Non-Neoplasia

Front 1

1. Condition caused by a mucous or mucopurulent plug, a foreign body, intrabroncial clot, tumor, or extrinsic compression
2. Caused by Hydrothorax, hemothorax, pneumothorax, basal atelectasis

Back 1

1. Resorption Atelectasis
2. Compression atelectasis - extra pleural accumulation of material or loss of pleural space

Front 2

Microatelectasis ( non obstructive) due to:
General loss of expansion, multifactorial (loss of surfactant, interstitial inflammation, poor expansion)
- seen in RDS & post surgical

Back 2

Contraction atelectasis - local or generalized fibrosis interfere w/ expansion of lungs and increase elastic recoil during expiration

Front 3

1. Goal of quick Rx in atelectasis?
2. Atelectasis that is not treatable?
3. The episodic reversible bronchospasm resulting from an exagerated bronchoconstrictor response to stimuli

Back 3

1. Reverse it, reduce hypoxemia, prevent pneumonia
2. Contraction atelectasis
3. Asthma

Front 4

Atopic/extrinsic asthma:
1. Type of hypersensitivity
2. CD cell that drives the process
*elevated IgE and eosinophils

Back 4

1. Type I to extrinsic antigen
2. CD4+ T-helper --- other asthma mb 8+

Front 5

1. What is the most common type of asthma?
-airway is hyperresponsive, exagerated bronchoconstrictor response
2. Cytokines induced by the asthma induce what?

Back 5

1. Atopic
2. Synthesis of IgE, Mast cell production, Eosinophil production and activation

Front 6

In the early asthma phase (30-60 min) describe;
1. Cytokine production
2. IgE action
3. effect of vagal receptors in central and local reflex

Back 6

1. IL -4 Stimulates IgE produciton
IL- 5 activates local eosinophils, IL-13 stimulates local mucous produciton
2. coats submucosal mast cells, repeat exposure is bad
3. Bronchoconstriction

Front 7

1. When is the late asthma phase?
2. What types of cells are recruited?
--Chemotactic factors, LT, PAF, TNF
- mast cells are activated
- epithelial damage occurs

Back 7

1. 4-8 hrs later
2. Leukocytes, basophils, neutrophils, eosinophils

Front 8

1. Eotaxin is produced by what lung cells?
2. 2 proteins directly toxic to epithelial cells
3. Effect of eosinophil peroxidase?
4. Effect of LT and platelet activating factor?

Back 8

1. bronchial epithelial cells, macrophages, and smooth m.
2.Major basic protein and eosinophil cationic protein
3. oxidative tissue damage
4. inflammatory response w/o fresh antigen

Front 9

1. What is a non-immune form of asthma, associated w/ aspirin, pulm. infec., stress, exercise, inhaled stuff
2. IgE levels?
3. What appears to remain a key component of it?

Back 9

1. Intrinsic asthma - no allergic manifestations
2. normal - just a constitution prone to bronchospasm
3. Eosinophils

Front 10

IN asthma what happens to:
1. bronchi and bronchioles
2. Eosinophils can produce what histo finding
**increase in submucosal mucous glands, ^ goblet cells; epithelial injury, thick collagen under basement membrane, hypertrophy and hyperplasia of smooth m in large & med airways

Back 10

1. occluded by mucous plugs
2. Charcot-Leyden crystals

Front 11

In asthma see:
-dyspnea and wheezing
- air trapping and hyperinflation of lungs
- ^CO2, acidosis, severe hypoxia mb fatal
- Rx w/ bronchodilators and corticosteroids

Back 11

Emphysema - airspace enlargement w/ fibrosis
Probable most common form 2ndary to healed scarring from previous insult

Front 12

1. Permanent enlargement of airspace distal to the terminal bronchioles with destruction of alveolar walls
2. What are the 3 types of 1?

