemic heart disease, HF< osteoporosis, diabetes metabolic syndrome, normocytic anemia, depression
Peripheral inflammation INFy, crp chronically elevated, serum amyloid a, surfactant up,
Skeletal muscle weakness and cachexia, at risk for lung cancer, ischemic HF, osteoporosis, metabolic syndrome
Also get chronic hypoxia and HB chronically elevated-secondary erythrocytosis**
Dyspnea scal 0-normal ppl
I only get breathlessness with strenuous exercise
Grade 1 dyspnea cycle
I get short of breath when hurrying on level grounf or walking up a slight hill
Grade 2 dyspnea scale
On level grounf, i walk slower than people of the same age bc of breathlessness, or I have to stop for breath when walking at my own pace on the level
Grade 3 dyspnea scale
I stop for breath after walking about 100 yards or after a few minutes on level ground
Grade 4 dyspnea
I am too breathless to leave the house or i am breathless when dressing
BODE-survival prediction,
BMI+airflow obstruction+dyspnea rating+exercise capacity (6 min walk test)
Higher worse
BMI>21
0 points
<21 1 point
—-why if don’t have as much lean Boyd mass it is a problem can affect mortality in this disease
FEV1>65% normal
0 points
FEV150-64%
1
FEV1 36-49%
2
FEV1<35%
3 points
^MWT >350 meters
0
6MWT 250-349 m
1 point
6MWT 150-249 m
2 points
<149 m 6MWT
3 points
0-2 points
80% 4 year survival
3-4 points
67%
5-6 points 4 year survival
57%
7-10 points
18% four year survival
Why get dyspnea in COPD
Increased dead space-increased PaCO2
Altered V/Q relationship-hypoxemia
Airflow obstruction-limits ability to meet increased demands
Reduced mechanical advantage of the diaphragm
-Hoover sign, accessory respiratory muscle use, paradoxical respiratory motion
Diaphragm flat so when breath it contracts and rams together out in periphery rib cage gets pulled in paradoxically,
Diaphragm doesn’t descend , get suck in rather than out
What Hoover sign is-
Normally tidal flow volume loops expand in both directions during exercise. I’m emphysema, the decreased expiratory time results in more air trapping and increases the FRC, shifting the tidal flow volume loop curves to the left, a phenomenon called
Dynamic hyperinflation
Asthma COPD similar
Weather may exacerbate
May have perennial symptoms
Exam-cough, sputum, wheeze, prolonged expiratory phase
Differences COPD asthma
Complete reversibility, may have seasonal variations , may have associated ENT allergic symptoms, usually younger at onset
Similarities COPD LVF
Progressive dyspnea, orthopnea
Exam-wheeze, cough, dyspnea
Differences LVF COPD
PND, history of heart disease,
Exam-crackles, edema, s3 gallop, JVD/HJR
Sama
Causes of COPD=a1at too much neutrophil elastase in lung destroy elastin early onset COPD, genes in detox of cig smoke, low birth weight, childhood, air pollution
Prevention-smoking stop causes bronchial mucous gland hypertrophy and goblet cell metaplasia with inflammatory cell infiltrate, squamous cell metaplasia, ciliary loss, SM prolif, …smoking cessation
Best prevent is stop prevent
Ium
Ipratropium
Saba
Screening-not recommended in not symptomatic
Screen early onset and strong family history of lung or liver disease for aat
Diagnose-sough, sputum production and dyspnea, smoking history, laryngeal height under 4 cm most predictive of copd
(Top of thyroid cartilage and suprasternal notch), hyperinflation, barrel crest, hyperresonant percussion , distant breath sound, prolonged expiration time, Cor pulmonar, neck vein distention,
Ol
Albuterol
LABA
Terol
Olodaterol
Lama
Ium
Tiotropium
ICS
Asone
Fluticasone
ICS
IDE
Budesonide
Metered dose inhaled (MDI)
Non breath activated-drug is released when you activate the inhaler
Breath activated-drug is released when you breathe
Dry powder inhaled or DPI
Single dose device-with a single dose the patient puts a capsule int he device
Multiunit device-dose built into the device
Multidose device-dose built into the device
Respiratory
Propellant free liquid inhaler creates a cloud
- proair respimat
- spiriva respimat
- siolto respimat
Mild and younger patients (FEV1>50% and age<65)
Doxycycline (macrolides may become the standard)
TMP-smx
Cephalosporin (ceftroxinme, cefdinir, cefopodoxine)
Advanced macrolides(azithromycin, clarithromycin)
Sicker older patient
Amoxicillin-clavulunate
Fluoroquinolones(Achilles tendon rupture)
Steroids
Prednisone, cheap, a range of starting doses
-1mg/kg, in practice adults are given 40-60mg/day
CHEAP
Methhylpredisolone-meh
Indications for supplemental O2
PaO2<56 or SpO2<89% measure twice over a 3 week period of time
PaO2>56<60 any time with evidence of
-pulmonary HTN, CHF, erythrocytosis HcT<55%
Gold I mild treat
SABA or SAMA prn; often together in same inhaler
FEV1/FVC <70% FEV1>80%
With or without chronic symtpoms
Gold II treatment
FEV1.FVC<70%; <50%FEV1<80%
With or without chronic symtpoms
LABA or LAMA
Need something take once or twice a day, every 12 hour basis
Add regular treatment with one or more LABA add pulmonary rehab
Gold III treatment severe disease
With or without chronic symtpoms
FEV1/FVC<70^; 30% FEV1<50%
ICS+LABA Ir ICS+ LAMA (never use ICS alone in COPD)
With or without either roflumilast or theophylline
Need to bring steroids in here. Use steroids wit LAMA or LABA. In COPD don’t just give steroid NEVER(acceptable in asthma but not acceptable in COPD)****
Add ICS if repeated exacerbations
Gold IV verysevere disease treat
FEV1/FVC<70%; FEV1<30% of predicted of FEV1<50% of predicted pluc chronic respiratory failure
ICS+LABA or ICS+LAMA or ICS+LAMA+LABA
With or without roflumilast or theophylline
As long term oxygen therapy if chronic respiratory failure; consider surgical
Pulmonary rehab
Exercise training, education, psychosocial training and support, nutritional support, breathing training, inspiratory muscle training and chest physical therapy, vaccination (flu, pneumococcal)
Helpful SOCIAL
Majority COPD
Smokers, former, a1AT-if young
Who should be evaluated for a1at
Unexplained dyspnea and cough
Young
Diagnose chronic bronchitis
Chronic productive cough some days for 3 months a year for 2 successive years without another explanation (blue bloater)
Emphysema-pink puddles
76 yo woman was fit now walks slower pace than ppl her age, episodic wheezing 70. Years. 9 year history of dyspnea , flattened diaphragm increased retrosternal space and barrel chest (increase AP) consistent with hyperinflation COPD
FVC 62%
FEV1 52%
FEV1 68%
Gold2
36 year old [rpgressive SOB-a1at
FEV 65%
FEV1/FVC 64%
GOlD moderate
MRD=1
Asthma-could be start at 6 Bronchiectasis sure CHF prob not Chronic bronchitis ok Emphysema Broad differential
LAMA/LABA -combination
Interstitial lung disease
DPLD-ILD-distal lung parenchyma on histopathology that is not COPD, lung malignancy, infections-always lung parenchyma, sometimes small airway, vasculature, and/or pleura—histo with inflammation and fibrosis vs granulomatous
Inflammation and fibrosis-epithelial surface injury inthe alveoli leads to spreading fibrotic change into the interstitial and vasculature, which can progress to interstitial fibrosis.
