Lung

Question 1

Community acquired pneumonia

Answer 1

Ok

Question 2

Hospital acquired pneumonia

Answer 2

Ok

Question 3

Healthcare acquired pneumonia

Answer 3

Ok

Question 4

Ventilator associated pneumonia

Answer 4

Ok

Question 5

Aspiration pneumonia

Answer 5

Ok

Question 6

Right factors PNA

Answer 6

Ok

Question 7

Patient population susceptible to PNA

Answer 7

Ok

Question 8

Aspiration PNA

Answer 8

Ok

Question 9

Local pneumonia

Answer 9

Alveoli
CXR/CT-dense consolidation , air bronchospasm

US-consolidation , dynamic air broncograms

Question 10

Micro of lobar

Answer 10

Strep pneumonia

Klebsiella pneumonia

Legionella

Question 11

Bronchopneumonia

Answer 11

Bronchi

CXR/CT-Patchy opacities

US-Patchy B lines

May have consolidation

Question 12

Micro of bronchopneumonia

Answer 12

Wide variety (mycoplasma, chlamydia, staph, pseudomonas

Question 13

Interstitial pneumonia

Answer 13

Interstitial

CT/CXR-diffuse hazy opacities, septal thickening

US-patchy B lines, may have some consolidation

Question 14

Micro interstitial pneumonia

Answer 14

Viruses, PJP, mycoplasma

Question 15

Discuss preventative practices for CAP. What are contraindications

Answer 15

Ok

Question 16

Two indices used to determine if a patient needs to be admitted to the hospital for PNA

Answer 16

Ok

Question 17

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

Answer 17

Ok

Question 18

Orthomyxovirus PNA

Answer 18

Ok

Question 19

Adenovirus PNA

Answer 19

Ok

Question 20

H5N1 PNA 240, 250

Answer 20

Avian flu virus great risk for human pandemics

Question 21

MPV PNA 303 -paramimyxoviridaevirus

Answer 21

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

Question 22

Hantavirus PNA 299, 308 a bunyviridae

Answer 22

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

Question 23

Define antigenic drift and shift, provide an example of each

Answer 23

Ok

Question 24

Outline diagnostic and treatment methods for influenza. Include in you discussion: supportive care and neuraminidase inhibitors

Answer 24

Ok

Question 25

Strep pneumonia morphology, metabolism, clincial presentation, diagnostics 33, 38

Answer 25

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

Question 26

Haemophilus influenza morphology, metabolism, clincial presentation, diagnostics 96 ,100

Answer 26

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

Question 27

Moraxella 68,71

Answer 27

Neisseriaceae Causes otitis media, and URI in patients with COPD or old COPD exacerbation

Question 28

Staph aureus 43, 46

Answer 28

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,

Question 29

Klebsiella 75, 94

Answer 29

Ok

Question 30

Pseudomonas 92, 94

Answer 30

Ok

Question 31

Coxiella burnetti 120

Answer 31

Ok

Question 32

Typical pneumonia

Answer 32

Strep p, HE< moraxella cat, klebsiella, pseudomonas, coxiella burnetti

Question 33

Atypical bacterial pneumonia

Answer 33

Mycoplasma, chlamydia pneumonia’s, legionella pneuophilia, chlamydia psittacosaurus, burkholderia cepacia

