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205 Cards in this Set

  • Front
  • Back
Strep pneumoniae - what kind of microbe?
Gram positive cocci. capsule; stains blue
What are the conditions to keep a patient with pneumonia as outpatient?
1. age < 50 years
2. none of these 5 conditions: neoplastic, liver, renal, CHF, stroke
3. vitals near normal and normal mental status
What is the empirical outpatient treatment of pneumonia?
Macrolide, Fluoroquinolone, or Doxycycline
3 main typical pneumonia pathogens
1) strep pneumoniae
2) haemophilus influenza
3) moraxella catarrhalis
describe haemophilus influenza
gram negative rod, small, pleomorphic; stains pink
moraxella catarrhalis
gram negative diplococcus
What are the atypical agents of pneumonia
Mycoplasma pneumoniae
Chlamydia pneumoniae
Legionella pneumophila
Mycoplasma pneumoniae
Lacks a cell wall (no gram stain, no cell wall Abx)
lives in water; gram negative aerobic bacilli
Chlamydia pneumoniae
Obligate intracellular bacteria; reticulate bodies
How does strep pneumoniae confer resistance to B lactams?
point mutations of the PBPs
How do H. influenzae and M. catarralis confer resistance to b lactams?
beta lactamase producers
Macrolides - main adverse effects?
GI, torsade de pointes
What is good against atypical pneumonia?
Bronchopulmonary Dysplasia - what is it?
Positive Pressure Ventilation during first two weeks of life

O2 requirement for more than 28 days to stay over 50

Ground glass appearance; one month of age - small cysts (fibroses); 7 mos - cysts coalesce into larger ones
What do you give to treat BPD?
O2 (because of V/Q mismatch), fluid restriction, diuretics (but must be careful because diuretics can cause hyponatremia, hypokalemia, renal problems), bronchodilators, nutrition
Infant with fever, cough, dyspnea, wheeze, cyanosis - bronchiolitis. What most likely caused it?

Which virus also has similar presentation?
Respiratory Syncytial Virus

hMPV - human metapneumovirus
Which serum Ab is affected when baby is born premature?
IgG - then babies are at a higher risk for chronic lung disease
bronchiolitis - obstructive or restrictive?
obstructive; acute inflammatory disease of lower respiratory tract caused by RSV
CXR - hyperinflation, peribronchial cuffing, atelectasis. Part of clinical symptoms is apnea. What is it?
bronchiolitis (infants)
What is ribavirin?
treatment of RSV
Best way to treat RSV?
mechanical ventilation and trial of B agonists; Synagis (Palivizumab) is monthly "vaccine" given during RSV season to high risk infants
What are three mechanisms of airflow limitation in asthma?
Acute bronchoconstriction (smooth muscle) - bronchial hyperresponsiveness; mucus plug; airway INFLAMMATION/edema
What is the bronchoprovacation test? What is used to test?
Methacholine given in increased increments to test at what point airways respond - asthmatics will respond much sooner than normal
Which cells are involved in the early response of asthma? Which cells are involved in the late response?
Early - IgE binds to mast cells upon exposure to allergen; reexposure triggers lymphocytes, mast cells, cytokines
Late - cytokines recruit eosinophils --> airway damage
What's the strongest predisposing factor to developing asthma?
atopy - genetic predisposition to have an IgE mediated response to allergens
What is the hygeine hypothesis?
Nurture part of asthma - exposures in early life move babies toward T1 phenotype. T2 phenotype is IgE mediated response, T1 phenotype is cell-mediated immunity so is less prone to asthma
CXR: diaphragm pushed down, heart looks "squeezed". What is it?
hyperinflation of lungs; possible sign of asthma
What do you give to treat bronchospasm?
Bronchodilators (B agonists). Short acting: albuterol, metaproterenol, terbutaline
Long acting: Salmeterol, formoterol
What do you give to treat asthmatics with inflammation?
inhaled corticosteroids - beclomethasone, flunisolide
In utero baby presents with meconium ileus. What does baby possibly have?
Cystic fibrosis; 90% of infants with meconium ileus have CF
Baby presents with rectal prolapse. What could it be and what does it indicate?
Indicates malabsorption; cystic fibrosis
Although respiratory problems determine survival in CF, what's the most common problem that occurs?
pancreatic insufficiency --> malabsorption. Patients need to be treated with pancreatic enzyme supplements.
What is measured in newborn screening for CF?
immunoreactive trypsinogen test - elevated levels indicate problem. Follow up with sweat test.
Name other problems associated with CF.
CF related diabetes
cholestasis/hepatobiliary disease (not common)
Bronchiectasis (due to infection --> inflammation of airways)
Azoospermia (90% of males with CF)
Which pathogen causes final disease of CF?
Pseudomonas aeruginosa
Most prevalent mutation in CF
DF508 phenylalanine nucleotide - affects CFTR channel; mainly affects conducting airways, not respiratory zone
Which CFTR mutations are severe? Which are mild?
Class 1,2,3 are severe (pancreatic insufficiency); class 4,5 are mild (pancreatic sufficiency)