Back 12

1. Emphysema
2. Centriacinar, panacinar, and distal acinar => acinar and lobule are synonymous

Front 13

Emphesema types:
1. Alveoli after bronchiole – Associated with antitrypsin def. in lower
2. – Associated with spontaneous pneumothorax in young adults with bullae
3. Central acinus with respiratory bronchiole – Associated with smoking and in upper lobe

Back 13

1. Pan acinar
2. Distal acinar
3. Centriacinar- in the middle of the lobule

Bullae - large cystic space around the pleura

Front 14

Emphysema pathogenesis:
- competing imbalance of protease-antiprotease activity
- imbalance of oxidant-antioxidant
- associated w/ heavy smoking

Back 14

Pathogenesis of Chronic Bronchitis
- air pollutants cause irritation and hyper secretion of bronchial mucous glands and hypertrophy of glands
- T cell infiltrate CD8 & lack of eosinophils

Front 15

1. What is the normal alpha 1 antitrypsin genotype
2. Abnormal?
3. Result of abnormal
4. How can you acquire high protease levels?

Back 15

1. PiMM
2. PiZZ
3. Drop in antitrypsin levels and get emphysema
4. Smoking - nicotine is a chemotractant of neutrophils through TNF and IL & smoking enhances Macro. elastase (not inhib by antitryp)

Front 16

1. 2 things that act as 1 antioxidants in the lungs
2. What does smoking do to this?
3. what will eventually happen w/ bronchitis or emphysema?
4. Dif between asthma and chronic bronchitis in T cells and eosinophils

Back 16

1. Superoxide dismutase & glutathione
2. depletes the natural antioxidants
3. Hypoxia induced vasospasm, loss of capilaries due to alveolar destruction
4. Asthma (CD4, eos +), Bronch (CD8+, eos-)

Front 17

1. less dyspnea and resp. drive, retain CO2, became hypoxic/cyanotic, develop CHF (cor pulmonale), blue bloaters
2. Dyspnea, normal FVC, minimally reduced FEV1/FVC; enlarged air spaces, low diffusing capacity, hyperventilation, poor oxygen, pink puffer

Back 17

1. chronic bronchitis - hyperplasia of bronchial glands, loss of ciliated cells w/ squamous metaplasia, goblet cell metaplasia, chronic inflammation
2. Emphysema

Front 18

1. A persistent cough for at least 3 consec. months in at least 2 consec. yrs
2. What do mucus glands do in large airways?
3. Airflow obstruction is due to?

Back 18

1. Chronic bronchitis
2. Hyper secretion, increase Reid index
3. inflammation and fibrosis of bronchioles

Front 19

1. Permanent dilation of bronchi and bronchioles caused by destruction of m. and supporting CT
2. Bronchiecstasis can be due to?

Back 19

1. Bronchiecstasis - can follow airways almost all way to the pleura
2. Obstruction, Congenital (CF, immunodeficiency or Kartageners syndrome), Necrotizing suppurative pneumonia

Front 20

1. What presents w/ a stiff lung, interstitial lung disease due to involvement of interstitium, alveolar wall, capillary unit,
2. effect of 1 on FVC and FEV1 and ratio

Back 20

1. Restrictive lung disease due to conditions:
Occupational/ environmental or Drug/Rx / Immunologic, / idiopathic
2. FVC and FEV1 is decreased, ratio is about normal

Front 21

1. Presents: Acute onset dyspnea, Low PaO2, bilateral pulmonary infiltrates, absence of clinical evidence of primary lt sided hrt failure
2. What is 1 due to?
Idiopathic of this is acute interstitial pneumonia

Back 21

1. Acute lung injury / Acute RDS -> type of Restrictive lung disease
2. imbalance of pro and antiinflammatory cytokines -> failure of microvascular endothelium and alveolar epithelium

Front 22

1. What are the 2 phases of acute RDS?
2. What is formed in 1st phase
3. What occurs in 2nd phase
**May resolve or progress to endstage honey comb lung

Back 22

1. Exudative (0-7 days) & proliferative (1-3 wks)
2. Hyaline membranes b/c of diffuse alveolar damag.
3. Proliferation of Alv. T2 cells & expansion of alveolar septae w/ fibroplasia

Front 23

Idiopathic Pulmonary fibrosis AKA Usual interstitial pneumonia AKA cryptogenic fibrosing alveolitis:
1. Age it occurs in?
2. TIme of onset
3. Predisposing injury?