Question 34

Mycoplasma pneumonia 156, 158

Answer 34

Ok

Question 35

Chlamydia pneumoniae 115, 122

Answer 35

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

Question 36

Legionella pneumophilia 99-101, 102

Answer 36

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,

Question 37

Chlamydia psittacosaurus 115 122

Answer 37

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

Question 38

Burkholderia cepacia 93, 94-95

Answer 38

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

Question 39

Pulmonary fungi

Answer 39

``` 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

Question 40

Aspergillus 201, 2140215

Answer 40

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

Question 41

Histoplasma capsulatum 205-207, 212

Answer 41

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

Question 42

Coccidiodes immitis 205-212

Answer 42

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

Question 43

Blastomycoses dermatidis 205-207

Answer 43

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

Question 44

Harrisons 132 pneumonia Nd lung abscess, | 101 influenza and other common viral respiratory infections

Answer 44

Ok

Question 45

What is pneumonia

Answer 45

Infection of lung parenchyma, classified as community acquired (CAP) or health care-associated (HCAP)

Question 46

HCAP

Answer 46

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

Question 47

How get pneumonia

Answer 47

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

Question 48

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

Answer 48

Macrophages

Question 49

Classic pneumonia presentation

Answer 49

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

Question 50

In VAP, respiratory bronchiolitis can __ a radiographically apparent infiltrate

Answer 50

Precede

Question 51

Typical community acquired pneumonia

Answer 51

S pneumoniae, haemophilus influenza, staph aureus, and gram negative bacteria like klebsiella p and pseudomonas a

Question 52

Atypical PNA

Answer 52

Mycoplasma pneumoniae, chlamydia pneumoniae, legionella, respiratory viruses (influenza, adenovirus, human metapneumovirus, RSV)

Question 53

A virus may be responsible for a large proportion fo CAP cases that require ____, even in adults

Answer 53

Hospital admission

Question 54

10-15% of PNA are ___

Answer 54

Polymicrobial Combo of typical and atypical

Question 55

When do anaerobes play a big role in CAP

Answer 55

Aspiration precedes presentation by days or weeks, often results in significant empyema

Question 56

CAP epidemiology

Answer 56

>5 million a year in US, 80% treated outpatient >55000 deaths annually 12 billion dollars

Question 57

Who gets CAP most

Answer 57

<4 >60

Question 58

Risk factors CAP

Answer 58

Alcoholism, asthma, immunosuppression, institutionalization, >70

Question 59

Factors CPA

Answer 59

Tobacco smoke, copd, colonization with MRSA, recent hospitalization or antibiotic therapy-influence the types of pathogens that should be considered in etiology disease

Question 60

Clincial manifestation CAP

Answer 60

Fevers, chills, sweat, cough, pleuritic chest pain, dyspnea Nausea, vomiting, diarrhea, fatigue, HA< myalgia, arthralgias

Question 61

Old patients with CAP presentation

Answer 61

Atypical, with confusion but few other manifestations

Question 62

PE CAP

Answer 62

Tachypnea, increased or decreased tactile fremitus; dull or flat percussion reflecting consolidation and pleural fluid, respectively; crackles; bronchial breath sounds ; pleural friction rub

Question 63

Diagnose CAP-want bc empiric tratment better for specific , also public safety implications

Answer 63

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

Question 64

What are the two sets of criteria that identify pts who will benefit from hostpail care

Answer 64

Pneumonia severity index CURB-65

Question 65

Complications CAP

Answer 65

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.

Question 66

Pleura effusion pH<7, glucose<2.2 LDH >1000 or if bacteria seen or cultured

Answer 66

Fluid should be drained, a chest tube is usually required

Question 67

Follow up CAP

Answer 67

CXR abnormalities may require 4-12 weeks to clear. Pts should receive influenza and pneumococcal vaccines, as appropriate

Question 68

Ventilator associated pneumonia micro

Answer 68

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

Question 69

Epidemiology VAP

Answer 69

-26-52 cases per 100 pts, with the highest hazard ration in the first 5 days of mechanical ventilation

Question 70

Three factors important in the pathogenesis of VAP

Answer 70

Colonization of the oropharynx with pathogenic microorganisms, aspiration of these organisms to the lower respiration tract, and compromise of normal host defense mechanism

Question 71

Clincial manifestation

Answer 71

Are similar to those in other forms of pneumonia

Question 72

Diagnosis VAP

Answer 72

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

Question 73

What if use wrong treatment

Answer 73

Higher mortality rate

Question 74

Treatment failrue VAP

Answer 74

Common, espicially MRSA, P aeruginos

Question 75

VAP complications

Answer 75

Prolonged mechanical ventilation, increased length of ICU stay and necrotizing pneumonia with pulmonary hemorrhage or bronchiectasis. VAP is associated with significant mortality risk

Question 76

Hostpital acquired pneumonia

Answer 76

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

Question 77

Bronchiectasis etiology

Answer 77

Irreversible airway dilation that involves the lung in either a focal or a diffuse manner

Question 78

Epidemiology bronchiectasis

Answer 78

Older age women 25-50% idiopathic disease

Question 79

Vicious cycle of bronchiectasis

Answer 79

Susceptibility to infection and poor mucocele are clearance results in microbial colonization of the bronchial tree.

Question 80

Noninfections bronchiectasis

Answer 80

Immune mediated reactions that damage the bronchial wall and parenchymal distortion as a result of lung fibrosis

Question 81

Clinical manifestation bronchiectasis

Answer 81

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

Question 82

Diagnose bronchiectasis

Answer 82

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

Question 83

Treat bronchiectasis

Answer 83

Control of active infection and at improving in secretion clearance

Question 84

Lung abscess what is it

Answer 84

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%)

Question 85

What causes primary lung abscesses

Answer 85

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.

Question 86

Secondary cloud abscesses

Answer 86

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

Question 87

Clinical manifestations lung abscess

Answer 87

Similar to pneumonia.

Question 88

Anaerobic lung abscess presentation

Answer 88

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

Question 89

Lung abscess from non anaerobic organisms (s aureus)

Answer 89

Present with a more fulminant course characterized by high fevers and rapid progression

Question 90

Diagnose lung abscess

Answer 90

Chest CT is the preferred radiographically study for precise delineation of the lesion

Question 91

Secondary lung abscess diagnosis

Answer 91

Sample collection (lovage, CT guided percutaneous aspiration) are recommended for secondary lung abscesses or when empirical therapy fails

Question 92

Treat primary lung abscess

Answer 92

Clindamycin or amoxacilllin

Question 93

Secondary lung abscess treat

Answer 93

Specific pathogen

Question 94

When stop treat lung abscess

Answer 94

When cleared or small scar

Question 95

Influenza A< B, C

Answer 95

Viruses RNA and orthomyxoviridae that have different nucleoprotein and matrix protein antigens

Question 96

Major human influenza

Answer 96

A and B (morphologically similar)

Question 97

A or B more severe

Answer 97

A

Question 98

Influenza A subtypes by ___ and ____

Answer 98

Hemagglutinin(H) and neuraminidase(N) antigens

Question 99

How does influenza infect

Answer 99

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

Question 100

What is major determinant of influenza a immunity

Answer 100

H antigen antibodies

Question 101

N antibodies

Answer 101

Limit viral spread and contribute to reduction of the infection

Question 102

How influenza a acquired

Answer 102

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

Question 103

Epidemiology influenza A

Answer 103

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

Question 104

Global pandemics

Answer 104

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

Question 105

Major changes

Answer 105

Antigenic shirt (INFLUENZa a only

Question 106

Minor variations

Answer 106

Antigenic drifts

Question 107

Avian influenza virus A/H51

Answer 107

Cause sporadic human cases, but sustained human to human transmission has not been observed; infection is linked to direct contact with infected poultry

Question 108

Swine

Answer 108

Can sustain simultaneous infection with swine, human, and avian Thesis multiple. Virus infections facilitate reassortment of genetic segments of different viruses.

Question 109

Pandemic A/H1N1 virus 2009-2010

Answer 109

Quadruple reassortment among swine, avian and human influenza viruses

Question 110

Interpandemic outbreaked

Answer 110

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

Question 111

Clincial manifestation influenza

Answer 111

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

Question 112

Complications influenza

Answer 112

Pneumonia and extrapulmonary | Common patients under 5 and over 65, pregnant women, or patients with chronic disease

Question 113

Pneumonia from influenza

Answer 113

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

Question 114

Secondary bacterial pneumonia

Answer 114

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

Question 115

Most common pneumonic complication involves aspects of viral and bacterial pneumonia

Answer 115

Extrapulmonary complications : Reyes’s, myositis, rhabdomyolysis, myoglobinuria, and CNS disease can occur as complications of influenza infection

Question 116

Reye’s syndrome

Answer 116

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

Question 117

Diagnose influenza

Answer 117

Reverse transcription PCR of respiratory samples

Question 118

Rapid tests that detect viral antigens

Answer 118

Fast results, can distinguish influenza a and b viruses, and are relatively specific but variably sensitive

Question 119

Serologic testing

Answer 119

Requires availability of acute and convalescent phase sera and is useful only retrospectively

Question 120

Prophylaxis influenza

Answer 120

Annual vaccination with either an inactivated or a live attenuated vaccine is the main public health measure for prevention

Question 121

How make vaccine

Answer 121

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

Question 122

Inactivated vaccines

Answer 122

50-80% protection against influenza is expected if the vaccine virus and the currently circulating viruses are closely related

Question 123

Who gets influenza vaccine

Answer 123

>6 months

Question 124

Chemoprophylaxis against influenza

Answer 124

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

Question 125

Acute viral respiratory illness

Answer 125

>50% of all acute illnesses; adults have 3-4 cases per person per year.

Question 126

Clincial presentation acute viral respiratory illness

Answer 126

Not specific enough to allow an etiology diagnosis, and viral illnesses are typically grouped into clinical syndromes

Question 127

Microbiology rhinovirus

Answer 127