1: no synthesis of CFTR
2: no maturation of CFTR
3,4,5: allow some degree of function

We CANNOT predict lung disease, only pancreatic enzyme problems
Pancreatic phenotype CF - what's the main determinant?
genotype (not as much genetic modifier or environmental influence)
Pulmonary dysfunction in CF - what's the main determinant of phenotype?
genetic, with lots of influence from genetic modifiers and environment
What is the most common cause of acute respiratory distress syndrome?
Sepsis secondary to pneumonia
What is obscured by right middle lobe pneumonia on CXR?
Right Heart Border
Bilateral "bat wing" infiltrate in AIDS pt CXR. What is it?
Pneumocystis Jiroveci (PCP)
Pneumonia. Proliferation in alveoli with necrosis/destruction. Which bacteria could it be?>
Staph. Aureous
Pneumonia. Proliferation in alveoli without destruction. What is the most likely bacteria?
Strep. Pneumoniae
Name three mechanisms of airway obstruction in COPD.
Secretions obstruct (obstructive bronchiolitis); airway wall inflammation and fibrosis (less radial traction); less elastic recoil of lungs
What is the main way to determine COPD?
Spirometry (FEV1/FVC) tests
By which mechanism does smoking lead to emphysema?
Smoking inhibits alpha 1 anti trypsin; al antitrypsin normally inhibits elastase from destroying the elastic recoil of the lung. Now elastase is free to destroy lung parenchyma --> emphysems
Where in the lungs do smokers usually get emphysema?
upper lobes; basilar lobe emphysema implies a1 antitrypsin deficiency
What is the pathophysiology of empysema, starting with mucus secretion and leading to cor pulmonale?
mucus hypersecretion --> airway obstruction --> pulmonary hyperinflation --> gas exchange problems --> pulmonary vasocontriction --> pulmonary htn --> cor pulm.
What leads to the hyperinflation seen in COPD?
increased compliance; dynamic compression during expiration (increased intrathoracic pressure collapses small airways w/no cartilage)
Smoker over age 45. Chronic cough, chronic sputum production, wheezing, DOE. What could it be and what test do you order?
COPD, order spirometry test. At any age, wheezing calls for spirometry test.
What is a pink puffer? Disease associated, symptoms, etc.
COPD patient whose main symptoms come from emphysema. Cachectic, not cyanotic. Major symptom is dyspnea. Decreased elastic recoil and diffusion capacity
What is a blue boater?
COPD patient whose main symptoms come from chronic bronchitis. Cough and sputum is main symptom. Obese, cyanotic, very low pO2. Normal diffusion capacity and elastic recoil.
What are the five steps to smoking cessation? What are the pharmacotherapies
Ask, Advise, Assess, Assist, Arrange

Bupropion, nicotine replacement
What is the mechanism of nicotine addiction?
Nicotine goes into alveoli --> alveolar capillaries --> brain

binds to nAch receptors and goes to reward centers
What is the main receptor for nicotine? Which drug is partial agonist for it?
a4b2 nicotinic receptor in ventral tegmental area; Chantix
In COPD which causes of airflow limitation are reversible? irreversible?
reversible: constriction of smooth muscle, mucus hypersecretion