Back 23

1. >60 yo
2. > 6 mo
3. no known

Front 24

Pathogenesis of idiopathic pulm. fibrosis
• Some form of persistent alveolar wall injury involving lymphocytes,
macrophages, neutrophils, and alveolar epithelial cells leading to proliferation of fibroblasts and interstitial fibrosis.
***• Temporally heterogeneous process ***

Back 24

Morphology
• Heterogeneous process histologically
• Fresh fibroplasia(recent injury)
• Old interstitial fibrosis (Remote injury)
• Lymphocytes, plasma cells, and alveolar type 2 cell hyperplasia
• Lead to end stage lung disease(Honeycomb lung disease)

Front 25

Presents with Insidious,gradual onset,cough, dyspnea • Dry velcro crackles of lung exam
• Progress to cyanosis and cor pulmonale
• CAT scan show lower lobe disease starting a the periphery • Mean survival 2-4 years

Back 25

Idiopathic pulmonary fibrosis
-nonspecific interstitial lung disease
- respiratory bronchiolitis/interstitial lung disease
- chronic organizing pneumonia

Front 26

1. A Multisystemic disease of unknown etiology with noncaseating granulomas • **Diagnosis of exclusion after infectious causes ruled out** Occurs in adults younger than 40, increased in Danish, Swedish, US blacks, higher incidence in non smokers

Back 26

1. Sarcoidosis Pathogenesis:
^ CD4/8 ratio; Oligoclonal T cells; Increased cytokines; Genetic - familial & racial clustering
Environmental - Tenuous association w/ infectious agents

Front 27

1. Presents w/ noncaseating granuloma rimmed by CD4 + cells, Schaumann bodies (calcifications) & asteroid bodies (proteinaceous precipitates), Hilar and paratracheal nodes involved in 85% of cases; lungs involved 90%;

Back 27

Sarcoidosis also can effect
skin, eye, salivary gland, spleen, liver, and bone marrow
**Often assymptomatic seen on Xray**, but if seen its for pulm. Sx

Front 28

1. Hypersensitivity pneumonitis is an immunologically mediated lung disease that targets the alveoli by?
2. What is 1 in response to?
Morpho: patchy mononuclear cell infiltrates w/ occasional small loose granulomas

Back 28

1. Type III (immune complex) & Type IV (cell mediated rxn) hypersensitivity
2. Inhaled antigens
Clinically: fever, cough, dyspnea 4-8 hrs post exposure, may present w/ chronic disease

Front 29

Hypersensitivity pneumonitis: Name the agent in
1. Bagassosis
2. Millers lung
3. Pigeon breeders lung
4. Rx for this?

Back 29

1. Moldy sugar gain w/ thermophilic a.
2. Cont. grain, wheat weevil
3. Pigeons, protein in poop
4. Steroids and removal of the offending Ag

Front 30

1. What do diffuse alveolar hemorrhage syndromes present as?
2. Histologic features?

Back 30

1. Triad of hemoptysis, anemia, and diffuse pulmonary infiltrates
2. Intraalveolar hemorrhage and hemosiderin laden macrophages a few days after onset

Front 31

1. Differential Dx for Diffuse alveolar hemorrhage syndromes
2. What is the most common cause of preventable death in hospitalized pts?, usu from deep v. of the leg, popliteal and above

Back 31

1. VICAR: Vasculitis (Wageners), Idiopathic pulmonary hemosiderosis, CT disorder (SLE), Anti-basement membrane Ab (goodpasture syndrome), Renal (pulmonary - renal syndrome)
2. Pulmonary thromboembolism,

Front 32

1. 3 causes of sudden death?
2. A smaller embolie causes a wedge shaped infarct in the lung, what is its progression?