Non enveloped, SsRNA viruses int he family picornaviridae that together are the major cause of the common cold

Question 128

Epidemiology rhinovirus

Answer 128

Spread by direct contact with infected secretions, usually respiratory droplets

Question 129

Clinical manifestations rhinovirus

Answer 129

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

Question 130

Diagnose rhinovirus

Answer 130

PCR and tissue availbe, but not ususlal attempted

Question 131

Treat rhinovirus

Answer 131

Symptom-antihistamines and decongestants

Question 132

Coronovirus

Answer 132

Pleomorphic, SsRNA viruses

Question 133

What coronavirus cause

Answer 133

Common cold SARS

Question 134

Incubation period coronavirus and duration

Answer 134

3 days | 6-7 days

Question 135

2002-2003

Answer 135

Coronavirus SARS developed in >8000 pts in 28 countries and was associated with 10% fatality rate, no case since 2004

Question 136

SARS incubation period and duration

Answer 136

2-7 days after which patients develop fever, malaise, HA< myalgia, and then a nonproductive cough and dyspnea

Question 137

SARS patients can develop what in second week of illness

Answer 137

ARDS and multiorgan dysfunction

Question 138

Middle East respiratory syndrome coronavirus

Answer 138

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

Question 139

Diagnose coronavirus

Answer 139

ELISA, IF< reverse transcription PCR SARS and MERS detected by R-PCR or viral culture of respiratory samples

Question 140

Treat coronavirus

Answer 140

Common cold-symptom relief SARS MERS-aggressive supportive care is most important . No specific therapy has been established as efficacious

Question 141

Human respiratory syncytial virus

Answer 141

Enveloped SsRNA and a member of the paramyxoviridae

Question 142

Epidemiology HRSV

Answer 142

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

Question 143

Transmission HRSV

Answer 143

Contact with contaminated fingers or fomites and by spread of coarse aerosols. Incubation 4-6 days

Question 144

Clincial manifestation HRSV

Answer 144

Infants typically develop rhinorrhea, low grade fever, cough, and wheezing; 35-40% of infections resul in lower tract disease, including pneumonia, bronchiolitis and tracheobronchitis

Question 145

In adults HRSV typically presents as the common cold, but is can cause

Answer 145

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

Question 146

Diagnosis HRSV

Answer 146

Rapid viral diagnosis available IF, ELISA, RTPCR of nasopharyngeal washes, aspirates or swabs

Question 147

Treat HSRV

Answer 147

Symptom based for upper tract disease and mild lower tract disease Incubation-if severe lower tract disease

Question 148

Prevention HRSV

Answer 148

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

Question 149

Human metapneumovius

Answer 149

Pleomorphic, single stranded RNA virus of the family paramyxoviridae

Question 150

Epidemiology Human metaneumovirus

Answer 150

1-5% of childhood upper respiratory tract infections and for 2-4% of acute respiratory illnesses in ambulatory adults

Question 151

Clincial human metapneumovirus

Answer 151

Disease manifestations are similar to those caused by HRSV

Question 152

Diagnose human HRSV

Answer 152

IF, PCR< tissue culture of nasal aspirates or respiratory secretions

Question 153

Treat human metapneumovirus

Answer 153

Supportive and symptom based

Question 154

Parainfluenza virus

Answer 154

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)

Question 155

Clinical manifestations parainfluenza virus

Answer 155

Infections are milder among children and adults, but severe , prolonged and fatal infection has been reported among pts with severe immunosuppression, including transplant recipients

Question 156

Diagnosis paramyxoviridae

Answer 156

Infections are milder among children and adults but severe prolonged and fatal infection has been reported among pts with severe immunosuppression, including transplant recipients

Question 157

Diagnoses paramyxoviridae

Answer 157

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

Question 158

Treat parainfluenza virus

Answer 158

Treat URI symptom based. For cases of croup with respiratory distress, intermittent racemis epinephrine and glucocorticoids are beneficial

Question 159

Adenovirus

Answer 159

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

Question 160

Clincial adenovirus

Answer 160

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

Question 161

Diagnose adenovirus

Answer 161

Isolation fo the virus in tissue culture; by rapid testing of nasopharyngeal aspirates, conjunctival or respiratory secretions, urine, or stool, or by PCR testing

Question 162

Treatment adenovirus

Answer 162

Supportive ribavirin cidofovir

Question 163

Tb Harrison

Answer 163

Ok

Question 164

Compare and contrast primary , progressice primary, latent and active Tb

Answer 164

Ok

Question 165

Outline signs and symtpoms indicative of pulmonary Tb

Answer 165

Ok

Question 166

Outline lab findings that are consistent with M Tb

Answer 166

Ok

Question 167

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

Answer 167

Ok

Question 168

Table 94-2

Answer 168

Ok

Question 169

Describe imaging finding for primary Tb, active Tb, and Millard Tb

Answer 169

Ok

Question 170

Define a nervy and discuss which patient populations are most likely to exhibit this phenomenon

Answer 170

Ok

Question 171

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

Answer 171

Ok

Question 172

In regards to monitoring treatment of TB, outline labs that are used to assess treatment progression and potential AE of medication

Answer 172

Ok

Question 173

Define MDR-TB and XDR TB

Answer 173

List reasons for resistance

Question 174

Mycobacterium TB

Answer 174

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)

Question 175

Mycobacterium Adium complex

Answer 175

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

Question 176

Mycobacterium kansaii

Answer 176

Gram positive acid fast, obligate aerobes, facultative intracellular organisms, Pulmonary: upper lung cavitary disease Disseminated disease in immunocompromised

Question 177

Microbiology TB

Answer 177

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

Question 178

Epidemiology TB

Answer 178

9 million new cases every year 1.5 million deaths-usually glow income, TB stable and falling worldwide

Question 179

US T

Answer 179

HIV, immigrants, old, poor

Question 180

MDR M TB

Answer 180

Resistant o at least rifampin and isoniazid and extensively drug resistant are increasing in frequency=480000 causes in 2013

Question 181

How spread T

Answer 181

Droplet nuclei that are aerosolized by coughing, sneezing or speaking <5-10 microV in diameter may be suspended in air for several hours

Question 182

How determine intimacy of Tb and duration of contact with pt

Answer 182

Degree of infectiousness of the pt, and the shared environment

Question 183

Cavitary or laryngeal disease

Answer 183

Most infectious, with as many as 10^5-10^7 acid fast bacilli in sputum

Question 184

Risk factors for active TB

Answer 184

Recent acquisition, comobidity (HIV..), malnutrition, tobacco smoking, and presence of fibrotic lesions

Question 185

Pathogenesis T

Answer 185

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

Question 186

2-4 weeks after Tb infection

Answer 186

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

Question 187

______ confers partial protection against BT. Cytokines secreted by alveolar ___c ontribute to disease manifestations, granula formation and mycobacteria killing

Answer 187

Cell mediated immunity Macrophages

Question 188

Clinical T

Answer 188

Pulmonary, extrapulmonary or both Extrapulmonary higher in HIV

Question 189

Pulmonary TB primary disease

Answer 189

No or mild in contrast to prolonged disease course that is common in post primary or adult type

Question 190

Primary Tb disease

Answer 190

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)

Question 191

Military disease

Answer 191

Hematogenous dissemination

Question 192

Adult type TB

Answer 192

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

Question 193

Extrapulmonary T

Answer 193

Any site, usually lymph nodes, pleura, GU, bones, joints, meninges, peritoneum, and pericardium,

Question 194

HIV and T

Answer 194

2.3 have extrapulmonary

Question 195

Lymphadenitis T

Answer 195

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%.

Question 196

Pleural TB

Answer 196

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

Question 197

GU T

Answer 197

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%

Question 198

Weight bearing joints T

Answer 198

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

Question 199

Meningitis T

Answer 199

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

Question 200

GI Tb

Answer 200

Can affect any portion of GI , ab pain, obstruction, hematochezia, palpable mass, peritonitis from ruptures lymph nodes

Question 201

Pericarditis Tb

Answer 201

Acute or subacute onset of fever, dull retrosternal pain and friction rub, effusion common, chronic is potentially fatal,

Question 202

Military disease

Answer 202

Hematogenous spread of M Tb through body. Small granulomas may develop in many organs. Hepatomegaly, splenomegaly, lymphadenopathy, and choroidal tubercles of eye

Question 203

HIV associated TB

Answer 203

Partial Cell mediated compromised-typical upper lobe | Late HIV-diffuse interstitial or Millard infiltrate

Question 204

Immune reconstitution inflammatory syndrome

Answer 204

1-3 mo after initiation antiretroviral, may exacerbate TB

Question 205

Diagnose TB

Answer 205

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

Question 206

Definitive diagnosis

Answer 206

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

Question 207

TST

Answer 207

Limited value active disease but mist widely used screening test for latent

Question 208

Interferon gamma release assays

Answer 208

Measure the release of interferon gamma by T cells after stimulation with TB specific antigens and more specific for M Tb that TST

Question 209

Prevent T

Answer 209

Vaccination Treat latent infection

Question 210

Tuberculin reaction size >5

Answer 210

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

Question 211

Tuberculin reaction size >10 mm

Answer 211

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

Question 212

Leprosy

Answer 212

Nonfatal chronic infectious disease from m leprae, an obligate intracellular bacterial species indistinguishable microscopically from other mycobacteria. In humans, armadillos, and sphagnum moss

Question 213

Can you culture M leprae

Answer 213

Not in vitro, has a doubling time in mice of 2 weeks

Question 214

What is leprosy associated with

Answer 214

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

Question 215

Transmission leprosy

Answer 215

Nasal drops maybe

Question 216

Clinical leprosy

Answer 216

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.

Question 217

Incubacliniincubation leprosy

Answer 217

2-40 years, usually 5-7

Question 218

Tuberculoid leprosy

Answer 218

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

Question 219

LL leprosy

Answer 219

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

Question 220

Complications leprosy

Answer 220

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

Question 221

Diagnosis TT

Answer 221

Biopsy, even in normal skin | Others not good

Question 222

What are nontuberculous mycobacteria

Answer 222

Mycobacteria not Tb or leprosy

Question 223

Miepidemiology NTM

Answer 223