irreversible: loss of elastic recoil, fibrosis
Pulmonary function test: Diffusion capacity of CO is increased. Is this emphysema, chronic bronchitis, or asthma?
emphysema. CB and asthma have normal DLCO
Pulmonary function test: FEV1/FVC goes back up to normal with bronchodilators. Is this emphysema, chronic bronchitis, or asthma
Asthma. Other two are only modestly affected.
When a patient continues to smoke with COPD, what is the course of decline?
FEV1 declines at 2-3 times the normal rate. Normal rate is 25-35cc decline per year
Are steroids more effective in COPD or in asthma?
asthma. THere is airway inflammation in both, but the mediators are different and respond better to steroids in asthma than COPD.
Acute Interstitial Pneumonia
diffuse alveolar damage (= adult respiratory distress syndrome). Homogenous appearance
Idiopathic Pulmonary Fibrosis
presentation: dyspnea and nonproductive cough; most patients die in 5-10 years

histology: temporal heterogeneity; mature fibrosis with collagen deposition and honeycombing - irreversible
Desquamative Interstitial Pneumonia
Macrophages in the alveolar spaces in diffuse, uniform manner.

Architecture of lung preserved, 90% of cases are smokers
Respiratory Brochiolitis Associated Interstitial Lung Disease
Strongly associated with cigarette smoking. More affinity for airways than DIP, not as diffuse. Accumulation of macrophages in alveoli and lymphocytic infiltrate in interstitium

Non specific interstitial pneumonitis
much lower mortality than UIP. Seen in patients with connective tissue disease

Histology: uniform pattern with mononuclear infiltrates and different grades of fibrosis
Hypersensitivity Pneumonitis
inhalation of particles (extrinsic allergic alveolitis)
Cushmann's spirals and Charcot-Leydan crystals are seen with what disease?
Wegener's Granulomatosis
necrotizing granulomatous inflammation and vasculitis. ANCA cells
granulomatous disease with histiocytes and multinucleated giant cells

T cell mediated granulomatous inflammation
Which type of emphysema is associated with smokers/nonsmokers.
Centrilobar is seen in smokers (proximal portion of terminal bronchiole)

Paracinar is in those with a1 antitrypsin deficiency (entire respiratory bronchiole)
What is Virchow's Triad?
for DVT - stasis, hypercoagulability, venous injury
What are the most common surgeries in which DVT can happen?
hip and knee replacement
Mortality of PE without treatment?
Pathophysiology of PE - what causes hypoxemia AND hypocarbia?
Hypocarbia is due to V/Q mismatch bc of bronchoconstriction, so hyperventilation causes pCO2 to go down.

Hypoxia is due to perfusion of poorly ventilated areas; "shunt" because of redistribution of blood flow --> hypoxia
Best choice to evaluate PE?

EKG can be done, but often shows nothing
What is the classic sign of pleural effusion on CXR?
meniscus (line where fluid goes over lung), costophrenic recess will be gone; also fluid more than 10mm in lateral decubitus position
How can you distinguish pleural thickening from pleural effusion?
Shift patient to a different position. Pleural effusion - fluid will shift, redistribute. Pleural thickening - nothing will move
What are the three possibilities if you have a transudate?
CHF, liver problem, renal problem.

Transudate is usually total protein < 3, LDH < 200, specific gravity < 1.016

Exudate is the opposite
What is the one thing that having eosinophils present in pleural effusion will rule out?
Tuberculosis. Everything else could have eosinophils.
CXR for plural effusion is best done during inspiration or expiration?
Expiration, because lung retracts from chest wall.
Inflammatory processes produce transudate or exudate in pleural effusion?
Most common causes of pleural effusion?
CHF, bacterial pneumonia, malignant disease (esp indicated by bloody pleural effusion)
Pertinent glucose levels on pleural effusion and what they indicate
less than 60 = bacterial, tb, or rheumatoid; less than 10 = rheumatoid arthritis; more than 60 = many possibilities
What are the best modalities of treatment for non small cell and small cell carcinoma (surgery, chemo, radiation)?
Small cell - responds best to chemo and radiation; cannot be resected by surgery

non small cell (squamous, adeno, large cell) - can be cured by surgery in early stages. Less responsive to chemo, radiation
True or false. Smokers can normalize lung cancer risk by cessation.
False - gradual drop in lung cancer risk, but never a complete normalization
What is the main problem if a lung tumor invades sympathetics? What can it invade if it is growing in apex of lung? What is SVC syndrome?
sympathetics - Horner's syndrome

apex - can obstruct brachial plexus

SVC syndrome - invades SVC, so blood can't return and you get swollen neck and face
What happens if tumor invades pericardium?

