Lung And Upper Resp. Tract I

Front 1

Pneumonia

Back 1

responsible for 1/6 of all deaths in the US

Front 2

What are the host defense mechanisms that filter out inhaled particulates and contaminated air?

Back 2

1. mucociliary clearance
2. macro. engulfment with help of complement
3. humoral IgA neutralization of bacteria and viruses

Front 3

What happens if you have a deficient humoral immune system in the pulm. system?

Back 3

leads to increased incidence of extracellular bacterial infection

Front 4

What happens if you ahve a deficient cellular immune system in the pulm. system?

Back 4

leads to increased incidence of intracellular viral and mycobacterial infection

Front 5

Community Acquired Pneumonia

Back 5

usually bacterial
-strep. pneumoniae
-haemophilus influenzae
-moraxella catarrhalis

Front 6

What groups and at increased risk for developing pneumonia?

Back 6

1. elderly
2. sickle cell anemia
3. COPD patients
4. diabetic patients
5. AIDs patients

Front 7

Pneumococcus

Back 7

usually aspiration of pharyngeal flora causes bronchopeumonia or lobar pneumonia
*RML and lower obes affected most

Front 8

What are the three types of pneumonia?

Back 8

1. lobar pneumonia
2. bronchopneumonia
3. hematogenous disemination of infection (infection some place else in body)

Front 9

What are the 4 phases in lobar pneumonia?

Back 9

1. congestion- boggy red lung w/ vascular congestion and prteinaceous fluid in the alveoli
2. red hepatizaiton- liver like consistency w/ the alveoli packed w/ neutrophils, red cells and fibrin
3. gray hepatization- dry, gray, and firm with fibrinous exudate persisting and lysis of red cells
4. resolution- exudates ingested by macro., resorbed and or expectorated

Front 10

Bronchopneumonia

Back 10

-inflamm. patches seen throughout one or several lobes
-well developed lesions appear as 3-4cm, yellow-whate and discrete

Front 11

What is the treatment for pneumococcal pneumonia?

Back 11

1. penicillin- except when resistant
2. clarithromycin- macrolide capable of concentrating the lung
3. cephalosporins- for resistant infections

Front 12

What is the prevention for pneumococcal pneumonia?

Back 12

vaccination for elderly and immune suppressed containing 23 common serotypes

Front 13

What are 4 complications from pulmonary infections?

Back 13

1. abscess formation with extension to the pleura
2. empyema- pleural space extension of abscess
3. organgization may convert the lung into solid fibrous tissue
4. bacterial dissemination leading to meningitis, arthritis, infective endo., bacteremia and resultant sepsis

Front 14

Haemophilus influenzae

Back 14

-both encapsulated and unencapsulated form cause CAP
-encapuslated type B H. influenzae have been eradicated with pediatric vaccination- caused epiglottitis

Front 15

Moraxella catarrhalis

Back 15

-cause pneumonia in elderly
-*2nd most common cause of pneumonia in adults with COPD
-cuase of otitis media infection w/ the other 3 CAP assoc.. bacteria

Front 16

Staph. aureus

Back 16

-important cause of secondary bacterial pneumonia in children follwoing viral pneumonia
-assoc. w/ abscess form and empyema
-more of a nosocomial pathogen

Front 17

Klebsiella pneumoniae

Back 17

-*most frequent g- bacterial pneumonia affecting malnourished, debilitated patients and alcoholics
-characterized by thick gelatinous (currant jelly) sputum from the exopolysaccharide capsule of the bacteria

Front 18

Pseudomonas aeruginose

Back 18

-assoc. w/ pneumonia of cystic fibrosis patients (more noscomial)
-common in patients who are neutropenic or burn patients
-more likely to go in bld stream w/ invasion of BV causing necrosis of lung parenchyma

Front 19

Legionella pneumophilia

Back 19

-Legionaire's disease causing fulminant pneumonia w/ a fatality rate of 30-50%
-affects elderly w/ chronic conditions and transplant patients
-natural in stagnant water where it attacks amoeba, but can be found in air ducts

Front 20

Pontiac Fever

Back 20

Legionella pneumophila infection in immunocompetent host

Front 21

What are the 4 community acquired atypical pneumonias?