Cause disease in humans only rarely unless some aspect of host defense impaired Mainly M kansasii, MAC M abscesses

Question 224

Clincial manifestations NTM

Answer 224

Broad Dieesminated Pulmonary disease Isolated cervical lymphadenopathy Skin and ST

Question 225

Disseminated NTM

Answer 225

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

Question 226

Pulmonary NTM

Answer 226

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

Question 227

Isolated cervical lymphadenopathy NTM

Answer 227

Most common in kids in NA, MAC | Nods typically firm and painless and develop in absence of systemic symptoms

Question 228

Skin ST NTM

Answer 228

Requires break in skin for introduction of organisms. Different NTM associated with exposures

Question 229

M fortuitous

Answer 229

Lined to pedicure bath-skin abrasions has imediatde pedicure (like if shaved legs before pedicure)

Question 230

M marinum

Answer 230

Acquires from fish tanks

Question 231

M ulverans

Answer 231

Waterborne tropical and africa

Question 232

Diagnose NTM

Answer 232

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

Question 233

MAC

Answer 233

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.

Question 234

Antibiotic NTM

Answer 234

Clarromycin, MAC Kansassi-rifampin

Question 235

MAC

Answer 235

Macrolides bc MDR

Question 236

Kansassi

Answer 236

Isoniazid.

Question 237

M Mary I’m

Answer 237

Rifamycin treat extrapulmonary disease

Question 238

Pulmonary htn

Answer 238

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

Question 239

Medication induced pulmonary HTN Fen-phen, the weight loss drug that suppresses appetites

Answer 239

Releases serotonin Fatigue dizzy, SOB, primary pulmonary HTN, idiopathic pulmonary arterial HTN, heart valve disease, HF Causes pulmonary HTN and heart disease

Question 240

.smoker, normal vitals, but low O2 sat. , bibasilar inspiratory crackles. No wheeze or prolongation of the expirations phase, no neck vein distention. S4

Answer 240

Normal vitals but low o2, has crackles, has s4 gallop Hypovascularoty peripheral Right descending pulmonary artery prominent central artery RV enlargement

Question 241

X ray of PAH

Answer 241

Peripheral hypovascularity, prominent central pulmonary artery (right and left prominent), right descending pulmonary artery, RV enlargement(see on lateral)-from increased workload

Question 242

Classic PFT pulmonary HTN

Answer 242

May have features of primary cause -severe COPD low DLCO | Low diffusion capacity for CO....

Question 243

Classis PAH with no DLCO

Answer 243

Normal PFT except isolated reduction in DLCO

Question 244

ECG PAH

Answer 244

RVH, RV strain, RAD Right axis deviation, right ventricular hypertrophy May see peaking of p wave—-right atrial enlargement .

Question 245

Echo PAH

Answer 245

Increased estimated PA pressure RA enlargement RV enlargement

Question 246

Is pulmonary HTN common

Answer 246

Pretty common Idiopathic uncommon

Question 247

Treat pulmonary HTN

Answer 247

Treatment is the treatment of underlying disease

Question 248

Idiopathic HTN is common?

Answer 248

No...specific therapies are changing very rapidly

Question 249

Group 1 pulmonary HTN

Answer 249

Idiopathic and CTD

Question 250

Group 2 pulmonary HTN

Answer 250

Heart

Question 251

Group 3 pulmonary HTN

Answer 251

Lung

Question 252

Group 4 pulmonary HTN

Answer 252

Pulmonary emboli

Question 253

Group 5 pulmonary HTN

Answer 253

All others

Question 254

Similarities between pulmonary HTN and ischemic heart disease

Answer 254

Both have exertional dyspnea, similar lack of associated symptoms, BNP elevated

Question 255

Differences between pulmonary HTN and ischemic heart disease

Answer 255

P2 increased in PAH CXR Other studies\-ECG, echo -ischemic, congestion, Kelley b lines, increased vasc May not see vascularity in pulmonary HTN

Question 256

Functional assessment of PAH Soo, how diagnose PH, how treat

Answer 256

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 ```

Question 257

OSA history clues

Answer 257

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

Question 258

Clincial findings OSA

Answer 258

Obesity, large neck circumference (short road), nasal obstruction( talk weird, short airway polyps and stuf congested), enlarged tonsils, narrow oropharynx, macroglossia, micrognathia, retrognathia

Question 259

Can non obese people get OSA. How diagnose OSA

Answer 259

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.

Question 260

Manage OSA goals

Answer 260

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

Question 261

Tools to manage OSA

Answer 261

Lifestyle modifications, CPAP

Question 262

Long term sequelae

Answer 262

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),

Question 263

Lifestyle modifications OSA

Answer 263

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

Question 264

When give CPAP

Answer 264

If symptoms persist after modifications Pneumatically props airway open -increased intraluminal airway presssure and FRC-after modifications Defer driving Continuous positive atrial airway pressure ,

Question 265

What is don’t adjust to CPAP

Answer 265

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.

Question 266

Oral device OSA

Answer 266

Mandibular assist device - can eliminate need for CPAP in mild/moderate cases - protrudes the jaw and/or holds tongue forward to prevent prolapse

Question 267

Upper airway surgery OSA

Answer 267

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

Question 268

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

Answer 268

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

Question 269

Symptoms obesity hypoventilation syndrome we need to do polysomnography!!!!!! Get ideas of what is going on and diagnose

Answer 269

decreased central respiratory drive Restrictive chest , pulmonary HTN, hypoxemia, Difficult airway, OSA CAD, congestive HF Difficult to position and bad vascular access

Question 270

Man sleepy during day stops breathing at night, doesn’t use alcohol, stopped smoking eight years ago, is sedentary, OBESSE

Answer 270

He’s fat

Question 271

Pink puffer

Answer 271

Emphysema thin burning so many calories as try to breathe

Question 272

Blue bloater

Answer 272

Chronic bronchitis

Question 273

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

Answer 273

Cyanosis, crackles and wheeze, obesity, peripheral edema, CO2 retention, chronic productive cough, purulent sputum Fat CO2 narcosis,

Question 274

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

Answer 274

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

Question 275

Extrapulmonary COPD

Answer 275

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****

Question 276

Dyspnea scal 0-normal ppl

Answer 276

I only get breathlessness with strenuous exercise

Question 277

Grade 1 dyspnea cycle

Answer 277

I get short of breath when hurrying on level grounf or walking up a slight hill

Question 278

Grade 2 dyspnea scale

Answer 278

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

Question 279

Grade 3 dyspnea scale

Answer 279

I stop for breath after walking about 100 yards or after a few minutes on level ground

Question 280

Grade 4 dyspnea

Answer 280

I am too breathless to leave the house or i am breathless when dressing

Question 281

BODE-survival prediction,

Answer 281

BMI+airflow obstruction+dyspnea rating+exercise capacity (6 min walk test) Higher worse

Question 282

BMI>21

Answer 282

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

Question 283

FEV1>65% normal

Answer 283

0 points

Question 284

FEV150-64%

Answer 284

1

Question 285

FEV1 36-49%

Answer 285

2

Question 286

FEV1<35%

Answer 286

3 points

Question 287

^MWT >350 meters

Answer 287

0

Question 288

6MWT 250-349 m

Answer 288

1 point

Question 289

6MWT 150-249 m

Answer 289

2 points

Question 290

<149 m 6MWT

Answer 290

3 points

Question 291

0-2 points

Answer 291

80% 4 year survival

Question 292

3-4 points

Answer 292

67%

Question 293

5-6 points 4 year survival

Answer 293

57%

Question 294

7-10 points

Answer 294

18% four year survival

Question 295

Why get dyspnea in COPD

Answer 295

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-

Question 296

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

Answer 296

Dynamic hyperinflation

Question 297

Asthma COPD similar

Answer 297

Weather may exacerbate May have perennial symptoms Exam-cough, sputum, wheeze, prolonged expiratory phase

Question 298

Differences COPD asthma

Answer 298

Complete reversibility, may have seasonal variations , may have associated ENT allergic symptoms, usually younger at onset

Question 299

Similarities COPD LVF

Answer 299

Progressive dyspnea, orthopnea Exam-wheeze, cough, dyspnea

Question 300

Differences LVF COPD

Answer 300

PND, history of heart disease, Exam-crackles, edema, s3 gallop, JVD/HJR

Question 301

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

Answer 301

Ium Ipratropium

Question 302

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,

Answer 302

Ol Albuterol

Question 303

LABA

Answer 303

Terol Olodaterol

Question 304

Lama

Answer 304

Ium Tiotropium

Question 305

ICS

Answer 305

Asone Fluticasone

Question 306

ICS

Answer 306

IDE Budesonide

Question 307

Metered dose inhaled (MDI)

Answer 307

Non breath activated-drug is released when you activate the inhaler Breath activated-drug is released when you breathe

Question 308

Dry powder inhaled or DPI

Answer 308

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

Question 309

Respiratory

Answer 309

Propellant free liquid inhaler creates a cloud - proair respimat - spiriva respimat - siolto respimat

Question 310

Mild and younger patients (FEV1>50% and age<65)

Answer 310

Doxycycline (macrolides may become the standard) TMP-smx Cephalosporin (ceftroxinme, cefdinir, cefopodoxine) Advanced macrolides(azithromycin, clarithromycin)

Question 311

Sicker older patient

Answer 311

Amoxicillin-clavulunate | Fluoroquinolones(Achilles tendon rupture)

Question 312

Steroids

Answer 312

Prednisone, cheap, a range of starting doses -1mg/kg, in practice adults are given 40-60mg/day CHEAP Methhylpredisolone-meh

Question 313

Indications for supplemental O2

Answer 313

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%

Question 314

Gold I mild treat

Answer 314

SABA or SAMA prn; often together in same inhaler FEV1/FVC <70% FEV1>80% With or without chronic symtpoms

Question 315

Gold II treatment FEV1.FVC<70%; <50%FEV1<80% With or without chronic symtpoms

Answer 315

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

Question 316

Gold III treatment severe disease With or without chronic symtpoms FEV1/FVC<70^; 30% FEV1<50%

Answer 316

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

Question 317

Gold IV verysevere disease treat | FEV1/FVC<70%; FEV1<30% of predicted of FEV1<50% of predicted pluc chronic respiratory failure

Answer 317

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

Question 318

Pulmonary rehab

Answer 318

Exercise training, education, psychosocial training and support, nutritional support, breathing training, inspiratory muscle training and chest physical therapy, vaccination (flu, pneumococcal) Helpful SOCIAL

Question 319

Majority COPD

Answer 319

Smokers, former, a1AT-if young

Question 320

Who should be evaluated for a1at

Answer 320

Unexplained dyspnea and cough | Young

Question 321

Diagnose chronic bronchitis

Answer 321

Chronic productive cough some days for 3 months a year for 2 successive years without another explanation (blue bloater) Emphysema-pink puddles

Question 322

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

Answer 322