Invades mediastinum? Phrenic?
Cardiac tamponade

Phrenic - diaphragm paralysis
What are the 4 clinical classifications of lung cancer?
1) growing locally
2) growing into adjacent structures
3) metastasis from another place
4) Paraneoplastic syndrome
Small cell carcinoma produces which hormones?
Squamous cell carcinoma can produce which hormone?
How do you decide if the patient is operable for resection of tumor in non small cell carcinoma? What are the values for FEV1 and DLCO?
Check cardiac status; check pulmonary function (FEV1 and DLCO)

FEV1 and DLCO pre op greater than 75% --> operable

FEV1 and DLCO predicted < 75% --> estimate post op

Post op FEV1 and DLCO > 40%, operable

ex: FEV1 = 1.8 L; 70% of lung will be left post op

1.8 x .7 = 45% --> operable
What are the three components of staging of lung cancer?

Extent of primary tumor (T)
Presence of regional metastases (N)
Presence of distant metastases (M)
Which levels of TNM staging are non resectable?
T4, N2, N3, M1
Solitary pulmonary nodule - what factors tell you if it is benign?
No growth for 2+ years; patient < 35 and non smoker; calcified - diffuse, popcorn, central, and laminar is fine; eccentric and stippled is bad
How is TB transmitted?
TB lives in cavities of lung. Eats through parenchyma and gets into airways suspended in the air and inhaled by others when a person coughs.
TB infection vs TB disease?
Infection - macrophages in alveoli, T cells have contained the cells

Disease - body cannot contain the cells and they become caseating granulomas (10% of those infected)
What is the main problem with PPD tests?
20% false positives (other mycobacteria, vaccine)
20% false negatives (immunosuppressed, recent infection)
What are the two conditions in which a PPD positive pregnant woman should receive immediate treatment?
HIV and recent infection, because these two conditions could have hematogenous spread of organisms through placenta
Why do we treat for 9 months?
We don't know when the TB is active or dormant (LTBI). Abx will only work during the active periods, so you have to give continuously to ensure they receive meds while it is active.
Where are you most likely to see TB in a CXR? Why?
upper lobes; TB likes O2 and the upper lobes are well ventilated so it activates there.
AFB smear. What does it test for. Sensitivity and specificity?
Acid fast bacilli. NOT sensitive or specific for TB (miss about 50% of cases if this is all we use). Results available in 24 hours.
TB culture. Pros and cons.
80% diagnosed. results take weeks. 20% of TB cases will be culture negative.
Nucleic Acid Amplification. What is it used for? How good is it?
8 hours results available. 99% specificity. If you are negative with PCR but positive with AFB smear, then you have nonTB mycobacterial infection.
What are the four drugs for TB treatment?
Isoniazid, Rifampin, Pyrazinamide, Ethambutol

Pansensitive, don't use ETH
Use PZA to shorten treatment time to 6 months
What is the definition of XDR TB?
resistant to INH, RIF, fluoroquinolone, and one of a set of aminoglycosides
Three main enzymes for HIV
reverse transcriptase
How does HIV replicate?
Host gets infection. Reverse transcriptase turns RNA viral strand into DNA template. In the CD4 cell, integrase helps it replicate, and protease cleaves it into functional unit. If protease does not work, it cannot spread the infection.
What is the pathogenesis of AIDS?
Loss of CD4 T cells causes immunosuppression, imbalance between CD4 and CD8 cells --> immune dysfunction. Leads to opportunistic infections.
How do TB and HIV work synergistically?
TB releases IFN gamma from T cells, which enhances viral replication of HIV.
What is the CD4 count that marks severe compromise of immune system?
CD4 < 200; opens door to opportunistic infections like PCP, Kaposi's sarcoma, sepsis
Most frequent pathogens of pneumonia in HIV patients?
Strep pneumoniae and haemophilus influenza
Most common AIDS indicator infection?

What are the presenting symptoms?