Can affect large lung area
Interstitial pleumonia vs idiopathic pulmonary fibrosis-
progression of interstitial changes over time in lung parenchyma, very difficult to reverse, can delay progression (reverse if hypersensitivity!)
Dyspnea, cough, crackles often describes as Velcro primarily developing in bases
Pan crackles, throughout all.
Digital clubbing (presence does not confirm and absence does not eliminate ILD) Exercise induced hypoxemia
PFT_reduced FRC, TLC normal, FEV1/FVC ration Normal, low DLCO
ILD FVC
Clincial diagnosis-history, physical, lab, imaging,
Progressive dyspnea:reduced exercise tolerance, and a persistent dry cough should raise DPLD . Some gradual usually-look for causes!!
50%
FEV1 ILD
50%
Restrictive! 8590% FEV1/FVC ration
FEV1/FVC ILD
90% predicted
FRC ILD
45%
RV ILD
35%
TLC ILD
65%
DLCO ILD
20%
Causes ILD
Drug
Inorganic dust-asbestosis, silicosis, coal workers, pneumoconiosis, berylliosis
Lymphangitis metastases from solid tumors
Hypersentivity pneumonitis-cat, med
Radiation
Idiopathic pulmonary fibrosis-often occurs in patients over 50 but interstitial lung disease associated with connective tissue disease, sarcoidosis, lymphangioleiomyomatosis, and langerhan cell histiocytosis usually occurs 20-40
Smoking associated
CT associated-erythema nodosum
Sarcoidosis-noncaseating granuloma-erythema nodosum,
History ILD
Radiograph-increased interstitial reticular or nodular infiltrates, often into e bases but the distribution can vary.
Smoking sure-usually COPD but can be
Occupation, hobby, environmental, travel, drugs both ex and non
Evaluation ILD
Chest ct-can often lead to a specific diagnosis
Pft
Ana and RA—-may be informative associated with sarcoidosis and CT
Scleroderma
Scleroderma
-pulmonary fibrosis-fibrosis
Pulmonary HTN-concentric fibrosis of the vessels
Aspiration-esophageal disease
Can be complaints in all
RA
Causes Interstitial pulmonary fibrosis
Bronchiectasis
Pulmonary rheumatoid nodules
Pulmonary vasculitis
*Pleural disense-very low pleural glucose is characteristic
SLE
Cause Interstitial lung disease
Extra-pulmonary restriction-shrinking lung syndrome
-decrease in all volumes over time, poorly Underwood and described
Pulmonary HTN
Pleural disease
Autoantibodies in scleroderma
High resolution CT_evaluare DPLD for distribution
-lab look for CT
Anticentromere: 20-40%
SCL-70; 30-70; more common in ILD
Antinucleolar:10-20% but predicts the worst prognosis
Autoantibodies in sle
Basal-IPF, asbestosis, NSIP
Upper lobe-hypersensitivity , sarcoidosis, silicosis
Peripheral-IPF, chronic eosinophilic pneumona, cryptogenic organizing pneumonia
Central-sarcoidosis, pulmonary alveolar proteinosis
Mosaic attenuation-small airways disease
DsDNA:550-75% (nephritis)
Ana:90-95%
Ro/la:60%/20%
Histone>90% drug induced SLE
Smith:10% white (30% aa and chinese)
Lupus anticoagulant : 20-30%
Drug and radiation induced lung disease
Bleomycin, bulsufan -treat patients with germ cell tumors causes drug induced lung disease
Bulsulfan-causes restrictive lung disease bulsulfan lun
PD1, PDL1 inhibitors -restore bodies immune competenance
Chemotherapeutic agents-largest category
Amiodarone-cardiac antiarrhythmic agent dose related, dose related
Nitrofurnation-antibiotic commonly used for UTI
Radiation induced
Radiation induced lung disease phases
PFT of DPLD-decreased volumes of all and decreased diffusing capacity
Early-1-3 months after
-acute
Late phase 6-12 months
-related end effect causing chronic fibrosis
Radiation recall reaction-more pneumonitis when had radiation disease occurs and u get rechallenged with something else
With newer radiation techniques it is less common
Inorganic dusts
Lung biopsy-sometimes required to confirm a diagnosis
Smoking-respiratory bronchiolitis interstitial lung disease, desquamative interstitial pneumonitis and langerhans cell histiocytosis
CT_RA, progressice systemic sclerosis, sjorgen-autoimmune or complication like aspiration. NSIP. Focus on CT disorder treat and prevention of reflux
Asbestosis, silicosis, coal, berylliosis
-decades after exposure,dyspnea on exertion, dry cough, exercise intolerance. Increase in basilar and subpleural bilateral linerar interstitial markings . Pleural plaques which are often calcified. Restriction
Acute form of hypersensitivity pneumonitis
*granulomatous
Put on antiviral and don’t get better….maybe something more going on
HIStoRY OF EXPOSURE
Can present as flu like. But most often occurs over time chronic.
Crackles, leukocytosis
Abrupt onset of dyspnea, cough, fever, with or without myalgia
CXR pulmonary infiltrates
Remove from agent
Chronic hypersensitivity oneumonitis
*granulomatous
Pulmonary fibrosis
IDL similar CHF
CHF and ILD-dyspnea, hypoxemia, similar chest x ray, crackles In base, pulm HTN
History difference,
Progressive dyspnea, exercise induced hypoxemia, cxr similar infiltrates
Exam crackles in base, may have evidence of pulmonary htn
Differences ILD versus CHF (LVF)
Idiopathic pulmonary fibrosis-poor prognosis, dyspnea on exertion, exercise intolerance, dry cough, crackles on inspiration, imaging shows lower lung zone and subpleural linear reticular markings, volume loss, honeycomb and traction bronchiectasis. UIP on histo. No trat. Poor. Evaluate exacerbation for infection or treatable things.