``` Asthma-could be start at 6 Bronchiectasis sure CHF prob not Chronic bronchitis ok Emphysema Broad differential ``` LAMA/LABA -combination

Question 323

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-

Answer 323

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

Question 324

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!!

Answer 324

50%

Question 325

FEV1 ILD

Answer 325

50% | Restrictive! 8590% FEV1/FVC ration

Question 326

FEV1/FVC ILD

Answer 326

90% predicted

Question 327

FRC ILD

Answer 327

45%

Question 328

RV ILD

Answer 328

35%

Question 329

TLC ILD

Answer 329

65%

Question 330

DLCO ILD

Answer 330

20%

Question 331

Causes ILD

Answer 331

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,

Question 332

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

Answer 332

Occupation, hobby, environmental, travel, drugs both ex and non

Question 333

Evaluation ILD

Answer 333

Chest ct-can often lead to a specific diagnosis Pft Ana and RA—-may be informative associated with sarcoidosis and CT

Question 334

Scleroderma

Answer 334

Scleroderma -pulmonary fibrosis-fibrosis Pulmonary HTN-concentric fibrosis of the vessels Aspiration-esophageal disease Can be complaints in all

Question 335

RA

Answer 335

Causes Interstitial pulmonary fibrosis Bronchiectasis Pulmonary rheumatoid nodules Pulmonary vasculitis *Pleural disense-very low pleural glucose is characteristic

Question 336

SLE

Answer 336

Cause Interstitial lung disease Extra-pulmonary restriction-shrinking lung syndrome -decrease in all volumes over time, poorly Underwood and described Pulmonary HTN Pleural disease

Question 337

Autoantibodies in scleroderma High resolution CT_evaluare DPLD for distribution -lab look for CT

Answer 337

Anticentromere: 20-40% SCL-70; 30-70; more common in ILD Antinucleolar:10-20% but predicts the worst prognosis

Question 338

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

Answer 338

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%

Question 339

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

Answer 339

Chemotherapeutic agents-largest category Amiodarone-cardiac antiarrhythmic agent dose related, dose related Nitrofurnation-antibiotic commonly used for UTI Radiation induced

Question 340

Radiation induced lung disease phases PFT of DPLD-decreased volumes of all and decreased diffusing capacity

Answer 340

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

Question 341

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

Answer 341

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

Question 342

Acute form of hypersensitivity pneumonitis *granulomatous Put on antiviral and don’t get better....maybe something more going on

Answer 342

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

Question 343

Chronic hypersensitivity oneumonitis | *granulomatous

Answer 343

Pulmonary fibrosis

Question 344

IDL similar CHF CHF and ILD-dyspnea, hypoxemia, similar chest x ray, crackles In base, pulm HTN History difference,

Answer 344

Progressive dyspnea, exercise induced hypoxemia, cxr similar infiltrates Exam crackles in base, may have evidence of pulmonary htn

Question 345

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.

Answer 345

Some specific history differences in onset and details CXR and ct have specific differences Differences -clubbing, edema, s3 in LVF

Question 346

Ild different from copd

Answer 346

More rapid decline, cough non productive

Question 347

Copd different from ild

Answer 347

Slower decline with more frequent exacerbations Weather and nsaids worsen symtpoms Productive cough

Question 348

Treat ILD

Answer 348

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

Question 349

Acute interstitial pneuma (Amman rich)

Answer 349

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 **********

Question 350

AIP not IPF (hamman rich)

Answer 350

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

Question 351

IPF not AIP

Answer 351

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

Question 352

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

Answer 352

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

Question 353

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,

Answer 353

Detailed history approached in a systemic way to guide the search for the underlying cause in an efficient manner

Question 354

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

Answer 354

In patients with a small amount of pleural fluid and associated heart failure, pneumonia, or heart surgery (<1cm thick on decubitus radiography or ultrasonography)

Question 355

Pleural fluid amylase

Answer 355

Should be measured only when pancreatic disease, esophagealrupture, or malignancy is considered

Question 356

Omalizumab

Answer 356

Binds IgE and reduce exacerbations in patients with severe persistent asthma who have evidence of allergies.

Question 357

Side effect omalizumab

Answer 357

Anaphylaxis Expensive Select patients who remain symptomatic despite other therapies

Question 358

Smoking cessation

Answer 358

Most clinically effective and most cost effective way to prevent and slow the progression of chronic COPD and improve disease related survival

Question 359

Screening for airway obstruction

Answer 359

In asymptomatic patients is not recommended as there is little evidence that making the diagnosis in setting

Question 360

Metered dose inhaler

Answer 360

With proper instruction and good technique, is as effective as a nebulizer

Question 361

Home tests

Answer 361

May be inaccurate

Question 362

Pulmonary arteries

Answer 362

Deliver mixed venous blood from the RV to the pulmonary capillary alveolar membrane where gas exchange occurs, while the bronchial directly from the aorta.

Question 363

Primary cause of pulmonary HTN

Answer 363

>25mmHg MAP during rest | Conditions causing elevation of left sided heart filing pressures or pulmonary disease(treat underling cause)

Question 364

Clincial findings pulmonary HTN

Answer 364

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

Question 365

Diagnose PH

Answer 365

Ok

Question 366

Common management principles in patents with pulmonary HTN

Answer 366

For condition

Question 367

Treat I PAH mPAP>25 and PCWP<15 | Idiopathic , heritable BMPR2, ALK1, enfolding with or without hereditary hemorrhagic telangiectasia

Answer 367

Drug and toxin induced Associated with ct diseases (scleroderma), HIV , portray HTN, congenital heart disease, schistomiasis, chronic hemolytic anemia

Question 368

Type II

Answer 368

Pulmonary veno occlusive disease and/or pulmonary capillary hemagiomatosis Systolic dysfunction Distaolic dysfunction Valvular disease MPAP>25 PCCWP up Left sided heart

Question 369

Type III

Answer 369

Secondary lung disease and/or hypoxia mPAP>25 with underlying lung disease COPD, ILD< pulmonary study, sleep disordered breathing, alveolar hypoventilation, high altitude

Question 370

Type 4

Answer 370

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

Question 371

Ph persist even with treatment

Answer 371

Ugh

Question 372

OSA symptoms

Answer 372

Habitual snoring, witnesssed apnea, nighttime awakening with grasping or choking, insomnia, nighttime diaphoresis, ED, daytime fatigue or sleepiness, alterations in mood, neurocognitive decline

Question 373

Physical finding osa

Answer 373

Fat, large neck circumference, nasal obstruction, enlarged tonsils, narrow oropharynx, macrflossia, retro or micrognathia

Question 374

Testing OSA

Answer 374

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

Question 375

Differential OSA

Answer 375

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

Question 376

Treat OSA goals

Answer 376

Improve daytime sleepiness and cognitive performance and to prevent long term sequelae

Question 377

Treat osa

Answer 377

Lifestyle and CPAP Oral devices or upper airway surgical procedures Don’t drive until resolved

Question 378

If persists despite preventions

Answer 378

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

Question 379

Bad CPAP

Answer 379

Hard to use Can get heated humidification, education, follow up

Question 380

If still can’t use CPAP

Answer 380

Bi level positive airway presssure nasal ventilation or auto-titrating positive pressure devices that modify airflow pressure to a more comfortable level.

Question 381

Mandibular advancement devices

Answer 381

Alternative therapy; however eliminate the need for CPAP in only mild to moderate

Question 382

Surgery

Answer 382

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.

Question 383

What do to document eddect of mandibular advancement device

Answer 383

Follow up polysomnogram

Question 384

Common causes of COPD

Answer 384

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

Question 385

DIFFERENTIAL for COPD

Answer 385

Asthma, bronchiectasis,CF

Question 386

Stage I GOLD

Answer 386

FEV1/FVC<70%; FEV1>80% of predicted With or without chronic symptoms (cough, sputumproduction)

Question 387

II COPD

Answer 387

FEV1/FVC<70%; 50%

Question 388

GOLD III severe

Answer 388

FEV1/FVC<70 30%

Question 389

State IV COPD

Answer 389

FEV1/FVC<70%; FEV1<30% or FEV1<50% plus chronic respiratory failure

Question 390

Treat mild

Answer 390

SABA

Question 391

Treat II

Answer 391

Add regular treatment with one or more long acting bronchodilators; add pulmonary rehabilitation

Question 392

Stage III treat

Answer 392

Add inhaled corticosteroids if repeated exacerbations

Question 393

TreatIV

Answer 393

Add long term oxygen therapy if chronic respiratory failrue; consider surgical treatments

Question 394

Difference between interstitial pneumonia’s and idiopathic pulmonary fibrotis

Answer 394

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.

Question 395

UIP

Answer 395

Hallmark different stages Starts subpleural Pneumoconiosis, radiation injury, end stage hypersensitivity, sarcoid

Question 396

NSIP

Answer 396

Uniforminvolvement of lung parenchyma with cellular infiltration or fibrosis. Bilateral, subpleural, correlating ground glass infiltrates on CT imaging andlittle honey combing. AutoimmuneCT

Question 397

BOOP

Answer 397

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

Question 398

Treatment DPLD

Answer 398

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

Question 399

Drugs DPLD

Answer 399

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),

Question 400

Anti fibrotic medications for DPLD

Answer 400

?