What enzyme is usually elevated?
PCP (fungus)

Gradual progression of fever, dry cough, shortness of breath, most common cause ARDS in HIV patients

LDH elevated in 90% (but non specific)
What is CXR appearance in PCP?
diffuse bilateral infiltrates (hazy)
What is the main treatment for PCP?
Bactrim (sulfamethoxazole + trimethoprim)

Adjunctive corticosteroids
fever, dry cough, SOB, diffuse infiltrates
How do you distinguish PCP from CMV?
Intranuclear or intracytoplasmic inclusions in BAL fluid, biopsy material

Treat with Gancyclovir or HAART
Cryptococcus Neoformans
most common fungus causing life threatening illness in AIDS patients

Foamy cells histologically, with India Ink see thick walls of organism

Treat with Amphotercin B
Where do you see Histoplasmosis the most?
Ohio, Mississippi River valleys, Central and S. Am, Carribean in immunocompromised patients

miliary infiltrates on CXR

Treat with Amphotercin B, long term suppressive therapy
Seen in AIDS patients with CD4 < 30.

Look for tissue invasion

CXR: upper lobe disease with cavitation and hemoptysis

Tx: Treat with amphotercin B but patients usually die
Kaposi's Sarcoma - what is it caused by?
Most common neoplasm in HIV patients; involves mainly skin

15% have lung cavitating lesions

What is the main pathogen that causes lobar pneumonia?
S. pneumoniae
What are the 4 stages of pneumonia without Abx treatment?
1. Congestion (few PMNs)
2. Red hepatization (numerous PMNs, RBCs, Fibrin)
3. Gray hepatization (Dry, lysed RBCs)
4. Resolution
Bronchiectasis - what causes it? How does it present clinically?
Results from chronic necrotizing infections; presents as severe persistent cough and lots of sputum

Primarily in lower lobes
Where is Histoplasmosis mostly found? It's symptoms parallel TB, but what is the main difference?
Ohio and Mississippi river valleys

Granulomas in histoplasmosis are non caseating; it is a fungus, while TB is an AFB
Aspergillosis - how can you tell it histologically? Who usually gets it? Necrotizing or no?
Septates and branches at acute angles

immunocompromised patients

presents as necrotizing pneumonia
What kind of fluid in PCP - transudate or exudate? Intra alveolar or interstitial?
Exudate (eosinophilic, "cotton candy"), intra alveolar
Cytomegalovirus - interstitial or intraalveolar pneumonia? What does it look like histologically?
interstitial pneumonia

"owl eye" intranuclear inclusions
Where in the lungs are you most likely to find TB? Why?
Primarily upper part of lower lobes and lower part of upper lobes. Because of O2 tension in these areas
What is the Ghon focus? What is the Ghon complex?
Ghon focus = area of caseating necrosis in the lung in TB

Ghon complex = lung necrosis + lymphadenopathy
What is the pathogenesis of miliary TB?
Organisms drain through lymphatics --> lymphatic duct --> right heart --> pulmonary artery --> systemic circulation
What kind of diseases would cause restrictive lung disease?
Pleural disease; chest wall disease (kyphosis), Neuromuscular disease - myasthenia gravis, polio)
What is the difference between intrinsic and extrinsic restrictive lung disease?
Intrinsic - diseases of lung parenchyma, air space filling defects (pneumonia, etc)

Extrinsic - disease of pleura (pneumothorax, pleural effusion, thickening); chest wall (scoliosis); neuromuscular (ALS, MG, Polio, Muscular dystrophy)
What layers does O2 pass to get from alveoli to bloodstream?
capillary endothelium
What is the pathogenesis of pulmonary fibrosis?
1. epithelial injury (acute inflammation)
2. Release of cytokines, growth factors --> basement membrane damage, oxidative stress
3. Apoptosis and impaired reepithelialization
4. Resistance to apoptosis via collagen matrix remodeling with tpye 3 collagen (instead of types 1 and 4)
5. Antibody mediated immunity --> fibroblast activation and matrix deposition --> fibrosis
When you see ground glass opacities on a CXR, is it acute or chronic?
Regional acute inflammation processes, acute
What are three factors that impact survival in patients with IPF?
Decline in DLCO, increase in pulmonary htn (>25mmHg), decline in FVC over time
which surgery causes more drop in vital capacity - upper or lower abdominal?
What is pancuronium?
Muscle paralyzer used in surgeries. Should not use because it increases risk of complications
What are the main health complications of mechanical ventilation?
hypotension, tension pneumothorax, alveolar damage
What are the three cycling methods in ventilation?
time, pressure, volume
Peak inspiratory pressure is determined by which factors? What about plateau pressure?
PIP - respiratory system compliance and airway resistance (below 35 is good)