Back 21

1. Mycoplasma pneumoniae
2. Chlamydiae pneumoniae
3. Coxiella burnetti (Q fever)
4. Viruses: RSV, parainfluenza virus, adenovirus, etc.

Front 22

Atypical CAP

Back 22

-most agents cause mild upper respiratory symptoms in children, adolescents, and young adults
-spread by airborn route in closed quarters
-usually self limited w/ life long immunity for that particular serotype (not commong in elderly

Front 23

What is the treatment for atypical CAP?

Back 23

-most mycoplasma treated w/ azithromycin
-sypmtomatic treatment
-isolation form work, school, etc.

Front 24

Tuberculosis

Back 24

-communicable, airborne disease causing caseating granulomas of the lung by mycobacterium tuberculosis
*leading cause of death worldwide

Front 25

What are the tuberculosis risk factors? (9)

Back 25

1. low socioeconomic status
2. diabetes mellitus
3. Hodgkin's Disease
4. HIV
5. chronic lung disease
6. chronic renal failure
7. malnutrition
8. alcoholism
9. immunosuppression

Front 26

What kind of immunitiy is vital to suppressing TB infection?

Back 26

T cell mediated immunity

Front 27

What is the pathogenesis of TB?

Back 27

1. inoculation from the environment
2. walling off of infection within the lung
3. dormancy of the mycobacteria

Front 28

PPD Test

Back 28

-TB leads to delayed hypersensitivity of the tuberculin antigen with peak induration, erythema, and itching in 48-72hrs
-immunosuppression may lead to a false negative test

Front 29

What is the etiology of TB?

Back 29

-acid fast slender rods w/ complex lipid shell w/ humans serving as the only natural resorvoir
-contraction is by direct airborne inoculum w/ active TB aerosol

Front 30

What is the pathogenisis of TB in an immunocompetent patient?

Back 30

-infection fo the lung parenchyma by the tubercle bacillus w/ form. or a single caseating granulom and adjacent calcified lymph node
-host repsone is to wall of teh infectiong and hypersinsitivity to the tuberculing Ag signfies acquisition of immunuity
-TB dorman for the remainder of life in host

Front 31

What is the Ghon Complex?

Back 31

calcified lymph nodes that occur with TB in immunocompetent host

Front 32

NRAMP1

Back 32

natural resistance assoc. macro. protein 1 gene polymorphisms especially amog black may have decreased microbicidal activity

Front 33

Primary TB

Back 33

TB in an unsensitized individual- elderly and immune-suppressed can lose their sensitized responses and develop primary TB more than once

Front 34

Ghon Focus

Back 34

lung parenchyma with caseous necrotic center

Front 35

Ghon Complex

Back 35

fibrotic lung parenchymal lesion with affected hilar lymph nodes

Front 36

Ranke Complex

Back 36

calcified lung parenchymal lesion w/ affected lymph nodes

Front 37

Secondary TB

Back 37

reactivation of TB arising in a sensitized host usually in the apical lobes b/c of high oxygen tension

Front 38

Progressive pulmonary TB

Back 38

erosion of lung parenchyma, vessels, and airways

Front 39

Miliary TB

Back 39

organisms drain into lymphatic channels w/ dissemination into thoracic duct and bld. stream producing diffuse abscesses in distant organs

Front 40

What is the clinical course of TB?

Back 40

asymptomatic to cachexia, dyspnea, malaise ad low grade fever and hemoptysis w/ erosion into BV and plerotic painw/ extension into pleura

Front 41

Plott's disease

Back 41

miliary TB of he spinal vertebral bodies with paraplegia if untreated

Front 42

How do you diagnose TB?

Back 42

-PCR amp. of TB DNA w/ as few as 10 organisms
-AFB pos. sputum
-cuture: 4-6 wks slow growth on 7H11 agar

Front 43

What is the treatment for TB?