Question 401

Usual interstitial pneumonitis UIP

Answer 401

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

Question 402

Nonspecific interstitial pneumonitis

Answer 402

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

Question 403

BOOP

Answer 403

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

Question 404

Diagnosis DPLD

Answer 404

History, PE, lab, imaging, lung biopsy

Question 405

Presentation DPLD

Answer 405

Progressice dyspnea, reduced exercise tolerance, and a persistent dry cough should raise the possibilty Gradual onset

Question 406

History DPLD

Answer 406

Meds, workplace, env exposures

Question 407

>50

Answer 407

Idiopathic pulmonary fibrosis

Question 408

20-40

Answer 408

Interstitial lung disease associated with CT disease, sarcoidosis, lymphangioleiomyomatosis, and langerhan

Question 409

Female DPLD

Answer 409

Lemphangioleiomyomatosis

Question 410

Smoking

Answer 410

Respiratory bronchiolitis associated with interstitial lung disease, desquamative interstitial pneumonia and langerhan

Question 411

Exposure to bird

Answer 411

Hypersensitivity

Question 412

Acute onset

Answer 412

Idiopathic pulmonary fibrosis, acute eosinophilic pneumonia, COP, hypersentivity, drug induced,

Question 413

Clubbing

Answer 413

Idiopathic pulmonary fibrosis

Question 414

Erythema nodosum

Answer 414

Associated with sarcoidosis, CT diseases

Question 415

Uveitis/conjunctivitis

Answer 415

Associated with sarcoidosis, CT disease

Question 416

CXR

Answer 416

Increase interstitial reticular or nodular infiltrates, often in bases

Question 417

HRCT

Answer 417

Detail about distribution and extend of disease

Question 418

Basal predominant

Answer 418

IPF< asbestosis, NSIP

Question 419

Upper lobe predominant

Answer 419

Hypersensitivity pneumonitis, sarcoidosis, silicosis

Question 420

Peripheral

Answer 420

IPF< chronic eosinophilic pneumonia, COP

Question 421

Central

Answer 421

Sarcoidosis, pulmonary elveolar proteinosis

Question 422

Mosaic attenuation

Answer 422

Small airways disease,

Question 423

PFT DPLD

Answer 423

Decreased lung volume and decreased diffusing capacity

Question 424

Smoking related

Answer 424

Interstitial in smokers, respiratory bronchiolitis interstitial lung disease, desquamative interstitial pneumonitis, langerhans

Question 425

CT associated DPLD

Answer 425

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

Question 426

Sarcoidosis

Answer 426

Granulomatous disease of unclear cause >18 Blacks Noncaseating granulomas involving lung and other organs

Question 427

Chronic bronchitis

Answer 427

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

Question 428

Asthma

Answer 428

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

Question 429

Bronchiectasis

Answer 429

Failure of the normal narrowing of the airway resulting in wider airways. Secondary to infection but may have a number of other causes

Question 430

Interstitial lung disease

Answer 430

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

Question 431

Pleural effusion

Answer 431

Sputum gets trapped between the visceral and parietal pleura. It can be from a number of different causes

Question 432

Pulmonary htn

Answer 432

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

Question 433

Common diagnosis in patients who present with cough acute

Answer 433

*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

Question 434

Chronic cough cause

Answer 434

Upper airway cough syndrome Asthma GERD Non asthmatic eosinophilic bronchitis Bronchiectasis Medication reaction (ACE-i_ Chronic bronchitis caused by smoking

Question 435

How upper viral infection cause cough

Answer 435

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

Question 436

Influenza symptoms

Answer 436

Sudden onset of fever and malaise followed by cough , HA, myalgia and nasal and pulmonary symptoms,

Question 437

Influenza signs

Answer 437

Fever, cough, pharyngitis, rhinorrhea

Question 438

How diagnose influenza

Answer 438

Secretion culture, IF, PCR,

Question 439

Chemoprophylaxis ho gets

Answer 439

Residents in assisted living

Question 440

H1N1 symtpoms

Answer 440

Cough, fever rhinorrhea, person to person transmission

Question 441

Nonviral caues of acute bronchitis

Answer 441

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

Question 442

Pneumonia

Answer 442

Most serious cause of cough Fever, diminished breadth sounds,

Question 443

Asthma cough

Answer 443

Acute cough

Question 444

Chronic bronchitis and bronchiectasis

Answer 444

Abrupt increase from baseline in cough, sputum production, sputum pursuance, and SOB

Question 445

Treat acute cough

Answer 445

Antitussive agents, expectorants, mucolytic agents, antihistamines, nasal anticholinergic agents.

Question 446

Indications for treatment with cough

Answer 446

Sleep disruption, painful cough, and debilitating cough

Question 447

That was all acute cough

Answer 447

Ok

Question 448

What is chronic cough

Answer 448

>8 weeks

Question 449

Common cause of chronic cough

Answer 449

Upper airway cough syndrome Asthma GERD Non asthmatic eosinophilic bronchitis Bronchiectasis I Ace-i Chronic bronchitis caused by smoking

Question 450

Evaluation chronic cough

Answer 450

History, PE, chest radiography* Smoking cessation and stop ace before more workup

Question 451

Most chronic cough in non smokers, normal chest x ray and not on ace

Answer 451

Upper airway cough syndrome Asthma GERD

Question 452

Upper airway cough syndrome

Answer 452

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.

Question 453

Cough variant asthma chronic

Answer 453

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)

Question 454

GERD cough

Answer 454

By aspiration Vaguely mediated distal esophageal tracheobronchial reflex 24 hour esophageal pH monitoring PPI if find symptom may not relieve for three months

Question 455

Nonasthmatic eosinophilic bronchitis chronic cough

Answer 455

Presence of airway eosinophilia Inhaled glucocorticosteroid

Question 456

Cough with sputum

Answer 456

Chronic bronchitis -stop smoking, inhaled anticholinergic agent , glucocorticoids, antibiotic,

Question 457

Bronchiectasis

Answer 457

Sputum with purulent Chest. Radiography and CT results tram line pattern Antibiotics based on sputum

Question 458

Smoke

Answer 458

Most have chronic cough, but don’t usually get medical attention Stop smoking resolve 94-100% Within 4 weeks!

Question 459

Cough caused by ACE i

Answer 459

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

Question 460

Hemoptysis

Answer 460

Acute or chronic cough Usually from infection (bronchitis or pneumonia) followed by malignancy

Question 461

What ekse may cause the hemoptysis

Answer 461

Elevated pulmonary pressure from left sided heart failure or pulmonary embolism

Question 462

Cryptogenic hemoptysis

Answer 462

Cause not known

Question 463

What do if hemoptysis

Answer 463

Chest radiography —-encobronchial lesion not always seen on CT do do bronchoscope too

Question 464

MASSSIVE HEMOPTYSIS

Answer 464

BLOOD LOSS GREATER THAN 200 ML.DAY. MASSIVE HEMOPTYSIS REQUIRES URGENT INPATIENT EVALUATION. AIRWAY MANAGEMENT AND VENTILATOION URGENT BRONCCHOSCOPY

Question 465

DYSPNEA

Answer 465

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”

Question 466

MOA dyanpnea

Answer 466

Impaired ventilator mechanics Increase in respiratory drive

Question 467

Impaired ventilator mechanics

Answer 467

Airflow obstruction, muscle weakness, decrease in chest wall compliance

Question 468

Impaired respiratory drive

Answer 468

Parenchymal or pulmonary vascular lung disease, congestive heart failure, chemoreceptor stimulation, impaired gas exchange, pregnant,

Question 469

Diagnose dyspnea

Answer 469

History and PE vitals -if tachypnea acute muscle use, or conversational dyspnea transfer to an acute setting

Question 470

Grade 1 dyspnea

Answer 470

Not troubled by breathlessness except on strenuous exercise

Question 471

Grade 2 dyspnea

Answer 471

Short of breath when hurrying on the level or walking up a sling hill

Question 472

Grade 3 dyspnea

Answer 472

Walks slowe than most people on the level, stops after a mile or so, or stops after 12 minutes walking at own pace

Question 473

Grade 4 dyspnea

Answer 473

Stops for breath after walking about 100 yards or after a few minutes on level grounf

Question 474

Grade 5 dyspnea

Answer 474

Too breathless to leave the house or breathless when undressing

Question 475

Acute dyspnea

Answer 475

Develops rapidly over minutes to a day

Question 476

Differentiat for acute dyspnea

Answer 476

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

Question 477

Patient presents with acute dyspnea

Answer 477

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

Question 478

Chronic dyspnea

Answer 478

Longer than 1 month

Question 479

Top causes chronic dyspnea

Answer 479

COPD, asthma, interstitial lung disease, HF Also maybe pulmonary vascular disorders, valvular and pericardial heart disease, anemia, and thyroid disease