PP - compliance only
How do you calculate tidal volume for someone on mechanical ventilation?
6-8 mL per kg of ideal body weight
What is normal minute ventilation for a patient? Why?
8-10 Liters; because of increased dead space of equipment
What are the three modes in mechanical ventilation?
Assist/Control, IMV, pressure support
What mmHg classifies as pulmonary arterial hypertension?
mPAP > 25 at rest, > 35 at exercise

Normal PCWP (LA)

Left heart not involved in idiopathic pulmonary htn, only right heart
What are the five types of pulmonary htn?
Pulmonary arterial htn (Right heart only)

Pulmonary venous htn (Left heart involved)

Pulmonary htn associated with hypoxemia (cor pulmonale, COPD, connective tissue disease, sleep related)

PH due to embolus

miscellaneous - sarcoidosis, compression of pulmonary vessels
What is the resistance and flow in pulm htn arteries?
Instead of high flow, low resistance, they are

LOW flow, HIGH resistance
histologically what would you see in pulmonary htn
smooth muscle proliferation, lumen filled with inflammatory cells, plexiform channeling through occlusion
What can arise as a complication to portal hypertension?
pulmonary hypertension - very high mortality rates
What are some of the physical findings often present in pulmonary htn?
permanent splitting of S2, S4 gallop, tricuspid regurg murmur (diastolic)
What is the main way to diagnose Pulmonary hypertension?
Echo with doppler pressures of pulmonary arteries, tests to determine causes like emboli, cardio, lung problems), sleep study

Definitive test: right heart catheterization
Does a drop in pulmonary arterial pressure always mean it's getting better?
NO! At end stage PH, CO is going down so much that PAP also starts going down. But PVR keeps going up.
How do you treat pulmonary hypertension?
O2, vasodilators, diuretics, sildenafil (viagra) PDE inhibitor
What do Epoprostenol and Bosentan both treat?
Pulmonary hypertension
What are the three pathways to target for pulmonary hypertension?
Nitric oxide pathway, endothelin pathway, prostacyclin pathway
What happens in REM sleep that causes apnea?
entire upper airway (nose, nasopharynx, oropharynx, laryngopharynx, larynx) relaxes; in snorers/apnea, tissues obstruct the airway

upper airway collapses or narrows
What is the Epworth Scale? What score is relevant?
Daytime sleepiness scale; above 9 means that a person has daytime sleepiness (may or may not be apnea)
Sleep History - what does BEARS stand for:
Epworth Scale
Regularity of Sleep
Physical exam findings in sleep apnea?
Obese, hypertensive
upper airway - tonsillar enlargement, large tongue, nasal obstruction; neck circumference > 16 female, > 17 male
What is the difference between obstructive and central apnea?
Obstructive - blocked upper airways, but still drive to breathe; paradoxical movement of abdomen and chest wall

Central - no drive to breathe (abd and chest wall not moving)
What is the difference between hypopnea and apnea?
Hypopnea - reduction in airflow to about 50%

Apnea - stoppage of airflow for more than 10 seconds
What is mixed apnea?
Central and obstructive apnea, then central turns on but still obstruction remains
What is the treatment for obstructive sleep apnea?
Mild - surgery
Diet and behavior modification, positional therapy, increase muscle tone with meds
Apnea Index - at what levels do you have apnea?
5-15 = normal
above 15 = mild apnea
above 30 = severe apnea
Which arteries are affected when you have a nose bleed?
Anterior - Kiesselbach plexus
Posterior - sphenopalatine artery
What are the two insertion points of the true epiglottis?

Only abductor of vocal cords?
arytenoids and epiglottis

posterior cricoarytenoids
Recurrent laryngeal nerve innervates all larynx muscles except?
cricothyroid (superior laryngeal)
What is polypoid corditis?
swelling of true vocal cords

History of tobacco, hoarseness, nodule right vocal cord
Intubation can cause posterior lesion in arytenoids
contact ulcers and granulomas
mechanism of Nexium, Prilosec?
Proton Pump inhibitor - use for reflux
Indications for tonsillectomy?
7 infections/i year; 5/yr two years; 3/yr three years
When there is a thromboembolus in the pulmonary artery, what do the lungs look like?
Sudden death (acute cor pulmonale)