Some specific history differences in onset and details
CXR and ct have specific differences
Differences
-clubbing, edema, s3 in LVF
Ild different from copd
More rapid decline, cough non productive
Copd different from ild
Slower decline with more frequent exacerbations
Weather and nsaids worsen symtpoms
Productive cough
Treat ILD
Remove or treat cause
Corticosteroids remain the mainstay or treatable non IPF causes
-meh
Idiopathic pulmonary fibrosis ONLY
- pirgenidone-antifibrotic and anti inflammatory-specific action is unknown
- nintedanib-tyrosine kinase inhibitor target inflammatory and profibrotic factors
Acute interstitial pneuma (Amman rich)
BAD
Idiopathic interstitial lung disease that is clinically characterized by sudden onset of dyspnea and rapid development of respiratory failure
Histologically characterized by diffuse alveolar damage with subsequent fibrosis
Very fast
Ham man rich
Rare, all age group, diffuse symmetrical bilateral **
AIP not IPF (hamman rich)
Occurs in all age, mainly adults
No specific etiology
Pattern is diffuse, symmetrical and bilateral
NEED BIOPSY
Abrupt onset with flu like symptoms biopsy establishes diagnosis
IPF not AIP
Occurs almost exclusively in adults
Often relatable to prior causative exposure
Pattern is often asymmetrical and favors upper or lower lobes**** tends to favor upper or lower ASYMMETRICAL
Granular onset, afebrile
Diagnosis based on history/clincial findings, imaging, and PFT, biopsy optional
Don’t usually biopsy
Sarcoidosis
-splunkers caves silicosis and bat poop can get hypersensitivity pneumonitis as result of hobby.
Chronic hypersensitivity-continued inhalation
Respiratory bronchiolitis associated interstitial lung disease-present ina cuticle smoker micronodular disease
Most asymptomatic of mild disease
Often found incidentally on chest radiograph
Bilateral hilar adenopathy!!!! Sarcoidosis
Symmetrical chest x ray
Chest c ray i fairly symmetrical (not so with chest CT)
In a small number of ppl can be devastating disease and can lead to severe disability and death
Prednisone is treatment of choice
Key to work up of chronic dyspnea
Dyspnea years-parasternal/lift heave and persistent split S2 -pulmonary HTN and ventricular hypertrophy right.
-not hyperinflated, restrictive, diffuse reticulat infiltrate upper lung zone. Hypersensitivity interstiital lung disease
Woman -6 month, SOB stairs, 32, shin lesion-sarcoidosis typical to have fever, painful red bumps 6 months ago (erythema nodosum), nodules, granulomas, blacks, Hillary adenopathy, cough dyspnea, chest heaviness, fever hilar adenopathy, interstitial infiltrates (nodular peribronchial), or patchy alveolar. NONCASEATING, nodular,
Detailed history approached in a systemic way to guide the search for the underlying cause in an efficient manner
Thoracentesis can be deferred
Organizing pneumona=small airway bronchiolitis with granulation tissue. CLINCIALLY flu like illness and has a radiographically appearance with peripheral opacities that change over time, among other findings when a proximate cause is identified, this syndrome is BOOP
-65 yo granular progressive SOB present with exertion occasionally productive cough 30 pack history ,shipyard asbestosis …chipper exposed to more
Clubbing , restrictive, posterior crackles. Pleural plaquesw thi asbestosis on parenchyma PLEURAL PLAQUES…asbestosis.
What do????? No further testing diagnosis made. Classic example of asbestosis in shipyard worker
In patients with a small amount of pleural fluid and associated heart failure, pneumonia, or heart surgery (<1cm thick on decubitus radiography or ultrasonography)
Pleural fluid amylase
Should be measured only when pancreatic disease, esophagealrupture, or malignancy is considered
Omalizumab
Binds IgE and reduce exacerbations in patients with severe persistent asthma who have evidence of allergies.
Side effect omalizumab
Anaphylaxis
Expensive
Select patients who remain symptomatic despite other therapies
Smoking cessation
Most clinically effective and most cost effective way to prevent and slow the progression of chronic COPD and improve disease related survival
Screening for airway obstruction
In asymptomatic patients is not recommended as there is little evidence that making the diagnosis in setting
Metered dose inhaler
With proper instruction and good technique, is as effective as a nebulizer
Home tests
May be inaccurate
Pulmonary arteries
Deliver mixed venous blood from the RV to the pulmonary capillary alveolar membrane where gas exchange occurs, while the bronchial directly from the aorta.
Primary cause of pulmonary HTN
> 25mmHg MAP during rest
Conditions causing elevation of left sided heart filing pressures or pulmonary disease(treat underling cause)
Clincial findings pulmonary HTN
Mortality, morbidity,
Group 1-restricted flow through pulmonary vasculature with elevation vascular resistance
Fatigue, dyspnea with exertion , palpitations,
Advance-RV decompensation, including syncope, edema, ascites, and hepatomegaly, left parasternal lift, increased jugular a wave and pulmonic component of S2 , murmurs of tricuspid regurgitation or pulmonic insuffiency, RV s3 or s4
Diagnose PH
Ok
Common management principles in patents with pulmonary HTN
For condition
Treat I PAH mPAP>25 and PCWP<15
Idiopathic , heritable BMPR2, ALK1, enfolding with or without hereditary hemorrhagic telangiectasia
Drug and toxin induced
Associated with ct diseases (scleroderma), HIV , portray HTN, congenital heart disease, schistomiasis, chronic hemolytic anemia
Type II
Pulmonary veno occlusive disease and/or pulmonary capillary hemagiomatosis
Systolic dysfunction
Distaolic dysfunction
Valvular disease
MPAP>25 PCCWP up
Left sided heart
Type III
Secondary lung disease and/or hypoxia mPAP>25 with underlying lung disease
COPD, ILD< pulmonary study, sleep disordered breathing, alveolar hypoventilation, high altitude
Type 4
Chronic thromboembolic pulmonary HTN
Secondary unclear or multifactorial causes
Hematologic disordersL myeloproliferative disorders, sickle cell
Systemic disorders: sarcoidosis, pulmonary langerhans cell histiocytosis, vasculitis
Metabolic disordersL glycogen storage disease, gaucherie, thyroid
Others: tumor obstruction, fibrosing mediastinitis, chronic kidney failure on dialysis
Ph persist even with treatment
Ugh
OSA symptoms
Habitual snoring, witnesssed apnea, nighttime awakening with grasping or choking, insomnia, nighttime diaphoresis, ED, daytime fatigue or sleepiness, alterations in mood, neurocognitive decline
Physical finding osa
Fat, large neck circumference, nasal obstruction, enlarged tonsils, narrow oropharynx, macrflossia, retro or micrognathia
Testing OSA
Polysomnography-test of choice
Reduced channel polysomnography-sensitivity 80-85%, less expensive and less accurate than polysomnography but may offer increased access to diagnosis
Overnight oximetry-sensitivity 90% specificity 65% overnight ocimetry is not an accurate OSA
Serum TSH-obtain with recent weight gain increased in 2-3%
CBC_secondary erythrocytosis can be a complication of severe osa with accompanying severe hypoxemia
CXR-obtain if coexisting heart failure is suspected based on physical exam. HF can be a complication
ECG-obtain if coexisting heart failrue is suspected based on PE
Arterial gas-if obese hypoventilation syndrome is suspected to look for hypercapnia and hypoxemia
Differential OSA
Central sleep apnea
Upper airway resistance syndrome Periodic limb movements of sleep Narcolepsy COPD Restrictive GERDsinusitis HF Epilepsy’s Sleep deprivation or short sleep schedule
Hypothyroidism
Acromegaly
Treat OSA goals
Improve daytime sleepiness and cognitive performance and to prevent long term sequelae
Treat osa
Lifestyle and CPAP
Oral devices or upper airway surgical procedures
Don’t drive until resolved
If persists despite preventions
Nocturnal CPAP
-pneumaticallt splinting the entire airway, presenting collapse bc it raises intraluminal airway pressure and increases functional residual capacity.