Back 43

-regimen of 3 drugs for nonresistant types insoniazid, pyrazinamide, rifampin
-4 drugs for resistant isoiazid, pyrazinamide, rifampin, and ethambutol with other meds

Front 44

Atypical Mycobacteria

Back 44

1. mycobacterium avium-intracellular
2. mycobacterium kansasii
3. mycobacterium chelonae-abscessus
-affect immunocompromised and treated w/ larger drug regimens

Front 45

Fungal Infections

Back 45

-classified as yeasts (budding) and molds (hyphal)
-all fungi can infect the lungs depending on host immune status

Front 46

What categories are fungal infections divided into? (4)

Back 46

1. superficial
2. subcutaneous
3. deep seated
4. opportunistic infections

Front 47

Candida

Back 47

*most frequent disease causing fungus, normally in GI tract and vagina
-has yeast and pseudohyphae in tissue
-may be diplayed in tissue with silver stains

Front 48

What is the most frequent disease causing fungus?

Back 48

Candida

Front 49

Thrush

Back 49

-candida
-superficial infection of the oral cavity in people taking inhaled steroids, HIV and antibiotics

Front 50

Vaginitis

Back 50

candida especially in diabetics

Front 51

Esophagitis

Back 51

candida; hemtolymphoid malignancies and HIV patients

Front 52

Cutaneous Candida Infections

Back 52

nail (onychomycosis), nail folds (paronychia), hair follicles (folliculitis), fingers and toe webs spaes (intertrigo), ad penile skin (balanitis)

Front 53

Chronic Mucocutaneous Candidiasis

Back 53

refractory disease affecting mucous membranes, hair, skin, and nails assoc. with autoimmune polyglandular syndrome (endocrinopathies) and iis rare

Front 54

Invasive Candidiasis

Back 54

bloodborne disease with dissemination to various organs with abscesses to multiple organs found in immunodeficient patients

Front 55

Cryptococcosis

Back 55

-pulmonary disease in immunocopetent patients- usually self limited
-meningitis in HIV/AIDs patients

Front 56

What is the morphology of cryptococcus?

Back 56

-5-10microns yeast in tissue that has a thick gelatinous capsule and reproduces by buding with no pseudohyphal form seen
-diagnosed with India Ink and PAS stains in tissue and cryptococcal Ag test in fluids

Front 57

What kind of reaction does cryptococcosis have in tisse?

Back 57

-creates a granulomatous reaction in tissues
-in immunosuppressed forms "soap bubble" lesions seen in the spaces of the sulci in the brain and perivascular virchow-robin space

Front 58

How is cryptococcosis transmitted?

Back 58

-it is inhaled from bird droppings and evades host via capsular polysaccharide, resistance to macro. killing and production of phenol oxidase enzyme that consumes epinephrine to protect form protective oxidative reactions
-mainly in lung and can causec granulomatous chronic inflammatory reactions
-gets into CNS and grows meninges

Front 59

Mucomycosis

Back 59

-opportunistic mold in diabetic patients and other immunocompromised

Front 60

Pulmonary Mucormycosis

Back 60

localizeddisease may present radiologically as miliary pattern

Front 61

Rhinocerebral Mucormycosis

Back 61

colonize nasal tact and invade into the brain parenchyma (surgical emergency)

Front 62

Aspergillosis

Back 62

-opportunistic mold in immunosuppressed producing a necrotizing pneumonia with systemic dissemination

Front 63

Allergic bronchopulmonary aspergilosis

Back 63

patients who develop asthma may develop type I hypersensitivity to noninvasive aspergillosis growing in the bronchi and haveperipheral eosinophilia

Front 64

Aspergilloma

Back 64

occurs with colonization of preexisting pulmonar cavities (bronchiectasis or post-tuberculous cavities) that grow as balls and obstruct the bronchus with no tissue invasion

Front 65

Dimorphic Fungal Infections (3)

Back 65

seen in immunocompetent individuals found in endemic areas
1. histoplasma capsulatum
2. coccidioides immitis
3. blastomyces dermatitidis

Front 66

Histoplasma capsulatum

Back 66

intracellular 2-5 microns yeast form in vivo

Front 67

Coccidioides immitis

Back 67

thick walled nonbudding spherules 20-60 microns filled with small endospores in vivo

Front 68

Blasomyces dermatitidis

Back 68

oval 5-15 micron extracellular broad based budding yeast in vivo

Front 69

Where is H. capsulatum found?