Question 480

Work up chronic dyspnea

Answer 480

History

Question 481

Worsening conditions chronic dyspnea

Answer 481

Natural disease progression, medication noncompliance, and exposure to environmental or dietary factors

Question 482

Chronic dyspnea with no chronic disease

Answer 482

Cardiac related volume overload-orthopnea, edema, or exertional symtpms —look at JVD, hepatojugular refluc, murmurs s2, or s4 gallop and pulmonary and peripheral Echo

Question 483

If no chronic disease or heart issues and chronic dyspnea

Answer 483

Pulmonary-wheezing, sough, smoking, env exposure

Question 484

What if no lung

Answer 484

Specific testing for issues

Question 485

Lung cancer major risk factors and etiology agents responsible

Answer 485

Cigarettes -mainly small cell is most bad Head neck-alcohol, tobacco ..synergistic

Question 486

Complaints and symptoms and clincial findings in patients with cancer of lung

Answer 486

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

Question 487

What is necessary for diagnosis of lung cancer

Answer 487

Histologic confirmation

Question 488

Sputum cytology

Answer 488

Reserved for poor pulmonary function who cant tolerate invasive procedures

Question 489

Acromegaly

Answer 489

Growth hormone releasing hormone

Question 490

Cushing syndrome

Answer 490

Adrenocorticotropic hormones (SSC)

Question 491

Lambert Eaton myasthenic syndrome

Answer 491

Proximal limb wewawkness and fatigue due to antibodies to voltage gated calcium channels (SSC)

Question 492

Hypercalcemia

Answer 492

PTH related peptide

Question 493

Hypertrophic pulmonary osteoarthropathy

Answer 493

Painful new periosteal bone growth and clubbing (adenocarcinoma)

Question 494

Hyponatremia

Answer 494

Syndrome of inappropriate antidiuretic hormone SSC)

Question 495

Pancoast syndrome

Answer 495

Shoulder pain, lower brachial plexopathy, and Horner syndrome from apical lung tumor (NSCC

Question 496

Superior vena cava syndrome

Answer 496

External compression of superior vena cava causing face and arm swelling (SCC)

Question 497

Trousseau syndrome

Answer 497

Hypercoagulable stae (most common with adenocarcinoma)

Question 498

Vocal cord paralysis

Answer 498

Entrapment of recurrent laryngeal nerve

Question 499

Horner syndrome

Answer 499

Ptosis, miosis, and anhidrosis, can be produced by a lesion anywhere along the sympathetic pathway that supplies the hand eye and neck

Question 500

Staging

Answer 500

Look for metastatic..eliminates surgery as option

Question 501

How find staging info

Answer 501

CT, PET-CT, brain imaging if neurologic symtpoms Bone scan if bone pain

Question 502

SSC

Answer 502

Systemic at diagnosis soncidered Sensitive to radiation and chemo CT PET-CT and serum electrolytes, aminotransferase and lactate DH also for staging

Question 503

Where does SCC spread

Answer 503

Liver bone, brain adrenal retroperitoneal lymph nodes, pancreas and subcutaneous ST

Question 504

What is an incidental pulmonary nodule

Answer 504

Asymptomatic discrete radiographically density<3 cm that is completely surrounded by aerated lung.

Question 505

Benign pulmonary nodule

Answer 505

No growth in two years Calcification in a diffuse central or laminar pattern

Question 506

Malignant nodules

Answer 506

>2 cm, have speculated edges, and are located int he upper lobes. The probability of malignancy increases with age over 40, smoking, asbestos, radon

Question 507

Manage pulmonary nodules

Answer 507

Determine behavior over time and stratify risk. Find previous radiography

Question 508

Nodule <4 mm

Answer 508

No follow up if never smoked and no other risk factors

Question 509

Nodules >4 mm

Answer 509

Follow up

Question 510

Solid nodules

Answer 510

In high risk require a consideration for immediate biopsy close interval CT scanning in another option in low risk patients

Question 511

T

Answer 511

Size

Question 512

N

Answer 512

Regional node status

Question 513

M

Answer 513

Metastatic

Question 514

Treatment 1 and II

Answer 514

Surgery Also some III And adjunct chemo in IB >3 vom

Question 515

Early stage non small cell if inoperable

Answer 515

Radiation but not helpful

Question 516

Stage III

Answer 516

Mediastinal lymphadenopathy Chemo to shrink prior to surgery

Question 517

Unresectable disease

Answer 517

Chemoradiation is superior to radiation alone. Encourage stop smoking

Question 518

Metastatic inoperable IV non small cell

Answer 518

Local radiation, palliative chemo Not beneficial with poor performance

Question 519

Decrease skeletal complications in patients with bony metastases

Answer 519

Monthly IV bisphosphonate therapy or monthly subcutaneous dosing of the RANK ligand inhibitos denosumab decreases skeletal complications in patients with bony metastases

Question 520

SSC

Answer 520

Chemo and platinum based agent and etoposide markedly improves survival

Question 521

SSC

Answer 521

MOST DIE | If tumor respond it will relapse explain that improvement is short lived

Question 522

Palliative treatment

Answer 522

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

Question 523

Cancers of the respiratory system

Answer 523

Epithelial-mucosal usually squamous cell -paranasal sinuses, oral cavity, and nasopharyngeal, oropharynx, Salivary gains-heterogenous and rate

Question 524

Identify the major risk factors for the development of cancer of the head and neck

Answer 524

Usually oral cavity, oropharynx, or larynx Oropharyngeal on rise Alcohol and tobacco!! Synergy stick together

Question 525

Smoking cancer

Answer 525

Older than 60

Question 526

HPV cancer

Answer 526

40s or 50s

Question 527

EBV

Answer 527

All ages

Question 528

Nasopharnx

Answer 528

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

Question 529

Carcinoma of oral cavity

Answer 529

Non healing ulcers Changes in fit of dentures or painful lesions Decreased tongue or speech HPV-neck lymphadenopathy at first sign

Question 530

Hoarseness

Answer 530

Laryngeal

Question 531

Advanced head and neck cancer

Answer 531

Severe pain, otalgia, airway obstruction, cranial neuropathies, trismus, enlarged nodes

Question 532

If enlarged nodes are located int he upper neck and the tumor cells are of squamous cell histology

Answer 532

Mucosal surface in the head or neck

Question 533

Supraclavicular node

Answer 533

Primary site in chest or abdomen

Question 534

PE head and neck cancer

Answer 534

Mucosal palpation and lymphnodes Leukoplakia or erythroplakia -premalignant biopsy them CT PET

Question 535

Staging

Answer 535

Anesthesia laryngoscopes, esophagoscope ad bronchoscopy with multiple

Question 536

T1-T3

Answer 536

Increasing size

Question 537

T4

Answer 537

Invasive

Question 538

Treat

Answer 538

Localized, locally or regionally advanced disease, recurrent and/or metastatic

Question 539

Localized treat

Answer 539

T1-T2 Curative intent with surgery or radiation

Question 540

Locally or regionally advanced disease

Answer 540

Large primary tumor and/or lymph. Node metastases Curative intent-combined modality thatpy surgery radiation, chemo

Question 541

Recurrent and or metastatic disease

Answer 541

Palliative intent 5-FU cisplatin, cabroplatin with 5-FU and cisplatin EGFR therapies including antibodies and TKI have activity against 10%

Question 542

Pneumothorax essentials of diagnosis

Answer 542

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

Question 543

Pleural effusion

Answer 543

Ok

Question 544

Transudative pleural effusion

Answer 544

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

Question 545

Symptoms of pleural effusion

Answer 545

Fever, dyspnea and chest pain

Question 546

Exudative

Answer 546

Inflammatory, infectious, malignant Collagen vascular disease, intraabdominal process

Question 547

Pathophysiology pneumothorax

Answer 547

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

Question 548

Describe management pneumothorac

Answer 548

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....

Question 549

# Define mediastinal compartments and their contents Medistinum-region between the pleural acs and has three compartments

Answer 549

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

Question 550

Anterior mediastinal

Answer 550

Thymomas, lymphomas, teratomas our neoplasms, thyroid masses

Question 551

Middle mediastinum

Answer 551

Vascular masses, lymph node enlargement from metastases or granulomatous disease and pleuropericardial and bronchogenic cysts

Question 552

Posterior mediastinum

Answer 552

Neurogenic tumors, meningoceles, meningomyeloceles, gastroenteritis cysts, and esophageal diverticula

Question 553

Squamous cell carcinoma head a neck region

Answer 553

5% of all cancers Higher incidence of death in african descent Men 50-60

Question 554

Risk factors

Answer 554

Smoke, alcohol, non smoke tobacco

Question 555

Field cancerization

Answer 555

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!!