CPAP willl increase daytime alertness, decrease HTN, and ap epic episodes
Bad CPAP
Hard to use
Can get heated humidification, education, follow up
If still can’t use CPAP
Bi level positive airway presssure nasal ventilation or auto-titrating positive pressure devices that modify airflow pressure to a more comfortable level.
Mandibular advancement devices
Alternative therapy; however eliminate the need for CPAP in only mild to moderate
Surgery
Unable CPAP. Resection or enlarged, obstructing tonsils may be beneficial in some.
Uvulopalatopharyngoplasty-alleviate obstruction of the hypoglossal space.
Variable success rates , depending on things.
What do to document eddect of mandibular advancement device
Follow up polysomnogram
Common causes of COPD
Emphysema and chronic bronchitis
, airflow limitation that is not fully reversible
A1 antitrypsin (too much neutrophil elastase)
Genes responsible for the production of enzymes involved in detoxification of cigarette smoke. Low birth weight, childhood illness (effect lung growth)
-tobacco smoke, occupational dist, chemical agents, air pollution
DIFFERENTIAL for COPD
Asthma, bronchiectasis,CF
Stage I GOLD
FEV1/FVC<70%; FEV1>80% of predicted
With or without chronic symptoms (cough, sputumproduction)
II COPD
FEV1/FVC<70%; 50%
GOLD III severe
FEV1/FVC<70 30%
State IV COPD
FEV1/FVC<70%; FEV1<30% or FEV1<50% plus chronic respiratory failure
Treat mild
SABA
Treat II
Add regular treatment with one or more long acting bronchodilators; add pulmonary rehabilitation
Stage III treat
Add inhaled corticosteroids if repeated exacerbations
TreatIV
Add long term oxygen therapy if chronic respiratory failrue; consider surgical treatments
Difference between interstitial pneumonia’s and idiopathic pulmonary fibrotis
Interstitial-inflammations Nd fibrosis pattern, it is believed that epithelial surface injury int he alveoli leads to spreading fibrotic change into the interstitial and vasculature
(UIP, NSIP, BOOP/COP)
Idiopathic-formof idiopathic DPLD. A diagnosis is important bc its poor prognosis. Dyspnea on exertion, exercise intolerance , dry cough, and crackles on inspiration. In typical cases, imaging shows lower lung zone and subpleural linear reticular markings, volume low, honeycombingand traction bronchiectasis. Histoplasma-UIP. Clincial course punctuated by acute declines due to exacerbation ofunderlying disease or overlay of infection , HF, or other comorbidity. Poor prognosis.
UIP
Hallmark different stages
Starts subpleural
Pneumoconiosis, radiation injury, end stage hypersensitivity, sarcoid
NSIP
Uniforminvolvement of lung parenchyma with cellular infiltration or fibrosis. Bilateral, subpleural, correlating ground glass infiltrates on CT imaging andlittle honey combing.
AutoimmuneCT
BOOP
Small airway bronchiolitis with granulation tissue and organizing pneumonia
With a granulomatous pattern,T cells, macrophages and epithelium cells accumulate to form granulomas int he lung parenchyma
GRANULOMAS
Treatment DPLD
Stop smoke
Supplemental oxygen
Symptomatic treatment for reactive airways or cough, maintenance of nutrition and fitness,and treatment of infections are also good.
Env exposure stop
Many get pulmonary HTN. Vasodilation agent to reduce right sided vascular resistance and pressures
Drugs DPLD
Amiodarone (dose dependent-any timetoseveral years after), methotrexate (treat CT disorder)and nitrofurantoin
(Antimicrobial)
Smoking
CT associated
Pneumoconiosis-asbestos, silicon, beryllium,IPF-asbestosis (decades after sign exposure and may be progressive),
Anti fibrotic medications for DPLD
?
Usual interstitial pneumonitis UIP
Hallmark pattern heterogenous involvement of the lung with different stages of progression of fibrosis in adjacent areas of the lung. The disease starts int he subpleural regions and honeycombing is seen. Associated with pneumoconiosis, radiation, end state hypersensitive, advanced sarcoid,
Idiopathic pulmonary fibrosis-no cause
Nonspecific interstitial pneumonitis
This pattern, there is uniform involvement of lung parenchyma with cellular infiltration or fibrosis. The process is often bilateral, subpleural, with correlating grounf glass infiltrates on ct imaging and little honeycombing. This pattern is typically seen in association with an underlying disease process such as autoimmune ct
BOOP
Small airway bronchiolitis with granulation tissue and organizing pneumonia.