Back 69

in the warm soil admixed with bird droppings in the Ohio and Mississippi rive valleys along the Appalachian mountains and southeast

Front 70

Where is C. immitis found?

Back 70

in the southwest paritcularly the San Joaquin valley in the soil

Front 71

Where is B. dermatitidis found?

Back 71

overlaps the Ohio and Mississippi river valleys where histoplasmosis is found

Front 72

Acute Pulmonary Infection

Back 72

resembles in most cases a flu like syndrome, self limited

Front 73

Chronic cavitary pulmonary disease

Back 73

cavitary lung disease with upper lobe involvement with cough, hemoptysis and chest pain

Front 74

Disseminated miliary disease

Back 74

infants, HIV patients takes the form of multiorgan disease witha minority of cases causing mouth and tongue lesions, cutaneous form iwht Bastomycosis mistaken for squamous cell carcinoma

Front 75

How do we diagnose dimorphic funal infections?

Back 75

1. skin test analogous to tuberculin hypersensitivity test
2. Histoplasmin, Coccidioidin PPD; o skin test exists for Blastomycosis
3. capsular Ag test for histoplasmin form the urin available

Front 76

Pneumocystis pneumonia (PCP)

Back 76

-opportunistic funal infection
-Pneumocystis jiroveci is causative org.
-serologic evidence of panexposure, however infection remains latent
-reactivation in the immunocompromised
-infection confined to lung producing hypoxia and interstitial pneumonitis with bibasilar infiltrates seen on CXR

Front 77

What is the histology of pneumocystis pneumonia?

Back 77

-intraalveolar foamy pink staining exudate with HandE stain
-GMS stain shows sup shaped org. (5-8microns) in alveoli

Front 78

How do we diagnose pneumocystis pneumonia?

Back 78

-mainly histology
-PCR based tests

Front 79

Cytomegalovirus

Back 79

member of herpesviridae

Front 80

How is CMV transmitted? (5)

Back 80

1. transplacental
2. perinatal infection through breast milk
3. preschool years asymptomatic to CMV mononucleosis
4. after 15yo verneral route
5. blood transfusions

Front 81

What is CMV produced from in the immunocopromised?

Back 81

-latent reactivated CMV due to depressed immune system
-CMV seroconversion from positive donor

Front 82

What does CMV produce?

Back 82

-pnumonitis developing into ARDS
-CMV retinitis

Front 83

What is the histology of CMV?

Back 83

parenchymal epithelial cells infected- produces "owls eye" nuclear changes

Front 84

How is CMV diagnosed?

Back 84

-histology
-Rising Ab titer- serology
-PCR based tests for CMV from DNA

Front 85

What is the number one cause of cancer related death in the US in both men and women?

Back 85

-carcinoma of the lung, rising in women

Front 86

Carcinoma of the lung

Back 86

-peak incidence 55-65
-at time of diagnosis 50% have metastasis w/ small cell at diagnoses 100% metastasis
-for all stages, 5yr survival = 14%

Front 87

Bronchogenic Carcinoma

Back 87

-non-small cell and small cell carcinoma

Front 88

Non-small cell carcinoma

Back 88

-amenable to surger, chemo and radiation
-squamous cell carcinoma
-adenocarcinoma
-large cell adenocarcinoma

Front 89

What is the most common primary tumor in women smakers and in patients <45yo?

Back 89

Adenocarcinoma

Front 90

Small cell carcinoma

Back 90

-not amenable to surgery, treated with chemo and radiation therapy
-may be combination of histological types

Front 91

Bronchogenic Carcinoma Mutations

Back 91

-early events: inactivation of tumor suppressor genes on 3p- found in normal epi cells exposed to carcinogens
-late events: TP53 mutations and K-RAS oncogene stimulation

Front 92

What percent of lung cancers is smoking assoc. with?

Back 92

90%

Front 93

What carcinomas show the stongest association with tobacco exposure? (2)

Back 93

1. squamous cell carcinoma
2. small cell carcinoma

Front 94

What is the pathology of carcinomas?