No changes in lung

when 60% or more of pulmonary artery is occluded
What is a saddle embolus?
Embolus at bifurcation of main pulmonary --> no alterations in lung

large emboli are 5% of emboli
Small emboli - what percentage of emboli are they?
70-95%; most clinically silent; 10-15% cause infarction - wedge shaped lesion
Histological appearance of small embolus that causes infarct?
Early: pulmonary hemorrhage
THen: Red infarct; coagulative necrosis of parenchyma + hemorrhage
Later: lysis of RBCs; hemosiderin and wedge shaped lesion
Then: organization of embolus, fibrosis, scar
Grades of pulmonary htn and what they mean.
Grade 1-2: proliferation of smooth muscle cells --> thickened intima and media in arteries (smaller lumen)

Grade 3: Smaller arteries and arterioles get thickened

Grade 4-5: (severe) plexiform lesions, organizing thromboembolus

Grade 6: necrotizing arteritis, fibrinoid necrosis
Where does a mesothelial tumor arise?
What is the most freqent carcinoma in non-smokers?
adenocarcinoma - usually peripherally located
How do you distinguish adenocarcinoma from squamous histologically?
special stain shows intracytoplasmic globules of mucin so you know it is adeno.
Squamous cell carcinoma - histology?
Centrally located; cavitations; keratin production

paraneoplastic - PTH
Small cell carcinoma - histology?
found in smokers; centrally located close to hilum; small amt of cytoplasm

cytoplasmic globules can contribute to paraneoplastic syndromes - ADH and ACTH
In order, which neuroendocrine tumors are the least to most aggressive?
Typical carcinoid (least) - homogenous tumor with no necrosis; Atypical carcinoid - neuroendocrine "gland" appearing; Small cell carcinoma
What's the most lung tumor in children?
Carcinoid - typical low grade malignant tumors; involves large bronchi with an endobronchial growth pattern
TB - which cells are you going to see?
multiple nodules in lung - is it more likely metastatic or primary tumor?
Metastatic - colon, breast, ovaries, liver
What is MEASURED by ABG? What is calculated?
Measured: pH, pCO2, pO2

Calculated: HCO3, SO2
What is normal A-a gradient? What is abnormal?
A-a between 5-10 is normal.

A-a > 20 is too high.

PAO2 = .21(760-47) x (pCO2/0.8)
Acute Lung Injury criteria: Oxygenation, CXR, PCWP
paO2/FiO2 < 300
CXR bilateral infiltrates
< 18mmHg
ARDS Criteria: Oxygenation, CXR, PCWP
paO2/FiO2 < 200
CXR bilateral infiltrates
< 18mmHg

NOT homogenous
What is the mechanism of hypoxemia when you have a normal A-a gradient?
How does the body try to respond to an acute increase in paCO2?
Decrease contractility, decrease resp. muscle contractility, increase arterial vasodilation, loss of consciousness

(body can't work right with such a low pH)
Acute vs Chronic cough? What's the difference?
Acute < 8 weeks
Chronic > 8 weeks
What's the most likely cause of chronic cough in a non-smoker?
post nasal drip
hemoptysis - most common three causes
What differentiates solitary fibrous tumor (pleural fibroma) from a malignant mesothelioma?
Tumor cells are CD34+ and no keratin (in contrast to mesothelioma)

No pleural effusion in pleural fibroma
What is the main cause of malignant mesothelioma?
asbestos exposure

histologically: CD34 - and Keratin+
You do an immunohistochemistry panel to differentiate between adenocarcinoma and mesothelioma. What will be the differences?
EMA: adeno - cytoplasm+
Meso - membrane+
CEA: adeno - positive
Meso - negative
Calretinin: adeno - negative
meso - positive
Meig syndrome?
right sided hydrothorax, ascites, ovarian fibroma
Shipyard, roofing, insulation.
Dyspnea, chronic dry cough, recurrent viral infections. Lower lobe interstitial fibrosis with honeycombing. Calcified parietal pleural plaques. What is it?
Exposure from dust, glass production, etc.

Increased risk for TB. CXR has calcified lymph nodes with "eggshell pattern"

Upper lobes and perihilar region.
lung biopsy shows lymphocytes, plasma cells, macrophages, interstitial fibrosis. What is it?
Hypersensitivity Pneumonitis (plasma cells are key)
Which one is NOT characterized by airflow obstruction?

A. Bronchiectasis
B. Kyphosis
C. Asthma
E. Emphysema
What is the mechanism of bronchodilation with beta agonists?
Increases intracellular cAMP, which aids in relaxation of smooth muscle