With a granulomatous patter, T cells, macrophages, and epithelium cells accumulate to form granules in the lung parenchyma. Granules hallmark of thess diseases but are not the sole finding and fibrotic change may be seen in the same patient. Granulomas
Well formed non caseating-sarcoid
Loosely-hypersensitivity
Diagnosis DPLD
History, PE, lab, imaging, lung biopsy
Presentation DPLD
Progressice dyspnea, reduced exercise tolerance, and a persistent dry cough should raise the possibilty
Gradual onset
History DPLD
Meds, workplace, env exposures
> 50
Idiopathic pulmonary fibrosis
20-40
Interstitial lung disease associated with CT disease, sarcoidosis, lymphangioleiomyomatosis, and langerhan
Female DPLD
Lemphangioleiomyomatosis
Smoking
Respiratory bronchiolitis associated with interstitial lung disease, desquamative interstitial pneumonia and langerhan
Exposure to bird
Hypersensitivity
Acute onset
Idiopathic pulmonary fibrosis, acute eosinophilic pneumonia, COP, hypersentivity, drug induced,
Clubbing
Idiopathic pulmonary fibrosis
Erythema nodosum
Associated with sarcoidosis, CT diseases
Uveitis/conjunctivitis
Associated with sarcoidosis, CT disease
CXR
Increase interstitial reticular or nodular infiltrates, often in bases
HRCT
Detail about distribution and extend of disease
Basal predominant
IPF< asbestosis, NSIP
Upper lobe predominant
Hypersensitivity pneumonitis, sarcoidosis, silicosis
Peripheral
IPF< chronic eosinophilic pneumonia, COP
Central
Sarcoidosis, pulmonary elveolar proteinosis
Mosaic attenuation
Small airways disease,
PFT DPLD
Decreased lung volume and decreased diffusing capacity
Smoking related
Interstitial in smokers, respiratory bronchiolitis interstitial lung disease, desquamative interstitial pneumonitis, langerhans
CT associated DPLD
Associated with RA< scleroderma, polymyosisis, dermatomyositis, sjorgen syndrome, and bechet
Autoimmune or from aspiration in progressice sclerosis or due to the medications she’d to modify
Sarcoidosis
Granulomatous disease of unclear cause >18
Blacks
Noncaseating granulomas involving lung and other organs
Chronic bronchitis
Diagnosis based on purely the patients history and symptoms. It requires a productive cough (regardless of how little or much) for 3 months out of the year for 2 consecutive years: and there is no other adequate explanation for the cough
Asthma
Is a completely reversible airway obstruction. It may have multiple triggers. These may be allergic or IgE mediated, medication medicated as int he case of asprin, may be non allergic, may be made worse with changes in season, humidity, temp, exposures to irritants
It may be occupationally related. May come from exercise
Bronchiectasis
Failure of the normal narrowing of the airway resulting in wider airways. Secondary to infection but may have a number of other causes
Interstitial lung disease
Group of diseases that have many different causes that result in interstitial thickening, restrictive pattern on pulmonary function tests, characteristics radiographically features that often present with dyspnea and/or severe often non productive cough
Pleural effusion
Sputum gets trapped between the visceral and parietal pleura. It can be from a number of different causes
Pulmonary htn
Bp int he pulmonary increases due to either another disease process secondary pulmonary HTN and this is fairly common or due to inherent HTN in the pulmonary artery known as primary pulmonary HTN, which is much less common
Common diagnosis in patients who present with cough acute
*Common cold or viral upper respiratory tract infection
Lower respiratory tract infections
Bacterial sinusitis
Rhinitis caused by allergens or env irritants
Asthma or copd exacerbation
Cardiogenic pulmonary edemaaspiration or foreign body
Meds (ACE i)
Pulmonary embolism
Chronic cough cause
Upper airway cough syndrome
Asthma
GERD
Non asthmatic eosinophilic bronchitis
Bronchiectasis
Medication reaction (ACE-i_
Chronic bronchitis caused by smoking
How upper viral infection cause cough
Protracted bronchial hyperactivity, with secondary cough lasting weeks to months
Airway cough receptors-in larynx, trachea, and bronchi and in rhinitis, rhinosinusitis, pharyngitis it is attributable to reflex stimulation from postnasal drainage or throat clearing.
-influenza a and b, parainfluenza , RSV, coronavirus, adenocirus, rhinovirus
Influenza symptoms
Sudden onset of fever and malaise followed by cough , HA, myalgia and nasal and pulmonary symptoms,
Influenza signs
Fever, cough, pharyngitis, rhinorrhea
How diagnose influenza
Secretion culture, IF, PCR,
Chemoprophylaxis ho gets
Residents in assisted living
H1N1 symtpoms
Cough, fever rhinorrhea, person to person transmission
Nonviral caues of acute bronchitis
Bordetella pertussis, mycoplasma pneumoniae and chlamydia
=cant diagnose pertussis treat with cough lasting more than 2 weeks during documented outbreak, known to contact a confirmed case
- PCR
- antimicrobial for pertussis to decrease shedding
Pneumonia
Most serious cause of cough
Fever, diminished breadth sounds,
Asthma cough
Acute cough
Chronic bronchitis and bronchiectasis
Abrupt increase from baseline in cough, sputum production, sputum pursuance, and SOB
Treat acute cough
Antitussive agents, expectorants, mucolytic agents, antihistamines, nasal anticholinergic agents.
Indications for treatment with cough
Sleep disruption, painful cough, and debilitating cough
That was all acute cough
Ok
What is chronic cough
> 8 weeks
Common cause of chronic cough
Upper airway cough syndrome
Asthma
GERD
Non asthmatic eosinophilic bronchitis
Bronchiectasis I
Ace-i
Chronic bronchitis caused by smoking
Evaluation chronic cough
History, PE, chest radiography*
Smoking cessation and stop ace before more workup
Most chronic cough in non smokers, normal chest x ray and not on ace
Upper airway cough syndrome
Asthma
GERD
Upper airway cough syndrome
Recurrent cough that occurs when mucus from the nose drains down the oropharynx and triggers cough receptors.
Confirmed when drug therapy eliminates discharge and cough.
Postnasal drainage, frequent throat clearing, nasal discharge, cobblestone appearance of oropharyngeal mucosa, or mucus dripping down the oropharynx.
Cough variant asthma chronic
Airway hyperresponsiveness and is confirmed when cough resolves with asthma meds. Cough variant asthma in 57% asthma
Can do bronchoprovocatative testing (but will also be pos for all copd)
GERD cough
By aspiration
Vaguely mediated distal esophageal tracheobronchial reflex
24 hour esophageal pH monitoring
PPI if find symptom may not relieve for three months
Nonasthmatic eosinophilic bronchitis chronic cough
Presence of airway eosinophilia
Inhaled glucocorticosteroid
Cough with sputum
Chronic bronchitis
-stop smoking, inhaled anticholinergic agent , glucocorticoids, antibiotic,
Bronchiectasis
Sputum with purulent
Chest. Radiography and CT results tram line pattern
Antibiotics based on sputum
Smoke
Most have chronic cough, but don’t usually get medical attention
Stop smoking resolve 94-100%
Within 4 weeks!