Back 94

-pseudostratified columnar epi
-squamous metaplasia
-dysplasia
-carcinoma
-may have central cavitation and necrosis of tumor
-form large bulky mass pushing into adjacent lungparenchyma, blood vessels and bronchi

Front 95

Squamous Cell Carcinoma

Back 95

-more common in men and tend to rise centrally from bronchus
-disseminate later than other histo. types
-transform from squamous metaplasia to dysplasia/carcinoma in situ to frank invasive carcinoma

Front 96

Keratinizing type of squamous cell carcinoma

Back 96

show keratin pearls and intercellular bridges (well differentiated) to poorly differentiated neoplasms with no squamous features

Front 97

Non-keratinizing type of squamous cell carcinoma

Back 97

-similar cells, no extracellular keratin
-intercelluar bridges

Front 98

Adenocarcinoma

Back 98

-more common in women and tend to arise peripherally from lung scars
-metastasize widely at presentation

Front 99

Which lung tumor has the weakest association with smoking?

Back 99

adenocarcinoma

Front 100

What is the histopathology of adenocarcinoma?

Back 100

shows intracellular mucin with vacuoloation indicating glandular differentiation to solid growth patterns

Front 101

Atypical Adenomatous Hyperplasia

Back 101

precursor lesion of the adenocarcinoma with cuboidal cells resembling Clara cells or type II pneumocytes and may be multifocal

Front 102

Bronchioalveolar Carcinoma

Back 102

subtype of adenocarcinoma with usually wideshpread involvement of the lung with growth along alveolar ducts that preserves alveolar architecture (can be multifocal)

Front 103

Large Cell Adenocarcinoma

Back 103

group of neoplasms which lackcytologic differentiation and represent squamous and adenocarcinomas

Front 104

What is the histopathology of large cell adenocarcinoma?

Back 104

may have osteoclast type giant cells (multinucleated) or sarcomatous type cells (spindle cells)

Front 105

Small Cell Carcinoma

Back 105

-appear as pale gray centrally located mass with extension into lung parenchyma and spreads beneath bronchi
-early involvement of the hilar and mediastinal nodes
-100% metastasis at presentation

Front 106

What is the histopathology of small cell carcinoma?

Back 106

-2-3X larger than lymphocytes
-monotonous appearance with high nuclear to cytoplasmic ratios and are derived from Kulchitsky cells (neuroendocrine cells)
-necrosis and mitotic figures
-nuclear molding

Front 107

What is nuclear molding?

Back 107

close apposition of tumor cells that makes nuclei appear to push each other (seen in small cell carcinoma)

Front 108

Malignant Mesothelioma

Back 108

-arise from parietal or visceral pleura with most cases occupational exposue to asbestos (25-40yrs after exposure)
-lifetime risk does not decrease with removal from asbestos exposure

Front 109

Combination of smoking and asbestos exposure increases the risk of ___________ but not ______________

Back 109

bronchogenic carcinoma
malignant mesothelioma

Front 110

What are the genetic mutations in malignant mesothelioma? (3)

Back 110

1. somatic mutations to p16/CDKN2A on chromosome 9p
2. neurofibromatosis gene 2 (NF2) on chromosome 22q
3. recently Simian virus 40 has been isolated in 60-80% malignant mesotheliomas

Front 111

Is surgery an option for malignant mesothelioma?

Back 111

-no because tumor is almost always unresectable
-chemo and radiation tried with little success

Front 112

What is the five year survival rate for malignant mesothelioma?

Back 112

>5%

Front 113

What is the progression of malignant mesothelioma?

Back 113

1. exposure to asbestos manifests as pleural fibrosis and plaque formation
2. lung ensheathed in a yelow-white firm tumor that obliterates the pleural space
3. invades the chest wall and subpleural lung tissue

Front 114

What is the histopathology of malignant mesothelioma?

Back 114

-normal mesothelial cells are biphasic giving rise to pleural lining cells and underlying fibrous tissue

Front 115

What are the three patterns that malignant cells confom to?

Back 115

1. epitheloid-line tubular and microcystic spaces with budding
2. sarcomatoid- spindle and fibroblastic appearing cells grow in nondistinctive sheets
3. biphasic- having both patterns