Question 556

Complaints of cancer head neck

Answer 556

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

Question 557

Viral cause head neck cancer

Answer 557

EBV -nasopharyngeal HPV western—-oropharync 16 16 Younger and sex a lot of partners ..better prognossi

Question 558

Assess nutritional and performance status of patient

Answer 558

How effected a patient is Few symtpoms vs cant work cant daily live need assistance Dietary factors-low fruit an veg Caretonoids-protective

Question 559

Laryngectomy

Answer 559

Remove vocal sound

Question 560

Treat cancer

Answer 560

Radiotherapy Surgery -laryngectomy Systemic therapy

Question 561

Electrolarynx

Answer 561

Placed in submandibular region Vibrates at constant pitch to allow speech

Question 562

Tracheostomy

Answer 562

Provides. Synthetic set of vocal cords for speech

Question 563

Squamous cell carcinoma types

Answer 563

Poorly differentiated, moderately, differentiated

Question 564

Worse prognosis

Answer 564

Poorly defined

Question 565

EBV

Answer 565

Undifferentiated

Question 566

Erythroplakia pre cancer

Answer 566

Red patch

Question 567

Leukoplakia pre cancer

Answer 567

White patch

Question 568

What do with nonspecific signs and symptoms in head and neck with symptoms more than 2-4 weeks

Answer 568

Thorough otolaryngologists exam

Question 569

Males or females HPV cancer neck

Answer 569

Males

Question 570

Symptoms nasopharynx cancer

Answer 570

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

Question 571

Carcinoma of oral

Answer 571

Nonhealing ulcers, change in fit of dentures, painful lesions. Decreased tongues mobility.

Question 572

Oropharynx or hypopharync cancer

Answer 572

Early early symptoms | Sore throat or otalgis

Question 573

HPV tumor sign

Answer 573

Lymphadenopathy first sign

Question 574

Laryngeal cancer

Answer 574

Hoarseness

Question 575

Advanced symptoms any head and neck

Answer 575

Pain, otalgia, airway obstruction, CN neuropathies, trismus, odynophagia, dysphagia

Question 576

Progressive issue swallow base in tongue, squamous cell carcinoma with no lymph node involvement and locally advanced disease-growing into adjacent structures How treat

Answer 576

Initial radiotherapy and chemo then surgery

Question 577

Enlarged nodes in upper neck and tumor cells are of squamous cell histology,

Answer 577

Probably squamous cell from mucosal surface

Question 578

What do if have lymph node involvement

Answer 578

CT of chest and upper abdomen

Question 579

Definitive statin

Answer 579

Endoscopic examination under anesthetics

Question 580

Stage I

Answer 580

T1 tumor <2cm without extra parenchymal extension NO No regional lymph node metastasis

Question 581

Stage II

Answer 581

T2 >2 cm but not more than 4 cm without extra parenchymal extension N-

Question 582

Stage III

Answer 582

Tumor >4 cm N1, metastasis in a single ipsilateral lymph node <3 cm in greater

Question 583

stave T4a

Answer 583

Tumor invades skin, mandible, ear canal, and or fascia nerve N2

Question 584

T4b

Answer 584

Tumor invades skill base and/or pterygoid plates and/or encases carotid artery N3

Question 585

35 yo man throat pain given antibiotics no improvement gets hoarseness, smokes and drinks, works in wood working shop

Answer 585

Occupational exposure can cause cancer wood working-inhaling things Increase risk

Question 586

What if lymph node involvment

Answer 586

Biopsy of all suspicious appearing ares and primary site

Question 587

Treat

Answer 587

Localized, locally or regional advanced disease, and recurrent and/or metasticize

Question 588

Treat localized disease

Answer 588

Curative intent surgery Laryngeal-radiation to preserve voice 60% survival Most recurrence in first two year

Question 589

Treat locally or regionally advanced disease

Answer 589

Curative intent with combined therapy including surgery radiation therapy and chemo or as concomitant

Question 590

Prevent

Answer 590

Avoid exposure

Question 591

Recurrent

Answer 591

Palliative Cisplastin with 5-FU EGFR therapies, antibodies, TKI

Question 592

Complications of treating dad and neck cancer

Answer 592

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

Question 593

Lung cancer top three causes

Answer 593

Smoking smoking smoking Second hand Radon Coal tars Agricultural farmers

Question 594

Majority lung cancer

Answer 594

Non small cell Rest are small cell

Question 595

Prevention

Answer 595

Stop smoking Give retinol, B carotene, N acetylcysteine, and selenium

Question 596

Screening

Answer 596

Low dose computed tomography scans to screen for early stage in former or current smokers

Question 597

Diagnosis lung cancer

Answer 597

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

Question 598

Bronchogenic carcinoma

Answer 598

Small cell Non small cell

Question 599

What need to diagnosis

Answer 599

Histology confirmation

Question 600

Pancoast

Answer 600

Superior sulcus tumor invade brachial plexus Shoulder pain paresthesia C7-T1

Question 601

Horner

Answer 601

Ipsilateral anhydrosis pupil constriction due to stellate ganglion Psosis, ahydrosis, superior sulcus

Question 602

Hypertrophic pulmonary osteoarthropay

Answer 602

Clubbing of distal phalanges and hypertrophy of joints Arthralgias, synovitis, and Facies furrowing of brow!! Painful, ner periosteal bone growth and cladding (adenocarcinoma) Hypoxemia...

Question 603

Superior vena cava

Answer 603

Extrinsic compression of SVC compression of by mass, adenopathy Distention of superficial veins and edema of face and neck Face and arm swelling

Question 604

What do

Answer 604

1.Chest x ray, guide thinking Will see node if >2 cm in size 2. 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

Question 605

Sputum cytology

Answer 605

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

Question 606

Mediastinoscope

Answer 606

Can see hilum and mediastinal structure for tumor resection...do it if thinking of remove to make sure we know

Question 607

Diagnose

Answer 607

Fine needle aspiration Done with radiograph or CT insert into tumor ..good for peripheral lung tumor Risk of pneumothorax.. Central-croncospocy FNA-peripheral

Question 608

SSC confined to one side, limited ok

Answer 608

Not extensive 15-25% cure

Question 609

Extensive SCC

Answer 609

95% die in few years

Question 610

Blood sputum in smoker

Answer 610

CT scan see if peripheral or central Central-bronchoscopy Peripheral-fine needle aspiration

Question 611

Tension pneumothorax

Answer 611

Mediastinal shift Can get in asbestosis

Question 612

Hydro pneumothorax

Answer 612

See water line

Question 613

Similarities pneumothorax or pleural effusion on exam

Answer 613

Sausculataion Absent or diminished breath sounds

Question 614

Differensions pneumothorax and pleural effusion

Answer 614

Percussion -hyperresonant in pneumothorax, dull in pleural effusion Auscultation -positional changes of breath sounds No change in pneumothorax May improve in effusion

Question 615

Causes of pneumothorax

Answer 615

Spontaneous-young men Traumatic -post procedural, direct trauma Disease related -numerous diseases

Question 616

Exudate

Answer 616

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

Question 617

Low pleural glucose

Answer 617

Parapneumonic effusion Malignant effusion Tb Hemothorax RA

Question 618

Pleural white cells

Answer 618

Normal pleural space | -macrophages 75% lymphocytes 25%

Question 619

Disease of pleural white cells Increase eosinophils

Answer 619

Increase eosinophils>10% Most often due to air in the pleural space Idiopathic parapneumonic Malignancy

Question 620

Pleural white cells lymphocytic effusion

Answer 620

Malignancy | Tb

Question 621

Transudate

Answer 621

LVF, CHF Other -misplaced central line, massive cirrhosis, nephrosis

Question 622

Exudate

Answer 622

Everything else

Question 623

Manage chronic pleural effusion pleurX

Answer 623

Indwelling catheter in pleural space allowing for at home drainage

Question 624

Pleurodesis

Answer 624

-closes potential space between parietal and visceral pleura -talc, tetracycline others Through thorascope on in IR

Question 625

What are mediastinal disease

Answer 625

Masses, inflammation/infection. Air or fluid collection

Question 626

4 t of the anterior mediastinum

Answer 626

Thymoma Teratomas Thyroid masses Terrible lymphoma-well there can be B cell lymphomas with mediastinal masses, as well as Hodgkin lymphoma

Question 627

MIDDLE MEDIASTINAL MASSESS

Answer 627

VAC VASCULAR masses, adenopathy, cysts-pleuropericardial, bronchogenic

Question 628

Posterior mediastinal massess

Answer 628

Nerves and guts - neurogenic tumors, - meningoceles, meningomyeloceles - gastroenteritis cysts and esophageal diverticula

Question 629

What causes pleural effusion

Answer 629

Increased