Cough caused by ACE i
Not dose related and may occur hours to weeks or months
Diagnose-on;y when cough stops with stop ace i
Can give angiotensin receptor blocker
Hemoptysis
Acute or chronic cough
Usually from infection (bronchitis or pneumonia) followed by malignancy
What ekse may cause the hemoptysis
Elevated pulmonary pressure from left sided heart failure or pulmonary embolism
Cryptogenic hemoptysis
Cause not known
What do if hemoptysis
Chest radiography
—-encobronchial lesion not always seen on CT do do bronchoscope too
MASSSIVE HEMOPTYSIS
BLOOD LOSS GREATER THAN 200 ML.DAY. MASSIVE HEMOPTYSIS REQUIRES URGENT INPATIENT EVALUATION. AIRWAY MANAGEMENT AND VENTILATOION
URGENT BRONCCHOSCOPY
DYSPNEA
Combination of symptoms of awareness of work and effort of breathing, tightness, and unsatisfactory inspirations. “My breath is short” “cant get enough air” “trouble breathing”
MOA dyanpnea
Impaired ventilator mechanics
Increase in respiratory drive
Impaired ventilator mechanics
Airflow obstruction, muscle weakness, decrease in chest wall compliance
Impaired respiratory drive
Parenchymal or pulmonary vascular lung disease, congestive heart failure, chemoreceptor stimulation, impaired gas exchange, pregnant,
Diagnose dyspnea
History and PE vitals
-if tachypnea acute muscle use, or conversational dyspnea transfer to an acute setting
Grade 1 dyspnea
Not troubled by breathlessness except on strenuous exercise
Grade 2 dyspnea
Short of breath when hurrying on the level or walking up a sling hill
Grade 3 dyspnea
Walks slowe than most people on the level, stops after a mile or so, or stops after 12 minutes walking at own pace
Grade 4 dyspnea
Stops for breath after walking about 100 yards or after a few minutes on level grounf
Grade 5 dyspnea
Too breathless to leave the house or breathless when undressing
Acute dyspnea
Develops rapidly over minutes to a day
Differentiat for acute dyspnea
Cardiovascular-acute decrease in left ventricular function or increase in pulmonary capillary pressure (acute coronary syndrome, tachycardia, cardiac tamponade)
Respiratory-airway destruction (bronchospasm,, aspiration, obstruction), disruption of gas exchange by parenchymal disease (pneumonia , acute respiratory distress syndrome), vascular disease, PE) or ventilator pump issue (pleural effusion, pneumothorax)
Panic disorder
Patient presents with acute dyspnea
Stabilization
PE
-low oxygen sat suggests asthma, exacerbation COPD, acute respiratory distress syndrome, heart failure, pulmonary fibrosis, or pulmonary vascular disease
Chest redaiography-Cause
Focal infiltrates-pneumonia
Air-pneumothorax
Basal opacity with.a meniscus-pleural effusion
Cardiomegaly and vascular engorgement-HF
Chronic dyspnea
Longer than 1 month
Top causes chronic dyspnea
COPD, asthma, interstitial lung disease, HF
Also maybe pulmonary vascular disorders, valvular and pericardial heart disease, anemia, and thyroid disease
Work up chronic dyspnea
History
Worsening conditions chronic dyspnea
Natural disease progression, medication noncompliance, and exposure to environmental or dietary factors
Chronic dyspnea with no chronic disease
Cardiac related volume overload-orthopnea, edema, or exertional symtpms —look at JVD, hepatojugular refluc, murmurs s2, or s4 gallop and pulmonary and peripheral
Echo
If no chronic disease or heart issues and chronic dyspnea
Pulmonary-wheezing, sough, smoking, env exposure
What if no lung
Specific testing for issues
Lung cancer major risk factors and etiology agents responsible
Cigarettes -mainly small cell is most bad
Head neck-alcohol, tobacco ..synergistic
Complaints and symptoms and clincial findings in patients with cancer of lung
New or persistent pulmonary symtpoms, lung abnormality finding, Horner syndrome , brachial plexopathy, chest wall tenderness, extrathoracic spread (wasting lymphadenopathy, focal neurologic findings, bone tenderness, skin nodules, hepatomegaly), paraneoplastic , get chest radiograph to look for masses, lymphadenopathy, and pleural effusions, smaller lung cancers may require ct detection
What is necessary for diagnosis of lung cancer
Histologic confirmation
Sputum cytology
Reserved for poor pulmonary function who cant tolerate invasive procedures
Acromegaly
Growth hormone releasing hormone
Cushing syndrome
Adrenocorticotropic hormones (SSC)
Lambert Eaton myasthenic syndrome
Proximal limb wewawkness and fatigue due to antibodies to voltage gated calcium channels (SSC)
Hypercalcemia
PTH related peptide
Hypertrophic pulmonary osteoarthropathy
Painful new periosteal bone growth and clubbing (adenocarcinoma)
Hyponatremia
Syndrome of inappropriate antidiuretic hormone SSC)
Pancoast syndrome
Shoulder pain, lower brachial plexopathy, and Horner syndrome from apical lung tumor (NSCC
Superior vena cava syndrome
External compression of superior vena cava causing face and arm swelling (SCC)
Trousseau syndrome
Hypercoagulable stae (most common with adenocarcinoma)
Vocal cord paralysis
Entrapment of recurrent laryngeal nerve
Horner syndrome
Ptosis, miosis, and anhidrosis, can be produced by a lesion anywhere along the sympathetic pathway that supplies the hand eye and neck
Staging
Look for metastatic..eliminates surgery as option
How find staging info
CT, PET-CT, brain imaging if neurologic symtpoms
Bone scan if bone pain
SSC
Systemic at diagnosis soncidered
Sensitive to radiation and chemo
CT PET-CT and serum electrolytes, aminotransferase and lactate DH also for staging
Where does SCC spread
Liver bone, brain adrenal retroperitoneal lymph nodes, pancreas and subcutaneous ST
What is an incidental pulmonary nodule
Asymptomatic discrete radiographically density<3 cm that is completely surrounded by aerated lung.
Benign pulmonary nodule
No growth in two years
Calcification in a diffuse central or laminar pattern
Malignant nodules
> 2 cm, have speculated edges, and are located int he upper lobes. The probability of malignancy increases with age over 40, smoking, asbestos, radon
Manage pulmonary nodules
Determine behavior over time and stratify risk.
Find previous radiography
Nodule <4 mm
No follow up if never smoked and no other risk factors
Nodules >4 mm
Follow up
Solid nodules
In high risk require a consideration for immediate biopsy close interval CT scanning in another option in low risk patients
T
Size
N
Regional node status
M
Metastatic
Treatment 1 and II
Surgery
Also some III
And adjunct chemo in IB >3 vom
Early stage non small cell if inoperable
Radiation but not helpful
Stage III
Mediastinal lymphadenopathy
Chemo to shrink prior to surgery
Unresectable disease
Chemoradiation is superior to radiation alone. Encourage stop smoking
Metastatic inoperable IV non small cell
Local radiation, palliative chemo
Not beneficial with poor performance
Decrease skeletal complications in patients with bony metastases
Monthly IV bisphosphonate therapy or monthly subcutaneous dosing of the RANK ligand inhibitos denosumab decreases skeletal complications in patients with bony metastases
SSC
Chemo and platinum based agent and etoposide markedly improves survival
SSC
MOST DIE
If tumor respond it will relapse explain that improvement is short lived
Palliative treatment
Severe pain need opioids, use glucocorticoids for brain metastases to decreased intracranial edema thoracic radiation for obstruction or superior vena cava syndrome
Targeted radiation-bone pain
, nerve pain
Cancers of the respiratory system
Epithelial-mucosal usually squamous cell
-paranasal sinuses, oral cavity, and nasopharyngeal, oropharynx,
Salivary gains-heterogenous and rate
Identify the major risk factors for the development of cancer of the head and neck
Usually oral cavity, oropharynx, or larynx
Oropharyngeal on rise
Alcohol and tobacco!!