Back 32

1. PE, MI, Cerebral infarct
2. Hemorrhage -> ischemic necrosis -> scar formation

Front 33

1. What is caused by a decrease in CSA of pulmonary vasculature?
2. Term for any infection of the lung
3. How can 2 be described by anatomic distriubiton

Back 33

1. Pulmonary HTN:: 2ndary to cardiac, inflammatory vascular or interstitial lung disease or recurrent thromboembolism; rarely idiopathic/primary
2. Pneumonia
3. Bronchopneumonia or lobar pneumonia

Front 34

Community Pneumonias; give group bothered by it
1. H. Influenza
2. Moraxella Catarrhalis
3. S. Pneumonia
4. Staphylococcus aureus

Back 34

1. most common exacerbation of COPD
2. elderly and COPD
3. most common, (90% of lobar), risk ^ in at risk ppl
4. Secondary pneumonia following virus

Front 35

Give bug for these community pneumonia
1. Most frequent gram -, frequent in alcoholics, malnourished
2. associated w/ CF, invades vessels
3. associated w/ artifical aquatic environments

Back 35

1. Klebsiella pneumonia
2. Pseudomonas aeruginosa
3. Legionella pneumophila

Front 36

1. Sequence of events in lobar pneumonia
Bronchonpneumonia - patch inflammation w/ No
Abscess formation - No accumulation w/ necrosis
Empyema - Suppurative material in pleural cavity

Back 36

1. Vascular Congestion -> Red hepatization, liver like consistency w/ neutrophils -> gray hepatization, dull gray, lysed RBC's, fibrin -> Resoluion, exudate resorbed and forms scar

Front 37

1. What are 5 community-acquired atypical pneum?
Morpho: widened alveolar septae w/ Mo, no sig. No response
2. Nosocomial pneumonia includes?

Back 37

1. Legionella, Chlamydia, Coxiella (Q fever) Mycoplasm pneumonia & Viral (most common)
2. PESKS - Pseudomonas sp., E. Coli, Serratia marcesens, Klebsiella sp, Staph A.

Front 38

Aspiration pneumonia
1. common to whom
2. Combo of what 2 things
3. presentation of it
4. 2 most common bronchi to aspirate stuff to

Back 38

1. Debilitated or unconscious patients
2. Aspiration of chemical & oral anaerobic bacteria
3. Necrotizing pneum. w/ frequent abscess formation
4. Posterior bronchus RUL, Apical bronchus RLL

Front 39

1. Most imp risk factor for TB?
Stuff: leading cause of death in poverty, crowdying. Spread person to person
2. hypersensitivity and time to rxn in PPD test
3. Type of staining for it?

Back 39

1. HIV infection,
2. Type IV T cell response, 48-72 hrs, will not tell if infection or disease
3. Acid fast, walls w/ a high lipid content, resists decolorization

Front 40

1. granuloma in TB
2. Where do inhaled mycobacterium bacilli go in lung
3. What is a Ghon complex

Back 40

1. a Caseating granuloma leading to cavitary lesion, Type IV T cell mediated immune response
2. upper part of lower lobe or lower part of upper lobe, near the pleura
3. bronchial lymph node involvement in TB

Front 41

1. When does progressive pulmonary TB occur? (enlargement, cavitation, erosion of vessels, miliary disease)
2. What is miliary disease (rice looking)

Back 41

1, immune response is inadequate
2. TB seeds beyond the lungs

Front 42

Funguses:
1. Mucocutaneous, superficial causes abscess
2. inhaled soil or bird droppings (thick capsule)
3. Associated w/ diabetics, invasive
4. Vascular invasion of immunosuppressed, acute angle branching, septated

Back 42

1. Candidiasis - budding yeast w/ pseudohyphae
2. Cryptococcus - budding yeast, mucicarmine stains well w/ thick capsule
3. Mucormycosis, right angle branching
4. Aspergillus

Front 43

1. Small budding yeast, Ohio, central Mississippi river valley, in bat and bird droppings
2. Nonbudding spherules w/ endospores, SW and far west (valley fever)
3. Similar location to 1, broad based budding yeast

Back 43

1. Histoplasmosis
2. Coccidioidomycosis
3. Blastomyces dermatiditis

Front 44

1. An owl's eye inclusion is indicative of?
- once infected always have it, immunosuppressed can redevelop it later, common in transplants
2. Morphology of the cells?

Back 44

1. Cytomegalovirus
2. Strikingly large w/ intranuclear basophilic or owl's eye inclusion

Front 45

1. PPl at risk of Pneumocystis Jiroveci disease
Morpho: foamy intra-alveolar exudate, minimal inflammation, GMS positive encysted trophozoite
2.Stain to use on it?

Back 45

1. Immunocompromised
2. Silver stain, see a cup shape