Synergy stick together
Smoking cancer
Older than 60
HPV cancer
40s or 50s
EBV
All ages
Nasopharnx
No early symptoms
Unilateral serous otitis media due to obstruction of ear tube, unilateral or bilateral nasal obstruction or epistaxis
Can damage CN at skull base
Carcinoma of oral cavity
Non healing ulcers
Changes in fit of dentures or painful lesions
Decreased tongue or speech
HPV-neck lymphadenopathy at first sign
Hoarseness
Laryngeal
Advanced head and neck cancer
Severe pain, otalgia, airway obstruction, cranial neuropathies, trismus, enlarged nodes
If enlarged nodes are located int he upper neck and the tumor cells are of squamous cell histology
Mucosal surface in the head or neck
Supraclavicular node
Primary site in chest or abdomen
PE head and neck cancer
Mucosal palpation and lymphnodes
Leukoplakia or erythroplakia -premalignant biopsy them
CT
PET
Staging
Anesthesia laryngoscopes, esophagoscope ad bronchoscopy with multiple
T1-T3
Increasing size
T4
Invasive
Treat
Localized, locally or regionally advanced disease, recurrent and/or metastatic
Localized treat
T1-T2
Curative intent with surgery or radiation
Locally or regionally advanced disease
Large primary tumor and/or lymph. Node metastases
Curative intent-combined modality thatpy surgery radiation, chemo
Recurrent and or metastatic disease
Palliative intent
5-FU cisplatin, cabroplatin with 5-FU and cisplatin
EGFR therapies including antibodies and TKI have activity against 10%
Pneumothorax essentials of diagnosis
Acute onset of unilateral chest pain and dyspnea
Minimal physical findings on mild cases;unilateral chest expansion, decreased tactile fremitus, hyperressonance, diminished breath sounds, mediastinal shift, cyanosis and hypotension in tension pneumothorax
Presence of pleural air on chest radiograph
Pleural effusion
Ok
Transudative pleural effusion
Atelectasis, constrictive pericarditis, duropleural fistula, extravasculr migration of central venous catheter, heart failure, hepatic hydrothorac, hypoalbuminemia, nephrotic syndrome, peritoneal dialysis, superior vena cava obstruction, trapped lung, urinothorac
Symptoms of pleural effusion
Fever, dyspnea and chest pain
Exudative
Inflammatory, infectious, malignant
Collagen vascular disease, intraabdominal process
Pathophysiology pneumothorax
Primary spontaneous pneumothorax-absence of an underlying lung disease
-tall thin men10-30 from rupture subpleural bless
Secondary spontaneous pneumothorac-complication of disease ,
Traumatic pneumothorac-penetrating or blunt trauma
Iatrogenic pneumothorac-follow procedures such as thoracentensis, pleural biopsy, subclavian or internal jugular vein catheter placement, percutaneous lung biopsy, bronchoscopy with transbronchial biopsy, positive pressure mechanical vent
Tension p-penetrating trauma ,lung infection, cardiopulmonary resuscitation, positive pressure-pressure of air in pleural space exceeds ambient pressure throughout the respiratory cycle-check valve mechanism allows air to enter the pleural space on inspiration and prevents egress or air on expiration
Describe management pneumothorac
Smal-observation, supplemental oxygen
Spontaneous primary-simple aspiration drain of air with small bore catheter
small bore chest tube to one way Heinrich valve protect against tension pneumo
Secondary, large, tension-ventilation mechanical (tube thoracostomy) under water seal drainage and suction applied until lung expands
Smoke-stop it
Thoracoscopy/open thoracotomy-recurrence of spontaneous, bilateral pneumothorac, failure of tube thoracostomy
Pneumocystis pneumonia-recurrence so hard. No best approach….
Define mediastinal compartments and their contents
Medistinum-region between the pleural acs and has three compartments
Anterior-from sternum anteriorly to the pericardium and brachiocephalic vessels posteriorly.-has thymus gland, anterior mediastinal lymph nodes, and the internal mammary arteries and veins
Middle mediastinum-lies between the anterior and posterior mediastinal and contains the heart; the ascending and transverse arches of the aorta; the venae cava; the brachiocephalic arteries and veins the phrenic nerves; the trachea the main bronchial and their contiguous lymph nodes and the pulmonary arteries and veins
Posterior mediastinum-bounded by the pericardium and the tracheaanteriorly and the vertebral column posteriorly-contains descending thoracic aorta, the esophagus, the thoracic duct, the AZt go’s and hemiazygos veins, and the posterior group of medications lymph
Anterior mediastinal
Thymomas, lymphomas, teratomas our neoplasms, thyroid masses
Middle mediastinum
Vascular masses, lymph node enlargement from metastases or granulomatous disease and pleuropericardial and bronchogenic cysts
Posterior mediastinum
Neurogenic tumors, meningoceles, meningomyeloceles, gastroenteritis cysts, and esophageal diverticula
Squamous cell carcinoma head a neck region
5% of all cancers
Higher incidence of death in african descent
Men 50-60
Risk factors
Smoke, alcohol, non smoke tobacco
Field cancerization
As a result of structure, the entire upper aerodigestive tract is exposed to carcinogens
- cancers may occur in any location
- the entire area needs to be investigated when malignancy is identified to excludes second primary cancer
Look at lung!!
Complaints of cancer head neck
Trouble swallowing, intermittent choking (aspiration too))
Trismus-inability to open the jaw from compression of trigeminal nerve or msucle invasion by the tumor
Ear pain-need evaluation of not responding to conventional treatment
Weight loss
Viral cause head neck cancer
EBV -nasopharyngeal
HPV western—-oropharync 16 16
Younger and sex a lot of partners ..better prognossi
Assess nutritional and performance status of patient
How effected a patient is
Few symtpoms vs cant work cant daily live need assistance
Dietary factors-low fruit an veg
Caretonoids-protective
Laryngectomy
Remove vocal sound
Treat cancer
Radiotherapy
Surgery
-laryngectomy
Systemic therapy
Electrolarynx
Placed in submandibular region
Vibrates at constant pitch to allow speech
Tracheostomy
Provides. Synthetic set of vocal cords for speech
Squamous cell carcinoma types
Poorly differentiated, moderately, differentiated
Worse prognosis
Poorly defined
EBV
Undifferentiated
Erythroplakia pre cancer
Red patch
Leukoplakia pre cancer
White patch
What do with nonspecific signs and symptoms in head and neck with symptoms more than 2-4 weeks
Thorough otolaryngologists exam
Males or females HPV cancer neck
Males
Symptoms nasopharynx cancer
Not really early symptoms
May cause unilateral serous otitis media due to obstruction of the Eustachian tube, unilateral or bilateral nasal obstruction or epistaxis.
Advances-neuropathies of CN due to skill base
Carcinoma of oral
Nonhealing ulcers, change in fit of dentures, painful lesions. Decreased tongues mobility.
Oropharynx or hypopharync cancer
Early early symptoms
Sore throat or otalgis
HPV tumor sign
Lymphadenopathy first sign
Laryngeal cancer
Hoarseness
Advanced symptoms any head and neck
Pain, otalgia, airway obstruction, CN neuropathies, trismus, odynophagia, dysphagia
Progressive issue swallow base in tongue, squamous cell carcinoma with no lymph node involvement and locally advanced disease-growing into adjacent structures
How treat
Initial radiotherapy and chemo then surgery
Enlarged nodes in upper neck and tumor cells are of squamous cell histology,
Probably squamous cell from mucosal surface
What do if have lymph node involvement
CT of chest and upper abdomen
Definitive statin
Endoscopic examination under anesthetics
Stage I
T1 tumor <2cm without extra parenchymal extension
NO No regional lymph node metastasis
Stage II
T2 >2 cm but not more than 4 cm without extra parenchymal extension
N-
Stage III
Tumor >4 cm
N1, metastasis in a single ipsilateral lymph node <3 cm in greater
stave T4a
Tumor invades skin, mandible, ear canal, and or fascia nerve
N2
T4b
Tumor invades skill base and/or pterygoid plates and/or encases carotid artery
N3
35 yo man throat pain given antibiotics no improvement gets hoarseness, smokes and drinks, works in wood working shop
Occupational exposure can cause cancer wood working-inhaling things
Increase risk
What if lymph node involvment
Biopsy of all suspicious appearing ares and primary site
Treat
Localized, locally or regional advanced disease, and recurrent and/or metasticize
Treat localized disease
Curative intent surgery
Laryngeal-radiation to preserve voice
60% survival
Most recurrence in first two year
Treat locally or regionally advanced disease
Curative intent with combined therapy including surgery radiation therapy and chemo or as concomitant
Prevent
Avoid exposure
Recurrent
Palliative
Cisplastin with 5-FU
EGFR therapies, antibodies, TKI
Complications of treating dad and neck cancer
Extent of surgery
Mucosistis, dysphagia
Xerostermia, loss of taste, decreased tongue mobility, second malignancies, dysphagia and neck fibrosis
Chemo-myelosuppression vomit nephrotoxicity
Mucosa-malnutrition dehydration
Lung cancer top three causes
Smoking smoking smoking
Second hand
Radon
Coal tars
Agricultural farmers
Majority lung cancer
Non small cell
Rest are small cell
Prevention
Stop smoking
Give retinol, B carotene, N acetylcysteine, and selenium
Screening
Low dose computed tomography scans to screen for early stage in former or current smokers
Diagnosis lung cancer
Hemoptysis, pulmonary infections, dyspnea, cough, chest pain
Abnormal lung finding-primary tumor
Intrathoracic spread-hoarse voice, Horner syndrome, brachial plexopathy, chest wall tenderness
Extrathoracic spread (wasting, lymphadenopathy), paraneoplastic syndromes, bone tenderness, masses, pleural effusions, CT
Bronchogenic carcinoma
Small cell
Non small cell
What need to diagnosis
Histology confirmation
Pancoast
Superior sulcus tumor invade brachial plexus
Shoulder pain paresthesia C7-T1
Horner
Ipsilateral anhydrosis pupil constriction due to stellate ganglion
Psosis, ahydrosis, superior sulcus
Hypertrophic pulmonary osteoarthropay
Clubbing of distal phalanges and hypertrophy of joints
Arthralgias, synovitis, and
Facies furrowing of brow!!
Painful, ner periosteal bone growth and cladding (adenocarcinoma)
Hypoxemia…
Superior vena cava
Extrinsic compression of SVC compression of by mass, adenopathy
Distention of superficial veins and edema of face and neck
Face and arm swelling
What do
1.Chest x ray, guide thinking
Will see node if >2 cm in size
- CT see mediastinum, lung arenchyma, liver,
MRI-more expensive and no better DONT
PET_when fused with CT, gives higher predictability for ancer vs benign disease oK USE
———fluoridinated glucose look for areas of increased uptake, if malignancies take up glucose more bc cancer more metabolically active
Sputum cytology
Screening…positive 60-90% of patients with lung cancer
Bronchoscope has replaced-can see stuff down to segmental bronchi, can collect and evaluate….required if hopeful of curative
Mediastinoscope
Can see hilum and mediastinal structure for tumor resection…do it if thinking of remove to make sure we know
Diagnose
Fine needle aspiration
Done with radiograph or CT insert into tumor ..good for peripheral lung tumor
Risk of pneumothorax..
Central-croncospocy
FNA-peripheral
SSC confined to one side, limited ok
Not extensive
15-25% cure
Extensive SCC
95% die in few years
Blood sputum in smoker
CT scan see if peripheral or central
Central-bronchoscopy
Peripheral-fine needle aspiration
Tension pneumothorax
Mediastinal shift
Can get in asbestosis
Hydro pneumothorax
See water line
Similarities pneumothorax or pleural effusion on exam
Sausculataion
Absent or diminished breath sounds
Differensions pneumothorax and pleural effusion
Percussion
-hyperresonant in pneumothorax, dull in pleural effusion
Auscultation
-positional changes of breath sounds
No change in pneumothorax
May improve in effusion
Causes of pneumothorax
Spontaneous-young men
Traumatic
-post procedural, direct trauma
Disease related
-numerous diseases
Exudate
If any of the following
-pleural protein/serum protein>.5
Pleural LDH/serum LDH?.6
Pleural fluid LDH>2/3 upper limits of serum LDH in the lab doing the measurement
Low pleural glucose
Parapneumonic effusion
Malignant effusion
Tb
Hemothorax
RA
Pleural white cells
Normal pleural space
-macrophages 75% lymphocytes 25%
Disease of pleural white cells
Increase eosinophils
Increase eosinophils>10%
Most often due to air in the pleural space
Idiopathic parapneumonic
Malignancy
Pleural white cells lymphocytic effusion
Malignancy
Tb
Transudate
LVF, CHF
Other
-misplaced central line, massive cirrhosis, nephrosis
Exudate
Everything else
Manage chronic pleural effusion pleurX
Indwelling catheter in pleural space allowing for at home drainage
Pleurodesis
-closes potential space between parietal and visceral pleura
-talc, tetracycline others
Through thorascope on in IR
What are mediastinal disease
Masses, inflammation/infection. Air or fluid collection
4 t of the anterior mediastinum
Thymoma
Teratomas
Thyroid masses
Terrible lymphoma-well there can be B cell lymphomas with mediastinal masses, as well as Hodgkin lymphoma
MIDDLE MEDIASTINAL MASSESS
VAC
VASCULAR masses, adenopathy, cysts-pleuropericardial, bronchogenic
Posterior mediastinal massess
Nerves and guts
- neurogenic tumors,
- meningoceles, meningomyeloceles
- gastroenteritis cysts and esophageal diverticula
What causes pleural effusion
Increased
